Unnamed: 0
int64
0
2.34M
titles
stringlengths
5
21.5M
abst
stringlengths
1
21.5M
1,500
Prevalence of drug-induced electrocardiographic pattern of the Brugada syndrome in a healthy population.
To determine the prevalence of drug-induced Brugada's syndrome (BrS) electrocardiograms (ECGs) in a healthy population, a sodium channel blockade challenge was performed in previously identified subjects with BrS-compatible (BrC) ECGs. These subjects were detected in 1,000 normal patients in whom first ECGs were systematically recorded. Because of the intermittent nature of electrocardiographic modifications in BrS, second ECGs were also recorded in a representative sample of the population presenting with first ECGs with normal results. The prevalence of typical drug-induced BrS ECGs was 5 of the 1,000 patients. This value was fivefold greater than the reported prevalence of spontaneous BrS ECGs in the healthy population.
1,501
Autonomic nervous system and paroxysmal atrial fibrillation: a study based on the analysis of RR interval changes before, during and after paroxysmal atrial fibrillation.
To evaluate the presence of an abnormal autonomic modulation before, during and immediately after paroxysmal atrial fibrillation (PAF).</AbstractText>We analysed Holter recordings of 65 patients with 110 PAF episodes lasting more then 30 s. Mean RR interval, co-efficient of variation and short-term heart rate variability were measured before, during and after PAF episodes. We observed a significant correlation between the coupling interval and both the cycle length measured from 30 min up to few cycles before PAF onset, and ventricular response. When comparing the heart rate variability (HRV) before and after PAF we observed a significant reduction of the low frequency/high frequency components (LF/HF) ratio (from 6.2+/-7.4 to 3.2+/-4.1). A short-long-short cycle sequence was detectable in 37 PAF onsets associated with a greater incidence of atrial ectopic beats and a greater LF component (62+/-25 vs. 53+/-27 normalised units) in comparison to the remaining episodes. When onsets were divided for a LF/HF ratio cut-off value of &gt; or = 2 to separate episodes with a predominant sympathetic, as opposed to those with a prevailing vagal (LF/HF&lt;2) modulation, we observed opposite changes (from 9.1+/-7.8 to 4+/-3.7 and from 0.8+/-0.5 to 2+/-3.6, respectively) consistent with a recovery of a more physiological sympatho-vagal balance immediately after recovery of sinus rhythm. No changes in co-efficient of variation of ventricular response were detectable before PAF termination.</AbstractText>A predominant sympathetic modulation characterises the majority of PAF onsets whereas a vagal predominance was detectable in about 30% of episodes. These patterns are no longer detectable after recovery of sinus rhythm.</AbstractText>
1,502
Safety and feasibility of high-dose dobutamine-atropine stress cardiovascular magnetic resonance for diagnosis of myocardial ischaemia: experience in 1000 consecutive cases.
To determine the safety of high-dose dobutamine-atropine stress cardiovascular magnetic resonance (stress-CMR), which recently emerged as a highly accurate modality for diagnosis of inducible myocardial ischaemia.</AbstractText>From 1997 to 2002, 1000 consecutive stress-CMR examinations were performed. Images were acquired at rest and during a high-dose dobutamine-atropine protocol in 3 short-axis, a 4- and a 2-chamber view. Stress testing was discontinued when &gt; or =85% of age-predicted heart rate was reached, on patient request, maximum pharmacologic infusion, or when new or worsening wall motion abnormalities, severe angina, dyspnoea, increase or decrease in blood pressure, or severe arrhythmias occurred. Stress-CMR was successfully performed in all but four patients (0.4%; insufficient ECG-triggering). Target heart rate was not reached in 95 cases (9.5%), due to maximum pharmacologic infusion in submaximal negative examinations in 21 cases (2.1%), and limiting side effects in 74 (7.4%). Side effects included one case (0.1%) of sustained and four cases (0.4%) of non-sustained ventricular tachycardia, 16 cases (1.6%) of atrial fibrillation, and two cases (0.2%) of transient second degree AV block.</AbstractText>The safety profile of stress-CMR is similar to other methodologies using dobutamine infusions. Patients must be closely monitored, and resuscitation equipment and trained personnel must be available.</AbstractText>
1,503
Differences between patients with a preserved and a depressed left ventricular function: a report from the EuroHeart Failure Survey.
Due to a lack of clinical trials, scientific evidence regarding the management of patients with chronic heart failure and preserved left ventricular function (PLVF) is scarce. The EuroHeart Failure Survey provided information on the characteristics, treatment and outcomes of patients with PLVF as compared to patients with a left ventricular systolic dysfunction (LVSD).</AbstractText>We performed a secondary analysis using data from the EuroHeart Failure Survey, only including patients with a measurement of LV function (n = 6806). We selected two groups: patients with LVSD (54%) and patients with a PLVF (46%). Patients with a PLVF were, on average, 4 years older and more often women (55% vs. 29%, respectively, p &lt; 0.001) as compared to LVSD patients, and were more likely to have hypertension (59% vs. 50%, p &lt; 0.001) and atrial fibrillation (25% vs. 23%, p = 0.01). PLVF patients received less cardiovascular medication compared to PLVF patients, with the exception of calcium antagonists. Multivariate analysis revealed that LVSD was an independent predictor for mortality, while no differences in treatment effect on mortality between the two groups was observed. A sensitivity analysis, using different thresholds to separate patients with and without LVSD revealed comparable findings.</AbstractText>In the EuroHeart Failure Survey, a high percentage of heart failure patients had PLVF. Although major clinical differences were seen between the groups, morbidity and mortality was high in both groups.</AbstractText>
1,504
Antithrombin administration during experimental cardiopulmonary resuscitation.
To determine whether antithrombin (AT) administration during cardiopulmonary resuscitation (CPR) increased cerebral circulation and reduced reperfusion injury.</AbstractText>Ventricular fibrillation was induced in 24 anaesthetised pigs. After a 5-min non-intervention interval, CPR was started. The animals were randomised into two groups. The treatment group received AT (250 U/kg) and the control group received placebo, after 7 min of CPR. Defibrillation was attempted after 9 min of CPR. If restoration of spontaneous circulation (ROSC) was achieved, the animals were observed for 4 h. Cortical cerebral blood flow was measured using laser-Doppler flowmetry. Cerebral oxygen extraction was calculated to reflect the relation between global cerebral circulation and oxygen demand. Measurements of eicosanoids (8-iso-PGF(2alpha) and 15-keto-dihydro-PGF(2alpha)), AT, thrombin-antithrombin complex (TAT) and soluble fibrin in jugular bulb plasma were performed to detect any signs of cerebral oxidative injury, inflammation and coagulation.</AbstractText>There was no difference between the groups in cortical cerebral blood flow, cerebral oxygen extraction, or levels of eicosanoids, TAT or soluble fibrin in jugular bulb plasma after ROSC. In the control group reduction of AT began 15 min after ROSC and continued throughout the entire observation period (P &lt; 0.05). Eicosanoids and TAT were increased compared to baseline in all animals (P &lt; 0.01).</AbstractText>In this experimental model of CPR, AT administration did not increase cerebral circulation or reduce reperfusion injury after ROSC.</AbstractText>
1,505
Vasopressin versus continuous adrenaline during experimental cardiopulmonary resuscitation.
To evaluate the effects of a bolus dose of vasopressin compared to continuous adrenaline (epinephrine) infusion on vital organ blood flow during cardiopulmonary resuscitation (CPR).</AbstractText>Ventricular fibrillation was induced in 24 anaesthetised pigs. After a 5-min non-intervention interval, CPR was started. After 2 min of CPR the animals were randomly assigned to receive either vasopressin (0.4 U/kg) or adrenaline (bolus of 20 microg/kg followed by continuous infusion of 10 microg/(kg min)). Defibrillation was attempted after 9 min of CPR.</AbstractText>Vasopressin generated higher cortical cerebral blood flow (P &lt; 0.001) and lower cerebral oxygen extraction (P &lt; 0.001) during CPR compared to continuous adrenaline. Coronary perfusion pressure during CPR was higher in vasopressin-treated pigs (P &lt; 0.001) and successful resuscitation was achieved in 12/12 in the vasopressin group versus 5/12 in the adrenaline group (P = 0.005).</AbstractText>In this experimental model, vasopressin caused a greater increase in cortical cerebral blood flow and lower cerebral oxygen extraction during CPR compared to continuous adrenaline. Furthermore, vasopressin generated higher coronary perfusion pressure and increased the likelihood of restoring spontaneous circulation.</AbstractText>
1,506
A predictive model for survival after in-hospital cardiopulmonary arrest.
In-hospital cardiopulmonary resuscitation (CPR) has seen a steady increase in the application of technology and techniques since the introduction of closed cardiac massage in 1960. Despite this progress, there has not been a demonstrated improvement in survival rates after in-hospital cardiac arrest over the last 40 years. Identification of prognostic factors associated with survival after a resuscitation attempt can help physician decisions and patients' end-of-life choices in a pre-arrest situation.</AbstractText>Using an Utstein-based template we analyzed 219 consecutive adult attempted resuscitations in a large urban teaching hospital over a 3-year period. The main outcome measures were survival to discharge, 1 and 3 months. Backwards stepwise logistic regression was used to select baseline variables that predict survival at discharge, 1 and 3 months.</AbstractText>Survival rates at discharge, 1 and 3 months were 15.1, 13.3, and 11.5%. Meaningful neurological status (cerebral performance score of 1) at discharge was achieved in 61% of survivors. Independent predictors of survival were: higher body-mass index (BMI), presence of chronic renal insufficiency (CRI), respiratory arrest, ventricular tachycardia/fibrillation (VT/VF) as initial rhythm and arrest early during the hospital stay. A risk model based on these variables demonstrated a significant fit between predicted and observed survival at discharge with goodness of fit test P-value of 0.87.</AbstractText>Survival after in-hospital cardiopulmonary arrest is poor and can be estimated by using clinical variables. If validated in a large prospective trial, this score could help physicians in attempting resuscitation, patients and families in making end-of-life decisions and hospitals in resource allocation.</AbstractText>
1,507
Measuring survival rates from sudden cardiac arrest: the elusive definition.
Measuring survival from sudden out-of-hospital cardiac arrest (OOH-CA) is often used as a benchmark of the quality of a community's emergency medical service (EMS) system. The definition of OOH-CA survival rates depends both upon the numerator (surviving cases) and the denominator (all cases).</AbstractText>The purpose of the public access defibrillation (PAD) trial was to measure the impact on survival of adding an automated external defibrillator (AED) to a volunteer response system trained in CPR. This paper reports the definition of OOH-CA developed by the PAD trial investigators, and it evaluates alternative statistical methods used to assess differences in reported "survival."</AbstractText>Case surveillance was limited to the prospectively determined geographic boundaries of the participating trial units. The numerator in calculating a survival rate should include only those patients who survived an event but who otherwise would have died except for the application of some facet of emergency medical care-in this trial a defibrillatory shock. Among denominators considered were: total population of the study unit, all deaths within the study unit, and documented ventricular fibrillation cardiac arrests. The PAD classification focused upon cases that might have benefited from the early use of an AED, in addition to the likely benefit from early recognition of OOH-CA, early access of EMS, and early cardiopulmonary resuscitation (CPR). Results of this classification system were used to evaluate the impact of the PAD definition on the distribution of cardiac arrest case types between CPR only and CPR + AED units.</AbstractText>Potential OOH-CA episodes were classified into one of four groups: definite, probable, uncertain, or not an OOH-CA. About half of cardiac arrests in the PAD units were judged to be definite OOH-CA events and therefore potentially treatable with an AED. However, events that occurred in CPR-only units were less likely to be classified as definite or probable OOH-CA events than those in CPR + AED units (43% versus 55%, odds ratio 0.78, 95% confidence interval 0.57-1.07). The study retained sufficient power to permit a statistical analysis of the alternative hypothesis that the CPR + AED method results in twice as many survivors as a CPR-only approach. The result is critically dependent on the denominator used for calculating survival rates; but the analysis does not require a denominator as the numerators will have identical Poisson distributions (counts for rare events) under the null hypothesis since randomization distributes the risk of cardiac arrest evenly between the two arms.</AbstractText>Reported OOH-CA rates and survival rates vary widely, depending upon the definitions applied to events. Rigorous assessment of treatments applied to improve survival can be obscured by inappropriate definitions. Large-scale randomized interventions designed to improve survival from OOH-CA can be evaluated based upon the absolute numbers of patients surviving, rather than a change in the proportion surviving.</AbstractText>
1,508
Brugada and long QT-3 syndromes: two phenotypes of the sodium channel disease.
Brugada and long QT-3 syndromes are two allelic diseases caused by different mutations in SCN5A gene inherited by an autosomal dominant pattern with variable penetrance. Both of these syndromes are ion channel diseases of the heart manifest on surface electrocardiogram by ST-segment elevation in the right precordial leads and prolonged QT(c) interval, respectively, with predilection for polymorphic ventricular tachycardia and sudden death, which may be the first manifestation of the disease. Brugada syndrome usually manifests during adulthood with male preponderance, whereas long QT3 syndrome usually manifests in teenage years, although it can also manifest in adulthood. Class IA and IC antiarrhythmic drugs increase ST-segment elevation and predilection for polymorphic ventricular tachycardia and ventricular fibrillation in Brugada syndrome, whereas these agents shorten the repolarization and QT(c) interval, and thus may be beneficial in long QT-3 syndrome. Beta-blockade also increases the ST-segment elevation in Brugada syndrome but decreases the dispersion of repolarization in long QT-3 syndrome. Mexiletine, a class IB sodium channel blocker decreases QT(c) interval as well as dispersion of repolarization in long QT-3 syndrome but has no effect on Brugada syndrome. The only effective treatment available at this time for Brugada syndrome is implantable cardioverter defibrillator, although repeated episodes of polymorphic ventricular tachycardia can be treated with isoproterenol. In symptomatic patients of long QT-3 syndrome in whom the torsade de pointes is bradycardia-dependent or pause-dependent, a pacemaker could be used to avoid bradycardia and pauses and an implantable cardioverter defibrillator is indicated where arrhythmia is not controlled with pacemaker and beta-blockade. However, the combination of new devices with pacemaker and cardioverter-defibrillator capabilities appear promising in these patients warranting further study.
1,509
Risk stratification using heart rate turbulence and ventricular arrhythmia in MADIT II: usefulness and limitations of a 10-minute holter recording.
We evaluated the usefulness of heart rate turbulence (HRT) parameters and frequency of ventricular premature beats (VPBs) for risk-stratifying postinfarction patients with depressed left ventricular function enrolled in Multicenter Automatic Defibrillator Trial II (MADIT II).</AbstractText>In 884 MADIT II patients, 10-minute Holter monitoring at enrollment was used to evaluate HRT parameters and frequency of VPBs. The primary endpoints were defined as all-cause mortality in patients randomized to conventional treatment and as appropriate therapy for ventricular tachycardia or fibrillation in patients randomized to implantable cardioverter defibrillator (ICD) therapy.</AbstractText>The median turbulence slope was lower in patients who died in comparison to survivors in the conventional arm (2.3 vs 4.5 ms/RR; P &lt; 0.05); but it was not a significant predictor of mortality after adjustment for clinical covariates (age, ejection fraction, beta-blocker use, and BUN levels). There was no association between HRT parameters and arrhythmic events in ICD patients. Conventionally treated patients who died and ICD patients who had appropriate ICD therapy had significantly more frequent VPBs than those without such adverse events. After adjustment for clinical covariates, frequent VPBs&gt;3/10 min were associated with death in the conventional arm (HR = 1.63; P = 0.070) and were predictive for appropriate ICD therapy in the ICD arm (HR = 1.75; P = 0.003).</AbstractText>In postinfarction patients with severe left ventricular dysfunction, frequent VPBs are associated with increased risk of mortality and with appropriate ICD therapy. HRT obtained from 10-min Holter ECG showed a trend toward the association with mortality in univariate analysis but HRT parameters were not predictive of the outcome in multivariate analyses.</AbstractText>
1,510
The increasing need for anticoagulant therapy to prevent stroke in patients with atrial fibrillation.
Ischemic stroke, a major complication of atrial fibrillation (AF), is believed to result from atrial thrombus formation caused by ineffective atrial contraction. Oral anticoagulant therapy effectively reduces the risk of ischemic stroke in patients with AF; this therapy is recommended for patients with any frequency or duration of AF and other risk factors for stroke, such as increased age (&gt;75 years), hypertension, prior stroke, left ventricular dysfunction, diabetes, or heart failure. Recently published data comparing rate-control and rhythm-control strategies in AF emphasized the importance of maintaining an international normalized ratio higher than 2.0 during warfarin therapy and the need for continuing anticoagulant therapy to prevent stroke in high-risk patients, even if the strategy is rhythm control. Hemorrhagic complications can be minimized by stringent control of the international normalized ratio (particularly in elderly patients) and appropriate therapy for comorbidities such as hypertension, gastric ulcer, and early-stage cancers. Undertreatment of patients with AF is a continuing problem, particularly in the elderly population. Patients perceived as likely to be noncompliant, such as the functionally impaired, are less likely to receive warfarin therapy. However, stroke prevention with anticoagulants is cost-effective and improves quality of life, despite the challenges of maintaining appropriate anticoagulation with monitoring and warfarin dose titration. New medications in development with more predictable dosing and fewer drug-drug interactions may reduce the complexities of achieving optimal anticoagulation and increase the practicality of long-term anticoagulant therapy for patients with AF at risk of stroke.
1,511
Sarafotoxin 6c (S6c) reduces infarct size and preserves mRNA for the ETB receptor in the ischemic/reperfused myocardium of anesthetized rats.
The aims of this study were to determine if the ETB receptor agonist, sarafotoxin 6c (S6c) reduces myocardial infarct size following myocardial ischemia and reperfusion and to investigate whether any changes in mRNA for endothelin receptors in the injured myocardium were modified by S6c pretreatment. Hypnorm/Hypnovel anesthetized rats were subjected to occlusion of the left main coronary artery for 30 minutes, followed by 120 minutes reperfusion. Animals were administered a bolus dose of S6c (0.24 nmol kg-1 i.v., n = 10) or saline (n = 15) 5 minutes prior to occlusion. At the end of reperfusion, hearts were stained with Evan's Blue dye to delineate area at risk. A 1.5- to 2.0-mm thick slice was cut transmurally 1 mm below the site of ligation for assessment of infarct size by triphenyltetrazolium chloride. A further transmural slice (2.5-3-mm thick) was cut for assessment of receptor mRNA levels by RTPCR. Administration of S6c caused a transient fall in mean arterial blood pressure (MABP) prior to occlusion and attenuated the fall in MABP induced by coronary occlusion. S6c significantly reduced infarct size (13 +/- 4% of area of slice at risk) compared with control hearts (35 +/- 5%; P &lt; 0.05). In control hearts, there was a marked reduction in mRNA content for both ETA (50% reduction) and ETB (70% reduction) receptors in the ischemic zone, compared with non-ischemic tissue. In hearts pre-treated with S6c there was a reduction in ETA, but not ETB receptor mRNA in the ischemic zone. This study has shown that S6c reduces myocardial infarct size and results in preservation of ETB receptor mRNA in ischemic/reperfused tissue.
1,512
Creation of a genetic calcium channel blocker by targeted gem gene transfer in the heart.
Calcium channel blockers are among the most commonly used therapeutic drugs. Nevertheless, the utility of calcium channel blockers for heart disease is limited because of the potent vasodilatory effect that causes hypotension, and other side effects attributable to blockade of noncardiac channels. Therefore, focal calcium channel blockade by gene transfer is highly desirable. With a view to creating a focally applicable genetic calcium channel blocker, we overexpressed the ras-related small G-protein Gem in the heart by somatic gene transfer. Adenovirus-mediated delivery of Gem markedly decreased L-type calcium current density in ventricular myocytes, resulting in the abbreviation of action potential duration. Furthermore, transduction of Gem resulted in a significant shortening of the electrocardiographic QTc interval and reduction of left ventricular systolic function. Focal delivery of Gem to the atrioventricular (AV) node significantly slowed AV nodal conduction (prolongation of PR and AH intervals), which was effective in the reduction of heart rate during atrial fibrillation. Thus, these results indicate that gene transfer of Gem functions as a genetic calcium channel blocker, the local application of which can effectively modulate cardiac electrical and contractile function.
1,513
[Anesthetic management of two patients with Brugada-type ECG and of different clinical severity].
Brugada syndrome is an arrhythmia syndrome characterized by typical electrocardiogram (Brugada-type ECG) and development of ventricular fibrillation (Vf) without any distinct structural heart diseases. The essential goal in the management of Brugada syndrome is to avoid the development of Vf. However, there has been no established consensus on pre-operative risk assessment of patients with Brugada-type ECG. We recently experienced two cases of anesthetic managements for patients with Brugada-type ECG. Based on these experiences and recent cardiological progress on the risk stratification of Brugada syndrome, we thoroughly discuss on the peri-operative managements for patients with Brugada-type ECG.
1,514
[Scuba diving and the heart. Cardiac aspects of sport scuba diving].
Diving with self-contained underwater breathing apparatus (scuba) has become a popular recreational sports activity throughout the world. A high prevalence of cardiovascular disorders among the population makes it therefore likely that subjects suffering from cardiovascular problems may want to start scuba diving. Although scuba diving is not a competitive sport requiring athletic health conditions, a certain medical fitness is recommended because of the physical peculiarities of the underwater environment. Immersion alone will increase cardiac preload by central blood pooling with a rise in both cardiac output and blood pressure, counteracted by increased diuresis. Exposure to cold and increased oxygen partial pressure during scuba diving will additionally increase afterload by vasoconstrictive effects and may exert bradyarryhthmias in combination with breath-holds. Volumes of gas-filled body cavities will be affected by changing pressure (Figure 1), and inert gas components of the breathing gas mixture such as nitrogen in case of air breathing will dissolve in body tissues and venous blood with increasing alveolar inert gas pressure. During decompression a free gas phase may form in supersaturated tissues, resulting in the generation of inert gas microbubbles that are eliminated by the venous return to the lungs under normal circumstances. Certain cardiovascular conditions may have an impact on these physiological changes and pose the subject at risk of suffering adverse events from scuba diving. Arterial hypertension may be aggravated by underwater exercise and immersion. Symptomatic coronary artery disease and symptomatic heart rhythm disorders preclude diving. The occurrence of ventricular extrasystoles according to Lown classes I and II, and the presence of atrial fibrillation are considered relative contraindications in the absence of an aggravation following exercise. Asymptomatic subjects with Wolff-Parkinson-White syndrome may be allowed to dive, but in case of paroxysmal supraventricular tachycardia they must refrain from diving. Pacemakers will fail with increasing pressure, but some manufacturers have proven their products safe for pressure equivalents of up to 30 m of seawater, so that patients may dive uneventfully when staying within the 0-20 m depth range. Significant aortic or mitral valve stenosis will preclude diving, whereas regurgitation only will not be a problem. Right-to-left shunts have increasingly gained attention in diving medicine, since they may allow venous gas microbubbles to spill over to the arterial side of the circulation enabling the possibility of arterial gas embolism. Significant shunts thus preclude diving. The highly prevalent patent foramen ovale is considered a relative contraindication only when following certain recommendations for safe diving (Table 2). Metabolic disorders are of concern, since adiposity is associated with both, higher bubble grades in Doppler ultrasound detection after scuba dives when compared to normal subjects, and an increased epidemiologic risk of suffering from decompression illness. In conclusion, cardiovascular aspects are important in the assessment of fitness to dive, and certain cardiovascular conditions preclude scuba diving. Any history of cardiac disease or abnormalities detected during the routine medical examination should prompt to further evaluation and specialist referral.
1,515
Cardiac sympathetic nerve biology and brain monoamine turnover in panic disorder.
Panic disorder serves as a clinical model for testing whether mental stress can cause heart disease. Our own cardiologic management of panic disorder provides case material of recurrent emergency room attendances with angina and electrocardiogram ischemia, triggered arrhythmias (atrial fibrillation, ventricular fibrillation), and documented coronary artery spasm, in some cases with coronary spasm being complicated by coronary thrombosis. Application of radiotracer catecholamine kinetics and clinical microneurography methodology suggests there is a genetic predisposition to panic disorder that involves faulty neuronal norepinephrine uptake, possibly sensitizing the heart to symptom generation. During panic attacks there are large sympathetic bursts, recorded by clinical microneurography in the muscle sympathetic nerve neurogram, and large increases in cardiac norepinephrine spillover, accompanied by surges of adrenal medullary epinephrine secretion. In other conditions such as heart failure and presumably here also, a high level of sympathetic nervous activation can mediate increased cardiac risk. The sympathetic nerve cotransmitter, neuropeptide Y (NPY), is released from the cardiac sympathetics during panic attacks, an intriguing finding given that NPY can cause coronary artery spasm. There is ongoing, continuous release of epinephrine from the heart in panic sufferers, perhaps attributable to epinephrine loading of cardiac sympathetic nerves by uptake from plasma during panic attacks, or possibly to in situ synthesis of epinephrine through the action of intracardiac phenylethanolamine-N-methytransferase (PNMT) activated by repeated cortisol responses. We have used internal jugular venous sampling and measurement of overflowing lipophilic brain monoamine metabolites to quantify brain norepinephrine and serotonin turnover in untreated patients with panic disorder. We find normal norepinephrine turnover but a marked increase in brain serotonin turnover in patients with panic disorder, in the absence of a panic attack, which presumably represents an underlying neurotransmitter substrate for the condition.
1,516
Three cases of sudden death due to butane or propane gas inhalation: analysis of tissues for gas components.
We report three cases of sudden death due to inhalation of portable cooking stove fuel (case 1), cigarette lighter fuel (case 2), and liquefied petroleum gas (LPG) (case 3). Specimens of blood, urine, stomach contents, brain, heart, lung, liver, kidney, and fat were collected and analyzed for propylene, propane, isobutane, and n-butane by headspace gas chromatography. n-Butane was the major substance among the volatiles found in the tissues of cases 1 and 2, and propane was the major substance in case 3. A combination of the autopsy findings and the gas analysis results revealed that the cause of death was ventricular fibrillation induced by hard muscle exercise after gas inhalation in cases 1 and 2, and that the cause of death in case 3 might be hypoxia. It is possible that the victim in case 3 was under anesthetic toxicity of accumulated isobutane which is a minor component of liquefied petroleum gas.
1,517
Long-term comparison of the implantable cardioverter defibrillator versus amiodarone: eleven-year follow-up of a subset of patients in the Canadian Implantable Defibrillator Study (CIDS).
The implantable cardioverter defibrillator (ICD) is superior to amiodarone for secondary prophylaxis of sudden cardiac death. However, the magnitude of this benefit over long-term follow-up is not known. Thus, our objective was to evaluate the long-term consequences of using amiodarone versus an ICD as first-line monotherapy in patients with a prior history of sustained ventricular tachycardia/ventricular fibrillation or cardiac arrest.</AbstractText>A total of 120 patients were enrolled at St Michael's Hospital in the Canadian Implantable Defibrillator Study (CIDS) and were randomly assigned to receive either amiodarone (n=60) or an ICD (n=60). The treatment strategy was not altered after the end of CIDS unless the initial assigned therapy was not effective or was associated with serious side effects. After a mean follow-up of 5.6+/-2.6 years, there were 28 deaths (47%) in the amiodarone group, compared with 16 deaths (27%) in the ICD group (P=0.0213). Total mortality was 5.5% per year in the amiodarone group versus 2.8% per year in the ICD group (hazard ratio of amiodarone: ICD, 2.011; 95% confidence interval, 1.087 to 3.721; P=0.0261). In the amiodarone group, 49 patients (82% of all patients) had side effects related to amiodarone, of which 30 patients (50% of all patients) required discontinuation or dose reduction; 19 patients crossed over to ICD because of amiodarone failure (n=7) or side effects (n=12).</AbstractText>In a subset of CIDS, the benefit of the ICD over amiodarone increases with time; most amiodarone-treated patients eventually develop side effects, have arrhythmia recurrences, or die.</AbstractText>
1,518
Ibutilide-induced alterations in electrocardiographic and spatial vectorcardiographic descriptors of ventricular repolarization.
Ibutilide is used for the pharmacologic cardioversion of atrial fibrillation (AF) or flutter (AFl). Ibutilide-induced QT interval prolongation has been demonstrated previously. However, its effects on vectorcardiographic (VCG) descriptors of ventricular repolarization (VR) have not been studied so far.</AbstractText>To evaluate the effects of ibutilide on electrocardiographic (ECG) and VCG descriptors of VR, one or two repeated 10-min infusions of 1 mg of ibutilide were given in 50 consecutively recruited patients (36 women, mean age 69.4 +/- 9.3 years) with AF or AFl of recent onset.</AbstractText>The maximum and the minimum QT intervals, QT dispersion, the rate-corrected QT maximum, and the spatial VCG descriptors, spatial T amplitude, and spatial QRS-T angle were calculated before (baseline ECG) and 30 min after the start of ibutilide infusion (postinfusion ECG).</AbstractText>After ibutilide infusion, 40 (80%) patients were cardioverted to sinus rhythm (Group 1), while in the remaining 10 (Group 2) AF or AFl persisted. In both study groups, temporal measures of VR were significantly increased from baseline to the postinfusion ECG. In Group 1, spatial T amplitude and spatial QRS-T angle did not differ between those two ECGs, while in Group 2 spatial T amplitude was significantly increased (p = 0.005) and spatial QRS-T angle was significantly decreased (p = 0.002) post infusion compared with baseline ECG.</AbstractText>While temporal measures of VR are significantly affected in all patients who receive ibutilide infusion for AF or AFl cardioversion, spatial VCG descriptors of VR are significantly altered only in those patients who fail to respond to the drug. A dose-related effect of ibutilide on the different aspects of VR should be suspected.</AbstractText>
1,519
Safety and efficacy of intravenously administered tedisamil for rapid conversion of recent-onset atrial fibrillation or atrial flutter.
The goal of the present study was to assess the efficacy and safety of intravenous tedisamil, a new antiarrhythmic compound, for conversion of recent-onset atrial fibrillation (AF) or atrial flutter (AFL) to normal sinus rhythm (NSR).</AbstractText>Tedisamil is a novel antiarrhythmic drug with predominantly class III activity. Its efficacy and safety for conversion of recent onset AF or AFL to NSR is not known.</AbstractText>This was a multicenter, double-blind, randomized, placebo-controlled, sequential ascending dose-group trial. A total of 201 patients with symptomatic AF or AFL of 3 to 48 h duration were enrolled in a two-stage study. During stage 1, patients were randomized to receive tedisamil at 0.4 mg/kg body weight or matching placebo; during stage 2, patients received tedisamil at 0.6 mg/kg body weight or matching placebo. Treatments were given as single intravenous infusions. The primary study end point consisted of the percentage of patients converting to NSR for at least 60 s within 2.5 h.</AbstractText>Of 175 patients representing the intention-to-treat sample, conversion to NSR was observed in 41% (25/61) of the tedisamil 0.4 mg/kg group, 51% (27 of 53) of the tedisamil 0.6 mg/kg group, and 7% (4/59) of the placebo group (p &lt; 0.001 for both tedisamil groups vs. placebo). Average time to conversion was 35 min in patients receiving tedisamil. There were two instances of self-terminating ventricular tachycardia: one episode of torsade de pointes and one of monomorphic ventricular tachycardia, both in patients receiving 0.6 mg/kg tedisamil.</AbstractText>Tedisamil at dosages of 0.4 and 0.6 mg/kg was superior to placebo in converting AF or AFL. Tedisamil has a rapid onset of action leading to conversion within 30 to 40 min in the majority of responders.</AbstractText>
1,520
Patient alert in implantable cardioverter defibrillators: toy or tool?
The purpose of this study was to analyze the utility of patient-alert features in implantable cardioverter defibrillators (ICDs).</AbstractText>Various alert features producing acoustic warning signals have been implemented in newer generation ICDs, but their role in early detection of system-related complications has not been systematically evaluated.</AbstractText>In 240 patients implanted with Medtronic ICD devices, the following alert features were routinely activated: pacing lead impedance &lt;200 or &gt;2,000 Omega, high-voltage lead impedance &lt;10 or &gt;200 Omega, low battery voltage (elective replacement indicator), long charge time (&gt;18 s), &gt;3 shocks delivered per episode, and all therapies in a zone delivered. Alert events occurring during follow-up were assessed in relation to actual findings (hospital charts, chest X-rays, ICD printouts including sensing/pacing/defibrillation threshold tests, episode data) to determine incidence, sensitivity, and specificity of the alert function.</AbstractText>During 12.2 +/- 8.9 months, 24 alert events occurred in the 240 patients (pacing lead impedance, n = 4; high-voltage lead impedance, n = 7; low battery voltage, n = 1; &gt;3 shocks, n = 6; all therapies, n = 6). A total of 22 serious complications (necessitating reprogramming or device/lead replacement) were observed, 14 of which were primarily identified through a patient alert (lead fracture, n = 11; connector defect, n = 1; T-wave oversensing, n = 1; battery depletion, n = 1). This reflects a sensitivity of 64% and a specificity of 96% of the alert function for serious complications. With 14 of 24 patient alerts being caused by serious complications, the positive predictive value reached 58%.</AbstractText>Patient-alert features are a useful additional tool facilitating early detection of serious ICD complications, but they do not substitute for regular ICD follow-up, because of their low sensitivity.</AbstractText>
1,521
Is defibrillation testing required for defibrillator implantation?
The assessment of defibrillation (DFT) efficacy has long been the standard of care during defibrillator implantation. To ensure an acceptable DFT safety margin, early defibrillator systems frequently required that the shock polarity and the location, type, or number of electrodes had to be altered. Advances in defibrillator and lead technology have resulted in lower and more consistent DFT thresholds in the range of 10 J, with an infrequent requirement to modify the DFT system. Yet, one can make an argument for and against continuation of DFT testing at the time of defibrillator implantation. The goal of this paper is to address both the data that do support and the data that do not support continuation of DFT testing at the time of device implantation. Scientifically, DFT testing should be abandoned only when prospective evidence demonstrates that defibrillator implantation without testing is as safe and has the same mortality benefits as implantation with testing. The most attractive aspect of eliminating DFT efficacy testing is that more patients may have the opportunity to be treated with this life-saving therapy. Perhaps there are alternative strategies to improve accessibility to defibrillator therapy without possibly eroding its effectiveness. In the end, will lives be saved or lost if we discontinue DFT efficacy testing and lower the barriers to implantable defibrillator therapy?
1,522
The Ashman phenomenon.
In the presence of atrial fibrillation, impulses of supraventricular origin that are transmitted through the ventricles during periods of relative refractoriness to impulse conduction exhibit anomalous configurations. These "aberrant beats" can be difficult to distinguish from ventricular ectopic beats, and groups of aberrant beats may be mistaken for ventricular tachycardia. Richard Ashman, PhD, a physiologist at Louisiana State University School of Medicine in New Orleans, noted that ventricular refractoriness varied with the lengths of cardiac cycles; that aberrant beats typically ended short cycles following long cycles; and that aberrant beats often have a right bundle branch block configuration. This observation, known as the "Ashman phenomenon," has become a principle of cardiology. Its recognition may allow clinicians to distinguish aberrant beats from ventricular ectopy. Ashman made a variety of other fundamental contributions to electrocardiography and was also an accomplished poet.
1,523
A prospective, population-based study of the epidemiology and outcome of out-of-hospital pediatric cardiopulmonary arrest.
This study reports the epidemiologic features, survival rates, and neurologic outcomes of the largest population-based series of pediatric out-of-hospital cardiopulmonary arrest patients with prospectively collected data.</AbstractText>Secondary analysis of data from a prospective, interventional trial of out-of-hospital pediatric airway management conducted from 1994 to 1997 (Gausche M, Lewis RJ, Stratton SJ, et al. JAMA. 2000;283:783-790). Consecutive out-of-hospital patients from 2 large urban counties in California &lt;12 years old or 40 kg in bodyweight who were determined by paramedics to be pulseless and apneic were included. Main outcome measures included survival to hospital discharge, patient demographics, arrest etiology, arrest rhythm, event intervals, and neurologic outcomes.</AbstractText>In 599 patients, 601 events were studied (54% were &lt;1 year old, 58% were male). Return of spontaneous circulation was achieved in 29%; 25% were admitted to the hospital, and 8.6% (51) survived to hospital discharge. The most prevalent etiologies were sudden infant death syndrome and trauma; these resulted in relatively higher mortality. Respiratory etiologies and submersions followed; these resulted in relatively lower mortality. Twenty-six percent of the arrests were witnessed by citizens, and an additional 8% were witnessed by rescue personnel. Witnessed arrests had a higher survival rate (16%). Thirty-one percent of patients received bystander cardiopulmonary resuscitation, which was not demonstrated to result in improved survival rates. Arrest rhythms were asystole (67%), pulseless electrical activity (24%), and ventricular fibrillation (9%); children with the latter 2 rhythms had better survival rates. One third of the survivors (16 of 51) had good neurologic outcome, none of whom received &gt;3 doses of epinephrine or were resuscitated for &gt;31 minutes in the emergency department.</AbstractText>The 8.6% survival rate after out-of-hospital pediatric cardiopulmonary arrest is poor. Administration of &gt;3 doses of epinephrine or prolonged resuscitation is futile.</AbstractText>
1,524
Nonsustained ventricular tachycardia: where do we stand?
The clinical approach to the patient with nonsustained ventricular tachycardia (NSVT) should always be considered within the particular clinical context in which the arrhythmia occurs. In the documented absence of heart disease, spontaneous NSVT does not carry any adverse prognostic significance. Exercise-induced NSVT may predict increased cardiac mortality. In ischaemic patients with a left ventricular ejection fraction (LVEF) &lt; 40%, NSVT has an adverse prognostic significance and electrophysiologic testing is indicated with a view to ICD implantation. In patients with LVEF &gt; 40% the independent prognostic significance of NSVT is unknown. The prognostic value of NSVT in patients with dilated cardiomyopathy is not known. NSVT in young patients with hypertrophic obstructive cardiomyopathy carries an adverse prognostic significance. The prognostic value of NSVT in conditions such as the long-QT syndromes, primary ventricular fibrillation, and Brugada syndrome, as well as in patients with hypertension and valvular disease, has not been established.
1,525
[Beneficial effect of reversion of atrial fibrillation to sinus rythm on the echocardiographic parameters in the elderly].
Atrial fibrillation (FA) is the most common arrhythmia, and frequency of its occurrence increases with age. The aim of this study was to assess the influence of sinus rhythm (SR) restoration on heart rate (HR) and ventricular arrhythmia (AEV) and pauses (PA) occurrence in patients in over 70 years age. Study group consists with 104 patients with nonrheumatic FA of different etiology, which were divided to two groups: in younger and older age. In group I (younger patients) were 52 patients (25 women and 27 men), 38 to 69 (mean 51.2 +/- 14.2) years old. In group II (older patients) were 52 patients (23 women and 29 men), 70 to 86, (mean 71.3 +/- 5.5) years old. In all patients Holter monitoring before reversion of atrial fibrillation was performed. Consequently sinus rhythm (SR) was restored using pharmacological or electrical cardioversion. After SR stabilization next Holter monitoring was performed. The following electrocardiographic parameters was assessed: mean heart rate (HR mean), maximal heart rate (HR max), minimal heart rate (HR min), occurrence of AEV and PA over 2000 ms duration time. The PA over 2000 ms duration time occurred significantly more often during FA than after SR restoration. HR max was significantly higher during FA compared to during SR. Similar changes in HR mean was noted. HR min was nearly constant both in FA and SR. The frequency of AEV occurrence was different according to Lown class. In clinically benign arrhythmia (class I and II) similar occurrence of ventricular ectopic beat either during FA and SR was observed. However ventricular arrhythmia Lown's class III and IV was observed more frequently during FA than after SR restoration. Ventricular arrhythmia Lown's class V only in one older patient during FA was recorded, and after reversion to SR wasn't observed. Reversion of FA to SR allows to better control HR and may prevent to arise or increase heart failure in the elderly. Number of PA during SR is considerably smaller compared to FA, which reduce risk of central nervous system ischemia in the elderly.
1,526
[Thrombocytopenia induced by type II heparin and myocardial infarct: 2 case reports].
Heparin-induced thrombocytopenia (HIT) type II is an acquired thrombophylic state and life-threatening immune complication of a heparin treatment mainly clinically manifested by marked thrombocytopenia, frequently by arterial and venous thrombosis, and sometimes by skin changes. Functional assay as heparin aggregation test and 14C-serotonin release assays are used in diagnostics as well as antigen assays of which detection tests for heparin-platelet factor 4 antibodies are most frequently used. Considering the fact that there is no single reliable assays for HIT II detection available, sometimes it is necessary to combine both of the above-mentioned types of assays. We present the case of a 57-year-old patient with an acute anterior myocardial infarction with cardiac insufficiency of III and IV degree according to Killip, recurrent ventricular fibrillation and diabetes mellitus type II developing thrombocytopenia to 37 x 10(9)/l accompanied with typical skin changes. The diagnosis was confirmed by the heparin aggregation test. The second patient aged 70 undergoing the treatment for anteroseptal myocardial infarction and reinfarction of the inferior wall complicated by a cardiogenic shock and acute right bundle branch block developed thrombocytopenia 59 x 10(9)/l on the third day of the heparin therapy, with the remark that he had received a heparin therapy during the first infarction as well. Antibodies against heparin-platelet factor 4 were detected by particle gel ID-HPF4 immuno-assay. In both patients, the disease had a lethal outcome despite all then available therapeutic measures applied. Further on we discuss advantages of certain types of tests, a therapy doctrine, need for urgent therapeutic measures, inclusive of the administration of antithrombins, avoidance of harmful procedures like low-molecular-weight heparins administration and prophylactic platelet transfusion as well as preventive measures.
1,527
[Severe heart failure due to toxic cardiomyopathy in a young patient--a case report].
A case of a 26-year-old male with a two-week history of increased dyspnea, weakness and depressed physical tolerance, is presented. Dilated cardiomyopathy due to cardiotoxic effects of toluene was diagnosed. Echocardiography showed left ventricular ejection fraction of 15%. Standard pharmacological treatment, including amiodarone administered due to atrial fibrillation, caused constant clinical improvement, return of sinus rhythm and increase in the ejection fraction to 45%.
1,528
[Amiodarone-induced torsade de pointes--five case reports].
Five patients with amiodarone-induced QT prolongation and torsade de pointes are described. Hypokalemia was present in three patients, marked bradycardia - in two, and T-wave alternans - also in two patients. Patients with negative T waves in precordial leads were at higher risk of ventricular fibrillation than the patients with positive T waves. Beta-blocker, lidocaine and, in two patients, tosylate bretylate were effective. All patients survived to hospital discharge, however, one patient died four months later.
1,529
Biochemical markers of myocardial damage after radiofrequency ablation.
Radiofrequency catheter ablation (RFCA) may cause myocardial injury.</AbstractText>To assess changes in myocardial enzymes levels following RFCA.</AbstractText>Creatine kinase (CK), CK-MB, aspartate aminotransferase (GOT), alanine aminotransferase (GPT), troponin I and myoglobin levels were assessed in 53 patients (33 females, 20 males, mean age 53 years, range 23-78 years) before and 20 hours after successful RFCA (WPW type A = 13, WPW type B = 10, atrio-ventricular nodal tachycardia n = 17, atrial fibrillation or flutter n = 5, atrial tachycardia n = 2 and complex arrhythmias n = 6).</AbstractText>The mean number of RF applications was 10.4, cumulative energy - 22 671 J, duration of application - 468 sec, and temperature - 58 degrees C. A significant post-RFCA increase in the troponin I and myoglobin levels was found whereas the changes in CK and GOT levels were less pronounced. A significant correlation between troponin I elevation and RFCA energy, particularly in males, was documented. There was a trend towards a decrease in the GPT and CK-MB levels. Troponin I and myoglobin levels increased regardless of the site of RF energy application.</AbstractText>Troponin I and myoglobin are useful for the assessment of RFCA-induced myocardial injury, regardless of the site of RFCA application.</AbstractText>
1,530
[Changes in the management of cardiac arrest].
NEW RECOMMENDATIONS: for cardio-pulmonary resuscitation Methods such as mouth to mouth or the search for a pulse, until now the fundamental preliminaries, have now become second line. Everything must be organised to allow for defibrillation as rapidly as possible. NEW MODALITIES FOR CARDIAC MASSAGE: The frequency of compressions recommended is currently 100 per minute in the adult with a rhythm of compression-ventilation reaching 15/2 before intubation. Concerning the haemodynamic agents for cardiac arrest, the efficacy of high doses of adrenalin is not greater than with conventional doses. Vasopressin is not superior to intravenous adrenalin regarding survival at 24 hrs exepet in case of asystoly. Dopamine at a "renal" dose is no longer used. ANTIARRYTHMICS: Amiodarone is part of the decisional tree in the case of ventricular fibrillation or ventricular tachycardia without a pulse. Semi-automatic defibrillator accessibility should be generalized. INFUSED SOLUTIONS: Sodium bicarbonate does not improve the survival except in particular cases. Physiological serum should be preferred to glucosed serum during reanimation.
1,531
Brugada syndrome-like ST-segment elevation increase exacerbated by vomiting.
The patient was a 53 year-old male who had 3 syncopal episodes over a 6-month period. In the electrophysiological study, ventricular fibrillation (VF) was repeatedly induced by the ventricular extrastimulus method. Intravenous pilsicainide was administered, and the J-point and ST-segment in the right precordial leads became slightly elevated just following drug administration. Five min later, the patient experienced severe nausea and then vomited twice, at which point the electrocardiogram (ECG) showed increased elevation of the J-point and ST-segment. These ECG changes recovered to normal 30 min later. The cause of his syncope was strongly suspected to be related to the VF associated with Brugada syndrome. An interesting aspect of this case was the particular type of J-point and ST-segment elevation that was induced when the patient experienced nausea and vomiting. It is proposed that this phenomenon originated from the vagal stimulation associated with the nausea and vomiting.
1,532
Different predictive values of electrophysiological testing and autonomic assessment in patients surviving a sustained arrhythmic episode.
Recent data suggest that the electrophysiological study (EPS) has limited value in the identification of high risk patients, so the aim of the present study was to evaluate if non-invasive measurement of baroreflex sensitivity (BRS), a marker of autonomic balance, provides additional prognostic information in patients surviving a sustained arrhythmic episode.</AbstractText>The study group comprised 112 post myocardial infarction patients consecutively referred for EPS following documented ventricular fibrillation (VF) (20), sustained ventricular tachycardia (VT) (74) or a syncopal episode with subsequently documented non-sustained VT at Holter monitoring (18). BRS was assessed according to the transfer function method. A cardioverter - defibrillator (ICD) was implanted in 97 patients. During follow-up (median 315 days), appropriate ICD discharge occurred in 53 patients, and 3 more patients died suddenly. Sustained VT was induced in 84% and 77% of patients who did or did not develop arrhythmia at follow-up (p=0.34). No differences were found in age, sex, infarct site, drug therapy, resting RR interval or cycle of induced VT. Left ventricular ejection fraction (LVEF) &lt; or =35%, New York Heart Association (NYHA) class &gt;2 and BRS &lt; or =3.3 ms/mmHg were found to be univariate predictors of arrhythmia recurrence. Multivariate models were obtained after grouping patients according to a moderately or severely depressed LVEF. Among the patients with LVEF &lt; or =35%, BRS &lt; or =3.3 ms/mmHg emerged as the only significant risk predictor of arrhythmia occurrence (sensitivity, specificity, positive and negative predictive value = 79%, 74%, 83% and 68%, respectively), whereas NYHA class &gt;2 was a significant predictor among patients with LVEF &gt;35%.</AbstractText>Noninvasive BRS, but not EPS, is of value in predicting VT/VF episode recurrence in patients surviving a major arrhythmic event.</AbstractText>
1,533
Measurement of end-tidal carbon dioxide in patients with cardiogenic shock treated using a percutaneous cardiopulmonary assist system.
We have reported that percutaneous cardiopulmonary assist systems (PCPS) are effective in treating life-threatening cardiogenic shock that is intractable to treatment with intraaortic balloon pumping (IABP). However, there are few clinical indices that can be used to evaluate the effectiveness of PCPS. End-tidal carbon dioxide (ET-CO(2)) content reflects pulmonary blood flow. We monitored ET-CO(2) continuously and determined whether we could use it as a new index to evaluate the effectiveness of PCPS. Seventeen patients with cardiogenic shock were intubated and evaluated by ET-CO(2) monitoring during PCPS. The etiology of shock included acute myocardial infarction (n=10), acute myocarditis (n=2), recent coronary artery bypass graft (n=1), cardiac rupture (n=1), hypertrophic obstructive cardiomyopathy complicated by ventricular fibrillation (n=1), left atrial myxoma (n=1) and artificial valve malfunction (n=1). PCPS was extremely effective in 10 of 17 patients (58.8%), and they recovered from the cardiogenic shock. The remaining 7 patients did not recover from shock, and died during PCPS. Six of ten patients who recovered from shock were successfully weaned from PCPS and 4 patients had good long-term survival. In the cases where PCPS was effective, the ET-CO(2) measured soon after the beginning of PCPS was significantly higher than in the cases in which PCPS was ineffective. Furthermore, the ET-CO(2) content increased gradually with the improvement in hemodynamics. In contrast, ET-CO(2) content remained low if PCPS was not effective. The ET-CO(2) represents a useful predictor of survival or death and is also a good index for weaning in patients treated with PCPS.
1,534
Heart failure and sudden death in patients with tachycardia-induced cardiomyopathy and recurrent tachycardia.
Tachycardia-induced cardiomyopathy is a reversible cause of heart failure. We hypothesized that although left ventricular ejection fraction measurements normalize after heart rate or rhythm control in patients with tachycardia-induced cardiomyopathy, recurrent tachycardia may have abrupt and deleterious consequences.</AbstractText>Patients with tachycardia-induced cardiomyopathy that developed over years were evaluated and treated. Tachycardia episodes and outcomes were assessed. Twenty-four patients were identified. All had NYHA functional class III heart failure or greater on presentation. One third were heart transplant candidates. There were 17 men and 7 women with a mean age of 46+/-16 years and mean left ventricular ejection fraction of 0.26+/-0.09 at the index visit. The cause was atrial fibrillation (n=13), atrial flutter (n=4), atrial tachycardia (n=3), idiopathic ventricular tachycardia (n=1), permanent junctional reciprocating tachycardia (n=2), and bigeminal ventricular premature contractions (n=1). Within 6 months of rate control or correction of the rhythm, left ventricular ejection fraction improved or normalized and symptoms abated in all. Five patients had tachycardia recur. In these patients, left ventricular ejection fraction dropped precipitously and heart failure ensued within 6 months, even though the initial impairment took years. Rate control eliminated heart failure and improved or normalized ejection fraction in 6 months. Three of 24 patients died suddenly and unexpectedly.</AbstractText>Tachycardia-induced cardiomyopathy develops slowly and appears reversible by left ventricular ejection fraction improvement, but recurrent tachycardia causes rapid decline in left ventricular function and development of heart failure. Sudden death is possible.</AbstractText>
1,535
The therapeutic approach to paroxysmal or persistent atrial fibrillation: rhythm control versus rate control. A review.
Atrial fibrillation (AFib) is the commonest form of arrhythmia in patients with or without cardiac disease. There is still controversy concerning the best treatment for paroxysmal or persistent atrial fibrillation: rhythm control (conversion of AFib to sinus rhythm) or rate control (control of ventricular rate with maintenance of AFib). This review aims to discuss the best evidence available on the initial approach to paroxysmal or persistent AFib. We found four major articles, whose results failed to prove the superiority of one approach over the other. However, there was a non-statistically significant tendency in favor of rate control in a set of clinically important results. Based on this data, we recommend rate control as the first approach to paroxysmal or persistent AFib.
1,536
Coronary surgery: which method to use?
To compare 4 methods of myocardial protection in GABG in terms of markers of myocardial ischemia, mortality, morbidity and mid-term results.</AbstractText><AbstractText Label="MATERIAL &amp; METHODS" NlmCategory="METHODS">Retrospective study of 241 consecutive patients undergoing isolated &gt; 1 CABG using one of 4 methods: off-pump (OFF, n = 108), cardiopulmonary bypass (CPB) and cardioplegia (CARD, n = 66), CPB and beating heart (BEAT, n = 47), or CPB and ventricular fibrillation (FIBR, n = 20). Mean age was 65.7 +/- 9.3 years and mean EuroSCORE was 3.2 +/- 2.3. The groups were similar in terms of age, gender distribution, body mass index, incidence of smoking, hypertension, renal insufficiency, CCS class, ventricular function and mean EuroSCORE. Serial blood samples were collected for CK-MB and troponin T, preoperatively and 1, 6, 12 and 24 hours after the procedure.</AbstractText>Mean number of distal anastomoses was 3.27 BEAT, 2.98 CARD, 2.90 FIBR and 2.55 OFF (p &lt; 0.05 OFF vs. the other 3 groups). Six patients died in hospital (2.5%), 2/47 BEAT (4.2%), 1/66 CARD (1.5%), 1/20 FIBR (5.0%), 2/108 (1.9% OFF) (p = 0.1). The incidence of atrial fibrillation, stroke/TIA and blood transfusion and length of stay were similar between groups (p = 0.1) but there was a tendency for increased incidence of Q-wave MI (p = 0.08) in OFF and combined adverse events in FIBR (p = 0.07). At 12 hours postoperatively, CK-MB and troponin T were significantly higher in FIBR than in CARD or OFF (p &lt; 0.05) and at 24 hours, troponin T remained higher in FIBR than in all other groups (p &lt; 0.05). After a mean follow-up of 19 months, no significant difference was observed between groups in mortality or relief of angina.</AbstractText>We were unable to demonstrate the superiority of any one revascularization method over another in terms of mortality, morbidity or length of stay. As shown by lower levels of myocardial markers of ischemia, better myocardial protection was obtained with OFF, BEAT and CARD compared to FIBR. Mid-term survival and relief of angina were similar between groups.</AbstractText>
1,537
Late incidence and determinants of stroke after aortic and mitral valve replacement.
Stroke is a devastating complication in patients with prosthetic valves, but characterization of its late occurrence from a large cohort is lacking.</AbstractText>Three thousand one hundred eighty-nine adult patients who underwent a total of 3,576 operations for left-heart valve replacement were managed with contemporary anticoagulation guidelines and prospectively followed in a dedicated clinic. Total follow-up was 20,096 patient years. Bootstrapped survival analysis was used to determine the impact of patient and valve related factors on the incidence of stroke.</AbstractText>Most strokes were embolic. Linearized embolic stroke rates were 1.3% +/- 0.2% per year for aortic bioprostheses, 1.4% +/- 0.2% per year for aortic mechanical valves, 1.3% +/- 0.3% per year for mitral bioprostheses, and 2.3% +/- 0.4% per year for mitral mechanical valves (p = 0.002, vs other implant types). Age more than 75 years, female gender, and smoking were independent risk factors after aortic and mitral valve replacement. Atrial fibrillation, coronary disease, and tilting-disc mechanical prostheses were independent predictors of embolic stroke after aortic valve replacement. Preoperative left ventricular (LV) dysfunction was an independent risk factor in patients with mitral prostheses. Primary operative indication, diabetes, redo status, or the presence of two prosthetic valves were not associated with an increased hazard. The addition of acetyl salicylic or dipyridamole to warfarin anticoagulation did not significantly lower embolic stroke risk in patients with mechanical prostheses.</AbstractText>Approximately 20% of patients with valve prostheses have an embolic stroke by 15 years after valve replacement. Some risk factors such as the avoidance of smoking, mitral mechanical prostheses, aortic tilting-disc valves, and proceeding to mitral surgery before LV dysfunction occurs are potentially modifiable.</AbstractText>
1,538
The mitral pulmonary autograft: assessment at midterm.
There is a dire need, especially in emergent societies, for a mitral substitute that does not require anticoagulation, and is not affected by early degeneration.</AbstractText>Between 1997 and 2003, 80 patients had successful mitral valve replacement with a pulmonary autograft. Fifty-five patients were female, and the mean age was 39.3 years. Seventy-eight patients had rheumatic mitral disease and 2 congenital. The autograft was placed inside a rigid Dacron tubing for support, and the right ventricular outflow was reconstructed with a xenograft or a homograft. Recently we have used microwave energy to ablate atrial fibrillation when present.</AbstractText>Intraoperative transesophageal echocardiography revealed adequate mitral valve areas (mean area 2.76 cm2) and acceptable mitral gradients (mean 4.3 mm Hg) in all 80 patients. There was no mitral regurgitation or trace amounts in 61 patients, and mild regurgitation in 19. Operative mortality was 5.0%, and late mortality clearly related to the procedure 6.25%. Follow-up was complete except for 2 lost patients, with a mean of 25 months, and echocardiographic findings were generally stable during follow-up. One patient developed uncritical mitral stenosis and another uncritical stenosis and insufficiency during 4 to 5.5 years. Four more patients had progression of mitral regurgitation from "mild" to "moderate" over a period from 8 months to 3 years. Uncritical xenograft pulmonic stenosis developed in 2 patients. Most of the surviving patients (83%) remain in class I status.</AbstractText>We believe the pulmonary autograft is a good mitral substitute at the disposal of cardiac surgeons, especially when patients are young and when life anticoagulation is contraindicated or impractical.</AbstractText>
1,539
Intravenous amiodarone for conversion of atrial fibrillation: misled by meta-analysis?
Therapeutic goals for atrial fibrillation (AF) include ventricular rate control, stroke prevention, conversion to normal sinus rhythm, and maintenance of normal sinus rhythm. The optimal strategy of rate versus rhythm control for acute management of patients with AF is a continuing debate. However, selected patients may require acute treatment with antiarrhythmic agents for conversion of symptomatic AF episodes to normal sinus rhythm. Recently published randomized controlled trials, qualitative systematic reviews, meta-analyses, and evidence-based international consensus guidelines have addressed the controversy regarding acute conversion of AF using antiarrhythmic therapy. Although meta-analyses often provide the highest level of evidence, the validity and application of their results are based on the quality of their methodology and accuracy of reporting. Authors of the most recent meta-analysis of amiodarone for conversion of AF state that the drug is effective and relatively rapid acting in converting AF to normal sinus rhythm in a wide range of patients, and they recommend it as a first-line drug. We feel that these conclusions are overstated and potentially misleading due to methodologic limitations of the analysis. The results of this meta-analysis and others concerning acute conversion of AF should be viewed as hypothesis generating and not the definitive answer to this question. Ultimately, well-designed, adequately powered, randomized placebo- or rate-controlled trials are needed in specific patient populations with AF to determine the absolute benefit of intravenous amiodarone for conversion of AF to normal sinus rhythm. Until more data are available, intravenous amiodarone cannot be promoted as a first-line agent for this purpose.
1,540
Percutaneous transatrial mitral commissurotomy by modified technique using a JOMIVA balloon catheter: a cost-effective alternative to the Inoue balloon.
Percutaneous transatrial mitral commissurotomy (PTMC) is an established non-surgical treatment of rheumatic mitral stenosis. The study aim was to assess the safety and efficacy of PTMC using the Joseph mitral valvuloplasty (JOMIVA) balloon catheter, with a modified technique.</AbstractText>PTMC was performed in 252 patients (88 males, 164 females; mean age 39.2 +/- 13.8 years; range: 10-76 years) with symptomatic mitral stenosis. Among patients, 52 (20.6%), 182 (72.2%) and 18 (7.2%) were in NYHA classes II, III and IV, respectively. Atrial fibrillation was present in 52 patients (20.6%), and mild mitral regurgitation (MR) in 26 (10.3%); 92 patients (36.5%) had a mitral valve echo score &gt; 8. Patients were followed up with detailed clinical and echocardiography studies at three-month intervals during the first year, and at six-month intervals thereafter.</AbstractText>The procedure was technically successful in 247 patients (98%), and an optimal result was achieved in 228 (90.5%), with mean mitral valve area increased from 0.81 +/- 0.32 to 1.92 +/- 0.39 cm2 (p &lt; 0.001). NYHA class was improved in most patients. Seven patients (2.8%) had cardiac tamponade during the procedure; one of these (0.4%) died from left ventricular tear. MR appeared (n = 10) or worsened (n = 20) in 30 patients (11.9%), among whom three (1.2%) developed severe MR. Each JOMIVA balloon catheter was used 10 to 20 times without being damaged. In total, 220 patients were followed up for between six and 54 months (mean 30 months). At follow up, 140 (63.6%) and 67 (30.5%) patients were in NYHA classes I and II, respectively. Seventeen patients (7.7%) developed mitral restenosis.</AbstractText>PTMC using the JOMIVA balloon catheter is a cost-effective and safe alternative to the Inoue balloon when treating symptomatic severe mitral stenosis. The hemodynamic benefits were sustained long term in a majority of patients. In particular, cost is important factor in a less wealthy country such as India.</AbstractText>
1,541
Antithrombotic therapy in native heart valve disease.
In establishing the indication for anticoagulation of patients with native heart valve disease, those with thromboembolic events and/or atrial fibrillation (AF) must be distinguished from patients with sinus rhythm. Anticoagulation should be started as a matter of principle in patients with thromboembolic events and/or AF who do not undergo valve replacement. However, a more differentiated procedure is mandatory for patients with sinus rhythm. If the left atrium is enlarged, spontaneous echo contrast is detected, and/or there is no atrial contraction and/or reduced left ventricular pump function (e.g., in patients with mitral valve stenosis), then anticoagulation with a target INR of 2.5 is indicated, even in those with sinus rhythm. Whereas rheumatic mitral valve stenosis predominates in developing countries, aortic stenosis (AS) predominates in developing countries. These AS patients mainly suffer microemboli that often determine the prognosis in patients with calcification of the mitral annulus. Anticoagulation is not recommended in calcific microemboli. If there are simultaneous atherothrombotic plaques of the aortic arch &gt; 5 mm in size owing to an often more complex cardiovascular risk profile, then warfarin treatment is indicated. Mitral valve prolapse (MVP), patient foramen ovale and atrial septal aneurysm are potential sources of embolism that may cause stroke. On their own, these congenital lesions do not entail an indication for anticoagulation. This applies in particular to patients with MVP in whom secondary prevention of stroke can be attained with 100 mg aspirin.
1,542
[Behcet disease: uncommon cause of myocardial infarction].
A 25-year-old man who was known to have Beh&#xe7;et's syndrome and who has no coronary risk factors suffered an acute anterior wall myocardial infarction which was complicated by a ventricular fibrillation. The diagnosis of Beh&#xe7;et's syndrome was based on recurrent thrombophlebitis, genital and oral aphtoses, posterior uveitis, positive pathergy test and HLAB51. About 20 cases of myocardial infarction were reported in the literature but the etiopathogeny, the causal relationship and the treatment are yet unknown.
1,543
[Does syncope change the results of programmed ventricular stimulation in patients with previous myocardial infarction?].
The induction of a ventricular tachycardia (VT) after myocardial infarction (MI) is associated with a high risk of VT and sudden death (SD) in asymptomatic patients; the purpose of the study was to know if syncope modifies the results of programmed ventricular stimulation (PVS) and the clinical consequences.</AbstractText>PVS using two and three extra stimuli delivered in two sites of right ventricle was performed in 1057 patients without spontaneous VT or resuscitated SD at least 1 month after an acute MI; 836 patients (group I) were asymptomatic and were studied for a low ejection fraction or nonsustained VT on Holter monitoring or late potentials; 228 patients (group II) were studied for unexplained syncope. The patients were followed up to 5 years of heart transplantation.</AbstractText>Sustained monomorphic VT (&lt; 280 b/min) was induced in 238 group I patients (28%) and 62 group II patients (29%); ventricular flutter (VT &gt; 270 b/min) or ventricular fibrillation (VF) was induced in 245 group I patients (29%) and 42 group II patients (18%) (P &lt; 0.05); PVS was negative in 353 group I patients (42%) and 124 (55%) group II patients (NS). The patients differ by their prognosis; cardiac mortality was 13% in group I patients and 34% in group II patients with inducible VT &lt; 280 b/min (P &lt; 0.01), 4% in group I patients and 13% in group II patients with inducible VF (P &lt; 0.05), 5% in group I patients and 7% in group II patients with negative study (NS). In conclusion, syncope did not change the results of programmed ventricular stimulation after myocardial infarction. However, syncope increased significantly cardiac mortality of patients with inducible ventricular tachycardia, flutter or fibrillation.</AbstractText>
1,544
Antiarrhythmic effect of ischemic preconditioning during low-flow ischemia. The role of bradykinin and sarcolemmal versus mitochondrial ATP-sensitive K(+) channels.
Short episodes of ischemia (ischemic preconditioning) protect the heart against ventricular arrhythmias during zero-flow ischemia and reperfusion. However, in clinics, many episodes of ischemia present a residual flow (low-flow ischemia). Here we examined whether ischemic preconditioning protects against ventricular arrhythmias during and after a low-flow ischemia and, if so, by what mechanism(s). Isolated rat hearts were subjected to 60 min of low-flow ischemia (12% residual coronary flow) followed by 60 min of reperfusion. Ischemic preconditioning was induced by two cycles of 5 min of zero-flow ischemia followed by 5 and 15 min of reperfusion, respectively. Arrhythmias were evaluated as numbers of ventricular premature beats (VPBs) as well as incidences of ventricular tachycardia (VT) and ventricular fibrillation (VF) during low-flow ischemia and reperfusion. Ischemic preconditioning significantly reduced the number of VPBs and the incidence of VT and of VF during low-flow ischemia. This antiarrhythmic effect of preconditioning was abolished by HOE 140 (100 nM), a bradykinin B(2) receptor blocker. Similar to preconditioning, exogenous bradykinin (10 nM) reduced the number of VPBs and the incidence of VT and of VF during low-flow ischemia. Furthermore, the antiarrhythmic effects of both ischemic preconditioning and bradykinin were abolished by glibenclamide (1 microM), a non-specific blocker of ATP-sensitive K(+) (K(ATP)) channels. Finally, the antiarrhythmic effects of both ischemic preconditioning and bradykinin were abolished by HMR 1098 (10 microM), a sarcolemmal K(ATP) channel blocker but not by 5-hydroxydecanoate (100 microM), a mitochondrial K(ATP) channel blocker. In conclusion, ischemic preconditioning protects against ventricular arrhythmias induced by low-flow ischemia, and this protection involves activation of bradykinin B(2) receptors and subsequent opening of sarcolemmal but not of mitochondrial K(ATP) channels.
1,545
Stretch-induced ventricular arrhythmias during acute ischemia and reperfusion.
Mechanical stretch has been demonstrated to have electrophysiological effects on cardiac muscle, including alteration of the probability of excitation, alteration of the action potential waveform, and stretch-induced arrhythmia (SIA). We demonstrate that regional ventricular ischemia due to coronary artery occlusion increases arrhythmogenic effects of transient diastolic stretch, whereas globally ischemic hearts showed no such increase. We tested our hypothesis that, during phase Ia ischemia, regionally ischemic hearts may be more susceptible to triggered arrhythmogenesis due to transient diastolic stretch. During the first 20 min of regional ischemia, the probability of eliciting a ventricular SIA (P(SIA)) by transient diastolic stretch increased significantly. However, after 30 min, P(SIA) decreased to a value comparable with baseline measurements, as expected during phase Ib, where most ventricular arrhythmias are of reentrant mechanisms. We also suggest that mechanoelectrical coupling may contribute to the nonreentrant mechanisms underlying reperfusion-induced arrhythmia. When coronary artery occlusion was relieved after 30 min of ischemia, we observed an increase in P(SIA) and the maintenance of this elevated level throughout 20 min of reperfusion. We conclude that mechanoelectrical coupling may underlie triggered arrhythmogenesis during phase 1a ischemia and reperfusion.
1,546
Usefulness of quantitative gated single-photon emission computed tomography to evaluate ventricular synchrony in patients receiving biventricular pacing.
Quantitative gated single-photon emission computed tomography was performed in 10 patients before and shortly after (&lt;1 month) receiving biventricular pacing (BVP). They were divided into 2 groups (responder and nonresponder groups) on the basis of clinical status and echocardiographic parameters 18 +/- 6 months later. In the responder group, left ventricular synchrony shortly after BVP improved significantly compared with that before BVP (p &lt;0.05), but there was no change in the nonresponder group.
1,547
Partial cardiac autotransplantation for reduction of the left atrium.
Various surgical procedures have been employed to treat a greatly enlarged left atrium. We review the use of partial cardiac autotransplantation to reduce left atrial volume in 7 patients with rheumatic mitral valve disease and left atrial and ventricular volume in 2 patients with idiopathic dilated cardiomyopathy. There were 5 males and 4 females aged 25 to 62 years. The patients with rheumatic etiology had atrial fibrillation, while those with dilated cardiomyopathy had sinus rhythm. The mitral valve was replaced in 6 patients and reconstructed in 3. Mean aortic cross clamp time in the operations involving isolated left atrial resection was 119 +/- 44 min. Mean left atrial volume fell from 331 mL to 92 mL, while mean left atrial diameter decreased from 8.6 cm to 4.7 cm. Sinus rhythm was restored in 5 of the 7 patients who had preoperative atrial fibrillation. There was no operative mortality. The patients with dilated cardiomyopathy died in the postoperative period, one on the 14th day from low cardiac output and the other on the 113th day from multiorgan failure. Partial cardiac autotransplantation can be effective in reducing heart chamber size in selected patients, especially those with giant left atrium.
1,548
A simulation study of the reaction of human heart to biphasic electrical shocks.
This article presents a study, which examines the effects of biphasic electrical shocks on human ventricular tissue. The effects of this type of shock are not yet fully understood. Animal experiments showed the superiority of biphasic shocks over monophasic ones in defibrillation. A mathematical computer simulation can increase the knowledge of human heart behavior.</AbstractText>The research presented in this article was done with different models representing a three-dimensional wedge of ventricular myocardium. The electrophysiology was described with Priebe-Beuckelmann model. The realistic fiber twist, which is specific to human myocardium was included. Planar electrodes were placed at the ends of the longest side of the virtual cardiac wedge, in a bath medium. They were sources of electrical shocks, which varied in magnitude from 0.1 to 5 V. In a second arrangement ring electrodes were placed directly on myocardium for getting a better view on secondary electrical sources. The electrical reaction of the tissue was generated with a bidomain model.</AbstractText>The reaction of the tissue to the electrical shock was specific to the initial imposed characteristics. Depolarization appeared in the first 5 ms in different locations. A further study of the cardiac tissue behavior revealed, which features influence the response of the considered muscle. It was shown that the time needed by the tissue to be totally depolarized is much shorter when a biphasic shock is applied. Each simulation ended only after complete repolarization was achieved. This created the possibility of gathering information from all states corresponding to one cycle of the cardiac rhythm.</AbstractText>The differences between the reaction of the homogeneous tissue and a tissue, which contains cleavage planes, reveals important aspects of superiority of biphasic pulses.</AbstractText>
1,549
Antiarrhythmic drugs in atrial fibrillation: an overview of new agents, their mechanisms of action and potential clinical utility.
Despite recent advances in our understanding of the mechanism of atrial fibrillation (AF), effective treatment remains difficult in many patients. Pharmacotherapy remains the mainstay of treatment and includes control of ventricular rate as well as restoration and maintenance of sinus rhythm. The currently available antiarrhythmic drugs are particularly effective in converting paroxysmal AF to sinus rhythm and in enhancing the positive effect of electrical cardioversion, but are limited in their efficacy in maintaining sinus rhythm. Moreover, there are limited options in the setting of co-existing ischaemic heart disease, left ventricular dysfunction and structural heart diseases. New drugs added to our clinical armamentarium have been, or are being, developed to combine better efficacy and lack of pro-arrhythmic effects. These developments have gained more interest particularly with the recent debate over rate control versus rhythm control for AF. Although some of these agents are promising, their uptake in clinical practice will not only depend on their efficacy as antiarrhythmic agents but also on their safety in acutely terminating AF and in long-term maintenance of sinus rhythm or rate control in the community.
1,550
QT prolongation in anaesthetized guinea-pigs: an experimental approach for preliminary screening of torsadogenicity of drugs and drug candidates.
Many non-cardiovascular drugs can prolong the QT interval of the electrocardiogram (ECG); this is an accessory property not necessary for their pharmacological action and generally linked to the block of the potassium HERG channels and delayed cardiac repolarization. The QT prolongation can lead to a dangerous tachyarrhythmia, called torsade de pointes, and potentially to fatal ventricular fibrillation. The experimental approaches, aimed at an early identification of this undesidered property, often require sophisticated and expensive equipment or the use of superior animal species (dog, primates) that cannot be employed easily for ethical and/or economic reasons. This work aimed to study drug-induced QT prolongation in anaesthetized guinea-pigs and to evaluate the reliability of such an experimental approach to obtain a satisfying predictive parameter of the torsadogenicity of drugs in humans. Seven drugs that were torsadogenic in humans (astemizole, cisapride, haloperidol, quinidine, sotalol, terfenadine and thioridazine) and two that were non-torsadogenic (chlorprotixene and diazepam) were administered i.v. to guinea-pigs under pentobarbital anaesthesia. The ECGs were recorded by four electrodes inserted in the subcutaneous layer of the limbs. Both RR and QT intervals were measured in Leads II and III and then the correct QT values were calculated by Bazett and Fridericia algorithms (QTcB and QTcF, respectively). All the drugs, with the exception of chlorprotixene and diazepam, produced a dose-dependent prolongation of the QT and RR intervals and a significant increase of QTcB and QTcF values. It can be concluded that this method represents a rapid and low-cost procedure to evaluate the cardiac safety pro fi le in the preliminary screening of a high number of drugs or drug candidates.
1,551
Effects of cardiopulmonary resuscitation on predictors of ventricular fibrillation defibrillation success during out-of-hospital cardiac arrest.
Early defibrillation is considered the most important factor for restoring spontaneous circulation in cardiac arrest patients with ventricular fibrillation. Recent studies have shown that, after prolonged ventricular fibrillation, the rates of return of spontaneous circulation (ROSC) and survival are improved if defibrillation is delayed so that CPR can be given first. To examine whether CPR improves myocardial readiness for defibrillation, we analyzed whether CPR causes changes in predictors of defibrillation success calculated from the ventricular fibrillation waveform.</AbstractText>ECG recordings were retrieved for 105 patients from an original study of 200 patients receiving CPR or defibrillation first. Altogether, 267 CPR sequences from 77 patients were identified on which the effect of CPR could be evaluated. Five predictors of ROSC (spectral flatness measure, energy, centroid frequency, amplitude spectrum relationship, and estimated probability of ROSC) were determined from a spectral analysis of the ventricular fibrillation waveform immediately before and immediately after each of the 267 sequences. CPR increased spectral flatness measure, centroid frequency, and amplitude spectrum relationship (P&lt;0.05, P&lt;0.001, P&lt;0.01). In an analysis of the effect of the duration of CPR, the probability of ROSC and amplitude spectrum relationship showed a positive change for CPR sequences lasting &gt;3 minutes (P&lt;0.001, P&lt;0.05).</AbstractText>During resuscitation from ventricular fibrillation, changes in the predictors calculated from the ventricular fibrillation waveform indicated a positive effect of CPR on the myocardium.</AbstractText>
1,552
Plasma B-type natriuretic peptide levels predict postoperative atrial fibrillation in patients undergoing cardiac surgery.
Postoperative (postop) atrial fibrillation (AF) occurs in up to 60% of patients after cardiac surgery, leading to longer hospital stays and increased healthcare costs. Recently, B-type natriuretic peptide (BNP) has been reported to predict occurrence of nonpostoperative AF. This study evaluates whether elevated preoperative (preop) plasma BNP levels predict the occurrence of postop AF.</AbstractText>One hundred eighty-seven patients with no history of atrial arrhythmia who had a preoperative BNP level and had undergone cardiac surgery were identified. Their records were reviewed, and postoperative ECG and telemetry strips were analyzed for AF until the time of discharge. Postop AF was documented in 80 patients (42.8%). AF patients were older (68+/-11 versus 64+/-14 years, P=0.04), but there was no difference in sex distribution, hypertension, left ventricular (LV) function, LV hypertrophy (LVH), left atrial size, history of coronary artery disease (CAD), or beta-blocker use. Preop plasma BNP levels were higher in the postop AF patients (615 versus 444 pg/mL, P=0.005). After adjustment for age, sex, type of surgery, hypertension, LV function, LVH, left atrial size, CAD, and beta-blocker use, the odds ratios of postop AF according to increasing quartiles, compared with patients with lowest quartile, were 1.8, 2.5, and 3.7 (P(trend)=0.03).</AbstractText>An elevated preop plasma BNP level is a strong and independent predictor of postop AF. This finding has important implications for identifying patients at higher risk of postop AF who could be considered for prophylactic antiarrhythmic or beta-blocker therapy.</AbstractText>
1,553
Ventricular fibrillation in hypercalcaemic crisis due to primary hyperparathyroidism.
We report the case of a 64-year-old man who presented with severe hypercalcaemia secondary to primary hyperparathyroidism. Soon after admission he developed ventricular fibrillation with no other cause than this severe hypercalcaemia. Although the occurrence of cardiac arrhythmias in hypercalcaemia is widely known, ventricular fibrillation has never been described before.
1,554
Iohexol contrast medium induces QT prolongation in amiodarone patients.
Amiodarone is widely used in ventricular tachyarrhythmias and atrial fibrillation, known to prolong QT-intervals. Concurrent administration of drugs prolonging QT- time can induce life-threatening ventricular tachyarrhythmia.</AbstractText>QT-interval changes following use of Iohexol contrast-medium for coronarangiography were observed comparing 21 patients taking long-term amiodarone therapy with 21 controls not taking amiodarone or QT-prolonging drugs retrospectively.</AbstractText>Concurrent use of Iohexol and amiodarone was associated with significant prolongation of QTc-interval (433, 95%CI: 419-448 ms vs. 480, 95%CI: 422-483 ms, P &lt; 0.001) the day after coronarangiograpgy. 6/21 patients showed severe prolonged QTc-interval of &gt;500 ms.</AbstractText>Caution is advised until more is known about pro-arrhythmic effects of Iohexol.</AbstractText>
1,555
Indications for an implantable cardioverter defibrillator (ICD).
Since the first clinical use of implantable defibrillator in human, the technology and the function of implantable cardioverter-defibrillator (ICD) have been much improved and now, ICD can be implanted within the chest wall. ICD is the most reliable therapy to prevent sudden cardiac death (SCD) in patients with documented VT/VF and the efficacy is most clear in patients with depressed heart function. It is now extended as a tool of the primary prevention of SCD in high risk patients after myocardial infarction. However, such beneficial effect is not applicable to DCM though patients might have depressed heart function. ICD is not free from procedure- or device-related problems which need to be resolved. From unknown causes, VT/VF might recur in an incessant form and an emergency admission is needed. Therefore, even during ICD therapy, patients often require antiarrhythmic drugs or catheter ablation.
1,556
Genuine effects of ventricular fibrillation upon myocardial blood flow, metabolism and catecholamines in patients with aortic stenosis.
Ventricular fibrillation (VF) is life-threatening because of its haemodynamic and metabolic effects. The purpose was to examine if VF also has primary effects per se. We therefore investigated the early effects of VF on myocardial blood flow, metabolic characteristics and catecholamine concentrations in patients undergoing surgery for aortic stenosis.</AbstractText>The immediate effects of up to 5 min of VF were studied in 21 patients during cardiopulmonary bypass (CPB) before valve replacement.</AbstractText>During VF the global myocardial oxygen consumption, coronary blood flow and vascular resistance were unchanged, and the mean arterial pressure (on CPB) decreased from 70 to 51 mmHg (p &lt; 0.02). Fibrillation induced a high myocardial tone and a probable functional aortic insufficiency, which instantly equilibrated left ventricular and aortic pressures. Signs of myocardial ischaemia and acidosis developed after 4 min: a decrease in the pH of coronary sinus blood from 7.38 to 7.32 (p &lt; 0.001), an increased release of lactate from 32 to 137 micromol/min (p &lt; 0.001) and potassium from 29 to 73 micromol/min (p &lt; 0.05). The noradrenaline net release increased from 0.021 to 0.58 nmol/min (p &lt; 0.02) after 1.5 min of VF and then decreased. The adrenaline net uptake remained low and unchanged (17-28%).</AbstractText>VF in patients with aortic stenosis was rapidly followed by myocardial ischaemia, acidosis and a transient increase in the myocardial noradrenaline net release despite sufficient coronary perfusion and unchanged global myocardial oxygen consumption. The VF instantly induced equilibration of left ventricular and aortic pressure and probably caused a relative underperfusion of the subendocardium. These factors all support persistence of VF.</AbstractText>
1,557
The calcium sensitizer levosimendan and cardiac arrhythmias: an analysis of the safety database of heart failure treatment studies.
Levosimendan is a calcium sensitizer that increases the contractility of the myofilaments and is considered not to affect cardiac electrophysiology. We assessed its potential to generate cardiac arrhythmias by analysing ECG recordings from clinical studies on intravenously administered levosimendan in heart failure patients.</AbstractText>The database consisted of continuous 1-day recordings, of which 366 were during levosimendan and 142 during placebo comparison. Supraventricular (SVT) and ventricular tachycardia (VT) were defined as &gt; or =3 premature complexes at a rate &gt; or = 120/min. No difference appeared between levosimendan and control groups in the occurrence of atrial fibrillation (12% vs 13%), SVT (28% vs 30%), or VT (41% vs 44% of all recordings; all p = NS). Also the frequency of VT was similar (0.55 +/- 3.89 vs 0.20 +/- 1.08 episodes/h; p = NS). No torsade de pointes or sustained VT occurred.</AbstractText>Short-term levosimendan therapy of heart failure showed no tendency to increase cardiac arrhythmias. Although assessing only surrogates of prognostically significant arrhythmias, the findings together with previously observed reduction of mortality in heart failure therapy studies support the presumption that levosimendan has an electrophysiologically neutral profile.</AbstractText>
1,558
Structure-affinity relationships of 5'-aromatic ethers and 5'-aromatic sulfides as partial A1 adenosine agonists, potential supraventricular anti-arrhythmic agents.
Atrial fibrillation (AF) is the most commonly encountered sustained clinical arrhythmia with an estimated 2.3 million cases in the US (2001). A(1) adenosine receptor agonists can slow the electrical impulse propagation through the atrioventricular (AV) node (i.e., negative dromotropic effect) resulting in prolongation of the stimulus-to-His bundle (S-H) interval to potentially reduce ventricular rate. Compounds that are full agonists of the A(1) adenosine receptor can cause high grade AV block. Therefore, it is envisioned that a compound that is a partial agonist of the A(1) adenosine receptor could avoid this deleterious effect. 5(') Phenyl sulfides (e.g., 17, EC(50)=1.26 microM) and phenyl ethers (e.g., 28, EC(50)=0.2 microM) are partial agonists with respect to their AV nodal effects in guinea pig isolated hearts. Additional affinity, GTPgammaS binding data suggesting partial activity of the A(1) adenosine receptor, and PK results for 5(') modified adenosine derivatives are shown.
1,559
A novel minimal-invasive model of chronic myocardial infarction in swine.
Most animal studies on myocardial infarction (MI) have used open-chest models with direct surgical coronary artery ligation, which imply local as well as generalized side effects of major surgery. Some closed-chest models of MI have been established, mainly using catheterization techniques with coronary artery embolization, balloon occlusion, and intracoronary injection of thrombogenic agents. The aim of this study was to develop a closed-chest technique of chronic coronary artery occlusion at a selected location with subsequent thrombus formation without use of balloon inflation or thrombotic chemical agents.</AbstractText>A coronary angiography via the carotid artery was performed using a 7 F guiding catheter in 21 pigs. After insertion of a percutaneous transluminal coronary angioplasty (PTCA) guide wire into the distal coronary artery, a vessel-size adapted flexible foreign body comprising an open-cell sponge was advanced into the coronary artery via the guide wire by a non-inflated PTCA balloon. Five min after removal of the guide wire and the balloon catheter, total coronary artery occlusion was documented by angiography. Retrograde thrombosis of the coronary artery occurred in three animals. After one week, total vessel occlusion at the previously selected location was visualized by coronary angiography in animals that had survived. Macroscopic analysis demonstrated the foreign body with subsequent thrombus formation in the coronary artery and distal MI. Post-mortem histological analysis revealed myocardial necrosis and granulocyte infiltration at the margin of the infarction, without damage to remote myocardium.</AbstractText>This new easy-to-perform closed-chest technique provides reproducible chronic coronary artery occlusion at a selected location with subsequent MI. It avoids major surgery and thoracotomy and does not require balloon inflation or intracoronary injection of thrombotic or chemical agents.</AbstractText>Copyright 2004 Lippincott Williams &amp; Wilkins</CopyrightInformation>
1,560
Management of chronic heart failure in the community: role of a hospital based open access heart failure service.
To evaluate the role of an open access heart failure service based at a teaching hospital for the diagnosis and treatment optimisation of patients with heart failure in the community and to identify measures that may further enhance the effectiveness of such a service.</AbstractText>963 patients with suspected heart failure seen over an eight year period referred by their general practitioners to the cardiology department at a district general hospital.</AbstractText>Presence or absence of left ventricular systolic dysfunction (LVSD) (left ventricular ejection fraction &lt; 50% on echocardiography), and determination of the risk factors and predictors of LVSD.</AbstractText>The majority of the patients were women (60% v 40%) and elderly (mean age 68.8 years). On echocardiography, only 30.8% were found to have LVSD. Patients were more likely to have LVSD if they were men (42.3% v 23.1%, p &lt; 0.001, relative risk (RR) 1.8), were &gt; 60 years of age (33.5% v 20.8%, p &lt; 0.001, RR 1.6), or had a history of diabetes (49.4% v 29.1%, p &lt; 0.001, RR 1.7), ischaemic heart disease (36.5% v 29.1%, p = 0.04, RR 1.3), or atrial fibrillation (52.6% v 27.8%, p &lt; 0.001, RR 1.9). An abnormal ECG (48.4% v 19.5%, p &lt; 0.001, RR 2.5) and cardiothoracic ratio &gt; 0.5 on chest radiograph (44.3% v 17.8%, p &lt; 0.001, RR 2.5) were found to be good predictors of LVSD. A normal ECG (negative predictive value 80.5%) and a cardiothoracic ratio of &lt; 0.5 (negative predictive value 82.2%) can be used as baseline measures to identify patients with lower risk of developing LVSD (combined negative predictive value 87.9%).</AbstractText>An open access heart failure clinic is effective for the diagnosis and management of chronic heart failure in community based patients. The presence of risk factors and simple baseline tests can be used to identify patients with LVSD in the community. The introduction of a protocol based on these findings into a referral system can improve the efficiency and cost effectiveness of such a service.</AbstractText>
1,561
Ventricular fibrillation: new insights into mechanisms.
Device therapy with implantable cardioverter-defibrillators is currently the only proven effective therapy against sudden cardiac death due to ventricular fibrillation. However, the expanded clinical indications for device therapy come at a staggering cost to an already overburdened health care system. Given these statistics, it is both highly desirable and economically imperative to develop alternative therapies. New insights into the mechanisms of ventricular fibrillation, particularly the role of dynamic factors causing wave instability, are providing a promising avenue for developing novel therapies to prevent sudden cardiac death.
1,562
[Severe anaphylactic reaction to metamizol during subarachnoid anesthesia].
A 59-year-old man with no relevant medical history underwent a right saphenectomy under subarachnoid anesthesia with mepivacaine. Administration of intravenous metamizol for postoperative analgesia was followed by severe anaphylactic reaction with respiratory failure and ventricular fibrillation. The patient recovered after orotracheal intubation and defibrillation. High serum tryptase levels 2 and 6 hours after the episode and positive skin prick tests confirmed the diagnosis of anaphylactic reaction mediated by immunoglobulin-E antibodies. Anaphylactic reactions to metamizol may be more common than would appear based on reports in the literature. When signs present suddenly with cardiovascular or respiratory involvement, symptomatic treatment should be started even in the absence of cutaneous or mucosal signs and allergy tests should be carried out immediately.
1,563
Enalapril treatment and hospitalization with atrial tachyarrhythmias in patients with left ventricular dysfunction.
Experimental and clinical evidence suggests a preventive role for agiotensin-coverting enzyme (ACE) inhibitors on the development of atrial fibrillation. However, the effect of ACE inhibition on hospitalization with atrial tachyarrhythmias in patients with left ventricular (LV) dysfunction is not known. We sought to determine whether enalapril treatment reduced hospitalizations with atrial tachyarrhythmias in patients with LV dysfunction.</AbstractText>We performed a retrospective analysis of the Studies of Left Ventricular Dysfunction (SOLVD) trial. Hospitalizations with atrial tachyarrhythmias were noted.</AbstractText>A total of 192 hospitalizations with atrial tachyarrhythmias occurred in 158 patients during a follow-up period of 34 months. The time to first hospitalization with atrial tachyarrhythmias or death was significantly lower in the enalapril group (P =.005). In a multivariate analysis adjusting for the presence of atrial fibrillation at study entry, enalapril treatment was associated with a reduction in the rate of hospitalization with atrial tachyarrhythmias or death (RR, 0.87; 95% CI, 0.79-0.96; P =.007). The incidence of hospitalization with atrial tachyarrhythmias was 7.9 hospitalizations per 1000 patient-years of follow-up in the enalapril group, compared with 12.4 per 1000 patient-years in the placebo group (RR, 0.64; 95% CI, 0.48-0.85; P =.002).</AbstractText>Enalapril is associated with a decreased incidence of hospitalization with atrial tachyarrhythmias in patients with LV dysfunction.</AbstractText>
1,564
[Perioperative heart rate control with landiolol for a patient with rapid atrial fibrillation complicated with low cardiac function].
A 62-year-old man complicated with old antero-septal wall myocardial infarction and atrial fibrillation suffered from lung and pancreas cancer. He underwent gastro-duodenum bypass surgery under epidural combined with general anesthesia. His ECG and echocardiogram revealed atrial fibrillation and his left ventricular ejection fraction was 35%. After the start of surgery under general anesthesia, EHR was stable between 80-100 beats x min(-1) but rapid atrial fibrillation developed with a rate of over 140 beats x min(-1) after epidural injection of 0.375% ropivacaine 3 ml. Treatment including continuous intravenous diltiazem and several bolus intravenous injections of verapamil failed to decrease the heart rate. Therefore we used landiolol, a short-acting beta blocker, to control heart rate. HR decreased without decreasing his blood pressure. Continuous landiolol infusion was maintained for 3 hours and 30 minutes in the ICU. After finishing infusion, his heart rhythm never became rapid atrial fibrillation. We conclude that landiolol is useful for heart rate control of rapid atrial fibrillation.
1,565
[A case of intraoperative hyperkalemia induced with administration of an angiotensin II receptor antagonist (AIIA) and intake of dried persimmons].
An 87-year-old man was scheduled for cervical laminectomy. Anesthesia was maintained with nitrous oxide, oxygen, sevoflurane, and fentanyl with tracheal intubation. Thirty minutes after the start of operation, serum potassium was 7.41 mEq x l(-1). We immediately administered potassium-free fluid, furosemide, bicarbonate, calcium gluconate and insulin. We stopped the operation and returned the patient to supine position, but he fell into ventricular fibrillation. Immediate CPR and countershock successfully restored sinus rhythm within 5 minutes. He was discharged from ICU without any neurological complications. Daily he took Losartan potassium, an AIIA, due to hypertension and ate preoperatively dried persimmons, a potassium-rich food. We suspect that hyperkalemia was induced by administration of an AIIA in combination with excessive intake of dried persimmons. AIIA may cause severe hyperkalemia inhibiting aldosterone activity. We should pay attention to the serum potassium level and a preoperative intake of food especially in a patient medicated with an AIIA.
1,566
Ventricular assist devices as a 'bridge to recovery': where do we stand?
The use of ventricular assist devices as a 'bridge to recovery' has a lot to promise. However, we are at a stage where there are more questions than answers. It is still difficult to predict who will be the right candidate and who will have sustained recovery after explantation of the device. In addition, we do not have a universally accepted protocol to wean patients from assist devices. A case that was successfully bridged to recovery with a left ventricular assist device is presented, together with a discussion of the literature. The search for precise markers of recovery should continue and a multicentre prospective study to validate weaning protocols is needed. At present, one should consider all available markers and look at the full clinical picture before allocating a patient to a bridge to recovery destination.
1,567
Electrophysiological findings in adolescents with atrial fibrillation who have structurally normal hearts.
Atrial fibrillation (AF) is uncommon in children, and its mechanisms are unknown. This study describes the electrophysiological findings in children and adolescents with AF and the outcome of catheter ablation.</AbstractText>Nine adolescents with symptomatic, lone AF who failed antiarrhythmic drug therapy were evaluated. All patients had ECG-documented AF and underwent invasive electrophysiological testing. Intracardiac mapping was performed to determine the site of spontaneous onset of AF and rapidly firing atrial foci. Only the triggering focus was targeted for ablation or isolation. The patients' mean age was 15.9+/-3.3 (range, 8 to 19 years). The most common finding was rapid, irregular atrial tachycardias in the region of the pulmonary veins (n=5), left atrium (n=2), or crista terminalis (n=3). One patient had foci in both the pulmonary veins and crista terminalis. The cycle lengths ranged from 108 to 280 ms. Catheter ablation was acutely successful in 8 patients (88.9%), whereas 1 patient with multiple left atrium foci was treated with the surgical maze operation. Over a mean of 35+/-22 months, 7 patients (77.8%) were arrhythmia free on no medications, while AF recurred in 2 patients who are controlled on antiarrhythmic medications. Two patients with tachycardia-induced cardiomyopathy had resolution of their left ventricular dysfunction after ablation.</AbstractText>AF in adolescents with structurally normal hearts is usually due to foci in the pulmonary veins, crista terminalis, or left atrium. These foci usually induce irregular atrial tachycardias. Catheter ablation of the foci is effective in eliminating recurrent AF.</AbstractText>
1,568
Atrial fibrillation and cardioembolic stroke.
The most disabling consequence of atrial fibrillation (AF) is stroke. In the elderly, AF is the single most important cause of stroke. The risk of stroke is increased at least 6-fold in subjects with AF. Strokes in patients with AF are in general severe, associated with higher risk of fatality and prone to early and long-term recurrence. The cardiac origin of stroke can be strongly suspected by anamnesis, clinical examination and findings on neuroimaging. Paroxysmal AF is an important cause of brain embolism, that is often difficult to document. Risk factors for stroke in AF include: previous embolism (including previous transient ischaemic attack (TIA), or ischaemic stroke), age &gt;65 years, structural cardiac disease, rheumatic or other significant valvular heart disease, valvular artificial prosthesis, hypertension, heart failure and significant left ventricular systolic dysfunction, diabetes and coronary disease. All AF patients with TIA or stroke have a formal indication for long-term anticoagulation. Only patients without risk factors or with contraindications to warfarin should be put on aspirin. Treating 1 000 patients with AF for 1 year with oral anticoagulants rather than aspirin would prevent 23 ischaemic strokes while causing 9 major bleedings. Despite its enormous preventive potential, oral anticoagulants are underused in AF, because treating physicians often have lack of knowledge about trials and guidelines, underestimate the benefits and overestimate the risks associated with continuous oral anticoagulation. The introduction of anticoagulants that do not need frequent control tests, such as ximelagatran, will increase the proportion of AF patients with risk factors for stroke who are anticoagulated. There is no evidence to support routine immediate anticoagulation in acute ischeamic stroke associated with AF.
1,569
Mapping and ablation of ventricular fibrillation.
Sudden cardiac death frequently results from ventricular fibrillation (VF). While VF is frequently the eventual mode of death in patients with abnormal ventricular substrates, it has also been described in patients with structurally normally hearts. Until recently, the management of patients who have survived sudden cardiac death has focused on treating the consequences by implantation of a defibrillator. However, such therapy remains restricted in many countries, is associated with a prohibitive cost to the community, and may be a cause of significant morbidity in patients with frequent episodes or storms of arrhythmia. Evidence emerging from the study of fibrillation both in the atria and the ventricle suggests an important role for triggers arising from the Purkinje network or the right ventricular outflow tract in the initiation of VF. Initial experience in patients with idiopathic VF and even those with VF associated with abnormal repolarization syndromes (LQT or Brugada syndrome) or myocardial infarction suggests that long term suppression of recurrent VF may be feasible by the elimination of these triggers. With the development of new mapping and ablation technologies, and greater physician experience, catheter ablation of VF, with the ultimate aim of curing such patients at risks of sudden cardiac death, may not be an unrealistic goal in the future.
1,570
Effect of optimizing the VV interval on left ventricular contractility in cardiac resynchronization therapy.
Simultaneous biventricular pacing improves left ventricular (LV) function in patients with heart failure and LV asynchrony. Proper timing of the interventricular pacing interval (VV interval) may further optimize LV function. We investigated the acute hemodynamic response of changing the VV interval using maximum LV dP/dt (LV dP/dt(max)) as a parameter for LV function. A biventricular pacemaker was implanted in 53 patients with severely impaired LV function, New York Heart Association class III and IV heart failure, left bundle branch block, LV asynchrony, and a QRS interval &gt;150 ms. Optimization of the atrioventricular and VV intervals was based on measurement of LV dP/dt(max) by a 0.014-in sensor-tipped pressure guidewire. Measurement of LV dP/dt(max) was obtained without complications in all patients. In patients in sinus rhythm with ischemic cardiomyopathy or idiopathic dilated cardiomyopathy, mean improvements by simultaneous biventricular pacing were 17% and 18%, respectively. Patients in atrial fibrillation showed an improvement of 21%. Optimizing the VV interval resulted in further absolute increases of 8%, 7%, and 3%, respectively, in dP/dt(max) in the 3 groups. Maximum dP/dt was achieved with LV pacing first in 44 patients, simultaneous right and left ventricular pacing in 6 patients, and right ventricular pacing first in 3 patients. The mean optimal VV intervals were 37 +/- 32 ms in the atrial fibrillation group, 28 +/- 30 ms in the idiopathic dilated cardiomyopathy group, and 52 +/- 31 ms in the ischemic cardiomyopathy group. Optimization of the VV interval significantly increased LV dP/dt(max) compared with simultaneous biventricular pacing, and such optimization could be easily, accurately, and reliably evaluated by a 0.014-in sensor-tipped pressure guidewire.
1,571
Changes in body surface potential distributions induced by isoproterenol and Na channel blockers in patients with the Brugada syndrome.
The characteristics of unique ECG findings in the Brugada syndrome have not been well explained.</AbstractText>To clarify their characteristics and mechanisms, body surface maps (BSM) were recorded from patients with the Brugada syndrome (13 cases; a mean age of 48 years) before and after administration of isoproterenol (ISP) or Na channel blockers (12 cases).</AbstractText>ST elevation in V1-V3 was decreased by 0.1 mV or more after ISP infusion in 8 of 11 cases and elevated after Na channel blockers in 8 of 12. In ventricular activation time (VAT) isochronal map, delayed conduction was noted on upper anterior chest in 11 and on anterior left chest in two. Delayed conduction areas were decreased by ISP and expanded by Na channel blockers. QRST isointegral map showed normal findings in baseline with minimal changes after ISP or Na channel blockers. Activation recovery interval (ARI) isochronal map showed prolonged area on upper anterior chest in baseline, being reduced by ISP and expanded by Na channel blockers. ARI dispersion (ARI-d), defined as difference between the maximum and minimum value of ARI, was larger in Brugada patients than that of normal subjects in baseline, and decreased after ISP and increased after Na channel blockers.</AbstractText>ST elevation in the Brugada syndrome is primarily caused by abnormality in depolarization rather than in repolarization. BSM can provide better information to clarify a mechanism of ECG changes adding its diagnostic value for this unique syndrome.</AbstractText>
1,572
Increase in QT/QTc dispersion after low energy cardioversion of chronic persistent atrial fibrillation.
The effects of atrial internal cardioversion on QT interval and QT dispersion (parameters associated with increased risk of ventricular tachyarrhythmias) are unknown. We investigated changes in QT interval, QTc and QT dispersion immediately after shock delivery for internal cardioversion in patients with chronic persistent atrial fibrillation.</AbstractText>Twenty-two patients with chronic persistent atrial fibrillation (mean duration, 17+/-23 months) underwent transvenous low-energy internal atrial cardioversion with a step-up protocol of shocks delivered between catheters in the right atrium and coronary sinus. (successful shock, 7.2+/-4.2 J). RR interval, QT interval, QTc interval, QT dispersion, and QTc dispersion were all measured on three consecutive beats (at 75 mm/s on at least 9 of 12 leads) and then averaged both before and after (1) the last unsuccessful shock, and (2) sinus rhythm restoration.</AbstractText>All parameters remained similar in the minute before and after the last unsuccessful shock. At 1 min after the successful shock, abrupt increases in QT dispersion (+43.8% vs. pre-shock; P&lt;0.001 at least significant difference analysis) and QTc dispersion (+30.0%; P&lt;0.05) were observed, followed by a gradual return to pre-shock values at 15 min.</AbstractText>These findings strongly suggest the likely existence of a brief period of increased electrical vulnerability immediately after restoration of sinus rhythm by internal cardioversion. Particular caution should therefore be applied whenever class III antiarrhythmic drugs are administered immediately after successful internal atrial cardioversion.</AbstractText>
1,573
Increased P wave dispersion after the radiofrequency catheter ablation in overt pre-excitation patients: the role of atrial vulnerability.
The pathogenesis of paroxysmal atrial fibrillation (PAF) in patients with overt pre-excitation and effect of elimination of accessory pathways on the appearance of AF are still controversial. We demonstrated the increased P max and P wave dispersion (PWD) reflecting more inhomogeneous and prolonged atrial conduction in patients with Wolff-Parkinson-White (WPW) syndrome and PAF attacks. One-hundred and fifty-one patients who underwent radiofrequency (RF) catheter ablation due to paroxysmal tachycardia medicated by accessory pathway were enrolled in this study. The patients were classified into two groups according to the presence of previous PAF attacks. We compared the clinical characteristics, echocardiograhic findings, P max and PWD values measured after normalization of PR intervals and disappearance of pre-excitation after ablation in overt pre-excitation patients. Although the differences in age, left atrial diameter and left ventricular ejection fraction (LVEF) were not significant in both groups, P maximum (130.0+/-8.4 vs. 122.3+/-8.7 ms, p=0.002) and P wave dispersion values measured after ablation (50.3+/-7.2 vs. 35.7+/-6.1 ms, p=0.001) were significantly higher in patients with previous PAF attacks. Accessory pathway (AP) antegrade and retrograde effective refractory period (ERP) values were shorter (276+/-27.3 vs. 321.0+/-48.7, p=0.001; 263.4+/-41.3 vs. 299.7+/-38.2, p=0.002, respectively) in patients with PAF attack when compared to those without PAF attacks. Higher P wave dispersion values in patients with previous PAF attacks suggest the important role of inhomogenous and discontinuous propagation of sinus impulses. Therefore, we concluded that not only the accessory pathway but also inhomogenous propagation of sinus impulses may play an important role in occurrence of AF in patients with pre-excitation.
1,574
Specific cardiac disorders in 402 consecutive patients with ischaemic cardioembolic stroke.
To determine the cardiological substrate in acute stroke patients presenting with a cardioembolic stroke subtype.</AbstractText>Data of 402 consecutive patients with cardioembolic stroke (cerebral infarction, n=347; transient ischaemic attack, n=55) were collected from a prospective hospital-based stroke registry in which data on 2000 stroke patients over a 10-year period were included. In all patients, specific cardiac disorders were identified by physical examination and results of electrocardiography and transthoracic echocardiography. Holter monitoring and more sensitive techniques of cardiac imaging were used in selected cases.</AbstractText>Cardioembolic cerebral ischaemia accounted for 20% of all acute strokes (25% of ischaemic cerebrovascular events). Cardiac sources of embolism included the following: (a) structural cardiac disorders associated with arrhythmia (n=232), the most frequent being left ventricular hypertrophic hypertensive disease (n=120) and rheumatic mitral valve disease (n=49); (b) structural cardiac disease with sustained sinus rhythm (n=81), the most frequent being systolic left ventricular dysfunction of both ischaemic (n=35) or non-ischaemic (n=24) aetiology; and (c) isolated atrial dysrhythmia (atrial fibrillation, n=88 and atrial flutter, n=1).</AbstractText>Hypertrophic hypertensive cardiac disease complicated with atrial fibrillation was the most frequent cardiac source of emboli in cardioembolic stroke. Other important cardiac sources were isolated atrial fibrillation, rheumatic mitral valve disease, and systolic left ventricular dysfunction of ischaemic and non-ischaemic cause. The incidence of traditional emboligenous-prone cardiac disorders, such as mitral valve prolapse and mitral annular calcification was low.</AbstractText>
1,575
Gender differences in ventricular arrhythmia recurrence in patients with coronary artery disease and implantable cardioverter-defibrillators.
We sought to determine whether men and women with coronary artery disease (CAD) and implantable cardioverter-defibrillators (ICDs) differ in frequency of arrhythmia recurrence and whether gender differences are independent of clinical, electrocardiographic, and electrophysiologic characteristics.</AbstractText>Epidemiologic studies show that women have a lower rate of sudden cardiac death (SCD) than men, even among patients with CAD. Whether this is due to differing susceptibilities to ischemia or to arrhythmia is unknown.</AbstractText>The clinical records and ICD data disks of 340 men and 59 women with CAD who received an ICD between June 1990 and June 2000 were reviewed. Ventricular tachycardia (VT) or ventricular fibrillation (VF) recurrences were compared between genders and relationship with other factors was analyzed.</AbstractText>Sustained VT/VF occurred in 52% of men and 34% of women (p &lt; 0.01). Men experienced more total VT/VF events (p &lt; 0.01), more shock-treated VT/VF events (p &lt; 0.03), more electrical storms (p &lt; 0.001), and had VT/VF on more days in follow-up (p &lt; 0.01). Gender differences were independent of measured clinical, electrocardiographic, and electrophysiologic factors. In stratified analyses, the gender differences in VT/VF recurrence were greatest in patients presenting with sustained monomorphic VT and those with inducible VT at electrophysiology study.</AbstractText>Women were less likely to experience VT/VF, and had fewer VT/VF episodes, than men. These findings were strongest in patients with evidence of a stable anatomic VT circuit: those with clinical or electrophysiologically induced VT. This study suggests that differing susceptibility to arrhythmia triggering may underlie the known differences in SCD rates between men and women.</AbstractText>
1,576
Effects of mechanical uncouplers, diacetyl monoxime, and cytochalasin-D on the electrophysiology of perfused mouse hearts.
Chemical uncouplers diacetyl monoxime (DAM) and cytochalasin D (cyto-D) are used to abolish cardiac contractions in optical studies, yet alter intracellular Ca(2+) concentration ([Ca(2+)](i)) handling and vulnerability to arrhythmias in a species-dependent manner. The effects of uncouplers were investigated in perfused mouse hearts labeled with rhod-2/AM or 4-[beta-[2-(di-n-butylamino)-6-naphthyl]vinyl]pyridinium (di-4-ANEPPS) to map [Ca(2+)](i) transients (emission wavelength = 585 +/- 20 nm) and action potentials (APs) (emission wavelength &gt; 610 nm; excitation wavelength = 530 +/- 20 nm). Confocal images showed that rhod-2 is primarily in the cytosol. DAM (15 mM) and cyto-D (5 microM) increased AP durations (APD(75) = 20.0 +/- 3 to 46.6 +/- 5 ms and 39.9 +/- 8 ms, respectively, n = 4) and refractory periods (45.14 +/- 12.1 to 82.5 +/- 3.5 ms and 78 +/- 4.24 ms, respectively). Cyto-D reduced conduction velocity by 20% within 5 min and DAM by 10% gradually in 1 h (n = 5 each). Uncouplers did not alter the direction and gradient of repolarization, which progressed from apex to base in 15 +/- 3 ms. Peak systolic [Ca(2+)](i) increased with cyto-D from 743 +/- 47 (n = 8) to 944 +/- 17 nM (n = 3, P = 0.01) but decreased with DAM to 398 +/- 44 nM (n = 3, P &lt; 0.01). Diastolic [Ca(2+)](i) was higher with cyto-D (544 +/- 80 nM, n = 3) and lower with DAM (224 +/- 31, n = 3) compared with controls (257 +/- 30 nM, n = 3). DAM prolonged [Ca(2+)](i) transients at 75% recovery (54.3 +/- 5 to 83.6 +/- 1.9 ms), whereas cyto-D had no effect (58.6 +/- 1.2 ms; n = 3). Burst pacing routinely elicited long-lasting ventricular tachycardia but not fibrillation. Uncouplers flattened the slope of AP restitution kinetic curves and blocked ventricular tachycardia induced by burst pacing.
1,577
Cardiovascular effects of beta-agonists in patients with asthma and COPD: a meta-analysis.
beta-Adrenergic agonists exert physiologic effects that are the opposite of those of beta-blockers. beta-Blockers are known to reduce morbidity and mortality in patients with cardiac disease. beta(2)-Agonist use in patients with obstructive airway disease has been associated with an increased risk for myocardial infarction, congestive heart failure, cardiac arrest, and acute cardiac death.</AbstractText>To assess the cardiovascular safety of beta(2)-agonist use in patients with obstructive airway disease, defined as asthma or COPD.</AbstractText>A meta-analysis of randomized placebo-controlled trials of beta(2)-agonist treatment in patients with obstructive airway disease was performed, to evaluate the short-term effect on heart rate and potassium concentrations, and the long-term effect on adverse cardiovascular events. Longer duration trials were included in the analysis if they reported at least one adverse event. Adverse events included sinus and ventricular tachycardia, syncope, atrial fibrillation, congestive heart failure, myocardial infarction, cardiac arrest, or sudden death.</AbstractText>Thirteen single-dose trials and 20 longer duration trials were included in the study. A single dose of beta(2)-agonist increased the heart rate by 9.12 beats/min (95% confidence interval [CI], 5.32 to 12.92) and reduced the potassium concentration by 0.36 mmol/L (95% CI, 0.18 to 0.54), compared to placebo. For trials lasting from 3 days to 1 year, beta(2)-agonist treatment significantly increased the risk for a cardiovascular event (relative risk [RR], 2.54; 95% CI, 1.59 to 4.05) compared to placebo. The RR for sinus tachycardia alone was 3.06 (95% CI, 1.70 to 5.50), and for all other events it was 1.66 (95% CI, 0.76 to 3.6).</AbstractText>beta(2)-Agonist use in patients with obstructive airway disease increases the risk for adverse cardiovascular events. The initiation of treatment increases heart rate and reduces potassium concentrations compared to placebo. It could be through these mechanisms, and other effects of beta-adrenergic stimulation, that beta(2)-agonists may precipitate ischemia, congestive heart failure, arrhythmias, and sudden death.</AbstractText>
1,578
Undersensing of VF in a patient with optimal R wave sensing during sinus rhythm.
We describe a case of potentially fatal undersensing of VF by a third generation ICD with predetermined automatic gain control. In this patient, ventricular sensing was optimal, as R wave amplitudes during sinus rhythm were at least 16 mV. Cyclical, high amplitude signals during VF elevated the sensing floor to such an extent that complete undersensing of subsequent lower amplitude local electrograms occurred. This led to bradypacing and complete ICD therapy failure. Therefore, high R wave amplitudes during sinus rhythm do not warrant flawless sensing during VF.
1,579
Successful use of quinidine in treatment of electrical storm in Brugada syndrome.
We report an adolescent with a malignant form of Brugada syndrome who presented with 15 episodes of ventricular fibrillation (VF) over 10 days, shortly after implantation of an implantable cardioverter defibrillator. Oral quinidine bisulphate at a dose of 1000 mg/day successfully suppressed the electrical storm and recurrence of VF over 18-month follow-up. It also normalized the ST-segment elevation in his right precordial leads, suppressed all ambient unifocal ventricular extrasystoles and induction of VF on programmed electrical stimulation. This case suggests that quinidine, by virtue of its blocking action on Ito, may be useful as adjunctive therapy in Brugada syndrome.
1,580
Remote monitoring of implantable cardioverter defibrillators: a prospective analysis.
A prospective study evaluating the functionality and ease of use of the Medtronic CareLink Network, "CareLink," was conducted at ten investigational sites. This internet-based remote monitoring service allows clinicians to remotely manage their patients' implantable cardioverter defibrillators (ICDs) and chronic diseases. The network is comprised of a patient monitor, a secure server, and clinician and patient websites. Under clinician direction, patients interrogated their ICDs at home, and transmitted data to secure servers via a standard telephone line. Comprehensive device data and a 10-second presenting rhythm electrogram were captured by the monitor and available for access and review on the clinician website. The information could also be printed using a standard desktop computer with internet access. During this study, patients were asked to transmit device data twice, at least 7 days apart, as scheduled by the clinic. Monitor functionality was assessed, and ease of using the system components was evaluated via questionnaires completed by patients and clinicians following each data transmission and review. Fifty-nine patients (64 +/- 14 years, range 22-85 years) completed 119 transmissions with only 14 calls to the study support center. Clinician review of data transmissions revealed several clinically significant findings, including silent AF discovery, assessment of antiarrhythmic drug efficacy in a previously diagnosed AF patient, previously unobserved atrial undersensing, and ventricular tachycardia. ICD patients found the monitor easy to use. Clinicians were pleased with the performance of the network and the quality of the web-accessed data, and found it comparable to an in-office device interrogation. CareLink is a practical tool for routine device management and may allow timely identification of clinically important issues.
1,581
Direct His-bundle pacing: present and future.
Direct His-bundle pacing (DHBP) produces rapid sequential multisite synchronous ventricular activation and, therefore, would be an ideal alternative to right ventricular apical (RVA) pacing. In 54 patients with cardiomyopathy, ejection fraction (EF) 0.23 +/- 0.11, persistent atrial fibrillation, and normal QRS &lt; 120 ms. DHBP was attempted. This was successful in 39 patients. In seven patients, the effect of increasing heart rate on contractility (Treppe effect) was investigated. Twelve patients who also received a RVA lead underwent cardiopulmonary testing. After a mean follow-up of 42 months, 29 patients are still alive with EF improving from 0.23 +/- 0.11 to 0.33 +/- 0.15. Functional class improved from 3.5 to 2.2. DP/dt increased at each pacing site (P &lt; 0.05) as the heart rate increased to 60, 100, and 120 beats/min. Rise in dP/dt by DHBP pacing at 120 beats/min was at least 170 +/- mmHg/s, greater than any other site in the ventricle (P &lt; 0.05). Cardiopulmonary testing revealed longer exercise time (RVA 255 +/- 110 s) (His 280 +/- 104 s) (P &lt; 0.05), higher O2 uptake (RVA 15 +/- 4 mL/kg per minute) (His 16 +/- 4 mL/kg minute) (P &lt; 0.05), and later anaerobic threshold (RVA 126 +/- 71 s) (His 145 +/- 74 s) (P &lt; 0.05) with DHBP compared to RVA pacing. Long-term DHBP is safe and effective in humans. DHBP is associated with a superior Treppe effect and increased cardiopulmonary reserve when compared to RVA pacing.
1,582
Precountershock cardiopulmonary resuscitation improves initial response to defibrillation from prolonged ventricular fibrillation: a randomized, controlled swine study.
To compare immediate countershocks (defibrillation 1st) with precountershock cardiopulmonary resuscitation (CPR 1st) for prolonged ventricular fibrillation (VF).</AbstractText>Randomized, controlled trial.</AbstractText>University animal laboratory.</AbstractText>Thirty swine (27 +/- 1 kg).</AbstractText>After 8 mins of untreated ventricular fibrillation, swine were randomly assigned to receive either immediate countershocks or CPR for 90 secs followed by countershocks.</AbstractText>After the first set of shocks, nine of 15 CPR 1st animals attained return of spontaneous circulation vs. 0 of 15 defibrillation 1st animals (p &lt;.001), and pulseless electrical activity occurred in only one of 15 CPR 1st animals vs. ten of 15 defibrillation 1st animals (p &lt;.01). The ultimate outcomes in the two groups were not different: Return of spontaneous circulation and 24-hr survival occurred in 15 of 15 CPR 1st and 13 of 15 defibrillation 1st animals. Good neurologic outcome at 24 hrs occurred in 12 of 15 CPR 1st and nine of 15 defibrillation 1st animals. None of the animals was successfully resuscitated with defibrillation alone; all successfully resuscitated animals were provided with chest compressions during the resuscitation. The ventricular fibrillation median frequency by fast Fourier transformation decreased during the untreated ventricular fibrillation interval in both groups (9.7 +/- 0.3 Hz and 10.1 +/- 0.2 Hz after 1 min vs. 8.8 +/- 0.3 Hz and 8.9 +/- 0.5 Hz at 8 mins, respectively). Because the ventricular fibrillation median frequency substantially increased after CPR 1st, it was much higher in the CPR 1st group before the first shock (15.1 +/- 0.9 Hz vs. 8.9 +/- 0.5 Hz, p &lt;.001). The ventricular fibrillation median frequency before the first countershock was much higher in the animals that attained return of spontaneous circulation after the first set of shocks vs. those that did not (16.1 +/- 1.3 Hz vs. 10.0 +/- 0.6 Hz, p &lt;.0001)</AbstractText>Precountershock CPR can result in substantial physiologic benefits and superior response to initial defibrillation attempts compared with immediate defibrillation in the setting of prolonged ventricular fibrillation.</AbstractText>
1,583
Non-invasive evaluation of ventricular refractoriness and its dispersion during ventricular fibrillation in patients with implantable cardioverter defibrillator.
Local ventricular refractoriness and its dispersion during ventricular fibrillation (VF) have not been well evaluated, due to methodological difficulties.</AbstractText>In this study, a non-invasive method was used in evaluation of local ventricular refractoriness and its dispersion during induced VF in 11 patients with VF and/or polymorphic ventricular tachycardia (VT) who have implanted an implantable cardioverter defibrillator (ICD). Bipolar electrograms were simultaneously recorded from the lower oesophagus behind the posterior left ventricle (LV) via an oesophageal electrode and from the right ventricular (RV) apex via telemetry from the implanted ICD. VF intervals were used as an estimate of the ventricular effective refractory period (VERP). In 6 patients, VERP was also measured during sinus rhythm at the RV apex and outflow tract (RVOT) using conventional extra stimulus technique.</AbstractText>Electrograms recorded from the RV apex and the lower esophagus behind the posterior LV manifested distinct differences of the local ventricular activities. The estimated VERPs during induced VF in the RV apex were significantly shorter than that measured during sinus rhythm using extra stimulus technique. The maximal dispersion of the estimated VERPs during induced VF between the RV apex and posterior LV was that of 10 percentile VF interval (40 +/- 27 ms), that is markedly greater than the previously reported dispersion of ventricular repolarization without malignant ventricular arrhythmias (30-36 ms).</AbstractText>This study verified the feasibility of recording local ventricular activities via oesophageal electrode and via telemetry from an implanted ICD and the usefulness of VF intervals obtained using this non-invasive technique in evaluation of the dispersion of refractoriness in patients with ICD implantation.</AbstractText>
1,584
Surgical options in ischemic cardiomyopathy.
The prevalence of ischemic dilated cardiomyopathy in western countries is increasing despite improvements in prevention, diagnosis, and treatment of cardiovascular disease. The management of patients with coronary artery disease and severe left ventricular dysfunction continues to be challenging and the mortality rate with medical therapy alone in this setting remains very high. Since heart transplantation represents a realistic option just for a very small number of patients, in recent years a variety of classic surgical interventions have been improved or optimized to address the complex and multifactorial pathophysiology of the ischemic heart failure picture. Myocardial revascularization, left ventricular restoration, mitral valve repair, passive containment device implantation, and surgical ablation of atrial fibrillation represent some of the "conventional" procedures which are currently in use or under development for the surgical treatment of ischemic cardiomyopathy. For several of them, the exact indications and results are not yet established and significant changes and improvements should reasonably be waited over the next few years. As techniques are refined and more data become available, the optimum surgical strategy for patients with advanced ischemic heart failure is likely to become clearer and more effective.
1,585
Effects of cardiac resynchronization therapy on disease progression in patients with congestive heart failure.
Cardiac resynchronization therapy (CRT) represents a new therapeutic modality of proven efficacy for selected patients with heart failure and ventricular asynchrony. The aim of this study was to assess the effects of CRT on clinical variables and cardiac remodeling in patients with moderate-to-severe congestive heart failure and inter/intraventricular conduction delays.</AbstractText>Thirty-seven patients (32 males, 5 females, mean age 73 +/- 7 years), in NYHA functional class III-IV, with left ventricular ejection fraction (LVEF) &lt; or = 35%, QRS &gt; or = 150 ms, and left ventricular end-diastolic diameter (LVEDD) &gt; or = 55 mm, underwent CRT by biventricular pacing (InSync, InSync III, InSync ICD; Medtronic Inc.). Fourteen (37.8%) had a previous pacemaker, and 11 (29.7%) were in permanent atrial fibrillation. The QRS width, NYHA functional class, LVEDD, left ventricular end-systolic diameter (LVESD), left ventricular end-diastolic volume (LVEDV), left ventricular endsystolic volume (LVESV), and LVEF were retrospectively evaluated in the period before CRT. For the purposes of the present study, the pre-CRT period was divided in two: T(-2) (from 6 to 3 years) and T(-1) (from 3 years to CRT). Moreover, these parameters were measured at the time of CRT (T0) and prospectively in the post-CRT follow-up (Tp).</AbstractText>Before CRT, a progressive worsening of the parameters was observed. The QRS duration steadily increased from T(-2) to T(-1) and T0 (both p = 0.000). The NYHA functional class increased from T(-2) to T(-1) and T0 (both p = 0.000). LVEDD and LVESD also increased and were higher at T(-1) (p = 0.001 and p = 0.000, respectively) and at T0 (both p = 0.000) compared to T(-2). Similar results were observed for LVEDV and LVESV. Finally, LVEF was higher at T(-2) than T(-1) and T0 (both p = 0.000). After CRT, there was a reduction in the QRS duration and an improvement in the NYHA functional class compared to T0 (both p = 0.000). LVEDD and LVESD were also reduced (p = 0.005 and p = 0.016, respectively), LVEDV and LVESV decreased (both p = 0.000), and LVEF increased (p = 0.000) with respect to T0. A highly significant correlation was found between LVEDD and LVESD both in the pre- and post-CRT time intervals, with a non-significant difference between the two linear regression lines. Similar results were obtained for the correlations between LVEDV and LVESV.</AbstractText>Congestive heart failure is associated with a progressive widening of the QRS complex and a worsening of the clinical status and results in anatomic remodeling with deterioration of the left ventricular function. CRT induces opposite changes in QRS duration, clinical status, and left ventricular remodelling.</AbstractText>
1,586
Transesophageal echocardiography-guided cardioversion of atrial fibrillation. Selection of a low-risk group for immediate cardioversion.
In patients (pts) with atrial fibrillation (AF) of more than 48 hours' duration, electrical cardioversion (ECV) should only be performed after 3 weeks of effective anticoagulation. Transesophageal echocardiography (TEE) allows earlier ECV; however, despite exclusion of thrombi in the atrium and left atrial appendage (LAA), cases of thromboembolism related to ECV have been documented in AF. To define a low-risk group for cardioversion without previous anticoagulation, pts were selected for immediate ECV if no thrombi or dynamic spontaneous echo contrast (auto-contrast) were found after TEE and if LAA velocity was more than 0.25 m/sec.</AbstractText>We performed TEE in 31 consecutive pts referred for ECV for AF of more than 48 hours' duration and without previous anticoagulation. After TEE the pts eligible for immediate ECV began anticoagulation with low molecular weight heparin (enoxaparin), subcutaneously in therapeutic doses, together with warfarin immediately before cardioversion. Enoxaparin was continued until an INR of over 2 was reached. Based on the TEE findings, the pts were divided in 2 groups: immediate ECV, group A, 20 pts with a mean age of 62 +/- 13 years, 6 female; and conventional therapy with warfarin before ECV, group B, 11 pts, mean age of 67 +/- 10 years (p &lt; 0.05), 2 female. None of the pts in either group had mitral stenosis or previous episodes of thromboembolism. The mean transverse diameter of the left atrium in the 31 pts was 47 +/- 4.5 mm, without statistically significant differences between the 2 groups. Of the 11 pts in group B, 3 had a thrombus in the LAA, 6 dynamic spontaneous echo contrast and the remainder LAA velocities of less than 0.25 m/sec. ECV was achieved in all the pts, with no complications. Oral anticoagulation was maintained for at least a month. At one month, sinus rhythm was maintained in 75% of group A and 45% of group B (p &lt; 0.01).</AbstractText>In pts with AF of more than 48 hours' duration and no previous history of thromboembolism, the use of our exclusion criteria during TEE enabled stratification of a low-risk population for immediate ECV, which was accomplished effectively and safely in 2/3 of the pts. This strategy is associated with early symptomatic improvement, and may contribute to maintenance of sinus rhythm after one month, which was significantly better than in the pts who had prolonged therapy with warfarin before ECV, despite the differences found in age and left ventricular function.</AbstractText>
1,587
Echocardiographic indices of left ventricular diastolic dysfunction in 647 individuals with preserved left ventricular systolic function.
Knowledge about the occurrence of isolated diastolic dysfunction (DD) in the general population is limited.</AbstractText>This population study was performed to assess the frequency and distribution pattern of echocardiographic indices of left ventricular (LV) DD in an elderly population aged 50-89 years in which LV systolic function is preserved.</AbstractText>The study population (n=764) recruited from the background population answered a heart failure questionnaire and underwent echocardiography. Excluding subjects with a LV ejection fraction &lt;50% or atrial fibrillation, diastolic function was evaluated in 647 subjects. The frequency of impaired relaxation according to earlier guidelines was 0.5%, vs. 2.5% using age- and gender-specific normal values of 'E/A-ratio' and 'deceleration time'. In a subpopulation of 167 participants, 6.6% had 'pseudonormalisation'. No difference was found in the frequency of dyspnea in subjects with impaired relaxation or 'pseudonormalisation' compared to subjects with normal filling pattern.</AbstractText>The prevalence of LV impaired relaxation was highly dependent on the choice of normal (cut-off) values for Doppler indices. Furthermore, our findings suggest that either isolated DD is often asymptomatic, or that Doppler flow derived parameters as a diagnostic method for assessing DD have a low specificity when used as a screening tool in the general population.</AbstractText>
1,588
Impact of atrial fibrillation on mortality and readmission in older adults hospitalized with heart failure.
Atrial fibrillation is common in older adults with heart failure. It is known to adversely affect outcomes.</AbstractText>To examine the associations of atrial fibrillation with 4-year mortality and 30-day readmission in older adults hospitalized with heart failure.</AbstractText>Patients were Medicare beneficiaries 65 years of age and older discharged with a primary diagnosis of heart failure. Baseline data were obtained by retrospective chart reviews and data on mortality and readmission were obtained from Medicare administrative files. Presence of atrial fibrillation was confirmed using electrocardiogram during hospital admission. Using Cox proportional hazards models we estimated bivariate and multivariable (adjusted for various patient and care covariates) hazards ratios (HR) and 95% confidence intervals (CI) for 4-year mortality and 30-day readmission of patients with atrial fibrillation compared with those without.</AbstractText>Patients (n=944) had a mean age (+/-S.D.) of 79 (+/-7) years, 61% were women, 18% African-Americans, 25% had atrial fibrillation by admission electrocardiogram, 64% died within 4 years, and 8% were readmitted. Patients with atrial fibrillation had a 52% increased risk of 4-year mortality (adjusted HR=1.52; 95%CI=1.11-2.07). Atrial fibrillation was also associated with higher risk of readmission (unadjusted HR=1.64; 95%CI=1.01-2.68). However, the association lost its statistical significance after adjustment for various patient and care variables (adjusted HR=2.09; 95%CI=0.94-4.65).</AbstractText>Presence of atrial fibrillation was associated with significant increased risk of long-term mortality in older adults hospitalized with heart failure and was associated with a non-significant higher risk of hospital readmission.</AbstractText>
1,589
[Ventricular arrhythmias].
Tachycardias arise from an arrhythmogenic substrate triggered by a random factor (generally an extrasystole) and modulated by the autonomic nervous system. The three components are interactive, but their intensity and conjunction vary continuously. During the last decade, major achievements have been made to clarify definition and classification of data reported in the literature, helping our understanding of the mechanisms of ventricular arrhythmias. Nowadays, the pathophysiology of cardiac arrhythmias is well-known at the cellular and molecular ion channel activity. The progress of epidemiology and molecular genetics have allowed a better knowledge of the genotype-phenotype correlation in young patients presenting syncopes due to torsades de pointes or polymorphic ventricular tachychardia episodes which may degenerate into ventricular fibrillation and cause sudden death. The data of numerous large prospective randomised studies have led to more rational treatments with the progressive withdrawal of class I antiarrhythmics and their replacement by betablocking agents. The surgical approach of ventricular tachycardia has been overcome by the automatic implantable defibrillator and in some well-defined clinical situations, catheter ablation is used.
1,590
A cardiac arrhythmia syndrome caused by loss of ankyrin-B function.
220-kDa ankyrin-B is required for coordinated assembly of Na/Ca exchanger, Na/K ATPase, and inositol trisphosphate (InsP(3)) receptor at transverse-tubule/sarcoplasmic reticulum sites in cardiomyocytes. A loss-of-function mutation of ankyrin-B identified in an extended kindred causes a dominantly inherited cardiac arrhythmia, initially described as type 4 long QT syndrome. Here we report the identification of eight unrelated probands harboring ankyrin-B loss-of-function mutations, including four previously undescribed mutations, whose clinical features distinguish the cardiac phenotype associated with loss of ankyrin-B activity from classic long QT syndromes. Humans with ankyrin-B mutations display varying degrees of cardiac dysfunction including bradycardia, sinus arrhythmia, idiopathic ventricular fibrillation, catecholaminergic polymorphic ventricular tachycardia, and risk of sudden death. However, a prolonged rate-corrected QT interval was not a consistent feature, indicating that ankyrin-B dysfunction represents a clinical entity distinct from classic long QT syndromes. The mutations are localized in the ankyrin-B regulatory domain, which distinguishes function of ankyrin-B from ankyrin-G in cardiomyocytes. All mutations abolish ability of ankyrin-B to restore abnormal Ca(2+) dynamics and abnormal localization and expression of Na/Ca exchanger, Na/K ATPase, and InsP(3)R in ankyrin-B(+/-) cardiomyocytes. This study, considered together with the first description of ankyrin-B mutation associated with cardiac dysfunction, supports a previously undescribed paradigm for human disease due to abnormal coordination of multiple functionally related ion channels and transporters, in this case the Na/K ATPase, Na/Ca exchanger, and InsP(3) receptor.
1,591
B-type natriuretic peptide for diagnosis of heart failure in emergency department patients: a critical appraisal.
The diagnosis of heart failure in the outpatient setting can be difficult. A rapid assay for B-type natriuretic peptide (BNP) has been advocated for the diagnosis of heart failure, using a single cutoff of 100 pg/mL. BNP is produced by both the right and left cardiac ventricles and is elevated in a variety of conditions, including heart failure, pulmonary hypertension, cor pulmonale, pulmonary embolism, left ventricular hypertrophy, renal failure, circulatory overload, acute coronary syndromes, atrial fibrillation, lung cancer, and sepsis. This multitude of causes of BNP elevation imposes limits on its diagnostic use for heart failure. The literature on the use of BNP testing for diagnosis of heart failure is reviewed, and improved guidelines for its interpretation are suggested.
1,592
A model of ischemically induced ventricular fibrillation for comparison of fixed-dose and escalating-dose defibrillation strategies.
Fixed- and escalating-dose defibrillation protocols are both in clinical use. Clinical observations suggest that the probability of successful defibrillation is not constant across a population of patients with ventricular fibrillation (VF). Common animal models of electrically induced VF do not represent a clinical VF etiology or reproduce clinical heterogeneity in defibrillation probability. The authors hypothesized that a model of ischemically induced VF would exhibit heterogeneous defibrillation shock strength requirements and that an escalating-dose strategy would more effectively achieve prompt defibrillation.</AbstractText>Forty-six swine were randomized to fixed, lower-energy (150 J) transthoracic shocks (group 1) or escalating, higher-energy (200 J-300 J-360 J) shocks (group 2). VF was induced by balloon occlusion of a coronary artery. After 1 or 5 minutes of VF, countershocks with a biphasic waveform were administered. The primary endpoint was successful defibrillation (termination of VF for 5 seconds) with &lt; or =3 shocks.</AbstractText>VF was induced with occlusion or after reperfusion in 35 animals. Only five of 17 group 1 animals (29%, 95% CI = 10 to 56) could be defibrillated with &lt; or =3 shocks; 15 of 18 group 2 animals (83%, 95% CI = 59 to 96) were defibrillated with &lt; or =3 shocks (p &lt; 0.002 vs. group 1). Nine of the group 1 animals (75%) that could not be defibrillated with 150-J shocks were rescued with &lt; or =3 shocks ranging from 200 to 360 J.</AbstractText>In this ischemic VF animal model, defibrillation shock strength requirements varied among individuals, and when defibrillation was difficult, an escalating-dose strategy was more effective for prompt defibrillation than fixed, lower-energy shocks.</AbstractText>
1,593
Vagal activity modulates spontaneous augmentation of ST elevation in the daily life of patients with Brugada syndrome.
In Brugada syndrome, ventricular fibrillation (VF) occurs mainly during sleep, and Brugada ECG signs are intensified by parasympathomimetic drugs; therefore, vagal activity could be a precipitating factor of VF. The aim of the present study was to elucidate the relation between spontaneous augmentation of ST elevation and changes in autonomic nervous activities in the daily life of patients with Brugada syndrome.</AbstractText>Twenty-three consecutive patients with Brugada syndrome were studied. Group VF(+) consisted of 7 symptomatic patients and 3 asymptomatic patients with inducible VF; group VF(-) consisted of 13 asymptomatic patients without documented or inducible VF. Two-channel unipolar lead (V(1) and V(2)) Holter ECG was recorded. Heart rate variability was analyzed by the maximum entropy method. Spontaneous augmentation of ST elevation (&gt;/=1.5 mm/20 min) occurred more frequently during 24 hours in group VF(+) than in group VF(-) (5.7 +/- 2.5 times vs 2.3 +/- 2.4 times, P &lt; 0.01). ST elevation was significantly greater in group VF(+) than in group VF(-) (2.1 +/- 0.2 mm vs 1.8 +/- 0.2 mm, P &lt; 0.05). Power of the high-frequency component (HF: 0.15-0.4 Hz) and RR interval increased progressively, and the ratio of low-frequency component (LF; 0.04- 0.15 Hz) to high-frequency component (LF/HF) gradually decreased toward the time of maximum ST elevation. During an entire day, daytime (0-5 P.M.), and nighttime (0-5 A.M.), both HF and LF/HF were not different between groups VF(+) and VF(-).</AbstractText>In Brugada syndrome, spontaneous augmentation of ST elevation in daily life occurred along with an increase in vagal activity. ST elevation was augmented more in patients with VF than in those without VF under similar vagal tone.</AbstractText>
1,594
Long-term outcome of patients who received implantable cardioverter defibrillators for stable ventricular tachycardia.
Evidence is inconclusive concerning the role of implantable cardioverter defibrillators (ICDs) to treat patients with hemodynamically stable ventricular tachycardia (VT). The goal of this study was to estimate future risk of unstable ventricular arrhythmias in patients who received ICDs for stable VT.</AbstractText>We reviewed complete ICD follow-up data from 82 patients (age 66.1 +/- 11.3 years; left ventricular ejection fraction 32.3%+/- 11.2%; mean +/- SD) who received ICDs for stable VT. During the follow-up period of 23.6 +/- 21.5 months (mean +/- SD), 15 patients (18%) died, and 10 (12%) developed unstable ventricular arrhythmia, 8 of whom had the unstable arrhythmia as the first arrhythmia after ICD placement. Estimated 2- and 4-year survival in the whole group was 80% and 74%, respectively. Estimated 2- and 4-year probability of any VT and unstable VT was 67% and 77% and 11% and 25%, respectively. There were no differences in age, ejection fraction, sex, underlying heart disease, cycle length, symptoms, baseline electrophysiologic study results, or QRS characteristics of qualifying VT between patients who developed unstable ventricular arrhythmia and patients who did not. Twenty-nine patients (35%) had at least one inappropriate shock, and 11 (13%) underwent further surgery for ICD-related complications.</AbstractText>Patients who present with hemodynamically stable VT are at risk for subsequent unstable VT. ICD treatment offers potential salvage of patients with stable VT who subsequently develop unstable VT/ventricular fibrillation, although complications and inappropriate shocks are considerable. No predictors could be found for high and low risk for unstable arrhythmias. These findings support ICD treatment for stable VT survivors.</AbstractText>
1,595
Clinical experience with a new detection algorithm for differentiation of supraventricular from ventricular tachycardia in a dual-chamber defibrillator.
Inadequate therapy for supraventricular tachyarrhythmias (SVT) is a frequent problem of implantable cardioverter defibrillators (ICD). Dual-chamber ICDs have been developed to improve discrimination of SVT from ventricular tachycardia (VT). We investigated the positive predictivity, sensitivity, and specificity of a new algorithm, the SMART detection trade mark algorithm, incorporated in the Phylax AV (Biotronik) dual-chamber ICD.</AbstractText>Two hundred nine patients (185 men, age 64 +/- 11 years) received a Phylax AV ICD with SMART detection trade mark activated. In 138 of these patients, 1,245 sustained tachycardia episodes with a detailed electrogram were stored in the device during a follow-up period of 10 +/- 6 months. Episodes were correctly classified as ventricular fibrillation (VF, n = 178) in 52 patients, VT (n = 641) in 98 patients, and SVT (n = 385) in 48 patients by the algorithm. Forty-one true SVT episodes (3.3%) were misclassified as VT: atrial fibrillation (n = 7) and flutter (n = 1), sinus tachycardia (n = 12), and other SVT (n = 21). The positive predictivity for VF/VT was 94.5% (95% CI 92.7-95.8) uncorrected and 94.5% (95% CI 92.9-95.8%) corrected with the generalized equation estimation (GEE) method. The positive predictivity for SVT was 100%. The specificity was 88.9% (95% CI 85.6-91.6%) uncorrected and 89.0% (95% CI 85.6-91.6%) corrected with the GEE method with a sensitivity of 100%.</AbstractText>The SMART detection trade mark algorithm was safe and reliable for the detection of all ventricular tachycardias. Although its specificity was high, it should be improved with regard to SVT to avoid inappropriate ICD therapies.</AbstractText>
1,596
The potential of Na+/Ca2+ exchange blockers in the treatment of cardiac disease.
The Na(+)/Ca(2+) exchanger (NCX), a surface membrane antiporter, is the primary pathway for Ca(2+) efflux from the cardiac cell and a determinant of both the electrical and contractile state of the heart. Enhanced expression of NCX has recently been recognised as one of the molecular mechanisms that contributes to reduced Ca(2+) release, impaired contractility and an increased risk of arrhythmias during the development of cardiac hypertrophy and failure. The NCX has also been implicated in the mechanism of arrhythmias and cellular injury associated with ischaemia and reperfusion. Hence, NCX blockade represents a potential therapeutic strategy for treating cardiac disease, however, its reversibility and electrogenic properties must be taken into consideration when predicting the outcome. NCX inhibition has been demonstrated to be protective against ischaemic injury and to have a positive inotropic and antiarrhythmic effect in failing heart cells. However, progress has been impaired by the absence of clinically useful agents. Two drugs, KB-R7943 and SEA-0400, have been developed as NCX blockers but both lack specificity. Selective peptide inhibitors have been well characterised but are active only when delivered to the intracellular space. Gene therapy strategies may circumvent the latter problem in the future. This review discusses the effects of NCX blockade, supporting its potential as a new cardiovascular therapeutic strategy.
1,597
Reperfusion strategy after regional ischaemia: comparative study of reperfusion conditions and compositions.
We investigated the effects of pressure, temperature and additives on aortic root reperfusion success. Cardiopulmonary bypass and heart arrest were initiated in mongrel dogs and sudden uncontrolled normothermic (group 1), pressure controlled substrate enriched normothermic (group 2a), pressure controlled unmodified normothermic (group 2b) and pressure controlled unmodified tepid (group 3) reperfusion compared. In group 1, the first cardiac rhythm was ventricular fibrillation, but dogs in the other groups showed spontaneous sinus rhythm. Recovery times were significantly longer and cardiac output levels significantly decreased in group 1 compared with the other groups. Prolonged lactate production and oxygen uptake failure were observed in group 1 compared with the other groups; oxidative stress markers and microscopic studies confirmed significant tissue injury in group 1. All parameters were similar between groups 2a, 2b and 3, indicating that low reperfusion pressure in the first 2 min is the most effective component of reperfusion.
1,598
Survival after out-of-hospital cardiac arrests in Katowice (Poland): outcome report according to the "Utstein style".
The purpose of this study was to evaluate the outcome of out-of-hospital cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) in the city of Katowice, Poland, during a period of 1 year prior to the planned reorganization of the national emergency system. Data were collected prospectively according to a modified Utstein style. To ensure accurate data collection, a special method of reporting resuscitation events with the use of a tape-recorder was introduced. Patients were followed for a 1-year period. Between 1 July 2001 and 30 June 2002, out-of-hospital cardiac arrest was confirmed in 1153 patients. Cardiopulmonary resuscitation was attempted in 188 patients. Cardiac arrest of presumed cardiac aetiology (147) was bystander witnessed in 105 (71%) cases and lay-bystander basic life support was performed in 35 (24%). In the group of bystander witnessed arrest ventricular fibrillation (VF) or tachycardia was documented in 59, asystole in 40 and other non-perfusing rhythms in six patients. Of 147 patients with cardiac aetiology, return of spontaneous circulation (ROSC) was achieved in 64 (44%) patients, 15 (10%) were discharged alive and 9 (6%) were alive 1 year later. Most of these patients had a good neurological outcome. Time to first defibrillatory shock was significantly shorter for survivors (median 7 min) compared to non-survivors (median 10 min). The most important resuscitation and patient characteristics associated with survival were VF as initial rhythm, arrest witnessed, and lay-bystander CPR.
1,599
A pilot randomised trial of thrombolysis in cardiac arrest (The TICA trial).
The outcome after out of hospital cardiac arrest is dismal. Thrombolysis during CPR has been advocated. Our hypothesis was that early administration of bolus thrombolysis could lead to improved survival from out of hospital cardiac arrest.</AbstractText>A prospective, randomised, double blind placebo controlled trial. All victims of out of hospital cardiac arrest brought to the Emergency Department (ED) by the emergency medical system were eligible for inclusion. All patients received standard advanced cardiac life support, except that the first drug the patient received was either tenecteplase 50 mg or placebo. The primary end point was return of spontaneous circulation (ROSC).</AbstractText>Of 35 patients enrolled, 19 received tenecteplase and 16 placebo. The tenecteplase group was younger (63 vs 72 years P = 0.04) and had significantly more ventricular fibrillation as the initial rhythm (63% versus 19%, 44% difference, 95% CI 15-73%). There was no difference in rhythm on arrival at the ED. ROSC occurred in 8 (42%) patients receiving tenecteplase and one (6%) placebo (36% difference, 95% CI 11-61%). Two tenecteplase and one placebo patient survived to leave ED, and one in each group survived to hospital discharge. Autopsy results were available on eight patients, five of whom had a thrombotic cause of death.</AbstractText>In this pilot study, we found the use of early bolus tenecteplase for OHCA to be feasible, and that it appears to increase the rate of ROSC. Larger studies are required to determine if this translates into a survival benefit. Appropriate patient selection for OHCA studies remains problematic.</AbstractText>