Fatal Ventricular Fibrillation Research Articles

Headache angina with fatal outcome.

We report 2 fatal cases of angina pectoris in patients who complained primarily of headache during the ischemic attack. The first patient, who was hospitalized because of headache and chest pain, demonstrated repeated ST-segment elevation and fatal ventricular fibrillation on ambulatory ECG monitoring. The second patient had post-infarction angina preceded by headache and by ST-segment elevation in the precordial leads. She eventually died of reinfarction. The mechanism of the headache in relation to the angina pectoris is discussed.

Dynamics of n-3 and n-6 fatty acids in phospholipids of heart muscle.

The purpose of this paper is to describe the dynamics of n-3 and n-6 polyunsaturated fatty acids in major phospholipids of heart muscle. The profile of n-3 and n-6 fatty acids was examined in rats in relation to various risk factors of coronary heart disease such as stress (catecholamines), ageing and dietary fat. The level of n-3 and n-6 fatty acids in cardiac phospholipids was also examined in relation to coronary heart disease and sudden cardiac death in man. Severe stress caused great changes in the fatty acid profile of phospholipids. Corresponding changes were observed during adaptation to neonatal stress. Rats fed diets containing cod liver oil, butter or corn oil showed different fatty acid composition of individual phospholipids in sarcolemma. Repeated epinephrine administration induced similar changes in the three dietary groups despite large differences in initial levels of individual n-3 and n-6 fatty acids. Fatal ventricular fibrillation in rats and sudden cardiac death in man were accompanied by a high ratio of 20:4 n-6/22:6 n-3. The balance between n-6 and n-3 fatty acids in cellular phospholipids seem to play an important role in sudden cardiac death.

Secondary prevention after myocardial infarction: effects of beta blocking agents and calcium antagonists.

Therapeutic interventions in patients with myocardial infarction, whether during the first hours after coronary occlusion or several days later, aim to reduce mortality and morbidity by several mechanisms: Prevention of fatal ventricular fibrillation, limitation of infarct size, and inhibition of platelet aggregation are some examples of such mechanisms. Results from early intervention trials with beta blocking agents, particularly from ISIS-I, suggest that 1-year mortality is significantly lower in selected patients randomized to active treatment. Late intervention studies also suggest a significant reduction in coronary mortality and morbidity with beta blockade, particularly when data are pooled. Studies with the calcium channel blockers nifedipine and verapamil were unable to demonstrate any beneficial effects of these drugs on mortality or reinfarction. In this review article, attention will be directed to the most recent information about the preventive value of beta adrenergic blocking drugs and slow calcium channel inhibitors.

MECHANISMS FOR THE EARLY MORTALITY REDUCTION PRODUCED BY BETA-BLOCKADE STARTED EARLY IN ACUTE MYOCARDIAL INFARCTION: ISIS-1

In a large randomised trial of early beta-blockade in acute myocardial infarction (ISIS-1), almost all the reduction in mortality associated with the use of atenolol occurred on the day of admission or on the subsequent day. To help determine the mechanisms that might be responsible for this retrospective observation, case notes were obtained for British, Irish, and Scandinavian patients who died during this early period. Of 217 early deaths adequate records were available for 193 (79 allocated atenolol and 114 allocated control). In the atenolol group, necropsy had shown cardiac rupture in 5 patients, and a further 15 in whom necropsy had not been done had had electro-mechanical dissociation (total, 20 early deaths from these causes); among control patients the corresponding numbers were 17 and 37 (total, 54 such deaths). Electro-mechanical dissociation was probably a manifestation of acute rupture, and the observed difference in the numbers with this complication was responsible for much of the difference in early mortality. There was a slightly higher incidence of fatal ventricular fibrillation and aortic dissection in the control group, and of bradycardia/asystole in the atenolol group. The data did not indicate any substantial contribution from mechanisms such as limitation of infarct size or prevention of reinfarction or cardiac arrest.

Fatal ventricular fibrillation following verapamil in Wolff-Parkinson-White syndrome with atrial fibrillation

A 29-year-old man with Wolff-Parkinson-White syndrome and atrial fibrillation developed fatal ventricular fibrillation shortly after receiving intravenous verapamil. The patient presented with an irregular pulse of 190. A total of 23 mg of verapamil was administered in small intravenous doses over 35 minutes. The ventricular rate accelerated as verapamil was administered, and fatal ventricular fibrillation followed. Three theoretical mechanisms by which verapamil may enhance conduction of atrial fibrillation in Wolff-Parkinson-White syndrome, predisposing to ventricular fibrillation, are mentioned.

Role of arachidonic acid metabolism in development of fatal ventricular fibrillation in rats

Role of arachidonic acid metabolism in development of fatal ventricular fibrillation in rats

Linoleic acid and susceptibility to fatal ventricular fibrillation in rats

The effect of linoleic acid on the induction of fatal ventricular fibrillation by intravenous CaCl 2 (10%), was studied in rats fed for a month from weaning on a diet with either a high or low content of linoleic acid. Studies were performed in the basal state and after pretreatment with noradrenaline, which increased the sensitivity to CaCl 2 equally in animals from both diet groups. Despite considerable differences in the linoleic acid levels in the plasma and myocardium, the two groups did not differ in the incidence of fatal ventricular fibrillation. Our conclusions concerning the effect of linoleic acid on cardiac arrhythmias, and sudden death in particular, are compared with those from other studies.

Cardiac arrest due to oral potassium administration

Cardiac arrest developed in two patients after the administration of oral potassium. Neither patient had renal insufficiency, but both had underlying heart disease. In one patient fatal ventricular fibrillation developed 4 days after he received an aortic valve replacement for aortic stenosis and while he was receiving oral potassium supplements. The serum potassium level before cardiac arrest was 8.1 meq. The second patient had angina and was given 40 meq of potassium orally 15 minutes after an exercise test which produced chest pain and S-T segment depression. One hour later, ventricular fibrillation developed. Resuscitation was successful. Both patients had electrocardiographic evidence of hyperkalemia. Oral administration of potassium may produce severe cardiac toxicity in patients with heart disease even when renal function is clinically normal.

Relative effectiveness of three antiarrhythmic agents in the treatment of ventricular arrhythmias in experimental acute myocardial ischemia

Since ventricular arrhythmias complicating acute myocardial infarction in man have an uncetain course, an animal model of acute ischemia was used to compare three commonly used agents—procainamide, lidocaine, and diphenylhydantoin. A total of 150 dogs were divided into “treatment only” and “prophylaxis plus treatment” groups for each of the three agents. Twenty additional dogs served as untreated controls. The arterial branch (left circumflex or anterior descending branch) had no effect on ultimate success in preventing ventricular fibrillation with drug therapy for at least 4 hours. Ninety per cent of untreated controls developed fatal ventricular fibrillation within 4 hours. Among the “treatment only” groups 4 hour survival with procainamide (80 per cent) was significantly higher than with lidocaine (45 per cent) or diphenylhydantoin (56 per cent). Prophylactic administration of drugs following S-T-segment elevation but preceding ventricular arrhythmias did not increase survival rate. Following acute myocardial ischemia in the previously undamaged heart, procainamide appears to afford greater protection against ventricular fibrillation than the other two agents.

Use of bretylium tosylate in the management of acute myocardial infarction

Sixty-two patients with acute myocardial infarction were treated for 4 days with bretylium tosylate. This agent was effective in suppressing and preventing ventricular fibrillation as well as other irritable arrhythmias and heart block. On admission 37 patients had arrhythmias and 2 complete atrioventricular (A-V) block; 23 had no rhythm disturbances and were treated prophylactically. Of the 37 patients with arrhythmias, 11 had been treated with lidocaine without success. Eight patients had from 1 to 5 episodes of ventricular fibrillation (not suppressed by lidocaine in 7) before treatment with bretylium, but no patient had ventricular fibrillation after bretylium therapy was started. Ventricular arrhythmias were suppressed in from 10 minutes to 12 hours on routine dose therapy; the response indicated a sharp dose-dependent effect for complete suppression. Twenty-two of the 23 patients treated prophylactically had no arrhythmias. One patient had fatal ventricular fibrillation 5 1 2 hours after the first dose was administered and just before the second dose was due; this was the only death due to arrhythmia in the 62 patients. Of the 60 patients without heart block on admission, only 1 had heart block of any degree during treatment. There were 8 deaths in the hospital (12.9 percent), 7 as a result of pump failure. If 2 patients who were in extremis before treatment was started, and who died before an effect could have occurred, are excluded, mortality was under 10 percent. Our previous mortality in the unit was 20 percent. The actions of bretylium in increasing contractile strength, impulse formation and conduction velocity in addition to suppressing rhythm disturbance make it a valuable agent for the management of the major complications of acute myocardial infarction.

Prevention of Ventricular Arrhythmias Related to Paired Pacing.

s1 May 1969Prevention of Ventricular Arrhythmias Related to Paired Pacing.Edwin L. Rothfeld, M.D., F.A.C.P., I. Richard Zucker, M.D.Edwin L. Rothfeld, M.D., F.A.C.P.Search for more papers by this author, I. Richard Zucker, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-70-5-1081_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptDespite the advent of coronary care units and more aggressive management of the patient with acute myocardial infarction, the mortality rate due to the cardiogenic-shock—low-output failure syndrome remains unacceptably high. Paired pacing has been suggested as a mode of therapy because of its powerful inotropic effects but has not been extensively used because of the hazard of producing ventricular fibrillation. Previous work in this laboratory has shown that paired pacing of the canine heart after coronary artery ligation results in fatal ventricular fibrillation. The purpose of this study was to observe the combined use of paired pacing and various antiarrhythmic... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Newark, New Jersey PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byDrug-pacemaker interactions 1 May 1969Volume 70, Issue 5Page: 1081-1081KeywordsAcute myocardial infarctionArrhythmiaCardiac care unitCoronary arteriesDeath ratesHeartLigation assayResearch laboratoriesVentricular fibrillation Issue Published: 1 May 1969 PDF downloadLoading ...

Ethyl-3-ethoxycarbonyl-4-hydroxy-2 H-1,2-benzothiazine-2-acetate-1,1-dioxide, a compound producing ventricular arrhythmias

Ethyl-3-ethoxycarbonyl-4-hydroxy-2 H-1,2-benzothiazine-2-acetate-1,1-dioxide (McN-2165), 5 mg/kg iv, administered to anesthetized dogs, consistently produced an increase in the QRS interval and venticular ectopic beats. These effects often terminated in ventricular tachycardia and ventricular fibrillation. Pretreatment with atropine sulfate, chlorisondamine chloride or propranolol HCl did not influence the occurrence of the arrhythmias although the latter compound did decrease the incidence of fatal ventricular fibrillation. The antiarrhythmic agents quinidine sulfate, procaine amide HCl, lidocaine HCl, and diphenylhydantoin sodium caused no significant effect on the ectopic beats produced by McN-2165, but they significantly decreased the occurrence of fatal ventricular fibrillation. The administration of McN-2165 may furnish a method for the detection of more effective ventricular antiarrhythmic agents.

Diphenylhydantoin Toxicity

<h3>To the Editor:—</h3> Two articles "Fatalities Following Intravenous Use of Sodium Diphenylhydantoin for Cardiac Arrhythmias" and "Fatal Ventricular Fibrillation Following Intravenous Sodium Diphenylhydantoin Therapy" (<b>200</b>:335-338, 1967) incriminate diphenylhydantoin sodium as the causative factor in the death of three patients. The three patients reported in the two articles were all rapidly deteriorating clinically despite intensive medical treatment at the time of diphenylhydantoin administration. In this setting, the incrimination of diphenylhydantoin as<i>the</i>causative factor in the death of at least two of these patients is questionable. In the initial report both patients had pulmonary edema, one with falling blood pressure. The third patient was semiconscious with sepsis and hypoxia. It would have been important to indicate the blood pressure during and after the diphenylhydantoin infusion since this is an important determinant of the rate of the drug's administration. In contrast to these three cases, a substantial clinical experience has been

Fatal ventricular fibrillation during carotid sinus stimulation∗

The third case of ventricular fibrillation (the first with autopsy) occurring during carotid sinus stimulation is reported. Although this patient received only moderate amounts of digoxin, had no obvious electrolyte derangement, and received carotid sinus stimulation for only a few seconds, a fatal outcome occurred. The heart was normal at necropsy. Although carotid sinus stimulation is an invaluable and usually a safe tool in the treatment and diagnosis of cardiac arrhythmias, it is suggested that caution be used in applying this maneuver to the critically ill patient who has received even modest amounts of cardiac glycosides.

Complications and Limitations of Direct-Current Countershock

Elective direct-current countershock was applied to 65 patients with chronic atrial fibrillation to define the most exact criteria for safe use of this method. The 35 patients of group 1 were selected because of uncontrollable ventricular rate, persistent congestive heart failure, or a disabling awareness of the irregular rhythm. Sinus rhythm was reestablished in 31 patients (88%), but was maintained for two months in only ten (32%). Conversion following open heart surgery for mitral stenosis was successful in 28 of 30 (93%) patients; only three (10%) remained in sinus rhythm for more than two weeks. Fatal ventricular fibrillation occurred 30 to 120 seconds following shock for paroxysmal atrial tachycardia with block in two patients and intermittent ventricular tachycardia in one. Digitalis intoxication was implied and must be identified as a potential hazard.

COMPLICATIONS AND LIMITATIONS OF DIRECT-CURRENT COUNTERSHOCK.

Elective direct-current countershock was applied to 65 patients with chronic atrial fibrillation to define the most exact criteria for safe use of this method. The 35 patients of group 1 were selected because of uncontrollable ventricular rate, persistent congestive heart failure, or a disabling awareness of the irregular rhythm. Sinus rhythm was reestablished in 31 patients (88%), but was maintained for two months in only ten (32%). Conversion following open heart surgery for mitral stenosis was successful in 28 of 30 (93%) patients; only three (10%) remained in sinus rhythm for more than two weeks. Fatal ventricular fibrillation occurred 30 to 120 seconds following shock for paroxysmal atrial tachycardia with block in two patients and intermittent ventricular tachycardia in one. Digitalis intoxication was implied and must be identified as a potential hazard.

Observations in patients with implanted pacemaker: III. Frequency of ventricular tachycardia as cause of Adams-Stokes attacks and rate of pacing required for its prevention

Thirty-eight patients with Adams-Stokes syndrome were treated with implanted pacemakers. In 28 the mechanism of syncope could be determined. Ventricular tachycardia was observed in 19, that is, in about 68 per cent. Because of the great frequency of this arrhythmia and the grave prognosis attached to it, prevention of ventricular tachycardia is the chief problem in the treatment of Adams-Stokes syndrome. The use of sympathomimetic and cardiac-depressant drugs is contraindicated. Stimulation of the ventricle by an electrical pacemaker is the only promising method of treatment. Pacing at a rate of 60 per minute was effective in the long-term prevention of ventricular tachycardia in 15 out of 19 patients. In 3 patients, ventricular arrhythmias recurred on the day of implantation. Raising the rate of pacing from 60 to 80 per minute prevented further attacks in 2 patients. In the third patient, however, fatal ventricular fibrillation recurred on the day of operation, after the rate of pacing had been stepped up to 96 per minute. A fourth patient succumbed to ventricular fibrillation on the ninth postoperative day while function of the implanted pacemaker at a rate of 60 per minute was unimpaired. It is suggested that implantable pacemakers, in order to yield full benefit, should have an inherent pacing rate of 90 per minute. Provision should be made, if possible, for increasing the rate of the pacemaker so that its function may be adapted to changing needs.

Cardiac ischemic changes and arrhythmias induced by hypothalamic stimulation

It has been shown that in cats, short periods of stimulation of discrete hypothalamic areas (anterior, posterior and lateral) can lead to temporary and repeatable pressor responses associated with consistent electrocardiographic ischemic-like changes (ST-T deviations) and arrhythmias (bradycardia, tachycardia and ectopic beats). Significant quantitative and qualitative differences in these responses are demonstrable, depending on whether succinylcholine or gallamine is used. The pressor responses from all areas are completely abolished by C2 spinal section and are therefore of sympathetic origin; but whether or not they are from specific hypothalamic areas or from some common sympathetic pathways traversing these areas has not been determined. Parasympathetic cardiac changes (bradycardia) appear to be specifically mediated only from the anterior hypothalamus, although with high intensity stimulation they can also arise from other areas. Sympathetic cardiac changes (tachycardia and ST-T deviations) ensue from all three areas, but appear to be specifically mediated only from the lateral hypothalamus. Intense, prolonged and repeated lateral stimulation enhances the development and persistence of ischemic-like electrocardiographic disturbances, and with bilateral stimulation can induce significant postmortem pathologic changes (distinct myocardial infarction in some animals), although acute fatal ventricular fibrillation was never observed. It is postulated that these sympathetic cardiac changes are mediated by norepinephrine rather than by epinephrine. The findings suggest that hypothalamic stimulations might be involved in some of the arrhythmias reported in patients with cerebrovascular accidents.

Supraventricular Tachycardia in Acute Myocardial Infarction : Review of the Literature and Report of Five Cases

1. This study of 360 recently hospitalized cases of acute myocardial infarction and a review of the literature confirms the impression that supraventricular tachycardia is a relatively rare complication of acute myocardial infarction. 2. Supraventricular tachycardia is of grave prognostic import in acute myocardial infarction. This is at least partially due to the fact that this arrhythmia seems to complicate infarction mostly in patients with severely damaged hearts. Only three recoveries were noted in the 19 cases studied. 3. Of our five cases reported, one was related to digitalis intoxication and four were not. The danger of inducing supraventricular tachycardia constitutes another reason for due caution when digitalis is given to patients with acute myocardial infarction, although it should, of course, be used when indicated. 4. In one of our cases the supraventricular tachycardia converted to a fatal ventricular fibrillation following an average dose of deslanoside.

Ventricular fibrillation during and after coronary artery occlusion: Incidence and protection afforded by various drugs ∗

The incidence of ventricular fibrillation during and after temporary experimental occlusion of the left anterior descending coronary artery or its branches was studied in 351 dogs. A standardized procedure of thirty-minute temporary occlusion of this artery was employed in 330. There is usually a critical period after twelve and up to fifteen minutes of ischemia which is characterized by a tendency to arrhythmia: extrasystoles, singly or in runs, ventricular tachycardia, or both extrasystoles and tachycardia if not a fatal ventricular fibrillation. Several instances of transient ventricular fibrillation were observed. Of 239 animals surviving thirty minutes of occlusion, 71 per cent developed ventricular fibrillation immediately after release of the artery, while only 28 per cent of 330 animals developed fibrillation during the occlusion. The re-establishment of blood flow to an area of the myocardium made ischemic for thirty minutes by occlusion of the anterior descending coronary artery is more likely to precipitate ventricular fibrillation than is the period of ischemia itself. Various drugs were evaluated in 324 dogs. Quinidine was the most effective drug in affording protection from ventricular arrhythmia during (7 per cent) and following (47 per cent) occlusion. Procaine, procaine amide and Apresoline offered good protection during the ischemic period. Apresoline and Regitine also reduced the incidence (44 and 37 per cent) of ventricular fibrillation upon reopening the ligature. Of the other drugs tested, only one, pendiomide, showed significant protection (52 per cent incidence). Systemic arterial pressures did not predict the onset of ventricular arrhythmia. Electrical countershock accomplished cardiac resuscitation in 75 per cent of the fibrillating dogs. From these experiments, quinidine appears to be the drug of choice in the prophylaxis of fatal ventricular arrhythmias.