Biomedical subjects
Publications and source records attributed to J Askenazi.
Origin of the left circumflex coronary artery from the right sinus of Valsalva or the right coronary artery is a well-described anomaly. We report 3 cases which suggest a familial association of this anomaly. The familial clustering that we report has not been previously demonstrated.
The efficacy and safety of esmolol, a titratable intravenous beta-adrenergic blocking agent with a short elimination half-life (t 1/2 = 9.0 min) was evaluated in a multicenter open-label study for the treatment of supraventricular tachyarrhythmias (heart rate greater than 100 bpm). The study also investigated the feasibility of transferring patients from esmolol to alternate oral antiarrhythmic agents without loss of therapeutic response. Of the 113 patients studied, 95 (84%) achieved therapeutic response (reduction in heart rate of 15% or more or conversion to sinus rhythm). Most of these patients (93%) achieved the therapeutic response at esmolol doses of 200 micrograms/kg/min or lower. Transfer from esmolol to an oral antiarrhythmic agent(s) was studied in 76 patients. Alternate antiarrhythmic agents used in this study were digoxin (N = 25), propranolol (N = 21), verapamil (N = 10), metoprolol (N = 11), quinidine (N = 2), and a combination of two antiarrhythmic agents (N = 7). Sixty-seven (88%) patients were successfully transferred to oral antiarrhythmic agents without loss of the therapeutic response obtained with esmolol. The most frequent adverse effect observed during the study was hypotension, which resolved quickly (16 +/- 14 min) either by decreasing the dose or by discontinuation of esmolol infusion. This study supports previous observations concerning the safety and efficacy of esmolol in the treatment of supraventricular tachyarrhythmias. Furthermore, it demonstrates that the majority of patients successfully treated with esmolol can be safely and effectively transferred to oral therapy with alternate antiarrhythmic agents.
The hemodynamic effects of esmolol were evaluated in 12 male patients at rest (mean age, 51 +/- 10 years) undergoing routine cardiac catheterization. Hemodynamic measurements were obtained during baseline (prior to esmolol), at steady state (during an intravenous infusion of esmolol 300 micrograms/kg/min), and at 30 minutes after stopping esmolol (postinfusion). Esmolol produced hemodynamic effects similar to the effects of other beta blockers. Significant reductions in rate-pressure product (mean decrease, 15%), cardiac index (mean decrease, 17%), stroke volume index (mean decrease, 13%), left ventricular stroke work index (mean decrease, 20%), and left ventricular ejection fraction (mean decrease, 18%) were observed. In contrast to other beta blockers, all hemodynamic effects of esmolol had returned to baseline values within 30 minutes after the infusion stopped. One patient exhibited hypotension during the esmolol infusion; this episode resolved without sequelae after discontinuation of esmolol. In summary, the effects of esmolol at rest on hemodynamic parameters and left ventricular function are similar to other beta-adrenergic blocking agents. Due to its ultrashort half-life, esmolol can be administered safely in critically ill patients whose disease status makes treatment with currently available beta blockers risky.
The effects of the digitalis glycosides on systemic vascular resistance (SVR) in patients with congestive heart failure (CHF) are controversial. Most investigators report a reduction in total SVR, an action that has been attributed primarily to withdrawal of elevated sympathetic tone. Direct proof of this hypothesis is lacking, however, and the roles played by the renin-angiotensin-aldosterone and vasopressin systems have not been fully explored. Moreover, in several studies of patients with CHF, SVR did not decrease after the administration of digitalis. To clarify these issues, the hemodynamic and hormonal effects of digoxin were correlated in 11 normotensive men in sinus rhythm with CHF due to dilated cardiomyopathy. Patients were evaluated at rest and during submaximal exercise before and 6 hours after the intravenous infusion of 1.0 mg of digoxin (mean serum concentration 1.7 ng/ml). With digoxin therapy, heart rate, pulmonary wedge pressure and right atrial pressure declined and cardiac output increased. Although vasopressin was unchanged, both plasma norepinephrine concentrations and plasma renin activity decreased, the reduction in norepinephrine correlating with the increase in cardiac output. Despite these hemodynamic and hormonal effects, there was no change in total SVR at rest or during exercise. It is concluded that the improvement in cardiac function with digoxin in this patient group was a result of the inotropic properties of the drug, without an associated reduction in impedance. The failure of total SVR to decrease despite decreases in plasma norepinephrine levels and plasma renin activity might be explained by concomitant digitalis-induced vasoconstriction, impaired ability of arterioles to dilate in CHF, or offsetting alterations in other vasoactive hormone systems.
The effects of atrioventricular (AV) sequential pacing-induced left bundle branch block (LBBB) on left ventricular (LV) performance were evaluated during cardiac catheterization in 9 randomly selected patients being investigated for chest pain. All patients were in normal sinus rhythm with a normal P-R interval and QRS duration. LV performance was assessed by both hemodynamic and angiographic measurements. The maximal rate of LV pressure increase (dP/dt), rate of maximal LV pressure decrease (-dP/dt), LV end-diastolic pressure (LVEDP), end-diastolic volume (LVEDV), end-systolic volume (LVESV), stroke volume and percent ejection (EF) were measured during right atrial and AV sequential pacing at a constant pacing rate. The average pacing rate was 97 +/- 3 beats/min (mean +/- standard error of the mean). In each patient, both dP/dt and -dP/dt decreased significantly (p less than 0.001) during AV sequential pacing compared with atrial pacing at the same rate, from 1,541 +/- 68 to 1,319 +/- 56 mm Hg/s for dP/dt and from 1,506 +/- 86 to 1,276 +/- 92 for -dP/dt. LVEDP did not change significantly when atrial (17 +/- 3 mm Hg) and AV sequential pacing (16 +/- 2 mm Hg) were compared. Mean LVEDV did not change during atrial (135 +/- 13 ml) or AV sequential pacing (137 +/- 14 ml). In contrast, the LVESV during AV sequential pacing was higher by 15 ml (23%) (from 48 +/- 10 to 63 +/- 12 ml) (p less than 0.001); as a result, the stroke volume was lower by 13 ml (15%) and the EF decreased by 10%, from 66 to 56% (-15%).(ABSTRACT TRUNCATED AT 250 WORDS)
In 25 patients with cardiac disease, but free of left ventricular inflow obstruction, the electrocardiogram and M-mode echocardiogram of the aortic root, left atrium and both the mitral and the aortic valves were obtained simultaneously with the pulmonary artery wedge pressure (PAWP) during right heart catheterization. The echocardiographic measurements of the left atrial size, PR-AC interval, left atrial emptying index and the ratio between the electrocardiographic Q wave to mitral valve closure (Q-MVC) and between aortic valve closure to the mitral E point (AVC-E) were correlated to the pulmonary artery wedge pressure by means of linear regression analysis. A formula in which PAWP = 36.6 (Q-MVC/AVC-E)-- 2 was prospectively used to study the measured pressure in the current group of patients. The pulmonary artery wedge pressure derived from these latter measurements correlated well with the invasive measurement of this pressure (r = 0.91). The pulmonary artery wedge pressure calculated by echocardiography differed from the pulmonary artery wedge pressure measured by catheterization by 3 mm Hg or less in 19 of the 25 patients, by 4 mm Hg or less in 22 patients and by 6 mm Hg or less in 24 patients. Although the correlation between the (Q-MVC/AVC-E) ratio and measured pulmonary artery wedge pressure was highly significant (r = 0.91, probability [p] less than 0.001, n = 25), the left atrial emptying index, PR-AC and left atrial size revealed poor correlation coefficients (r = 0.45, r = 0.45 and r = 0.56 [p less than 0.05]), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Carcinoid syndrome was diagnosed in a 48-year-old man by urinary 5-hydroxyindoleacetic acid test results and liver biopsy findings. Cardiac catheterization disclosed tricuspid stenosis and mild pulmonic stenosis. The distinctive echocardiographic findings included a tricuspid valve moving in unison with the annulus and thickened immobile tricuspid leaflets. Unlike in rheumatic heart disease, diastolic doming of the tricuspid leaflets was not seen.
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Fifty patients were examined with phonocardiograms, carotid pulse tracings, and M-mode echocardiograms to evaluate the ability of noninvasive tests to identify the severity of aortic valvular disease as determined at cardiac catheterization. Linear and multivariate analysis showed these noninvasive approaches to have only fair correlation with the severity of the disease. A binary division of the population under study into severe and nonsevere subgroups based on aortic valvular area (less than or equal to 0.8 sq cm in severe group [n = 25]; greater than 0.8 sq cm in nonsevere group [n = 25]) allowed sensitivity, specificity, and likelihood ratios to be determined. The likelihood ratio increased fourfold as the interval from the ECG Q wave to the murmur's peak (Q-MP) prolonged to 320 msec and increased sevenfold when the rate-corrected left ventricular ejection time (delta LVET) was more than 40 msec beyond values predicted from standard regression equations. Echocardiographic measurements were less helpful. Prolonged values of Q-MP and delta LVET proved to be the best discriminators of severe aortic valvular disease in this population where the prevalence of severe and nonsevere disease was equal.
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Frequent use of central venous lines has led to an increasing problem with embolized catheter fragments which have become lodged in the right heart and pulmonary vasculature. Removal of catheter fragments is justified because of a high complication rate when they are left in situ. Using a snare retrieval apparatus catheter fragments may be quickly and easily removed. In the past year we have seen 3 patients with embolized catheter fragments. One case was unusual in that its transverse position in the pulmonary vasculature required initial dislodgement with a pigtail catheter before it could be successfully snared. The literature and our experience suggest that most, if not all, catheter fragments in the right heart and pulmonary circulation can be successfully retrieved without resorting to thoracotomy.
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The relation between electrocardiographic findings and the angiographic left ventricular ejection fraction and the augmented ejection fraction after a premature ventricular contraction was investigated in 73 patients with documented chronic coronary artery disease. The patients were separated into four groups according to the presence or absence of abnormal Q waves. Twenty-four patients had diaphragmatic myocardial infarction, 21 had anterior myocardial infarction, 15 had both and 13 had no myocardial infarction. There was no statistically significant differences in cardiac index, left ventricular end-diastolic pressure or number of coronary vessels showing critical narrowing in the four groups. The sum of R waves (in mv) in leads aVL, aVF and V1 to V6 (sigmaR) was correlated with the ejection fraction (EF) and the augmented ejection fraction (EFa). EF in percent = 6.6 sigmaR mv + 9.4 (no. =73, r = 0.61); and EFa in percent = 8.6 sigmaR mv + 11.0 (no. = 73, r = 0.77). Among patients with sigmaR of less than 4.0 mv, augmented ejection fraction was less than 0.45 in 73 percent; among patients with sigmaR of 4.0 mv or more the augmented ejection fraction was greater than 0.45 in 93 percent (P less than 0.001). Thus, the sigmaR, calculated from six precordial and two augmented leads in patients with chronic coronary artery disease, correlated with both ejection fraction and augmented ejection fraction. The electrocardiogram in patients with coronary artery disease may prove useful as a simple, readily available and noninvasive guide in the assessment of left ventricular function in patients with coronary artery disease.
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To evaluate hyaluronidase's effect in reducing post-infarction myocardial necrosis, we randomized 91 patients with anterior infarction to control (45) or to hyaluronidase-treatment (46) groups. A 35-lead precordial electrocardiogram was recorded on admission and seven days later. Hyaluronidase was administered intravenously after the first electrocardiogram and every six hours for 48 hours. QRS-complex changes were analyzed to assess the drug's effect. Precordial sites with ST-segment elevation (larger than or equal to 0.15 mV) on the initial electrocardiogram that retained an R wave were considered vulnerable for the development of electrocardiographic signs of necrosis. The sum of R-wave voltages of vulnerable sites fell more in the control group than in the hyaluronidase group (70.9 +/- 3.6 per cent [+/- 1 S.E.M.] vs 54.2 +/- 5.0 per cent P less than 0.01). Q waves appeared in 59.3 +/- 4.9 per cent of the vulnerable sites in control versus 46.4 +/- 4.9 per cent in hyaluronidase-treated patients (P less than 0.05). Thus, hyaluronidase reduced the frequency of electrocardiographic signs of myocardial necrosis.
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