Ventricular fibrillation incidence

Cardiac arrhythmias are an important cause of morbidity and mortality approximately 400,000 people per year die from myocardial infarctions (MI) in the United States alone. Individuals with MI exhibit some form of dysrhythmia within 48 h. Post-mortem examinations of MI victims indicate that many die in spite of the fact that the mass of ventricular muscle deprived of its blood supply is often quite small. These data suggest that the cause of death is ventricular fibrillation and that the immediate availability of a safe and efficacious antiarrhythmic agent could have prolonged a number of Hves. The goals of antiarrhythmic therapy are to reduce the incidence of sudden death and to alleviate the symptoms of arrhythmias, such as palpitations and syncope. Several excellent reviews of the mechanisms of arrhythmias and the pharmacology of antiarrhythmic agents have been pubflshed (1,2). 

Kanashiro, M., Matsubara, T., Goto, T., and Sakamoto, N. (1993). Cyprid-ina luciferin analog reduces the incidence of ischemia/reperfusion-induced ventricular fibrillation. Jpn. J. Pharmacol. 63 47-52. 

First, drug-induced lengthening of the QT interval has been associated with the occurrence of ventricular tachyarrhythmias, namely TdP, a polymorphous ventricular arrhythmia that may cause syncope and degenerate into ventricular fibrillation and sudden death although the incidence of TdP is a rare event (usually, less than 1 in 100 000) [32], even a low risk is not justified for drugs with uncertain benefits or drugs providing only symptomatic improvement of a mild disease. 

The major toxic reactions to disopyramide administration include hypotension, congestive heart failure, and conduction disturbances. These effects are the result of disopyramide s ability to depress myocardial contractility and myocardial conduction. Although disopyramide initially may produce ventricular tachyarrhythmias or ventricular fibrillation in some patients, the incidence of disopyramide-induced syncope in long-term therapy is not known. Most other toxic reactions (e.g., dry mouth, blurred vision, constipation) can be attributed to the anticholinergic properties of the drug. 

Cardiovascular effect. Coconut and coconut oil, administered to 32 coronary heart disease patients in 16 age- and sex-matched healthy controls with no difference in the fat, saturated fat, and cholesterol consumption, produced no effecC h Hydrogenated oil, administered to young male Wistar rats, at a dose of 10% of diet for 10 weeks, produced an increase in the risk of ventricular arrhythmias under conditions of both ischemia and reperfusion. The incidence of ventricular fibrillation was 67% in the oil-... 

Lidocaine is the agent of choice for termination of ventricular tachycardia and prevention of ventricular fibrillation after cardioversion in the setting of acute ischemia. However, routine prophylactic use of lidocaine in this setting may actually increase total mortality, possibly by increasing the incidence of asystole, and is not the standard of care. Most physicians administer IV lidocaine only to patients with arrhythmias. 

Intake of dietary sources of n-3 fatty acids is associated with reduced incidence and severity of inflammatory disorders, cardiovascular diseases, and some cancers in humans (12, 98-103). Populations consuming fish that are rich in n-3 fatty acids are known to have a low incidence of atherosclerotic disorders (104). Dietary fish oil, which is high in EPA and DHA, also was shown to reduce myocardial ischemic damage (105) and ventricular fibrillation (106). The antitumorigenic effect of n-3 fatty acids was demonstrated in breast cancer (107), colon cancer (108-110), and pancreatic neoplasm (111). In addition to their beneficial influence on cardiovascular disorders and cancers, n-3 fatty acids are also known to decrease the severity and minimize symptoms of inflammatory diseases, including rheumatoid arthritis (15) and inflammatory bowel disease (16), and may be of benefit in correcting psychological disorders (17). 

The incidence of major adverse reactions to dipyridamole was determined in a multicenter retrospective study, involving 73 806 patients who underwent intravenous dipjridamole stress imaging in 59 hospitals and 19 countries (4). The main conclusion was that the risk of serious dipjridamole-induced adverse effects is very low, a conclusion that is in line with other reports (5), and comparable to that reported for exercise testing in a similar patient population. Combined major adverse events among the entire patient population included 7 cardiac deaths (0.95 per 10000), 13 non-fatal myocardial infarctions (1.76 per 10000), 6 non-fatal sustained ventricular dysrhythmias (0.81 per 10000) (ventricular tachycardia in 2 and ventricular fibrillation in 4), 9 transient cerebral ischemic attacks (1.22 per 10000), 1 stroke, and 9 severe cases of bronch-ospasm (1.22 per 10000). Minor non-cardiac adverse effects were less frequent among the elderly and more frequent in women and patients taking maintenance aspirin. 

Reperfusion dysrhythmias can occur when thrombolytic drugs are used to treat myocardial infarction. The most common is transient ventricular tachycardia. However, controlled trials have failed to show an increase in serious ventricular dysrhythmias, the incidence of ventricular fibrillation being actually reduced by thrombolytic therapy in myocardial infarction (11). 

Intravenous administration of (+)-isocorydine hydrochloride to anesthetized rats at a dosage of 5-20 mg/kg significantly counteracted the arrhythmias induced by intravenously administered barium chloride (3 mg/kg) or aconitine (20 mg/kg), and decreased the incidence of ventricular fibrillation, as well as the mortality rate [332]. 

Estrogens induced cardioprotection seems to involve the ERa receptor. In fact, hearts from estrogens receptor-alpha knock out mice were sensitive to ischemia and reperfusion injury". Furthermore, estrogens receptor modulators which lack some of the estrogens side effects are shown to be cardioprotective raloxifene limited infarct size and incidence of ventricular fibrillation in an in vivo canine model of coronary occlusion and reperfusion. This effect was attenuated by the inhibition of NO synthase (NOS) or calcium activated potassium channels and completely abolished by both blocking NOS and Ca2+-activated K+ channels. Ischemia and reperfusion induced p38 MAPK activation was also attenuated in raloxifene treated hearts.12... 

Cobb LA, Fahrenbruch CE, Olsufka M, Copass MK. Changing incidence of out-of-hospital ventricular fibrillation, 1980-2000. JAMA 2002 288 3008-3013. 

Kuisma M, Repo J, Alaspaa A. The incidence of out-of-hospital ventricular fibrillation in Helsinki, Finland, from 1994 to 1999. Lancet 2001 358 473 74. 

In contrast, patients who have ventricular fibrillation associated with acute MI (i.e., during the first 24 hours after symptom appearance) usually have little risk of recurrence. Of all patients who die from an acute MI, approximately 50% die suddenly prior to hospitalization. Ventricular fibrillation associated with acute MI can be subdivided into two types primary ventricular fibrillation and complicated or secondary ventricular fibrillation. Primary ventricular fibrillation occurs in an uncomplicated MI not associated with heart failure secondary ventricular fibrillation occurs in an MI complicated by heart failure. The time course, incidence, mechanisms, treatment, and com-... 

Antman EM, BerUn JA. Declining incidence of ventricular fibrillation in myocardial infarction ImpUcations for the prophylactic use of Udocaine. Circulation 1992 86 764-773. 

Atrial fibrillation is commonly associated with heart failure, and the prevalence of atrial fibrillation is related to the severity of heart failure, with less than 5% affected with very mild heart failure to nearly 50% affected with advanced heart failure [66]. Heart failure and atrial fibrillation are both common cardiovascular disorders and share the same demographic risk factors, including age, history of hypertension, prior myocardial infarction, and valvular heart disease [67, 68]. Further, the incidence of heart failure increases dramatically after the diagnosis of atrial fibrillation [69]. Progression of LV dysfunction can clearly be associated with rapid ventricular rates [70-76]. Conversely, conversion to normal sinus rhythm or control of ventricular response in atrial fibrillation can improve LV function [71-74, 77]. Accordingly, rate control becomes very important in patients with heart failure and dilated cardiomyopathy, and likely even more so when ischemia from rapid rates complicate the patient s course. 

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