Although the class Ic drugs, encainide and flecainide, were effective in suppressing VEBs, arrhythmic death was more common in those treated with the drugs (4.5%) than placebo with a relative risk of 3.6. 7 CAST was a randomised, placebo‐controlled study which tested the hypothesis that suppression of asymptomatic or minimally symptomatic VEBs after myocardial infarction would reduce arrhythmic death. Furthermore, results of the Cardiac Arrhythmia Suppression Trial (CAST) published in 1989 questioned the causal importance of VEBs in increasing risk and revolutionised the thinking behind the necessity to suppress VEBs. 5 Both the increased prevalence of VEBs and the higher incidence of heart disease are likely to contribute towards the low specificity and predictive value of VEBs for arrhythmic death in this population. The incidence and frequency of VEBs increase with age but studies had failed to establish a firm association between VEBs and arrhythmic death in older persons. These results had been criticised for the lack of rigorous measures to exclude underlying heart disease which may have confounded the outcome. Similar outcomes were reported in apparently healthy subjects in the Framingham Heart Study 6 whereby VEBs were associated with a twofold increase in the risk of all cause mortality, myocardial infarction and cardiac death. 4 Later, the study on a cohort of the Multiple Risk Factor Intervention Trial (MRFIT), 5 reported that the presence of VEB identified on a rest two‐minute ECG rhythm strip was associated with a high risk for sudden death in apparently healthy subjects over a 7.5 year follow‐up. However, the study by Kennedy in 1985 suggested that in the absence of structural heart disease, even frequent and complex VEBs are associated with a benign prognosis. 4 These latter phenomena are often seen in patients with heart disease and are widely accepted as markers of increased risk of malignant arrhythmias and death. Even frequent (> 60/h or 1/min) and complex VEBs occur in apparently healthy subjects, with an estimated prevalence of 1–4% of the general population. The study by Kostis et al 3 in 1981 in subjects free of recognisable heart disease, verified by the above list of investigations including right‐ and left‐heart catheterisation and coronary arteriography, showed that 39 out of 101 subjects had at least one VEB over a 24 hour period and four subjects had > 100/24 hours, with five having > 5 VEBs in any given hour and four having multiform VEBs. Early studies had been criticised as the presence of heart disease was not investigated with stress testing, echocardiography or invasive tests. VEBs have been described in 1% of clinically normal people as detected by standard ECG and 40–75% of apparently healthy persons as detected by 24–48 hour ambulatory (Holter) ECG recording. This triggered the widely accepted dogma that increasing “severity” of ventricular ectopic activity was directly related to the risk of malignant ventricular arrhythmias and considerable effort had been spent in developing and employing antiarrhythmic drugs to suppress ectopics in the 1960s and '70s. Lown and colleagues 2 proposed a classification and grading of ventricular ectopics based on their frequency and complexity. This was shown to be so in more recent times where patients who have had a myocardial infarct were more prone to sudden death if they had frequent ventricular ectopics. 1 He noted that these irregularities did not interfere with normal lifespan when they were occasional but an ominous prognosis was implied if they were frequent. The first recorded description of intermittent perturbations interrupting the regular pulse, that could be consistent with VEBs, was from the early Chinese physician Pien Ts'Io, around 600 BC, who was the master in pulse palpation and diagnosis. VENTRICULAR ECTOPIC BEATS: PAST, PREVALENCE AND PROGNOSIS
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