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4,600 | Successful resuscitation from recurrent ventricular fibrillation secondary to butane inhalation. | Resuscitation from cardiac arrest caused by volatile substance abuse is rarely successful. Large doses of catecholamines given during resuscitation, in the presence of butane, may cause recurrent ventricular fibrillation. We report a case of prolonged resuscitation in a young man who had inhaled butane. Cardiac output was restored 10 min after the administration of intravenous amiodarone. We suggest that antiarrhythmic agents should be used early during resuscitation to prevent recurrent arrhythmias. |
4,601 | Dangerous impact--commotio cordis. | Sudden death following blunt chest trauma is a frightening occurrence known as 'commotio cordis' or 'concussion of the heart'. It is speculated that commotio cordis could be caused by ventricular fibrillation secondary to an impact-induced energy that was transmitted via the chest wall to the myocardium during its vulnerable repolarization period. We describe a survivor of commotio cordis caused by a baseball. In this patient, an initial ventricular fibrillation was documented and converted by direct current defibrillation. Serial electrocardiographic changes (bifascicular conduction block and T wave inversion in precordial leads) were noticed in this patient. Our case suggested that coronary vasospasm might also play a role in commotio cordis. |
4,602 | Recurrent ventricular fibrillation in a marathon runner during exercise testing. | We report a case of a marathon runner who presented with chest tightness, ST-segment depression, and ventricular fibrillation following treadmill exercise testing. At cardiac catheterization, the patient was found to have an isolated lesion in the left anterior descending (LAD) artery that was hemodynamically insignificant by accepted angiographic and coronary flow reserve standards. Ventricular fibrillation was thought to be idiopathic, and an implantable cardioverter defibrillator was placed. Chest pain and ST-segment depression followed by ventricular fibrillation was reproduced during follow-up treadmill testing, prompting reconsideration of the original diagnostic hypothesis. A coronary stent was deployed in the LAD artery. The patient has been asymptomatic and arrhythmia free during follow-up treadmill testing and recreational running. |
4,603 | Alpha-human atrial natriuretic peptide, carperitide, reduces infarct size but not arrhythmias after coronary occlusion/reperfusion in dogs. | Carperitide, a recombinant form of alpha-hANP, possesses potent diuretic, natriuretic, and vasodilatory activity, and inhibits the renin-aldosterone system and sympathetic nervous activity. However, its beneficial effects on ischemic myocardium have not been studied fully. We examined carperitide's effects on infarct size, hemodynamics, and arrhythmia frequency in anesthetized dogs (n = 20) subjected to a 90-min coronary artery occlusion/6-h reperfusion protocol. Intravenous infusion of carperitide (0.2 microg/kg/min) commenced 15 min after occlusion and continued during occlusion/reperfusion. Ventricular fibrillation developed in two of 10 control versus three of 10 treated dogs (p = NS). Hemodynamics, collateral blood flow to the ischemic wall measured 10 min after occlusion, and extent of area at risk were comparable for the two groups. Infarct size/area at risk was smaller in treated than in control dogs (4.5 +/- 2.1% vs. 27.8 +/- 7.8%, respectively; p < 0.05). During occlusion, carperitide tended to increase collateral blood flow (+39%) and significantly decreased left ventricular systolic pressure (-13%) and end-diastolic pressure (-40%) compared with baseline. In control dogs, collateral blood flow tended to decrease (-8.3%), whereas most hemodynamic parameters did not change significantly with respect to baseline. The number of arrhythmias recorded during occlusion/reperfusion was similar in the two groups. Intravenous administration of carperitide limited infarct size, but did not reduce incidence of ventricular arrhythmias after 90-min coronary occlusion/6-h reperfusion in anesthetized dogs. Although the beneficial effects of carperitide may be attributable to concomitant changes in hemodynamics and collateral blood flow, the precise mechanisms require further investigation. |
4,604 | Seasonal variation in sudden death in the Negev desert region of Israel. | Previous studies have documented an increased incidence of cardiac mortality and sudden death during winter months.</AbstractText>To evaluate seasonal variation in sudden death in a hot climate such as the desert region of southern Israel.</AbstractText>We analyzed the files of 243 consecutive patients treated for out-of-hospital sudden death by the Beer Sheva Mobile Intensive Care Unit during 1989-90. Daily, monthly and seasonal incidence of sudden death was correlated with meteorological data, including temperature, heat stress, relative humidity and barometric pressure.</AbstractText>The seasonal distribution of sudden death was 23% in spring, 21% in summer, 25% in autumn and 31% in winter (not significant). In patients with known heart disease there were more episodes of sudden death in cold weather (< 15.4 degrees C) than hot (> 34.2 degrees C) (16 vs. 3, P < 0.05). Resuscitation was less successful in cold compared with hot weather (28 vs. 11, P < 0.05). Of patients older than 65 years, 11 sustained sudden death when heat stress was below 12.4 degrees C compared to 2 patients when heat stress was above 27.5 degrees C (P = 0.05).</AbstractText>Despite the warm desert climate, there were more cases of sudden death in older patients and in those with known heart disease during the winter season and on particularly cold days.</AbstractText> |
4,605 | Endotracheal versus intravenous epinephrine and atropine in out-of-hospital "primary" and postcountershock asystole. | Pulmonary blood flow during cardiac arrest and cardiopulmonary resuscitation (CPR) is <20% of normal, and transalveolar drug absorption is likely to be minimal. Animal and clinical CPR studies have not addressed the use of endotracheal (ET) epinephrine in doses currently recommended for adults (twice the intravenous dose). The purpose of this study was to compare the effects of ET and intravenous drugs on cardiac rhythm in the prehospital setting.</AbstractText>A 3-yr (1995-1997) retrospective review of all cardiac arrests transported to a single, municipal teaching institution was performed.</AbstractText>Patients >18 yrs in atraumatic cardiac arrest whose first documented field rhythm was asystole with time-to-definitive care of < or =10 mins (primary asystole) and patients found in ventricular fibrillation who developed postcountershock asystole (secondary asystole) were included. Patients were grouped according to route of drug administration (i.v., ET, or no drug therapy) as well as rhythm (primary or secondary asystole). A positive response to drug therapy was defined as any subsequent rhythm other than asystole during continued prehospital resuscitation.</AbstractText>A total of 136 patients met inclusion criteria. The following groups were defined: group 1, primary asystole/i.v. drugs (n = 39); group 2, postcountershock asystole/i.v. drugs (n = 39); group 3, primary asystole/ET drugs (n = 25); group 4, postcountershock asystole/ET drugs (n = 18); and group 5, primary or secondary asystole/no drug therapy (n = 15). Significant differences were not observed between groups with respect to age, gender, witnessed arrest, frequency of bystander CPR, or time-to-definitive care. The positive rhythm response rate was significantly greater in group 1 (64%) and group 2 (69%) (both p < .01) than in Group 3 (12%) or group 4 (11%). The response rate in the control group was 20% and not significantly different from either ET group. The intravenous groups also had a significantly greater rate of return of spontaneous circulation (17%) when compared with the ET groups (0%) (p = .005).</AbstractText>We conclude that the currently recommended doses of epinephrine and atropine administered endotracheally are rarely effective in the setting of cardiac arrest and CPR.</AbstractText> |
4,606 | Molecular basis of electrical remodeling in atrial fibrillation. | Atrial fibrillation (AF) is the most common cardiac arrhythmia, and is often associated with other cardiovascular disorders and diseases. AF can lead to thromboembolism, reduced left ventricular function and stroke, and, importantly, it is independently associated with increased mortality. AF is a progressive disease; numerous lines of evidence suggest that disease progression results from cumulative electrophysiological and structural remodeling of the atria. There is considerable interest in delineating the molecular mechanisms involved in the remodeling that occurs in the atria of patients with AF. Cellular electrophysiological studies have revealed marked reductions in the densities of the L-type voltage-gated Ca2+ current, I(Ca,L), the transient outward K+ current, I(TO), and the ultrarapid delayed rectifier K+ current, I(Kur), in atrial myocytes from patients in chronic AF. Similar (but not identical) changes in currents are evident in myocytes isolated from a canine model of AF and, in this case, the changes in currents are correlated with reduced expression of the underlying channel forming subunits. In both human and canine AF, the reduction in I(Ca,L) appears to be sufficient to explain the observed decreases in action potential duration and effective refractory period that are characteristic features of the remodeled atria. In addition, expression of the sarcoplasmic reticulum Ca2+ ATPase is reduced, suggesting that calcium cycling is affected in AF. These recent studies suggest that calcium overload and perturbations in calcium handling play prominent roles in AF-induced atrial remodeling. Although considerable progress has been made, further studies focused on defining the detailed structural, cellular and molecular changes that accompany the different stages of AF in humans, as well as in animal models of AF, are clearly warranted. It is anticipated that molecular insights gleaned from these studies will facilitate the development of improved therapeutic approaches to treat AF and to prevent the progression of the arrhythmia. |
4,607 | The effects of high-dose epinephrine combined with isoprenaline on isolated rabbit heart and cardiomyocytes after cardioversion of ventricular fibrillation. | The effects of high-dose epinephrine (HDE) combined with isoprenaline (Iso) on myocardial hemodynamics of isolated rabbit heart were studied. The electrophysiology and L-type Ca2+ channel of single ventricular myocyte after cardioversion of ventricular fibrillation were determined. The results suggest that parameters of hemodynamics were significantly enhanced by HDE+Iso than that of HDE (p < 0.01). The OS and Vmax of HDE+Iso increased 83.7 and 10.15% respectively compared to HDE alone. The APF of HDE+Iso is much more rapid than that of HDE (138.38 +/- 9.96 vs. 55.58 +/- 8.63 min(-1), p < 0.001). The APD50 and APD90 of HDE+Iso were significantly decreased; HR was increased (134.16 +/- 1.48 vs 62.20 +/- 6.25 min(-1)); and the amplitude current of through L-type Ca2+ channel was reduced but was significantly higher than the control. We conclude that HDE+Iso can improve the hemodynamics and improve electrophysiology of cardiomyocytes after cardioversion of ventricular fibrillation which is likely interrelated with I(Ca). The combined use of epinephrine and isoprenaline for cardiopulmonary resuscitation of primary ventricular fibrillation may be beneficial when employed in clinical situations. |
4,608 | Drug-induced torsade de pointes: from molecular biology to bedside. | A progressively increasing number of cardiac and noncardiac drugs prolong the ventricular action potential duration (QT interval of the electrocardiogram) and cause a distinctive polymorphic ventricular tachycardia termed torsades de pointes (TdP) that can degenerate into ventricular fibrillation and sudden cardiac death. Drugs prolong the QT interval and cause TdP by blocking cardiac K+ channels in general and selectively blocking the rapidly activating delayed rectifier channel IKr. Coassembly of HERG (human-ether-a-go-go-related gene) alpha-subunits and MiRP1 (MinK-related peptide 1) beta-subunits recapitulate the behavior of native human IKr and mutations of HERG and MiRP1 decrease the repolarizing current, delay ventricular repolarization and prolong the QT. Thus, drug-induced QT prolongation and TdP might represent an iatrogenic reproduction of the congenital LQTS. In patients with silent forms of the congenital LQTS associated with mutations in IKr, arrhythmic symptoms developed almost exclusively after exposure to QT-prolonging drugs. This review centers on the possible cellular mechanisms underlying drug-induced QT prolongation and TdP, the description of specific drugs and risk factors facilitating the development of TdP, and the recommendations for preventing and treating this potentially fatal arrhythmia. |
4,609 | Integrated backscatter assessment of left atrial spontaneous echo contrast in chronic nonvalvular atrial fibrillation: relation with clinical and echocardiographic parameters. | Integrated backscatter (IB) provides the quantitative assessment of left atrial spontaneous echo contrast (SEC). The IB intensity of the left atrial cavity relative to the left ventricular cavity is related to atrial thrombus in patients with atrial fibrillation (AF) or sinus rhythm. However, little is known about the relation between the quantitative SEC value of the left atrial cavity and variables implying thromboembolism in nonvalvular AF. To examine this relation, we performed transesophageal echo-cardiography with IB analysis in 65 patients with chronic nonvalvular AF. The quantitative SEC value of the left atrial cavity was defined as the difference between atrial IB intensity and ventricular IB intensity (corrected IB intensity). The corrected IB intensity was correlated with the left atrial dimension (r = 0.25, P =.049), the left atrial appendage velocity (r = -0.41, P <.001), and the duration of AF (r = 0.23, P =. 023). The corrected IB intensity was higher in patients who had a history of hypertension (3.2 +/- 2.2 dB versus 2.0 +/- 1.6 dB, P =. 018), SEC (3.9 +/- 1.9 dB versus 1.4 +/- 1.1 dB, P =.002), and left atrial thrombus (4.5 +/- 2.7 dB versus 2.2 +/- 1.7 dB, P <.001) when compared with those who did not have these abnormalities. The corrected IB intensity was significantly lower in patients with significant mitral regurgitation than in those without it (1.1 +/- 1. 2 dB versus 2.7 +/- 2.0 dB, P =.036). When the cutoff value of the corrected IB intensity was set at >/=2.0 dB, the sensitivity for left atrial thrombus was 78% and the specificity was 55%. In patients with chronic nonvalvular AF, the quantitative SEC value of the left atrial cavity depends on the duration of AF as well as the left atrial dimension and appendage velocity. Although IB may be capable of identifying patients with higher risk of cardiogenic embolism, a large-scale prospective study is needed to actually establish this. |
4,610 | [Alcoholic heart disease]. | Alcoholic heart disease is caused by a lifestyle in which alcoholics are continue to consume an excessive amount of alcohol over a long period of time. Total abstinence is a very effective way to treat them to prevent the development of the final stage of this disease. In contrast, repetitive drinking of massive amount of alcohol is very harmful and causes exacerbation of this disease. From our clinical studies, six candidates were nominated as symptoms of alcoholic heart disease, namely(1) tachyarrhythmias (incidence: 33%), (2) left ventricular hypokinesis(17%), (3) QT interval prolongation(17%), (4) hyperthickened LV wall(13%), (5) LV dilatation with pump failure: alcoholic cardiomyopathy(0.1%), and (6) sudden cardiac death (unknown %). In the beginning of alcoholic heart disease, the patient usually complains of no symptoms, and physical signs are quite poor. Ordinarily, either transient atrial fibrillation and/or left ventricular hypertrophy which is initially documented by electrocardiography or echocardiography is one of the first signals in the diagnosis. Without such early signals, an early diagnosis is impossible. To make a definite diagnosis of alcoholic heart disease, a clinical follow-up is by all means necessary. Improvement of cardiac function after total abstinence, it's worsening after drinking again, and again improvement after abstinence a second time is a diagnostic clue. In this follow-up study, electrocardiography and echocardiography were employed as important ways to gather date. In treatment, total abstinence is essential. To achieve this therapeutic goal, education of the patient is necessary, because approximately 70 per cent of patients with alcoholic heart disease fail to continue abstinence within two years even if they have good training. |
4,611 | [Symptoms and electrocardiographic findings in cardiomyopathies]. | Based on the national surveys in Japan, the most common symptoms of dilated cardiomyopathy(DCM) were dyspnea, palpitation, general fatigue and edema. Palpitation, dyspnea, general fatigue and anginal pain were common in hypertrophic obstructive cardiomyopathy(HOCM) and hypertrophic non-obstructive cardiomyopathy (HNOCM). Dyspnea was the most common symptom in constrictive cardiomyopathy (RCM). Electrocardiographic findings in DCM were not specific, and ST-T change, wide QRS complex, left ventricular hypertrophy and abnormal Q wave were frequently observed. In both of HOCM and HNOCM, frequent electrocardiographic abnormalities were ST-T abnormality, left ventricular hypertrophy and wide QRS complex. Moreover, abnormal Q wave was frequently observed in HOCM. Ventricular arrhythmia, including fatal ventricular tachycardia or ventricular fibrillation, was frequently found in patients with any type of cardiomyopathy. |
4,612 | Investigating the dual nature of endothelin-1: ischemia or direct arrhythmogenic effect? | Endothelin-1 (ET-1) is a potent vasoconstrictor peptide, which may also elicit severe ventricular arrhythmias. The aims of our study were to compare the effects of total left anterior descending coronary artery (LAD) occlusion to intracoronary (ic.) ET-1 administration and to investigate the pathomechanism of ET-1 induced arrhythmias in 3 groups of anesthetized, open-chest mongrel dogs. In group A (n=10) a total LAD occlusion was carried out for 30 min, followed by a 60 min reperfusion period. In groups B and C ET-1 was administered into LAD for 30 min at a rate of 30 pmol/min (n=6) and 60 pmol/min (n=8). Epi- and endocardial monophasic action potential (MAP) recordings were performed to detect electrophysiologic changes and ischemia Blood samples for lactate measurements were collected from the coronary sinus (CS) and from the femoral artery. Infrared imaging was applied to follow epimyocardial heat emission changes. At the end of the ET-1 infusion period coronary blood flow (CBF) was reduced significantly in groups B and C (deltaCBF30MIN B: 21+/-2%, p<0.05; C: 35+/-2%, p<0.05), paralleled by a significant epimyocardial temperature decrease in group C (deltaT30MIN: -0.65+/-0.29 degrees C, p<0.05). Two dogs died of ventricular fibrillation (VF) in the reperfusion period in group A. Ventricular premature contractions and non-sustained ventricular tachycardic episodes appeared in group B, whereas six dogs died of VF in group C. Significant CS lactate level elevation indicating ischemia was observed only in group A from the 30th min occlusion throughout the reperfusion period (control vs. 30 min: 1.3+/-0.29 vs. 2.2+/-0.37 mmol/l, p<0.05). Epi- and endocardial MAP durations (MAPD90) and left ventricular epicardial (LV(EPI)) upstroke velocity decreased significantly in group A in the occlusion period. ET-1 infusion significantly increased LV(EPI) MAPD90 in group B and both MAPD90-s in group C. In conclusion, ischemic MAP and CS lactate changes were observed only in group A. Although ET-1 reduced CBF significantly in groups B and C, neither MAP nor lactate indicated ischemic alterations. ET-1 induced major ventricular arrhythmias appeared before signs of myocardial ischemia developed, though reduced CBF presumably contributed to sustaining the arrhythmias. |
4,613 | Dynamic cardiomyoplasty: long-term clinical results in patients with dilated cardiomyopathy. | Dynamic cardiomyoplasty has been considered to be an effective method of surgical treatment of patients with end-stage heart failure, and is an alternative to heart transplantation.</AbstractText>We critically evaluated the long-term course of 52 patients with dilated cardiomyopathy who underwent dynamic cardiomyoplasty and were followed-up for up to 110 months.</AbstractText>Dilated cardiomyopathy was due to undetermined cause in 42 patients (80.8%), Chagas disease in 8 (15.4%), viral infection in 1 (1.9%), and peripartum cardiomyopathy in 1 (1.9%). In the nonchagasic group the survival rates were 79.5% +/- 6.1%, 67.8% +/- 7.1%, 53.7% +/- 8.3%, 49.9% +/- 8.3%, 14.9% +/- 12.2%, and 14.9% +/- 12.2%, respectively, at 12, 24, 48, 60, 80 and 110 months of follow-up. In the chagasic patients the survival rates were 37.5% +/- 17.1%, 12.5% +/- 11.7%, 12.5% +/- 11.7% and 0%, respectively, at 12, 24, 48, and 60 months of follow-up, making chagasic cardiomyopathy a possible contraindication for dynamic cardiomyoplasty.</AbstractText>There was no correlation between the clinical improvement and hemodynamic data. Ventricular fibrillation was a frequent cause of immediate and late death, suggesting the need for prophylactic use of antiarrhythmic drugs or implantable cardioverter/ defibrillators.</AbstractText> |
4,614 | Intraoperative amiodarone as prophylaxis against atrial fibrillation after coronary operations. | New onset of atrial fibrillation is a frequent complication after coronary artery bypass grafting and is a major cause of postoperative morbidity. Preoperative oral treatment with amiodarone hydrochloride has been shown to be efficacious as prophylaxis. The present study investigated whether intraoperative use of intravenous amiodarone has a preventive effect on the incidence of atrial fibrillation after coronary revascularization.</AbstractText>In a prospective study, 150 consecutive patients (mean age, 63 +/- 8 years; 132 men and 18 women) undergoing coronary artery bypass grafting were randomly assigned to one of three groups. Two groups received different doses of intravenous amiodarone (group I, 300-mg bolus and 20 mg x kg(-1) x day(-1) for 3 days; group II, 150-mg bolus and 10 mg x kg(-1) x day(-1) for 3 days) after aortic cross-clamping and one group, placebo (group III). Continuous electrocardiographic online monitoring was performed for 10 days. Arrhythmias were analyzed with respect to type, frequency, duration, and clinical relevance.</AbstractText>New onset of atrial fibrillation occurred in 24% of patients in group I, 28% in group II, and 34% in group III (p = not significant). Atrial fibrillation with a rapid ventricular response (>120 beats per minute) was significantly more frequent in the control group (group I, 14%; group II, 24%; group III, 32%; p < 0.05, group I versus group III) and appeared significantly earlier (group I, day 4.3 +/- 2.5; group II, day 4.8 +/- 2.9; group III, day 2.6 +/- 1.3; p < 0.05, group III versus groups I and II). Temporary atrial pacing because of bradycardia (<60 beats per minute) was necessary significantly more often in group I (group I, 48%; group II, 40%; group III, 28%; p < 0.05, group I versus group III). Early mortality rate (group I, 4%; group II, 2%; group III, 4%), rate of perioperative complications (group I, 14%; group II, 20%; group III, 14%), and duration of hospital stay (group I, 14.0 days; group II, 14.4 days; group III, 14.7 days) were not different between groups.</AbstractText>Intraoperative prophylactic use of amiodarone does not prevent new onset of atrial fibrillation in patients undergoing coronary artery bypass grafting and had no effect on outcome. Therefore, intraoperative prophylactic treatment with amiodarone at the tested doses does not appear to be justified.</AbstractText> |
4,615 | Involvement of Ca(2+) in antiarrhythmic effect of ischemic preconditioning in isolated rat heart. | We investigated the relationship between the effects of ischemic preconditioning (IPC) and Ca(2+) preconditioning (CPC) on reperfusion-induced arrhythmias. In the control group (noPC), Langendorff-perfused rat hearts were subjected to 5-min zero-flow global ischemia (I) followed by 15-min reperfusion (I/R). In ischemic preconditioning groups (IPC), the hearts were subjected to three cycles of 3-min global ischemia and 5-min reperfusion. In the CPC group, the hearts were exposed to three cycles of 3-min perfusion of higher Ca(2+) (2.3 mmol/l Ca(2+)) followed by 5-min perfusion of normal 1.3 mmol/l Ca(2+), and the hearts were then subjected to I/R. Verapamil was administered in several hearts of the IPC group (VR+IPC). Ventricular arrhythmias upon reperfusion were less frequently seen in the IPC and CPC groups than in the noPC and VR+IPC groups. IPC and CPC could attenuate conduction delay and enhance shortening of the monophasic action potential duration during ischemia. The ventricular fibrillation threshold measured at 1-min reperfusion was significantly higher in the IPC and CPC groups than in the noPC and VR+IPC groups. Verapamil completely abolished the salutary effects of IPC. These results demonstrate that Ca(2+) plays an important role in the antiarrhythmic effect of IPC during reperfusion. |
4,616 | Contrasting efficacy of dofetilide in differing experimental models of atrial fibrillation. | Rapid atrial pacing (RAP) and congestive heart failure (CHF) produce different experimental substrates for atrial fibrillation (AF). We tested the hypothesis that AF maintained by different substrates responds differently to antiarrhythmic-drug therapy.</AbstractText>The class III antiarrhythmic agent dofetilide was given intravenously at doses of 10 (D10) and 80 (D80) microg/kg to dogs with AF induced either (1) after 7 days of RAP at 400 bpm or (2) in the presence of CHF induced by rapid ventricular pacing. Dofetilide terminated AF in all CHF dogs, but D10 failed to terminate AF in any RAP dog, and D80 terminated AF in only 1 of 5 RAP dogs (20%) (P<0.01 for efficacy in CHF versus RAP dogs). Dofetilide was highly effective in preventing AF induction by atrial burst pacing in dogs with CHF but was totally ineffective in dogs with RAP. Dofetilide increased atrial effective refractory period and AF cycle length to a greater extent in CHF dogs. Epicardial mapping with 248 bipolar electrodes showed that CHF-related AF was often due to macroreentry, with dofetilide terminating AF by causing block in reentry circuits. RAP-related AF was due to multiple-wave front reentry, with dofetilide slowing reentry and decreasing the number of simultaneous waves, but not sufficiently to stop AF.</AbstractText>The mechanism underlying AF importantly influences dofetilide efficacy. The dependence of drug efficacy in AF on the underlying mechanism has potentially significant implications for antiarrhythmic drug use and development and may explain the well-known therapeutic resistance of longer-duration AF.</AbstractText> |
4,617 | How previous angina influences early prognosis of patients with acute myocardial infarction. | There is little information about how previous angina influences the complications of myocardial infarction and also contradictory results have been reported.</AbstractText>To compare the risk factors for myocardial infarction, complications, performance of left ventricle, and coronary angiography findings of patients who had suffered acute myocardial infarction with those for patients who had not.</AbstractText>We studied 600 patients diagnosed to have suffered acute myocardial infarction. Patients are grouped into those having previously had angina for at least 1 month preceding acute myocardial infarction (group I, n = 308 patients; 223 men and 85 women, mean age 60.4 +/- 10.6 years) and those who had not had angina (group II, n = 292 patients; 221 men and 71 women, mean age 58 +/- 9 years). The risk factors, complications (cardiogenic shock, heart failure, disturbances of rhythm and conduction, cardiac rupture and death), left-ventricle ejection fraction, and echocardiography and coronary angiographic findings during hospitalization are compared.</AbstractText>There was no difference with respect to localization of myocardial infarction (anterior, inferior, and non-Q) between groups I and II (P> 0.05). Hypertension in members of group I was higher (P < 0.05). There was no statistically significant difference with respect to diabetes mellitus, hypercholesterolemia and cigarette smoking (P > 0.05). Heart failure (P< 0.05), cardiogenic shock (P< 0.01), incidence of ventricular premature systole > 3/min (P< 0.001) and atrial fibrillation (P< 0.05) were seen more prevalently in group II than they were in group I. There was no difference between the two groups with respect to bundle-branch blockage and third-degree atrioventricular blockage. Incidences of ventricular fibrillation, rupture of interventricular septum (IVS) and death in hospital were higher in group II (6.2 versus 3.6%, 6.2 versus 3.2%, 2.1 versus 0.6%) but were not statistically significant. Coronary angiography detected no statistically significant difference with respect to disease in left main coronary artery, and one-vessel and two-vessel disease; but three-vessel disease was significantly more prevalent in group II (P < 0.01).</AbstractText>Heart failure, cardiogenic shock, arrhythmia (more than three VPS within 1 min and atrial fibrillation), and three-vessel disease detected by coronary angiography were found more often in the myocardial infarct patients without previous angina and these differences were statistically significant. In-hospital mortality and cardiac rupture were also found more commonly in this group and ejection fractions measured by echocardiography were found to be less, but these differences were statistically insignificant.</AbstractText> |
4,618 | Inappropriate shock delivery by implantable defibrillators with dual chamber pacing during nonsustained ventricular tachycardia in patients with heart block. | Transvenous implantable cardioverter defibrillators (ICDs) have improved the management of patients with ventricular tachycardia/ventricular fibrillation (VT/VF). Many patients with sustained VT/VF have bradyarrhythmias and nonsustained VT. Shock delivery due to nonsustained VT would be an undesirable feature. Abortive shock capability (noncommitted shocks) is a feature available in devices to prevent delivery of shocks for nonsustained VT. Recently, the availability of dual chamber pacing capability has improved the efficacy of ICDs by obviating the need of separate pacemaker implantation in patients with VT/VF and concomitant bradyarrhythmias. However, interaction between bradyarrhythmias and VT/VF has not been described and has important clinical implications. We report a case in which a patient with complete atrioventricular (AV) block and ventricular arrhythmias received an inappropriate shock following spontaneous termination of nonsustained VT, showing an important shortcoming of devices with these features. |
4,619 | Safety of pacemaker implantation prior to radiofrequency ablation of atrioventricular junction in a single session procedure. | RF current delivery may cause acute and chronic dysfunction of previously implanted pacemakers. The aim of this study was to assess prospectively the effects of RF energy on Thera I and Kappa pacemakers in 70 consecutive patients (mean age 70 +/- 11 years, mean left ventricular ejection fraction 48 +/- 15%) who underwent RF ablation of the AV junction for antiarrhythmic drug refractory atrial fibrillation (permanent in 42 patients, paroxysmal in 28). These pacing systems incorporate protection elements to avoid electromagnetic interference. The pacemakers (Thera DR 7960 I in 20 patients, Thera SR 8960 I in 30, Kappa DR 600-601 in 8, Kappa SR 700-701 in 12) were implanted prior to RF ablation in a single session procedure and were transiently programmed to VVI mode at a rate of 30 beats/min. Capsure SP and Z unibipolar leads were used. During RF application there was continuous monitoring of three ECG leads, endocavitary electrograms, and event markers. Complete AV block was achieved in all cases after 3.6 +/- 2.9 RF pulses and 100 +/- 75 seconds of RF energy delivery. The mean time of pacemaker implantation and RF ablation was 60 +/- 20 minutes. Transient or permanent pacemaker dysfunction including under/oversensing, reversion to a "noise-mode" pacing, pacing inhibition, reprogramming, or recycling were not observed. Leads impedance, sensing, and pacing thresholds remained in the normal range in the acute and long-term phase (average follow-up 18 +/- 12 months). In conclusion, Thera I and Kappa pacemakers exhibit excellent protection against interference produced by RF current. The functional integrity of the pacemakers and Capsure leads was observed in the acute and chronic phases. Thus, the implantation of these pacing systems prior to RF ablation of the AV junction can be recommended. |
4,620 | Initial results with left ventricular pacemaker lead implantation using a preformed "peel-away" guiding sheath and "side-wire" left ventricular pacing lead.<Pagination><StartPage>985</StartPage><EndPage>990</EndPage><MedlinePgn>985-90</MedlinePgn></Pagination><Abstract><AbstractText>We report our preliminary experience with the use of preformed "peel-away" guiding sheaths and "side-wire" pacing leads for permanent biventricular pacemaker insertion in 13 patients with heart failure. Three of these patients were undergoing an upgrade of a preexistent VVIR pacing system after prior His ablation for medically refractory atrial fibrillation. Six of the patients had undergone attempted biventricular pacemaker insertion, but required left ventricular lead repositioning after total implantation failure or late displacement of the lead. The remaining patients were undergoing new system implantation. Target vessel cannulation was achieved in all patients. However, in one patient, diaphragmatic pacing throughout the target vessel length prevented successful implantation. All other implants were ultimately successful (92% success rate). We conclude that device implantation using a preformed sheath and side-wire pacing lead is feasible and may offer significant benefits over implantation with currently available technology.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Walker</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Harefield Hospital, United Kingdom. [email protected]</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Levy</LastName><ForeName>T</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Rex</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Paul</LastName><ForeName>V</ForeName><Initials>V</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Pacing Clin Electrophysiol</MedlineTA><NlmUniqueID>7803944</NlmUniqueID><ISSNLinking>0147-8389</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004867" MajorTopicYN="N">Equipment Design</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="N">Heart Failure</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010138" MajorTopicYN="Y">Pacemaker, Artificial</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2000</Year><Month>7</Month><Day>6</Day><Hour>11</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2001</Year><Month>2</Month><Day>28</Day><Hour>10</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2000</Year><Month>7</Month><Day>6</Day><Hour>11</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">10879383</ArticleId><ArticleId IdType="doi">10.1111/j.1540-8159.2000.tb00885.x</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10878969</PMID><DateCompleted><Year>2000</Year><Month>09</Month><Day>14</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>18</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1019-5297</ISSN><JournalIssue CitedMedium="Print"><Issue>1</Issue><PubDate><Year>2000</Year><Season>Jan-Feb</Season></PubDate></JournalIssue><Title>Likars'ka sprava</Title><ISOAbbreviation>Lik Sprava</ISOAbbreviation></Journal>[The structural changes in the lungs in the acute period of a myocardial infarct in the wake of ventricular fibrillation]. | We report our preliminary experience with the use of preformed "peel-away" guiding sheaths and "side-wire" pacing leads for permanent biventricular pacemaker insertion in 13 patients with heart failure. Three of these patients were undergoing an upgrade of a preexistent VVIR pacing system after prior His ablation for medically refractory atrial fibrillation. Six of the patients had undergone attempted biventricular pacemaker insertion, but required left ventricular lead repositioning after total implantation failure or late displacement of the lead. The remaining patients were undergoing new system implantation. Target vessel cannulation was achieved in all patients. However, in one patient, diaphragmatic pacing throughout the target vessel length prevented successful implantation. All other implants were ultimately successful (92% success rate). We conclude that device implantation using a preformed sheath and side-wire pacing lead is feasible and may offer significant benefits over implantation with currently available technology.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Walker</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Harefield Hospital, United Kingdom. [email protected]</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Levy</LastName><ForeName>T</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Rex</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Paul</LastName><ForeName>V</ForeName><Initials>V</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Pacing Clin Electrophysiol</MedlineTA><NlmUniqueID>7803944</NlmUniqueID><ISSNLinking>0147-8389</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004867" MajorTopicYN="N">Equipment Design</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="N">Heart Failure</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010138" MajorTopicYN="Y">Pacemaker, Artificial</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2000</Year><Month>7</Month><Day>6</Day><Hour>11</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2001</Year><Month>2</Month><Day>28</Day><Hour>10</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2000</Year><Month>7</Month><Day>6</Day><Hour>11</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">10879383</ArticleId><ArticleId IdType="doi">10.1111/j.1540-8159.2000.tb00885.x</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10878969</PMID><DateCompleted><Year>2000</Year><Month>09</Month><Day>14</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>18</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1019-5297</ISSN><JournalIssue CitedMedium="Print"><Issue>1</Issue><PubDate><Year>2000</Year><Season>Jan-Feb</Season></PubDate></JournalIssue><Title>Likars'ka sprava</Title><ISOAbbreviation>Lik Sprava</ISOAbbreviation></Journal><ArticleTitle>[The structural changes in the lungs in the acute period of a myocardial infarct in the wake of ventricular fibrillation].</ArticleTitle><Pagination><StartPage>25</StartPage><EndPage>28</EndPage><MedlinePgn>25-8</MedlinePgn></Pagination><Abstract>Time-related course was studied of structural changes in the lung tissue in acute myocardial infarction having developed in the wake of secondary ventricular fibrillation, using investigational methods common in biology, histochemistry, and electron-microscopy. It has been found out that development in patients with acute myocardial infarction of ventricular fibrillation greatly aggravates the course of the illness inducing origination of profound and even irreversible alternative changes in all constituents of the aerohematic barrier. The above patients developed structural as well as functional pulmonary insufficiency which is at its greatest within 2 to 4 days of the onset of ventricular fibrillation. |
4,621 | Corrected QT interval prolongation associated with intravenous haloperidol in acute coronary syndromes. | We report on three patients with acute coronary syndromes who developed QT interval prolongation associated with intravenous haloperidol use. One developed ventricular fibrillation. We also review 21 such patients from the literature. Haloperidol should be used with caution and QT intervals monitored closely in patients with coronary ischemia who may be prone to ventricular ectopy. |
4,622 | Electrophysiological effect of adenosine triphosphate and adenosine on atrial and ventricular action potential duration in humans. | Bolus injection of adenosine triphosphate (ATP) or adenosine is widely used clinically for terminating supraventricular tachycardia. However, bolus injection of these drugs has been reported to provoke atrial fibrillation (Afib). The effects of ATP and adenosine on the monophasic action potential duration (MAPD) of atrial and ventricular muscle was investigated, as well as the changes in the spatial distribution of atrial functional refractoriness caused by adenosine. Bolus injection of ATP and adenosine shortened atrial MAPD; no change was observed in the ventricle. Because local f-f intervals during atrial fibrillation correlate with the atrial refractory period, changes in mean f-f intervals in the right atrial appendage, His bundle region, coronary sinus ostium and distal coronary sinus were compared before and after injection of adenosine during induced Afib. Maximal shortening of f-f intervals was observed in the right atrial appendage. Inhomogeneous shortening of atrial refractoriness may account for the Afib following bolus injection of ATP or adenosine. |
4,623 | Esmolol versus diltiazem in the treatment of postoperative atrial fibrillation/atrial flutter after open heart surgery. | Supraventricular tachyarrhythmias are common after open heart surgery. Possible causative factors for these arrhythmias include operative trauma, atrial ischemia, electrolyte imbalances, pericardial irritation, and excess catecholamines. Two agents commonly used to control ventricular rate in atrial fibrillation or atrial flutter (AF/AFL) are beta-blockers and calcium channel blockers.</AbstractText>This randomized study was designed to compare the safety and efficacy of intravenous diltiazem versus intravenous esmolol in patients with postoperative AF/AFL after coronary bypass surgery and/or valve replacement surgery. A comparative cost analysis was also performed. Thirty patients received either esmolol (n = 15) or diltiazem (n = 15) for AF/AFL. During the first 6 hours of treatment, 66.6% of esmolol-treated patients converted to sinus rhythm compared with 13.3% of the diltiazem-treated patients (P <.05). At 24 hours, 66.6% of the diltiazem group converted to SR compared with 80% of the esmolol group (not significant). Drug-induced side effects, time to rate control (<90 beats/min), number of patients requiring cardioversion, and length of hospitalization were similar for the two groups. The drug cost/successfully treated patient for esmolol versus diltiazem was $254 versus $437 at 6 hours and $529 versus $262 at 24 hours.</AbstractText>Although this is a small study, it suggests that esmolol is more effective in converting patients to normal sinus rhythm than diltiazem during the initial dosing period. No differences in conversion rates were observed between the two groups after 24 hours. Additional studies are needed to confirm whether esmolol is the initial drug of choice in patients with postoperative AF/AFL after coronary bypass surgery.</AbstractText> |
4,624 | Arrhythmia risk stratification in idiopathic dilated cardiomyopathy based on echocardiography and 12-lead, signal-averaged, and 24-hour holter electrocardiography. | To date, considerable controversy exists regarding noninvasive arrhythmia risk stratification in idiopathic dilated cardiomyopathy (IDC). Methods and Results Between 1992 and 1997, 202 patients with IDC without a history of sustained ventricular tachycardia (VT) underwent echocardiography, signal-averaged electrocardiogram (ECG), and 24-hour Holter ECG in the absence of antiarrhythmic drugs. During 32 +/- 15 months of prospective follow-up, major arrhythmic events, including sustained VT, ventricular fibrillation, or sudden death, occurred in 32 (16%) of 202 patients. After adjusting for baseline medical therapy and antiarrhythmic therapy during follow-up, multivariate Cox regression analysis identified a left ventricular (LV) end-diastolic diameter >/=70 mm and nonsustained VT on Holter as the only independent arrhythmia risk predictors. The combination of an LV end-diastolic diameter >/=70 mm and nonsustained VT was associated with a 14. 3-fold risk for future arrhythmic events (95% confidence interval 2. 3-90). To further elucidate the prognostic value of LV ejection fraction, multivariate Cox analysis was repeated with ejection fraction forced to remain in the model. In the latter model, an ejection fraction </=30% combined with nonsustained VT on Holter was found to be a significant arrhythmia risk predictor with a relative risk of 14.6 (95% confidence interval 2.2-97).</AbstractText>The combination of an LV end-diastolic diameter >/=70 mm and nonsustained VT on Holter, and the combination of LV ejection fraction </=30% and nonsustained VT on Holter, identify a subgroup of patients with IDC with a 14-fold risk for subsequent arrhythmic events. These findings have important implications for the design of future studies evaluating the role of prophylactic defibrillator therapy in patients with IDC.</AbstractText> |
4,625 | A prospective, randomized controlled trial comparing the efficacy and safety of sotalol, amiodarone, and digoxin for the reversion of new-onset atrial fibrillation. | A prospective, randomized controlled trial of new-onset atrial fibrillation was conducted to compare the efficacy and safety of sotalol and amiodarone (active treatment) with rate control by digoxin alone for successful reversion to sinus rhythm at 48 hours.</AbstractText>We prospectively randomly assigned 120 patients with atrial fibrillation of less than 24 hours' duration to treatment with sotalol, amiodarone, or digoxin using a single intravenous dose followed by 48 hours of oral treatment. Patients had ECG monitoring for 48 hours, and time of reversion, adequacy of rate control, and numbers of adverse events were compared. After 48 hours, those still in atrial fibrillation underwent cardioversion according to a standardized protocol. After 48 hours of therapy and attempted cardioversion, the number of patients whose rhythms had successfully reverted were compared.</AbstractText>There was a significant reduction in the time to reversion with both sotalol (13. 0+/-2.5 hours, P <.01) and amiodarone (18.1+/-2.9 hours, P <.05) treatment compared with digoxin only (26.9+/-3.4 hours). By 48 hours, the active treatment group was significantly more likely to have reverted to sinus rhythm than the rate control group (95% versus 78%, P <.05; risk ratio 5.4, 95% confidence interval [CI] 1.5 to 19.2 ). In those patients whose rhythms did not revert to sinus rhythm, there was superior ventricular rate control in the sotalol group at both 24 and 48 hours compared with those who received either amiodarone or digoxin. There were also fewer adverse events in the active treatment group compared with the rate control group.</AbstractText>Immediate pharmacologic therapy for new-onset atrial fibrillation with class III antiarrhythmic drugs (sotalol or amiodarone) improves complication-free 48-hour reversion rates compared with rate control with digoxin.</AbstractText> |
4,626 | The Framingham Study: ITS 50-year legacy and future promise. | The Framingham Study was initiated in 1948 to investigate an epidemic of coronary disease in the USA, using a prospective epidemiological approach. Insights were provided into the prevalence, incidence, full clinical spectrum and predisposing factors. The major "risk factors" (a term coined by the Framingham Study) for coronary disease, stroke, peripheral artery disease and heart failure were identified and clinical misconceptions dispelled about isolated systolic hypertension, left ventricular hypertrophy, dyslipidemia, atrial fibrillation and glucose intolerance. Average values for blood lipids, blood pressure, body weight, glucose and fibrinogen were shown to be dangerously suboptimal and to have a continuous graded relationship to cardiovascular disease without critical values. Dyslipidemia, glucose intolerance and elevated fibrinogen were shown to have smaller hazard ratios in the elderly, but this was offset by a higher absolute risk. Diabetes was shown to operate more strongly in women, eliminating their advantage over men. Serum total cholesterol was shown to derive its atherogenic potential from its LDL component and also to reflect cholesterol being removed in the HDL fraction. The total/HDL-cholesterol ratio was demonstrated to be the most efficient lipid profile for predicting coronary disease. LDL was shown to be correlated with hemostatic factors, suggesting that there would be additional benefits to lowering LDL. High triglyceride associated with reduced HDL, indicating insulin resistance and small dense LDL, was shown to be associated with excess coronary disease. All the risk factors tended to cluster, and this was shown to be promoted by insulin resistance induced by weight gain. Multivariate risk profiles were produced to facilitate risk stratification of candidates for coronary disease, stroke, peripheral artery disease and heart failure. The Framingham Study is now engaged in quantifying the independent contributions of homocysteine Lp(a), insulin resistance, small dense LDL, C reactive protein, clotting factors and genetic determinants of cardiovascular disease. We are now able to estimate the lifetime risk of all the atherosclerotic cardiovascular disease outcomes. |
4,627 | Evaluation of the indirect revascularization method after 3 months chronic myocardial ischemia. | The long-term effectiveness of transmyocardial laser revascularization (TMLR) was evaluated in the setting of a severe left anterior descending artery (LAD) stenosis.</AbstractText>To employ the chronic ischemic model, pigs underwent three operative procedures over a 13-week period. In the first operation, an operative stenosis of the LAD was created. One week later, the animals were studied at baseline by analyzing different parameters of perfusion (microspheres), function and ECG changes. Afterwards, pigs were randomized into one of three different experimental groups: animals in laser group 1 received one laser channel (n=9) and laser group 2 two channels per cm(2) (n=6) in the LAD territory (using a CO(2)-laser). Animals of the ischemic group (n=12) underwent the same procedures without TMLR-treatment. Twelve weeks later, the animals were re-studied (third operation) and killed. Additional analysis of myocardial water content and histochemistry was performed.</AbstractText>Chronic myocardial ischemia and regional myocardial blood flow (RMBF) in laser group 2 revealed relatively higher RMBF values compared with the ischemic group (P=0.015), after 3 months, but no absolute improvement of perfusion at rest compared with baseline was observed in all experimental groups. Left ventricular stroke work index (LVSWI) at rest and under stress did not show any improvement compared with initial values in all study groups (P not significant). However, laser group 1 demonstrated relatively higher LVSWI(max) values in comparison with the ischemic group (P=0.013) as did laser group 2 (P=0.017). Regional contractility of the laser groups recovered after 3 months (which was deteriorated shortly after TMLR, P<0.001) and increased under stress compared with baseline (laser 1: P=0.015, laser 2: P=0.017). In contrast, the ischemic group did not show any difference from initial values (P not significant). The lased pigs of group 2 were less prone to intractable ventricular fibrillation (P=0.036 vs. ischemic group), and showed a significant smaller area of necrosis in the area at risk (P=0.012 vs. ischemic group).</AbstractText>This model of chronic regional ischemia demonstrates that CO(2)-laser revascularization significantly ameliorates microperfusion and regional contractility, and diminishes the incidence of ventricular fibrillation and necrosis in the area at risk. However, it does not change the overall perfusion and global LV function.</AbstractText> |
4,628 | Hypermagnesemia-induced cardiopulmonary arrest before induction of anesthesia for emergency cesarean section. | We describe a 42-yr-old woman scheduled for emergency cesarean section who had sudden cardiopulmonary arrest just before induction of general anesthesia. Hypermagnesemia, caused by accidental overdose of magnesium sulfate during transportation to the operating room, was the primary cause of this life-threatening event. Anesthetic management after such events and a brief summary of the literature regarding iatrogenic hypermagnesemia in obsteric patients are provided. |
4,629 | Increased connexin43 gap junction protein in hamster cardiomyocytes during cold acclimatization and hibernation. | The physiology of hibernation is characterized by dramatic reductions of heart rate, respiration, metabolism, blood pressure and body temperature and by resistance to ventricular fibrillation. Gap junctions in the heart provide low resistance pathways, facilitating electrical and metabolic coupling between cardiac muscle cells for coordinated action of the heart and tissue homeostasis. The conductance of these junctions, and therefore their function, is likely to be affected by the physiological changes that take place during hibernation. Our objective was to quantitate gap junction protein levels in cold acclimatization, hibernation and arousal.</AbstractText>We have used specific antibodies to connexins 43 and 40, in combination with confocal microscopy, to quantitatively analyze the expression of connexin protein in hamster (Mesocricetus auratus) left ventricles in four animal groups: normal controls at euthermy, cold controls (cold-exposed animals that did not undergo hibernation), hibernating animals and animals aroused from hibernation for 2 h.</AbstractText>Connexin40 immunostaining was not detected in ventricular cardiomyocytes in any animal group but connexin43 was found in all groups. Connexin43 expression was significantly enhanced in hibernation and cold control ventricular cardiomyocytes. Total plaque area, numerical density and plaque size were higher in the cold controls and hibernating hamsters compared to normal controls and animals aroused from hibernation.</AbstractText>It is possible that the increased size and number of connexin43 gap junction plaques in the cold controls may represent a compensatory response in order to maintain sufficient gap junction communication during physiological conditions that would reduce conductance. These changes may represent a mechanism by which the hamster avoids ventricular fibrillation during hibernation and arousal.</AbstractText> |
4,630 | Resuscitation after prolonged ventricular fibrillation with use of monophasic and biphasic waveform pulses for external defibrillation. | Survival after prolonged ventricular fibrillation (VF) appears severely limited by 2 major factors: (1) low defibrillation success rates and (2) persistent post-countershock myocardial dysfunction. Biphasic (BP) waveforms may prove capable of favorably modifying these limitations. However, they have not been rigorously tested against monophasic (MP) waveforms in clinical models of external defibrillation, particularly where rescue from prolonged VF is the general rule.</AbstractText>We randomized 26 dogs to external countershocks with either MP or BP waveforms. Hemodynamics were assessed after shocks applied during sinus rhythm, after brief VF (>10 seconds), and after resuscitation from prolonged VF (>10 minutes). Short-term differences in percent change in left ventricular +dP/dt(max) (MP -16+/-28%, BP +9.1+/-24%; P=0.03) and left ventricular -dP/dt(max) (MP -37+/-26%, BP -18+/-20%; P=0.05) were present after rescue from brief VF, with BP animals exhibiting less countershock-induced dysfunction. After prolonged VF, the BP group had lower mean defibrillation thresholds (107+/-57 versus 172+/-88 J for MP, P=0.04) and significantly shorter resuscitation times (397+/-73.7 versus 488+/-74.3 seconds for MP, P=0.03).</AbstractText>External defibrillation is more efficacious with BP countershocks than with MP countershocks. The lower defibrillation thresholds and shorter resuscitation times associated with BP waveform defibrillation may improve survival after prolonged VF arrest.</AbstractText> |
4,631 | Long QT syndrome: ionic basis and arrhythmia mechanism in long QT syndrome type 1. | Long QT syndrome type 1 (LQT1) causes torsades de pointes arrhythmia, ventricular fibrillation, and sudden death. It usually is inherited as an autosomal dominant trait (Romano-Ward syndrome). The primary defect in LQT1 is a mutation in KVLQT1, a gene that encodes the pore-forming alpha-subunit of a K+ channel. KvLQT1 alpha-subunits coassemble with minK beta-subunits to form channels that conduct the slow delayed rectifier K+ current (I(Ks)) in the heart. Recessive mutations in KVLQT1 cause Jervell and Lange-Nielsen syndrome, which is characterized by more severe arrhythmias and congenital neural deafness. Heterologous expression studies demonstrated that mutations in KVLQT1 reduce I(Ks) by causing loss of channel function, altered channel gating, and/or a dominant-negative effect. It remains to be proven that an understanding of the molecular basis of LQT1 will lead to more effective therapy. |
4,632 | Evidence for a cardiac ion channel mutation underlying drug-induced QT prolongation and life-threatening arrhythmias. | The aim of this study was to test the hypothesis that some cases of drug-induced arrhythmias depend on genetic predisposition. Excessive prolongation of the QT interval and life-threatening arrhythmias (torsades de pointes or ventricular fibrillation) may occur in response to a variety of cardiac and noncardiac drugs, with detrimental effects on patient safety and the investments made by the pharmaceutical industry. Moss and Schwartz hypothesized that some drug-induced arrhythmias might represent cases of "forme fruste" of the congenital long QT syndrome (LQTS). The availability of molecular screening techniques for LQTS genes allowed us to test this hypothesis. An elderly female patient with documented cardiac arrest related to cisapride, a prokynetic drug that blocks I(Kr), and transiently prolonged QT interval underwent mutational analysis of the known LQTS-related genes performed by single-strand conformational polymorphism and DNA sequencing. Double-electrode voltage clamp in Xenopus oocytes as the expression system was used to study the in vitro cellular phenotype caused by the genetic defect in coexpression with the wild-type (WT) gene. Molecular analysis revealed a heterozygous mutation leading to substitution of a highly conserved amino acid in the pore region of KvLQT1. This mutation was present not only in the patient with ventricular fibrillation but also in her two adult asymptomatic sons who have a normal QT interval. In vitro expression of the mutated KvLQT1 protein showed a severe loss of current with a dominant negative effect on the WT-KvLQT1 channel. Our findings demonstrate that some cases of drug-induced QT prolongation may depend on a genetic substrate. Molecular screening may allow identification among family members of gene carriers potentially at risk if treated with I(Kr) blockers. Evolving technology may lead to rapid screening for mutations of candidate genes that cause drug-induced life-threatening arrhythmias and allow early identification of individuals at risk. |
4,633 | Successful catheter ablation in a patient with polymorphic ventricular tachycardia. | We describe a patient with polymorphic ventricular tachycardia (PVT)/ventricular fibrillation (VF) without organic heart disease who was cured by radiofrequency catheter ablation. The patient was a 65-year-old woman with a 10-year history of recurrent syncope. There was no evidence of organic heart disease, and the QT interval during sinus rhythm was borderline normal (corrected QT interval = 0.45 sec1/2). ECG recording during syncope showed PVT. On one occasion, PVT degenerated into VF. This PVT was always induced by a premature ventricular complex (PVC) originating from the right ventricular (RV) outflow tract. Rapid pacing (220 beats/min) at the site of PVC origin reproduced polymorphic change of the QRS wave on surface ECG that was similar to PVT. This suggests that the PVT originated from a single focus in the RV outflow tract. Catheter ablation was performed at the site of PVC origin. During 18-month follow-up, PVT/VF was not documented. |
4,634 | Electrophysiologic deterioration after one-minute fibrillation increases relative biphasic defibrillation efficacy. | The probability of survival decreases to 70% after 2 minutes of ventricular fibrillation. Biphasic shocks are more effective than monophasic shocks in terminating short-duration (<30 sec) ventricular fibrillation. We tested the hypotheses that developing ischemia changes the electrophysiologic characteristics of fibrillation and that the relative efficacy of biphasic shocks increases as electrophysiologic characteristics deteriorate.</AbstractText>Monophasic (12 msec) and biphasic (6/6 msec) shocks (1 to 4 A) were tested in random order in isolated rabbit hearts after 1-minute ischemic fibrillation. Monophasic action potentials showed only a sporadic occurrence of electrical diastole after 5 seconds of fibrillation (24% of action potentials in the right ventricle and 18% in the left ventricle). After 60 seconds of fibrillation, diastole (17.83+/-1.14 msec in the right ventricle and 21.52+/-1.16 msec in the left ventricle) appeared after almost every action potential (P < 0.0001 compared with 5 sec), despite a lack of change in fibrillation cycle length and dominant frequency. Monophasic I50 was 2.89 A, and biphasic I50 was 1.4 A (77% reduction in energy). Normalized curve width decreased 28%. Retrospective analysis showed that shocks delivered early in the fibrillation action potential had a greater probability of succeeding (89%) than shocks delivered late (30%; P < 0.001).</AbstractText>After 1-minute ischemic fibrillation, diastolic intervals occur during fibrillation. Therefore, defibrillation shocks have an approximately 29% probability of interacting with the fibrillation action potential during diastole. At this time, biphasic shocks produced a more deterministic defibrillation threshold and became even more efficacious (I50 B/M = 0.48) than at short fibrillation durations (I50 B/M = 0.7).</AbstractText> |
4,635 | Regional hyperkalemia increases ventricular defibrillation energy requirements: role of electrical heterogeneity in defibrillation. | Increased spatial electrical heterogeneity has been associated with impaired defibrillation efficacy. The current study investigated the relationship between electrical heterogeneity and defibrillation efficacy by manipulating spatial electrical heterogeneity.</AbstractText>We increased spatial electrical heterogeneity by infusing potassium chloride (2 to 4 mEq/hour) or placebo in the left anterior descending artery in 13 pentobarbital anesthetized swine. Electrophysiologic measurements at five myocardial sites and defibrillation energy requirement (DER) values were determined at baseline and during regional hyperkalemia (n = 7) or placebo (n = 6). Regional potassium infusion was titrated to a 20% reduction in action potential duration in the perfused region. Regional hyperkalemia increased biphasic DER values by 87% (P = 0.02), whereas infusion of placebo did not alter defibrillation efficacy. Regional hyperkalemia decreased myocardial repolarization and refractoriness in the perfused region by 21% (P < 0.001) and 18% (P = 0.01), respectively. However, regional hyperkalemia increased ventricular fibrillation cycle length (VFCL) by 39% (P = 0.008). Consequently, dispersions of repolarization, refractoriness, and VFCL were significantly increased by 169%, 92%, and 200%, respectively. Regional hyperkalemia also increased ventricular conduction time to the perfused region by 54% (P = 0.006), indicating conduction velocity dispersion, while not affecting local pacing threshold or local voltage gradient.</AbstractText>Regional hyperkalemia increased DER values. Regional hyperkalemia likely impairs defibrillation by increasing myocardial electrical heterogeneity, which supports the theory that electrical heterogeneity promotes nonuniform propagation of early postshock activations, thereby inhibiting defibrillation.</AbstractText> |
4,636 | Left ventricular diastolic dysfunction in patients with so-called lone atrial fibrillation. | Lone atrial fibrillation (AF) is defined by the absence of identifiable causes of AF, but its hemodynamics have not been investigated. Twenty-eight patients with lone AF were compared with 14 control patients referred for Wolff-Parkinson-White ablation. Transthoracic and transesophageal echocardiography were performed to rule out structural heart disease, followed by transseptally performed complete hemodynamic evaluation of the left heart systolic and diastolic function. There was no evidence of diastolic dysfunction according to echocardiographic criteria in AF and control patients. There was no difference in echocardiographic measurements, except for a significantly higher inferosuperior left atrial dimension seen in the four-chamber apical view in AF patients (51+/-10 vs 40+/-6 mm, P = 0.03). Hemodynamic evaluation showed that end-diastolic left ventricular pressure and the nadir of the left atrial Y descent were significantly higher in lone AF patients versus controls: 13+/-5 versus 8+/-3 mmHg (P = 0.001) and 6.7+/-3 versus 4.6+/-2.7 mmHg (P = 0.05). Our results demonstrated the presence of diastolic left heart dysfunction in patients with so-called lone AF. |
4,637 | [Variable late potentials in long-term ECG of the post-infarct patient at risk for ventricular fibrillation]. | Ventricular late potentials are found more readily in post-infarction patients who had sustained ventricular tachycardia than in those who survived ventricular fibrillation. Hypothetically, a daytime variability of late potentials might be responsible for this finding.</AbstractText>Therefore a conventional late potential analysis only performed once a day was compared to a late potential analysis in time and frequency domain repeatedly performed every hour in the Holter-ECG of 160 post-infarction patients (50 patients (= VT-group) with documented, sustained ventricular tachycardia (cycle-length > 230 ms), 50 patients (= VF-group) who survived, documented ventricular fibrillation and 60 patient, without ventricular arrhythmias (= O VT/VF-group)).</AbstractText>The conventional analysis showed late potentials in time domain in 72% of the patients in the VT-group, in 40% of patients in the VF-group and in 20% of the patients in the O VT/VF-group. The Holter-ECG showed late potentials to be permanently present in frequency domain in 66% of the patients in the VT-group, in only 6% in the patients in the VF-group and in no patient in the O VT/VF-group. However, in at least one analysis we detected late potentials in 84% of patients of the VF-group, in 90% of patients in the VT-group and in 18% of patients in the O VT/VF-group. Transiently detectable late potentials in patients of the VF-group were predominantly seen at heart rate accelerations in the morning hours, ST-segment shifts or transitory decreased heart rate variability.</AbstractText>Post-infarction patients with sustained ventricular tachycardia predominantly have constantly detectable late potentials over 24 hours. In these patients conventional late potential is successful for post-infarction risk stratification at any time of the day. However, in post-infarction patients who survived ventricular fibrillation, late potentials are found to be transitory and only detectable by Holter-ECG. Thus, late potential analysis performed in the Holter-ECG might improve post-infarction risk stratification in patients prone to sudden cardiac death.</AbstractText> |
4,638 | [Ventricular fibrillation in intra-atrial cardioversion of atrial fibrillation]. | Recently intra-atrial defibrillation has become an interesting alternative to external defibrillation and drug therapy for the treatment of atrial fibrillation. Low-energy intra-atrial defibrillation can be used to restore sinus rhythm f.ex. after a failed external cardioversion or during an electrophysiologic study when the administration of antiarrhythmic drugs should be avoided. Additionally this new technique has led to the development of implantable atrial defibrillators for the treatment of selected patients suffering from chronic atrial fibrillation. Intra-atrial defibrillation seems to be a highly effective and safe method, but little experience exists concerning the outcome so far. Especially the potential risk of inducing ventricular pro-arrhythmia is subject of current controversy. We report the case of a 79-year-old patient suffering from WPW syndrome with a concealed bypass tract who was subject to an intra-atrial defibrillation during an electrophysiologic study. At the beginning of the study atrial fibrillation could be converted to sinus rhythm by a single low-energy atrial defibrillation (3 J.). After a short period of time a second intra-atrial defibrillation had to be performed in the same way because of recurrent atrial fibrillation. By this atrial shock ventricular fibrillation was induced, so that high energy external defibrillation became necessary. Analyzing the ECG a correct R-wave synchronization was found, but a rather short preceding RR interval (252 ms). In conclusion, low energy atrial defibrillation is gaining importance as a highly effective new technique to restore sinus rhythm in patients suffering from atrial fibrillation resistant to conventional therapies. Nevertheless potential risks have to be considered such as the induction of ventricular pro-arrhythmia. Therefore, a correct R-wave synchronization is obligatory and shock delivery should be withheld after short RR intervals. Future prospective randomized studies will have to show whether this new technique is really safe enough and superior to the conventional methods for restoring sinus rhythm in patients suffering from atrial fibrillation. |
4,639 | [Projection of new antihistamines]. | The metabolic fate of most antihistamines is not clearly established. The drugs usually appear to be extensively metabolized,mainly in the liver. Some second generation antihistamines are metabolized principally by the cytochrome P-450 microsomal enzyme system, mainly by the isoenzyme 3A4 (CYP3A4), although other isoenzyme,including CYP1A2 and CYP2D6, also may be involved. However,other second generation antihistamines appear to be only minimally metabolized in the liver. Serious cardiac effects (prolongation of the QT interval, arrhythmias, torsades de pointes, ventricular fibrillation, arrest, hypotension, palpitations, syncope, dizziness, and/or death) have been reported rarely in patients receiving terfenadine or astemizole. Cardiotoxic effects ussually were associated with higher than recommended dosages and/or increased plasma concentrations of the drugs and their active metabolites. No clinically important adverse effects or changes in the QT intervals were reported after concomitant administration of ketoconazole with fexofenadine. Patients receiving an azole, antifungal, a macrolide, quinine or grapefruit juice also appear to be at substantial risk of such toxicity, probably secondary to interference with metabolism of the antihistamine. Second-generation H1 receptor antagonist have been studied extensively in the treatment of asthma. Many of these drugs have been reported to inhibit eosinophil and basophil chemotaxis and therefore might have an effect on the inflammatory reactions that characterise this disease. Safe use of antihistamines during pregnancy has not been established; therefore, the drugs should not be used in women who are or may become pregnant unless the potential benefits justify the possible risks to the fetus. Antihistamines should not be administered to premature or full-term neonates. Young children may be more susceptible than adults to the toxic effects of antihistamines. |
4,640 | Effective arterial elastance of irregular beats during atrial fibrillation in canine left ventricle. | Effective arterial elastance (E(a)) was originally defined as the end-systolic pressure (ESP)/stroke volume (SV) ratio of the left ventricle (LV). E(a) combined with LV contractility (E(max)), E(a)/E(max), proved to be powerful in analyzing the ventriculo-arterial coupling of normal and failing hearts in regular beats. However, E(a) sensitively changes with LV E(max), preload, and afterload widely changing among irregular beats. This has discouraged the use of E(a) during arrhythmia. However, we hypothesized that E(a) could serve as the effective afterload (not always arterial) elastance against ventricular ejection under arrhythmia. We tested this hypothesis by analyzing beat-to-beat changes in E(a) of irregular beats during electrically induced atrial fibrillation (AF) in normal canine in situ hearts. We newly found that during AF in each heart: 1) E(a) changed widely among irregular beats and became markedly high in weak beats with small SVs; 2) E(a) and E(a)/E(max) distributed non-normally with large skewness but 1/E(a) distributed more normally; 3) 1/E(a) correlated closely with end-diastolic volume, E(max) and preceding beat intervals; and 4) the reciprocal of mean 1/E(a) closely correlated with mean ESP/mean SV. These results support our hypothesis that E(a) can serve as the effective afterload elastance against ventricular ejection on a per-beat basis during AF. E(a)/E(max) can also quantify the ventriculo-afterload (not arterial) coupling on a per-beat basis. This study, however, warns that mean E(a) and mean E(a)/E(max) of irregular beats cannot necessarily represent their averages during AF. |
4,641 | Capture and fusion beats during atrial fibrillation and ventricular tachycardia. | Two patients were presented, and two previously unreported observations were made. Patient 1, a 50 year old man with episodic palpitations and dizziness for 10 years, exhibited initiation of idiopathic ventricular tachycardia (VT) by atrial fibrillation (AF). Patient 2, a 43 year old woman with a structurally normal heart but recurrent palpitations for one year, demonstrated fusion and capture beats during simultaneous VT and AF. An explanation is given as to why the latter phenomenon is rarely observed. |
4,642 | Prevalence of the Brugada sign in idiopathic ventricular fibrillation and healthy controls. | To determine the prevalence of the Brugada sign (right bundle branch block with ST elevation in V1-V3) in idiopathic ventricular fibrillation and in an age matched healthy population.</AbstractText>ECGs from 39 consecutive patients with idiopathic ventricular fibrillation and 592 healthy controls were reviewed. They were classified as definite, questionable, and no Brugada sign (according to predetermined criteria) by four investigators blinded to the subjects' status.</AbstractText>Eight patients (21%) with idiopathic ventricular fibrillation but none of the 592 controls had a definite Brugada sign (p < 0.005). Thus the estimated 95% confidence limits for the prevalence of a definite Brugada sign among healthy controls was less than 0.5%. A questionable Brugada sign was seen in two patients with idiopathic ventricular fibrillation (5%) but also in five controls (1%) (p < 0.05). Normal ECGs were found following resuscitation and during long term follow up in 31 patients with idiopathic ventricular fibrillation (79%). Patients with idiopathic ventricular fibrillation and a normal ECG and those with the Brugada syndrome were of similar age and had similar spontaneous and inducible arrhythmias. However, the two groups differed in terms of sex, family history, and the incidence of sleep related ventricular fibrillation.</AbstractText>A definite Brugada sign is a specific marker of arrhythmic risk. However, less than obvious ECG abnormalities have little diagnostic value, as a "questionable" Brugada sign was observed in 1% of healthy controls. In this series of consecutive patients with idiopathic ventricular fibrillation, most had normal ECGs.</AbstractText> |
4,643 | Reoperative coronary artery bypass via left thoracotomy. | The patient was a 49-year-old woman. When she was 39 years old, she underwent coronary artery bypass grafting (left internal thoracic artery to left anterior descending artery, saphenous vein graft to first diagonal branch). At the age 48, she had effort angina. On coronary angiography, triple-vessel disease was found, and she was treated conservatively. Progression of the disease was confirmed with detection of the left circumflex artery associated with jeopardized collateral to the right coronary artery showing total occlusion. The patient underwent reoperation. Since the left internal thoracic artery was patent despite occlusion of the saphenous vein graft, the approach of left thoracotomy was employed. Under cardiopulmonary bypass with ventricular fibrillation and left vent through left atrial appendage, the right radial artery was anastomosed to the left circumflex artery from the descending thoracic aorta, and the right gastroepiploic artery was anastomosed to the right coronary artery (4AV branch). Patency of the bypass was confirmed postoperatively. We consider this operative technique was especially useful for reoperation in cases of a patent internal thoracic artery in which left thoracotomy can be conducted safely. |
4,644 | Cardiac K+ channels and drug-acquired long QT syndrome. | The hallmark of long QT syndromes (LQTS) is an abnormal ventricular repolarization characterized by a prolonged QT interval on the electrocardiogram and a propensity to the occurrence of syncopes resulting from polymorphic ventricular tachycardia, called torsades de pointes. They may degenerate to ventricular fibrillation, possibly causing sudden death. Congenital LQTS, which implicates at least six chromosomal loci, LQT1 to LQT6, three of them corresponding to mutations concerning the coding of K+ channel proteins, give useful information about the mechanism underlying the arrhythmia. One of the potassium channel genes implicated in congenital LQTS is HERG, which encodes the IKr current channel protein. This current has provided a relevant insight into the occurrence of drug-acquired LQTS, since all drugs associated with torsades, such as erythromycin, terfenadine, haloperidol, or cisapride, also block IKr. |
4,645 | [Antiarrhythmic therapy in patients with heart failure]. | In patients with severe chronic heart failure, many deaths are sudden due to life-threatening ventricular arrhythmias. Supraventricular arrhythmias such as paroxysmal or chronic atrial fibrillation may also cause serious complications in those patients due to acute loss of atrial contraction, pump failure during rapid ventricular response and embolic events. Two therapeutic strategies are currently available for therapy and prevention of malignant ventricular arrhythmias and subsequent sudden arrhythmic death: antiarrhythmic drug therapy and implantable defibrillators. However, selection of the most beneficial strategy for the individual patient to reduce the risk of sudden death remains a major challenge in cardiology. Betablockers exert a favorable antiarrhythmic action without increasing proarrhythmia, thus betablockers may serve as a basic medication in patients at risk for sudden death. However, the general use of antiarrhythmic drug therapy for symptomatic ventricular arrhythmias is not recommended, as these drugs have been shown to increase mortality in patients with severe congestive heart failure due to proarrhythmic or negative inotropic effects (e.g. class Ia antiarrhythmics). Even class III antiarrhythmic drugs such as amiodarone, which has been studied sufficiently in patients with left ventricular dysfunction, is not effective enough for significant reduction of cardiac mortality in patients with symptomatic ventricular arrhythmias and depressed ventricular function (e.g. EMIAT, CAMIAT). But as a positive result of available studies, amiodarone does not increase mortality in those patients. Dofetilide has also not been shown to prolong life significantly by suppressing malignant ventricular arrhythmias (DIAMOND-Study). In patients with symptomatic ventricular arrhythmias or aborted sudden death, ICD therapy has been proven to be superior to antiarrhythmic drug therapy in cardiac mortality reduction as a secondary prevention strategy (e.g. AVID, CASH, CIDS). For primary prevention of sudden arrhythmic death in high risk patients, 2 studies (MADIT, MUSST) have already demonstrated favorable results, decreasing mortality by ICD therapy in selected patient populations with partly-reduced ventricular function and unsustained but inducible ventricular tachycardias. This topic is, however, undergoing further evaluation by ongoing trials (e.g. MADIT II, SCD-HeFT). From available data, antiarrhythmic drug therapy in high risk patients is not justified on a routine basis, whereas ICD therapy as a secondary and perhaps primary prevention strategy will significantly reduce cardiac mortality in patients with severe heart failure. Sotalol, a class III antiarrhythmic agent, has recently been shown to reduce ICD-shock delivery which indicates that concomitant drug therapy in patients with an ICD device already implanted may be beneficial in terms of reducing ICD discharges due to ventricular and supraventricular tachycardias. In patients with paroxysmal atrial fibrillation and congestive heart failure, restitution of sinus rhythm is the primary therapeutic goal which can be safely achieved by amiodarone and dofetilide (DIAMOND). In the latter, continuous monitoring of the patient is mandatory because of increased risk of torsade de pointes arrhythmias during the first days of drug administration. In patients with chronic atrial fibrillation rate control and anticoagulation with warfarin is the primary therapeutic option, which can be achieved with either drug treatment (Digoxin, betablockers, amiodarone) or by His bundle ablation with subsequent pacemaker insertion. |
4,646 | Effect of atrial fibrillation on pulmonary venous flow patterns assessed by Doppler transesophageal echocardiography. | To investigate the effect of atrial fibrillation (AF) on pulmonary venous flow (PVF) patterns in a cohort with nonrheumatic AF.</AbstractText>A prospective and controlled study undertaken at a tertiary referral medical center.</AbstractText>The echocardiographic parameters of left superior PVF as assessed by Doppler transesophageal echocardiography in 40 patients with chronic AF (group 1) were compared to those of 33 volunteers with sinus rhythm (group 2) and well-matched baseline characteristics.</AbstractText>: All group 1 patients presented with single systolic forward flow (SFF) patterns. In contrast, single and double SFF patterns were found equally in group 2. With regard to reverse flow (RF), most group 1 patients (33 of 40) had an early systolic RF and none had atrial RF; however, most group 2 subjects (29 of 33) had an atrial RF. Some of the group 1 patients (17%) had a late systolic RF in the absence of significant mitral regurgitation. In group 1, the SFF appeared later and disappeared earlier than in group 2. The mean systolic peak velocity and time-velocity integral (TVI) of the SFF were significantly lower in group 1 compared to group 2. The diastolic peak velocity and TVI were not significantly different between groups.</AbstractText>: Our data indicate that AF independently and significantly affects the PVF and leads to characteristic flow patterns different from sinus rhythm. The presence of AF reduces SFF in addition to the absence of atrial RF. These changes in the flow patterns should be taken into account while interpreting the implications of PVF in the presence of AF.</AbstractText> |
4,647 | Long-term prognosis of acute pulmonary oedema--an ominous outcome. | Acute pulmonary oedema (APOE) is a major health problem, leading to poor hospital and long-term outcomes. There is a relative paucity of studies describing prognosis of consecutive unsolicited patients diagnosed with APOE and hospitalized in internal medicine departments.</AbstractText>To describe the clinical profile and outcome (in hospital and 1-year prognosis) of successive unselected patients with APOE, in a prospective observational study.</AbstractText>The study population included 150 consecutive unsolicited patients (90 men, 60 women; median age 75 years) with APOE all hospitalized in an internal medicine department, in a 900-bed care centre. Ischaemic heart disease (IHD), hypertension and diabetes were present in 85%, 70% and 52% of patients, respectively. The most common precipitating factors for APOE included high blood pressure (29%), rapid atrial fibrillation (29%), unstable angina pectoris (25%), infection (18%) and acute myocardial infarction (MI; 15%). Eighteen patients (12%) died in hospital, with 82% of these deaths attributed to cardiac pump failure. Predictors for an increased in-hospital mortality included: diabetes (P<0.05), orthopnoea (P<0. 05), echocardiographic finding of depressed global left ventricular systolic function (P<0.001), acute MI during hospital stay (P<0.001), hypotension/shock (P<0.05), and the need for mechanical ventilation (P<0.001). After a median hospital stay of 10 days, 132 patients were discharged home. The 1-year mortality was 40%. Only the presence of pleural effusion was found as a predictor for 1-year mortality.</AbstractText>Most patients with APOE in this study are elderly, and have IHD, hypertension, diabetes and a previous history of APOE. The overall mortality is high (in-hospital, 12%: 1-year, 40%). Left ventricular dysfunction was associated with high in-hospital mortality, but not with long-term prognosis.</AbstractText> |
4,648 | Homicidal commotio cordis in two children. | This paper's objective is to describe two cases of fatal commotio cordis resulting from the deliberate striking of children's chests by adults with their fists. These deaths involve two male children, ages 3 years and 14 months. The clinical histories, events in the households prior to the deaths, behaviors of the children, autopsy findings, and investigation results are all similar. In both cases, fatal blows were delivered to the anterior chest with a closed fist. Both children collapsed immediately, unable to be resuscitated. Confessions were obtained in both cases by investigators soon after the children's deaths. Autopsies showed chest contusions in only one child, presumably due to knuckle impact. The cardiac rhythms noted by paramedics were ventricular fibrillation and asystole. Due to the lack of physical findings, an immediate and thorough investigation is critical. An accurate history of events preceding death must be obtained. |
4,649 | Effects of the I(K.ATP) blockers glibenclamide and HMR1883 on cardiac electrophysiology during ischemia and reperfusion. | Clinical evidence indicates an antiarrhythmic effect of sulfonylureas, which might be blunted by their vascular action. We wanted to investigate the effect of glibenclamide and the new sulfonylthiourea compound 1-[[5-[2-(5-chloro-o-anisamido)ethyl]-2-methoxyphenyl]-sulfonyl]-3 -me thylthiourea (HMR1883) on cardiac electrophysiology in the course of regional ischemia and reperfusion. Isolated rabbit hearts (Langendorff-technique) were pretreated with either vehicle (n=14), 3 micromol/l glibenclamide (n=7) or 3 micromol/l HMR1883 (n=7) before regional ischemia was induced by left coronary artery branch occlusion (45 min) followed by 45 min reperfusion. Unipolar epicardial electrocardiograms were recorded from 256 epicardial AgCl electrodes. Coronary ligation resulted in a decrease in coronary flow (CF) by 35% and in left ventricular pressure (LVP) by 40% in all series. The occluded zone was 23+/-3% in all series. Ischemia led to shortening of the epicardial activation-recovery interval (ARI) in the ischemic area, which was inhibited by both drugs especially in the early phase. In the non-ischemic area, ARIs remained stable and there was no effect of the drugs. Ischemia led to an increase in the regional difference in ARI between ischemic center and border zone. This increase was significantly inhibited by both substances during late ischemia and early reperfusion (until 15 min reperfusion). In addition, the dispersion of ARIs was reduced by both drugs during late ischemia and reperfusion. Ventricular fibrillation was observed in 7/14 (control), 0/7 (glibenclamide), and 0/7 (HMR1883). All ventricular fibrillation occurred during reperfusion. In glibenclamide but not in HMR1883-treated hearts recovery of CF upon reperfusion was significantly depressed (control: 25.5+/-4; HMR1883: 23+/-2.5; glibenclamide: 16+/-1 ml/min, values at 2 min reperfusion), while the elevation of ST-segments of the electrograms in early ischemia was fully prevented by both treatments. We conclude that both glibenclamide and HMR1883 exert an antiarrhythmic effect in this model, and reduce the shortening of the ARIs in the ischemic area, thus attenuating regional differences in ARIs between ischemic and non-ischemic area. Furthermore, unlike glibenclamide HMR1883 does not interfere with postischemic hyperemia. |
4,650 | [Legal aspects in early defibrillation by trained lay respondents]. | Ventricular fibrillation is the main reason for cardiac arrest. The probability for survival decreases by 10% every minute, therefore immediate resuscitation is necessary. Cardiopulmonary Resuscitation (CPR) by trained first responders is already established, when a doctor is not available. Today automated external defibrillators (AED) are available to first responders for an effective therapy of ventricular fibrillation. Thanks to the high reliability of today's automated external defibrillators they can be used by trained first responders without any legal reservations. If a defibrillator is available, a trained first responder is obliged to use it in an emergency. |
4,651 | Acute heart failure in the parturient--do not forget phaeochromocytoma. | Phaeochromocytoma is a rare condition and extremely rare in pregnancy. Diagnosis is notoriously difficult, as phaeochromocytoma may present a broad spectrum of clinical manifestations. The key to a successful outcome is a high index of suspicion of its existence and its early diagnosis. |
4,652 | The use of calcium salts in the prevention and management of verapamil-induced hypotension. | To review the available literature on the use of intravenous calcium salts for the prevention of hypotension associated with intravenous verapamil.</AbstractText>A MEDLINE search (1966-June 1999) identified pertinent articles; references from these articles were identified to serve as additional resources.</AbstractText>Verapamil is effective in inhibiting atrioventricular nodal conduction, thereby controlling ventricular rate in patients with atrial fibrillation/flutter and terminating paroxysmal supraventricular tachycardia. However, hypotension may be caused by the negative inotropic and vasodilating effects of verapamil. In vitro and animal data suggest that calcium pretreatment may minimize the effects of verapamil on cardiac output and blood pressure. Case reports suggest that intravenous calcium may be useful for both prevention and reversal of the hemodynamic effects of verapamil. A number of small clinical trials have been performed, suggesting that calcium administered prior to intravenous verapamil results in a decreased incidence of hypotension. The most common adverse effect of intravenous calcium is flushing.</AbstractText>Calcium pretreatment prior to intravenous calcium-channel blocker administration should be considered in patients in whom further reductions in blood pressure may precipitate hypoperfusion or worsen underlying cardiovascular status. A dose of calcium gluconate 1 g (ionized calcium 90 mg) administered over three minutes is recommended for preventing or lessening the hypotensive effect of verapamil without affecting the antiarrhythmic effects of verapamil.</AbstractText> |
4,653 | The antihypertensive and cardioprotective effects of (-)-MJ-451, an ATP-sensitive K(+) channel opener. | ATP-sensitive K(+) (K(ATP)) channel openers have been shown to be a potential class of therapeutic agents for the control of cardiovascular diseases, including angina, arrhythmias, and hypertension. In this study, the pharmacological activity of 6-cyano-3S,4R-dihydro-2, 2-dimethyl-2H-3-hydroxy-4-[5S-(1-hydroxymethyl)-2-oxo-1-pyrrolidinyl] -1-benzopyran ((-)-MJ-451), a synthetic K(ATP) opener, was evaluated in anesthetized rat models and in isolated rat thoracic rings. Results demonstrated that intravascular injection of (-)-MJ-451 (0. 02, 0.05 and 0.1 mg/kg) produced an immediate, dose-related reduction in mean arterial blood pressure in anesthetized spontaneously hypertensive rats (SHR), which persisted for more than 3 h and was not accompanied by reflex tachycardia. The hemodynamic changes were completely abolished by pretreatment with glibenclamide (4 mg/kg, i.v. bolus), a selective K(ATP) channel blocker. In isolated thoracic aorta, (-)-MJ-451 (10 nM-3 microM) produced a concentration-dependent vasodilator effect on the phenylephrine (0.3 microM)-induced vasoconstriction. Moreover, (-)-MJ-451 relaxed the thoracic aorta contracted by low (5, 20 and 30 mM), but not high (40 and 60 mM) concentrations of extracellular potassium. In addition, (-)-MJ-451 showed cardioprotective effects in the rat model of 45-min left coronary artery occlusion followed by 1-h reperfusion. In myocardial ischemia, pretreatment with (-)-MJ-451 (2, 5 and 10 microg/kg, i.v. bolus) significantly reduced the incidence of ventricular fibrillation and the mortality, also reducing the total number of ventricular premature contractions, total duration of ventricular tachycardia and ventricular fibrillation. A significant reduction in infarct size was noted in three (-)-MJ-451 (2, 5 and 10 microg/kg)-treated groups. Also, the cardioprotective effects of (-)-MJ-451 were virtually abolished by pretreating the rats with glibenclamide (4 mg/kg, i.v. bolus). In conclusion, (-)-MJ-451, through opening the K(ATP) channel, exerted antihypertensive and cardioprotective effects. Therefore, it is suggested that (-)-MJ-451 has potential in the treatment of hypertension or acute myocardial infarction. |
4,654 | Nicotine increases ventricular vulnerability to fibrillation in hearts with healed myocardial infarction. | The vulnerability of the infarcted hearts to ventricular fibrillation (VF) was tested in in situ canine hearts during nicotine infusion. The activation pattern was mapped with 477 bipolar electrodes in open-chest anesthetized dogs (n = 8) 5-6 wk after permanent occlusion of the left anterior descending coronary artery. Nicotine (129 +/- 76 ng/ml) lengthened (P < 0.01) the pacing cycle length at which VF was induced from 171 +/- 8.9 to 210 +/- 14. 7 ms. Nicotine selectively amplified the magnitude of conduction time and monophasic action potential (MAP) amplitude and duration (MAPA and MAPD, respectively) alternans in the epicardial border zone (EBZ) but not in the normal zone. With critical reduction of the MAPA and MAPD in the EBZ, conduction block occurred across the long axis of the EBZ cells. Block led immediately to reentry formation in the EBZ with a mean period of 105 +/- 10 ms, which, after one to two rotations, degenerated to VF. Nicotine widened the range of diastolic intervals over which the dynamic MAPD restitution curve had a slope >1. We conclude that nicotine facilitates conduction block, reentry, and VF in hearts with healed myocardial infarction by increasing the magnitude of depolarization and repolarization alternans consistent with the restitution hypothesis of vulnerability to VF. |
4,655 | Experimental study of the effects of multi-site sequential ventricular pacing on the prophylaxis of ventricular fibrillation. | Previous studies report a significant prophylactic effect on the occurrence of atrial fibrillation by simultaneous multi-site atrial pacing. We investigated the effects of multi-site sequential ventricular pacing (MSVP), which may be preferable to simultaneous multi-site pacing in terms of the prophylaxis of the occurrence of ventricular fibrillation (VF). Needle electrodes were inserted at ten different epicardial sites on both ventricles for MSVP in 12 adult beagle dogs. Four premature ventricular extrastimuli (PVE) were introduced to provoke VF reproducibly from a separate electrode in the left ventricle. The 4 PVE were applied to try to provoke VF during MSVP in a comparable fashion to the activation sequence during sinus rhythm. We compared the prophylactic effects of MSVP on the inducibility of VF by changing the number of stimulation sites to either 1, 3, 5, or 10 epicardial sites. We performed a total of 363 trials of induction and suppression of VF. The occurrence rates of VF by the 4 PVE for the various number of epicardial stimulation sites of MSVP, i.e., at 1, 3, 5, and 10 sites, were 0.8263, 0.4286, 0.4450, and 0.2857, respectively (p < 0.05). There was a significant prophylactic effect of MSVP on the inducibility of VF, and this effect became stronger as the number of MSVP sites was increased from 3 to 10. The hemodynamic state was relatively stable during MSVP. MSVP seems to be a promising method with which to reduce the occurrence of VF, and a larger number of stimulation sites would be more effective in terms of the prophylaxis of VF. |
4,656 | Drug therapy of sustained ventricular tachyarrhythmias. Is there still a role? | This article provides a review of the risks faced by patients with sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) in the absence of a reversible or transient cause so that the goals of therapy can be clearly defined. The therapeutic approaches that have been proposed to achieve these goals are outlined and evidence comparing these various approaches to therapy is then summarized in order to propose an algorithm for the optimal use of antiarrhythmic drug therapies as primary therapy for selected VT/VF patients. Options for the ancillary uses of antiarrhythmic drug therapies in ICD patients are considered. |
4,657 | Application of noninvasive and invasive tests for risk assessment in patients with ventricular arrhythmias. | Sudden cardiac death remains a major public health problem in western society. Because most patients who experience cardiac arrest are not successfully resuscitated, primary prevention of sudden death remains an important challenge. A number of noninvasive risk stratification techniques have been suggested as providing useful information in patients with underlying structural heart defects. Unfortunately, the positive predictive value of most of these techniques has been limited. Left ventricular ejection fraction, the presence of nonsustained ventricular tachycardia on Holter monitoring, and inducible sustained ventricular tachycardia at electrophysiologic testing in patients with coronary artery disease remain the best established prognostic test. However, with the exception of two ICD studies using the combination of these markers, prospective studies have not yet completely validated the use of these and other prognostic markers. Further understanding of the pathophysiology of ventricular fibrillation and other risk stratification techniques will be necessary before a clear algorithm can be developed for application to patients at risk for sudden death. |
4,658 | [Transportation of patients with acute myocardial infarction]. | The aim of this study was to describe the results and experiences from a local hospital concerning transports with patients with acute myocardial infarction to primary PTCA. Our material includes 27 patients who had primary PTCA. There were no complications during the transports. None of the patients had hypotension or arrythmia requiring treatment during the transports. One patient had ventricular fibrillation before the transport. None of the patients died during the transports. Two patients died in the period following PTCA. The transport delay was 1 hour and 40 minutes on average. Future randomized studies like DANAMI 2 will show if PTCA with delayed treatment, or immediate thrombolysis, give better results for the patient. |
4,659 | [A surgical case of atrial septal defect with myotonic dystrophy]. | A case report is presented of a 16-year-old woman with myotonic dystrophy, who required open-heart surgery for an atrial septal defect. We successfully repaired an atrial septal defect using normothermic cardiopulmonary bypass and electrically maintained ventricular fibrillation. Anesthesia using fentanyl, vecronium and isoflurane was uneventful and there were no postoperative complications. Anesthetic agents must be selected with care, and ventilation requires meticulous attention. |
4,660 | Basic mechanisms of atrial fibrillation--very new insights into very old ideas. | Atrial fibrillation (AF) was recognized and studied extensively in the early twentieth century, but many fundamental aspects of the arrhythmia were poorly understood until quite recently. It is now recognized that AF can be initiated by a variety of mechanisms that share the ability to cause extremely rapid, irregular atrial electrical activity. Once initiated, AF causes alterations in atrial electrical properties (electrical remodeling), including both rapid functional changes and slower alterations in ion channel gene expression, which promote the maintenance of AF and facilitate reinitiation of the arrhythmia should it terminate. Electrical remodeling decreases the atrial refractory period in a heterogeneous way, thus decreasing the size and stability of potential functional atrial reentry waves and promoting multiple-circuit reentry. Whatever the initial cause of AF, electrical remodeling is likely to be a final common pathway that ultimately supervenes. Recent advances in understanding ion channel function, regulation, and remodeling at the molecular level have allowed for a much more detailed appreciation of the basic determinants of AF. Improvements in the clinical management of AF will inevitably follow the recent advances in our understanding of its detailed pathophysiology. |
4,661 | Ventricular fibrillation: mechanisms of initiation and maintenance. | Ventricular fibrillation (VF) is the major immediate cause of sudden cardiac death. Traditionally, VF has been defined as turbulent cardiac electrical activity, which implies a large amount of irregularity in the electrical waves that underlie ventricular excitation. During VF, the heart rate is too high (> 550 excitations/minute) to allow adequate pumping of blood. In the electrocardiogram (ECG), ventricular complexes that are ever-changing in frequency, contour, and amplitude characterize VF. This article reviews prevailing theories for the initiation and maintenance of VF, as well as its spatio-temporal organization. Particular attention is given to recent experiments and computer simulations suggesting that VF may be explained in terms of highly periodic three-dimensional rotors that activate the ventricles at exceedingly high frequency. Such rotors may show at least two different behaviors: (a) At one extreme, they may drift throughout the heart at high speeds producing beat-to-beat changes in the activation sequence. (b) At the other extreme, rotors may be relatively stationary, activating the ventricles at such high frequencies that the wave fronts emanating from them breakup at varying distances, resulting in complex spatio-temporal patterns of fibrillatory conduction. In either case, the recorded ECG patterns are indistinguishable from VF. The data discussed have paved the way for a better understanding of the mechanisms of VF in the normal, as well as the diseased, human heart. |
4,662 | Clinical and echocardiographic predictors of left atrial clot and spontaneous echo contrast in patients with severe rheumatic mitral stenosis: a prospective study in 200 patients by transesophageal echocardiography. | The objective of this study was to prospectively investigate various clinical and echocardiographic variables to predict the left atrial and left atrial appendage clot and spontaneous echo contrast in patients with severe rheumatic mitral stenosis. We studied 200 consecutive patients (112 males and 88 females; mean age 29.6+/-9.6 years). Left atrial clot and spontaneous echo contrast were present in 26 and 53.5% of cases, respectively. There were no significant differences in the mitral valve area, mean transmitral diastolic gradient and left ventricular ejection fraction between patients with and without clot. Patients with clot were older (34.4+/-11.4 vs. 28.2+/-8.5 years, P<0.001), had longer duration of symptoms (41. 4+/-36.0 vs. 28.8+/-22.9 months, P<0.001), more frequent atrial fibrillation and spontaneous echo contrast (69.2 vs. 16.9%, P<0. 00001 and 76.9 vs. 45.3%, P<0.00001, respectively) and larger left atrial area and diameter (41.0+/-12.7 vs. 29.9+/-7.4 cm(2), P<0.00001 and 53.9+/-8.3 vs. 47.6+/-7.4 mm, P<0.0001, respectively) as compared to patients without clot. Similarly patients with spontaneous echo contrast were older (31+/-10.4 vs. 27.8+/-8.3 years, P<0.01), had more frequent atrial fibrillation (48.6 vs. 9.7%, P<0.0001), left atrial clot (37.4 vs. 12.9%, P<0.0001), larger left atrial area and diameter (37.6+/-11.2 vs. 28.1+/-6.7 cm(2), P<0.00001 and 52.2+/-8.3 vs. 45.9+/-6.5 mm, P<0.00001, respectively) and smaller mitral valve area (0.77+/-0.14 vs. 0.84+/-0.13 cm(2), P<0.01) as compared to patients without spontaneous echo contrast. There were no significant differences in the mean transmitral diastolic gradient and left ventricular ejection fraction. On multiple regression and discriminant function analysis, atrial fibrillation and left atrial area were independent predictors of left atrial clot formation. In a subgroup of patients with sinus rhythm, larger left atrial area and presence of spontaneous echo contrast were significantly associated with the presence of clot in left atrium and appendage. We conclude that in patients with severe mitral stenosis, the presence of atrial fibrillation and in the subgroup of the patients with sinus rhythm the presence of large left atrium (> or =40 cm(2)) and spontaneous echo contrast were associated with higher risk of clot formation in the left atrium and might be benefited by prophylactic anticoagulation. |
4,663 | Automatic external defibrillators: changing the way we manage ventricular fibrillation. | To discuss recent developments in automatic defibrillation and to review the evidence that first-responders equipped with automatic external defibrillators (AEDs) improve survival from out-of-hospital cardiac arrest.</AbstractText>MEDLINE search from 1966 to 1999 (articles in English only) and examination of bibliographies.</AbstractText>Published studies of out-of-hospital cardiac arrest and first-responders equipped with AEDs. Studies had to have a control group and to report survival to hospital discharge from ventricular fibrillation (VF).</AbstractText>Six studies met the selection criteria (two prospective randomised trials, two prospective controlled trials, and one cohort study and one retrospective study, both with historical controls).</AbstractText>A random effects meta-analysis of odds ratios for survival from VF.</AbstractText>Meta-analysis suggests that equipping first-responders with AEDs increases the probability of survival to hospital discharge after out-of-hospital cardiac arrest (odds ratio, 1.74; 95% CI, 1.27-2.38; P < 0.001). However, most of the studies lacked sufficient power to draw definitive conclusions. Until the impact of wide deployment of AEDs is fully understood, first-responder defibrillation in Australia should only occur as part of coordinated multicentre research studies.</AbstractText> |
4,664 | Time course and mechanism of myocardial catecholamine release during transient ischemia in vivo. | Elevated concentrations of norepinephrine (NE) have been observed in ischemic myocardium. We investigated the magnitude and mechanism of catecholamine release in the myocardial interstitial fluid (MIF) during ischemia and reperfusion in vivo through the use of microdialysis.</AbstractText>In 9 anesthetized pigs, interstitial catecholamine concentrations were measured in the perfusion areas of the left anterior descending coronary artery (LAD) and the left circumflex coronary artery. After stabilization, the LAD was occluded for 60 minutes and reperfused for 150 minutes. During the final 30 minutes, tyramine (154 nmol. kg(-1). min(-1)) was infused into the LAD. During LAD occlusion, MIF NE concentrations in the ischemic region increased progressively from 1. 0+/-0.1 to 524+/-125 nmol/L. MIF concentrations of dopamine and epinephrine rose from 0.4+/-0.1 to 43.9+/-9.5 nmol/L and from <0.2 (detection limit) to 4.7+/-0.7 nmol/L, respectively. Local uptake-1 blockade attenuated release of all 3 catecholamines by >50%. During reperfusion, MIF catecholamine concentrations returned to baseline within 120 minutes. At that time, the tyramine-induced NE release was similar to that seen in nonischemic control animals despite massive infarction. Arterial and MIF catecholamine concentrations in the left circumflex coronary artery region remained unchanged.</AbstractText>Myocardial ischemia is associated with a pronounced increase of MIF catecholamines, which is at least in part mediated by a reversed neuronal reuptake mechanism. The increase of MIF epinephrine implies a (probably neuronal) cardiac source, whereas the preserved catecholamine response to tyramine in postischemic necrotic myocardium indicates functional integrity of sympathetic nerve terminals.</AbstractText> |
4,665 | Effects of experimental heart failure on atrial cellular and ionic electrophysiology. | Congestive heart failure (CHF) is frequently associated with atrial fibrillation (AF), but little is known about the effects of CHF on atrial cellular electrophysiology.</AbstractText>We studied action potential (AP) properties and ionic currents in atrial myocytes from dogs with CHF induced by ventricular pacing at 220 to 240 bpm for 5 weeks. Atrial myocytes from CHF dogs were hypertrophied (mean+/-SEM capacitance, 89+/-2 pF versus 71+/-2 pF in control, n=160 cells per group, P<0.001). CHF significantly reduced the density of L-type Ca(2+) current (I(Ca)) by approximately 30%, of transient outward K(+) current (I(to)) by approximately 50%, and of slow delayed rectifier current (I(Ks)) by approximately 30% without altering their voltage dependencies or kinetics. The inward rectifier, ultrarapid and rapid delayed rectifier, and T-type Ca(2+) currents were not altered by CHF. CHF increased transient inward Na(+)/Ca(2+) exchanger (NCX) current by approximately 45%. The AP duration of atrial myocytes was not altered by CHF at slow rates but was increased at faster rates, paralleling in vivo refractory changes. CHF created a substrate for AF, prolonging mean AF duration from 8+/-4 to 535+/-82 seconds (P<0.01).</AbstractText>Experimental CHF selectively decreases atrial I(to), I(Ca), and I(Ks), increases NCX current, and leaves other currents unchanged. The cellular electrophysiological remodeling caused by CHF is quite distinct from that caused by atrial tachycardia, highlighting important differences in the cellular milieu characterizing different clinically relevant AF substrates.</AbstractText> |
4,666 | Termination of asynchronous contractile activity in rat atrial myocytes by n-3 polyunsaturated fatty acids. | A protective effect of the n-3 polyunsaturated fatty acids (PUFAs) in preventing ventricular fibrillation in experimental animals and cultured cardiomyocytes has been demonstrated in a number of studies. In this study, a possible role for the n-3 PUFAs in the treatment of atrial fibrillation (AF) was investigated at the cellular level using atrial myocytes isolated from young adult rats as the experimental model. Electrically-stimulated, synchronously-contracting myocytes were induced to contract asynchronously by the addition of 10 microM isoproterenol. Asynchronous contractile activity was reduced following acute addition of the n-3 PUFAs docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) at 10 microM, compared with no fatty acid addition (from 99.0+/-1.0% to 30.7+/-5.2% (p < 0.05) for DHA and 23.8+/-2.8% (p < 0.01) for EPA), while the saturated fatty acid, docosanoic acid (DA) and the methyl ester of DHA (DHA m.e.) did not exert a significant effect on asynchronous contractile activity. Asynchronous contractile activity was also reduced to 1.7+/-1.7% in the presence of the membrane fluidising agent, benzyl alcohol (p < 0.001 vs no fatty acid addition). Cell membrane fluidity was determined by steady state fluorescence anisotropy using the fluorescent probe, TMAP-DPH. Addition of DHA, EPA or benzyl alcohol significantly increased sarcolemmal membrane fluidity (decreased anisotropy, r(ss)) of atrial myocytes compared with no addition of fatty acid (control) (from r(ss) = 0.203+/-0.004 to 0.159+/-0.004 (p < 0.01) for DHA, 0.166+/-0.001 (p < 0.01) for EPA and 0.186+/-0.003 (p < 0.05) for benzyl alcohol, while DA and DHA m.e. were without effect. It is concluded that the n-3 PUFAs exert anti-asynchronous effects in rat atrial myocytes by a mechanism which may involve changes in membrane fluidity. |
4,667 | Controlled postcardioplegia reperfusion: mechanism for attenuation of reperfusion injury. | Controlled reperfusion and secondary cardioplegia are used to minimize reperfusion injury. The mechanisms for their benefit are incompletely defined and may include attenuation of myocyte sodium uptake.</AbstractText>Pigs had 1 hour of cardioplegic arrest followed by reperfusion with blood (control) or warm cardioplegic solution followed by blood (test). Reperfusion injury in the control and test groups was quantified by measuring changes of intramyocyte ion content with atomic absorption spectrometry and by analyzing electrophysiologic recovery from recordings of reperfusion arrhythmias.</AbstractText>Control animals had an increase in intramyocyte sodium content at 5 minutes after initiating reperfusion (+20.2 micromol/g dry weight, P <.04), whereas the test group had an insignificant decrease (-14.0 micromol/g dry weight, P =.33). The first rhythm after initiating reperfusion was more often ventricular fibrillation in the control group (100% vs 50%, P <.02), and the control group required more defibrillations to establish a nonfibrillating rhythm (4.5 +/- 1.2 vs 1.1 +/- 0.3, P <.03).</AbstractText>Controlled reperfusion eliminated the increase in intramyocyte sodium that was observed in the control group at 5 minutes after cardioplegic arrest. This improvement in myocyte ion homeostasis during postcardioplegia reperfusion was associated with fewer reperfusion arrhythmias. These data support the hypothesis that attenuation of myocyte sodium gain during postischemic reperfusion is a mechanism by which controlled reperfusion and secondary cardioplegia are beneficial.</AbstractText> |
4,668 | Comparison of retrograde vs simultaneous ante/retrograde cold blood cardioplegia. | To evaluate the homeostasis of myocardium during simultaneous continuous retrograde and antegrade cardioplegia vs retrograde continuous cardioplegia.</AbstractText>40 patients who underwent elective operation of coronary arteries bypass grafting were randomly assigned to 2 groups: group one consisted of 24 patients who received retrograde continuous blood cardioplegia; group two consisted of 16 patients who received simultaneous continuous ante/retrograde cardioplegia. The following measurements were taken: acidosis, oxygen content, oxygen extraction and oxygen consumption; they were taken before and after cross-clamp releasing from coronary sinus effluent and from arterial line. Incidence of low cardiac output, ventricular fibrillation, raised cardiac enzymes and ischemic changes on ECG was noted.</AbstractText>In simultaneous group such parameters as acidosis, oxygen content, oxygen extraction and myocardial oxygen consumption recovered after cross-clamping and changes of their values were respectively: 0.0005, 0.87 ml/100 ml, 0.098 and 1.4 ml/min. The same parameters didn't recovered in retrograde group and changes were respectively: 0.05 - p=0.2; 3.7 ml/100 ml - p=0.006, 0.29 p=0.006 and 7.4 ml/min - p=0.03. These changes were significant between groups.</AbstractText>Metabolic viability of myocardium measured with oxygen utilisation is better preserved with simultaneous antegrade and retrograde cardioplegia.</AbstractText> |
4,669 | Left ventricular myocardial adenosine triphosphate changes during reperfusion of ventricular fibrillation: the influence of flow and epinephrine. | To determine whether epinephrine in combination with high flow worsens left ventricular (LV) myocardial high-energy phosphate stores during reperfusion of ischemic ventricular fibrillation (VF).</AbstractText>Blinded, prospective block randomized, placebo controlled study.</AbstractText>University medical center research laboratory.</AbstractText>A total of 22 mixed breed swine weighing 22.0+/-3.3 kg (SD).</AbstractText>Open-chest swine, anesthetized with alpha-chloralose, underwent 10 mins of nonperfused VF followed by reperfusion with cardiopulmonary bypass for 90 mins and then defibrillation. Animals were block randomized to four groups for reperfusion: Group 1 (n = 5), high flow (100 mL/kg/min) and epinephrine (2.5 microg/kg/min); Group 2 (n = 5), high flow and placebo; Group 3 (n = 6), low flow (30 mL/kg/min) and epinephrine; and Group 4 (n = 6), low flow and placebo.</AbstractText>In vivo LV creatine phosphate (CP) and adenosine triphosphate (ATP) were determined using whole wall and spatially localized 31P NMR spectroscopy at 4.7 Tesla. During perfusion of the fibrillating myocardium, epinephrine significantly increased aortic pressure (p < .05) and improved defibrillation rates (p < .01). ATP levels during reperfusion were significantly decreased within all groups compared with baseline. There were no differences in ATP levels between groups. High flow, independent of epinephrine, was associated with increased preservation of ATP (p < .05), increased CP/ATP ratios (p < .02) in all layers of the LV wall, and decreased aortic and cardiac vein lactates (p < .001).</AbstractText>Epinephrine, in combination with flow higher than standard cardiopulmonary resuscitation flows, increased perfusion pressure and defibrillation rates, but did not significantly alter myocardial ATP during VF reperfusion in the in vivo heart Reperfusion flow, independent of epinephrine, is a critical determinant of myocardial ATP preservation.</AbstractText> |
4,670 | Adverse effects of high-dose epinephrine on cerebral blood flow during experimental cardiopulmonary resuscitation. | To study the effects of high-dose epinephrine, compared with standard-dose epinephrine, on the dynamics of superficial cortical cerebral blood flow as well as global cerebral oxygenation during experimental cardiopulmonary resuscitation. We hypothesized that high-dose epinephrine might be unable to improve cerebral blood flow during cardiopulmonary resuscitation as compared with standard-dose epinephrine.</AbstractText>Randomized controlled study.</AbstractText>University hospital research laboratory.</AbstractText>A total of 20 male anesthetized piglets.</AbstractText>Ventricular fibrillation was induced. A nonintervention interval of 8 mins was followed by open-chest cardiopulmonary resuscitation. The animals were randomized to receive repeated bolus injections of either 20 microg/kg (standard-dose group, n = 10) or 200 microg/kg (high-dose group, n = 10) of epinephrine.</AbstractText>Focal cortical cerebral blood flow was measured continuously by using laser Doppler flowmetry. The duration of blood flow increase was significantly shorter in the high-dose group after the second dose of epinephrine. In the high-dose group there was also a consistent tendency for lower peak levels and shorter duration of flow increase in response to repeated bolus doses of epinephrine. Cerebral oxygen extraction ratio was significantly lower in the high-dose group after administration of epinephrine.</AbstractText>Repeated bolus doses of epinephrine 200 microg/kg, as compared with 20 microg/kg, do not improve superficial cortical cerebral blood flow during experimental open-chest cardiopulmonary resuscitation. High-dose epinephrine appears to induce vasoconstriction of cortical cerebral blood vessels resulting in redistribution of blood flow from superficial cortex. This might be one explanation for the failure of high-dose epinephrine to improve overall outcome in clinical trials.</AbstractText> |
4,671 | Time averaged spatial distribution of epicardial dominant frequencies during ventricular fibrillation. | Recent evidence suggests that the dominant frequencies during ventricular fibrillation (VF) may be used as indicators of dispersion in repolarization and in activation patterns. In the present study, we quantified dominant frequencies from multiple epicardial electrodes to investigate if there are differences in the averaged frequencies within the electrograms recorded from the left and the right ventricles. Further, we quantified whether the difference in average frequency between the two ventricles changed during 30 seconds of VF. Results from eighteen trials in two pigs showed that during the entire duration of VF the average dominant frequencies of all electrodes over the left ventricle were higher than those over the right ventricle (p < 0.005). The dominant frequencies are reciprocal of cycle periods or activation intervals during VF. Our results show that on average, activations in the left ventricle occurred at a faster rate than those in the right ventricle. Activation intervals at any site are determined by the refractory period at that site and the arrival time of next activation. Although differences in cellular properties may have contributed to the observed differences in activation intervals between the ventricles, it is possible that activation arrival times may be different as well. It is possible that the increased tissue mass of the left ventricle may increase the probability that any site will get excited at a faster rate after it is recovered from previous activation. |
4,672 | Time-frequency representation of epicardial electrograms during ventricular fibrillation. | In the present study we quantified changes in dominant frequency, which is reciprocal of activation interval or cycle period, during ventricular fibrillation (VF). We used a Smoothed Pseudo Wigner Distribution (SPWD) to estimate time-frequency representations of epicardial electrograms recorded in swines. We used a sock with 64 electrodes spaced equally to record electrograms during 30 seconds of electrically induced VF. Results from 29 trials in three animals showed a mean dominant frequency of 6.64 Hz. We observed considerable variation in dominant frequencies during VF. Temporally, the frequencies varied by as much as +/- 1.24 Hz (2 standard deviations). Spatial variation in frequencies was +/- 1.20 Hz. Cycle periods were computed as the reciprocal of dominant frequencies obtained from the SPWD. These cycle periods were verified to be numerically similar to the cycle periods estimated using activation times detected from differentiated electrograms. Results of recent studies by others have shown that cycle periods during VF are correlated with refractory periods. Our results show that a non-stationary analysis technique such as the SPWD can be used to track spatio-temporal variation in cycle periods. These changes can be used to investigate spatio-temporal variation in cellular properties such as the effective refractory periods during VF. The substantial temporal variation in dominant frequencies that we observed suggest the possibility that the excitable gap at any epicardial location also varies considerably from one instance to another during a VF episode. |
4,673 | [Long-term outcome of pharmacological and nonpharmacological treatment for ventricular arrhythmias]. | Recent advances of nonpharmacological therapy such as catheter ablation and implantable cardioverter defibrillator and lessons from the Cardiac Arrhythmia Suppression Trial(CAST) have changed the strategy for ventricular arrhythmias. The safety and efficacy of radiofrequency catheter ablation of symptomatic sustained monomorphic ventricular tachycardia without structural heart disease has made ablation the firstline curative therapy. In idiopathic ventricular fibrillation such as Brugada syndrome, an implantable cardioverter defibrillator is the most effective treatment to prevent sudden cardiac death. In patients with asymptomatic ventricular tachyarrhythmias in heart failure, class I antiarrhythmic drugs should be avoided due to proarrhythmic and negative inotropic effects that may be responsible for increased mortality in some trials. In such patients, amiodarone and beta-blocker may reduce sudden cardiac death. For patients with sustained ventricular tachycardia or ventricular fibrillation in heart failure, amiodarone or implantable cardioverter defibrillator should be considered. In comparison with amiodarone, implantable cardioverter defibrillator markedly reduced sudden death in ventricular tachycardia and ventricular fibrillation survivors in Antiarrhythmics Versus Implantable Defibriltors(AVID). Although better patient selection and clarification of mapping criteria improved the successful ablation rate in patients with structural heart disease, candidates of ablation are few. In patients with extensive structural heart disease, multiple ventricular tachycardias are often present. Catheter ablation of a single ventricular tachycardia may be only palliative. Therefore, implantable cardioverter defibrillator is the most effective treatment to prevent sudden cardiac death, with amiodarone and ablation as the adjunctive therapy to prevent frequent ventricular tachycardia. Furthermore, an implantable cardioverter defibrillator improved survival in selected patients with depressed ventricular function after myocardial infarction, who also have nonsustained and inducible sustained ventricular tachycardia in Multicenter Automatic Defibrillator Implantation Trial(MADIT) and Multicenter Unsustained Tachycardia Trial(MUSTT). |
4,674 | [Treatment of choice and long-term prognosis for ventricular arrhythmias]. | Treatment of choice and long-term prognosis of the patients with ventricular arrhythmias are described in terms of prevention of sudden cardiac death and/or recurrence of life-threatening arrhythmias(ventricular tachycardia and ventricular fibrillation). 1) As to the long-term prognosis of ventricular tachyarrhythmias, presence of organic heart disease and degree of cardiac dysfunction are major determining factors. 2) The prognosis of patients with ventricular arrhythmias depends on how sudden cardiac death and life-threatening arrhythmias can be prevented. Among various methods, the electrophysiological test and its guided-therapy for antiarrhythmic drugs are now believed to be the most effective method for the prediction and prevention of the life-threatening events. We propose that the signal averaged electrocardiography is the best screening method as non-invasive approach for the selection of patients undergoing the electrophysiological test. 3) There are still certain limitations as to the prediction of sudden cardiac death and/or prevention of recurrent life-threatening arrhythmias by antiarrhythmic drug treatments in the certain numbers of patients depending on their basal cardiac disease and functional impairment. At present, catheter ablation procedure and implantable cardioverter defibrillator are the choice of the treatment in these cases. 4) In addition to conventional antiarrhythmic drugs, the treatment for the basal cardiac condition is mandatory for the long-term prognosis in the patients with ventricular arrhythmias. |
4,675 | [The electrocardiology of atrial fibrillation]. | Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and it is associated mainly with a significant mortality and morbidity. The purpose of this report is to focus on the major electro-cardiological aspects of AF and to provide some elements useful in the understanding of its pathophysiology. Experimental and clinical studies have shown that AF is maintained by multiple reentrant wavelets within the atrial muscle. It has been estimated that a critical number of wavelets (from 3 to 6) is necessary for perpetuation of AF. The short duration of the atrial effective refractory period (ERP) usually favors the onset of AF. Two different kinds of reentry have been observed during AF: random reentry and leading circle reentry. The presence of an adequate substrate is critical for the beginning of AF. Although this event is possible even in a normal atrium, atrial dilation and/or structural heterogeneity enhance the atrial propensity to develop AF. Even uniform or non-uniform anisotropy is now believed to play an important role in the genesis of AF. Finally, ionic channel disorders, some of which are genetically transmitted, may represent a possible substrate of AF. An important modulating role of the autonomic nervous system in the genesis of AF is universally accepted. In particular, many observations support the hypothesis that patients without heart disease tend to have vagally-mediated AF, whereas patients with structural heart disease tend to have adrenergic-mediated AF. In the presence of an opportunely modulated substrate, a third prerequisite for the triggering of a multiple atrial reentry is the presence of an adequate "trigger" factor. This is represented, in most cases, by ectopic atrial beats, commonly originating in the pulmonary veins. AF may cause atrial changes, either in an electrophysiological behavior and anatomy or both, that may favor its irreversibility and/or its frequent recurrence. Some of these changes are: atrial ERP disease, paradoxical shortening of ERP at a lower rate (inversed rate adaptation), accumulation of glycogen within atrial cells, apoptosis, and cellular dedifferentiation. The ventricular rate during AF has a pivotal role in its pathophysiology. The ERP of the atrioventricular node, the concealed conduction through the atrioventricular node, the autonomic neural balance and the drug's action are the most important factors that regulate ventricular rate during AF. In the presence of an atrioventricular accessory pathway, with fast anterograde conduction, AF is a very dangerous arrhythmia. During AF, aberrant conduction may often be seen, especially after long cycles (Ashman phenomenon). In patients with dilated cardiomyopathy and AF, arrhythmia is not always a secondary phenomenon. In fact, there is current evidence that AF may be the cause of cardiomyopathy. |
4,676 | Infarct related artery patency: relation to serial electropharmacological studies and outcome in patients with previous myocardial infarction and ventricular tachyarrhythmias. | Evidence suggests that infarct related artery (IRA) patency may improve survival after acute myocardial infarction, which is thought to be partially due to a lower incidence of malignant ventricular tachyarrhythmias. However, little is known about the effect of IRA patency on antiarrhythmic drug response and long-term outcome in patients with previous infarction who already experienced sustained ventricular tachyarrhythmias. A total of 152 patients with remote myocardial infarction and documented ventricular tachycardia (VT) or ventricular fibrillation (VF) underwent coronary angiography and programmed ventricular stimulation before and after oral administration of d,l-sotalol (240-640 mg/day). D,l-sotalol suppressed inducibility of VT/VF in 37 (25.2%) patients. The IRA was patent in 38.1% of all patients. There was no significant difference in the frequency of drug response between patients with patent or occluded IRAs (26.8% vs 24.2%, P = 0.87). In patients with a patent IRA, d,l-sotalol tended to be more effective in the absence of a left ventricular aneurysm, although this difference did not reach statistical significance (P = 0.38). Ejection fraction and collateral blood flow had no effect on drug response in the presence or absence of IRA patency. During follow-up (13.0 +/- 19.9 months) of 29 patients discharged on oral d,l-sotalol, 3 patients experienced symptomatic VT and 4 sudden death. Arrhythmia recurrence and death of all cause (n = 6) and cardiac death (n = 4) were independent of IRA patency status. IRA patency had no effect on short-term drug response to d,l-sotalol in patients with remote myocardial infarction and documented VT/VF. Long-term outcome of patients with sustained ventricular tachyarrhythmias is independent of IRA patency status. In contrast to a previous report, outcome of electropharmacological testing was not predicted by the patency of the IRA. |
4,677 | Factors affecting the frequency of subcutaneous lead usage in implantable defibrillators. | Subcutaneous leads (SQ) add complexity to the defibrillation system and the implant procedure. New low output devices might increase the requirement for SQ arrays, although this might be offset by the effects of active can and biphasic technology. This study sought to assess the impact of these technologies on SQ lead usage, and to determine if clinical variables could predict the need for an SQ lead. Patients receiving nonthoracotomy systems (n = 554) at our institution underwent step-down-to-failure DFT testing with implant criteria of a 10-J safety margin. SQ leads were used only after several endovascular configurations failed. Use of biphasic waveforms significantly lowered the frequency of use of SQ leads from 48% to 3.7% (P < 0.000001). SQ leads were required in 4.4% of patients with cold can devices and 2.6% of patients with active can devices (P = NS). There was no increase in SQ lead usage with low energy (< 30-J delivered energy) devices. Clinical variables (including EF, heart disease, arrhythmia, and prior bypass) did not predict the need for an SQ lead. The implant DFT using SQ arrays (14.5 +/- 6.5 J) was not significantly lower than that for SQ patches (16.6 + 6.0 J). We conclude that biphasic waveforms significantly reduce the need for SQ leads. Despite this reduction, 3.7% of implants still use an SQ lead to achieve adequate safety margins. The introduction of lower output devices has not increased the need for SQ leads, and when an SQ lead is required, there is not a significant difference in the implant DFT of patches versus arrays. Clinical variables cannot predict which patients require SQ leads. |
4,678 | Is automatic mode switching effective for atrial arrhythmias occurring at different rates? A study of the efficacy of automatic mode and rate switching to simulated atrial arrhythmias by chest wall stimulation. | Automatic mode switching (AMS) is a useful means to avoid rapid ventricular response during atrial fibrillation (AF), but AMS cannot occur if the detected atrial rate during AF is below the mode switching criteria. This may be the result of antiarrhythmic medications, or when the atrial events fall within the atrial blanking period, or if the atrial amplitudes during AF are too small to be sensed. We hypothesize that the addition of an automatic rate switching (ARS) algorithm may complement AMS response during AF with different detected atrial rates. We studied the Marathon DDDR pacemaker (Model 294-09, Intermedics Inc.) with the AMS and ARS algorithms that are independently programmable but can also operate in combination. AF sensed above the AMS rate (160 beats/min) will lead to VDIR pacing, whereas AF below AMS rate will be tracked at an interim rate as dictate by the ARS, at a ventricular response that is 20 beats/min above the sensor indicated rate. Atrial tachyarrhythmias were simulated by chest wall stimulation (CWS). CWS was applied to 33 patients (16 men, 17 women, mean age 69 +/- 11 years) with a Marathon DDDR pacemaker using an external pacer to simulate AF occurring at two rate levels: above the AMS rate (programmed at 160 beats/min) at 180 beats/min and below the AMS rate at 120 beats/min. The maximum, minimum, and mean ventricular rates during CWS in DDDR mode with AMS alone, ARS alone, and their combination were compared. During CWS at 120 beats/min, the AMS plus ARS setting showed a mean ventricular rate of 79 +/- 3 beats/min and 124 +/- 14 beats/min in the AMS setting alone (P < 0.01). With CWS at 180 beats/min, the mean ventricular rate in the AMS plus ARS setting compared to the AMS setting alone was not significantly different. However, the variation in ventricular pacing rate was 7 +/- 14 beats/min in the AMS plus ARS setting and 40 +/- 42 beats/min in the AMS setting (P < 0.05). In conclusion, AMS is effective for simulated atrial tachyarrhythmias sensed above the AMS rate. Combined AMS with ARS is useful to handle simulated atrial tachyarrhythmia at a slower rate and to avoid rate fluctuation during AMS. There is also a possibility that this can be applied to the naturally occurring atrial tachyarrhythmias. |
4,679 | Regional differences in arrhythmogenic aftereffects of high intensity DC stimulation in the ventricles. | Regional differences of the aftereffects of high intensity DC stimulation were investigated in isolated rabbit hearts stained with a voltage-sensitive dye (di-4-ANEPPS). Optical action potential signals were recorded from the epicardial surface of the right and left ventricular free wall (RVep, LVep) and from the right endocardial surface of the interventricular septum (IVS). Ten-millisecond monophasic DC stimulation (S2, 20-120 V) was applied to the signal recording spots during the early plateau phase of the action potential induced by basic stimuli (S1, 2.5 Hz). There was a linear relationship between S2 voltage and the S2 field intensity (FI). S2 caused postshock additional depolarization, giving rise to a prolongation of the shocked action potential. With S2 > or = 40 V (FI > or = approximately 20 V/cm), terminal repolarization of action potential was inhibited, and subsequent postshock S1 action potentials for 1-5 minutes were characterized by a decrease in the maximum diastolic potential and a decrease in the amplitude and a slowing of their upstroke phase. The higher the S2 voltage, the larger the aftereffects. The changes in postshock action potential configuration in RVep were significantly greater than those observed in LVep and IVS when compared at the same levels of S2 intensity. In RVep, 12 of 20 shocks of 120 V resulted in a prolonged refractoriness to S1 (> 1 s), and the arrest was often followed by oscillation of membrane potential. Ventricular tachycardia or fibrillation ensued from the oscillation in five cases. No such long arrest or serious arrhythmias were elicited in LVep and IVS. These results suggest that RVep is more susceptible than LVep and IVS for arrhythmogenic aftereffects of high intensity DC stimulation. |
4,680 | Cardioversion of persistent atrial flutter in non-anticoagulated patients at low risk for thromboembolism. | The true risk of thromboembolic events after cardioversion of atrial flutter was not addressed carefully. Nevertheless, thromboembolic events were thought to be rare and less likely to occur after cardioversion of atrial fibrillation. The aim of this study was to prospectively evaluate if the interruption of persistent typical atrial flutter could be safely performed without anticoagulation in a group of patients at low risk for thromboembolic events.</AbstractText>We studied 64 subjects selected among 138 consecutive patients with persistent typical atrial flutter (minimal duration 72 hours) in whom a transesophageal atrial pacing was performed in our electrophysiology laboratory from October 1994 to May 1999. Exclusion criteria included: anticoagulation therapy during the previous 4 weeks; previous history of atrial fibrillation; recent (< 1 month) myocardial infarction; history of thromboembolic events; left ventricular ejection fraction < 40%; presence of moderate or severe mitral regurgitation or stenosis; induction of sustained (> 6 hours) atrial fibrillation during transesophageal atrial pacing. Patients in whom atrial flutter persisted in spite of transesophageal atrial pacing underwent external direct current cardioversion or right atrial overdrive pacing within 24 hours. Thromboembolic events were checked for 4 weeks after the restoration of sinus rhythm.</AbstractText>Sinus rhythm was restored in 54 patients by transesophageal atrial pacing, in 8 patients by electrical cardioversion, and in 2 by right atrial pacing. The mean duration of atrial flutter was 18 +/- 19 days, the mean left atrial size 41.3 +/- 6.2 mm, and the mean left ventricular ejection fraction 54.8 +/- 7.3%. During the study period no episodes of thromboembolism were recorded.</AbstractText>Cardioversion of persistent typical atrial flutter in non-anticoagulated patients at low risk for thromboembolic events appears safe.</AbstractText> |
4,681 | Echocardiographic evaluation of left ventricular function in pure mitral stenosis. | Echocardiographic evaluation of left ventricular function was performed in 22 cases of pure rheumatic mitral stenosis and 22 age matched normal persons. Cases with any evidence of rheumatic activity in the preceding six months, those with gross tricuspid regurgitation and paradoxical movement of the interventricular septum and cases with atrial fibrillation were excluded. None of the patients showed systolic left ventricular dysfunction. Left ventricular end diastolic dimension was also not affected. Echocardiographic parameters did not have any relation for mitral valve area. Our observations show that mitral stenosis per se does not affect left ventricular function. |
4,682 | [The chain of survival]. | Coronary artery disease remains the leading cause of death in Italy as in most developed countries. Many of the victims die from sudden cardiac arrests, most commonly resulting from out-of-hospital ventricular fibrillation. The epidemiological evidence of the high incidence of sudden deaths in the small subgroup of high-risk patients and of the low incidence of events in the large subgroup of low- and intermediate-risk patients which are contributing to most of the deaths has suggested the development of emergency services and to the chain of survival concept. With the development of the automatic external defibrillator, early recognition and treatment of ventricular fibrillation by non-skilled rescuers has significantly improved the outcome of sudden death. Training is essential to provide the numerous skills required for those regularly exposed to resuscitation and also to provide the diffusion of cardiopulmonary resuscitation competence in the general population. This paper reviews the past, present and future development of the epidemiological, organizational, training, and research issues related to the chain of survival. |
4,683 | Orthotopic heart transplantation: standard versus bicaval technique. | We compared orthotopic heart transplantation (HT) by bicaval technique with the standard technique. Between January 1995 and December 1997, 117 patients underwent 118 HTs; 71 patients (15 women and 56 men) had 72 HTs by standard technique and 46 patients (9 women, 37 men) underwent HT using bicaval procedures. Preoperative parameters were similar in both groups; 5 patients who underwent the standard technique and no patients who underwent bicaval procedures required permanent pacemakers (p = NS). Isoproterenol infusion was significantly longer in the standard technique. Major perioperative arrhythmias (ventricular tachycardia and fibrillation, asystole) appeared in 8.2% and 7.0% of standard and bicaval HTs, respectively; atrial fibrillation appeared in 13.1% and 4.6%, respectively (p = NS). At 1 month, mitral and tricuspid regurgitation rates were higher in the standard group (p = NS); at 1 year only tricuspid regurgitation was still higher (p = NS). Right atrial pressure, Wood units, cardiac output, and cardiac index were examined (p = NS). At multivariate analysis, interaction between preoperative Wood units and transplant type was elicited for Wood units at 1 month and for right atrial pressure at 1, 3, and 6 months. In the high resistance subgroup, the patients who underwent bicaval procedures had higher resistances at 1 month. In the low resistance subgroup, right atrial pressure was higher in patients who underwent standard techniques at 1, 3, and 6 months follow-up. Thus, bicaval HT was found to be safe, without surgically related complications, it provoked significantly less blood loss, and required less isoproterenol use. No significant advantages were observed in conduction disturbances and major arrhythmias or regarding the need for temporary or permanent pacemakers. |
4,684 | Left ventricular apex ablation decreases the upper limit of vulnerability. | After shocks with an approximately 50% probability of success for the upper limit of vulnerability (ULV(50)) of strength, the first few activations appear focally on the epicardium at almost the same site at the left ventricular (LV) apex in both successful and failed induction of ventricular fibrillation (VF). We tested the hypothesis that subendocardial ablation at this early site would decrease the shock strength required for the ULV(50).</AbstractText>Ten S1 stimuli were delivered from the right ventricular apex at a 300-ms coupling interval in 5 pigs. Biphasic shocks were delivered from right ventricular-superior vena cava electrodes after the last S1 stimulus. The ULV(50) was determined using an up/down protocol with T-wave scanning. Radiofrequency ablation was performed endocardially at the apical LV. The ULV(50) was determined again 30 minutes after ablation. To determine the importance of the ablation region, this protocol was repeated in another 5 pigs with ablation at the LV base. Delivered voltage (401+/-60 versus 323+/-50 V) and energy (11+/-3 versus 7+/-2 J) for the ULV(50) were significantly decreased after LV apex ablation by 19% and 34%, respectively. However, no difference existed in ULV(50) before and after LV base ablation. Lesions at both the LV apex and base were subendocardial and ranged from 0.8 to 1.1 cm in diameter.</AbstractText>Subendocardial ablation at the apical LV markedly decreases ULV(50), which suggests that the activation originating from this postshock early site is responsible for VF initiation and that interventions to electrically silence this site can influence the outcome of VF induction by ULV shocks.</AbstractText> |
4,685 | [Cardiac insufficiency: prevention of ventricular arrhythmias]. | Ventricular arrhythmias are particularly common in cardiac failure and their mechanisms are very complex. The prevention of these ventricular arrhythmias is only worthwhile if it results in benefits in terms of reduction of the risk of sudden death and in improvement in life expectancy. However, the relationship between complex ventricular arrhythmias and sudden death is far from established. The first problem is, therefore, to select the patients at high risk of sudden death. Unfortunately, there are no reliable markers of arrhythmic risk; only patients at low risk can be reasonably well identified on clinical and haemodynamic assessment and the results of ambulatory and signal averaged ECG. When an antiarrhythmic treatment seems to be required, the choice is very limited in practice. There is no role for Class I antiarrhythmics to play in this indication. Amiodarone, with its complex electrophysiological profile enabling an interaction with all potential mechanisms of ventricular arrhythmias, is a first-line drug in cardiac failure because of its efficacy and good myocardial tolerance. However, the benefits of amiodarone therapy in terms of reduction of global mortality have not been demonstrated, especially in view of the discordance between the results of the GESICA and CHF STAT trials. On the other hand, the value of betablockers, whether conventional molecules like bisoprolol (CIBIS II study) or metoprolol (MERIT-HF study), or molecules with a special profile such as carvedilol, has been clearly established. In association with conventional diuretics and angiotensin converting enzyme inhibitors, they reduce global mortality by about 35% and sudden death by 40%. However, the future possibly lies with non-pharmacological approaches such as the implantable defibrillator, at least in patients clearly identified as being at high risk of arrhythmic death, resuscitated from cardiorespiratory arrest due to documented ventricular fibrillation or presenting with haemodynamically poorly tolerated ventricular tachycardia. The automatic defibrillator could improve the prognosis of these patients, irrespective of their functional status (NYHA, Classes I, II or III). In practice, "rhythmological" management of cardiac failure cannot be dissociated from the haemodynamic and neuro-hormonal aspects of the affection, and only a multi-factorial approach is being realistic. |
4,686 | Scroll wave dynamics in a three-dimensional cardiac tissue model: roles of restitution, thickness, and fiber rotation. | Scroll wave (vortex) breakup is hypothesized to underlie ventricular fibrillation, the leading cause of sudden cardiac death. We simulated scroll wave behaviors in a three-dimensional cardiac tissue model, using phase I of the Luo-Rudy (LR1) action potential model. The effects of action potential duration (APD) restitution, tissue thickness, filament twist, and fiber rotation were studied. We found that APD restitution is the major determinant of scroll wave behavior and that instabilities arising from APD restitution are the main determinants of scroll wave breakup in this cardiac model. We did not see a "thickness-induced instability" in the LR1 model, but a minimum thickness is required for scroll breakup in the presence of fiber rotation. The major effect of fiber rotation is to maintain twist in a scroll wave, promoting filament bending and thus scroll breakup. In addition, fiber rotation induces curvature in the scroll wave, which weakens conduction and further facilitates wave break. |
4,687 | [The cumulative risk index in stroke prevention]. | The screening and special management of high risk patient, is possible strategy to reduce the high morbidity and mortality of stroke. In the II. district of Budapest we examined high vascular risk patients cooperating with general practitioners. We let the severity of risk with arithmetic of the cumulative risk index. Significant relation was found between of high cumulative risk index and 50% or higher carotis stenosis, as well as the cumulative risk index and low Se HDL level. Increased blood pressure level has been found in among the treated hypertonic patient. Reduction of high blood pressure was documented in the 6 month control examination. Finally there was very low level of smoking in the high vascular risk patient group. |
4,688 | Changes over time in the incidence and case-fatality rates of primary ventricular fibrillation complicating acute myocardial infarction: perspectives from the Worcester Heart Attack Study. | Limited population-based data are available that describe temporal and recent trends in the incidence and case-fatality rates in patients with primary ventricular fibrillation (VF) complicating acute myocardial infarction (AMI). The purpose of this study was to describe changes over a 22-year period (1975 through 1997) in the incidence and hospital case-fatality rates of primary VF complicating AMI from a multihospital, community-wide perspective.</AbstractText>This was an observational study of metropolitan Worcester residents hospitalized with a validated uncomplicated AMI (n = 5020) in all hospitals in the Worcester, Massachusetts, metropolitan area (1990 census population = 437,000) during 11 1-year periods between 1975 and 1997. The overall incidence rate of primary VF complicating AMI was 4.7%. The crude as well as multivariable adjusted odds of the development of VF did not change significantly over the 22-year period under study. The overall in-hospital case-fatality rate of patients with primary VF was 44%, which was significantly greater in comparison with AMI patients in whom VF did not develop (5%). Hospital mortality rates associated with primary VF declined over time. Improved survival was observed in patients who had primary VF in the 1990s after adjusting for potential prognostic confounders.</AbstractText>The results of this community-wide study failed to indicate changes over time in the incidence rates of primary VF in patients hospitalized with AMI between 1975 and 1997. On the other hand, hospital death rates in patients with primary VF have shown encouraging declines during more recent periods. These mortality trends are likely to be the results of improvements in the treatment and more careful surveillance of patients with AMI.</AbstractText> |
4,689 | Left atrial fibrillation with regular right atrial activation and a single left-to-right electrical interatrial connection: multisite mapping of dissimilar atrial rhythms. | We report two patients who had isolated atrial fibrillation in the left atrium and regular activation of the entire right atrium. Mapping of the arrhythmia was performed using a 64-electrode basket catheter that was inserted intravenously and deployed in the right and left atria. Both patients manifested a single, stable interatrial electrical connection conducting in a left-to-right direction, consistent with Bachmann's bundle location. The right and left sides of the interatrial septum were activated discordantly, each reflecting activation characteristics of the respective atria. A filtering effect at the level of interatrial septum was demonstrated by calculating the fibrillation intervals on both sides of the operative interatrial connection. It was concluded that differences in activation of the left and right surfaces of the interatrial septum and preferential use and the filtering effect of the interatrial connections play a significant role in explaining the differences in activation patterns of the left and right atria in patients with atrial fibrillation. |
4,690 | Focal ablation of chaotic atrial rhythm in an infant with cardiomyopathy. | Chaotic atrial rhythm in infants has been defined similar to multifocal atrial tachycardia in adults, implying a multifocal etiology. However, its ECG appearance resembles atrial fibrillation, which sometimes has a unifocal ectopic mechanism amenable to catheter ablation. Curative focal radiofrequency ablation was performed in a 4-month-old infant with chaotic atrial rhythm and dilated cardiomyopathy. Left ventricular function subsequently returned to normal. Reversibility of associated cardiomyopathy supports aggressive rhythm management of chaotic atrial rhythm. In this patient, the unifocal origin allows insight into the pathophysiology of the rhythm and demonstrates the potential utility of catheter ablation for refractory cases. |
4,691 | Spatial and temporal heterogeneity of depolarization and repolarization may complicate implantable cardioverter defibrillator therapy in Brugada syndrome. | Dynamic variations in electrophysiologic phenomena inherent to the Brugada syndrome may complicate therapy with implantable cardioverter defibrillators (ICDs).</AbstractText>Between 1997 and 1999, 3 of 7 patients with Brugada syndrome (1 man and 2 women, mean age 42 years) received an ICD. During follow-up, 2 patients experienced multiple inappropriate shocks. Simultaneously with dynamic changes in the surface ECG, endocardial ECGs revealed a dynamic decrease in the right ventricular R wave and an increase in the corresponding T wave, resulting in T wave oversensing. With ajmaline administration, these dynamic changes in endocardial signals were reproducible at different right ventricular sites, whereas left ventricular epicardial signals remained stable. Incremental AAI pacing and exercise stress testing resulted in similar changes in right ventricular endocardial signals, but normalization of the surface ECG apart from progressively increasing S waves in leads II, V5, and V6. Orciprenaline administration had no effect on ECG phenomena. After implantation of a left ventricular epicardial lead for sensing and pacing, no inappropriate tachycardia detection recurred.</AbstractText>These findings demonstrate that, in Brugada syndrome, spontaneous or ajmaline-induced changes in the surface ECG may be paralleled by significant variations in the right ventricular endocardial electrogram that may result in ICD malfunction. Implantation of a left ventricular epicardial lead for sensing and pacing may be the ultimate successful approach in certain patients. To assure proper ICD function, ajmaline testing during ICD implantation appears to be helpful.</AbstractText> |
4,692 | Bimodal RR interval distribution in chronic atrial fibrillation: impact of dual atrioventricular nodal physiology on long-term rate control after catheter ablation of the posterior atrionodal input. | Radiofrequency (RF) catheter modification of the AV node in patients with atrial fibrillation (AF) is limited by an unpredictable decrease of the ventricular rate and a high incidence of permanent AV block. A bimodal RR histogram has been suggested to serve as a predictor for successful outcome but the corresponding AV node properties have never been characterized. We hypothesized that a bimodal histogram indicates dual AV nodal physiology and predicts a better outcome after AV node modification in chronic AF.</AbstractText>Thirty-seven patients were prospectively subdivided into two groups according to the RR histogram of 24-hour ECG monitoring. Before to RF ablation, internal cardioversion and programmed stimulation were performed. Among the 22 patients (group I) with a bimodal RR histogram, dual AV nodal physiology was found in 17 (77%) patients. Ablation significantly decreased ventricular rate with loss of the peak of short RR cycles after ablation (mean and maximal ventricular rates: 32% and 35% rate reduction, respectively; P < 0.01). In 15 patients with a unimodal RR histogram (group II), dual AV nodal physiology was found in 2 (13%), and rate reductions were 16% and 17%, respectively. At 6 months, 3 (14%) patients in group I and 6 (40%) in group II underwent elective AV nodal ablation with pacemaker implantation due to intolerable rapid ventricular response to AF.</AbstractText>Bimodal RR interval distribution during chronic AF suggests the presence of dual AV nodal physiology and predicts a better outcome of RF ablation of the posterior atrionodal input.</AbstractText> |
4,693 | Inappropriate shocks diagnosed by stored electrograms of implantable cardioverter defibrillators--two case reports. | An implantable cardioverter defibrillator is an important therapeutic option for patients with high risk of life-threatening ventricular arrhythmias. However, their use is also associated with several complications including inappropriate shock. Although the most frequent cause of inappropriate shock is supraventricular tachyarrhythmias, lead fracture can also be associated with inappropriate shock. Diagnosis of lead fracture can be made by chest x-ray radiography, fluoroscopic examination, interrogation of the device, and intracardiac electrograms. In this report, the authors present two cases of inappropriate shock due to lead fractures in the costoclavicular region that could only be diagnosed by the help of stored intracardiac electrograms. Methods for diagnosis of lead fractures and modalities to avoid recurrences are also discussed. |
4,694 | Pulmonary embolism as a cause of cardiac arrest: presentation and outcome. | Pulmonary embolism (PE) is a possible noncardiac cause of cardiac arrest. Mortality is very high, and often diagnosis is established only by autopsy.</AbstractText>In a retrospective study, we analyzed clinical presentation, diagnosis, therapy, and outcome of patients with cardiac arrest after PE admitted to the emergency department of an urban tertiary care hospital.</AbstractText>Within 8 years, PE was found as the cause in 60 (4.8%) of 1246 cardiac arrest victims. The initial rhythm diagnosis was pulseless electrical activity in 38 (63%), asystole in 19 (32%), and ventricular fibrillation in 3 (5%) of the patients. Pronounced metabolic acidosis (median pH, 6.95, and lactate level, 16 mmol/L) was found in most patients. In 18 patients (30%), the diagnosis of PE was established only postmortem. In 42 (70%) it was diagnosed clinically, in 24 of them the diagnosis of PE was confirmed by echocardiography. In 21 patients, 100 mg of recombinant tissue-type plasminogen activator was administered as thrombolytic treatment, and 2 (10%) of these patients survived to hospital discharge. Comparison of patients of the thrombolysis group (n = 21) with those of the nonthrombolysis group (n = 21) showed a significantly higher rate of return of spontaneous circulation (81% vs 43%) in the thrombolysis group (P=.03).</AbstractText>Mortality related to cardiac arrest caused by PE is high. Echocardiography is supportive in determining PE as the cause of cardiac arrest. In view of the poor prognosis, thrombolysis should be attempted to achieve return of spontaneous circulation and probably better outcome.</AbstractText> |
4,695 | The heart-brain connection. | We have long known that patients with vascular disease in one system are at risk for vascular disease in other systems. Beyond this, we are recognizing the increased risk for cardiovascular patients to develop stroke not only as the result of arrhythmia, but also at the time of cardiovascular events or procedures. This presents clinical challenges to nurses with either neurological or cardiovascular expertise, requiring development of new awareness, clinical and critical thinking skills, and collaboration with their colleagues in other specialties. Three case studies illustrate patient presentations ranging from the subtle to the obvious. Pathophysiology of stroke is reviewed. Leading-edge management strategies and supporting literature highlight the benefits of prompt identification and management of the stroke patient. The Stroke Watch Action Team (SWAT) has proved to be an effective means of expediting patient identification and access to effective stroke treatment. |
4,696 | Use of an inspiratory impedance threshold valve during cardiopulmonary resuscitation: a progress report. | Building upon studies on the mechanism of active compression-decompression (ACD) cardiopulmonary resuscitation, a new inspiratory impedance threshold valve has been developed to enhance the return of blood to the thorax during the decompression phase of CPR. Use of this device results in a greater negative intrathoracic pressure during chest wall decompression. This leads to improved vital organ perfusion during both standard and ACD CPR. Animal and human studies suggest that this simple device increases cardiopulmonary circulation by harnessing more efficiently the kinetic energy of the outward movement of the chest wall during standard CPR or active chest wall decompression. When used in conjunction with ACD CPR during clinical evaluation, addition of the impedance valve resulted in sustained systolic pressures of greater than 100 mmHg and diastolic pressures of greater than 55 mmHg. The new valve may be beneficial in patients in asystole or shock refractory ventricular fibrillation, when enhanced return of blood flow to the chest is needed to 'prime the pump'. The potential long-term benefits of this new valve remain under investigation. |
4,697 | Successful recovery after ventricular fibrillation in a patient with Kawasaki disease. | Kawasaki disease (KD) is an uncommon cause of sudden death in young adults in Europe. Angiographically, the disease is characterized by coronary artery aneurysms which can be fully obstructed by acute thrombosis or by progression of the disease. If diagnosis of KD is made, immediate investigation should be made to determine whether ischemia is occurring and if so, to establish optimal time for revascularisation or cardiac transplantation. We describe an 18-year-old Caucasian male who was not previously known to have KD and who suffered from an acute myocardial infarction complicated by ventricular fibrillation, caused by acute thrombosis of a coronary artery aneurysm. |
4,698 | Reliability of ECG monitoring with a gel pad/paddle combination after defibrillation. | Recent warnings have highlighted the possibility of unreliable monitoring through gel pads and paddles when using manual defibrillators. Occasionally, this causes an apparent asystole to be displayed when the true rhythm is ventricular fibrillation. We investigated this phenomenon in the laboratory using defibrillator-testing devices with two different impedances and with two defibrillators (Physio-Control LIFEPAK 9 and Hewlett Packard XL). After delivery of a 200 J shock, the time taken for the original ECG test signal to return to the defibrillator monitor was measured. Measurements were made after each of a series of ten shocks delivered with each defibrillator and gel pad/ testing device combination. Additional measurements were made using self-adhesive combination defibrillator electrodes. When using a low-impedance testing device with gel pads, on all occasions the initial rhythm reappeared immediately. When using the high-impedance testing device, the post shock rhythm was initially displayed as 'no signal' (Hewlett Packard XL) or 'asystole' (Physio-Control LIFEPAK 9). Over the series of ten shocks, the time to return of the original signal ranged between 24 and 154 s with the Hewlett Packard and 17-61 s with the Physio-Control LIFEPAK 9. The time for return of the signal increased with successive shocks. When using Fast-Patch electrodes, the original test signal always returned immediately. We conclude that after the delivery of a shock, monitoring through gel pads may result in the display of spurious asystole being displayed. This is more likely to occur in the presence of high chest impedance and with an increasing number of shocks delivered through the same gel pads. If defibrillator paddles and gel pads have been used for 'quick-look' monitoring, and 'asystole' is displayed after delivery of a shock, the rhythm should be confirmed immediately with monitoring leads. |
4,699 | Early defibrillation and the chain of survival in 'in-hospital' adult cardiac arrest; minutes count. | To report the outcomes from and the impact of the chain of survival in 'in-hospital' cardiac arrest where the presenting rhythm was VF/VT, the arrest was witnessed, defibrillation was conducted rapidly and no other resuscitation interventions were required.</AbstractText>Any return of spontaneous circulation and discharge from hospital.</AbstractText>A 2-year prospective resuscitation audit using the Utstein style was conducted within a major London NHS Hospital Group.</AbstractText>There were 124 patients who had primary VF/VT arrest. Eight were excluded from the study and 14 had non-witnessed cardiac arrest. Twenty one patients had witnessed VF/VT arrest but with delayed defibrillation, 81 patients had witnessed VF/VT arrest with rapid defibrillation, 69 patients had witnessed VF/VT arrest with rapid defibrillation, CPR and other additional interventions. There were 15 patients that had witnessed cardiac arrest with a presenting rhythm of VF/VT, who received rapid defibrillation and had no ventilation or chest compression prior to or following defibrillation. All 15 patients achieved a return of spontaneous circulation, and 12 were discharged alive.</AbstractText>Rapid defibrillation prior to any other resuscitation intervention is associated with increased survival from witnessed VF/VT arrest in in-hospital cardiac arrest victims, and that the time to first shock is critical in enhancing the prospects of long-term survival in these patients.</AbstractText> |
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