To assess the role of ventricular premature beats in influencing mortality of coronary patients, 1739 men with prior myocardial infarction were monitored for ectopic activity for one hour at a standard base-line examination, and followed for mortality for periods up to four years (average, 24.4 months). Analyses of survival taking into account other important prognostic variables establish that the presence of complex premature beats (R on T, runs of 2 or more, multiform or bigeminal premature beats) in the monitoring hour is associated with a risk of sudden coronary death three times that of the men free of complex ventricular premature beats. The corresponding risk of death from any cause is twice that of men without such complex beats in the hour. These arrhythmias make an independent contribution to increased risk of death that persists over the length of this observation period.

tended to develop 5-year mortality rates. Accumulation of a total of 349 deaths, 149 of them sudden (deaths within minutes in the absence of symptoms or signs of acute MI), permits both examination of course of disease over the longer period and more detailed study of the role of specified qualitative features of the ventricular premature complexes in relation to risk of sudden death. MethodsOver a period of almost 4 years (March 1972 through December 1975, 2155 CHD patients were identified from a population of 120,000 men ages 35-74 years, insured in HIP, a prepaid group-practice plan providing comprehensive medical services. Standard baseline observations included interviews to establish personal characteristics and medical history, physical examination and laboratory determinations, a 12-lead ECG and 1 hour of single-lead ECG monitoring recorded on tape. A baseline examination was performed in 87% of the men identified as potential study subjects from case-finding procedures. Of those examined, 83% satisfied the study criteria for CHD12 and entered the follow-up phase of the study. Of these, 1739 men had had at least one MI before the baseline date and 416 had had unequivocal effort angina in the absence of historical or ECG evidence of MI.Computer processing of the monitoring tapes produced writeouts on ECG paper of all possibly abnormal beats. Double reading these sections by trained technicians and physicians then provided the basis for classification of patients by ventricular ectopic activity during the monitoring hour. Details of the method and data on validation have been published.7, 13 Follow-up of all patients is now complete, and mortality status as of the last observation due before April 1, 1978 is known for all patients. The final data, presented for the MI patients in this report, are based on an average observation period of 3.5 years. Patients have been followed for mortality up to periods of 5.5 years,

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In the past thirty years, numerous observations have been made on the hemodynamic effects of arteriovenous fistulae. Arteriovenous fistulae of variable size and location have been studied in patients as well as in animals. Such studies have consisted a) in observing the effect of suddenly opening and closing a fistula in acute experiments, b) in studying the effects of suddenly closing and opening a fistula in an animal or a patient who had had such a fistula for a relatively long time, and c) in recording the effect of complete surgical eradication of a long-standing fistula. While some agreement has been reached on many points, there persists some controversy about most of them (1). It is now generally agreed that an acute as well as a chronic arteriovenous fistula increases the cardiac output (1-8). However, Lewis and Drury (9) came to the conclusion that the cardiac output is not increased unless the arteriovenous shunt is very large. Van Loo and Heringman (10) concluded that acute arteriovenous fistulae increase the cardiac output although the flow of blood in certain vascular areas outside the fistula circuit is decreased. The venous pressure is definitely increased near the site of the arteriovenous communication, but most investigators have found that the increment of venous pressure decreases rapidly as the pressure is measured further down the venous bed toward the right atrium, and in the venae cavae and right atrium the pressure is elevated little or not at all I This work was made possible by a grant-in-aid from the New York Heart Association, the Sidney A. Legendre Gift, and the Charles A. Frueauff Gift. It was presented at the Annual Meeting of the American Physiological Society in New York City in 1952.2Fellow of the New York Heart Association. (3, 4, 11). However, one group of workers (12) has reported more striking increases of right atrial pressure in dogs with an arteriovenous fistula. The blood volume seems to be increased by an arteriovenous fistula of a certain size and duration (3, 13) although some observers (4) suggest that this increase in blood volume occurs only in the presence of an incipient or frank cardiac failure.Since the magnitude of the effects of an arteriovenous fistula would seem a priori to depend upon the volume of blood shunted through the abnormal pathway, it is rather surprising that in no study has any attempt been made to measure simultaneously the rate of flow through the fistula and the other functions of interest such as cardiac output, arterial and venous pressures. The present study was undertaken in an attempt to determine the acute cardiovascular adjustments to arteriovenous fistulae of different sizes, by recording simultaneously and continuously the flow of blood through the fistula, the flow of blood into the systemic circulation exclusive of the arteriovenous fistula circuit, the mean arterial blood pressure and the mean central venous pressure. METHODSFifteen dogs weighing between 13 and 28 kilograms were anesthetized by the intravenous infusion of 100 m...

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