Exercise testing early after myocardial infarction.

A consecutive series of 179 survivors of acute myocardial infarction had a symptom-limited 12-lead electrocardiographic treadmill exercise test, coronary angiographic studies, and left ventriculograms six to eight weeks after infarction. The exercise-induced ST-segment responses were correlated with the presence of multivessel disease, the presence of advanced left ventricular wall motion abnormalities (LVWMA), and ejection fraction. Each type of ST-segment response in patients after infarction has its own specific predictive value. ST-segment depression indicated multivessel disease. ST-segment elevation indicated advanced LVWMA and low ejection fraction. Concomitant ST-segment depression and ST-segment elevation indicated both multivessel disease and advanced LVWMA.

Prognostic value of exercise testing, coronary angiography and left ventriculography 6--8 weeks after myocardial infarction.

This study provides data on a consecutive series of 179 survivors of acute myocardial infarction (MI) who had symptom-limited treadmill exercise testing, coronary angiography and left ventriculography within 6--8 weeks after infarction. No patient died. The prevalence of multivessel disease was higher in the symptomatic survivors (79%) (p less than 0.001). The prevalence of multivessel disease in inferior MI was 63% and in anterior MI 42% (p less than 0.001). Left ventricular impairment was more severe in anterior and preexisting MI than in inferior and nontransmural MI (p less than 0.005). During a mean follow-up of 28 months, 11 cardiac deaths and 12 reinfarctions occurred. The total mortality rate was 22% (10 of 46) in patients with an ejection fraction less than 30% or three-vessel disease and 1% (one of 133) in patients with an ejection fraction greater than or equal to 30% and one- or two-vessel disease (p less than 0.001). A group at high risk of mortality is thus identified by angiography. The total reinfarction rate was 9% (11 of 121) in patients with an exercise tolerance of less than 10 minutes (Bruce protocol) and 2% (one of 58) in patients with an exercise tolerance of 10 minutes or more (p less than 0.1). The 58 patients who had an exercise tolerance of 10 minutes or more had a very low risk for cardiac death or reinfarction.

Sympathetic and parasympathetic cardiac control in athletes and nonathletes at rest.

A simple model to characterize sympathetic and parasympathetic effects on heart rate (R) was tested during rest in 10 nonathletes and 8 world-class oarsmen. The model states that R = mnR0, where R0 is the intrinsic cardiac rate, and m and n depend only on sympathetic and parasympathetic activity, respectively. The multipliers, m and n, were determined by dual pharmacological blockade in two sessions under similar conditions, but in one session propranolol and in the other atropine was given first. In agreement with the model, when corrections were made for atropine-induced blood pressure changes, m and n did not depend on which blocking agent was administered first. In athletes the control heart rate [55 +/- 3.3 (SD) beats/min] and R0 (81 +/- 8.3 beats/min) were lower than in nonathletes (62 +/- 6.0, P less than 0.01 and 102 +/- 11, P less than 0.001, respectively). The sympathetic multiplier, m, was similar (1.18 +/- 0.06 vs. 1.20 +/- 0.05, P greater than 0.4) in the two groups, but n, the parasympathetic multiplier, was closer to 1 in the athletes (0.57 +/- 0.03 vs. 0.51 +/- 0.05, P less than 0.01). We conclude that the model is suitable for the quantitative study of sympathetic/parasympathetic heart rate control in humans, and that the lower resting heart rate in oarsmen is solely due to a reduction in intrinsic cardiac rate, and not to an increase in parasympathetic tone.

Complete heart block. Studies of atrial and ventricular pacemaker site and function.

Atrial and ventricular pacemaker function was studied in 20 patients with idiopathic chronic complete heart block using the rate response to an intravenous bolus dose of isoprenaline (5 mug/70 kg bodyweight). Pacemaker responses were compared with those of 16 normal control subjects. None of the patients was having syncopal attacks at the time of admission and they were therefore selected in that none required immediate pacing. Ten of the patients had His bundle electrograms; all were shown to have a pre-His type of atrioventricular block. Two major groups emerge from the responses to isoprenaline. (a) High risk group: 11 of the 14 patients with reduced ventricular pacemaker responses had frequent syncopal attacks; 8 of the patients with Adams-Stokes syncope had a bundle-branch block pattern, while 3 had a narrow QRS. These patients require pacing. (b) Low risk group: a low risk asymptomatic group (5 patients) was identified with atrial and ventricular responses to isoprenaline within normal range. One of these patients had a bundle-branch block pattern, while 4 had a narrow QRS. These patients might be managed without pacing. The atrial response to isoprenaline was reduced in 12 of the 20 cases, 10 of whom also had reduced ventricular responses. All 9 patients with bundle-branch block had reduced ventricular responses, while 7 had reduced atrial responses. This evidence indicates that cardiac conducting tissue pathophysiology is widespread in complete heart bolck. The present work suggests that consideration of the ventricular pacemaker function is important in assessing liability to syncope in complete heart block. While patients with Adams-Stokes attacks require pacing it is suggested that all asymptomatic patients with complete heart block and those with minor symptoms are assessed using studies of both ventricular pacemaker function and site. A low risk group not requiring a pacemaker may emerge after sufficient follow-up assessment.

Sinoatrial block. Autonomic influences and clinical assessment.

Seventeen patient with sinoatrial block and 16 healthy volunteers were investigated with recently developed autonomic tests of atrial pacemaker function. Only one patients was found to be entirely normal in comparison with normal subjects, while another patients had supernormal responses. Fifteen patients had reduced responses relative to the controls implying impaired atrial pacemaker function or sinoatrial disease. It is suggested that while in some cases sinoatrial block may be of physiological origin, it is more often due to sinoatrial disease. The latter group are liable to Adams-Stokes syncope and may have additional atricventricular conduction abnormalities. The possible mechanisms and treatment of sinoatrial block are discussed relative to the autonomic and pacemaker function abnormalities described.