Irwin Hoffman

Left bundle branch block: A predictor of poor left ventricular function in coronary artery disease

Clinical, coronary arteriographic, and hemodynamic studies were performed in 55 patients with left bundle branch block (LBBB) and coronary artery disease and were compared with 110 patients consecutively matched for age and sex with ischemic heart disease but without LBBB. No significant differences were found in duration of symptoms or frequency of prior myocardial infarction, hypertension, or diabetes mellitus; however, the LBBB patients had a significantly (p less than 0.001) higher frequency of congestive heart failure (38.2% vs 11.8%) and cardiomegaly (63.6% vs 25.5%). An evaluation of severity of the coronary disease on the basis of subtotal vs total obstructive lesions, number of vessels involved, total coronary score, and individual coronary arteries involved revealed no significant differences between the groups. The LBBB patients had significantly (p less than 0.001) greater impairment of left ventricular function as reflected by the end-diastolic volume (107 +/- 43 vs 79 +/- 30 ml/m2), ejection fraction (0.35 +/- 0.19 vs 0.59 +/- 0.18), and frequency of an abnormal contractile pattern (91% vs 61%). Evaluating the LBBB patients on the basis of the QRS width and axis revealed no significant intragroup differences in clinical profile, severity of coronary disease, or left ventricular dysfunction. A prolonged PR interval (greater than or equal to 0.20 second) was associated with more severe coronary artery disease and an enlarged heart. This study indicates that coronary artery disease associated with LBBB identifies patients with severe left ventricular dysfunction.

Atrial transport function in coronary artery disease: Relation to left ventricular function

The atrial contribution to ventricular stroke volume was evaluated in 50 patients with coronary artery disease and found to be related to left ventricular function. All patients underwent complete hemodynamic and angiographic studies. Angiographic volume studies were utilized to determine atrial contribution to the stroke volume, end-systolic volume and ejection fraction. In 11 patients without heart disease, atrial contribution to stroke volume was (mean value +/- standard deviation) 9.3 +/- 6 ml/m2 compared with 13.5 +/- 6 ml/m2 in the patients with coronary disease (probability [p] less than 0.05). The percent of atrial contribution to stroke volume was 20 +/- 7 and 33 +/- 11%, respectively, in normal subjects and patients with coronary disease (p less than 0.05). The combination of congestive heart failure and cardiomegaly was the only clinical aspect associated with a significantly higher (p less than 0.05) atrial contribution to stroke volume than that in the remaining patients with coronary disease (46 versus 31%). Relating the atrial contribution to stroke volume to the left ventricular end-diastolic pressure, stroke volume, end-systolic volume and ejection fraction revealed correlation coefficients of 0.30, -0.44, 0.56 and -0.64, respectively. No patient with a normal ejection fraction (greater than 0.50) had an atrial contribution greater than 40% of stroke volume. The ratio of peak left ventricular systolic pressure/end-systolic volume (mm Hg/ml) was 2.7 +/- 1.5 in patients (n = 14) with an atrial contribution greater than 40% of stroke volume compared with 5.3 +/- 3.4 in patients having an atrial contribution of 40% or less (p less than 0.01). These findings indicate that atrial contribution to stroke volume is inversely related to left ventricular function.

Significance of new Q waves after bypass grafting: Correlations between graft patency, ventriculogram, and surgical venting technique

New postoperative electrocardiographic Q waves have been described in eight of 40 per cent of patients undergoing bypass grafting for coronary artery disease. Various theories have been proposed to explain these new Q waves. Correlations of new Q waves to vein bypass occlusion, prolonged pump time or aortic cross-clamping time are controversial. Indeed, whether or not the appearance of new postoperative Q waves means real transmural myocardial infarction is not clear. We report herein our experience with postoperative Q waves in 56 patients with vein bypass grafts and the relationship of new Q waves to ventricular venting, graft patency, and the postoperative ventriculogram. Our observations indicate that: (1) Not all Q waves are due to occlusion of the saphenous bypass grafts (as noted by others). (2) A certain percentage of new Q waves may not reflect true transmural myocardial infarction, especially when all the vein grafts are patent and the postoperative ventriculograms show improvement. (3) Some new Q waves reflect true transmural infarction due to occlusion of grafts or of distal coronary arteries with deteriorated left ventriculograms. (4) The high incidence of new Q waves in patients with ventricular vents is probably due to direct myocardial trauma at the apex of the left ventricle.

ABERRANT BEATS OF WOLFF-PARKINSON-WHITE CONFIGURATION IN ARTERIOSCLEROTIC HEART DISEASE

Evidence has been presented by Prinzmetal et al. (1952) and Borduas et al. (1955) that electrocardiographic beats characterized by short P-R and long QRS intervals may occur in the absence of an accessory pathway by-passing the A-V node. In animal experiments, Prinzmetal observed beats ofWPW type after repeated electrical stimulation of the A-V node, and noted in these same animals the spontaneous occurrence of various supraventricular tachycardias. Several arteriosclerotic patients studied by Prinzmetal demonstrated similar electrocardiographic phenomena, and at necropsy were found to have fibrotic disease of the A-V node and no accessory conduction system. These clinical and experimental observations indicate that WPW beats may occur on an acquired basis, secondary to nodal disease. In other experiments, Prinzmetal induced beats ofWPW type in dogs after repeated ventricular stimulation with the A-V node intact. These observations harmonize with those of Kossman et al. (1950) who recorded such beats during cardiac catheterization when the catheter was in direct contact with the endocardial surface. Similar complexes have been observed by Prinzmetal during the course of acute myocardial infarction, frequently in association with ventricular premature beats and ventricular arrhythmias. On the basis of his extensive studies, including high-speed cinematographic techniques, Prinzmetal has deduced that accelerated conduction through part of the A-V node is responsible for aberrant complexes. He believes this to be true both in instances of nodal disease ( nodal accelerated conduction) and ventricular irritability ( ventricular accelerated conduction). In this latter type, the accelerated conduction through the A-V node may be on a reflex basis. Five instances of WPW aberration have been seen during the past two years in patients with arteriosclerotic heart disease. Of these, four are considered to be of acquired type, and only one an example of classical, congenital, Wolff-Parkinson-White syndrome (1954).

The response of arrhythmias and tachycardias of supraventricular origin to oral procaine amide.

The introduction of procaine amide for the control of cardiac arrhythmias in man has been recent (Mark et al., 1950). There are relatively few reports at present concerned with it. Those published have dealt chiefly with the use of the preparations of the drug given by intravenous injection and have emphasized its value in arrhythmias of ventricular origin (Mark et al., 1950; Joseph et al., 1951; Garlett et al., 1951; Kinsman et al., 1951; Miller et al., 1951; Kayden et al., 1951; and Stearns and Callahan, 1951). Thus, it has been stated that procaine amide is of value in ventricular arrhythmias but that its effect on auricular function appears to be minimal (Joseph et al., 1951). With the advent of the preparation for use by mouth,* a study of the action of orally administered procaine amide upon supraventricular disturbances of the heart beat was undertaken.

Functional and anatomic correlates of markedly abnormal stress tests

The functional state and coronary anatomy of 120 patients evaluated primarily because of a markedly positive ischemic exercise stress test (greater than 2 mm ST depression) is presented. Twenty-seven patients were asymptomatic (group A), 36 patients (group B) had type I angina (Canadian classification) and 57 patients (group C) had angina with only minor limitations (type II angina). All patients underwent exercise stress testing (Bruce protocol) within 2 months of cardiac catheterization. No significant intergroup differences were observed in exercise variables including time of onset of ischemia, maximal heart rate achieved, rate-pressure product, duration of exercise or mean change in blood pressure. Two patients in group A had normal coronary arteriograms. Comparison of the remaining asymptomatic patients in group A with patients in groups B and C revealed no significant differences in the number of coronary arteries involved, main left coronary artery disease, coronary score or the frequency of collateral circulation. In group A, 18% of collateral vessels were in jeopardy compared with 52% in groups B and C (p less than 0.05). Triple vessel disease was present in 57% and left main coronary artery disease in 16% of the total group. The only exercise variable useful in identifying patients with severe coronary disease was an abnormal exercise blood pressure response. This study indicates that a markedly ischemic stress test, regardless of the functional state of the patient, identifies patients, including those without symptoms, who have severe coronary disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Errors in unipolar limb leads caused by unbalanced skin resistances, and a device for their elimination.

Abstract 1.1. Unbalanced or dissimilar skin resistances may seriously alter deflections in the unipolar limb leads and lead to important clinical errors. These changes are due to potential variations at the so-called indifferent electrode and may occur in either augmented or nonaugmented unipolar extremity leads. 2.2. Changes in amplitude, contour, and direction of P, QRS, and T waves were produced experimentally by altering skin resistances. These changes included the inversion of normally upright T waves and the production of Q waves not present with resistances balanced. 3.3. These errors result from an inadvertent shift in axis of the unipolar leads clockwise or counterclockwise to a maximum of 30 degrees. The amount of shift in axis depends on the degree of imbalance. Thus, aV R (or V R ) may then erroneously resemble Lead I inverted or Lead II inverted; aV L (or V L ) may resemble Lead I or Lead III inverted; and aV F (or V F ) may resemble Lead II or Lead III. 4.4. An electronic coupling device is described which prevents errors in unipolar limb leads due to dissimilar skin resistances even when the imbalance is extreme.

The T loop in right bundle branch block: A vectorcardiographic study of 82 cases☆

ectorcardiographic studies of QRS loops in right bundle branch block (RBBB) have been reported by many authors, and the classic abnormalities are discussed in texts and symposium proceedings.l-6 The T loop in RBBB has received scant attention thus far, except for Chou and associates’g who reported the incidence of abnormal T loop wideness in 10 per cent of RBBB cases. The rotational characteristics of T loops in RBBB, as encountered in ischemic heart disease, in right ventricular enlargement, and in healthy persons have not been explored. The purpose of this investigation was to survey T-loop characteristics in a series of patients whose RBBB was of diverse etiology.

Effect of procaine amide on anomalous conduction and paroxysmal tachycardia in a case resembling the Wolff-Parkinson-White syndrome

Abstract 1. 1. Recurrent paroxysmal tachycardia occurred in a patient with intermittent aberrant atrioventricular conduction. 2. 2. A pathway bypassing part, but not all, of the atrioventricular node is suggested as an explanation for the somewhat shortened P-R interval and the somewhat lengthened QRS. 3. 3. Both the presenting nodal tachycardia and the aberrant conduction mechanism were easily controlled by oral procaine amide.

Oscillation-Free Ballistocardiography A Simple Technic and a Demonstration of Its Validity

Body motion resulting from cardiac forces may be recorded as displacement, velocity or acceleration by a variety of methods. None of these is identical with the cardiac force curve because of distortion due to body oscillations. Schwarzschild devised an electronic mixer that combines displacement, velocity, and acceleration in any proportion desired. This device permits recording ballistocardiograms that are free of oscillations due to body resonance. Validity of the technic was established by the identity of strain gage records of forces applied to a log phantom with simultaneous records obtained with the method presented.