Transient S-T segment elevation in unstable angina: prognostic significance

The clinical and prognostic significance of the direction of the S-T segment shift on the 12-lead electrocardiogram was evaluated in medically treated patients with unstable angina pectoris. Long-term mortality and morbidity of 11 patients with transient S-T segment elevation (group I) were compared to that of 21 patients with transient S-T segment depression (group II). The average follow-up duration was 62 months. There was no significant difference between groups I and II with respect to survival or nonfatal myocardial infarction over a five-year period. Mortality was related to the extent of coronary artery disease and left venticular ejection fraction rather than to the direction of the S-T segment shift.     

Plasma norepinephrine and epinephrine responses to glucagon in patients with suspected pheochromocytomas

Plasma norepinephrine and epinephrine levels were measured before and after glucagon administration in 28 patients suspected of having a pheochromocytoma: three patients were subsequently found to have tumors. The norepinephrine response predicted the presence or absence of a tumor in 27 of the 28 patients. Epinephrine levels doubled, on the average, in patients who did not have pheochromocytomas, and were not useful in distinguishing the patients with or without tumors. A comparison of the response to glucagon and a placebo indicated that changes in plasma catecholamine levels were hormone-related and not the result of side-effects accompanying injection. The glucagon provocation test, with measurement of plasma norepinephrine and epinephrine levels, may be a useful adjunctive tool for evaluating patients suspected of having a pheochromocytoma when performed according to a standardized protocol and interpreted in relation to appropriate controls.     

Acute changes in infranodal conduction time following left ventriculography and sublingual nitroglycerin administration in man

During diagnostic cardiac catheterization for the evaluation of chest pain, His bundle electrograms were obtained in 32 male patients before and 2 to 5 minutes after each of two interventions known to acutely affect left ventricular volume and left ventricular end-diastolic pressure (the injection of 40 to 60 cc of contrast medium during left ventriculography and the administration of 0.4 mg of sublingual nitroglycerin). Changes in left ventricular end-diastolic pressure (18 +/- 6 vs 30 +/- 7 mm Hg, p less than 0.001 following ventriculography and 32 +/- 8 vs 19 +/- 8 mm Hg, p less than 0.005 following nitroglycerin administration) were accompanied by parallel alterations in HQ (48 +/- 8 vs 54 +/- 10 msec, p less than 0.005 following ventriculography and 57 +/- 10 vs 53 +/- msec, p less than 0.005 following nitroglycerin administration), but there were no significant changes in atrioventricular (AV) nodal conduction (AH). Significantly greater changes in HQ were seen in patients with triple-vessel coronary artery disease than in the remainder of the population, although there was clinical and/or ECG evidence of ischemia in only one patient. We conclude that factors other than progression of intrinsic conduction system disease may affect infranodal conduction. HQ should be interpreted cautiously in situations with rapidly changing hemodynamics, especially in patients with severe coronary artery disease.     

Rest angina with transient S-T segment elevation correlation of clinical features with coronary anatomy

In 44 consecutive patients with angina at rest associated with transient S-T segment elevation, clinical features were correlated with angiographic coronary anatomy. Patients were divided into three groups depending on the number of major vessels having ?70 per cent luminal narrowing: Group I = no or minimal disease (six patients); group II = single vessel disease (13 patients); and group III = multiple vessel disease (25 patients).The following features did not differ significantly among groups I, II or III: age, sex, risk factors, time from onset of episodes of pain at rest to study or arrhythmias during ischemic episodes. Patients in group III were more likely to have angina on effort (p < 0.001) and an abnormal base line electrocardiogram (p < 0.001) than patients in groups I or II. However, the absence of these features did not separate patients in group I from those in group II.In patients with angina at rest associated with transient S-T segment elevation, clinical features identify patients with multiple vessel disease but do not allow differentiation of patients with no or minimal coronary disease from patients with single vessel disease.     

Quinidine therapy in hospitalized patients with ventricular arrhythmias.

Quinidine serum levels and pharmacokinetic data were assessed during steady state therapy with oral quinidine sulfate in 19 hospitalized patients who were being treated for ventricular arrhythmias. A new high performance liquid chromatography assay was employed. Four patients were studied both after the first dose of quinidine and at steady state, and the initial dose pharmacokinetic values were found not to be predictive of steady state. The mean half-life of quinidine was 4.5 hours, but there was wide individual variation. The elimination rate constant for quinidine was significantly lower in patients with echocardiographic evidence of left ventricular dilatation than in patients with normal echocardiographic left ventricular size. The average urinary excretion of quinidine was only 11.3%. The pharmacokinetic data in seven chronic alcoholic patients without clinical or laboratory evidence of hepatic insufficiency did not differ from the data obtained in nonalcoholic patients. However, with severely impaired liver function, there may be marked prolongation of quinidine half-life predisposing to quinidine toxicity. The possible clinical implications of these findings are discussed.     

Intrinsic sympathomimetic activity of pindolol. Evidence for interaction with pretreatment sympathetic tone

Eighty-six hypertensive patients were treated with pindolol, a beta-adrenergic blocking drug with intrinsic sympathomimetic activity. To evaluate the interactions between beta-blockade, intrinsic sympathomimetic activity, and the level of pretreatment sympathetic activity, blood pressure, heart rate, and forced expiratory volume in one second (FEV1) were examined before and during a 15-week treatment program. The response of patients with a relatively higher pretreatment sympathetic tone reflected by a resting heart rate equal to or greater than 80 beats per minute (Group I) was compared with the response of patients with a lower pretreatment heart rate (less than 80 beats per minute) (Group II). Decreases in mean blood pressure were similar in the two groups. In patients in Group I, the net effect of pindolol was a modest decrease in heart rate and FEV1, supporting the concept that when sympathetic tone is relatively high, the beta-blocking effect is dominant. In contrast, patients in Group II showed little change in heart rate or FEV1 during pindolol treatment, reflecting a balance between the intrinsic sympathomimetic activity and beta-blocking effects of pindolol. Thus, the intrinsic sympathomimetic activity of pindolol is physiologically evident, and relative impact is dependent on the pretreatment level of sympathetic tone.     

The electrophysiologic effects of oral cibenzoline

Five male patients with chronic stable ventricular arrhythmias underwent a placebo controlled ascending dose study with oral cibenzoline, a new type 1 antiarrhythmic drug. Ambulatory ECG (Holter) recordings and electrophysiologic studies were done while on placebo and on the maximum dose of cibenzoline. Drug toxicity, manifested by vomiting and QRS widening, accompanied by very high serum cibenzoline concentrations, was seen in two patients. A major reduction (greater than 85% in ventricular premature beats occurred in three patients including two in whom only relatively low serum concentrations had been achieved. Cibenzoline caused significant increases in AH (97 +/- 26 vs. 110 +/- 23 msec, p less than 0.01) and HV (59 +/- 7 vs. 78 +/- 7 msec, p less than 0.02), a major but statistically not significant increase in QRS (99 +/- 12 vs. 128 +/- 27 msec, NS) but QT (38 +/- 2 vs. 38 +/- msec) and QTc (42 +/- 1 vs. 44 +/- 3 msec) were essentially unchanged, even in toxic patients. Cibenzoline had no consistant effect on sinus cycle length, sinus node recovery time, or the relative, functional or effective refractory periods of the atrium and AV node. We conclude that cibenzoline has potent type 1 effects in prolonging HV but may be unique in not affecting QT or QTc, even at toxic levels. Its effects upon AH were unexpected and warrant further study.     

Improvement in depressed cardiac function in hypertensive patients during pindolol treatment

To assess changes in left ventricular function during antihypertensive treatment using pindolol, a beta-adrenocepter blocking drug with potent intrinsic sympathomimetic activity, serial echocardiographic measurements were obtained in 70 hypertensive patients before and during 15 weeks of treatment with pindolol. For analysis, the patients were separated into three groups on the basis of their baseline left ventricular fractional shortening (Group I, 35 patients with normal fractional shortening of 28 percent or more; Group II, 16 patients with abnormal fractional shortening of 21 to 27 percent; and Group III, 19 patients with markedly abnormal fractional shortening of 20 percent or less). More than half of the patients in Group I and Group II had decreases in mean blood pressure of 10 percent or more in response to pindolol, but only one fourth of Group III patients had similar responses (p < 0.05). Patients with normal pretreatment fractional shortening had a mild decrease in fractional shortening during pindolol treatment, whereas patients with either abnormal or markedly abnormal fractional shortening had an increase in fractional shortening. This increase in fractional shortening suggests the possibility that the partial agonist or intrinsic sympathomimetic activity of pindolol may play a role in preserving left ventricular function in patients with borderline or impaired function.     

Regional myocardial perfusion at rest and during intracoronary papaverine in patients with coronary artery disease

Regional myocardial perfusion was measured in 32 patients with the xenon-133 washout technique at rest and after 5 mg of intracoronary papaverine. Areas of decreased perfusion and/or decreased vasodilation were identified visually from computer-generated functional images. The locations of arteries and stenoses, obtained from identically positioned cineangiograms, were overlaid on the functional images. Perfusion rates for 62 myocardial regions were calculated and correlated with the percentage of stenosis. There was no association between degree of stenosis and perfusion at rest. Regional myocardial perfusion increased after papaverine in regions supplied by coronary arteries without stenoses (0% to 25%), 88.6 ± 4.7 ml/min/100 gm. This increase was significantly greater (p < 0.001) than the increase in regions supplied by 51% to 75% stenoses (23.7 ± 6.3 ml/min/100 gm), or 76% to 99% stenoses (12.9 ± 6.3 ml/min/100 gm), or 100% stenoses (2.5 ± 3.8 ml/min/100 gm). Thus there was an inverse relationship between the increase in myocardial perfusion stimulated by papaverine and the degree of coronary artery stenosis measured angiographically. In regions supplied by two stenoses in series, vasodilation produced less of an increase than a single stenosis of a similar degree.     

Left anterior fascicular block: electrocardiographic criteria for its recognition in the presence of inferior myocardial infarction.

Although the vectorcardiographic criteria for recognizing left anterior fascicular block in the presence of inferior myocardial infarction are well established, comparable electrocardiographic criteria have not been studied. From vectorcardiographic criteria, it was hypothesized that in patients with left axis deviation but without bundle branch block the presence of a deep negative terminal deflection (S wave) in lead II accompanied by a positive terminal deflection (r wave) in lead aVR should indicate left anterior fascicular block whether or not inferior infarction is present. The electrocardiograms of 75 patients with unequivocal vectorcardiographic evidence of either left anterior fascicular block or inferior infarction, or both, were reviewed. Of the 47 patients who met strict vectorcardiographic criteria for left anterior fascicular block, 44 (94 percent) showed the predicted electrocardiographic pattern, including 24 of 26 (92 percent) who had both this conduction defect and inferior myocardial infarction. There was only one patient with vectorcardiographic evidence of inferior myocardial infarction alone with the findings of left axis deviation and the electrocardiographic pattern of combined infarction and fascicular block (that is, only one false positive). Thus, if bundle branch block is excluded, the proposed electrocardiographic pattern permits recognition of left anterior fascicular block whether or not there is coexistent inferior myocardial infarction.     

Effect of propafenone in patients with stable ventricular arrhythmias

Thirty patients with clinically significant ventricular ectopy were treated with propafenone, a new potent antiarrhythmic agent with membrane stabilizing action. Patients had a minimum mean of greater than 30 ventricular premature beats per hour documented by continuous 48-hour ambulatory ECG recording. Twenty-five patients qualified as responders, defined as greater than 85% reduction of ventricular ectopy compared to baseline, and completed a double-blind placebo-crossover phase. Significant reduction in single ventricular ectopy per hour, paired ventricular ectopy per hour, and ventricular tachycardia beats per hour were observed. Almost total abolition of ventricular tachycardia and paired ventricular ectopy was achieved. Side effects were minimal and well tolerated. A significant prolongation of the PR interval occurred. QRS prolongation and prolongation of the corrected QT interval was observed in some patients, with new left bundle branch block developing in two patients. Long-term efficacy and safety studies will be necessary to determine the ultimate role of this new agent in the selection of antiarrhythmic therapy, but these inital results are encouraging.     

Comparative hemodynamic effects of dopamine and dobutamine in patients with acute cardiogenic circulatory collapse

The hemodynamic effects of dopamine (DPM) and dobutamine (DBM) were compared in 13 patients with acute cardiogenic circulatory collapse. All patients presented with acute pump failure and inadequate systemic perfusion, and most were hypotensive. Nine patients had an acute myocardial infarction (AMI); the other four patients had an acute decompensation of a previously stable ischemic cardiomyopathy, and presented with a low-output syndrome in the absence of documented AMI. Patients were studied with a randomized single crossover design using each patients as his own control. Both drugs were given at doses of 2.5, 5, and 10 μg/kg/min for periods of 10 minutes at each dose while hemodynamics were monitored. No other vasoactive drugs were used during the study. Because of advanced age or severe peripheral vascular disease, no patient was considered suitable for intra-aortic balloon counterpulsation. There were no significant differences between the two drugs with regard to heart rate, mean arterial pressure, systemic vascular resistance, stroke work index, or mean right atrial pressure. DBM improved stroke index and cardiac index significantly (p < 0.05) more than DPM at doses of 5 μg/kg/min. DPM increased left ventricular filling pressure (LVFP) more than DMB at 5 μg/kg/min (p < 0.001) and at 10 μg/kg/min (p < 0.05). Although both DPM and DBM are useful in acute cardiogenic circulatory collapse, there appear to be important differences in their effect on LVFP and in the mechanisms whereby they increase blood pressure.     

Variability of electrocardiographic responses to repeated ergonovine provocation in variant angina patients with coronary artery spasm

We reviewed our experience with serial ergonovine provocative tests for coronary artery spasm (CAS) in ten variant angina patients with angiographically proved CAS. Of the 26 ergonovine tests performed in the ten patients, only four patients exhibited reproducible ECG response to ergonovine. The remaining six patients had variable and unpredictable ECG responses to ergonovine. All patients were in an active phase of their disease. The variability of ST segment directional response to ergonovine is considered to be on the basis of disparate sensitivity of the coronary circulation to intravenous ergonovine. Because of this variable response, the ECG response alone should not be considered as the standard indicator for CAS presence but should be utilized with other hemodynamic and angiographic criteria.     

Current problems in the recognition and management of patients with tuberculosis in a general hospital

Our series of 62 patients points out several features in the current management of tuberculosis. First, if there is a high index of suspicion for tuberculosis, protection of other health care personnel can be achieved to a large degree. Second, it is imperative that results of positive cultures for M. tuberculosis be channeled through a centralized registry so that patients with positive cultures are not overlooked because of the delay in obtaining culture results and the lack of continuity of care in certain clinical settings. This will help ensure the appropriate treatment for patients and, through public health authorities, the initiation of contact screening.     

The acute response of plasma norepinephrine, renin activity, and arginine vasopressin to short-term nitroprusside and nitroprusside withdrawal in patients with congestive heart failure

Activation of the sympathetic nervous system, manifested by an increase in heart rate and circulating plasma norepinephrine, can occur in normal subjects when they are given vasodilators. The extent to which this activation occurs in patients with congestive heart failure (CHF) and whether this activation could account for the hemodynamic rebound sometimes observed following abrupt withdrawal of nitroprusside in such patients are unclear. We prospectively and retrospectively studied the effects of nitroprusside on plasma norepinephrine in 38 patients with CHF to determine if acute vasodilator therapy activates this vasoconstrictor system during or following such treatment. Thirty-six of these patients also had plasma renin activity (PRA) measured and plasma arginine vasopressin was measured in 12 patients. Baseline supine plasma norepinephrine (714 +/- 72 pg/ml, +/- SEM), PRA (15 +/- 2 ng/ml/hr), and arginine vasopressin (10 +/- 1 pg/ml) were increased at least twofold in the CHF patients. Nitroprusside (96 +/- 11 micrograms/min) was infused for 63 +/- 5 minutes after achieving an optimal hemodynamic response: cardiac index increased (2.01 +/- 0.08 to 2.67 +/- 0.1 L/min/m2, p less than 0.001), pulmonary artery wedge pressure decreased (25 +/- 1 to 16 +/- 1 mm Hg, p less than 0.001), mean arterial pressure decreased (83 +/- 1 to 72 +/- 1 mm Hg, p less than 0.001), and heart rate was unchanged. Plasma norepinephrine (632 +/- 43 pg/ml), PRA (18 +/- 3 ng/ml/hr), and arginine vasopressin (11 +/- 1 pg/ml) did not change significantly for the group during peak effect of the vasodilator.(ABSTRACT TRUNCATED AT 250 WORDS)