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6,100 | Targeted SERCA2a gene expression identifies molecular mechanism and therapeutic target for arrhythmogenic cardiac alternans. | Beat-to-beat alternans of cellular repolarization is closely linked to ventricular arrhythmias in humans. We hypothesized that sarcoplasmic reticulum calcium reuptake by SERCA2a plays a central role in the mechanism of cellular alternans and that increasing SERCA2a gene expression will retard the development of cellular alternans.</AbstractText>In vivo gene transfer of a recombinant adenoviral vector with the transgene for SERCA2a (Ad.SERCA2a) was performed in young guinea pigs. Isolated myocytes transduced with Ad.SERCA2a exhibited improved sarcoplasmic reticulum Ca(2+) reuptake (P<0.05) and were markedly resistant to cytosolic calcium alternans (P<0.05) under repetitive constant action potential clamp conditions (ie, when alternation of action potential duration was prevented), proving that sarcoplasmic reticulum Ca(2+) cycling is an important mechanism in the development of cellular alternans. Similarly, SERCA2a overexpression in the intact heart demonstrated significant resistance to alternation of action potential duration when compared with control hearts (heart rate threshold, 484+/-25 bpm versus 396+/-11 bpm, P<0.01), with no change in action potential duration restitution slope. Importantly, SERCA2a overexpression produced a 4-fold reduction in susceptibility to alternans-mediated ventricular arrhythmias (P<0.05).</AbstractText>These data provide new evidence that sarcoplasmic reticulum Ca(2+) reuptake directly modulates susceptibility to cellular alternans. Moreover, SERCA2a overexpression suppresses cellular alternans, interrupting an important pathway to cardiac fibrillation in the intact heart.</AbstractText> |
6,101 | Coronary perfusion pressure and return of spontaneous circulation after prolonged cardiac arrest. | The amount of myocardial perfusion required for successful defibrillation after prolonged cardiac arrest is not known. Coronary perfusion pressure (CPP) is a surrogate for myocardial perfusion. One limited clinical study reported that a threshold of 15 mmHg was necessary for return of spontaneous circulation (ROSC), and that CPP was predictive of ROSC. A distinction between threshold and dose of CPP has not been reported.</AbstractText>To test the hypothesis that swine achieving ROSC will have higher preshock mean CPP and higher preshock area under the CPP curve (AUC) than swine not attaining ROSC.</AbstractText>Data from four similar swine cardiac arrest studies were retrospectively pooled. Animals had undergone 8-11 minutes of untreated ventricular fibrillation, 2 minutes of mechanical cardiopulmonary resuscitation (CPR), administration of drugs, and 3 more minutes of CPR prior to the first shock. Mean CPP +/- standard error of the mean (SEM) was derived from the last 20 compressions of each 30-second epoch of CPR and compared between ROSC/no-ROSC groups by repeated-measures analysis of variance (RM-ANOVA). AUC for all compressions delivered over the 5 minutes was calculated by direct summation and compared by Kruskal-Wallis test. Prediction of ROSC was assessed by logistic regression.</AbstractText>Throughout the first 5 minutes of CPR (n = 80), mean CPP +/- SEM was consistently higher in animals with ROSC (n = 63) (maximum CPP 41.2 +/- 0.6 mmHg) than animals with no ROSC (maximum CPP 20.1 +/- 0.3 mmHg) (p = 0.0001). Animals with ROSC received more total reperfusion (43.9 +/- 17.6 mmHg x 10(2)) than animals without ROSC (21.4 +/- 13.7 mmHg x 10(2)) (p < 0.001). Two regression models identified CPP (odds ratio [OR] 1.11; 95% confidence interval [CI] 1.05, 1.18) and AUC (OR 1.10; 95% CI 1.05, 1.16) as predictors of ROSC. Experimental study also predicted ROSC in each model (OR 1.70; 95% CI 1.15, 2.50; and OR 1.59; 95% CI 1.12, 2.25, respectively).</AbstractText>Higher CPP threshold and dose are associated with and predictive of ROSC.</AbstractText> |
6,102 | Comparison of low-energy versus high-energy biphasic defibrillation shocks following prolonged ventricular fibrillation. | Since the initial development of the defibrillator, there has been concern that, while delivery of a large electric shock would stop fibrillation, it would also cause damage to the heart. This concern has been raised again with the development of the biphasic defibrillator.</AbstractText>To compare defibrillation efficacy, postshock cardiac function, and troponin I levels following 150-J and 360-J shocks.</AbstractText>Nineteen swine were anesthetized with isoflurane and instrumented with pressure catheters in the left ventricle, aorta, and right atrium. The animals were fibrillated for 6 minutes, followed by defibrillation with either low-energy (n = 8) or high-energy (n = 11) shocks. After defibrillation, chest compressions were initiated and continued until return of spontaneous circulation (ROSC). Epinephrine, 0.01 mg/kg every 3 minutes, was given for arterial blood pressure < 50 mmHg. Hemodynamic parameters were recorded for four hours. Transthoracic echocardiography was performed and troponin I levels were measured at baseline and four hours following ventricular fibrillation (VF).</AbstractText>Survival rates at four hours were not different between the two groups (low-energy, 5 of 8; high-energy, 7 of 11). Results for arterial blood pressure, positive dP/dt (first derivative of pressure measured over time, a measure of left ventricular contractility), and negative dP/dt at the time of lowest arterial blood pressure (ABP) following ROSC were not different between the two groups (p = not significant [NS]), but were lower than at baseline. All hemodynamic measures returned to baseline by four hours. Ejection fractions, stroke volumes, and cardiac outputs were not different between the two groups at four hours. Troponin I levels at four hours were not different between the two groups (12 +/- 11 ng/mL versus 21 +/- 26 ng/mL, p = NS) but were higher at four hours than at baseline (19 +/- 19 ng/mL versus 0.8 +/- 0.5 ng/mL, p < 0.05, groups combined).</AbstractText>Biphasic 360-J shocks do not cause more cardiac damage than biphasic 150-J shocks in this animal model of prolonged VF and resuscitation.</AbstractText> |
6,103 | Public Access Defibrillation. | In the United States, 250,000 people die from a cardiac arrest every year. Despite a well established emergency medical response system, survival from out-of-hospital cardiac arrest remains poor in United States cities. Paramount to achieving successful resuscitation of a cardiac arrest victim is provision of early defibrillation. Among patients that arrest due to a ventricular fibrillation, the likelihood of survival decreases by 10% for every minute of delay in defibrillation. In 1995, the American Heart Association challenged the medical industry to develop a defibrillator that could be placed in public settings, used safely by lay responders, and provide earlier defibrillation to cardiac arrest victims. Over the last decade, there have been significant technological advancements in automated external defibrillators (AEDs), and clinical studies have demonstrated their benefits and limitations in various public locations. This article discusses the technologic features of the modern AED and the current data available on the use of AEDs in public settings. |
6,104 | Study of resuscitated in- and out-hospital cardiorespiratory arrest patients undergoing therapeutic hypothermia. | To determine the characteristics of patients undergoing standard institutional protocol for management of resuscitated patients after a cardiac arrest episode, including therapeutic hypothermia.</AbstractText>This was a retrospective analysis of 26 consecutive patients admitted following cardiac arrest, between January 2007 and November 2008.</AbstractText>All cases underwent therapeutic hypothermia. Average age was 63 years, and the patients were predominantly male. Cardiac arrest event was out-of-hospital in 8 cases, in the emergency room in 3 cases, in the wards in 13 cases and in the operation room in 2 cases. The cardiac arrest rhythm was ventricular fibrillation in seven patients, asystolia in 11, pulseless electrical activity in 5 cases, and was undetermined in 3 patients. The interval between the cardiac arrest and return of spontaneous circulation was 12 minutes (SD ± 5 min). The time to reach the target temperature was 5 ± 4 hours, the hypothermia time was 22 ± 6 hours and time to rewarming 9 ± 5.9 hours. Fourteen patients died in the intensive care unit, a 54% mortality, and three patients died during the in-hospital stay, a 66% in-hospital mortality. There was statistically significant reduction in hemoglobin (p<0.001), leukocytes (p=0.001), platelets (p<0.001), lactate (p<0.001) and potassium (p=0.009), values and increased C reactive protein (p=0.001) and INR (p=0.004) after hypothermia.</AbstractText>The creation of a standard operative protocol for therapeutic hypothermia in post cardiac arrest patients management resulted in a high use of therapeutic hypothermia. The clinical results of this protocol adapted from randomized studies are similar to the literature.</AbstractText> |
6,105 | A Case of Amiodarone-Induced Thyrotoxicosis: A diagnostic and therapeutic dilemma. | Amiodarone is an iodine rich agent widely used for the treatment of ventricular arrhythmias, paroxysmal supraventricular tachycardia, atrial fibrillation and flutter. However 14-18% of patients treated with amiodarone develop overt thyroid dysfunction in the form of either amiodarone-induced thyrotoxicosis (AIT) or amiodaroneinduced hypothyroidism (AIH). Two different types of AIT have been recognised and designated as Type 1 and Type 2. Distinguishing between the two is often difficult, but necessary for instituting appropriate treatment. We report a case of a 56 year-old male patient who was started on amiodarone for atrial fibrillation and then developed AIT. The challenges in the diagnosis and management of these patients are discussed. |
6,106 | History of surgery for atrial fibrillation. | There is a rich history of surgery for atrial fibrillation. Initial procedures were aimed at controlling the ventricular response rate. Later procedures were directed at converting atrial fibrillation to normal sinus rhythm. These culminated in the Cox Maze III procedure. While highly effective, the complexity and morbidity of the cut and sew Maze III limited its adoption. Enabling technology has developed alternate energy sources designed to produce a transmural atrial scar without cutting and sewing. Termed the Maze IV, this lessened the morbidity of the procedure and widened the applicability. Further advances in minimal access techniques are now being developed to allow totally thorascopic placement of all the left atrial lesions on the full, beating heart, using alternate energy sources. |
6,107 | The effects of phase duration on defibrillation success of dual time constant biphasic waveforms. | The effects of first and second phase duration of biphasic waveforms on defibrillation success were evaluated in a guinea pig model of ventricular fibrillation (VF). We hypothesized that waveform duration, and especially the first phase duration, played a main role on defibrillation efficacy in comparison to energy, current and voltage, when a dual time constant biphasic shock was employed.</AbstractText>VF was induced and untreated for 5s in 30 male guinea pigs, prior to attempting a single defibrillatory shock with one of 5 defibrillation waveforms which had different durations of the first and second phase. A five step up-down protocol was utilized for determining the defibrillation efficacy. After a 3-min interval, the procedure was repeated. A total of 25 cardiac arrest events and defibrillations were investigated for each animal.</AbstractText>The defibrillation waveforms with an intermediate first phase of 5 ms, yielded the highest defibrillation success (p<0.05). These waveforms also presented significantly lower energy, current and voltage in comparison to waveforms with shorter or longer first phase durations (p<0.001). However, no differences on defibrillation success were observed among waveforms with different second phase durations varying from 1.5 ms to 3.5 ms.</AbstractText>For dual time constant biphasic waveforms, the first phase duration played a main role on defibrillation success. The intermediate first phase duration of 5 ms, yielded the best defibrillation efficacy compared with shorter or longer first phase durations. While the second phase duration did not affect defibrillation outcomes.</AbstractText>Copyright 2009 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
6,108 | Predicting survival after out-of-hospital cardiac arrest: role of the Utstein data elements. | Survival after out-of-hospital cardiac arrest depends on the links in the chain of survival. The Utstein elements are designed to assess these links and provide the basis for comparing outcomes within and across communities. We assess whether these measures sufficiently predict survival and explain outcome differences.</AbstractText>We used an observational, prospective data collection, case-series of adult persons with nontraumatic out-of-hospital cardiac arrest from December 1, 2005, through March 1, 2007, from the multisite, population-based Resuscitation Outcomes Consortium Epistry-Cardiac Arrest. We used logistic regression, receiver operating curves, and measures of variance to estimate the extent to which the Utstein elements predicted survival to hospital discharge and explained outcome variability overall and between 7 Resuscitation Outcomes Consortium sites. Analyses were conducted for all emergency medical services-treated cardiac arrests and for the subset of bystander-witnessed patient arrests because of presumed cardiac cause presenting with ventricular fibrillation or ventricular tachycardia.</AbstractText>Survival was 7.8% overall (n=833/10,681) and varied from 4.6% to 14.7% across Resuscitation Outcomes Consortium sites. Among bystander-witnessed ventricular fibrillation or ventricular tachycardia, survival was 22.1% overall (n=323/1459) and varied from 12.5% to 41.0% across sites. The Utstein elements collectively predicted 72% of survival variability among all arrests and 40% of survival variability among bystander-witnessed ventricular fibrillation. The Utstein elements accounted for 43.6% of the between-site survival difference among all arrests and 22.3% of the between-site difference among the bystander-witnessed ventricular fibrillation subset.</AbstractText>The Utstein elements predict survival but account for only a modest portion of outcome variability overall and between Resuscitation Outcomes Consortium sites. The results underscore the need for ongoing investigation to better understand characteristics that influence cardiac arrest survival.</AbstractText>Copyright (c) 2009. Published by Mosby, Inc.</CopyrightInformation> |
6,109 | Vasospastic heart failure: multiple spasm may cause transient heart failure? | There have been no reports concerning the correlation between heart failure and coronary artery spasm.</AbstractText>From January 2000 to December 2007, 201 patients with heart failure were hospitalized at our institution. We could perform coronary arteriography and spasm provocation tests in 37 (22 men, 67±11 years) out of 201 patients with heart failure before discharge. Atrial fibrillation was observed in 13 patients (35%). After controlling heart failure and 24h cessation of vasoactive drugs, pharmacological spasm provocation tests were performed. Positive spasm was defined as >90%. Coronary spasm was observed in 12 patients (32%) and multiple spasm was recognized in 10 (83%) out of 12 patients. Though ejection fraction on admission was not different between the two groups (42±18% vs. 43±11%, ns), left ventricular end-diastolic and end-systolic dimension after medical therapy over 1 year was significantly smaller in patients with positive spasm than that in patients with negative spasm. There was no difference concerning medications except the administration of nitrate and nicorandil between two groups.</AbstractText>Coronary artery spasm, especially multiple spasm, may cause transient heart failure in a small part of unknown origin heart failure in Japan.</AbstractText> |
6,110 | Determinant factors of plasma B-type natriuretic peptide levels in patients with persistent nonvalvular atrial fibrillation and preserved left ventricular systolic function. | Plasma B-type natriuretic peptide (BNP) levels are determined by several factors. The presence of atrial fibrillation (AF) is one of these factors. Meanwhile, plasma BNP levels are well correlated with left ventricular (LV) filling pressure in patients with sinus rhythm. Furthermore, LV filling pressure can be estimated by the ratio of early diastolic transmitral velocity to early diastolic mitral annular velocity (E/e' ratio) in patients with sinus rhythm or with AF. However, it is still unclear if elevated plasma BNP levels reflect increases in LV filling pressure in patients with AF, especially with preserved LV systolic function. This study was designed to examine which factors determine plasma BNP levels in patients with persistent nonvalvular AF and preserved LV systolic function.</AbstractText>We examined 195 clinically stable outpatients with persistent nonvalvular AF and preserved LV systolic function. They underwent comprehensive 2-dimensional and Doppler echocardiography, plasma BNP and creatinine levels, clinical history, and heart rate were determined. Then we statistically analyzed the correlation between plasma BNP levels and several variables including E/e' ratio. On univariate analyses, plasma BNP levels were significantly correlated with age, LV diastolic diameter (LVDd), E/e' ratio, and mitral E wave deceleration time. In addition, plasma BNP levels were significantly higher in males and in patients with a history of congestive heart failure and those who had been administered a ß-blocker. On multiple linear regression analyses, E/e' ratio, age, LVDd, and administration of ß-blocker were independent determinant factors of plasma BNP levels.</AbstractText>Plasma BNP levels in patients with persistent AF and preserved LV systolic function are affected by E/e' ratio, age, LVDd, and administration of ß-blockers.</AbstractText> |
6,111 | Improving cardiac gap junction communication as a new antiarrhythmic mechanism: the action of antiarrhythmic peptides. | Co-ordinated electrical activation of the heart is maintained by intercellular coupling of cardiomyocytes via gap junctional channels located in the intercalated disks. These channels consist of two hexameric hemichannels, docked to each other, provided by either of the adjacent cells. Thus, a complete gap junction channel is made from 12 protein subunits, the connexins. While 21 isoforms of connexins are presently known, cardiomyocytes typically are coupled by Cx43 (most abundant), Cx40 or Cx45. Some years ago, antiarrhythmic peptides were discovered and synthesised, which were shown to increase macroscopic gap junction conductance (electrical coupling) and enhance dye transfer (metabolic coupling). The lead substance of these peptides is AAP10 (H-Gly-Ala-Gly-Hyp-Pro-Tyr-CONH(2)), a peptide with a horseshoe-like spatial structure as became evident from two-dimensional nuclear magnetic resonance studies. A stable D: -amino-acid derivative of AAP10, rotigaptide, as well as a non-peptide analogue, gap-134, has been developed in recent years. Antiarrhythmic peptides act on Cx43 and Cx45 gap junctions but not on Cx40 channels. AAP10 has been shown to enhance intercellular communication in rat, rabbit and human cardiomyocytes. Antiarrhythmic peptides are effective against ventricular tachyarrhythmias, such as late ischaemic (type IB) ventricular fibrillation, CaCl(2) or aconitine-induced arrhythmia. Interestingly, the effect of antiarrhythmic peptides is higher in partially uncoupled cells and was shown to be related to maintained Cx43 phosphorylation, while arrhythmogenic conditions like ischaemia result in Cx43 dephosphorylation and intercellular decoupling. It is still a matter of debate whether these drugs also act against atrial fibrillation. The present review outlines the development of this group of peptides and derivatives, their mode of action and molecular mechanisms, and discusses their possible therapeutic potential. |
6,112 | Relationships of CRP and P wave dispersion with atrial fibrillation in hypertensive subjects. | Although inflammation has been shown to be implicated in the pathophysiology of atrial fibrillation (AF), little is known about its involvement in the accompanying atrial electrical remodeling expressed by P wave dispersion (P(disp)).</AbstractText>Fifty hypertensive subjects with documented paroxysmal AF (AF group) and 50 matched for body mass index, sex and office systolic blood pressure (BP) subjects with no history of AF (SR group) were subjected to electrocardiogram (ECG) and P(disp) assessment, hs-CRP determination, a complete echocardiographic study and 24-h ambulatory BP monitoring.</AbstractText>The AF as compared to the SR subjects were older by 14 years (P < 0.0001) and they exhibited lower office and 24-h diastolic BP (7 mm Hg, P < 0.0001 and by 8 mm Hg, P < 0.0001, respectively) and higher office and 24-h pulse pressure (by 4 mm Hg, P = 0.03 and 6 mm Hg, P = 0.001, respectively) mean values. A higher mean of left atrial (LA) diameter index (by 1.9 mm/m(2), P < 0.0001) and left ventricular mass index (by 16 g/m(2), P < 0.0001) were observed in the AF vs. SR group. P(disp) mean and hs-CRP median values were higher in the AF group (by 22 ms, P < 0.0005 and by 4.63 mg/l, P < 0.0005, respectively). Standard multiple and multiple logistic regression analysis identified log(10)(hs-CRP) as independent determinant of P(disp) and log(10)(CRP) and P(disp) as independent determinants of AF.</AbstractText>In hypertensive subjects hs-CRP and P(disp) are interrelated and associated with AF, suggesting an active implication of inflammation in the atrial electrophysiological remodeling predisposing to AF.</AbstractText> |
6,113 | The effect of open-chest cardiac resuscitation on mitral regurgitant flow: an on-line transesophageal echocardiographic study in dogs. | We sought to determine the effect of cardiac massage on a pre-existing regurgitant mitral valve during open-chest cardiopulmonary resuscitation (OCCPR) in an animal experiment.</AbstractText>Our study included 29 dogs that were used as experimental models. We anesthetized them and inserted a transesophageal echocardiographic (TEE) probe. Then we performed a transverse thoracotomy, attempting to produce acute mitral regurgitation (MR). In models that showed cardiac arrest we initiated OCCPR to restore cardiac function. The regurgitant area of mitral jet and left ventricular (LV) diameters and volumes were calculated before and during OCCPR using TEE.</AbstractText>Ventricular fibrillation and/or electromechanical dissociation occurred in 13 animals (45%). In 4 models without preexisting MR, no additional regurgitation was detected during OCCPR, while in another 5 with preexisting MR we noticed a slight increase in the regurgitant flow. The regurgitant flow area changed from 0.62 +/- 1 cm2 before to 1.1 +/- 0.36 cm2 during OCCPR (p<0.008). In the 4 animals that had severe damage to the mitral apparatus after the attempts, the regurgitant flow increased from 4.01 +/- 0.93 cm2 to 7.7 +/- 2.6 cm2 (p<0.002). The LV transverse diameter decreased from 4.39 +/- 0.62 cm to 1.54 +/- 0.5 cm and its volume from 60.5 +/- 7.14 cm3 to 17.02 +/- 4.14 cm3 (both p<0.001), thus showing the effectiveness of OCCPR.</AbstractText>Given the presence of preexisting mitral regurgitation, direct cardiac massage during OCCPR would probably be less effective than expected, because of an increase in the amount of the regurgitant.</AbstractText> |
6,114 | Incidence and predictors of silent embolic cerebral infarction following diagnostic coronary angiography. | Coronary angiography (CAG) is an invasive diagnostic procedure, which could lead to procedure related complications. One of the well known post-procedural complications is cerebral embolic infarction with or without symptoms. Silent embolic cerebral infarction (SECI) has clinical significance because it can progress to a decline in cognitive function and increase the risk of dementia in the long term. The aim of this study was to detect the incidence and predictors of SECI after diagnostic CAG using diffusion-weighted magnetic resonance imaging (DW-MRI).</AbstractText>A total of 197 patients with coronary artery disease who underwent DW-MRI for evaluation of intracranial vasculopathy before coronary artery bypass graft surgery were retrospectively enrolled in the present study. DW-MRI was performed within 48 h after diagnostic CAG. SECI was diagnosed as presence of focal bright high signal intensity in DW-MRI. Patients were divided into groups according to presence/absence of SECI (+ SECI vs. - SECI, respectively). The clinical and angiographic characteristics were analyzed and independent predictors were evaluated.</AbstractText>Of the 197 patients, SECI occurred in 20 patients (10.2%) after diagnostic CAG. Age, female gender, frequency of underlying atrial fibrillation, extent of coronary disease, and fluoroscopic time during diagnostic CAG were not different between the + SECI and - SECI groups. Left ventricular ejection fraction was significantly lower in the + SECI group than in the - SECI group (45.9 ± 8.5% vs. 51.4 ± 13.1%, p=0.014) and performance rate of internal mammary artery (IMA) angiography was significantly higher in the + SECI group compared with the - SECI group (85% vs. 37.2%, p<0.001). By multivariate analysis, performing IMA angiography was the only predictor of SECI (OR=14.642; 95% CI=3.201 to 66.980, p=0.001).</AbstractText>The incidence of SECI after diagnostic CAG was not infrequent. Diagnostic CAG with IMA angiography may increase the risk of SECI.</AbstractText>Copyright © 2009 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
6,115 | Prevalence of inappropriate use of digoxin in 136 patients on digoxin and prevalence of use of warfarin or aspirin in 89 patients with persistent or paroxysmal atrial fibrillation. | Of 136 patients, mean age 72 years, receiving digoxin in the hospital or in the medical clinic, 47 (35%) had heart failure with reduced left ventricular ejection fraction and symptoms despite optimal medical therapy, 82 (60%) had persistent atrial fibrillation (AF), and 7 (5%) had paroxysmal AF. The prevalence of inappropriate use of digoxin was 5%. Of 89 patients with persistent or paroxysmal AF, 70 (79%) were being treated with warfarin to maintain an International Normalized Ratio between 2.0 and 3.0, 15 (17%) were being treated with aspirin 325 mg daily, and 4 (4%) were not being treated with warfarin or aspirin. The prevalence of nonuse of warfarin or aspirin in patients with persistent or paroxysmal AF was 4%. |
6,116 | Left atrial pressure reduction for mitral stenosis reverses left atrial direction-dependent conduction abnormalities. | Left atrial (LA) stretch-associated electrophysiological changes in patients with mitral stenosis (MS) predispose to atrial fibrillation. We hypothesized that the normalization of the pressure gradient by percutaneous transvenous mitral balloon valvotomy (PTMV) affects LA but not right atrial (RA) conduction, depending on the site of stimulation. Because direction-dependent (asymmetric) changes of conduction may contribute to arrhythmogenesis, we assessed conduction symmetry in MS patients and tested whether it is restored by PTMV.</AbstractText>In nine patients with MS, atrial effective refractory period and local activation times (ATs) were determined during stimulation before and after PTMV, with up to four decapolar catheters (LA and RA). Eight patients with ventricular pre-excitation served as controls. ATs at basic cycle length were similar before and after PTMV. With stimulation from either atrium, they were about 45 ms in the ipsilateral atrium and about 115 ms in the contralateral atrium. With premature stimulation, ATs increased dramatically. The shortest ATs were found in the RA with RA stimulation (78 +/- 9 and 80 +/- 6 ns, before and after PTMV). PTMV caused a shortening in LA-ATs (following LA stimulation) from 118 +/- 14 to 82 +/- 5 ms (before and after; P < 0.05). Asymmetry in conduction properties was therefore normalized by PTMV. PTMV led to a decrease in RA-ATs (following LA stimulation) from 196 +/- 11 to 174 +/- 13 ms (P < 0.02). In addition, following RA stimulation, the dispersion in ATs in the LA decreased significantly by PTMV (from 66 +/- 10 to 34 +/- 7 ms; P < 0.02).</AbstractText>MS is associated with LA conduction delay, increased LA dispersion of conduction, and conduction asymmetry. These changes are immediately reversible by PTMV.</AbstractText> |
6,117 | RR-interval irregularity precedes ventricular fibrillation in ST elevation acute myocardial infarction. | Sudden cardiac arrest is a leading cause of death in industrialized countries, and ischemic ventricular fibrillation (VF) is a frequent cause.</AbstractText>The purpose of this study was to determine whether patients with ST elevation myocardial infarction (STEMI) who develop ischemic VF show more overall RR-interval irregularity (RRI) than do STEMI patients without ischemic VF.</AbstractText>Ischemic VF was identified in 41 patients from 1,473 digital 12-lead Holter recordings from three separate STEMI studies. Continuous 3-lead and 12-lead electrocardiogram (ECG) snapshots recorded every minute were compared between all ischemic VF patients and 123 random patients without ischemic VF. Time intervals from start of Holter to ischemic VF and equivalent intervals in the controls were used for calculations. ECG variables related to conduction intervals and severity of ischemia were measured using the most ischemic 12-lead ECG. RRI was calculated as the square root of the mean squared differences of successive RR intervals. For RRI, all QRS complexes, including ventricular ectopic beats, were used.</AbstractText>No baseline differences were observed between the study and control groups, except for male preponderance among ischemic VF patients (90% vs 72%, P = .019). QRS interval, ECG ischemia severity, RRI, and number of ventricular ectopic beats were significantly associated with ischemic VF. Multivariate analysis revealed RRI (odds ratio 1.006, 95% confidence interval 1.001-1.010, P = .016) and ST deviation score (odds ratio 1.073, 95% confidence interval 1.041-1.106, P <.001) as the only statistically significant predictors of ischemic VF.</AbstractText>In the period before ischemic VF, RRI and ST deviation score are associated with ischemic VF in STEMI patients. These findings could have important pathophysiologic and clinical implications.</AbstractText> |
6,118 | The impact of dopamine on hemodynamics, oxygen metabolism, and cerebral resuscitation after restoration of spontaneous circulation in pigs. | Restoration of spontaneous circulation after cardiopulmonary resuscitation in cardiac arrest patients does not always signal a completely successful outcome. Functional deficiencies of the nervous system are found in many survivors of cardiac arrest.</AbstractText>To study the effects of dopamine-induced elevated blood pressure on the hemodynamics, oxygen metabolism, and cerebral resuscitation in different perfusion conditions in a resuscitated animal model.</AbstractText>There were 18 pigs included in the study. Ventricular fibrillation (VF) was induced with a programmed electrical stimulation device. After 4 min of untreated ventricular fibrillation followed by 9 min of CPR, 12 animals were resuscitated successfully, and were then randomly assigned to either the study group (dopamine group) or the control group (normal perfusion group). All animals in the two groups received normal saline through continuous intravenous guttae for 4 h at a rate of 15 mL/kg/h. In the study group, dopamine was added to raise the animals' blood pressure. Four hours of intensive monitoring was performed for all study animals. Finally, 24-h evaluation of neurological function was conducted in surviving animals in accordance with the standard of the Cerebral Performance Category Score.</AbstractText>In animals in the dopamine group, the cardiac output, mean aortic pressure, coronary perfusion pressure, oxygen delivery, and oxygen consumption were higher than those found in the animals in the normal perfusion group (p < 0.05). Oxygen metabolism was remarkably improved in animals in the dopamine group. Furthermore, cerebral perfusion was better in the dopamine group than in the control group and thus, results of the evaluation of nervous system function were better in animals treated with dopamine (p < 0.05).</AbstractText>Dopamine improved systemic perfusion, cerebral blood supply, and oxygen metabolism after successful resuscitation from VF in a porcine model. All of these factors have profound effects on the cerebral resuscitation.</AbstractText>Copyright © 2011 Elsevier Inc. All rights reserved.</CopyrightInformation> |
6,119 | Vernakalant hydrochloride for the treatment of atrial fibrillation. | Atrial fibrillation (AF) is the most common arrhythmia encountered in clinical practice. Rhythm control strategy for AF is limited by drug toxicity and side effects, and recent trials have shown that this strategy is not superior to a rate control one. New antiarrhythmic drugs, free of undesired effects, would enhance rhythm control, with the possibility of sinus rhythm restoration and maintenance. A promising find in the search for new antiarrhythmic therapies is atrial-tissue specific ion channels. The findings that the ultrarapid delayed rectifier (I(Kur)) and the inwardly rectifying, acetylcholine-regulated current (I(K-Ach)) exist in atrial but not ventricular tissue increase the probability that atrioselective drugs without ventricular proarrhythmic toxicity can be developed for treatment of patients with AF. There are also other potential targets for atrial-selective therapy: transient outward current (I(to)), rapidly and slowly activating delayed rectifier currents (I(Kr) and I(Ks)), atrial sodium current (I(Na)) and atrially expressed connexins. New drugs under development with promising atrial-selectivity include: tertiapin, NIP-142, NIP-141, JTV-519, AVE0118, AVE1231, DPO-1, AZD7009 and many others. Among such new agents, vernakalant hydrochloride is currently in an advanced phase of development and has already been evaluated in clinical trials. In this overview, we describe the history and current state of developmental process of the drug, as well as its mechanism of action and influence on electrophysiological parameters. Vernakalant seems to be effective in terminating recent-onset AF, but is not efficacious in long-lasting AF and atrial flutter. The drug may be relatively free of proarrhythmic effects, and exerts a protective effect on ventricular tissue and ventricular repolarization. It is expected that the intravenous formulation will soon be approved for the pharmacological termination of recent-onset AF. |
6,120 | [Effect of shensongyangxin capsule on myocardial remodeling and ventricular fibrillation threshold value in rat with coronary artery ligation]. | To study the effect of shensongyangxin capsule on myocardial remodeling and ventricular fibrillation characteristics in rat with coronary artery ligation.</AbstractText>Twenty-three male rats were randomly divided into sham-group (n = 5), model group (n = 6), anmiodarone group (n = 6) and shensongyangxin capsule group (n = 6). Drugs were administrated after modeling of 2 days, lasting four weeks. Two dimensional and Doppler images were acquired by a 15 MHz high-frequency linear ultrasound transducer at 4 weeks after operation, and chest was opened to detect ventricular fibrillation threshold value and persistent time.</AbstractText>After administration of four weeks, echocardiogram was detected. Compared with model group, shensongyangxin capsule group diastasis interventricular septum thickness (IVSTd) and left ventricle diameter (LVDd) were significiently different between them (1.20 +/- 0.49) vs (0.78 +/- 0.08) mm and (6.77 +/- 1.34) vs (7.95 +/- 0.92) mm, (P < 0.01 and 0.05); echocardiogram result had no difference in amiodarone and model groups (P > 0.05). LVMI measured by practicion was different between shensongyangxin capsule and model groups: (17.12 +/- 1.91) vs (18.95 +/- 1.41) g x m(-2), (P < 0.05), while amiodarone group had no difference compared with model group. Electrophysiology was used to detect ventricular fibrillation threshold value and 1-5, 6-10, 11-15 V three stages' ventricular fibrillation threshold persistent time were significiently different among each group (P < 0.01), 16-20 V stage's ventricular fibrillation persistent time were also different among each group (P <0.05). Sample "average ranks" showed ventricular fibrillation threshold value of amiodarone group and shensongyangxin capsule group were four times than model group; and amiodaron group had best effect of holding-back ventricular fibrillation persistent time.</AbstractText>The coronary artery ligation can result in myocardial remodeling by increasing volume load, and at the same time influencing electrophysiology function of heart. Amiodaron elevated ventricular fibrillation threshold of heart, this effect maybe relate to influencing many ion channels of myocardial cellular membrane; shensongyangxin capsule also elevate ventricular fibrillation threshold of heart, this effect maybe also relate to influencing many ion channels of myocardial cellular membrane, and on the other hand this effect maybe relate to hold-back ventricular remodeling after coronary artery was ligated, accordingly improve electrophysiological base material of heart.</AbstractText> |
6,121 | Cardiac resynchronization therapy is effective even in elderly patients with comorbidities. | The purpose of this study was to compare the effects of cardiac resynchronization therapy (CRT) in elderly patients (> or =65 years) with younger patients and to assess the impact of comorbidities in CRT remodeling response.</AbstractText>This is a prospective study of 87 consecutive patients scheduled for CRT who underwent clinical and echocardiographic evaluation before and 6 months after CRT. A reduction in left ventricular end-systolic volume (LVESV) > or =15% after CRT defined remodeling responders, and a reduction of at least one New York Heart Association class defined clinical responders. Multivariate analysis was used to identify independent predictors of non-response to CRT in terms of reverse remodeling.</AbstractText>The mean age was 62 +/- 11 years, with 36 elderly patients (41%). The baseline QRS duration was 145 +/- 32 ms. After CRT, there were significant and similar improvements of left ventricular (LV) ejection fraction, LVESV, LV dP/dt, and mitral regurgitation jet area (JA) between elderly (> or =65 years) and younger (<65 years) patients. The number of clinical and remodeling responders was comparable, and we found no significant differences in unplanned cardiac hospitalizations at 6 months between groups. Independent predictors of lack of remodeling response to CRT were QRS duration <120 ms, LV diastolic diameter >74 mm, and JA >10 cm(2) before CRT, but not comorbidities.</AbstractText>This work suggests that being elderly is not an impediment to CRT success even in the presence of comorbidities.</AbstractText> |
6,122 | Catheter ablation of arrhythmic storm triggered by monomorphic ectopic beats in patients with coronary artery disease. | Frequent episodes of polymorphic ventricular tachycardias/ventricular fibrillation (VT/VF) in patients with coronary artery disease can be triggered by monomorphic ventricular premature beats (VPBs) and thus, amenable to catheter ablation. The goal of this study was to review single-center experience in catheter ablation of electrical storm caused by focally triggered polymorphic VT/VF.</AbstractText>Catheter ablation of electrical storm due to focally triggered polymorphic VT/VF was performed in nine patients (mean age, 62+/-7 years; two females). All patients had previous myocardial infarction (interval of 3 days to 171 months). Mean left ventricular ejection fraction was 27+/-6 percent. All patients presented with repeated runs of polymorphic VT/VF triggered by monomorphic VPBs.</AbstractText>Based on mapping data, the ectopic beats originated from scar border zone on interventricular septum (n=5), inferior wall (n=3), and lateral wall (n=1). Catheter ablation was performed to abolish the triggering ectopy and to modify the arrhythmogenic substrate by linear lesions within the infarct border zone. The ablation procedure was acutely successful in eight out of nine patients. During the follow-up of 13+/-7 months, two patients died due to progressive heart failure. One patient had late recurrence of electrical storm due to ectopic beats of different morphology and was successfully reablated.</AbstractText>Electrical storm due to focally triggered polymorphic VT/VF may occur either in subacute phase of myocardial infarction or substantially later after index event. Catheter ablation of ectopic beats triggering these arrhythmias can successfully abolish electrical storm and become a life-saving procedure.</AbstractText> |
6,123 | Experimental and clinical research findings on the cardiovascular benefits of consuming flaxseed. | Functional foods and nutraceuticals are becoming popular alternatives to pharmacological treatments by providing health benefits and (or) reducing the risk of chronic diseases. Flaxseed is a rich source of 3 components with demonstrated cardioprotective effects: the omega-3 fatty acid alpha-linolenic acid (ALA), dietary fibre, and phytoestrogen lignans. Multiple clinical dietary intervention trials report that consuming flaxseed daily can modestly reduce circulating total cholesterol (TC) by 6%-11% and low-density lipoprotein (LDL) cholesterol by 9%-18% in normolipemic humans and by 5%-17% for TC and 4%-10% for LDL cholesterol in hypercholesterolemic patients, as well as lower various markers associated with atherosclerotic cardiovascular disease in humans. Evidence to date suggests that the dietary fibre and (or) lignan content of flaxseed provides the hypocholesterolemic action. The omega-3 ALA found in the flaxseed oil fraction also contributes to the antiatherogenic effects of flaxseed via anti-inflammatory and antiproliferative mechanisms. Dietary flaxseed may also protect against ischemic heart disease by improving vascular relaxation responses and by inhibiting the incidence of ventricular fibrillation. |
6,124 | PKA and PKC partially rescue long QT type 1 phenotype by restoring channel-PIP2 interactions. | Long-QT syndrome causes torsade de pointes arrhythmia, ventricular fibrillation, and sudden death. The most commonly inherited form of long-QT syndrome, LQT1, is due to mutations on the potassium channel gene KCNQ1, which forms one of the main repolarizing cardiac K(+) channels, IKs. IKs has been shown to be regulated by both beta-adrenergic receptors, via protein kinase A (PKA), and by Gq protein coupled receptors (GqPCR), via protein kinase C (PKC) and phosphatidylinositol 4,5-bisphosphate (PIP(2)). These regulatory pathways were shown to crosstalk, with PKA phosphorylation increasing the apparent affinity of IKs to PIP(2). Here we study the effects of LQT1 mutations in putative PIP(2)-KCNQ1 interaction sites on regulation of IKs by PKA and GqPCR. The effect of the LQT1 mutations on IKs regulation was tested for mutations in conserved, positively charged amino acids, located in four distinct cytoplamic domains of the KCNQ1 subunit: R174C (S2-S3), R243C (S4-S5), R366Q (proximal c-terminus) and R555C (distal c-terminus). Mutations in the c-terminus of IKs (both proximal and distal) enhanced channel sensitivity to changes in membrane PIP(2) levels, consistent with a decrease in apparent channel-PIP(2) affinity. These mutant channels were more sensitive to inhibition caused by receptor mediated PIP(2)-depletion and more sensitive to stimulation of PIP(2) production, by overexpression of phosphatidylinositol-4-phosphate-5-kinase (PI5-kinase). In addition, c-terminus mutants showed a potentiated regulation by PKA. On the other hand, for the two cytoplasmic-loop mutations, an impaired activation by PKA was observed. The effects of the mutations on PKC stimulation of the channel paralleled the effects on PKA stimulation, suggesting that both regulatory inputs are similarly affected by the mutations. We tested whether PKC-mediated activation of IKs, similarly to the PKA-mediated activation, can regulate the channel response to PIP(2). After PKC activation, channel was less sensitive to changes in membrane PIP(2) levels, consistent with an increase in apparent channel-PIP(2) affinity. PKC-activated channel was less sensitive to inhibition caused by block of synthesis of PIP(2) by the lipid kinase inhibitor wortmannin and less sensitive to stimulation of PIP(2) production. Our data indicates that stimulation by PKA and PKC can partially rescue LQT1 mutant channels with weakened response to PIP(2) by strengthening channel interactions with PIP(2). |
6,125 | Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial. | Intravenous access and drug administration are included in advanced cardiac life support (ACLS) guidelines despite a lack of evidence for improved outcomes. Epinephrine was an independent predictor of poor outcome in a large epidemiological study, possibly due to toxicity of the drug or cardiopulmonary resuscitation (CPR) interruptions secondary to establishing an intravenous line and drug administration.</AbstractText>To determine whether removing intravenous drug administration from an ACLS protocol would improve survival to hospital discharge after out-of-hospital cardiac arrest.</AbstractText><AbstractText Label="DESIGN, SETTING, AND PATIENTS" NlmCategory="METHODS">Prospective, randomized controlled trial of consecutive adult patients with out-of-hospital nontraumatic cardiac arrest treated within the emergency medical service system in Oslo, Norway, between May 1, 2003, and April 28, 2008.</AbstractText>Advanced cardiac life support with intravenous drug administration or ACLS without access to intravenous drug administration.</AbstractText>The primary outcome was survival to hospital discharge. The secondary outcomes were 1-year survival, survival with favorable neurological outcome, hospital admission with return of spontaneous circulation, and quality of CPR (chest compression rate, pauses, and ventilation rate).</AbstractText>Of 1183 patients for whom resuscitation was attempted, 851 were included; 418 patients were in the ACLS with intravenous drug administration group and 433 were in the ACLS with no access to intravenous drug administration group. The rate of survival to hospital discharge was 10.5% for the intravenous drug administration group and 9.2% for the no intravenous drug administration group (P = .61), 32% vs 21%, respectively, (P<.001) for hospital admission with return of spontaneous circulation, 9.8% vs 8.1% (P = .45) for survival with favorable neurological outcome, and 10% vs 8% (P = .53) for survival at 1 year. The quality of CPR was comparable and within guideline recommendations for both groups. After adjustment for ventricular fibrillation, response interval, witnessed arrest, or arrest in a public location, there was no significant difference in survival to hospital discharge for the intravenous group vs the no intravenous group (adjusted odds ratio, 1.15; 95% confidence interval, 0.69-1.91).</AbstractText>Compared with patients who received ACLS without intravenous drug administration following out-of-hospital cardiac arrest, patients with intravenous access and drug administration had higher rates of short-term survival with no statistically significant improvement in survival to hospital discharge, quality of CPR, or long-term survival.</AbstractText>clinicaltrials.gov Identifier: NCT00121524.</AbstractText> |
6,126 | Atrial tachycardia with 1:1 atrioventricular conduction precipitated by propafenone. | A 58-year-old man presented to the emergency department with sudden onset rapid palpitations and significant presyncope while walking on the flat. The previous day he had undergone DC cardioversion for atrial fibrillation (AF) which had been initially successful. However, 6 h after cardioversion he was aware of intermittently raised but regular heart rates. On arrival at the emergency department (ED) he was well with no haemodynamic compromise. The ECG showed an atrial tachycardia instead of AF. Medications consisted of propafenone 300 mg twice daily, bisoprolol 5 mg at night and warfarin. Bisoprolol was increased to 5 mg twice daily and he was discharged with a plan for outpatient ablation. He collapsed in the hospital car park with rapid palpitations, chest tightness and vagal symptoms. On return to the ED he was hypotensive with a heart rate of 200 bpm. The ECG showed 1:1 atrioventricular conduction (AV) of the atrial tachycardia which promptly improved after administering intravenous atenolol. Class 1c antiarrhythmic agents such as propafenone can precipitate 1:1 AV conduction of atrial tachycardias resulting in dangerous exacerbations of ventricular rate or even malignant tachyarrhythmias. It is therefore essential that concomitant AV blocking agents are used both prophylactically or acutely in suspected cases. |
6,127 | Incidence and predictors of silent cerebral embolism during pulmonary vein catheter ablation for atrial fibrillation. | Left atrial catheter ablation of the pulmonary veins (PV) has evolved as an important therapeutic option for the treatment of atrial fibrillation (AF). We aimed to investigate the incidence and predictors of silent cerebral embolism associated with PV catheter ablation, detected by diffusion-weighted magnetic resonance imaging (DW-MRI).</AbstractText>We performed a prospective analysis of 53 consecutive patients with persistent or paroxysmal AF that underwent PV ablation and post-procedural cerebral MRI 1 day after lasso catheter-guided ostial PV ablation. Patients were analysed for possible demographical, medical, echocardiographical, and procedural predictors of embolic events. A mean of 3.5 +/- 0.5 PVs were ablated per patient. In six patients, DW-MRI depicted new clinically silent microembolism after PV ablation (11%). The number of ineffective medical antiarrhythmic agents prior to ablation procedure was significantly higher in the embolism group (3.3 +/- 0.5 vs. 2.2 +/- 1.4, P = 0.014). Coronary heart disease (CAD) was more frequent in patients with cerebral embolisms (33 vs. 2%, P = 0.031); left ventricular volume (130 +/- 12 vs. 103 +/- 26 mL, P = 0.002), and septal wall thickness (13.0 +/- 1.4 vs. 7.9 +/- 4.8 mm, P = 0.025) were significantly increased.</AbstractText>This study shows a high incidence of silent micro-embolic events after PV ablation. CAD, left ventricular dilatation, and hypertrophy were potential predictors of this complication.</AbstractText> |
6,128 | Should patients with asymptomatic severe mitral regurgitation with good left ventricular function undergo surgical repair? | A best evidence topic in cardiac surgery was written according to a structured protocol. The question addressed was, 'Does severe asymptomatic mitral regurgitation (MR) require surgery or is watch and wait the optimal strategy?'. Over 103 papers were found using the reported search, and 10 represented the best evidence to answer this clinical question. The authors, journal, date and country of publication, patient group studied, study type, relevant outcomes and results of these papers are tabulated. No studies in the modern era have shown significant survival benefit for patients undergoing surgery for asymptomatic severe MR if they have good left ventricular (LV) function. The progression rate to surgery on developing symptoms is 10% per year in these patients. Ling et al. reported a 63% incidence of congestive heart failure and 30% incidence of chronic atrial fibrillation (AF) at 10 years for conservative treatment, during which period 90% either underwent surgery or died. In addition, one study of 478 patients with good LV operated on in the 1980s showed a 76% 10-year survival in patients who were NYHA I/II but only a 48% 10-year survival in patients with NYHA III/IV although this group was older and had more AF. Early surgery has very good peri- and postoperative survival rates, and the American Heart Association currently recommend that these patients may be operated on if the chance of repair is >90%. Patients may, therefore, be reassured that either strategy is acceptable. |
6,129 | Frequency of cardiac death in children with idiopathic dilated cardiomyopathy. | The prognosis in children with idiopathic dilated cardiomyopathy (IDC) is guarded, with the 5-year mortality rate ranging from 14% to 50%, owing to sudden cardiac death (SCD) or pump failure. The risk factors for SCD in adults with IDC include asymptomatic nonsustained ventricular tachycardia and poor left ventricular function. It is unclear whether these findings can be extrapolated to the pediatric population. A retrospective review of all patients with the diagnosis of IDC seen at a single institution from 1990 to 2004 was performed. A total of 85 patients (46 males), with a median age of 3.8 years (0 days to 17.3 years) were studied. The mean left ventricular ejection fraction was 25 +/- 12% (median 23%, range 45% to 45%) at presentation. The following arrhythmias occurred at presentation or during the initial hospitalization: nonsustained ventricular tachycardia in 6, sustained ventricular tachycardia or fibrillation in 1, supraventricular arrhythmias in 6, and both atrial and ventricular arrhythmias in 1. During a subsequent hospitalization or outpatient follow-up, 7 patients had the following arrhythmias: supraventricular arrhythmias in 2, nonsustained ventricular tachycardia in 4, and both atrial and ventricular arrhythmias in 1. The cumulative survival rate was 40% at a mean follow-up of 6.2 years (95% confidence interval 4.4 to 8.1). One single episode of SCD occurred in 1 patient without a history of sustained arrhythmias. In conclusion, in children with IDC, despite the low left ventricular ejection fraction and presence of ventricular arrhythmias, only one episode of SCD occurred in this group of patients. Given the 1% incidence of SCD in this cohort, the use of implantable cardioverter-defibrillators as primary prevention in children with IDC might not be indicated. |
6,130 | Lethal arrhythmia and corticosteroid insufficiency. | We describe a case of isolated adrenocorticotropic hormone deficiency that showed ventricular fibrillation associated with QT prolongation. A 72-year-old man was admitted because of consciousness disorder caused by severe hypoglycemia. On the second hospital day, QT intervals were unexpectedly prolonged and ventricular fibrillation occurred. Electrical defibrillation was performed and restored hemodynamically stable condition without neurologic deficits. He was diagnosed with endocrine tests as having isolated adrenocorticotropic hormone deficiency. QT prolongation was improved after hydrocortisone replacement therapy. We considered the QT prolongation was caused by corticosteroid insufficiency. We should be aware that corticosteroid insufficiency may provoke QT prolongation responsible for sudden cardiac death. |
6,131 | Pharmacological modulations of cardiac ultra-rapid and slowly activating delayed rectifier currents: potential antiarrhythmic approaches. | Despite the emerging new insights into our understandings of the cellular mechanisms underlying cardiac arrhythmia, medical therapy for this disease remains unsatisfactory. Atrial fibrillation (AF), the most prevalent arrhythmia, is responsible for significant morbidity and mortality. On the other hand, ventricular fibrillation results in sudden cardiac deaths in many instances. Prolongation of cardiac action potential (AP) is a proven principle of antiarrhythmic therapy. Class III antiarrhythmic agents prolong AP and QT interval by blocking rapidly activating delayed rectifier current (I(Kr)). However, I(Kr) blocking drugs carry the risk of life-threatening proarrhythmia. Recently, modulation of atrial-selective ultra-rapid delayed rectifier current (I(Kur)), has emerged as a novel therapeutic approach to treat AF. A number of I(Kur) blockers are being evaluated for the treatment of AF. The inhibition of slowly activating delayed rectifier current (I(Ks)) has also been proposed as an effective and safer antiarrhythmic approach because of its distinguishing characteristics that differ in remarkable ways from other selective class III agents. Selective I(Ks) block may prolong AP duration (APD) at rapid rates without leading to proarrhythmia. This article reviews the pathophysiological roles of I(Kur) and I(Ks) in cardiac repolarization and the implications of newly developed I(Kur) and I(Ks) blocking agents as promising antiarrhythmic approaches. Several recent patents pertinent to antiarrhythmic drug development have been discussed. Further research will be required to evaluate the efficacy and safety of these agents in the clinical setting. |
6,132 | Non-atheroprotective effects of statins: a systematic review. | Since the introduction of HMG-CoA reductase inhibitors (statins) for lowering lipids, a large amount of data has been published demonstrating their potential benefits in conditions as varied as cancer, osteoporosis, and Alzheimer's dementia. We reviewed the published literature on MEDLINE from articles between 1950 and 2008 on the non-atheroprotective effects of statins and noted consistent benefits of statin use in improving outcomes of ventricular arrhythmias, sudden cardiac death, cardiac transplant rejection, chronic obstructive pulmonary disease, and sepsis. However, for these conditions, the level of evidence was inadequate to recommend statin use. The evidence for improving outcomes in atrial fibrillation, mortality in heart failure, contrast-induced nephropathy, cataract, age-related macular degeneration, sub-arachnoid hemorrhage, osteoporosis, dementia, and cancer incidence was conflicting and inconclusive. Furthermore, we found that most of the literature consists of small observational studies and their conclusions are often not corroborated by results from larger or randomized studies. Pending large, well designed, randomized trials, we conclude that there is no definite evidence for the use of statins in any condition besides hyperlipidemia and atherosclerosis. |
6,133 | Diastolic intracellular calcium-membrane voltage coupling gain and postshock arrhythmias: role of purkinje fibers and triggered activity. | Recurrent ventricular arrhythmias after initial successful defibrillation are associated with poor clinical outcome.</AbstractText>We tested the hypothesis that postshock arrhythmias occur because of spontaneous sarcoplasmic reticulum Ca release, delayed afterdepolarization (DAD), and triggered activity (TA) from tissues with high sensitivity of resting membrane voltage (V(m)) to elevated intracellular calcium (Ca(i)) (high diastolic Ca(i)-voltage coupling gains).</AbstractText>We simultaneously mapped Ca(i) and V(m) on epicardial (n=14) or endocardial (n=14) surfaces of Langendorff-perfused rabbit ventricles. Spontaneous Ca(i) elevation (SCaE) was noted after defibrillation in 32% of ventricular tachycardia/ventricular fibrillation at baseline and in 81% during isoproterenol infusion (0.01 to 1 micromol/L). SCaE was reproducibly induced by rapid ventricular pacing and inhibited by 3 mumol/L of ryanodine. The SCaE amplitude and slope increased with increasing pacing rate, duration, and dose of isoproterenol. We found TAs originating from 6 of 14 endocardial surfaces but none from epicardial surfaces, despite similar amplitudes and slopes of SCaEs between epicardial and endocardial surfaces. This was because DADs were larger on endocardial surfaces as a result of higher diastolic Ca(i)-voltage coupling gain, compared to those of epicardial surfaces. Purkinje-like potentials preceded TAs in all hearts studied (n=7). I(K1) suppression with CsCl (5 mmol/L, n=3), BaCl(2) (3 micromol/L, n=3), and low extracellular potassium (1 mmol/L, n=2) enhanced diastolic Ca(i)-voltage coupling gain and enabled epicardium to also generate TAs.</AbstractText>Higher diastolic Ca(i)-voltage coupling gain is essential for genesis of TAs and may underlie postshock arrhythmias arising from Purkinje fibers. I(K)(1) is a major factor that determines the diastolic Ca(i)-voltage coupling gain.</AbstractText> |
6,134 | A comparison of atrial arrhythmias after heart or double-lung transplantation at a single center: insights into the mechanism of post-operative atrial fibrillation. | We compared the incidence of atrial arrhythmias in double-lung transplant patients versus heart transplant patients to gain insight into factors that contribute to post-operative atrial fibrillation (AF).</AbstractText>Atrial fibrillation is a common complication after thoracic surgery. Pulmonary vein isolation is an effective treatment for AF. Heart or double-lung transplantation surgery both involve pulmonary vein isolation because of suture lines.</AbstractText>We reviewed the records of 174 consecutive heart transplant patients and 122 double-lung transplant patients at the Columbia Presbyterian Medical Center between January 2005 and June 2008. Electrocardiograms during atrial arrhythmia episodes were reviewed by an electrophysiologist. Clinical variables, biopsy results, immunosuppressive regimens, and echocardiographic measurements were collected from the perioperative time period and at the time of arrhythmia occurrence.</AbstractText>In the heart transplant group, 8 (4.6%) patients had AF (group A). In the lung transplant group, 23 (18.9%) patients had AF (group B; p < 0.001). The incidence of AF in a comparison group of 131 patients with normal left ventricular function who underwent coronary artery bypass graft surgery was 19.8%. Immunosuppressive regimens and clinical variables were similar for both groups. Echocardiographic data revealed no significant cardiac abnormalities in 74% of group B compared with 25% of group A (p < 0.05), and 78% of biopsy results in group B were normal, whereas only 25% of group A results were normal (p < 0.05).</AbstractText>In heart transplant recipients, AF is uncommon and occurs in the setting of myocardial dysfunction and graft rejection. In contrast, AF is more common after lung transplantation despite the absence of graft rejection and cardiac dysfunction. Pulmonary vein isolation alone cannot explain the discrepancy in AF incidence between heart transplant recipients and double-lung transplant recipients. Cardiac autonomic denervation may have a protective effect for heart transplant patients in the post-operative setting.</AbstractText> |
6,135 | Role of the CHADS2 score in the evaluation of thromboembolic risk in patients with atrial fibrillation undergoing transesophageal echocardiography before pulmonary vein isolation. | The goals of this study were to determine: 1) if low-risk patients assessed by a CHADS(2) score, a clinical scoring system quantifying a risk of stroke in patients with atrial fibrillation (AF), require a routine screening transesophageal echocardiogram (TEE) before pulmonary vein isolation (PVI); and 2) the relationship of a CHADS(2) score with left atrial (LA)/left atrial appendage (LAA) spontaneous echo contrast, sludge, and thrombus.</AbstractText>There is no clear consensus of whether a screening TEE before catheter ablation of AF should be performed in every patient.</AbstractText>Initial TEEs for pre-PVI of 1,058 AF patients (age 57 +/- 11 years, 80% men) were reviewed and compared with a CHADS(2) score.</AbstractText>CHADS(2) scores of 0, 1, 2, 3, 4, 5, and 6 were present in 47%, 33%, 14%, 5%, 1%, 0.3%, and 0% of patients, respectively. The prevalence of LA/LAA thrombus, sludge, and spontaneous echo contrast were present in 0.6%, 1.5%, and 35%. The prevalence of LA/LAA thrombus/sludge increased with ascending CHADS(2) score (scores 0 [0%], 1 [2%], 2 [5%], 3 [9%], and 4 to 6 [11%], p < 0.01). No patient with a CHADS(2) score of 0 had LA/LAA sludge/thrombus. In a multivariate model, history of congestive heart failure and left ventricular ejection fraction <35% were significantly associated with sludge/thrombus.</AbstractText>The prevalence of LA/LAA sludge/thrombus in patients with AF undergoing a pre-PVI screening TEE is very low (<2%) and increases significantly with higher CHADS(2) scores. This suggests that a screening TEE before PVI should be performed in patients with a CHADS(2) score of >or=1, and in patients with a CHADS(2) score of 0 when the AF is persistent and therapeutic anticoagulation has not been maintained for 4 weeks before the procedure.</AbstractText> |
6,136 | Atrial fibrillation at baseline and during follow-up in ALLHAT (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial). | The ALLHAT (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial) determined that treatment with amlodipine, lisinopril, or doxazosin was not superior to thiazide-like diuretic (chlorthalidone) in preventing coronary heart disease (CHD) or other cardiovascular events. This subanalysis examines baseline prevalence and in-trial incidence of new-onset atrial fibrillation (AF) or atrial flutter (AFL) and their influence on clinical outcomes.</AbstractText>Limited information is available on whether atrial fibrillation incidence is affected differentially by different classes of antihypertensive medications or treatment with statins.</AbstractText>AF/AFL was identified from baseline and follow-up electrocardiograms performed biannually. Analyses were performed to identify characteristics associated with baseline AF/AFL and its subsequent incidence.</AbstractText>AF/AFL was present at baseline in 423 participants (1.1%), more frequent in men (odds ratio: 1.72; 95% confidence interval [CI]: 1.37 to 2.17) and nonblacks (odds ratio: 2.09; 95% CI: 1.58 to 2.75). Its prevalence increased with age (p < 0.001) and was associated with CHD, cardiovascular disease, obesity, and high-density lipoprotein cholesterol <35 mg/dl. New-onset AF/AFL was associated with the same baseline risk factors plus electrocardiogram left ventricular hypertrophy. It occurred in 641 participants (2.0%) and, excluding doxazosin, did not differ by antihypertensive treatment group or, in a subset of participants, by pravastatin versus usual care. Baseline AF/AFL was associated with increased mortality (hazard ratio [HR]: 2.82; 95% CI: 2.36 to 3.37; p < 0.001), stroke (HR: 3.63; 95% CI: 2.72 to 4.86; p < 0.001), heart failure (HR: 3.17; 95% CI: 2.38 to 4.25; p < 0.001), and fatal CHD or nonfatal myocardial infarction (HR: 1.64; 95% CI: 1.22 to 2.21; p < 0.01). There was a nearly 2.5-fold increase in mortality risk when AF/AFL was present at baseline or developed during the trial (HR: 2.42; 95% CI: 2.11 to 2.77; p < 0.001).</AbstractText>In this high-risk hypertensive population, pre-existing and new-onset AF/AFL were associated with increased mortality. Excluding doxazosin, treatment assignment to either antihypertensive drugs or pravastatin versus usual care did not affect AF/AFL incidence. (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial [ALLHAT]; NCT00000542).</AbstractText> |
6,137 | Appropriate evaluation and treatment of heart failure patients after implantable cardioverter-defibrillator discharge: time to go beyond the initial shock. | Multiple clinical trials support the use of implantable cardioverter-defibrillators (ICDs) for prevention of sudden cardiac death in patients with heart failure (HF). Unfortunately, several complicating issues have arisen from the universal use of ICDs in HF patients. An estimated 20% to 35% of HF patients who receive an ICD for primary prevention will experience an appropriate shock within 1 to 3 years of implant, and one-third of patients will experience an inappropriate shock. An ICD shock is associated with a 2- to 5-fold increase in mortality, with the most common cause being progressive HF. The median time from initial ICD shock to death ranges from 168 to 294 days depending on HF etiology and the appropriateness of the ICD therapy. Despite this prognosis, current guidelines do not provide a clear stepwise approach to managing these high-risk patients. An ICD shock increases HF event risk and should trigger a thorough evaluation to determine the etiology of the shock and guide subsequent therapeutic interventions. Several combinations of pharmacologic and device-based interventions such as adding amiodarone to baseline beta-blocker therapy, adjusting ICD sensitivity, and employing antitachycardia pacing may reduce future appropriate and inappropriate shocks. Aggressive HF surveillance and management is required after an ICD shock, as the risk of sudden cardiac death is transformed to an increased HF event risk. |
6,138 | Spontaneous pericardial hematoma with familial amyloid polyneuropathy. | There are more than a few risks of hemorrhage complication in patients with amyloidosis. Although most cases with amyloidosis exhibit minor bleeding manifestations, they can be occasionally associated with life-threatening problems. To our knowledge, there are only a few cases of spontaneous pericardial hematoma associated with amyloidosis. We here report a patient who suddenly died of cardiac tamponade with massive pericardial hematoma 7 years after the diagnosis of familial amyloid polyneuropathy (FAP). A 69-year-old female with FAP with cardiogenic shock was admitted to our emergency room. Although she previously underwent permanent pacemaker implantation for atrial fibrillation with slow ventricular response, electrocardiogram showed a critical pacing failure. Emergent telemetry check revealed a sudden extreme increase of pacing capture threshold in the right ventricle. Maximum pacing voltage could not improve the critical condition, and she died 7 h after arrival. Autopsy showed a massive pericardial hematoma in the right ventricular free wall, and microscopic examination revealed typical amyloid deposition in the arterial wall of the pericardium. In this case, it is assumed that a sudden rupture of fragile pericardial vessels with amyloid deposition led to the lethal pericardial hematoma. |
6,139 | Prevalence, clinical correlates and treatment of permanent atrial fibrillation among the elderly: insights from the first prospective population-based study in rural Greece. | To investigate the prevalence of permanent atrial fibrillation (AF), its clinical associated conditions and treatment status in the elderly population in rural Greece. 720 people (46.1% males) older than 65 years (mean age: 72.5 +/- 5.7 years) living in four villages in rural Greece were screened with an electrocardiogram (response rate: 90.5%) for the presence of permanent AF. They underwent a physical examination, including blood pressure (BP) measurement, and body mass index (BMI) calculation, in addition to an interview about their medical history, physical activity, smoking habits, alcohol consumption and medication use. Subjects with AF for whom anticoagulants were contraindicated were identified and stroke risk stratification was performed using the CHADS2 algorithm. The prevalence of permanent AF was 5% (6.6% among men and 3.6% among women) and it increased with age. In the entire population, ECG evidence of myocardial ischaemia and ventricular premature beats were independently associated with the presence of permanent AF (OR 5.266; 95% CI 2.22-12.49, P = 0.0001 and OR 2.61; 95% CI 1.059-6.432, P = 0.037, respectively), while female sex was independently associated with the absence of the AF (OR 0.327; CI 0.147-0.729, P = 0.006). From those patients who were eligible for anticoagulation, 40.6% were treated with anticoagulants, 34.3% were given antiplatelets therapy and the rest received no antithrombotic treatment. This is the first prospective study demonstrating the prevalence, clinical correlates and treatment status of permanent AF in Greece. These results confirm the high prevalence of permanent AF among the elderly and underscore the issue regarding anticoagulants underutilization. |
6,140 | Remote monitoring of cardiovascular implantable electronic devices: prerequisite or luxury? | The number of patients implanted with cardiovascular electronic devices (CIED) like implantable defibrillators (ICD), cardiac resynchronisation (CRT) devices, and pacemakers continues to grow. These devices require regular follow-up interrogation in dedicated device clinics. Contemporary CIED are capable of wireless remote interrogation and monitoring. This technology has been proven to be technically reliable and helpful in certain conditions. It is of particular benefit in monitoring devices that are under a safety alert since it allows early identification of device malfunction and minimises the risk of under-reporting. There is also strong evidence that it helps to reduce heart failure hospitalisations in CRT and ICD patients. Furthermore, this technology proves to be very helpful in the early detection of arrhythmias like atrial fibrillation or ventricular tachyarrhythmias. Remote monitoring significantly reduces the number of follow-up visits, patients' and physicians' time spent per visit, and increases patients' adherence to follow-up visits. Future studies are needed to determine how to best allocate this new technology in a cost-effective manner. |
6,141 | Implantable cardioverter-defibrillators. | The automatic implantable cardioverter-defibrillator (AICD) is the most effective treatment for patients with life-threatening ventricular tachycardia or ventricular fibrillation. The American College of Cardiology/American Heart Association class I, IIa, and III indications for an AICD are discussed. Patients with AICDs should be treated with biventricular pacing, not with dual-chamber rate-responsive pacing at a rate of 70/minute. Patients with AICDs should be treated with beta blockers, statins, and angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. |
6,142 | Long-term outcome associated with early repolarization on electrocardiography. | Early repolarization, which is characterized by an elevation of the QRS-ST junction (J point) in leads other than V(1) through V(3) on 12-lead electrocardiography, has been associated with vulnerability to ventricular fibrillation, but little is known about the prognostic significance of this pattern in the general population.</AbstractText>We assessed the prevalence and prognostic significance of early repolarization on 12-lead electrocardiography in a community-based general population of 10,864 middle-aged subjects (mean [+/-SD] age, 44+/-8 years). The primary end point was death from cardiac causes, and secondary end points were death from any cause and death from arrhythmia during a mean follow-up of 30+/-11 years. Early repolarization was stratified according to the degree of J-point elevation (> or = 0.1 mV or > 0.2 mV) in either inferior or lateral leads.</AbstractText>The early-repolarization pattern of 0.1 mV or more was present in 630 subjects (5.8%): 384 (3.5%) in inferior leads and 262 (2.4%) in lateral leads, with elevations in both leads in 16 subjects (0.1%). J-point elevation of at least 0.1 mV in inferior leads was associated with an increased risk of death from cardiac causes (adjusted relative risk, 1.28; 95% confidence interval [CI], 1.04 to 1.59; P=0.03); 36 subjects (0.3%) with J-point elevation of more than 0.2 mV in inferior leads had a markedly elevated risk of death from cardiac causes (adjusted relative risk, 2.98; 95% CI, 1.85 to 4.92; P<0.001) and from arrhythmia (adjusted relative risk, 2.92; 95% CI, 1.45 to 5.89; P=0.01). Other electrocardiographic risk markers, such as a prolonged QT interval corrected for heart rate (P=0.03) and left ventricular hypertrophy (P=0.004), were weaker predictors of the primary end point.</AbstractText>An early-repolarization pattern in the inferior leads of a standard electrocardiogram is associated with an increased risk of death from cardiac causes in middle-aged subjects.</AbstractText>2009 Massachusetts Medical Society</CopyrightInformation> |
6,143 | High-resolution electrical mapping of depolarization and repolarization alternans in an ischemic dog model. | Cardiac electrical alternans have been associated with spontaneous ventricular arrhythmias during myocardial ischemia. The study aims were to use a new algorithm to measure depolarization and repolarization alternans from epicardial electrograms in an ischemia model and to evaluate which features are predictive of ventricular fibrillation (VF). The left anterior descending coronary artery was occluded in 21 dogs, of which 6 developed spontaneous VF. Four seconds of unipolar epicardial electrograms was recorded before and 5 min after occlusion from an 8 x 14-electrode plaque placed on the anterior left ventricle. Alternans amplitudes were estimated with a triangular wave-fitting algorithm and for each unipolar electrogram for various measurements of the QRS and ST-T wave amplitude. The root mean square error was computed for each fit. Receiver-operator characteristic curves were used to determine whether prevalence of alternans having estimated alternans amplitude-to-error ratio (A/E) above a given threshold could distinguish the dogs who had and did not have spontaneous VF. The prevalence of alternans after ischemia was highly predictive of VF when measured both during depolarization (sensitivity of 83% and specificity of 87%) and during repolarization (sensitivity of 100% and specificity of 73%). The optimal alternans A/E ranged from 1 to 4. There were no differences in the level of discordance or alternans amplitude between dogs who developed VF versus dogs who did not. The prevalence of alternans in the ventricles may be the key risk factor for developing VF during myocardial ischemia when short-term recordings are used. |
6,144 | Avoiding medical error during electrical cardioversion of atrial fibrillation: prevention of unsynchronized shock delivery. | Electrical cardioversion of atrial fibrillation is now commonly performed in veterinary medicine. Successful timing of the delivery of energy is important in order to avoid ventricular fibrillation. This brief communication describes how to ensure that proper energy delivery is performed. |
6,145 | Nifekalant versus lidocaine for in-hospital shock-resistant ventricular fibrillation or tachycardia. | To compare the efficacy and safety of nifekalant, a pure class III anti-arrhythmic drug, and lidocaine in patients with shock-resistant in-hospital ventricular fibrillation (VF) or ventricular tachycardia (VT).</AbstractText>Between August 2005 and March 2008, we conducted a prospective, two-arm, cluster observational study, in which participating hospitals were pre-registered either to the nifekalant arm or the lidocaine arm. Patients were enrolled if they had in-hospital VF or VT resistant to at least two defibrillation shocks. Congenital or drug-induced long QT syndrome was excluded. The primary end-point was termination of VF or VT with/without additional shock. The secondary end-points were return of spontaneous circulation (ROSC), 1-month survival and survival to hospital discharge. We also assessed the frequency of adverse events, including asystole, pulseless electrical activity and torsade de pointes.</AbstractText>In total, 55 patients were enrolled. After nifekalant, 22 of 27 patients showed termination of VF or VT, as compared with 15 of 28 patients treated with lidocaine with/without additional shock (odds ratio (OR): 3.8; 95% confidence interval (CI): 1.1-13.0; P=0.03). Twenty-three of 27 patients given nifekalant showed ROSC, as compared with 15 of 28 patients given lidocaine (OR: 5.0; 95% CI: 1.4-18.2; P=0.01). There was no difference in 1-month survival or survival to hospital discharge between the nifekalant and lidocaine arms. There was a higher incidence of asystole with lidocaine (7 of 28 patients) than with nifekalant (0 of 27 patients) (P=0.005). Torsade de pointes was not observed.</AbstractText>Nifekalant was more effective than lidocaine for termination of arrhythmia and for ROSC in patients with shock-resistant in-hospital VF or VT (umin-CTR No. UMIN 000001781).</AbstractText>Copyright 2009 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
6,146 | The feasibility of inducing mild therapeutic hypothermia after cardiac resuscitation using iced saline infusion via an intraosseous needle. | This study was done, using a swine model of prolonged ventricular fibrillation out-of-hospital cardiac arrest, to determine the feasibility of inducing therapeutic hypothermia after successful resuscitation by giving an intraosseous infusion of iced saline.</AbstractText>This study was IACUC approved. Liter bags of normal saline, after being refrigerated for at least 24h, were placed in an ice filled cooler. Female Yorkshire swine weighing between 27 and 35 kg were sedated and instrumented under general anesthesia. A temperature probe was inserted 10 cm into the esophagus. Ventricular fibrillation was electrically induced and allowed to continue untreated for 10 min. Animals were randomized to one of two resuscitation schemes for the primary study (N=53). One group had central intravenous access for drug delivery and the other had an intraosseous needle inserted into the proximal tibia for drug administration. Animals in which spontaneous circulation was restored were immediately cooled, for this secondary study, by means of a rapid, pump-assisted infusion of 1L of iced saline either through the intraosseous needle (n=8), the central access (n=6), or a peripheral intravenous catheter (n=7) in a systematic, non-randomized fashion. Room, animal, and saline temperatures were recorded at initiation and upon completion of infusion. The data were analyzed descriptively using Stata SE v8.1 for Macintosh.</AbstractText>The baseline characteristics of all three groups were mathematically the same. The average ambient room temperature during the experimental sessions was 25.5 degrees C (SD=1.3 degrees C). There were no statistically significant differences between the three groups with regard to saline temperature, rate of infusion, or decrease in core body temperature. The decrease in core temperature for the intraosseous group was 2.8 degrees C (95% CI=1.8, 3.8) over the infusion period.</AbstractText>Mild therapeutic hypothermia can be effectively induced in swine after successful resuscitation of prolonged ventricular fibrillation by infusion of iced saline through an IO needle.</AbstractText>Copyright 2009 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
6,147 | Intranasal cooling with or without intravenous cold fluids during and after cardiac arrest in pigs. | Intranasal balloon catheters circulated with cold saline have previously been used for the induction and maintenance of selective brain cooling in pigs with normal circulation. In the present study, we investigated the feasibility of therapeutic hypothermia initiation, maintenance and rewarming using such intranasal balloon catheters with or without addition of intravenous ice-cold fluids during and after cardiac arrest treatment in pigs.</AbstractText>Cardiac arrest was induced in 20 anaesthetised pigs. Following 8 min of cardiac arrest and 1 min of cardiopulmonary resuscitation (CPR), cooling was initiated after randomisation with either intranasal cooling (N) or combined with intravenous ice-cold fluids (N+S). Hypothermia was maintained for 180 min, followed by 180 min of rewarming. Brain and oesophageal temperatures, haemodynamic variables and intracranial pressure (ICP) were recorded.</AbstractText>Brain temperatures reductions after cooling did not differ (3.8 +/- 0.7 degrees C in the N group and 4.3 +/- 1.5 degrees C in the N+S group; P=0.47). The corresponding body temperature reductions were 3.6 +/- 1.2 degrees C and 4.6 +/- 1.5 degrees C (P=0.1). The resuscitation outcome was similar in both groups. Mixed venous oxygen saturation was lower in the N group after cooling and rewarming (P=0.024 and 0.002, respectively) as compared with the N+S group. ICP was higher after rewarming in the N group (25.2 +/- 2.9 mmHg; P=0.01) than in the N+S group (15.7 +/- 3.3 mmHg).</AbstractText>Intranasal balloon catheters can be used for therapeutic hypothermia initiation, maintenance and rewarming during CPR and after successful resuscitation in pigs.</AbstractText> |
6,148 | Statins as antiarrhythmics: a systematic review part I: effects on risk of atrial fibrillation. | Recent studies have demonstrated that statins may possess antiarrhythmic properties in addition to their lipid-lowering effects.</AbstractText>Studies which reported the association of statins with the incidence of atrial arrhythmias were identified through a systematic review of published literature.</AbstractText>One randomized, placebo-controlled trial of 200 patients undergoing cardiac surgery showed that atorvastatin decreased the incidence of postoperative atrial fibrillation by 61%. Observational studies in patients with stable coronary disease, left ventricular dysfunction, or those undergoing cardiac or noncardiac surgery show that statin therapy is associated with an approximately 50% lower rate of atrial fibrillation. Two small randomized trials reported conflicting results: one showing that atorvastatin reduced the recurrence of AF after electrical cardioversion and the other finding that pravastatin did not.</AbstractText>Published data suggests that statins may possess antiarrhythmic properties that reduce the propensity for atrial fibrillation. Most of this data is observational; more randomized, placebo-controlled trials are needed.</AbstractText> |
6,149 | Transcatheter closure of postsurgical residual ventricular septal defects: early and mid-term results. | The incidence of residual ventricular septal defects (VSDs) after surgery is 5-25%. Redo surgery is associated with higher risks.</AbstractText>Between January 2000 to December 2008, 170 patients underwent percutaneous VSD closure in our centre: 22(16M) of these had 23 closures for residual VSDs. Median age was 32.5 yrs (1.4-79). All patients had echocardiographic signs of left ventricle volume overload (Q(p)/Q(s) >or= 1.5). Nine patients had previous VSD closure, 6 tetralogy of Fallot repair, and 7, other procedures. There were 15 muscular, 6 perimembranous and 2 apical VSDs.</AbstractText>Amplatzer VSD devices were used in all. Median VSD size was 8 mm (4.3-16). Median fluoroscopy time was 33 minutes (15-130). There were three adverse events: 1 ventricular fibrillation requiring DC cardioversion; 1 transient complete atrio-ventricular block reverting to sinus rhythm at 24-hours; one patient had transient atrial flutter during the procedure. All procedures were successful; no additional procedures were required. Trivial residual shunts were seen in 3 patients at follow-up. There were no late events. One patient experienced arrhythmic death 5-yrs after procedure. One patient was reoperated due to dehiscence of VSD patch 2-yrs after the second successful percutaneous closure.</AbstractText>Transcatheter closure of postsurgical residual VSD is safe and efficacious management option and obviates the need for further surgery and by-pass.</AbstractText> |
6,150 | Antiarrhythmic and cardioprotective effects of remifentanil in anesthetized dogs. | To study the antiarrhythmic effect of remifentanil in experimental arrhythmias in dogs.</AbstractText>We used dogs weighing 12 kg-18 kg anesthetized with 30 mg/kg sodium pentobarbital given intravenously. Ventricular arrhythmia, ventricular fibrillation and death were induced with digoxin (9 microg/kg/min). In another model, two types of arrhythmia were induced in the right atrium, one of them with aconitine crystals placed on the right atrium and the other was induced in the basement of the right atrium by electrical stimulation. The potential antiarrhythmic action of remifentaniL was investigated in ventricular and atrial arrhythmias by the administration of an intravenous bolus after toxic signs were evident. Thus, two arrhythmias with different mechanisms were generated. Leads DII, unipolar left intraventricular and right atrial leads, and left ventricular pressure were used to record control tracings and tracings in presence of remifentanil, during ventricular arrhythmia.</AbstractText>Remifentanil abolished toxic effects of digoxin, it eliminated the A-V dissociation and ventricular extrasystoles, reverting to sinus rhythm in each case. Remifentanil extended the time to reach lethal doses from 63.25 +/- 11.3 to 100 +/- 11.8 min. These effects were blocked by naloxone (0.01 microg/kg) applied before remifentanil. In the two arrhythmias model, remifentanil suppressed both, ectopic focus and atrial flutter.</AbstractText>Remifentanil elicits antiarrhythmic and cardioprotective effects in experimental ventricular arrhythmias induced by digoxin and in a model of two atrial arrhythmias induced by aconitine and by electrical stimulation.</AbstractText> |
6,151 | Preservation of neurological function following therapeutic hypothermia in a patient of in-hospital cardiac arrest with non-ventricular fibrillation. | A 76-year-old woman with a diagnosis of dilated-phase hypertrophic cardiomyopathy was admitted to our hospital for exacerbation of congestive heart failure. After admission, she developed cardiac arrest and the electrocardiogram showed pulseless electrical activity. Cardiopulmonary resuscitation was started immediately; however, return of spontaneous circulation was achieved 56 min after cardiopulmonary arrest. Therapeutic hypothermia was considered as an adjunct therapy, together with intensive treatment. The target temperature of 33.0 °C was achieved 10 h after cardiopulmonary arrest. Core temperature was maintained between 33.0 and 35.0 °C for 72 h with no cardiac arrhythmia detected during this period. Re-warming was initiated at a rate of 1 °C/day. On day 6, the core temperature returned to 37 °C and recovery of consciousness was achieved on day 9. No impairment of neurological function was noted. She had no heart failure-related symptoms and B-type natriuretic peptide level decreased from 4174 pg/mL on admission to 450 pg/mL at discharge. Therapeutic hypothermia may be a promising post-resuscitation therapy for comatose survivors of in-hospital cardiac arrest with non-ventricular fibrillation leading to improvement in neurological outcome. |
6,152 | Defibrillation efficacy of a subcutaneous array lead: A case report. | We report a case of Brugada syndrome with a high defibrillation threshold (DFT) in whom a subcutaneous array lead was used to lower the DFT in combination with a transvenous right ventricular defibrillation lead. The patient had previously received pacemaker implantation due to sick sinus syndrome. An implantable cardioverter defibrillator (ICD) with a transvenous right ventricular defibrillation lead alone required a high DFT. A subcutaneous array lead improved defibrillation efficacy in combination with a right ventricular lead. These data suggest that a subcutaneous array lead facilitates implantation of an effective ICD lead system in patients requiring a high DFT. |
6,153 | Inward rectifier potassium channels control rotor frequency in ventricular fibrillation. | Ventricular fibrillation (VF) is the most important cause of sudden cardiac death. While traditionally thought to result from random activation of the ventricles by multiple independent wavelets, recent evidence suggests that VF may be determined by the sustained activation of a relatively small number of reentrant sources. In addition, recent experimental data in various species as well as computer simulations have provided important clues about its ionic and molecular mechanisms, particularly in regards to the role of potassium currents in such mechanisms. The results strongly argue that the inward rectifier current, I(K1,) is an important current during functional reentry because it mediates the electrotonic interactions between the unexcited core and its immediate surroundings. In addition, I(K1) is a stabilizer of reentry due to its ability to shorten action potential duration and reduce conduction velocity near the center of rotation. Increased I(K1) prevents wave front-wave tail interactions and thus averts rotor destabilization and breakup. Other studies have shown that while the slow component of the delayed rectifier potassium current I(Ks) does not significantly modify rotor frequency or stability, it plays a major role in postrepolarization refractoriness and wave break formation. Therefore, the interplay between I(K1) and the rapid sodium inward current (I(Na)) is a major factor in the control of cardiac excitability and thus the stability and frequency of reentry, while I(Ks) is an important determinant of fibrillatory conduction. |
6,154 | Performance of a consensus scoring algorithm for assessing pediatric advanced life support competency using a computer screen-based simulator. | To develop a computer screen-based simulator that may be used as a pediatric advanced life support (PALS) cognitive skill assessment tool and to pilot test a consensus-based scoring system for the simulator.</AbstractText>Development of an evaluation tool, followed by prospective, observational study of tool performance.</AbstractText>Tertiary care pediatric hospital.</AbstractText>A total of 100 PALS providers from multiple disciplines.</AbstractText>Using a consensus process with a group of six experts in pediatric emergency and critical care medicine, we developed scoring algorithms to measure performance on four interactive PALS scenarios (supraventricular tachycardia, pulseless electrical activity, ventricular fibrillation, and bradycardia). PALS providers (n = 100) completed the scenarios on the simulator and the computer assessed their performance using the scoring algorithm.</AbstractText>Case management scoring audits agreed 100% with computer scoring during pilot testing, indicating excellent reliability. The mean time to complete all four cases was 13.8 mins. Performance scores were highest for supraventricular tachycardia management and lowest for pulseless electrical activity management. Survival was significantly more common than death in the supraventricular tachycardia and ventricular fibrillation scenarios, whereas death was more common in the pulseless electrical activity scenario (p < .004). Physician status predicted a higher aggregate score as well as higher scores in the supraventricular tachycardia (p < .001), pulseless electrical activity (p = .041), and bradycardia (p = .006) scenarios. Participants who completed the PALS course on the same day as their assessment scored higher on the supraventricular tachycardia scenario (p = .041).</AbstractText>Personal computer-based simulation can be used to evaluate performance against consensus criteria in a large number of PALS providers. This technology could supplement traditional curricula by facilitating frequent knowledge assessments as part of a PALS competency maintenance regimen.</AbstractText> |
6,155 | The influence of endotoxemia on the electroencephalographic and antinociceptive effects of isoflurane in a swine model. | We have previously reported that hemorrhagic shock decreases the minimum alveolar anesthetic concentration (MAC) of isoflurane but minimally alters the electroencephalographic (EEG) effect. In this study, we investigated the influence of endotoxemia on the EEG effect and the MAC of isoflurane.</AbstractText>Eighteen swine (25.7 +/- 2.3 kg) were anesthetized by inhalation of isoflurane. The inhaled concentration was decreased to 0.5% and maintained for 20 min, before being returned to 2% and maintained for a further 20 min. End-tidal isoflurane concentrations and spectral edge frequencies were recorded. Analysis of the pharmacodynamics was performed using a sigmoidal inhibitory maximal effect model for spectral edge frequencies versus effect-site concentration. After measurement of the EEG effect, MAC was determined using the dewclaw clamp technique in which movement in response to clamping is recorded. After completion of control measurements, infusion of lipopolysaccharide (LPS, 1 microg x kg(-1) x h(-1)) was started after a 100-microg bolus administration. After 1 h, the inhaled concentration of isoflurane was varied as in the control period, and the MAC was assessed again (LPS1h). The same procedures were also performed after 3 h of LPS infusion (LPS3h).</AbstractText>Endotoxemia decreased the effect-site concentration that produced 50% of the maximal effect from 1.31% +/- 0.22% to 1.13% +/- 0.14% (LPS1h) and 1.03% +/- 0.22% (LPS3h) and decreased the MAC from 2.05% +/- 0.20% to 1.51% +/- 0.30% (LPS1h) and 1.21% +/- 0.29% (LPS3h).</AbstractText>Endotoxemia increases both the hypnotic and antinociceptive effects of isoflurane, in contrast to hemorrhagic shock, and the extent of these alterations increases with progression of endotoxemia.</AbstractText> |
6,156 | Predictive value of electrical restitution in hypokalemia-induced ventricular arrhythmogenicity. | The ventricular action potential (AP) shortens exponentially upon a progressive reduction of the preceding diastolic interval. Steep electrical restitution slopes have been shown to promote wavebreaks, thus contributing to electrical instability. The present study was designed to assess the predictive value of electrical restitution in hypokalemia-induced arrhythmogenicity. We recorded monophasic APs and measured effective refractory periods (ERP) at distinct ventricular epicardial and endocardial sites and monitored volume-conducted ECG at baseline and after hypokalemic perfusion (2.5 mM K(+) for 30 min) in isolated guinea pig heart preparations. The restitution of AP duration measured at 90% repolarization (APD(90)) was assessed after premature extrastimulus application at variable coupling stimulation intervals, and ERP restitution was assessed by measuring refractoriness over a wide range of pacing rates. Hypokalemia increased the amplitude of stimulation-evoked repolarization alternans and the inducibility of tachyarrhythmias and reduced ventricular fibrillation threshold. Nevertheless, these changes were associated with flattened rather than steepened APD(90) restitution slopes and slowed restitution kinetics. In contrast, ERP restitution slopes were significantly increased in hypokalemic hearts. Although epicardial APD(90) measured during steady-state pacing (S(1)-S(1) = 250 ms) was prolonged in hypokalemic hearts, the left ventricular ERP was shortened. Consistently, the epicardial ERP measured at the shortest diastolic interval achieved upon a progressive increase in pacing rate was reduced in the hypokalemic left ventricle. In conclusion, this study highlights the superiority of ERP restitution at predicting increased arrhythmogenicity in the hypokalemic myocardium. The lack of predictive value of APD(90) restitution is presumably related to different mode of changes in ventricular repolarization and refractoriness in a hypokalemic setting, whereby APD(90) prolongation may be associated with shortened ERP. |
6,157 | Combined resynchronization therapy and automatic defibrillator in advanced non-ischaemic heart failure: the importance of QRS width. | The combined use of an automatic defibrillator in resynchronization therapy for primary prevention in patients with idiopathic dilated cardiomyopathy is controversial.</AbstractText>We assessed a series of 46 patients (61 +/- 10 years, 64% male) with idiopathic dilated cardiomyopathy undergoing resynchronization therapy combined with a defibrillator in primary prevention and the potential relationship between baseline characteristics and the onset of ventricular arrhythmic events. Of the 46 patients included, eight (17%) presented episodes of ventricular tachycardia/fibrillation during follow-up (19 +/- 12 months). There were no baseline differences among these patients, except the proportion of males (57.9 vs. 100%, P = 0.02) and QRS width (162 +/- 24 vs. 189 +/- 26 ms, P = 0.008), which was the only independent predictor of arrhythmic events (OR 1.42, 95% CI 1.12-1.68; P = 0.03).</AbstractText>In patients with idiopathic dilated cardiomyopathy undergoing resynchronization therapy combined with a defibrillator, baseline QRS is an independent predictor of arrhythmic events.</AbstractText> |
6,158 | Biometal muscle to restore atrial transport function in a permanent atrial fibrillation animal model: a potential tool in the treatment of end-stage heart failure. | Half of the patients with end-stage heart failure suffer from persistent atrial fibrillation (AF). Atrial kick (AK) accounts for 10-15% of the ejection fraction. A device restoring AK should significantly improve cardiac output (CO) and possibly delay ventricular assist device (VAD) implantation. This study has been designed to assess the mechanical effects of a motorless pump on the right chambers of the heart in an animal model.</AbstractText>Atripump is a dome-shaped biometal actuator electrically driven by a pacemaker-like control unit. In eight sheep, the device was sutured onto the right atrium (RA). AF was simulated with rapid atrial pacing. RA ejection fraction (EF) was assessed with intracardiac ultrasound (ICUS) in baseline, AF and assisted-AF status. In two animals, the pump was left in place for 4 weeks and then explanted. Histology examination was carried out. The mean values for single measurement per animal with +/-SD were analysed.</AbstractText>The contraction rate of the device was 60 per min. RA EF was 41% in baseline, 7% in AF and 21% in assisted-AF conditions. CO was 7+/-0.5 l min(-1) in baseline, 6.2+/-0.5 l min(-1) in AF and 6.7+/-0.5 l min(-1) in assisted-AF status (p<0.01). Histology of the atrium in the chronic group showed chronic tissue inflammation and no sign of tissue necrosis.</AbstractText>The artificial muscle restores the AK and improves CO. In patients with end-stage cardiac failure and permanent AF, if implanted on both sides, it would improve CO and possibly delay or even avoid complex surgical treatment such as VAD implantation.</AbstractText>Copyright (c) 2009 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved.</CopyrightInformation> |
6,159 | Clinical, echocardiographic and histopathologic findings in nine patients with surgically explanted ASD/PFO devices: do we know enough about the healing process in humans? | Atrial septal defects (ASD) and persistent foramen ovale (PFO) are managed in increasing numbers by catheter interventions as an attractive alternative to surgery. Early complications have been described in clinical series whereas late complications are rare. No series are reported with clinical, echocardiographic and histological data.</AbstractText>We collected clinical, echocardiographic, and histolological data of nine patients with surgically explanted devices. Occlusion devices were explanted after a mean interval of 3.4 ± 2.4 years (range 0.9-8.3). Indications were recurrent thromboembolic events in five, residual shunt/dislocation in three, and growing mass on echocardiography despite oral anticoagulation in one patient. Two patients suffered potentially live threatening events due to coronary embolism. One of them had to be resuscitated due to ventricular fibrillation. Histologically, residues of superficial thrombus formation could be demonstrated in two of the devices. In another patient, hyperplastic tissue formation was related to a local inflammatory process but not to a thrombus as suspected by echocardiography.</AbstractText>Late complications after device implantation may occur up to 8 years after device implantation and may be potentially live threatening. Echocardiographic controls should be prolonged beyond the first year after implantation and every explanted device should be histologically worked up in an experienced center. Up to now, the mechanisms of late thrombogenesis are not fully understood.</AbstractText>Crown Copyright © 2009. Published by Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
6,160 | Renal function and long-term survival after hospital discharge in heart failure with preserved ejection fraction. | Baseline renal function and worsening of renal function (WRF) during hospitalization for heart failure (HF) have a major prognostic impact in patients with left ventricular systolic dysfunction.</AbstractText>We sought to prospectively investigate the impact of reduced baseline renal function and WRF during hospitalization on the 7-year outcome in 358 patients surviving a first admission to hospital for heart failure with preserved (≥ 50%) ejection fraction (HFPEF).</AbstractText>Mean baseline estimated glomerular filtration rate (eGFR) was 59.4 ± 23.6 ml/min/1.73 m². Low admission eGFR (<60 ml/min/1.73 m²) was frequently observed (190 patients--53% of the study population). Low baseline eGFR was associated with an increased risk of 7-year overall mortality (unadjusted hazard ratio [HR] 1.43[1.10-1.86]; p = 0.007) and cardiovascular mortality (unadjusted HR 1.57[1.13-2.19]; p = 0.007). After adjustment for covariates, the relationships remained significant. During hospitalization, WRF occurred in 43 patients (12%). History of renal failure, baseline systolic blood pressure >160 mm Hg, and baseline atrial fibrillation were independent predictors of the development of WRF during hospitalization. WRF was independently predictive of 7-year overall mortality (adjusted HR 2.10[1.24-3.58]; p = 0.006) and cardiovascular mortality (adjusted HR 2.54[1.35-4.78]; p = 0.004) in patients with low baseline eGFR but not in those with baseline eGFR ≥ 60 ml/min/1.73 m².</AbstractText>In patients admitted for the first time for HFPEF, low baseline eGFR is a potent predictor of long-term mortality. Patients with impaired renal function at baseline who develop WRF during hospitalization have particularly poor prognosis.</AbstractText>Copyright © 2009 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
6,161 | Right ventricular rupture induced by cardiopulmonary resuscitation. | Right ventricular rupture is a rare complication of cardiopulmonary resuscitation and could be fatal. We report a survival case of right ventricular rupture induced by cardiopulmonary resuscitation in a patient with acute myocardial infarction. A 57-year-old man was admitted to our hospital with ventricular fibrillation. Although chest compression and defibrillation were performed, ventricular fibrillation continued. We inserted a percutaneous cardiopulmonary system and performed coronary angiography, which revealed occlusion of the left anterior descending artery. After coronary stenting and intra-aortic balloon pumping, we succeeded in defibrillation and vital signs became stable. Twenty hours after the intervention, systolic blood pressure dropped to 60 mmHg. Ultrasonic cardiogram at that time revealed massive pericardial effusion. We diagnosed cardiac tamponade, and 8Fr drainage tube was placed in the pericardial space. We determined that emergent operation was necessary because we suspected left ventricular rupture due to acute myocardial infarction or coronary rupture induced by percutaneous coronary intervention. However, operative findings revealed right ventricular free wall rupture, which could have been induced by chest compression. In these cases, we should consider the possibility of not only the rupture of left ventricle and coronary artery but also the rupture of right ventricle induced by cardiopulmonary resuscitation. |
6,162 | Induced moderate hypothermia after cardiac arrest. | The use of induced hypothermia has been considered for treatment of head injuries since the 1900s. However, it was not until 2 landmark studies were published in 2002 that induced hypothermia was considered best practice for patients after cardiac arrest. In 2005, the American Heart Association included recommendations in the postresuscitation support guidelines recommending consideration of mild hypothermia for unconscious adult patients with return of spontaneous circulation following out-of-hospital cardiac arrest due to ventricular fibrillation. This article provides an overview on the history and supportive research for inducing mild hypothermia after cardiac arrest, the pathophysiology associated with cerebral ischemia occurring with hypothermia, nursing management for this patient population, and the development of a protocol for induced hypothermia after cardiac arrest. |
6,163 | Ability of terminal QRS notching to distinguish benign from malignant electrocardiographic forms of early repolarization. | Recent studies have suggested that early repolarization (ER) might be associated with up to 1/3 of idiopathic ventricular tachycardia/ventricular fibrillation (VT/VF) cases ("malignant" ER). We sought to identify electrocardiographic features to distinguish benign from malignant variants of ER. We reviewed the medical records for implantable-cardioverter defibrillators implanted at a single institution (1988 to 2008) to identify cases of idiopathic VT/VF. The electrocardiograms were scored for ER, defined as a >or=0.1-mV elevation of the QRS-ST junction manifesting as J-point slurring or notching in 2 contiguous leads. We also identified a cohort of 200 healthy age- and gender-matched controls with electrocardiographic findings previously identified as normal ER ("benign" ER cohort). Of 1,224 consecutive implantable-cardioverter defibrillator implants, we identified 39 cases of idiopathic VT/VF. Of the 39 cases, 9 (23%) demonstrated ER. During a mean follow-up of 7.2 +/- 4.6 years, the combined end point of appropriate implantable-cardioverter defibrillator shocks or all-cause mortality occurred less frequently in cases of idiopathic VT/VF with ER than in those without ER (11% vs 30%, odds ratio 0.29, 95% confidence interval 0.03 to 2.69, p = 0.40). A comparison of the electrocardiograms between those with malignant ER and controls demonstrated that QRS notching was significantly more prevalent among cases when present in leads V4 (44% vs 5%, p = 0.001) and V5 (44% vs 8%, p = 0.006), with a similar trend in lead V6 (33% vs 5%, p = 0.013). In conclusion, left precordial terminal QRS notching is more prevalent in malignant variants of ER than in benign cases. These findings could have important implications for risk stratification of patients with ER. |
6,164 | The acute effect of Metoprolol upon NT-proBNP level in patients with congestive heart failure. | Brain natriuretic peptide (BNP) is a sensitive and specific marker of left ventricular (LV) function. The acute effect of beta blockers upon plasma BNP levels in CHF patients has been less studied but it is important because of the initial possible depressing effect upon LV function.</AbstractText>To investigate the acute effect of oral Metoprolol upon plasma proBNP levels in CHF patients.</AbstractText>There were included 56 patients with congestive heart failure, 38 with ischemic heart disease and 18 with idiopathic dilated cardiomyopathy, 40 males and 16 females, aged between 25 and 65 years, who were compared with 19 healthy individuals, 12 males and 7 females, of the same age. All patients were free of beta blockers treatment. Plasma Nt-proBNP was determined in fasting state using ELISA method (NV <250 fmol/mL). After this, every patient received 50 mg Metoprolol succinate and at three hours (considered as peak plasmatic concentration) venous blood samples were again obtained and Nt-proBNP determined.</AbstractText>NT-pro BNP was increased (1400 +/- 130 fmol/mL) in heart failure patients and normal (187 +/- 17.2 fmol/mL) in healthy controls. After Metoprolol the plasmatic level of NT-proBNP was not significantly different in both healthy controls (162 +/- 13.3 fmol/mL) and heart failure patients (1419 +/- 133 fmol/ml) in comparison with baseline values. After Metoprolol NT-proBNP decreased (from 1266 +/- 121 to 1120 +/- 107, p>0.05) in III NYHA class patients and increased (from 1457 +/- 142 to 1530 +/- 150, p<0.05) in IV NYHA class patients. It remained unchanged in patients with LVEF >30% (1384 +/- 140 vs 1389 +/- 129 fmol/mL) and increased (from 1480 +/- 134 to 1690 +/- 161 fmol/mL, p<0.05) in patients with LVEF <30%; it was not significantly modified in patients with atrial fibrillation in comparison with those in sinus rhythm (1348 +/- 132 vs 1516 +/- 168 fmol/mL).</AbstractText>Beta blockers do not have a severe depressant effect on left ventricular performance in all patients with systolic heart failure. A LVEF>30% suggests, but the lack of modification of NT-proBNP levels after administration of 50 mg Metoprolol confirm, that the beta blocking treatment can be initiated with higher doses than those recommended until now.</AbstractText> |
6,165 | Cardiac resynchronization therapy in heart failure patients with atrial fibrillation. | Cardiac resynchronization therapy (CRT) is an important device-based, non-pharmacological approach that has shown, in large randomized trials, to improve left ventricular (LV) function and reduce both morbidity and mortality rates in selected patients affected by advanced heart failure (HF): New York Heart Association (NYHA) functional class III-IV, reduced LV systolic function with an ejection fraction (EF) <or=35%, QRS duration >or=120 ms, on optimal medical therapy, and who were in sinus rhythm. For the first time, the latest ESC and AHA/ACC/HRS Guidelines have considered atrial fibrillation (AF) patients, who constitute an important subgroup of HF patients, as eligible to receive CRT. Nevertheless, these Guidelines did not include a strategy for defining differentiated approaches according to AF duration or burden. In this review, the authors explain in which way AF may interfere with adequate CRT delivery, how to manage different AF burden, and finally present a brief overview on the effects of CRT in AF patients. |
6,166 | Dronedarone: a novel antiarrhythmic agent for the treatment of atrial fibrillation. | To describe the electrophysiological profile and the clinical portfolio of dronedarone, a new multichannel-blocking antiarrhythmic drug developed for the treatment of atrial fibrillation.</AbstractText>Dronedarone is a derivative of amiodarone that is free of iodine and less lipophilic. The drug has - as its predecessor - multichannel-blocking efficacy and in addition vasodilating effects. It reduces the incidence of ventricular fibrillation in several experimental models. Dronedarone has undergone thorough clinical evaluation in various patient populations. In two large trials, the drug was shown to postpone the recurrence of atrial fibrillation after cardioversion relative to placebo. In a trial in unstable heart failure patients, there was excess mortality in the dronedarone arm. This trial was stopped prematurely and prompted the conduct of a large outcome study. The ATHENA trial demonstrated a significant reduction in cardiovascular hospitalizations and death in atrial fibrillation patients randomly assigned to receive dronedarone or placebo. This large trial in more than 4600 patients revealed no signs of excess mortality or morbidity in patients receiving dronedarone.</AbstractText>On the basis of the results of five international, multicenter, randomized clinical trials involving nearly 6300 patients, dronedarone was approved by the FDA for treatment of nonpermanent atrial fibrillation to reduce the risk of cardiovascular hospitalization.</AbstractText> |
6,167 | Fragmented QRS and other depolarization abnormalities as a predictor of mortality and sudden cardiac death. | Several invasive and noninvasive tests for risk stratification of sudden cardiac death (SCD) have been studied. Tests such as microwave T wave alternans (repolarization abnormality) and signal-averaged ECG (depolarization abnormality) have high negative predictive values but low positive predictive values in patients with heart disease. The presence of a fragmented QRS (fQRS) complex on a routine 12-lead ECG is another marker of depolarization abnormality. The purpose of this review is to discuss the potential utility of tests to detect depolarization abnormalities of the heart for the risk stratification of mortality and SCD with main emphasis on fQRS.</AbstractText>fQRS is associated with increased mortality and arrhythmic events in patients with coronary artery disease. fQRS has also been defined as a marker of arrhythmogenic right ventricular cardiomyopathy and Brugada syndrome. In Brugada syndrome, the presence of fQRS predicts episodes of ventricular fibrillation during follow-up.</AbstractText>fQRS may be of value in determining the risk for SCD and guiding selection for device therapy in patients with structural heart disease and Brugada syndrome. It is possible that the predictive value of fQRS for SCD can be enhanced further by combining a marker of repolarization abnormality such as microwave T wave alternans.</AbstractText> |
6,168 | Left ventricular systolic dysfunction by itself does not influence outcome of atrial fibrillation ablation. | The objective of the study was to analyse the influence of left ventricular (LV) ejection fraction (EF) on the outcomes of atrial fibrillation (AF) ablation after a first procedure. Pre-procedural predictors of recurrences after AF ablation can be useful for patient information and selection of candidates. The independent influence of LV systolic dysfunction on recurrence rate has not been studied.</AbstractText>A case-control study (1:1) was conducted with a total of 72 patients: 36 cases (depressed LVEF) and 36 controls (normal LVEF). Patients were matched by left atrial diameter (LAD), the presence of arterial hypertension, and other variables that might influence the results (age, gender and paroxysmal vs. persistent AF). There were no statistical differences in the variables used to perform the matching. Patients with depressed LVEF had higher LV end diastolic diameter (55.6 +/- 6.2 vs. 52.4 +/- 5.5, P = 0.03), higher LV end systolic diameter (40.3 +/- 6.9 vs. 32.6 +/- 4.3, P < 0.001), lower LVEF (41.4 +/- 8.0 vs. 63.1 +/- 5.5, P < 0.001) and were more likely to have structural heart disease. After a mean follow-up of 16 +/- 13 months, survival analysis for AF recurrences showed no differences between patients with depressed vs. normal LVEF (50.0 vs. 55.6%, log rank = 0.82). Cox regression analysis revealed LAD to be the only variable correlated to recurrence [OR 1.11 (1.01-1.22), P = 0.03]. Analysis at 6 months showed a significant increase in LVEF (43.23 +/- 7.61 to 51.12 +/- 13.53%, P = 0.01) for the case group.</AbstractText>LV systolic dysfunction by itself is not a predictor of outcome after AF ablation. LAD independently correlates with outcome in patients with low or normal LVEF.</AbstractText> |
6,169 | Mode of onset of ventricular fibrillation in patients with early repolarization pattern vs. Brugada syndrome. | The aim of the present study was to identify specific electrocardiogram (ECG) features that predict the development of multiple episodes of ventricular fibrillation (VF) in patients with an early repolarization (ER) pattern and to compare the mode of VF initiation with that observed in typical cases of Brugada syndrome (BrS).</AbstractText>The mode of the onset and the coupling intervals of the premature ventricular contractions (PVCs) initiating VF episodes were analysed in patients with BrS (n = 8) or ER who experienced sudden cardiac death/syncope or repeated appropriate implantable cardioverter defibrillator shocks. Among the 11 patients with ER, 5 presented with electrical storm (ES, four or more recurrent VF episodes/day). The five ES patients displayed a dramatic but very transient accentuation of J waves across the precordial and limb leads prior to the development of ES. Ventricular fibrillation episodes were more commonly initiated by PVCs with a short-long-short (SLS) sequence in ER (42/58, 72.4%) vs. BrS patients (13/86, 15.1%, P < 0.01). Coupling intervals were significantly shorter in the ER group compared with those with BrS [328 (320, 340) ms vs. 395 (350, 404) ms, P < 0.01].</AbstractText>Our study provides additional evidence in support of the hypothesis that ER pattern in the ECG is not always benign. Transient augmentation of global J waves may be indicative of a highly arrhythmogenic substrate heralding multiple episodes of VF in patients with ER pattern. Ventricular tachycardia/VF initiation is more commonly associated with an SLS sequence, and PVCs display a shorter coupling interval in patients with ER pattern compared with those with BrS.</AbstractText> |
6,170 | Role of ischemic preconditioning and inflammatory response in the development of malignant ventricular arrhythmias after reperfused ST-elevation myocardial infarction. | Sustained ventricular tachycardia and ventricular fibrillation (VT/VF) are major complications of ST-elevation myocardial infarction (STEMI), even in the era of reperfusion therapy. We sought to clarify the determinants of VT/VF after reperfused STEMI.</AbstractText>Consecutive STEMI patients treated with primary percutaneous coronary intervention (n=457) were divided into 2 groups by the presence or absence of VT/VF during hospitalization. Serum C-reactive protein (CRP) level and peripheral white blood cell (WBC) count were serially measured. VT/VF was observed in 54 patients (12%). Prior infarction was more common and preinfarction angina was less in patients with VT/VF than those without. Peak CRP level (P < .0001), WBC count on admission (P=.008), and maximum WBC count (P=.0014) were higher in patients with VT/VF than those without. VT/VF, especially VT/VF later than 48 hours after onset, was associated with greater left ventricular (LV) dimension during convalescence. Kaplan-Meier curves and log-rank test revealed VT/VF to be a significant determinant of long-term major adverse cardiac events. Multivariate analysis revealed that prior infarction, absence of preinfarction angina, and peak CRP >or=10mg/dL were independent determinants of VT/VF.</AbstractText>Lack of ischemic preconditioning, enhanced inflammatory response, and subsequent LV dysfunction are related to the development of VT/VF after STEMI.</AbstractText> |
6,171 | Ventricular fibrillation by hypothermia in spinal fusion surgery: A case report. | A 63-year-old man was scheduled for T12-S1 posterolateral spinal fusion surgery. The patient's vital signs were stable and there were no specific laboratory findings except for high triglycerides. In addition, echocardiography showed mild left ventricular hypertrophy, but normal left ventricular function, no regional wall abnormal contractility and normal ejection fraction. During the operation, a warming blanket and fluid warmer were applied. Near the end of the operation, the blood pressure waveform from the radial artery and pulse oxymeter became flat. Cardiotonics were administered and an infusion of intraoperative salvage of blood was administered using the cell-saver. However, the hemodynamic status of the patient deteriorated to severe hypotension, with ventricular fibrillation. The patient's vital signs with temperature became stabilized after warming for 4 hours using active warming methods, including a forced air warming blanket and warming of the fluids and blood components with a rapid infusion system. |
6,172 | A case of myotonic dystrophy presenting with ventricular tachycardia and atrial fibrillation. | Myotonic dystrophy type 1 (MD1) is an autosomal dominant disorder characterized by myotonia, progressive muscular weakness, cataract, and cardiac involvement. Cardiac involvement is common and includes conduction system abnormalities, supraventricular and ventricular arrhythmias, and less frequently, myocardial dysfunction and ischemic heart disease. A 54-year-old woman with a previous diagnosis of MD1 was admitted with palpitation, blood pressure of 157/118 mmHg, and a heart rate of 220 beats/min. Electrocardiography (ECG) showed ventricular tachycardia. Within minutes, hemodynamic collapse developed and electrical cardioversion was performed. Immediately following cardioversion, ECG showed atrial fibrillation, a slightly prolonged QT interval, and intraventricular conduction delay. After intravenous infusion of amiodarone, the rhythm converted to sinus. Transthoracic echocardiography showed significantly depressed left ventricular function, an ejection fraction of 25%, and normal coronary arteries. During electrophysiological study, atrium-His interval and His-ventricle interval were 120 msec was 54 msec, respectively, and monomorphic ventricular flutter was induced. An implantable cardioverter-defibrillator was placed. She was discharged in sinus rhythm. |
6,173 | Tissue Doppler evaluation of the effects of major lung resection on cardiac functions. | The aim of our study was to evaluate the influence of lung resection on cardiac functions by using tissue Doppler echocardiography.</AbstractText>Nineteen consecutive patients (15 males, 4 females; mean age 55+/-8 years) undergoing major lung surgery (16 lobectomy, 3 pneumonectomy) were evaluated in a prospective design. Malignant lung cancer (n=15, 79%) was the major cause for lung surgery. Exclusion criteria were a history of myocardial infarction, angina, atrial fibrillation, valvular heart disease, major arrhythmias, diastolic dysfunction, heart surgery, and FEV1/FVC ratio lower than 60%. Two-dimensional Doppler echocardiography and tissue Doppler imaging (TDI) were performed one or two days before surgery and 4+/-2 weeks postoperatively.</AbstractText>Compared to the preoperative measurements, right and left atrial and ventricular dimensions did not differ after surgery (p>0.05). Left ventricular ejection fraction, left ventricular end-systolic and end-diastolic volumes were preserved postoperatively. The following Doppler parameters showed significant changes after surgery: mitral A wave (92+/-23 cm/sec vs. 105+/-27 cm/sec, p=0.005), mitral E/A ratio (1.0+/-0.2 vs. 0.8+/-0.2, p=0.001), tricuspid A wave (65+/-19 cm/sec vs. 80+/-30 cm/sec, p=0.006), and tricuspid E deceleration time (327+/-68 msec vs. 274+/-51 msec, p=0.01). Concerning TDI parameters, there were significant differences in mitral E'/A' ratio (1.0+/-0.4 vs. 0.8+/-0.3, p=0.03) and tricuspid E' wave (9+/-2 cm/sec vs. 8+/-3 cm/sec, p=0.03) after surgery.</AbstractText>Findings of our study suggest that systolic functions are preserved but diastolic functions are affected after major lung resection in a relatively short time period.</AbstractText> |
6,174 | Changes in connexin expression and the atrial fibrillation substrate in congestive heart failure. | Although connexin changes are important for the ventricular arrhythmic substrate in congestive heart failure (CHF), connexin alterations during CHF-related atrial arrhythmogenic remodeling have received limited attention.</AbstractText>To analyze connexin changes and their potential contribution to the atrial fibrillation (AF) substrate during the development and reversal of CHF.</AbstractText>Three groups of dogs were studied: CHF induced by 2-week ventricular tachypacing (240 bpm, n=15); CHF dogs allowed a 4-week nonpaced recovery interval after 2-week tachypacing (n=16); and nonpaced sham controls (n=19). Left ventricular (LV) end-diastolic pressure and atrial refractory periods increased with CHF and normalized on CHF recovery. CHF caused abnormalities in atrial conduction indexes and increased the duration of burst pacing-induced AF (DAF, from 22+/-7 seconds in control to 1100+/-171 seconds, P<0.001). CHF did not significantly alter overall atrial connexin (Cx)40 and Cx43 mRNA and protein expression levels, but produced Cx43 dephosphorylation, increased Cx40/Cx43 protein expression ratio and caused Cx43 redistribution toward transverse cell-boundaries. All of the connexin-alterations reversed on CHF recovery, but CHF-induced conduction abnormalities and increased DAF (884+/-220 seconds, P<0.001 versus control) remained. The atrial fibrous tissue content increased from 3.6+/-0.7% in control to 14.7+/-1.5% and 13.3+/-2.3% in CHF and CHF recovery, respectively (both P<0.01 versus control), with transversely running zones of fibrosis physically separating longitudinally directed muscle bundles. In an ionically based action potential/tissue model, fibrosis was able to account for conduction abnormalities associated with CHF and recovery.</AbstractText>CHF causes atrial connexin changes, but these are not essential for CHF-related conduction disturbances and AF promotion, which are rather related primarily to fibrotic interruption of muscle bundle continuity.</AbstractText> |
6,175 | Triggering of nocturnal arrhythmias by sleep-disordered breathing events. | This study sought to evaluate respiratory disturbances as potential triggers for arrhythmia in patients with sleep-disordered breathing (SDB).</AbstractText>SDB is associated with an increased risk of atrial fibrillation and nonsustained ventricular tachycardia (NSVT) as well as a predilection for sudden cardiac death during nocturnal sleeping hours. However, prior research has not established whether respiratory disturbances operate as triggers for nocturnal arrhythmias.</AbstractText>Overnight polysomnograms from the Sleep Heart Health Study (n = 2,816) were screened for paroxysmal atrial fibrillation and NSVT. We used the case-crossover design to determine whether apneas and/or hypopneas are temporally associated with episodes of paroxysmal atrial fibrillation or NSVT. For each arrhythmia, 3 periods of sinus rhythm were identified as control intervals. Polysomnograms were examined for the presence of respiratory disturbances, oxygen desaturations, and cortical arousals within a 90-s hazard period preceding each arrhythmia or control period.</AbstractText>Fifty-seven participants with a wide range of SDB contributed 62 arrhythmias (76% NSVT). The odds of an arrhythmia after a respiratory disturbance were nearly 18 times (odds ratio: 17.5; 95% confidence interval: 5.3 to 58.4) the odds of an arrhythmia occurring after normal breathing. The absolute rate of arrhythmia associated with respiratory disturbances was low (1 excess arrhythmia per 40,000 respiratory disturbances). Neither hypoxia nor electroencephalogram-defined arousals alone increased arrhythmia risk.</AbstractText>Although the absolute arrhythmia rate is low, the relative risk of paroxysmal atrial fibrillation and NSVT during sleep is markedly increased shortly after a respiratory disturbance. These results support a direct temporal link between SDB events and the development of these arrhythmias.</AbstractText> |
6,176 | Ventricular arrhythmia in coronary artery disease: limits of a risk stratification strategy based on the ejection fraction alone and impact of infarct localization. | Estimates of the left ventricular ejection fraction (LVEF) in patients with life-threatening ventricular arrhythmias related to coronary artery disease (CAD) have rarely been reported despite it has become the basis for determining patient's eligibility for prophylactic defibrillator. We aimed to determine the extent and distribution of reduced LVEF in patients with sustained ventricular tachycardia or ventricular fibrillation.</AbstractText>252 patients admitted for ventricular arrhythmia related to CAD were included: 149 had acute myocardial infarction (MI) (Group I, 59%), 54 had significant chronic obstructive CAD suggestive of an ischaemic arrhythmic trigger (Group II, 21%) and 49 patients had an old MI without residual ischaemia (Group III, 19%). 34% of the patients with scar-related arrhythmias had an LVEF > or =40%. Based on pre-event LVEF evaluation, it can be estimated that less than one quarter of the whole study population had a known chronic MI with severely reduced LVEF. In Group III, the proportion of inferior MI was significantly higher than anterior MI (81 vs. 19%; absolute difference, -62; 95% confidence interval, -45 to -79; P < or = 0.0001), though median LVEF was higher in inferior MI (0.37 +/- 10 vs. 0.29 +/- 10; P = 0.0499).</AbstractText>Patients included in defibrillator trials represent only a minority of the patients at risk of sudden cardiac death. By applying the current risk stratification strategy based on LVEF, more than one third of the patients with old MI would not have qualified for a prophylactic defibrillator. Our study also suggests that inferior scars may be more prone to ventricular arrhythmia compared to anterior scars.</AbstractText> |
6,177 | Incidence of paroxysmal atrial tachycardias in patients treated with cardiac resynchronization therapy and continuously monitored by device diagnostics. | Little is known about the incidence of paroxysmal atrial tachycardias (PAT) in patients with heart failure (HF). The availability of cardiac resynchronization therapy (CRT) devices with extended diagnostics for AT enables continuous monitoring of PAT episodes. The aim of the study was to assess the incidence over time of PAT in HF patients treated with CRT.</AbstractText>Consecutive patients in NYHA functional class III or IV despite optimal drug therapy, QRS duration > or = 130 ms, left ventricular ejection fraction < or = 35%, and left ventricular end-diastolic dimension > or = 55 mm were eligible for enrolment. Patients with permanent or persistent atrial fibrillation (AF) were not included in the study. The first follow-up examination was performed 2 weeks after implantation, to optimize atrial sensing and CRT. Subsequent follow-up examinations were carried out 15 and 28 weeks after implantation, to collect the telemetric data. A total of 173 patients (67 +/- 11 years, M 116) were enrolled. Complete arrhythmia monitoring data were available from 120 patients over a mean follow-up of 183 +/- 23 days. Atrial tachycardia episodes were detected through telemetry in 25 of 120 patients (21%) during at least one follow-up examination. Atrial tachycardia episodes were recorded in 29 and 17% (P = NS) of patients with and without previous history of AF, respectively.</AbstractText>More than 20% of the overall HF patient population treated with CRT suffer PAT episodes. Paroxysmal atrial tachycardia may interfere with response to CRT. Therefore, telemetric data may be relevant to drive the appropriate therapy in each patient.</AbstractText> |
6,178 | Thrombus formation due to flow competition after apico-aortic conduit. | We report a case of unusual thrombus formation and describe the risk of perioperative myocardial infarction or stroke in severe aortic stenosis after apico-aortic conduit. An 86-year-old woman was admitted with aggravation of dyspnoea on exertion and chest pain. She was complicated with severe aortic stenosis and liver cirrhosis. Echocardiography demonstrated a peak pressure gradient of 50 mmHg across the aortic valve with ejection fraction of 51%. Since she had porcelain aorta and severe liver dysfunction, we selected an apico-aortic conduit under left ventricular fibrillation as treatment. Postoperative computed tomography showed a large thrombus in the descending aorta. Using strict anticoagulation therapy, the thrombus almost disappeared and thrombo-embolic events did not occur after surgery. |
6,179 | Hypertension and atrial fibrillation. | Atrial fibrillation (AF) is an emerging public health problem. The most important risk factor for developing chronic AF is uncontrolled hypertension. Uncontrolled hypertension promotes the initiation and perpetuation of AF through atrial remodeling. Experimental evidence has demonstrated the important role of the renin-angiotensin system in atrial remodeling. Retrospective analysis of several large clinical trials and small prospective trials suggests the beneficial role of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in preventing the onset and recurrence of AF in different populations. Several large prospective trials with longer follow-up periods are in progress. These trials may provide definitive evidence for the use of these agents in the prevention of AF. |
6,180 | The genetic basis of long QT and short QT syndromes: a mutation update. | Long QT and short QT syndromes (LQTS and SQTS) are cardiac repolarization abnormalities that are characterized by length perturbations of the QT interval as measured on electrocardiogram (ECG). Prolonged QT interval and a propensity for ventricular tachycardia of the torsades de pointes (TdP) type are characteristic of LQTS, while SQTS is characterized by shortened QT interval with tall peaked T-waves and a propensity for atrial fibrillation. Both syndromes represent a high risk for syncope and sudden death. LQTS exists as a congenital genetic disease (cLQTS) with more than 700 mutations described in 12 genes (LQT1-12), but can also be acquired (aLQTS). The genetic forms of LQTS include Romano-Ward syndrome (RWS), which is characterized by isolated LQTS and an autosomal dominant pattern of inheritance, and syndromes with LQTS in association with other conditions. The latter includes Jervell and Lange-Nielsen syndrome (JLNS), Andersen syndrome (AS), and Timothy syndrome (TS). The genetics are further complicated by the occurrence of double and triple heterozygotes in LQTS and a considerable number of nonpathogenic rare polymorphisms in the involved genes. SQTS is a very rare condition, caused by mutations in five genes (SQTS1-5). The present mutation update is a comprehensive description of all known LQTS- and SQTS-associated mutations. |
6,181 | A comparison between monophasic and biphasic defibrillation for the cardioversion of persistent atrial fibrillation in patients with and without heart failure. | Atrial fibrillation (AF) and heart failure commonly coexist. Restoring sinus rhythm using external direct current cardioversion (DCCV) may improve left ventricular function, exercise capacity and quality of life (QoL). However, DCCV may be less successful at restoring sinus rhythm in patients with heart failure. We aimed to determine whether biphasic DCCV was superior to monophasic DCCV for the restoration of sinus rhythm in patients with heart failure.</AbstractText>592 consecutive cardioversion procedures were performed on 503 patients for persistent AF, 261 (44%) procedures using monophasic defibrillation and 331 (56%) using biphasic. Patients with symptomatic heart failure were identified for further analysis.</AbstractText>173 cardioversions were performed on 149 patients with heart failure. The overall success rate of cardioversion in this group was 82.7% (83.3% and 82.2% for monophasic and biphasic respectively). There was no difference in the success rate of cardioversion for those with heart failure compared to those without heart failure (p = 0.141). Furthermore, there was no substantial difference in success rates according to defibrillation type (83.3% v. 84.2% for monophasic and 82.2% v. 88.5% for biphasic, p = 0.502 and 0.085 respectively).</AbstractText>External defibrillation is similarly effective at restoring SR in patients with and without HF and both mono- and biphasic shocks have a high rate of success. However, significantly less energy (maximal and cumulative) is required to restore SR using biphasic defibrillation.</AbstractText>Copyright © 2009 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
6,182 | Relationship of indices of inflammation and thrombogenesis to arrhythmia burden in paroxysmal atrial fibrillation. | Atrial fibrillation (AF) is associated with a high risk of stroke. The contribution of arrhythmia to events is clear in sustained forms of AF, but in paroxysmal AF, presently available data have yet to identify what proportion of time spent in AF (ie, arrhythmia burden [AFB]) is of clinical relevance. We aimed to assess this relationship using surrogate blood markers for the hypercoagulable state associated with AF.</AbstractText>One hundred twenty-one consecutive outpatients (mean age 74.7 +/- 7.8 years; 73 [60.3%] men) with pacemakers capable of arrhythmia detection were recruited. AFB was assessed over a 1-month period and classified as AFB = 0%, 0.1% to 10%, 10.1% to 50%, or > 50%.</AbstractText>Baseline characteristics and comorbidities were comparable between groups. There were no significant differences in levels of soluble E-selectin (sE-selectin), von Willebrand factor (vWf), high-sensitivity C-reactive protein, interleukin-6, soluble P-selectin (sP-selectin), or tissue factor (TF) across the four patient groups. Levels of plasma brain natriuretic peptide (BNP) were approximately twofold greater in the group with the highest AFB (P < .001). Following a stepwise multiple linear regression analysis, age was a significant predictor of vWf (P = .010), sP-selectin (P = .042), and BNP (P = .012). Left ventricular fractional shortening was predictive of BNP (P = .001) and sE-selectin (P = .012). Anticoagulation was a predictor of vWf levels (P = .005), and hypertension was predictive of TF (P < .001).</AbstractText>Given no appreciable difference in levels of prothrombotic markers in relation to AFB in this study, it is plausible that these abnormalities do, in fact, relate to underlying risk factors, and that such patients should be anticoagulated if risk factors dictate. Thus, AFB per se should probably not influence the decision to anticoagulate, but rather the presence of AF combined with clinical risk scoring should remain the predominant tool for stroke risk assessment.</AbstractText> |
6,183 | Hypothermia and postconditioning after cardiopulmonary resuscitation reduce cardiac dysfunction by modulating inflammation, apoptosis and remodeling. | Mild therapeutic hypothermia following cardiac arrest is neuroprotective, but its effect on myocardial dysfunction that is a critical issue following resuscitation is not clear. This study sought to examine whether hypothermia and the combination of hypothermia and pharmacological postconditioning are cardioprotective in a model of cardiopulmonary resuscitation following acute myocardial ischemia.</AbstractText><AbstractText Label="METHODOLOGY/PRINCIPAL FINDINGS" NlmCategory="RESULTS">Thirty pigs (28-34 kg) were subjected to cardiac arrest following left anterior descending coronary artery ischemia. After 7 minutes of ventricular fibrillation and 2 minutes of basic life support, advanced cardiac life support was started according to the current AHA guidelines. After successful return of spontaneous circulation (n = 21), coronary perfusion was reestablished after 60 minutes of occlusion, and animals were randomized to either normothermia at 38 degrees C, hypothermia at 33 degrees C or hypothermia at 33 degrees C combined with sevoflurane (each group n = 7) for 24 hours. The effects on cardiac damage especially on inflammation, apoptosis, and remodeling were studied using cellular and molecular approaches. Five animals were sham operated. Animals treated with hypothermia had lower troponin T levels (p<0.01), reduced infarct size (34+/-7 versus 57+/-12%; p<0.05) and improved left ventricular function compared to normothermia (p<0.05). Hypothermia was associated with a reduction in: (i) immune cell infiltration, (ii) apoptosis, (iii) IL-1beta and IL-6 mRNA up-regulation, and (iv) IL-1beta protein expression (p<0.05). Moreover, decreased matrix metalloproteinase-9 activity was detected in the ischemic myocardium after treatment with mild hypothermia. Sevoflurane conferred additional protective effects although statistic significance was not reached.</AbstractText><AbstractText Label="CONCLUSIONS/SIGNIFICANCE" NlmCategory="CONCLUSIONS">Hypothermia reduced myocardial damage and dysfunction after cardiopulmonary resuscitation possible via a reduced rate of apoptosis and pro-inflammatory cytokine expression.</AbstractText> |
6,184 | Treatment and outcome of patients after cardiopulmonary resuscitation admitted to the intensive cardiac care unit. | Sudden circulatory arrest is most often of cardiac origin. Our aim was to evaluate circulatory arrest etiology and treatment strategies in patients after cardiopulmonary resuscitation (CPR) with persistent impairment of consciousness in relation to survival and the subsequent quality of life.</AbstractText>Retrospective analysis of patients after CPR treated according to the local protocol including mild hypothermia in the intensive cardiac care unit.</AbstractText>Over 2 years, we admitted 57 mechanically ventilated patients after CPR. 47 patients (82%) were resuscitated outside the hospital. In 33 patients (58%) the initial rhythm was ventricular fibrillation; in the remaining patients (42%) asystole/pulseless electrical activity. Urgent coronary angiography was performed in 36 patients and percutaneous coronary intervention in 25 of them. The admission APACHE II score was 32,4 +/- 3,4 with predicted mortality of 77,1%. The hospital survival rate was 54% and 47% of the patients were discharged home in a good state of health (Glasgow outcome score 4-5).</AbstractText>Our results suggest that comprehensive post-resuscitation care including therapeutic hypothermia and percutaneous coronary intervention in selected cases may have a positive impact on the prognosis of patients after CPR.</AbstractText> |
6,185 | Predictors of sudden cardiac death change with time after myocardial infarction: results from the VALIANT trial. | To determine whether predictors of sudden cardiac death (SCD) vary with time after myocardial infarction (MI).</AbstractText>We analysed 11 256 patients enrolled in VALIANT. Landmark analysis and Cox proportional hazards modelling were used to predict SCD during hospitalization, from discharge to 30 days, 30 days to 6 months, and 6 months to 3 years. The cumulative incidence of SCD was 8.6% (n = 965). Initially, higher baseline heart rate [HR 1.20 per 10 b.p.m. (95% CI 1.06-1.37)] and impaired baseline creatinine clearance [HR 0.82 per 10 mL/min (95% CI 0.74-0.91)] were stronger predictors of SCD. With long-term follow-up, prior MI [HR 1.71 (95% CI 1.39-2.10)], initial left ventricular ejection fraction <40% [HR 0.67 per 10% (95% CI 0.58-0.78)], and recurrent cardiovascular events [HR 1.47 for rehospitalization (95% CI 1.17-1.86)] were more robust risk stratifiers for SCD. Atrial fibrillation post-MI was associated with an increased risk of SCD over the entire follow-up period. As time passed, the associations between baseline clinical characteristics and SCD decreased and time-updated assessments became more important.</AbstractText>Predictors of SCD change with time after MI. Future studies of risk stratification for SCD should account for changes in these factors with time after MI.</AbstractText> |
6,186 | Cariporide given during resuscitation promotes return of electrically stable and mechanically competent cardiac activity. | Episodes of ventricular fibrillation (VF) and myocardial dysfunction commonly occur after cardiac resuscitation compromising the return of stable circulation. We investigated in a pig model of VF whether limiting Na(+)-induced cytosolic Ca(2+) overload using the sarcolemmal sodium-hydrogen exchanger isoform-1 (NHE-1) inhibitor cariporide promotes resuscitation with stable circulation.</AbstractText>VF was electrically induced in 20 male pigs and left untreated for 6 min after which CPR was initiated and continued for 8 min before attempting defibrillation. Pigs were randomized to receive 3-mg/kg cariporide (n=10) or 0.9%-NaCl (n=10) before chest compression.</AbstractText>Seven of 10 pigs in each group were successfully resuscitated and survived 2h. Cariporide ameliorated post-resuscitation ventricular ectopic activity such that fewer singlets (5+/-5 vs. 26+/-21; p<0.05) and fewer bigemini (1+/-3 vs. 33+/-25; p<0.05) were observed during the initial 5 min post-resuscitation. Additionally, cariporide-treated pigs did not require additional post-resuscitation shocks for ventricular tachycardia or recurrent VF (0.0+/-0.0 vs. 5.3+/-7.8 shocks; p=0.073). During the initial 60 min cariporide-treated pigs had higher, cardiac index (6.1+/-0.7 vs. 4.4+/-1.1L/min/m(2); p<0.01), left ventricular stroke work index (45+/-9 vs. 36+/-10 gmm/beat/m(2); p<0.05), and numerically higher mean aortic pressure (104+/-11 vs. 91+/-12 mmHg; p=0.054).</AbstractText>Cariporide administered at the start of chest compression may help restore electrically and mechanically stable circulation after resuscitation from cardiac arrest.</AbstractText>Copyright 2009 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
6,187 | Benefit of facilitated percutaneous coronary intervention in high-risk ST-segment elevation myocardial infarction patients presenting to nonpercutaneous coronary intervention hospitals. | We hypothesized that patients most likely to benefit would be those at high risk with a shorter duration of acute ischemia and who required transfer for percutaneous coronary intervention (PCI).</AbstractText>The FINESSE (Facilitated Intervention with Enhanced Reperfusion Speed to Stop Events) study failed to demonstrate an improvement in the 90-day composite clinical end point of early treatment with abciximab plus half-dose reteplase (combination-facilitated PCI) or abciximab alone.</AbstractText>We performed a retrospective analysis of 2,452 patients in this double-blind, placebo-controlled study. Patients were stratified by Thrombolysis In Myocardial Infarction (TIMI) risk score for ST-segment elevation myocardial infarction (STEMI), presentation to a spoke (no PCI available) or hub site, and symptom-to-randomization time. Outcomes included the primary composite end point of death, ventricular fibrillation after 48 h, cardiogenic shock, and congestive heart failure through day 90 as well as 1-year mortality.</AbstractText>Mortality for all patients at 1 year was directly related to TIMI risk score (23 of 1,223 = 1.9% in patients with score <3 and 145 of 1,229 = 11.8% with score > or =3, p < 0.001). Patients with TIMI risk score > or =3 and presentation to a spoke site with a symptom-to-randomization time < or =4 h had significantly better 1-year survival if treated with combination-facilitated PCI (hazard ratio [HR]: 0.351, p = 0.01) as well as 90-day composite outcome (HR: 0.45, p = 0.009). A trend for improved survival was also observed in patients with TIMI score > or =3 and spoke site alone (HR: 0.549, p = 0.06).</AbstractText>Facilitation of PCI with a combination of abciximab and half-dose reteplase improved survival at 1 year in high-risk patients presenting to a spoke hospital with symptom-to-randomization time < or =4 h. Further prospective study of facilitated PCI in this subgroup of patients is warranted.</AbstractText> |
6,188 | The utility of transoesophageal echocardiography to determine management in suspected embolic stroke. | Assessment for source of stroke is a common indication for transoesophageal echocardiography (TOE). Although an abnormality is frequently found, it remains uncertain how frequently the findings alter patient management. Also, the role of transthoracic echocardiography (TTE) prior to or instead of TOE is not well defined. We sought to determine the use of TTE prior to TOE, the outcome of the TOE and its impact on management.</AbstractText>We retrospectively reviewed the records and echocardiography results of 100 consecutive patients who underwent TOE for any reason at a tertiary hospital. In 35 subjects (35%), the indication was evaluation for source of stroke. Among these, we determined clinical risk factors for stroke, if a TTE was performed prior to their TOE, the results of the TOE and its effect on management.</AbstractText>The mean age of the stroke patients was 64.6 years (17-90) and 49% were women. Eighty per cent had at least one risk factor for stroke and 17% had atrial fibrillation. A TTE, performed in 40% prior to the TOE, found an abnormality in 14% (2/14). The TOE showed an abnormality in 71% of patients; 54% had aortic atheroma; 17% PFO; 14% spontaneous echo contrast; 6% left atrial appendage thrombus, 3% left ventricular thrombus and 3% vegetation. In only one patient (3%) the management was altered based on the abnormal TOE findings.</AbstractText>An abnormality on TOE, although common (71%) and more sensitive than TTE, altered management in only 3% of subjects referred for stroke assessment. Its role requires further consideration.</AbstractText>© 2010 The Authors. Internal Medicine Journal © 2010 Royal Australasian College of Physicians.</CopyrightInformation> |
6,189 | Prime time use of tissue Doppler echocardiography: what have we gained? | In daily practice, Tissue Doppler Echocardiography (TDI) is used to estimate left ventricular filling pressures, categorize diastolic dysfunction, identify patients with heart failure (HF) with normal ejection fraction, differentiate constrictive pericarditis from restrictive cardiomyopathy, to prognosticate acute coronary syndrome, valvular heart disease syndrome of HF etc, correlate exercise capacity and symptoms, differentiate physiological versus pathological hypertrophy, assessment of intraventricular dyssynchrony, regional and global systolic and diastolic properties, detection of right ventricular function and possible carriers of genetic cardiomyopathies like Fabry's disease and hypertrophic cardiomyopathy, etc. Its role in adding incremental value to stress echocardiography, subclinical dysfunction evaluation, cardiac transplant rejection, cardiotoxicity of anti-cancer drugs, predicting occurrence and reversion of atrial fibrillation, predicting aortic catastrophies etc, although very encouraging has not found many users. It was intuitively considered invaluable in detecting subclinical myocarditis, acute rheumatic fever, Chaga's disease and localization of atrioventricular accessory pathways with manifest conduction, but could not find prime time readiness. In a similar manner, tissue-velocity derived deformation parameters have not found prime time use, despite making great inroads into the mysteries of muscle mechanics. Part of the problem lies in their emphasis on unidirectional information of a structure which is essentially multidimensional. The other problems have been angle-dependency and low signal-to-noise ratio in deformation imaging which has restricted its use to highly experienced operators rather than more democratic use. Validation studies did indicate its great potential. TDI-derived imaging paved the way for non-Doppler multidimensional deformation imaging which is slowly gaining ground. |
6,190 | Inherited cardiac diseases caused by mutations in the Nav1.5 sodium channel. | A prerequisite for a normal cardiac function is a proper generation and propagation of electrical impulses. Contraction of the heart is obtained through a delicate matched transmission of the electrical impulses. A pivotal element of the impulse propagation is the depolarizing sodium current, responsible for the initial depolarization of the cardiomyocytes. Recent research has shown that mutations in the SCN5A gene, encoding the cardiac sodium channel Nav1.5, are associated with both rare forms of ventricular arrhythmia, as well as the most frequent form of arrhythmia, atrial fibrillation (AF). In this comprehensive review, we describe the functional role of Nav1.5 and its associated proteins in propagation and depolarization both in a normal- and in a pathophysiological setting. Furthermore, several of the arrhythmogenic diseases, such as long-QT syndrome, Brugada syndrome, and AF, reported to be associated with mutations in SCN5A, are thoroughly described. |
6,191 | Limited response to cardiac resynchronization therapy in patients with concomitant right ventricular dysfunction. | Patients with left ventricular dysfunction (LVD) and LV dyssynchrony may respond to cardiac resynchronization therapy (CRT). However, right ventricular dysfunction (RVD) is a predictor of decreased survival in patients with LVD, and its influence on clinical response to CRT is unknown. The purpose of this study was to examine the effect of RVD on the clinical response to CRT.</AbstractText>A retrospective cohort of consecutive patients who underwent implantation of a CRT implantable cardioverter-defibrillator (ICD) were included and deemed to have RVD based on a RV ejection fraction <0.40. A lack of response to CRT was defined as: death, heart transplantation, implantation of an LV assist device, absent improvement in NYHA functional class at 6 months or hospice care. Among 130 patients included (mean age 58 +/- 11 years, 68.5% male, 87.7% Caucasian, 51.5% nonischemic cardiomyopathy), 77 (59.2%) had no response to CRT as defined above. Of the nonresponders, 43 (56%) had RVD and 34 (44%) did not have RVD (P = 0.02). After adjustment for age, race, gender, cardiomyopathy type, atrial fibrillation, serum sodium, and severe mitral regurgitation, RVD (adjusted OR = 0.34, 95%CI 0.14-0.82), female gender (adjusted OR = 0.36, 95%CI 0.14-0.95), and serum creatinine (adjusted OR = 0.25, 95%CI 0.09-0.71) were independently associated with decreased odds of response to CRT. There was a significant difference in survival of patients with and without RVD after CRT (log rank P = 0.01).</AbstractText>RVD represents a strong predictor of lack of clinical response to CRT in patients with CHF due to LVD and should be considered when prescribing CRT.</AbstractText> |
6,192 | Identification of hemodynamically unstable arrhythmias using subcutaneous photoplethysmography. | Determination of hemodynamic status is central to arrhythmia management in the inpatient setting. In contrast, therapy decisions in implantable cardioverter defibrillators (ICDs) are based exclusively on the arrhythmia's electrical signature. Hemodynamic sensing in ICDs would allow tailoring of therapy according to perfusion status. Subcutaneous photoplethysmography (PPG) is an attractive technology for this application because it responds to changes in arterial pressure and can be readily incorporated into the housing of implanted devices. This study evaluated the accuracy of PPG in identifying hemodynamically unstable simulated arrhythmias in an animal model.</AbstractText>Rapid atrial and ventricular pacing was used to simulate arrhythmias in an acute preparation of 7 healthy dogs. Aortic pressure and subcutaneous PPG were simultaneously recorded. Simulated arrhythmias were defined as hemodynamically unstable if aortic pressure decreased by >or=15 mmHg, marginally unstable if pressure decreased by 5-15 mmHg, and hemodynamically stable if pressure either increased or decreased by no more than 5 mmHg. An average of 56 arrhythmias were simulated in each animal. Changes in pressure and PPG output were highly correlated, with correlation coefficient of 0.7-0.9. Subcutaneous PPG identified hemodynamically unstable episodes with a sensitivity of 100% for 6 subjects and 80% for 1 subject. Specificity was more than 90% for 6 subjects and was 50% for 1 subject.</AbstractText>Subcutaneous PPG detects hemodynamically unstable simulated arrhythmias in an acute canine preparation. If successfully validated in humans, this technology may allow ICD therapy to be specifically tailored according to the hemodynamic status of the arrhythmia.</AbstractText> |
6,193 | Automatic detection and classification of human epicardial atrial unipolar electrograms. | This paper describes an unsupervised signal processing method applied to three-channel unipolar electrograms recorded from human atria. These were obtained by epicardial wires sutured on the right and left atria after coronary artery bypass surgery. Atrial (A) and ventricular (V) activations had to be detected and identified on each channel, and gathered across the channels when belonging to the same global event. The algorithm was developed and optimized on a training set of 19 recordings of 5 min. It was assessed on twenty-seven 2 h recordings taken just before the onset of a prolonged atrial fibrillation for a total of 1593697 activations that were validated and classified as normal atrial or ventricular activations (A, V) and premature atrial or ventricular activations (PAA, PVA). 99.93% of the activations were detected, and amongst these, 99.89% of the A and 99.75% of the V activations were correctly labelled. In the subset of the 39705 PAA, 99.83% were detected and 99.3% were correctly classified as A. The false positive rate was 0.37%. In conclusion, a reliable fully automatic detection and classification algorithm was developed that can detect and discriminate A and V activations from atrial recordings. It can provide the time series needed to develop a monitoring system aiming to identify dynamic predictors of forthcoming cardiac events such as postoperative atrial fibrillation. |
6,194 | Short-term memory and restitution during ventricular fibrillation in human hearts: an in vivo study. | Action potential duration (APD) variation is an important determinant of wave break and reentry. The determinants of APD variability during early ventricular fibrillation (VF) in myopathic human hearts have not been studied. The objective of this study was to study the role of APD restitution and short-term cardiac memory on variation in human VF.</AbstractText>The study consisted of 7 patients (67+/-9 years old) with ejection fraction <35%. Monophasic action potentials were recorded from the right and/or left ventricular septum during VF. APD(60/90) was measured in sinus beat preceding induction of VF, and its amplitude was used to define 60%/90% repolarization in VF. The monophasic action potential upstroke (dV/dt(max)) was used to characterize local excitability. Simple linear regression showed that variability in APD(n60) was determined by APD/diastolic interval restitution (R(2)=0.48, P<0.0001) and short-term memory (APD(60) n-1, n-2, n-3, n-4; R(2)=0.55, 0.40, 0.33, and 0.27 respectively; P<0.001). Using multiple stepwise regression, short-term memory and restitution accounted for 62% of variance in APD(60) (P<0.001). Individually, memory effect had the greatest contribution to APD variability (R(2)=0.55, P<0.0001).</AbstractText>In early human VF, short-term memory and APD/diastolic interval restitution explain most of the APD variability, with memory effects predominating. This suggests that in early human VF, short-term cardiac memory may provide a novel therapeutic target to modulate progression of VF in myopathic patients.</AbstractText> |
6,195 | Long-term prognosis of probands with Brugada-pattern ST-elevation in leads V1-V3. | The prognosis of patients with saddleback or noncoved type (non-type 1) ST-elevation in Brugada syndrome is unknown. The purpose of this study was to clarify the long-term prognosis of probands with non-type 1 ECG and those with coved (type 1) Brugada-pattern ECG.</AbstractText>A total of 330 (123 symptomatic, 207 asymptomatic) probands with a coved or saddleback ST-elevation > or = 1 mm in leads V(1)-V(3) were divided into 2 ECG groups-type 1 (245 probands) and non-type 1 (85 probands)-and were prospectively followed for 48.7+/-15.0 months. The absence of type 1 ECG was confirmed by drug provocation test and multiple recordings. The ratio of individuals with a family history of sudden cardiac death (14%) was lower than previous studies. Clinical profiles and outcomes were not notably different between the 2 groups (annual arrhythmic event rate of probands with ventricular fibrillation; type 1: 10.2%, non-type 1: 10.6%, probands with syncope; type 1: 0.6%, non-type 1: 1.2%, and asymptomatic probands; type 1: 0.5%, non-type 1: 0%). Family history of sudden cardiac death at age <45 years and coexistence of inferolateral early repolarization with Brugada-pattern ECG were independent predictors of fatal arrhythmic events (hazard ratio, 3.28; 95% confidence interval, 1.42 to 7.60; P=0.005; hazard ratio, 2.66; 95% confidence interval, 1.06 to 6.71; P=0.03, respectively, by multivariate analysis), although spontaneous type 1 ECG and ventricular fibrillation inducibility by electrophysiological study were not reliable parameters.</AbstractText>The long-term prognosis of probands in non-type 1 group was similar to that of type 1 group. Family history of sudden cardiac death and the presence of early repolarization were predictors of poor outcome in this study, which included only probands with Brugada-pattern ST-elevation.</AbstractText> |
6,196 | Relationship of paroxysmal atrial tachyarrhythmias to volume overload: assessment by implanted transpulmonary impedance monitoring. | Clinical experience suggests that atrial tachyarrhythmias (ATs) are a frequent comorbidity in heart failure patients with left ventricular systolic dysfunction and that volume overload may increase AT susceptibility. However, substantiating this apparent relationship in free-living patients is difficult. Recently, certain implantable cardioverter-defibrillators provide, by measuring transpulmonary electric bioimpedance, an index of intrathoracic fluid status (OptiVol index [OI]). The goal of this study was to determine whether periods of greater intrathoracic fluid congestion (as detected by OI) correspond with increased AT event frequency.</AbstractText>This analysis retrospectively assessed the relation between AT events and OI estimate of volume overload in patients with left ventricular systolic dysfunction and OI-capable implantable cardioverter-defibrillators. OI values were stratified into 3 levels: group 1, <40; group 2, 40 to 60; and group 3, >60. An OI threshold-crossing event was defined as OI > or = 60, a value previously associated with clinically significant volume overload. Findings in 59 patients (mean left ventricular ejection fraction, 24%) with 225 follow-up visits (mean, 3.8 visits per patient) were evaluated. AT prevalence was 73%. AT frequency (percent of patients visits with at least 1 episode of AT since previous device interrogation) was greater in group 3 versus group 1 (P=0.0342). Finally, in terms of temporal sequence, AT episodes preceded OI threshold-crossing event in 43% of incidences, followed threshold-crossing event in 29%, and was simultaneous or indeterminate in the remainder.</AbstractText>These findings not only support the view that worsening pulmonary congestion is associated with increased AT frequency in patients with left ventricular dysfunction but also suggest that AT events may be responsible for triggering episodic pulmonary congestion more often than previously suspected.</AbstractText> |
6,197 | Complete loss of murine Xin results in a mild cardiac phenotype with altered distribution of intercalated discs. | Xin is a striated muscle-specific F-actin binding protein that has been implicated in cardiomyopathies. In cardiomyocytes, Xin is localized at intercalated discs (IDs). Mice lacking only two of the three Xin isoforms (XinAB(-/-) mice) develop severe cardiac hypertrophy. To further investigate the function of Xin variants in the mammalian heart, we generated XinABC(-/-) mice deficient in all Xin isoforms.</AbstractText>XinABC(-/-) mice showed a very mild phenotype: heart weight, heart weight to tibia length ratios, and cardiac dimensions were not altered. Increased perivascular fibrosis was only observed in hearts of young XinABC(-/-) mice. Striking differences were revealed in isolated cardiomyocytes: XinABC(-/-) cells demonstrated a significantly increased number of non-terminally localized ID-like structures. Furthermore, resting sarcomere length was increased, sarcomere shortening, peak shortening at 0.5-1 Hz, and the duration of shortening were decreased, and shortening and relengthening velocities were accelerated at frequencies above 4 Hz in XinABC(-/-) cardiomyocytes. ECG showed a significantly shorter HV interval and a trend towards shorter QRS interval in XinABC(-/-) mice, suggesting a faster conduction velocity of the ventricular-specific conduction system. In human cardiac tissue, expression of XinC protein was detected solely in samples from patients with cardiac hypertrophy.</AbstractText>Total Xin deficiency leads to topographical ID alterations, premature fibrosis and subtle changes in contractile behaviour; this is a milder cardiac phenotype than that observed in XinAB(-/-) mice, which still can express XinC. Together with the finding that XinC is detected solely in cardiomyopathic human tissues, this suggests that its expression is responsible for the stronger dominant phenotype in XinAB(-/-) mice. Furthermore, it indicates that XinC may be involved in the development of human cardiac hypertrophy.</AbstractText> |
6,198 | Role of transesophageal echocardiography among patients with atrial fibrillation undergoing electrophysiology testing. | External or internal shocks administered to terminate ventricular arrhythmias as a part of electrophysiology or implantable cardioverter-defibrillator testing, can inadvertently cardiovert atrial fibrillation (AF). Moreover, anticoagulation therapy is often withheld in these patients in anticipation of an invasive procedure. The risk of embolic events during these procedures has not been well described. Accordingly, the present study was a prospective evaluation of the incidence of left atrial (LA) thrombus and AF cardioversion among patients undergoing ventricular arrhythmia assessment. Transesophageal echocardiography was routinely performed on 44 consecutive patients in AF with subtherapeutic anticoagulation undergoing electrophysiology or implantable cardioverter-defibrillator testing. Arrhythmia induction was not performed when LA thrombus was present. The incidence and clinical predictors of thrombus, the inadvertent cardioversion of AF, and adverse events related to the procedure were assessed during the subsequent 4 to 6 weeks. Left atrial thrombus was observed in 12 patients (27%). Sinus rhythm was restored in 29 patients (91%), at least transiently, who underwent testing with a shock delivered. No adverse neurologic or hemorrhagic complications were observed. Univariate analysis identified no predictors of LA thrombus or cardioversion to sinus rhythm. In conclusion, LA thrombus and cardioversion to sinus rhythm are common among patients with AF undergoing an evaluation of ventricular arrhythmias. Transesophageal echocardiography performed before the procedure in patients with subtherapeutic anticoagulation is warranted to minimize embolic complications. This strategy appears to be a safe method to guide diagnostic testing in this patient population. |
6,199 | Predictors of the atrial fibrillation occurrence in patients with Wolff-Parkinson-White syndrome. | Atrial fibrillation (AF) in WPW syndrome occurs earlier and is more common than in the general population.</AbstractText>To evaluate the predisposing factors for the first episode of AF in patients with WPW.</AbstractText>We analysed data on 930 patients (510 males, 420 females) with WPW treated in our centre during 1988-2007. AF was diagnosed in 236 patients (25% - 161 males, 75 females, aged 36 +/- 15 years). The AF group was divided into two subgroups - patients with AF and atrio-ventricular reentrant tachycardia (AVRT), and patients with AF only. The analysis included subjects' age and gender, the presence of AVRT, the number and properties of accessory pathways, left ventricular ejection fraction (LVEF) and concomitant cardiovascular diseases.</AbstractText>The groups did not differ in terms of concomitant diseases and LVEF. In the whole group of patients with AF, arrhythmia occurred earlier in men than in women (34 +/- 14 vs. 40 +/- 15 years of age, p = 0.013). In the subgroup with AF and AVRT, AF was documented earlier compared to patients with AF only (34 +/- 15 vs. 41 +/- 15 years of age, p = 0.0072). AVRT was more common in patients with AF compared to those without AF (69 vs. 53%, p < 0.001). In the whole group of 930 patients, AF was observed more often in patients with overt pre-excitation compared to concealed WPW (29 vs. 12%, p < 0.001).</AbstractText>In patients with WPW syndrome, AF occurs earlier in patients with AVRT compared to patients with AF and without documented AVRT, earlier in men compared to women, and is more common in patients with overt WPW.</AbstractText> |
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