Infarction-associated pericarditis. Rarity of diagnostic electrocardiogram.

To examine how often pericarditis is associated with myocardial infarction and how often it is diagnosable by electrocardiographic changes, we determined the frequency of diagnostic (Stage I) ST-segment changes in 423 consecutive patients admitted to the coronary-care unit. Careful auscultation and electrocardiography were performed at least once daily in all patients and at least twice daily in those presenting with new chest pain of any description or a pericardial rub. Thirty-one patients had pericardial rubs, usually detected within the first four days after admission. Only 1 of the 31 had diagnostic electrocardiographic changes. The 31 patients with pericarditis differed significantly from the 392 patients without pericarditis in several respects: male predominance; Killip Classes II, III, and IV; and Q-wave infarcts. However, differences in the location of the infarct and in mortality were not statistically significant. We conclude that during acute infarction-associated pericarditis the pericardial rub is the most frequent clinical sign, and ST-segment changes diagnostic of pericarditis are rare. Our findings are consistent with the confinement of pericardial involvement to the infarct zone.

Association of acute respiratory symptoms with onset of acute myocardial infarction: prospective investigation of 150 consecutive patients and matched control patients.

Among 150 prospectively investigated patients with acute myocardial infarction (MI) and 150 control patients matched for age, sex and admission date, acute respiratory symptoms occurred in 42 MI patients and in 23 control patients (p less than 0.02). Matched-pairs analysis gave an odds ratio for a respiratory syndrome of 2.2:1 for MI. The statistically significant association of minor respiratory syndromes and the onset of MI must be further investigated to determine whether there is any pathogenetic relation of respiratory symptoms, presumably virally induced, to the onset of MI.

Efficacy of mexiletine in chronic ventricular arrhythmias compared with quinidine: a single-blind, randomized trial.

This single-blind, randomized study was designed to evaluate the efficacy and safety of oral mexiletine compared with oral quinidine in suppressing premature ventricular contractions (PVCs). Fifty-one patients were studied for less than or equal to 12 weeks; 26 patients were randomized to the mexiletine group and 25 to the quinidine group. The drugs were administered in an increasing dose regimen to suppress the PVCs by 70% from the baseline value in both groups. Mexiletine reduced the average number of PVCs by 70% of the baseline number in a comparable fashion to quinidine; 69% in the mexiletine group vs 70% in the quinidine group (p greater than 0.05). There was a comparable reduction (greater than or equal to 50%) of ventricular couplets from the baseline value in the 2 groups, 78% in the mexiletine group vs 86% in the quinidine group (p greater than 0.05). The effect of mexiletine on suppression of ventricular tachycardia was also similar, 72% in the mexiletine group vs 71% in the quinidine group (p greater than 0.05). There was no significant difference in the 2 groups in side effects. This study shows the comparable efficacy and tolerance of mexiletine and quinidine for the control of ventricular arrhythmias in a large number of patients with diverse forms of heart diseases.

Respiratory effects on systolic time intervals during pericardial effusion.

Pericardial effusion without cardiac tamponade is defined by the detection of excessive pericardial fluid without clinical manifestations, particularly pulsus paradoxus (inspiratory decrease in systolic blood pressure greater than 10 mm Hg) and jugular venous distention. Nineteen consecutive patients without heart or lung disease who had pericardial findings and no evidence of tamponade were investigated by echocardiography: 14 with pericardial effusion and 5 with noneffusive ("dry") pericarditis. Patients with effusion had an inspiratory decrease in left ventricular ejection time (delta LVET) of 17.9 +/- 5.78 ms and an increase in preejection period (delta PEP) of 12.1 +/- 3.78 ms, each well beyond the respective respiratory changes measured in normal subjects. The 5 control patients with dry pericarditis had a mean delta LVET and delta PEP of only 8.0 and 7.0 ms, respectively. Of the 14 patients with effusion, 6 whose systolic pressure showed no respiratory change had mean delta LVET of 13.7 ms and delta PEP of 11.2 ms, comparable to the other 8 patients with effusion who had a respiratory change of 2 to 10 mm Hg. We conclude that although pulsus paradoxus was not present, excessive pericardial fluid is not physiologically inert. If a satisfactory echocardiogram is not available, exaggerated respiratory fluctuation in systolic time intervals may be evidence of excessive pericardial fluid.

Effects of nitroglycerin on isometric exercise.

Eight patients with ischemic heart disease performed isometric handgrip of five minutes' duration at 30% of their maximum voluntary contraction, before and after administration of 0.4 mg sublingual nitroglycerin (NTG). Although isometric exercise resulted in similar rise of left ventricular systolic pressure (LVSP) before and after NTG, the level of LVSP during the post NTG effort was lower. Heart rate, cardiac index, stroke index, left ventricular stroke work index, and systemic resistance were not different during the pre- and post NTG exercise. Left ventricular end-diastolic pressure rose to a significantly lower level (18.3 +/- 14.4 mm Hg) during the post NTG handgrip than during the pre NTG effort (31.4 +/- 17.6 mm Hg, P less than 0.005). It is concluded that NTG reduces preload and afterload both at rest and during isometric exercise and improves left ventricular performance during isometric exercise.

Atropine-induced cardioacceleration in patients on chronic propranolol therapy: comparison with the positive chronotropic effect of isometric exercise.

The hemodynamic effects of intravenous atropine administration were examined in 24 patients on chronic propranolol therapy. In the first 13 patients the safety of atropine administration was tested by giving the drug in small increments to a total dose of either 1.2 mg (five patients) or 1.7 mg (eight patients). The heart rate after atropine administration in these patients varied between 57 and 82 bpm and no adverse effects were noted. The other 11 patients received 1.2 mg atropine intravenously with hemodynamic measurements obtained prior to and 3 minutes after administration of the drug. Heart rate increased from 57.5 +/- 8.7 to 72.8 +/- 13.9 bpm, mean pulmonary arterial and left ventricular end-diastolic pressure declined, and cardiac index increased. Total systemic resistance decreased in most of the patients. Isometric exercise performed prior to atropine administration in the same 11 patients accelerated heart rate from 57.4 +/- 8.6 to 68.4 +/- 10.8 bpm. A close correlation, r = 0.909, was demonstrated between the postatropine heart rate and the rate during isometric exercise. It is concluded that atropine in a dose of 1.2 to 1.7 mg may be administered safely in patients on chronic propranolol therapy. Isometric exercise may be useful in unmasking vagal tone in beta-blocked patients.

Cardiovascular responses to isometric exercise in patients with mitral stenosis. Comparison with normal subjects and patients with depressed ejection fraction.

The hemodynamic response to isometric handgrip was evaluated in 15 patients with mitral stenosis (MS), 12 normal subjects, and 13 patients with severe left ventricular failure (LVF). Acceleration of heart rate and rise in left ventricular systolic pressure were not significantly different between the three groups. Left ventricular end-diastolic pressure did not change in normal subjects and patients with MS during handgrip, but it was raised markedly in patients with LVF. Cardiac index increased in normal subjects but did not change in patients with MS and LVF. Stroke index declined in patients with LVF. In all groups there was a modest and similar increase in oxygen consumption and significant widening of the arteriovenous oxygen difference in patients with LVF. In patients with MS, pulmonary capillary pressure increased by an average of 10.6 mm Hg, with a parallel rise in mean pulmonary vascular resistance. It is concluded that patients with MS demonstrate a normal chronotropic and pressor response to isometric exercise. Normal left ventricular end-diastolic pressure response to isometric handgrip stress in patients with MS suggests good left ventricular performance.

Left ventricular diastolic capacity in man.

Plasma volume expansion with 500 ml of low-molecular-weight dextran was used in 27 patients (nine normal subjects, 13 patients with ischemic heart disease, four with aortic stenosis and one with cardiomyopathy) to increase left ventricular end-diastolic pressure (LVEDP) from a control value of 12.4 +/- 7.0 mm Hg (mean +/- SD) to 23.3 +/- 7.0 mm Hg and end-diastolic volume (EDV) from 84.0 +/- 23.8 ml/m2 to 97.6 +/- 22.9 ml/m2. EDV-LVEDP curves constructed for 12 patients from multiple angiograms at progressively increasing LVEDPs during plasma volume expansion showed an initial part where EDV increased in parallel with LVEDP and a final steep or perpendicular part where EDV increased minimally or not at all as LVEDP exceeded 20 mm Hg. Exponential equations were used to fit diastolic volume-pressure data obtained with catheter-tip manometers in seven patients: the exponential constant, k, was 0.012-0.044 ml-1 and was inversely related to EDV (Spearman's rank correlation coefficient = -1). For comparable EDV, there were no differences in k values between normal subjects and patients with a variety of heart diseases.

Responses of peak ear-pulse derivative to changing left ventricular function.

The ear densitograph displacement pulse derivative (dD/dtear) is the analog of the arterial pressure derivative (dP/dt) and behaves comparably under a variety of cardiocirculatory challenges. Technical reliability and uniform application of the transducer are advantages that make it ideal for intrasubject monitoring. With atrial fibrillation as a model of functional variability in eight subjects, peak dD/dtear (P) tracked echocardiographic stroke volume, ejection fraction, ejection rate, and velocity of circumferential fiber shortening quite closely with the exception of some values in three subjects, two of whom had mitral regurgitation and one paradoxic septal movement. In all subjects, P showed good to excellent correlations with cycle length, preejection period (PEP), LVET (left ventricular ejection time), and PEP/LVET. The method appears to be ideally suited to intrasubject monitoring for changing ventricular function.

Angiotensin II inhibition. Treatment of congestive cardiac failure in a high-renin hypertension.

A patient with intractable congestive cardiac failure secondary to renovascular hypertension and severe coronary artery disease was infused with the competitive antagonist of angiotensin II, saralasin acetate. The infusion produced an impressive increase in cardiac output and left ventricular stroke work index in parallel with a striking decrease in the systemic and pulmonary vascular resistance, the coronary resistance, and the myocardial oxygen consumption. It is suggested that angiotensin inhibition may present advantages over other forms of treatment of congestive cardiac failure in selected cases.

Psychological correlates of coronary angiographic findings.

Prior to undergoing diagnostic coronary angiography, 94 men responded to tests for the coronary-prone behavior pattern, anxiety, depression, and neuroticism. Independently, cardiologists rated cineangiograms by the percent of atheromatous luminal obstruction in four major coronary arteries. The patients with greater atheromatous obstruction scored significantly higher than those with lesser disease on all four scales of the test for the type A coronary-prone behavior pattern. Those with more seriously diseased vessels also scored significantly higher on anxiety and depression scales but significantly lower on a denial scale. Men rated as having more frequent and intense angina pain scored significantly higher on hypochondriasis, depression, and admission of symptoms than men less subject to ischemic pain. Multivariate statistical analyses revealed that the findings regarding extent of atherosclerosis are independent of anginal pain or congestive heart failure.

Effects of isometric exercise on the end-diastolic pressure, volumes, and function of the left ventricle in man.

Changes induced in left ventricular (LV) hemodynamics by isometric exercise were analyzed in 43 patients: 30 with coronary heart disease (CAD), four with noncoronary heart disease, nine normal. Volumes were angiographically determined and correlated with left ventricular end-diastolic pressure (LVEDP) both at rest and during the fifth minute of 30% sustained handgrip (HNG). All normals and eight with CAD improved LV function during HNG. LVEDP decreased or remained constant, end-diastolic volume (EDV) decreased, end-systolic volume (ESV) decreased, as ejection fraction (EF) remained constant. None of these eight CAD cases altered their regional LV contraction pattern during HNG. Twenty-five patients, 21 CAD and four nonCAD, showed diminished LV function during HNG. LVEDP increased, EDV decreased, ESV increased, as EF declined. In these 21 CAD patients, at least one major coronary vessel was narrowed 70% or more and, with but two exceptions, was not supported by adequate collaterals. In 18, new asynergic zones developed in previously normally contracting areas or pre-existing asynergic zones extended during HNG.

Vectorial characteristics of ventricular extrasystoles stimulated during cardiac catheterization.

Ventricular extrasystoles (VES) from different areas of the ventricular muscle mass were obtained by mechanical stimulation of inflow and outflow regions of the right ventricle (RV) and apical and basal portions of the left ventricle (LV) during cardiac catheterization. Cube system vectorcardiogram (VCG) patterns of VES from each location were analyzed to determine the specificity of vector orientation from each site. Transverse plane VCG distinguished between nonseptal LVES and RVES, while a combination of transverse and either sagittal or frontal planes permitted further localization of septal VES to inflow or outflow regions of the RV and apical and basal areas of the LV.

Atropine dose in acute myocardial infarction in man.

Heart rate response to intravenous atropine therapy in acute myocardial infarction (MI) was assessed from detailed studies performed on 18 of 492 consecutively admitted coronary care unit patients. Atropine was given for extreme bradycardia (less than 40/min) or bradycardia (less than 60/min) coincident with hypotension or ventricular premature beats. 14 patients had posterior and 4 anterior infarction. Degree of cardioacceleration evoked by atropine depended upon drug dose and route of administration. Atropine, 0.0053-0.0088 mg/kg, given within 15 sec increased heart rate by 20-72/min but never beyond a peak rate of 120. Larger atropine doses, 0.120-0.148 mg/kg, increased heart rate by 51-92/min and, in four to five instances to a peak rate exceeding 120/min. Intramuscular atropine was associated with paradoxical slowing of heart rate in one case. Multiple neural, hormonal, and circulatory factors can modify heart rate response to fixed amounts of intravenous atropine but 0.008 mg/kg represents a safe and suitable initial drug dose for use in acute MI.