Long-term Prognosis following Ventricular Fibrillation in Acute Ischaemic Heart Disease

Of 160 patients who survived ventricular fibrillation complicating acute ischaemic heart disease, 80 had had a clinically mild coronary attack. Most of the long-term survivors had ventricular fibrillation within 24 hours of the onset of symptoms. The longterm prognosis of the survivors was similar to that of patients whose myocardial infarction was not complicated by ventricular fibrillation. Those patients who survived ventricular fibrillation which occurred within four hours of the onset of symptoms were younger, usually had had a mild coronary attack, and had the most favourable longterm prognosis. The number of episodes of ventricular fibrillation did not affect adversely the long-term prognosis. Of those who at the time of review were eligible to work, 86% were fit to work and 68% were actually at work.     

Lignocaine Therapy for Ventricular Ectopic Activity after Acute Myocardial Infarction: A Double-blind Trial

The effectiveness of intravenous lignocaine in suppressing ventricular ectopic activity after acute myocardial infarction was examined in a double-blind trial in 82 patients. Whereas suppression of unifocal ventricular ectopics was achieved by lignocaine in 90% of patients, other forms of potentially more dangerous ectopic activity (multifocal or R-on-T ectopics) seemed more resistant to therapy. Cessation of ectopic activity was also observed in about one-third of the patients in the control group. The incidence of ventricular tachycardia and fibrillation and the mortality during and after the trial period were similar in the lignocaine-treated and control groups, whether or not the initial ventricular ectopics had been suppressed.This study provides no evidence to support the routine use of intravenous lignocaine in the management of ventricular ectopic activity after acute myocardial infarction.     

Five hundred patients with myocardial infarction monitored within one hour of symptoms.

Of 2886 patients monitored during acute myocardial infarction, 500 were observed within one hour of the onset of symptoms. Half of the early admission group were admitted in response to emergency 999 calls and 435 of them travelled in resuscitation ambulances, where surveillance for arrhythmias was instituted. Pulmonary oedema occurred in 130 patients (26%), cardiogenic shock supervened in 60 (12%), and 115 (23%) died in hospital. Ventricular fibrillation was observed in 98 patients (20%). Forty two of them survived to be discharged, including 20 of the 24 with primary fibrillation which had occurred first in hospital. In only one case did primary ventricular fibrillation occur after the first 10 hours of onset of illness. Sinus bradycardia, atrial fibrillation, ventricular tachycardia, and ventricular fibrillation were all observed more frequently in patients admitted within one hour after the onset of symptoms than in those admitted later. An element of selection is inevitable when early admission is encouraged by the existence of a resuscitation ambulance system; this will depend in part on the early recognition of risk and the geographical location of the attack. These factors may bias the group towards relatively high risk. Nevertheless, prompt admission after myocardial infarction should improve survival by permitting successful management both of ventricular fibrillation and of other arrhythmias which may influence short term and long term prognosis.     

Bretylium Tosylate in the Management of Refractory Ventricular Fibrillation

Nine patients who had recurrent ventricular fibrillation following acute myocardial infarction or angina were given bretylium tosylate in a dose of 5 mg./kg. intramuscularly every eight hours after other measures had proved ineffective. Provided the patients were not in shock or in heart failure, there was a considerable reduction in the episodes of ventricular fibrillation.A second group of nine patients who developed recurrent ventricular fibrillation following open heart surgery were given bretylium intravenously, which controlled the arrhythmia in every instance.Bretylium did not completely abolish ventricular premature beats but the latter did not initiate ventricular fibrillation even when they occurred on the T wave.     

Sexual activity after myocardial infarction.

Questionnaires on sexual activity were completed by 161 patients attending an exercise-centred rehabilitation program an average of some 3 years after a myocardial infarction. In almost half the group, sexual activity was unchanged or increased compared with the period before the infarction. In the remainder it was reduced; this group included 29 men who had adopted a more passive sexual role and 26 who were now having angina or ventricular premature beats during intercourse. Although the patients with diminished activity could not be distinguished by means of formal personality test, questionnaires completed by their wives suggested that they were less willing to assume responsibility, had increased difficulty in adjusting to life at home and at work and were more neurotic and depressed than those with normal or increased activity. Furthermore, those with decreased sexual activity had a poorer response to training in terms of attendance, final average jogging distance and gains in physiologic status. Since the frequency of angina and ventricular premature beats was less during intercourse than during standard laboratory exercise, it was concluded that normal sexual relations carry no special risk for the average postcoronary patient; indeed, by enhancing self-esteem and encouraging effective participation in an exercise programm, acceptance of normal sexual activity may improve the prognosis.     

Risk-benefit stratification as a guide to lidocaine prophylaxis of primary ventricular fibrillation in acute myocardial infarction: an analytic review.

Early investigators suggested that ventricular fibrillation without heart failure in acute myocardial infarction was reliably preceded by warning arrhythmias, and that suppression of such arrhythmias with intravenous lidocaine could avoid the need for resuscitation. While the efficacy and safety of lidocaine have been substantiated, the reliability of warning arrhythmias as predictors for primary ventricular fibrillation has not. We present data showing that the risk of primary ventricular fibrillation is most dependent on the patient''s age and the interval since the onset of his symptoms, rather than on the presence of warning arrhythmias. We have estimated that lidocaine prophylaxis would have to be given to about 12 patients in the highest risk group (patients under age 50 and within six hours of the onset of symptoms), compared to about 400 patients in the lowest risk group (patients above age 70 and more than 24 hours since the onset of symptoms), to prevent one episode of primary ventricular fibrillation in each group. We propose that these risk stratifications, as adapted to the conditions in specific hospitals, provide the most rational approach to lidocaine prophylaxis of primary ventricular fibrillation.     

Late ventricular fibrillation following successful resuscitation from postinfarction cardiogenic shock with intraaortic balloon pumping

Early ventricular fibrillation occurs in approximately 5% of patients admitted for acute myocardial infarction. Although late ventricular fibrillation (> 48 hours postinfarction) may occur in stable patients, it occurs more commonly when severe left ventricular power failure is present. We have encountered late ventricular fibrillation in three of 42 (7%) patients treated with intraaortic balloon pumping (IABP) for profound cardiogenic shock secondary to myocardial infarction. These patients progressed to our hemodynamic Class A prior to weaning, and were thought to be stable prior to IABP removal. They were the only ones who expired after achieving Class A status. The episodes of late ventricular fibrillation occurred after the patients had been successfully weaned from IABP and were free of arrhythmias. This experience suggests that prolonged antiarrhythmic therapy may be indicated for postinfarction patients who have had ventricular dysrhythmias during IABP support.     

Mobile Intensive Care in Myocardial Infarction

In the first six months of its existence a mobile intensive care unit was used to admit 95 patients with definite or probable myocardial infarction to the local district hospital. Though the area served was a rural one, with a radius of about 25 miles from the hospital, the average interval between receiving a call and starting intensive care was less than 30 minutes. Five patients with ventricular fibrillation were successfully resuscitated by the mobile team outside hospital. The mobile unit has made it possible to admit many more patients with myocardial infarction to hospital than before, and we believe its cost and use of skilled staff are justified by the results. The unit reduces the delay between the onset of symptoms and initiation of intensive care and thus diminishes the risk of primary ventricular fibrillation, which is maximal soon after the onset of symptoms. Since mobile intensive care removes the risk of transport it allows concentration of cases of acute myocardial infarction in the larger hospitals.     

80例急性心肌梗死患者心电监护及护理

目的总结急性心肌梗死患者心电监护及护理经验。方法对本院性心肌梗死患者及时进行心电监护,对出现的心律失常者进行对症处理。结果本组80例患者中出现心律失常55例,其中室性心律失常48例,临床治愈45例;出现心室颤动7例,4例及时电复律转为窦性心律,3例抢救无效死亡。本组心律失常均发生在心肌梗死后1周内,尤其是发病24小时内,出现最多。结论心律失常是心肌梗死患者常见的并发症,也是患者死亡的主要原因,持续心电监护对患者心律失常的及时发现、明确诊断、指导抢救有重要意义。     

Paroxysmal atrial fibrillation triggered by a monomorphic ventricular couplet in a patient with acute coronary syndrome

Atrial fibrillation is a common arrhythmia in patients suffering from acute myocardial infarction, however its pathophysiological mechanisms are not fully understood. We describe the unusual case of a 76-year old woman admitted for non-ST-segment elevation myocardial infarction, who developed multiple episodes of paroxysmal atrial fibrillation triggered by monomorphic ventricular couplets. Beta-blocking and amiodarone therapy resulted efficacious in preventing arrhythmic recurrences. We then discuss the possible arrhythmogenic mechanisms, with special emphasis on the unique electrophysiological, hemodynamic, cellular and anatomical milieu created by acute myocardial ischemia.     

Transthoracic ventricular defibrillation in adults.

A prospective study of the energy required for transthoracic ventricular defibrillation in adults showed that in 42 (81%) out of 52 episodes of ventricular fibrillation shocks of 100 watt-seconds (Ws) of stored energy were successful. Out of 233 episodes, 222 (95%) were converted by 200 W s shocks. Among patients in whom primary ventricular fibrillation occurred within one hour of the onset of acute myocardial infarction, 200 W s shocks were successful in 40 (98%) out of 41 episodes. When low-energy shocks failed, a stored energy of 400 W s invariably succeeded. The need for large and expensive defibrillators that store more than 400 W s and are less readily available is therefore questioned.     

Reduced risk of death at 28 days in patients taking a beta blocker before admission to hospital with myocardial infarction.

OBJECTIVE--To see whether patients taking an oral beta blocker at the time of admission to hospital with myocardial infarction have a reduced risk of death at 28 days. DESIGN--Retrospective analysis of data collected on patients admitted over four years. SETTING--Community based study. PATIENTS--2430 Consecutive patients living in the Perth statistical division admitted to hospital with myocardial infarction during 1984-7. MAIN OUTCOME MEASURE--Survival at 28 days among patients taking a beta blocker at onset of myocardial infarction. RESULTS--Patients were grouped into those who were and were not taking a beta blocker at the time of admission. Though patients taking a beta blocker were older and more likely to have a history of myocardial infarction, angina, or hypertension, the overall mortality at 28 days was similar in the two groups. A logistic regression model used to adjust for factors predictive of cardiac death at 28 days confirmed that patients taking a beta blocker at the time of admission had a significantly reduced risk of death (relative risk 0.50; 95% confidence interval 0.34 to 0.76). Though the incidence of fatal ventricular fibrillation was similar in the two groups, mean peak creatine kinase activity was significantly lower in the beta blocker group. CONCLUSIONS--These data support the value of long term use of beta blockers in patients at risk of myocardial infarction. They suggest that patients taking these agents before admission to hospital with myocardial infarction have a significant survival advantage at 28 days, which may be due to a reduction in infarct size.     

The effect of bretylium tosylate on ventricular arrhythmias in patients with acute myocardial infarction]

Sixty three patients with the acute myocardial infarction, aged between 34 and 85 years, admitted to the Intensive Cardiological Care Unit during the first 12 hours following the infarction were randomly divided into two groups. Patients of group I (20 subjects) were treated with nitroglycerin and additional intravenous infusions of bretylium tosylate in the dose of 5 mg/kg administered every 6 hours for 48-72 hours. Patients of group II (33 subjects) were mainly treated with intravenous nitroglycerin. A type and incidence of the ventricular arrhythmias, conduction disorders in AV node, and hemodynamic complications were analysed during the first 72 hours. It was found that bretylium tosylate reduces the incidence of ventricular arrhythmias accompanying myocardial infarction but after 2-3 hours following its administration (p < 0.05). Therefore, bretylium tosylate should be administrated to patients with the acute myocardial infarction in combination with other rapidly acting anti-arrhythmic drug. Bretylium tosylate increases also the effectiveness of electric defibrillation in patients with ventricular fibrillation or ventricular tachyarrhythmia. No evidence of the effectiveness of bretylium tosylate on atrio-ventricular conduction and hemodynamic complications of myocardial infarction was found.     

Prevention of disorders of the electric stability of the heart in experimental infarct using adaptation to hypoxia

It has been shown on rats preadapted to hypoxia in an altitude chamber that myocardial infarction induced by ligation of the coronary artery was accompanied by less disturbances in the electrical stability of the heart, namely by a twofold decrease in ventricular fibrillation threshold and a considerable decrease in the heart ectopic activity. Preliminary adaptation provided the maintenance of myocardial contractility in infarction.     

Indications for admission to a coronary care unit in patients with unstable angina.

One hundred cases with an admission diagnosis of acute coronary insufficiency or unstable angina were reviewed to establish criteria for admission to a coronary care unit. Myocardial infarction was subsequently diagnosed in 20 of the patients. Ventricular tachycardia occurred in 16 patients and ventricular fibrillation in 1 patient. Clinical features found to predict an increased risk of myocardial infarction included chest pain for more than 30 minutes within 24 hours prior to admission, new nonspecific electrocardiographic abnormalities consistent with ischemia, and diaphoresis. All patients with ventricular tachydysrhythmias had presented with both prolonged chest pain prior to admission and new electrocardiographic changes. The sensitivity, specificity and predictive value of various clinical criteria for identifying patients likely to have a myocardial infarction were calculated, and criteria with very high (greater than 90%) sensitivity were identified. These could be used to establish which patients are at increased risk of myocardial infarction and therefore require admission to a coronary care unit.     

The Brighton resuscitation ambulances: review of 40 consecutive survivors of out-of-hospital cardiac arrest.

In three years 40 patients were resuscitated by ambulancemen after out-of-hospital cardiac arrest and survived to be discharged. Twenty-six of these had had circulatory arrest before an ambulance arrived and a further three had developed ventricular fibrillation before they were moved. Thirty-two patients were alive at the time of review six months to three and a half years later. Resuscitation by ambulancemen can be effective for patients with unheralded sudden cardiac arrest as well as for patients with recent myocardial infarction. Survivors of out-of-hospital ventricular fibrillation may have a favourable long-term prognosis.     

Isolated left ventricular noncompaction in a patient presenting with a subacute myocardial infarction

Isolated left ventricular noncompaction is a rare cardiomyopathy that is often not recognised. So far, it is not well established how best to manage this abnormality. We describe a patient in whom the diagnosis of isolated left ventricular noncompaction was made after presentation with a subacute myocardial infarction. Because of nonsustained ventricular tachycardias during hospitalisation, which were inducible and deteriorated into ventricular fibrillation on electrophysiological examination after coronary artery bypass grafting, he received an implantable defibrillator. Whether the ventricular tachycardias were due to the myocardial infarction or to the noncompacted myocardium remains uncertain. (Neth Heart J 2007; 15:109-11.)     

Effect of myocardial infarction and ischemia on induction of cardiac reentries and ventricular fibrillation

The present work is aimed at investigating the effects of myocardial infarction and ischemia on induction of ventricular fibrillation. Electrophysiologic effects of global and local ischemia (variation of the dispersion of refractory periods as well as conduction velocity) on initiation of reentry mechanisms was studied by means of computer simulations based on a cellular automata model of propagation of activation wave through a ventricular surface element. A local area of ischemia where effects of the dispersion of refractory periods are investigated is then simulated. This is made using a Gaussian distribution characterized by its mean and standard deviation. These simulations show that ischemia is capable of initiating reentry phenomena which propagate through the whole ventricle; they are responsible for ventricular fibrillation which causes sudden cardiac death, even when ischemia only involves limited parts of the myocardium. Statistical study of the probability of reentries as a function of both of the size of ischemic zones and the rate of dispersion of refractory periods shows that the latter parameter is of primary importance in triggering cardiac reentries.     

Lignocaine Therapy after Acute Myocardial Infarction

Thirty-five patients with ventricular dysrhythmias and seven with other dysrhythmias after acute myocardial infarction were treated with intravenous lignocaine.Satisfactory initial suppression of ventricular ectopic beats was achieved in 27 (82%) of 33 patients after either a 50-mg. bolus or a 50-mg. bolus followed by a 100-mg. bolus of intravenous 2% lignocaine. Continuous suppression of ventricular ectopic beats was accomplished in 21 (78%) of these 27 patients by continuous intravenous lignocaine infusions of 1 to 2 mg. per minute. Recurrence of ventricular ectopic beats occurred in four patients despite lignocaine infusion rates of up to 6 mg. per minute. Six patients with ventricular ectopic beats developed ventricular fibrillation despite satisfactory initial suppression of their dysrhythmia by lignocaine. In three of them ventricular fibrillation supervened while they were receiving a lignocaine infusion and two subsequently died. Unheralded ventricular fibrillation occurred in three other patients between four and seven days after completing the full course of lignocaine therapy.Toxic effects of lignocaine were minimal in patients receiving 1 to 2 mg. per minute.     

Implantable cardioverter defibrillator: an update

Automatic implantable cardioverter defibrillator is now a well established therapy to prevent sudden cardiac death. In secondary prevention (patients with a previous cardiac arrest) defibrillator can be considered as a class I indication, if there is no transient or reversible cause. The level of proof is A. in primary prevention the defibrillator is indicated in coronary artery disease patients with or without symptoms of mild to moderate heart failure (NYHA II or III), an ejection fraction lower than 30 %, measured at least one month after a myocardial infarction and 3 months after a revascularisation, surgery or angioplasty (level of proof B). It is also indicated in symptomatic spontaneous sustained ventricular tachycardias with underlying heart disease (level of proof B), in patients with spontaneous sustained ventricular tachycardia, poorly tolerated, without underlying heart disease for which pharmacological treatment or ablation can not be performed or failed (level of proof B). Finally it is also indicated in patients with syncope of unknown cause with sustained ventricular tachycardia or inducible ventricular fibrillation, with an underlying heart disease (level of proof B). The guidelines proposed by the different societies have also proposed class IIa recommendations which are the following: coronary artery disease patients with left ventricular dysfunction (ejection fraction between 31 or 35 %) measured at least one month after a myocardial infarction and 3 months after a revascularisation with an inducible ventricular arrhythmia. It can be also indicated in idiopathic dilated cardiomyopathies with an ejection fraction lower than 30% and NYHA class II or III. It can be also indicated in familial or inherited conditions with a high risk of sudden cardiac death by ventricular fibrillation without any other efficient known treatment and finally in heart failure patients remaining symptomatic, in class III or IV NYHA, with an optimal medical therapy, an ejection fraction lower than 35 % and a QRS complex duration higher than 120 ms: in this case it is an indication of cardiac resynchronization therapy device associated to the defibrillator. All these class IIa indications have a level of proof B.