Prevalence and reproducibility of exercise-induced ventricular arrhythmias during maximal exercise testing in normal men.

The occurrence of ventricular arrhythmias at rest or during ordinary daily activities has been implicated as a risk factor for future coronary-related events and sudden death. However, the clerical significance of exercise-induced ventricular arrhythmias remains uncertain. To assess the prevalence and reproducibility of such arrhythmias, two serial maximal treadmill exercise tests were performed in a study population of 543 male Indian State policemen at an average interval of 2.9 years. Four hundred sixty-two subjects were clinically free of evidence of cardiovascular disease, and 81 had evidence of definite or suspected cardiovascular disease. The prevalence of exercise-induced ventricular arrhythmias during the first test was 30% in men aged 25 to 34 years, 32% in those aged 35 to 44 years and 36% in those aged 45 to 54 years. The prevalence rate in these age groups with repeat testing was 36, 38 and 42%, respectively. These differences were not statistically significant. The group with definite or suspected cardiovascular disease had a greater prevalence of exercise-induced ventricular arrhythmias than normal subjects during both tests but the prevalence rate with repeat testing remained constant. The occurrence of exercise-induced ventricular arrhythmias was reproducible in individual subjects during the second test in 55% of 25 to 34 year olds, 58% of 35 to 44 year olds and 62% of 45 to 54 year olds. Thus, individual reproducibility in two consecutive tests was only slightly greater than reproducibility by chance alone. The group with known or suspected cardiovascular disease demonstrated a trend toward greater reproducibility with repeat testing. Exercise-induced ventricular arrhythmias were not reproducible by type or complexity. The marked variability of exercise-induced ventricular arrhythmias during repeat maximal exercise testing in a clinically normal population appears to negate the usefulness of this finding during a single test as a marker of future cardiovascular disease. Nevertheless, subjects whose arrhythmias were reproducible may form a group destined to manifest clinical cardiovascular disease in long-term follow-up studies.     

Atropine-induced cardioacceleration and myocardial blood flow in subjects with and without coronary artery disease

Thirty-five patients being studied by coronary cineangiography for diagnosis or evaluation of coronary atherosclerotic occlusive disease had myocardial blood flow determinations at rest and after intravenous administration of atropine sulfate, 1.0 mg. Myocardial blood flow was determined by a coincidence counting system and a single bolus injection of ⁸⁴rubidium chloride.In 10 patients without coronary occlusive disease, heart rate increased by 52 percent and myocardial blood flow by 48 percent (P < 0.001, r = 0.888). In 14 patients with single vessel disease or partial occlusion of two vessels, myocardial blood flow increased by 44 percent and heart rate by 37 percent (P <0.05, r = 0.553). In 11 patients with two or three vessel occlusive disease, heart rate increased by 30 percent whereas myocardial blood flow increased by only 15 percent (r = ?0.172).We conclude that patients with two and three vessel involvement by atherosclerotic occlusive disease are unable to increase nutrient myocardial blood flow in response to atropine-induced Cardioacceleration to the same degree as patients without coronary disease or with less extensive disease. The observation may be of therapeutic importance because of the potential that administration of atropine may have for inducing myocardial ischemia in such patients.     

Role of echocardiography in patients with coronary artery disease.

Impaired left ventricular performance, one of the hallmarks of coronary artery disease, can be detected by echocardiography in various ways. One of these approaches is the recording of abnormal wall motion. Because of the way in which the left ventricle can be examined echocardiographically, this technique has the capability of detecting regional wall abnormalities. In fact echocardiography is probably the most sensitive technique available, including even contrast ventriculography, for the detection of akinetic, hypokinetic or dyskinetic wall segments. With increasing experience it is apparent that more areas of the left ventricle can be examined echocardiographically than had previously been thought possible. Newer techniques include directing the ultrasonic beam not only through the body of the left ventricle but also toward the apical portion of the ventricle near the vicinity of the papillary muscles. In addition the true anterior left ventricular wall can be examined by moving the transducer laterally away from the left sternal border. Yet another approach utilizes a subxiphoid position for the transducer while the ultrasonic beam is directed through the medial portion of the septum and posterolateral wall of the left ventricle. M-mode scanning techniques together with recently developed cross-sectional echocardiographic instruments give great promise of improved detection of abnormalities of ventricular shape, especially the presence of aneurysms. The cross-sectional approach makes it possible to examine the left ventricular apex, an area virtually impossible to record with M-mode echocardiography. Recording of left ventricular dimensions and abnormal mitral valve motion may help in assessing overall left ventricular performance. A dilated left ventricular dimension in the vicinity of the mitral valve seems to be an ominous finding both in patients with acute myocardial infarction and in patients with chronic coronary disease being considered for possible surgery. Another echocardiographic sign of abnormal ventricular performance is altered closure of the mitral valve, which reflects a significantly elevated left ventricular diastolic pressure. These echocardiographic techniques are still in the investigational stages and are more technically difficult than the usual echocardiographic applications. However, the preliminary data are encouraging and make us hopeful that echocardiography will prove to be an important tool in the overall evaluation of the left ventricle in patients with coronary artery disease.     

Anterior left ventricular wall echoes in coronary artery disease. Linear scanning with a single element transducer

The feasibility and usefulness of obtaining anterior left ventricular wall echoes were studied using a linear cardiac scan with a single element tranducer and M mode recordings. One hundred four patients were examined: 50 with acute myocardial infarction and 54 who underwent left ventricular angiography and coronary cineangiography for evaluation of chest pain. Of the 54 patients with cardiac catheterization studies, 11 had no evidence of cardiac disease, 42 had 50 percent or greater obstruction in one or more of the three major coronary arteries and one had aortic insufficiency. Anterior left ventricular wall echo motion toward the transducer or absence of motion during ejection was called abnormal, and motion away from the transducer during ejection was interpreted as normal. Abnormal motion was seen in four of four patients with an isolated lesion of the anterior descending coronary artery, in one of three with an isolated lesion of the right coronary artery and in neither of two with an isolated lesion of the left circumflex artery. Of the 20 patients with obstructive coronary artery disease by arteriography and abnormal left ventricular wall echo motion, 18 had obstruction of the left anterior descending artery with or without other disease. Correlation of the anterior left ventricular echograms with the left ventricular angiograms was poor, with agreement in only 66 percent (33 of 50) of cases. Twenty-five of 26 patients with acute infarction and abnormal anterior left ventricular wall echo motion had electrocardiographic changes indicative of anterior or lateral wall infarction, or both. Twenty-five of 34 patients with electrocardiographic changes indicative of anterior wall infarction had an abnormal anterior wall motion echo. This study shows that obtaining the anterior left ventricular wall echo is feasible and useful in patients with coronary artery disease since abnormal anterior left ventricular wall motion is closely associated with anterior wall ischemia or infarction in these patients.     

Coronary angiographic, echocardiographic, and electrocardiographic studies on a patient with variant angina due to coronary artery spasm.

A 45-year-old Caucasian female patient with a clinical rehistory and ECG's conforming to the syndrome of variant angina as characterized by Prinzmetal is presented. ECG's recorded during spontaneous pain demonstrated ST-segment elevation and symmetrical peaking of the T-waves in the lateral precordial leads and short runs of ventricular tachycardia. Similar ECG changes were recorded during treadmill exercise- and hand-grip exercise-induced chest pain. An echocardiogram recorded during angina induced by hand-grip exercise demonstrated progressive flattening of septal motion. Multiple views of the coronary system by selective coronary cineangiography were normal with the patient at rest. Angina was then induced by hand-grip exercise and a repeat right anterior oblique view of the left coronary system revealed marked spasm of the left anterior descending artery proximal to the first septal perforator.     

Diastolic heart sound produced by mid-diastolic closure of the mitral valve

Mid-diastolic closure of the mitral valve is suggested as the source for an audible diastolic sound in a patient with aortic valve and coronary artery disease. On the apex cardiogram the sound followed the rapid filling wave by 60 msec and preceded the a wave. On the echocardiogram the sound corresponded to premature closure of the mitral valve in mid-diastole. In this case an audible diastolic sound that appeared to originate from mid-diastolic closure of the mitral valve indicated a rapidly increasing left ventricular diastolic pressure with severe left ventricular failure. After treatment of the congestive heart failure, the sound diminished in intensity.     

Echocardiographic patterns of pulmonary valve motion in valvular pulmonary stenosis

Echocardiographic tracings of the pulmonary valve were examined in 14 patients with isolated pulmonary stenosis, 20 normal subjects, 26 patients with pulmonary hypertension, 10 patients with a left to right shunt and 28 patients with various forms of heart disease other than pulmonary stenosis. Because of the plane of pulmonary valve motion and the angle of the ultrasonic beam, usually the echoes from only one posterior pulmonary leaflet were recorded. In normal patients atrial systole caused slight posterior motion of the pulmonary valve leaflet in late diastole (average 3, range 0 to 7 mm). The degree of valvular motion after atrial systole (the a wave) increased with inspiration. The position of the leaflet at the onset of ventricular systole varied with the depth of the a wave and the length of the P-R interval, but in the normal subjects the leaflet always returned to a base line or closed position at some time during the respiratory cycle. In 10 patients with moderate or severe pulmonary stenosis (gradient 50 to 142 mm Hg) the depth of the a wave increased markedly (average 10, range 8 to 13 mm). In patients with a gradient of more than 65 mm Hg (8 of 10) the leaflet never returned to a base line or closed position before ventricular systole. In three of four patients with mild pulmonary stenosis (gradient less than 50 mm Hg) and all patients with a left to right shunt or heart disease without pulmonary involvement the a wave was within the normal range. In 25 of 26 patients with pulmonary hypertension no a wave was present. In moderate to severe pulmonary stenosis, the exaggerated leaflet motion after atrial systole probably reflects increased right ventricular end-diastolic pressure and force of atrial contraction which, in the face of a normal or reduced pulmonary arterial pressure, produces a positive gradient across the valve in end-diastole.     

Role of exercise stress testing in healthy subjects and patients with coronary heart disease. Controversies in cardiology--I.

The value of the exercise stress test in the evaluation of clinically healthy subjects and patients with coronary heart disease is not limited to the isolated interpretation of abnormalities of the S-T segment. Other measurable parameters which are of diagnostic and prognostic importance include: (1) a decrease in systolic blood pressure during exercise; (2) the appearance of complex ventricular arrhythmias of low exercise heart rates; (3) the appearance of inverted U waves during or after exercise; (4) the patient's maximal exercise capacity; and (5) new auscultatory findings postexercise. The reliability of the exercise test as a diagnostic tool is futher enhanced by proper patient selection and careful attention to exercise techniques. Subjects with labile ST-T wave changes during standing hyperventilation, fixed ST-T changes at rest, and intraventricular conduction defects are not ideal candidates for "diagnostic" stress testing and the examining physician must rely more heavily on nonelectrocardiographic findings. The criteria used to define an abnormal S-T response will vary according to the lead system used. However, in both symptomatic and asymptomatic subjects the appearance of marked degrees of S-T depression at low exercise heart rates significantly increases the probability of finding advanced coronary disease, particularly if the S-T depression is seen in multiple monitoring leads and is of prolonged duration postexercise.     

Nonparoxysmal junctional tachycardia in acute myocardial infarction: Computer-assisted detection

Thirty consecutive patients with acute myocardial infarction had continuous magnetic tape recording of their electrocardiograms (lead II) for the period of their stay in the coronary care unit. Analysis of the 24 hour tape recordings was implemented on a Honeywell model 316 digital computer.

In the first 24 hours after admission to the coronary care unit, 12 of the 30 patients (40 percent) exhibited nonparoxysmal junctional tachycardia; in 5 the arrhythmia was not recognized by conventional monitoring techniques. For the subsequent 3 days, the incidence rate of the arrhythmia was 13 percent for the first 48 hours and 3 percent for 72 hours. Although the mortality rate in patients with nonparoxysmal junctional tachycardia was greater than in patients not demonstrating the arrhythmia (33 versus 6 percent), there was a greater percentage of patients with anterior infarction in the former group; therefore, mortality may have been related to site of infarction rather than being reflective of the arrhythmia or its associated pathophysiologic state. Of possible significance is the association of a greater degree of sinus arrhythmia with nonparoxysmal junctional tachycardia.

The incidence of nonparoxysmal junctional tachycardia in this group of patients was greater than previously reported. It is possible that computer tape analysis may have provided more accurate recognition of the arrhythmia and, thus, more realistic incidence data. The association of nonparoxysmal junctional tachycardia with sinus arrhythmia could only have been recognized by computer technique. The computer system is not a diagnostic system but rather a tape review method.     

Echocardiographic manifestations of discrete subaortic stenosis

The echocardiographic manifestations of discrete membranous subaortic stenosis are described in three cases. The diagnosis was confirmed by cardiac catheterization in all and at operation in two. The characteristic finding in these patients was abnormal movement of the aortic valve leaflets. The leaflets opened rapidly with the onset of systole, then exhibited abrupt premature closure shortly after ventricular ejection. The valve remained partially closed throughout the remainder of systole. This premature leaflet closure Is believed to be caused by obstruction to aortic valve flow produced by the band-like fibrous subaortic tissue. The valve leaflets also exhibited a gross fluttering motion possibly caused by a jet stream effect of the turbulent blood hitting the leaflets. In the two patients treated surgically, postoperative echograms continued to show premature leaflet closure but the degree of closure was decreased. The echocardlogram of one patient had the characteristic systolic anterior bulge of the mitral valve observed in muscular subaortic stenosis or idiopathic hypertrophic subaortic stenosis. Our data suggest that the following echocardiographic findings are suggestive if not specific for discrete subaortic stenosis: aortic valve closure early in systole, persistent valve closure throughout the remainder of systole, coarse fluttering of the leaflets, and absence of asymmetric septal hypertrophy.     

Evaluation of abnormal exercise electrocardiogram in apparently healthy subjects: Labile repolarization (ST-T) abnormalities as a cause of false positive responses

Long-term follow-up studies were carried out in 121 apparently healthy men with an abnormal S-T segment response to exercise—49 Indiana State policemen and 72 subjects from a large occupational health center. The mean follow-up periods were 66 months and 43 months, respectively, for the two groups of subjects. A tendency toward labile S-T or T wave abnormalities were documented during standing rest or with hyperventilation in 61 of these 121 subjects and there was only one new coronary event in this subgroup. The labile ST-T wave changes and the abnormal S-T segment responses to exercise were not consistently reproducible in these subjects, and it was not unusual to see an abnormal S-T segment response at a time when the labile repolarization changes could not be demonstrated. Many of the subjects exhibited labile ST-T wave changes only after oral glucose loading. Significant coronary artery disease was documented in 34 (57 percent) of the remaining 60 subjects during the follow-up period.Coronary cineangiographic studies, obtained in 21 of the 35 subjects from the health center who had had no evidence of labile ST-T wave abnormalities, revealed coronary arterial stenoses of 75 percent or greater in 19. A statistical analysis was carried out in the 35 subjects without labile ST-T abnormalities to determine if there were exercise test variables that would differentiate the true positive from the false positive responses. A set of criteria were identified that yielded a specificity of 92 percent, a sensitivity of 82 percent and a predictive value of 95 percent. The entire group of 72 from the health center subjects had undergone an average of 3.8 exercise tests before their referral to the authors' laboratory. A review of these records revealed that a serial conversion from a normal to an abnormal S-T segment response was not more predictive of underlying coronary artery disease than an initially abnormal test result.     

Cross-sectional echocardiography in evaluating patients with discrete subaortic stenosis

Ten patients with discrete subvalvular aortic stenosis were examined using a real time, high resolution cross-sectional echocardiographic scanner. There were two patients (Group I) with a thin discrete subvalvular membrane, five (Group II) with a more extensive area of subvalvular narrowing and three with a residual area of outflow tract obstruction after surgical revision (Group III). In patients with a thin obstructing membrane (Group I), two distinct linear echoes were observed in the outflow tract. These echoes were not continuous with the walls of the outflow tract and showed some dynamic motion during the cardiac cycle. In four of the five patients with diffuse outflow tract narrowing (Group II), a relatively extensive area of inward bowing of both the anterior and posterior margins of the outflow tract was noted. In the fifth case, there was a prominent localized shelf-like increase in thickness of the basal portion of the muscular septum with a corresponding echo projecting anteriorly from the mid-portion of the anterior mitral leaflet. The three cases examined after surgical revision of the outflow tract (Group III), had different patterns of outflow tract narrowing, but narrowing was clearly demonstrated. This study suggests that cross-sectional echocardiography offers an alternative and probably improved method for the noninvasive visualization of the left ventricular outflow tract.     

Computer detection of premature ventricular complexes: A modified approach

The accuracy of a data reduction system for arrhythmia detection in identifying premature ventricular complexes was evaluated in continuous tape records of 30 patients in a coronary care unit. Computer analysis was performed with a Honeywell 316 digital computer. Threshold values for dominant complexes were automatically determined and recognition of premature ventricular complexes was based on differences in QRS configuration, timing and T wave configuration from the dominant complexes. Verification of the computer accuracy in detecting premature ventricular complexes was made with visual beat by beat inspection using a two channel strip chart recorder with simultaneous recording of the electrocardiogram and computer signal. This procedure allowed for exact beat to beat correlation and, thus, absolute determination of false positive and false negative identifications.From 0.5 to 6 continuous hours of monitoring per patient (average 3.5 hours) were analyzed for a total of 105 monitoring hours. The basic cardiac rhythms noted were normal sinus rhythm, sinus arrhythmia, sinus tachycardia, demand pacemaker rhythm, atrial fibrillation and atrioventricular (A-V) dissociation with junctional rhythm. Premature ventricular complexes were evident in 28 tapes (93 percent) including 12 (43 percent) with multifocal premature ventricular complexes and 3 (11 percent) with ventricular tachycardia. The visual count of premature ventricular complexes totaled 7,921. Of these, 7,542 (95 percent) were properly classified by the computer. The total computer count was 8,717, representing a 13 percent false positive and 5 percent false negative identification rate. The false positive identifications of premature ventricular complexes occurred during periods of 10 seconds or more of continuous noise artifact and in the presence of atrial premature complexes conducted aberrantly. When these sections of tape were excluded, the computer had a less than 2 percent false negative and 3 percent false positive rate of identification of premature ventricular complexes.     

Dissociation of the inotropic effect of digitalis from its effect on atrioventricular conduction.

The relation between sequential changes in left ventricular contractility and atrioventricular (A-V) nodal conduction and refractoriness was assessed in open chest dogs during intravenous administration of acetylstrophanthidin (5 mug/kg) at 5 minute intervals until toxic arrhythmias developed. At each time interval, high fidelity left ventricular pressure, its electronic derivative (dP/dt) and a His bundle electrogram were simultaneously recorded and the A-V nodal refractory period was measured by graded trains of stimuli. Animals were studied with an intact autonomic state (Group I), with pharmacologic blockade of both the beta adrenergic and parasympathetic system (Group II) and with parasympathetic blockade (Group III). Whereas contractility increased in response to small doses of digitalis, displaying a linear dose-response relation independent of autonomic tone, A-V nodal transmission indexes responded minimally to less than 50 percent of the toxic dose of digitalis, and the response was dependent upon autonomic tone. These results indicate a dissociation between the effects of digitalis on contractility and A-V transmission in that the major drug action on the ventricular contractile mechanism is a direct, linear one in contrast to the nonlinear response of A-V nodal transmission, which is predominantly mediated through the autonomic system. Clinically, these observations imply that the optimal dose and serum level of digitalis required to treat congestive heart failure may differ significantly from those required to treat supraventricular tachycardias, the therapeutic response of the latter being largely determined by the underlying autonomic tone.     

"Presystolic" augmentation of diastolic heart sounds in atrial fibrillation.

In the presence of atrial fibrillation, the diastolic murmur of mitral stenosis can appear augmented during early systole before the mitral valve closure sound. This phenomenon has previously been thought to be due to increased blood flow velocity across the narrowing mitral valve orifice. We have observed patients in whom the third heart sound (S3) gallop, the diastolic flow murmur of atrial septal defect and mitral insufficiency and the initial muscular component of the first heart sound become more intense during this period with short, critically timed cycle lengths. This phenomenon appears to be neither peculiar to nor indicative of mitral stenosis and is probably a direct result of the initial muscular contraction of an underfilled ventricle. Either the contraction itself or the sudden deceleration of the rapidly moving flow of blood across the atrioventricular orifice may produce the sound.     

Echocardiographic differentiation of infundibular from valvular pulmonary stenosis.

Echocardiographic tracings of the pulmonary valve were examined in 24 normal subjects, 16 patients with valvular pulmonary stenosis and 3 patients with infundibular pulmonary stenosis. In normal subjects, atrial contraction produced a slight posterior opening motion of the pulmonary valve leaflet (a wave). This presystolic opening motion (a wave) varied with respiration, and maximal a wave depth recorded during quiet inspiration (Amax) averaged 3.7 plus or minus 1.2 (standard error of the mean) mm (range 2 to 7 mm). In the 10 cases with moderate or severe valvular pulmonary stenosis, increased force of right atrial contraction and elevated right ventricular end-diastolic pressure resulted in an increased posterior or opening motion of the pulmonary valve leaflet, and Amax averaged 9.6 plus or minus 2.0 mm (range 8 to 13 mm, P less than 0.001 versus normal). When both anterior and posterior leaflets were recorded, presystolic opening or doming of the valve was observed. In six cases of mild valvular pulmonary stenosis, Amax averaged 4 plus or minus 2.5 mm (not significant). In patients with infundibular pulmonary stenosis, marked chaotic systolic fluttering of the valve leaflet, which lies in the turbulent stream of blood distal to the obstruction, was recorded. This finding was never seen with valvular pulmonary stenosis. In two cases of mild infundibular pulmonary stenosis, the amplitude of presystolic opening motion was within the normal range of 3 and 7 mm. In one case of severe infundibular pulmonary stenosis, no presystolic opening motion was recorded, thus suggesting that the small pressure changes produced by atrial systole failed to reach the valve leaflets. Echocardiography, therefore, should be of use in differentiating valvular from infundibular pulmonary stenosis.