A six-week program of intensive training in seven patients with angina was carried out to determine the relative contributions to the improved exercise performance of altered circulatory response and enhanced myocardial oxygen delivery. Training resulted in a marked increase in exercise capacity: time to onset of angina (± S.E.M.) rose an average of 6.8 ± 1.5 minutes (p less than 0.01), and the intensity of exercise (measured by total body oxygen consumption) attained before the onset of angina increased 56 ± 19 per cent (p less than 0.005). The "triple product" (an index of myocardial oxygen consumption) at any level of exercise was less after training, thus accounting for part of the improved exercise capacity. In addition after training, a higher triple product could be achieved at the onset of angina, 4885 vs. 4300 (p less than 0.05), suggesting that training might improve myocardial oxygen delivery. Physical training thus seems to improve exercise performance consistently by reducing the responses of heart rate and arterial pressure to exercise. The data also suggest that myocardial oxygen delivery may be enhanced.
In contrast to previous opinions, recent investigations have suggested that increasing heart rate (HR) with atropine when moderate sinus bradycardia accompanies acute myocardial infarction is not necessarily beneficial. To further characterize the influence of vagally mediated changes in HR during ischemia, we evaluated the effects of atropine and of electric stimulation of the vagus nerves on the incidence of ventricular arrhythmias during acute coronary occlusion in closed-chest dogs. Protection from occlusion-induced arrhythmia was not observed when 28 dogs receiving atropine were compared with 27 control dogs. Rather, the total incidence of ventricular arrhythmias was significantly higher ( P < 0.05) and ventricular fibrillation tended to occur more frequently in the atropine-treated group. Moreover, fewer ventricular arrhythmias (and total absence of ventricular fibrillation or close-coupled premature beats) were noted in 12 control animals with spontaneous bradycardia (HR<60 beats/min) compared with 15 nonbradycardic animals. When vagal stimulation produced bradycardia (HR = 40-60 beats/min) during coronary occlusion, occurrence and character of ventricular arrhythmias were the same as in dogs with normal rates (HR = 80-100 beats/min). Although these results may not necessarily apply to man, further studies are needed before it can be assumed that all individuals with moderate bradycardia during acute myocardial infarction should receive vagolytic agents.
An ECG-gated, scintigraphic imaging procedure is described in which a complete, average cardiac cycle is visualized with high temporal resolution. The ability of this method to detect wall motion abnormalities and quantitate left ventricular function is illustrated in a patient with severe coronary artery disease. These results are compared to (contrast) angiographic findings in the same patient.
Diurnal patterns of plasma euglobulin fibrinolytic activity, estimated by the fibrin plate method, were determined in groups of young normal and older normal subjects, in subjects with type IV hyperlipoproteinemia, and in subjects with coronary artery disease who had normal lipid profiles. The marked diurnal increases in fibrinolytic activity observed in the young normal subjects were significantly reduced in a large percent of the older normal subjects and in most of the subjects with coronary artery disease or type IV hyperlipoproteinemia. Although not conclusive, these findings were compatible with the hypothesis that an impairment in the responsiveness of the fibrinolytic system may be related to the development of coronary artery disease.
Previous investigations have shown that a slower heart rate (HR) and myocardial ischemia independently diminish the electrical stability of the heart. It therefore was suggested that increasing heart rate during myocardial infarction might diminish the incidence of serious ventricular arrhythmias. However, since increased HR during experimental acute myocardial ischemia augments the degree of ischemia, an evaluation of the presumed "protective" effects of increased HR on the electrical stability of acutely ischemic myocardium was undertaken. The differences in refractory periods (RP) of eight contiguous areas of the left ventricle were determined as a function of HR. In nonischemic myocardium, the disparity of RP was less at an HR of 180 than 60. However, in ischemic myocardium the disparity increased in three of six animals as the HR was increased from 60 to 90, in seven of 10 animals as HR was increased from 60 to 120, and in all animals when the HR was increased from 60 to 180. The increased disparity of RP is believed to favor development of reentrant arrhythmia. The vulnerability of the heart to develop ventricular fibrillation was assessed by determining ventricular fibrillation threshold (VFT). During ischemia, VFT was not only an inverse function of HR but also was found to be independently influenced by electrical stimulation of the cervical vagus nerves. In the absence of vagal stimulation VFT was lowered in only one of four dogs as HR was increased from 50 to 90, but decreased 30% ( P < 0.01) as HR reached 120 and 74% at 180 beats/min. When vagal stimulation was used to control HR VFT was lowered 37% as HR was increased from 50 to 60 to 90 ( P < 0.05). We conclude that increasing HR within a physiologic range by diminishing vagal tone during myocardial ischemia decreases electrical stability of the ventricle by (1) increasing ischemia consequent to the rate-induced increase in myocardial oxygen requirements, and (2) a direct electrophysiologic action of the vagus on the ventricular myocardium.
Echocardiographic studies have demonstrated that the characteristic anatomic defect in idiopathic hypertrophic subaortic stenosis (IHSS) is asymmetric septal hypertrophy (ASH). Although echocardiographic diagnosis of ASH is extremely sensitive, occasionally adequate echocardiograms cannot be obtained. Moreover, echocardiographic assessment of the extent of the underlying cardiomyopathic process, known to be distributed nonuniformly, is limited to evaluation of the upper part of the ventricular septum and the posterobasal left ventricular (LV) free wall. To determine if a specific angiographic marker of ASH can be identified even in the absence of LV outflow obstruction, and to delineate the extent and degree of cardiomyopathic involvement of the ventricular septum and LV free wall in patients with ASH, septal and LV wall configuration and thickness were measured using simultaneous biventricular cineangiography. The ventricular septum was thicker in 16 patients with ASH (avg. 15.2 ± 1.5 mm) and in six patients with concentric left ventricular hypertrophy (LVH) due to aortic valve disease (avg. 12.8 ± 1.1 mm) than in seven normal subjects (avg. 6.7 ± 0.4 mm, P < 0.001). In normal subjects and in patients with concentric LV hypertrophy, the walls of the ventricular septum were parallel. In contrast, the walls diverged in ASH so that septal width increased significantly inferiorly. Thus, the ratio of upper to lower septal width was greater than 0.8 (avg. 1.04 ± 0.06 mm) in normals and LVH patients but less than 0.77 (avg. 0.70 ± 0.01 mm, P < 0.001) in ASH patients. Furthermore, upper septal width and the ratio of upper to lower septal width in ASH were significantly greater in seven patients with LV outflow obstruction than in six patients without obstruction, suggesting that the upper septum bulges into the LV outflow tract to a greater extent in obstructive ASH. In addition, the LV free wall in ASH was nonuniformly thickened, whereas in LVH the hypertrophy was uniform. We conclude that angiographic delineation of the septum and LV free wall 1) demonstrates abnormalities that distinguish ASH from normal and concentrically hypertrophied hearts, 2) demonstrates abnormalities that distinguish obstructive from nonobstructive ASH, and 3) aids in characterizing the distribution of myopathic involvement in patients with ASH.
The electrocardiographic response to exercise was compared with the results of coronary angiography in 89 patients with Type II hyperlipoproteinemia who had previous myocardial infarction or typical angina or both (43 patients) (Group A), "atypical angina" (16 patients) (Group B) or positive electrocardiographic response to exercise without other evidence of cardiac disease (30 patients) (Group C). Thirty-nine of 43 in Group A had ≥50 per cent stenosis, and 26 (67 per cent) of these 39 had negative exercise tests. In Group B, five of 16 had ≥50 per cent Stenosis, and three had positive exercise tests (one patient had a false-positive test). In Group C, eleven of 30 (37 per cent) had ≥50 per cent stenosis; however, nine (30 per cent) had minor stenoses (≤50 per cent), and 10 (33 per cent) normal coronary arteries. The diagnostic usefulness of exercise electrocardiography is limited. False-negative responses are frequent in patients with clinically suspected coronary disease, and false-positive responses frequent in asymptomatic patients. (N Engl J Med 293:367–371, 1975)
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