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Biomedical subjects

J Kluger

Publications and source records attributed to J Kluger.

105 records · Page 6Linked to original sources
PubMed1984

Possible recurrence of amiodarone pulmonary toxicity following corticosteroid therapy.

Amiodarone hydrochloride, a new antiarrhythmic agent, has been associated with pulmonary toxicity characterized by cough, dyspnea and diffuse pulmonary infiltrates. We describe a case of fibrosing alveolitis, diagnosed by lung biopsy, in a patient receiving amiodarone which responded to corticosteroid therapy. The pulmonary symptoms recurred after discontinuing corticosteroids, five months after amiodarone was stopped, and were associated with a persistent amiodarone level. To our knowledge, this recurrence of amiodarone pulmonary toxicity has not been reported previously.

Adrenal Cortex Hormones↗
PubMed1982

The contributions of sympathetic tone and the renin-angiotensin system to severe chronic congestive heart failure: response to specific inhibitors (prazosin and captopril).

The contribution of sympathetic tone and the renin-angiotensin system to the pathogenesis of chronic heart failure was evaluated. In 20 paired studies of the same 10 patients, the baseline hemodynamic and humoral correlates of congestive heart failure, and the response to alpha adrenergic blockade (prazosin) and angiotensin converting enzyme inhibition (captopril) were assessed. Despite the extent of failure, baseline plasma renin activity ranged from normal to very high. In contrast, baseline plasma catecholamine levels were always elevated. Baseline plasma norepinephrine reflected the severity of heart failure, correlating inversely with baseline cardiac index before administration of both drugs. Comparable improvement in left ventricular function was noted after acute therapy. Baseline renin and norepinephrine did not predict the response to prazosin, but baseline renin did predict the response to captopril: pulmonary wedge pressure (r=-0.776, p less than 0.01), stroke index (r=0.752, p less than 0.02), systemic vascular resistance (r=-0.673, p less than 0.05). In summary, elevated levels of plasma norepinephrine were inversely correlated with baseline cardiac function but norepinephrine levels did not change despite improved hemodynamics with specific prazosin therapy. The renin-angiotensin system exhibited a wide spectrum of activity and hemodynamic improvement with captopril was related to this activity. Absence of a correlation between plasma norepinephrine and plasma renin activity suggested that their contributions to vasoconstriction were not interdependent. Increased sympathetic tone was consistent in severe heart failure, whereas renin-angiotensin activity differed widely. The response to captopril can be used to identify a subset of patients with severe heart failure and adverse angiotensin-mediated vasoconstriction.

Aged↗
PubMed1982

Sympathetic responsiveness and plasma norepinephrine during therapy of chronic congestive heart failure with captopril.

The interaction of cardiac function and sympathetic tone in severe chronic heart failure was evaluated in 24 patients by assessing the cardiac index/plasma norepinephrine relationship. Potential changes were assessed during first-dose and long-term captopril therapy including sympathetic responsiveness to the gravitational stress of head-up tilt. Because cardiac index and norepinephrine levels demonstrated a significant inverse correlation (r = -0.640, p less than 0.001). Norepinephrine decreased from 803 +/- 116 to 635 +/- 76 pg/ml following first-dose captopril therapy (p less than 0.02), with overall hemodynamic improvement. However significant first-dose correlations were not observed. During long-term therapy, norepinephrine decreased from 694 +/- 118 to 457 +/- 106 pg/ml, associated with improvement of symptoms and exercise tolerance. The extent of cardiac index increase was matched by norepinephrine reduction, so that their correlation was maintained (r = -0.540, p less than 0.02). First-dose and long-term therapy were associated with improved responsiveness of sympathetic tone to the reduction of cardiac index induced by the gravitational stress of tilt. In summary, sympathetic tone was increased in severe heart failure, correlating inversely with cardiac function. Although there was improvement of cardiac function with first-dose captopril therapy, significant correlations of supine improvement with reduction of sympathetic tone were noted primarily with long-term therapy. Responsiveness of sympathetic tone to the stress of tilt however, was evident during first-dose and long-term therapy.

Adult↗
PubMed1982

Mechanisms governing the postural response and baroreceptor abnormalities in chronic congestive heart failure: effects of acute and long-term converting-enzyme inhibition.

We assessed the hemodynamic and hormonal response to tilt and the baroreceptor response in 12 patients in sinus rhythm with severe chronic congestive heart failure. We also assessed the response to acute (n = 12) and chronic (n = 8) converting-enzyme inhibition with captopril. The control tilt was characterized by high cardiac filling pressures, absence of significant peripheral pooling and apparent absence of afferent stimuli for hemodynamic and hormonal response. After acute captopril, the hemodynamic response to tilt was improved, but not normalized. The chronic response was characterized by the absence of a reflex increase of systemic vascular resistance on tilt despite peripheral pooling. Five patients developed orthostatic hypotension, but responded to acute infusion of 0.9% sodium chloride. Efferent sympathetic activity (response to cold pressor) was abnormal during the control study, but indistinguishable from normal subjects by the time of chronic captopril therapy. This paralleled an improved responsiveness of plasma catecholamines during chronic tilt. The Valsalva maneuver remained abnormal. There was a distinct absence of the normally anticipated heart rate increase on tilt, suggesting a parasympathetic abnormality.

Adult↗
PubMed1981

Anterior S-T segment depression in acute inferior myocardial infarction: indicator of posterolateral infarction.

Although patients with acute inferior myocardial infarction often manifest S-T segment depression in precordial electrocardiographic leads, the pathophysiologic abnormalities associated with this finding are poorly understood. To examine this problem, electrocardiographic findings on admission were compared with results of radionuclide cineangiography performed within 38 hours of the onset of symptoms in 25 patients with inferior infarction. Summation of S-T depression in leads V1 through V4 permitted the separation of patients into two groups: Group A (11 patients with 0.20 mV or less of S-T depression) and Group B (14 patients with 0.45 vM or more of S-T depression). The radionuclide cineangiogram revealed inferior wall dysfunction in all patients. Additional posterolateral dysfunction was seen in 13 patients, all in Group B. Patients in Group B had a relatively larger infarction (peak creatine kinase Units - 756 +2- 358 in Group A versus 1,566 +/- 983 units in Group B, p less than 0.01) and greater functional impairment (ejection fraction - 45 +/- 12 in Group A versus 33 +/- 12 in Group B, p less than 0.01). The relation between precordial S-T segment depression and posterolateral dysfunction appears to be largely independent of electrocardiographic evidence of "true posterior infarction." Thus moderate or severe anterior precordial S-T depression in patients with acute inferior infarction is a sensitive and specific indicator of relatively extensive myocardial damage, primarily involving the posterolateral region.

Adrenergic beta-Antagonists↗
PubMed1981

Long-term antiarrhythmic therapy with acetylprocainamide.

Nineteen patients whose arrhythmias were initially suppressed with acetylprocainamide underwent long-term treatment with this drug. Eleven patients were still taking the drug at the end of 12 months. Drug withdrawal with substitution of a placebo caused an increase in ventricular premature beats. Thus, suppression of ventricular premature beats persisted for 1 year. The eight withdrawals from the study were due to death during the year (n = 6) or recurrence of arrhythmias. The deaths occurred in patients who were in New York Heart Association functional class II (one patient), III (three patients) and IV (two patients). Ventricular performance, assessed from systolic time intervals, improved with drug therapy and declined during drug withdrawal. Symptomatic effects were common, with seven patients requiring a reduction in dosage or discontinuation of therapy. Three patients treated for 3 years continued to show drug suppression of ventricular premature beats compared with the level during placebo substitution. Small amounts of procainamide were present in all patients because of in vivo deacetylation of acetylprocainamide. Many patients with good initial responses to this drug had recurrent arrhythmias during long-term therapy. For this reason, the usefulness of acetylprocainamide as an antiarrhythmic drug appears to be limited.

Acecainide↗
PubMed1981

Acetylprocainamide therapy in patients with previous procainamide-induced lupus syndrome.

Acetylprocainamide was used to treat 11 patients with previous procainamide-induced lupus syndrome for their cardiac arrhythmias. Three patients from whom procainamide had been withdrawn and whose lupus was in remission did not have a recurrence during a course of acetylprocainamide therapy of a longer average duration than their prior procainamide therapy. Lupus symptoms subsided during treatment in two patients who had symptoms when acetylprocainamide was started. Drug fever developed in one patient, and another had a mild recurrence of lupus symptoms during high-dose acetylprocainamide therapy that regressed with dosage reduction. All patients had small amounts of circulating procainamide from in-vivo deacetylation of acetylprocainamide. These observations strongly support the hypothesis that the aromatic amino group on procainamide is important for induction of the lupus syndrome and that acetylating this amino group blocks the lupus-inducing effect.

Acecainide↗
PubMed1980

The clinical pharmacology and antiarrhythmic efficacy of acetylprocainamide in patients with arrhythmias.

The actions of acetylprocainamide, the major metabolite of procainamide in man, were studied in a placebo-controlled oral-dose-ranging trial in 16 persons with arrhythmias. The occurrences of arrhythmias decreased in 15 patients receiving acetylprocainamide and increased subsequently in 10 of 13 patients given placebo. The frequency of arrhythmias was reduced by more than 75 percent in nine patients. Antiarrhythmic effects were dependent on dose and serum drug concentrations, with levels of 10 to 24 microgram/ml observed in patients with a reduction of more than 70 percent in premature ventricular complexes. The ratio of preejection period to left ventricular ejection time decreased during therapy. Side effects of light-headedness, insomnia, nausea and diarrhea occurred in six patients at serum levels ranging from 11 to 22 microgram/ml. The serum half-life of acetylprocainamide lengthened from 7 to 21 hours as the creatinine clearance decreased from 105 to 35 ml/min. Acetylprocainamide has antiarrhythmic efficacy, but causes side effects in human beings. This compound appears to contribute to the effects of procainamide therapy and may be useful as an antiarrhythmic drug.

Acecainide↗
PubMed1980

Aging and renal clearance of procainamide and acetylprocainamide.

Thirty-two patients had blood and urine collected simultaneously for measurement of procainamide, acetylprocainamide, and creatinine. The ratios of drug clearance to creatinine clearance were calculated for each. The procainamide:creatinine clearance ratio averaged 2.9 +/- 1.6 (SD) and fell as age of the patients rose (r = 0.5, p < 0.01). The acetylprocainamide:creatinine clearance ratio averaged 1.7 +/- 0.8 and also fell with age. The combination of decline in overall renal function with age with this decrease in the rate of renal tubular secretion of these drugs led to a progressive age-related rise in the steady-state serum level of procainamide (r = 0.56, p < 0.01) and acetylprocainamide (r = 0.36, p < 0.1) achieved by any dose of procainamide. Thus, the dosage of procainamide must be individualized for both overall renal function (GFR) and the age-related variations in renal tubular secretion that are of most note in children and the elderly.

Acecainide↗
PubMedDate not supplied

Changes in P-wave dispersion and P-wave duration after open heart surgery are associated with the peak incidence of atrial fibrillation.

BACKGROUND: Increased P-wave dispersion (P-disp) and maximum P-wave duration (P-max) predict the development of atrial fibrillation (AF) in the general population. The present study evaluates the time-dependent relationship of P-disp and P-max after open heart surgery. METHODS AND RESULTS: P-disp and P-max were measured in the perioperative period of open heart surgery (one day before surgery through postoperative day 4). Compared with the baseline, P-max decreased immediately after open heart surgery (112.63 +/- 7.4 ms vs 106.9 +/- 8.2 ms, P =.005). An increase in P-disp was observed between postoperative days 1 and 2 (37.5 +/- 6.8 ms vs 43.1 +/- 4.5 ms, P <.05), and postoperative days 1 and 3 (37.5 +/- 6.8 ms vs 44.1 +/- 6.6 ms, P <.05). There was also an increase in the P-max between postoperative day 1 and 3 (103 +/- 8.3 ms vs 110 +/- 7.7 ms, P <.05). CONCLUSIONS: Nonuniform atrial conduction (P-disp) is greatest on days 2 and 3 after open heart surgery, and the longest atrial conduction time (P-max) is greatest on day 3 after open heart surgery, findings that coincide with the time of greatest risk for AF. (Heart Lung((R)) 2001;30:466-71.)

Aged↗