Number Of Sudden Deaths Research Articles

Amiodarone: a late comer

Amiodarone is useful in the treatment of patients with ventricular arrhythmias after acute myocardial infarction and was equally useful when these arrhythmias were associated with CHF. Amiodarone prolongs repolarization and lowers heart rate, actions that are beneficial in treating symptomatic arrhythmias. The absence of proarrhythmic effects distinguishes amiodarone from other antiarrhythmic agents. No excess mortality was seen in any of the amiodarone trials, and in fact, a definite trend toward a decrease in the number of sudden deaths was noted. For many years, amiodarone has been the antiarrhythmic drug of choice in Europe. Only in recent years has this drug gained respectability in the United States. Amiodarone is truly a late comer to our shores.

Therapy of Sustained Ventricular Arrhythmias With Amiodarone: Prediction of Efficacy With Serial Electrophysiologic Studies.

BACKGROUND: Programmed electrical stimulation early during amiodarone therapy has poor prognostic capabilities; and persistent inducibility has been associated with a favorable outcome in a majority of patients. These observations result from studies that differed significantly in methodology. METHODS AND RESULTS: The authors prospectively enrolled 121 patients in a standardized amiodarone dosing protocol in which amiodarone was the only antiarrhythmic agent. Electrophysiologic testing was done after 2 and 6 weeks to determine noninducibility, predictive value, and the significance of drug-induced prolongation of tachycardia cycle length. The mean age of the patients in the study was 63.2 +/- 11.5 years, and their ejection fraction was 32.8 +/- 11.9%. Coronary artery disease was present in 103 (85%). At 2 weeks 17 patients (14%) were no longer inducible, whereas 104 patients (86%) remained inducible. Patients in these groups were similar in age and ejection fraction. During follow-up evaluation, recurrences (35% vs 24%; P =.44) and sudden death (12% vs 13.5%) were similar in the two groups. Thirty-five of 95 patients (32%) with sustained monomorphic ventricular tachycardia had more than 100 ms prolongation of their cycle length, which was hemodynamically well tolerated (partial response), but 60 did not (nonresponse). Patients with a partial response were older (66.5 vs 61.1 years; P =.02) and had longer QRS durations (143.2 vs 129.4 ms; P =.03). They also had increased recurrences (37% vs 17%; P =.01) and more sudden deaths (23% vs 8%; P =.02). At 6 weeks 11 of 76 patients studied were noninducible. They had a lower recurrence rate than those who remained inducible (8% vs 27%; P =.02) but a similar number of sudden deaths (8% vs 16%; P =.27). Thirty-two patients partially responded, and 31 patients did not respond. During follow-up examination these two groups had a similar number of recurrences (25% vs 29%; P =.76) and sudden deaths (16% vs 16%). CONCLUSIONS: Noninducibility at 2 or 6 weeks of amiodarone therapy did not identify patients at low risk of sudden death. In inducible patients, tachycardia cycle length prolongation, even when well tolerated, was not a marker for favorable outcome. Electrophysiologically guided therapy, therefore, offers little benefit over empiric amiodarone.

France: The incidence has risen

The French government, concerned with a steady increase in sudden infant deaths over the past 10 years, has launched a public campaign to inform parents and doctors of the risk. The number of sudden deaths of infants aged under 1 year has nearly doubled, from 1.03/1000 in 1980 to 1.93/1000 in 1991. Some of this increase may …

THE NORWEGIAN MULTICENTER STUDY ON TIMOLOL AFTER MYOCARDIAL INFARCTION

ABSTRACTThe reduction in mortality induced by timolol was seen in all three risk groups. Thus the cumulative probability of death at 33 months (analyzed «per protocol») was reduced by 25 % in risk group I (p<0.05), 50 % in risk group II (p<0.01) and by 19 % in risk group III (ns). When number of deaths was analyzed «as randomized», a statistically significant reduction in mortality was seen also in risk group III.93 % of all deaths on treatment or within 28 days after withdrawal were cardiac deaths, 113 in the placebo group versus 58 in the timolol group (p<0.001). The number of sudden deaths (death < 24 hrs after onset of symptoms) was 95 in the placebo group versus 47 in the timolol group (p<0.001). Only 13 deaths were non‐cardiac (cerebrovascular disease (5), malignancies (4), other (4)).When the cause of death (in the per protocol period) was classified as instant, primary arrhythmia, cardiac failure, found dead, new MI or non‐cardiac, statistically significant fewer deaths in the timolol group were found in the following categories: instant death (38 versus 11, p<0.001), primary arrhythmia (7 versus 0, p<0.05), found dead (26 versus 9, p<0.01).Among patients withdrawn from the study there was no difference in deaths occurring later than 28 days after withdrawal. In the first 28 days after withdrawal a tendency to reduction in mortality in the timolol‐treated patients was still seen.In «the per protocol period» there were 52 episodes of witnessed heart arrest in the placebo group versus 19 in the timolol group (p<0.001). The total number of all probable heart arrests and instant deaths (witnessed and non‐witnessed) was 77 in the placebo group versus 26 in the timolol group (p<0.001).The number of initial re‐infarctions in «the per protocol period» was lower in the timolol‐ than in the placebo‐treated patients in all risk groups, the difference being statistically significant in risk group II and in all risk groups combined. The cumulative re‐infarction rate at 33 months was 20.1 % in the placebo group and 14.4 % in the timolol group ‐ a reduction of 28.4 % (p<0.001). The difference in cumulative reinfarction rate between placebo and timolol was almost unchanged after 6 months of follow‐up. Relatively few severe adverse experiences were seen. Heart failure was reported in 63 patients in the placebo group versus 73 in the timolol group. The difference between placebo‐ and timolol‐treated patients reached levels of statistical significance for the following adverse experiences: bradycardia, hypotension, asthenia, cold hands and feet, bronchial obstruction ‐ all appearing more frequently in the timolol group.Arrhythmias requiring treatment were seen more frequently in the placebo group, 38 versus 13 (p<0.001). Need for beta‐blocker was also seen more frequently in the placebo group, 68 versus 32 (p<0.001).In conclusion, the study has shown that when conventional contraindications to beta‐blockade are respected, a large proportion of patients surviving a MI can be given timolol 7–28 days after onset of symptoms and that timolol reduces mortality and re‐infarction rates substantially in these patients.

The toxicity of cassava

is a high-carbohydrate, low-protein staple food in many tropical countries. It grows well in tropical climates - as much as 2.5 kcal of food value can be produced from each hec- tare per day, compared with 1.76 kcal for rice. Against this undoubted advantage must be set a major drawback - cassava is poisonous. Although the local populations have developed ways of reducing the toxic effects of cassava, deaths and illnesses can still be attributed to the consumption of this plant. The ill effects of eating cassava can be a result of either the harmful components of the plant (most notably linamarin, a cyanogenic glycoside) or they can be caused by toxins produced by organisms that have infected the food during prepara- tion. Preparation of cassava Both the tuber and the leaves of cassava are eaten, although the tuber is considered the more palatable. There are two major methods for preparing the tuber for food. In the first method, mainly used in rural areas of Nigeria, the tuber is fermented in a large quantity of water and then reduced to a pulp, known as 'akpu'. The akpu is usually wet when prepared and it provides good conditions for the growth of organ- isms, some of which may be toxic. Thus, in addition to the food's inherent toxicity a number of sudden deaths in Nsukka vil- lages in Nigeria have been attributed to the consumption of infected akpu. The second method of preparing cassava tubers, more popular in urban Nigeria, involves fermentation and frying to pro- duce cassava flour or 'garri'. Garri may contain as much as 35 mg of HCN in the average daily consumption of 750 g - almost half the lethal dose of HCN. Con- centrations of this magnitude are said to occur only in the bitter strains of cassava, but unfortunately there is no clear differen- tiation between 'bitter' and 'sweet' strains. As garri is produced in a dry form, the growth of toxic microorganisms is not the problem as it is with akpu. Cassava leaves are also used as food in West Africa, New Guinea and Central Java. As well as the cyanogenic glycosides, the leaves contain hydrogen sulphide. The fresh leaves contain between 491 and 624

REDUCTION IN SUDDEN DEATHS BY A MULTIFACTORIAL INTERVENTION PROGRAMME AFTER ACUTE MYOCARDIAL INFARCTION

375 consecutive patients below 65 years who had an acute myocardial infarction (AMI) took part in a randomised rehabilitation and secondary prevention trial (part of a W.H.O.-coordinated project) designed to study the effects of a multifactorial intervention programme on morbidity, mortality, return to work, &c. After three years' follow-up the cumulative coronary mortality was significantly smaller in the intervention group than in the controls (18·6% versus 29·4%, p=0·02). This difference was mainly due to a reduction of sudden deaths in the intervention group (5·8% versus 14·4%, p<0·01). The reduction was greatest during the first six months after AMI. 18·1% in the intervention group and 11·2% in the controls (p<0·10) presented with non-fatal reinfarctions. The number of patients with new Q-QS findings at the end of the three years was, however, almost the same in both groups. The results suggest that organised aftercare during the first six months after AMI with special emphasis on optimum medical control and health education contributes significantly to a reduction in the number of sudden deaths.

Enzymatic indices of myocardial necrosis: influence on short- and long-term prognosis after myocardial infarction.

The prognostic effect of the peak level of serum creatine kinase (CK) and aspartate transaminase (AST), estimated daily for 3--5 days after acute myocardial infarction, was studied in 560 patients who survived the first day in hospital. In a subgroup of 54 patients, peak enzyme levels correlated well with the cumulated CK release (r = 0.90 with peak CK, r = 0.74 with peak AST), thus reflecting the extent of myocardial necrosis. Total mortality within a year after infarction was not significantly different in the lower three quintiles of peak serum enzyme level, but increased from 15.5% to 27.9% (p less than 0.001) when peak CK level exceeded eight times the upper limit of normal (8 X N) and form 13.1% to 34.8% (p less than 0.001) when peak AST level exceeded five time the upper limit of normal (5 X N). The effect of high enzyme levels was more marked in patients with a prior history of myocardial infarction; mortality increased from 14.7% for first infarctions to 18.2% for recurrent infarctions, with peak CK greater than 8 X N, and from 27.0% for first infarctions to 38.0% for recurrent infarctions with peak CK greater than 8 X N. Early mortality was more significantly affected (p less than 0.0001) than late mortality (p less than 0.05). In hospital survivors, late deaths from cardiac decompensation were three times (p less than 0.05) more frequent in the high enzyme group as in the low enzyme group, but the number of sudden deaths was unaffected. These findings have important implications for studies of reduction of myocardial infarct size.

Lancisi] De Subitaneis Mortibus (On Sudden Death)

Giovanni Maria Lancisi (1654-1720) is little remembered today, although the "striae of Lancisi" may strike a familiar chord in the physician who is not too far removed from his neuroanatomy. But Lancisi, contemporary of Ramazzini, was a leading Italian physician who contributed markedly to our knowledge of aneurysms (his work on this subject was translated almost 20 years ago), and heart disease; and he substantially advanced the correlation of clinical and autopsy findings. In 1705 and 1706 a great number of sudden deaths in Rome attracted considerable attention. Lancisi investigated many of the cases, carefully recorded the clinical history and the clinical course, and described the autopsy findings. He often was able to make significant clinicopathological correlations and he casually introduced much information about medical doctrine and theory at the beginning of the 18th century. In a great many cases the heart was either primarily or secondarily involved, and Lancisi's

Myocardial infarctions in the practices of a group of private physicians-III: Causes of death among patients who have survived a myocardial infarction

An analysis was made up of the causes of death during a five year period following recovery from a documented acute myocardial infarction. Forty-four per cent of the deaths were sudden and unexpected. An additional 33 per cent were due to congestive heart failure or subsequent myocardial infarction. Twenty-one per cent were neither cardiac nor sudden. The number of sudden deaths following a first myocardial infarction was about twice as great as in a matched sample of deaths which occurred in the general population.

Ultrastructure of Cardiac Myocytes from The Inner and Outer Zones of Fibrillating Bovine Hearts

Ventricular fibrillation is a clinical event which probably accounts for untold numbers of sudden deaths. The very nature of this arrhythmia, which prevents effective pumping of blood, has precluded the morphologic study of hearts that have fibrillated for appreciable periods. Current cardiac assist devices now provide the means of studying prolonged ventricular fibrillation. The circulation of 150 to 200-pound calves was maintained with left ventricular bypass pumps for as long as 40 hours of continuous ventricular fibrillation. Seven calves were studied histologically; one preparation that fibrillated for 24 hours was suitably preserved for ultrastructural study. Tissue was fixed in 5 % cacodylate buffered glutaraldehyde, rinsed in buffer for 48 hours, post-fixed in OsO4, and embedded in a mixture of Maraglas, D.E.R. 732, and DDSA.

EFFECT OF QUINIDINE SULPHATE IN INHIBITING VENTRICULAR FIBRILLATION

It has been quite definitely established that quinidine prolongs the refractory period of heart muscle; this has been regarded as the mechanism by which quinidine stops conditions due to circus movement of the heart such as auricular flutter and fibrillation. From clinical experience it has also been known that repeated administration of quinidine by mouth prevents the inception of these disturbances in the auricle which otherwise would be recurring in transient form.1Because fibrillation of the ventricles is also regarded as due to a circus movement, a similar method of therapy might become available as a preventive measure. Morawitz,2on empiric grounds, successfully used the drug as a prophylactic agent in patients whom he regarded as liable to sudden cardiac death; his figures showed a distinct diminution in the number of sudden deaths under the quinidine regimen. It is the general opinion at the present time that ventricular

THE "DOCTOR'S HEART"

The extensive propaganda for periodic health examinations and the alarming increase in the number of sudden deaths from heart disease in persons apparently enjoying good health have brought unconsciously, perhaps, into the busy life of the average physician a feeling akin to apprehension when the problems of middle age are considered. Whether there is an actual increase in heart disease or whether the increase is only apparent has been the point of discussion in a recent editorial inThe Journal; 1 without doubt, however, the physician is becoming more aware and increasingly cognizant of the number of cardiovascular deaths. While the question may be of general interest, it becomes more sharply focused when the number of physicians meeting cardiovascular deaths is considered. One has only to scan the death columns in the current medical journals both in this country and abroad to realize the significance and truth of this observation,