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Biomedical subjects

A S Jaffe

Publications and source records attributed to A S Jaffe.

At least 127 records · Page 7Linked to original sources
PubMed1986

Importance of continued activation of thrombin reflected by fibrinopeptide A to the efficacy of thrombolysis.

Factors responsible for initial success or failure of coronary thrombolysis and persistent recanalization or early reocclusion have not been thoroughly elucidated. Both adequate initial clot lysis and preclusion of rethrombosis are required. Failure may reflect clot lysis followed immediately or somewhat later by rethrombosis. To determine whether differences in the intensity and persistence of the activation of thrombin are determinants of success or failure of recanalization, plasma fibrinopeptide A, a fibrinogen product liberated by thrombin, was serially assayed in 19 patients treated with intravenous streptokinase. In patients exhibiting recanalization (n = 9), plasma fibrinopeptide A decreased after administration of streptokinase but before administration of heparin. In patients without initially apparent recanalization, fibrinopeptide A increased, suggesting ongoing thrombosis, and subsequently decreased promptly after heparin. In patients with initial recanalization followed by overt reocclusion the pattern was different. Despite recanalization, fibrinopeptide A continued to rise markedly. Elevations persisted despite administration of heparin. Thus, inhibition of activation of thrombin is associated with successful recanalization. Conversely, persistent activation of thrombin may be a predisposing factor to both apparent initial failure of recanalization and overt early reocclusion.

Coronary Disease↗
PubMed1986

Prognostic significance of the treadmill exercise test performance 6 months after myocardial infarction.

A submaximal treadmill exercise test performed before hospital discharge after an uncomplicated myocardial infarction is often utilized to estimate prognosis and guide management, but there is little experience with a maximal exercise test performed 6 months after infarction to identify prognosis later in the convalescent period. The performance characteristics during an exercise test 6 months after myocardial infarction were related to the development of death, recurrent nonfatal myocardial infarction and coronary artery bypass surgery in the subsequent 12 months (that is, 6 to 18 months after infarction) in 473 patients. Mortality was significantly greater in patients who exhibited any of the following: inability to perform the exercise test because of cardiac limitations, the development of ST segment elevation of 1 mm or greater during the exercise test, an inadequate blood pressure response during exercise, the development of any ventricular premature depolarizations during exercise or the recovery period and inability to exercise beyond stage I of the modified Bruce protocol. By utilizing a combination of four high risk prognostic features from the exercise test, it was possible to stratify patients in terms of risk of mortality, from 1% if none of these features were present to 17% if three or four were present. Recurrent nonfatal myocardial infarction was predicted by an inability to perform the exercise test because of cardiac limitations, but not by any characteristics of exercise test performance. Coronary artery bypass surgery was associated with the development of ST segment depression of 1 mm or greater during the exercise test. Although clinical evidence of angina and heart failure 6 months after infarction was predictive of subsequent mortality among all survivors, among the low risk group without severely limiting cardiac disease, the exercise test provided unique prognostic information not available from clinical assessment alone. Therefore, a maximal exercise test performed 6 months after myocardial infarction is a valuable, noninvasive tool to evaluate prognosis. It provides information that is independent of and additive to clinical evaluation performed at the same time.

Adrenergic beta-Antagonists↗
PubMed1986

Abrupt withdrawal of beta-blockade therapy in patients with myocardial infarction: effects on infarct size, left ventricular function, and hospital course.

The effects of abrupt withdrawal or continuation of beta-blockade therapy during acute myocardial infarction were evaluated in 326 patients participating in the Multicenter Investigation of the Limitation of Infarct Size (MILIS). Thirty-nine patients previously receiving a beta-blocker and randomly selected for withdrawal of beta-blockers and placebo treatment during infarction (group 1) were compared with 272 patients previously untreated with beta-blockers who were also randomly assigned to placebo therapy (group 2). There were no significant differences between the two groups in MB creatine kinase isoenzyme (15.8 +/- 10.9 vs 18.2 +/- 14.4 g-eq/m2, respectively) estimates of infarct size, radionuclide-determined left ventricular ejection fractions within 18 hr of infarction (0.44 +/- 0.15 vs 0.47 +/- 0.16) or 10 days later (0.42 +/- 0.14 vs 0.47 +/- 0.16), creatine kinase-determined incidence of infarct extension (13% vs 6%), congestive heart failure (43% vs 37%), nonfatal ventricular fibrillation (5% vs 7%), or in-hospital mortality (13% vs 9%). Patients in group 1 had more recurrent ischemic chest pain (p = .002) within the first 24 hr after infarction, but not thereafter. However, this did not appear to be related to a rebound increase in systolic blood pressure, heart rate, or double product. In a separate analysis, 20 propranolol-eligible group 1 patients randomly selected for withdrawal of beta-blockade (group 3) were compared with 15 patients randomly selected for continuation of prior beta-blockade therapy (group 4). This comparison yielded similar results. These data indicate that the beta-blockade withdrawal phenomenon is not a major clinical problem in patients with acute myocardial infarction. beta-Blockade therapy can be discontinued abruptly during acute myocardial infarction if clinically indicated.

Aged↗
PubMed1986

Diagnostic changes in plasma creatine kinase isoforms early after the onset of acute myocardial infarction.

Conventional plasma isoenzyme and enzyme values usually are normal during the first few hours of acute myocardial infarction. Thus definitive diagnosis may be delayed. We have shown recently that infarction in dogs can be detected within 1 hr after coronary occlusion by analysis of relative activities of MM creatine kinase (CK) isoforms in plasma. Isoforms of MM CK evolve through posttranslational modifications in plasma of the form released from tissue (MMA) to MMB and MMC. In this study we quantified changes in isoform profiles in the first available plasma samples from patients with evolving myocardial infarction, from patients with angina, and from normal subjects. In the 26 control subjects, the ratio of MMA to MMC was 1.09 +/- 0.4 (SE) (range 0.31 to 3.1; upper limit of normal [defined as the mean plus 2 SD] 2.5). In the seven control patients with coronary artery disease, the ratio of MMA to MMC was 1.3 +/- 0.3 with a range of 0.5 to 2.5. In contrast, among the 28 patients with acute myocardial infarction, the ratio of MMA to MMC in the first available plasma sample averaged 14.6 +/- 4.5 (p less than .01 compared with both control groups). First available samples were obtained 3.9 +/- 0.4 hr after the onset of pain. In 24 of 28 patients (86%) the ratio of MMA to MMC was greater than 2.5.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Acute myocardial infarction: state of the art.

The proper management of patients with acute myocardial infarction changes frequently as new data develop in this complex area. The present recommendations concerning the use of oxygen and morphine and the treatment of hypotension and congestive heart failure require little change save the addition of new agents. However, considerable new data have been derived in the area of limitation of myocardial infarct size. Several studies suggest that the early administration of beta-blockers or intravenous nitroglycerin may benefit patients with acute infarction. We must seriously consider whether the data supporting the use of these agents justify a recommendation that they be used routinely for patients with acute infarction. The role of thrombolytic agents, although widely used already, must also be addressed as data supporting its use build. Additionally, there are suggestive data that the aggressive treatment of hypertension is beneficial, and this approach may well merit advocacy. The prophylactic use of lidocaine and the ubiquitous use of nitrates necessitate reevaluation, although presently both agents are widely used. The aggressive use of electrical therapy for supraventricular arrhythmias and the lack of indication for the treatment of asymptomatic bradycardia with atropine in patients with acute infarction must be added to the previous National Conference standards.

Adrenergic beta-Antagonists↗
PubMed1986

Cardiovascular pharmacology. I.

The use of bicarbonate during cardiopulmonary resuscitation remains controversial. The present standards, suggested in large part by the investigations of Bishop and Weisfeldt, and the acknowledged toxicity of treatment with bicarbonate led to aggressive use of hyperventilation, the frequent monitoring of pH, and a reduction in bicarbonate administration. However, to date no studies have indicated an improvement in outcome to support the importance of these changes. Instead, controversy continues concerning the most appropriate buffer and whether the pH gradient induced between venous and arterial beds during CPR is of importance. To date, a viable alternative regimen has not been proposed. Thus, at present there is little new data upon which to base a major change in strategy, although the logic of reducing further the use of bicarbonate seems compelling. The choice of antiarrhythmic therapy is equally difficult. Initially, experimental studies suggested a more potent antifibrillatory effect for bretylium than for lidocaine. Subsequent studies have challenged these initial experimental results and clinical data have failed to indicate the benefit of one drug over the other. There is little information to suggest that these agents are more effective than the aggressive use of defibrillation alone in patients with ventricular fibrillation. It therefore seems improbable that a definitive decision concerning the use of one or another of these agents can be made.

Anti-Arrhythmia Agents↗
PubMed1986

Increased creatine kinase MB in the absence of acute myocardial infarction.

Although measurement of CK-MB is a very sensitive, specific, and cost-effective test for use in diagnosis or exclusion of acute myocardial infarction, it should not be used as the sole diagnostic indicator, and all positive values must be critically analyzed to exclude other causes of increased values in serum. This is particularly important when the population being tested consists of patients with multiple medical problems, with low to medium probability of myocardial infarction, and without clinical or other biochemical (i.e., LDH 1) evidence of acute myocardial infarction. When the temporal pattern and absolute CK-MB values are considered together with the patient's clinical status, the diagnostic specificity is dramatically increased. In addition, one must be familiar with the limitations of individual assay systems in order to exclude method-related artifactual values.

Adult↗
PubMed1985

Electrocardiographic, enzymatic and scintigraphic criteria of acute myocardial infarction as determined from study of 726 patients (A MILIS Study).

Methods for detecting acute myocardial infarction (AMI) were compared in a prospective study of 726 patients with pain presumed to be caused by ischemia that lasted 30 minutes or longer and was associated with electrocardiographic changes (ST-segment deviation greater than or equal to 0.1 mV and/or new Q waves or left bundle branch block). Using MB-CK values of more than 12 IU/liter as the standard criterion for detection of AMI, 639 patients (88%) were judged to have AMI. Total plasma CK values, technetium-99m stannous pyrophosphate images 48 to 72 hours after admission, and serial 12-lead electrocardiograms over 10 days were analyzed by investigators blinded to other clinical and laboratory data. For detection of AMI, total CK, electrocardiograms (ECGs) and pyrophosphate imaging were all highly accurate and sensitive (total CK accuracy 97%, ECG 92%, pyrophosphate 88%; total CK sensitivity 98%, ECG 96% and pyrophosphate 91%). However, both pyrophosphate and ECG were less specific than total CK (p less than 0.01) (total CK specificity 89%, pyrophosphate 64% and ECG 59%). The sensitivity (p less than 0.05) and accuracy (p less than 0.01) of total CK and pyrophosphate for those patients with Q-wave development were slightly greater than for those in whom Q waves did not evolve. The ECG was less accurate (p less than 0.02) and pyrophosphate was less specific (p less than 0.04) in patients with prior MI compared with those with initial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Creatine Kinase↗
PubMed1985

Chest pain after nontransmural infarction: the absence of remediable coronary vasospasm.

To assess the contribution of coronary vasospasm to chest pain in patients with nontransmural myocardial infarction, we performed a controlled trial of prophylactic antivasospastic therapy. Fifty patients with nontransmural infarction received either nifedipine or placebo in a double-blind randomized trial. Chest pain occurred in 52% of treated patients (38 episodes on 35 days) compared to 48% of control patients (42 episodes on 33 days). Concurrent therapy was comparable in the two groups. Recurrent infarction occurred in 12% and was comparable between groups. Ejection fraction was similar and was unchanged throughout the study in both groups. Logistic regression failed to identify predictors for recurrent chest discomfort. These data indicate that potent antivasospastic therapy does not reduce the incidence of recurrent chest pain or infarction. Thus, remediable coronary vasospasm is not likely to be a major cause of post infarction ischemia in patients with nontransmural infarction.

Aged↗
PubMed1985

Adverse effects due to morphine sulfate. Challenge to previous clinical doctrine.

Despite a lack of clinical data in this area, conventional wisdom holds that morphine sulfate induces vagally mediated conduction defects, especially in patients with inferior myocardial infarction. To assess the accuracy of this "clinical pearl," the records of 244 patients admitted to the Barnes Hospital Cardiac Care Unit with suspected acute myocardial infarction were reviewed to determine the frequency of deleterious cardiovascular effects related to the administration of morphine sulfate. Of 184 patients (156 subsequently documented to have infarction) who received morphine sulfate, four patients had symptomatic hypotension temporally associated with morphine sulfate administration. This represented a frequency of 2.2 percent for all patients treated with morphine sulfate and a frequency of 2.6 percent in those with proved infarction. In each instance, the heart rate response was inappropriate, i.e., decreased or less markedly accelerated than might be expected given the reduced blood pressure, suggesting a vagal mechanism for the adverse effects. Only one of the four patients had inferior infarction, and in three of four instances, the adverse effect occurred after the first dose. All patients subsequently received morphine sulfate without evidence of toxicity. No case of narcotic-induced conduction abnormality was identified. This series, which is the most extensive evaluation of the topic, documents that adverse cardiovascular effects due to morphine sulfate are rare and do not conform to preconceived clinical doctrine. They consist of inappropriate heart rate responses to hypotension rather than conduction defects and are not particularly associated with inferior myocardial infarction.

Aged↗
PubMed1985

Fibrinopeptide A: a marker of acute coronary thrombosis.

To determine whether coronary thrombosis in vivo is reflected by elevations in levels of fibrinopeptide A (FPA) in plasma, we sequentially characterized plasma FPA levels associated with evolving infarction in patients admitted to the cardiac care unit early after the onset of symptoms, in patients with transmural infarction admitted later, and in patients with nontransmural infarction. Studies were also performed in patients in whom the diagnosis of infarction was suspected but subsequently excluded. FPA values were significantly higher in patients with transmural infarction (42.3 +/- 11.2 ng/ml [mean +/- SEM], n = 53) compared with those in patients with nontransmural infarction (4.8 +/- 1.6 ng/ml, n = 17) or with those in patients in whom infarction was subsequently excluded as a diagnosis (3.5 +/- 0.6 ng/ml, n = 17, p less than .01 for both). Elevations in FPA level were greatest in patients with transmural infarction from whom samples were obtained soon after the onset of symptoms. Thus, in 39 patients from samples were obtained within 10 hr after the onset of symptoms, FPA levels were significantly higher than in 14 patients from whom samples were obtained initially more than 10 hr after the onset of symptoms (55.5 +/- 14.7 vs 4.9 +/- 1.4 ng/ml, p less than .01). In 30 of the 39 patients with evolving transmural infarction from whom samples were obtained within the first 10 hr after the onset of symptoms, the level of FPA was greater than 8 ng/ml.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Disease↗
PubMed1985

Quantification of myocardial infarction: a comparison of single photon-emission computed tomography with pyrophosphate to serial plasma MB-creatine kinase measurements.

Single photon-emission computed tomography (SPECT) with 99mTc-pyrophosphate (PPi) has been shown to estimate size of myocardial infarction accurately in animals. We tested the hypothesis that SPECT with 99mTc-PPi and blood pool subtraction can provide prompt and accurate estimates of size of myocardial infarction in patients. SPECT estimates are potentially available early after the onset of infarction and should correlate with estimates of infarct size calculated from serial measurements of plasma MB-creatine kinase (CK) activity. Thirty-three patients with acute myocardial infarction and 16 control patients without acute myocardial infarction were studied. Eleven of the patients had transmural anterior myocardial infarction, 16 had transmural inferior myocardial infarction, and six had nontransmural myocardial infarction. SPECT was performed with a commercially available rotating gamma camera. Identical projection images of the distribution of 99mTc-PPi and the ungated cardiac blood pool were acquired sequentially over 180 degrees. Reconstructed sections were color coded and superimposed for purposes of localization of infarct. Areas of increased PPi uptake within myocardial infarcts were thresholded at 65% of peak activity. The blood pool was thresholded at 50% and subtracted to determine the endocardial border for the left ventricle. Myocardial infarcts ranged in size from 1 to 126 gram equivalents (geq) MB-CK. The correlation of MB-CK estimates of size of infarct with size determined by SPECT (both in geq) was good (r = .89 with a regression line of y = 13.1 + 1.5x).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Effect of propranolol on myocardial-infarct size in a randomized blinded multicenter trial.

A multicenter randomized single-blind study was performed to evaluate the effects of propranolol administered during the evolution of myocardial infarction. Five centers enrolled a total of 269 patients, with 134 receiving propranolol and 135 placebo. Propranolol or placebo was given intravenously upon randomization (0.1 mg per kilogram of body weight) and then orally for nine days to keep the heart rate between 45 and 60 beats per minute. Less than 2 per cent of patients were treated within 4 hours after the onset of symptoms, but 50 per cent received therapy within 8 hours of onset of chest pain, and the remainder between 8 and 18 hours. The heart rates in the propranolol-treated group were significantly lower than those in the placebo group (P less than 0.001). Base-line characteristics, including the mean heart rate (79.6 vs. 81.3) and the left ventricular ejection fraction (49.0 vs. 49.5), were similar in the two groups. The primary end point evaluated--infarct size as estimated from plasma MB creatine kinase activity--was virtually identical in the two groups, averaging 13.3 and 13.6 gram-equivalents of MB creatine kinase per square meter of body-surface area. Peak plasma levels of the enzyme were also similar in the two groups. No significant difference was observed between the propranolol and placebo groups in the change in left ventricular ejection fraction, extent of area involved in pyrophosphate uptake, R-wave loss on electrocardiograms, or mortality (after three years). These results do not support the use of propranolol administered four or more hours after the onset of symptoms to limit infarct size.

Administration, Oral↗
PubMed1984

Risk factors for sudden death after acute myocardial infarction: two-year follow-up.

The risk of sudden coronary death after myocardial infarction (MI) was assessed in 533 patients who survived 10 days after MI and were followed for up to 24 months (mean 18) in the Multicenter Investigation of the Limitation of Infarct Size. Analysis of multiple clinical and laboratory variables determined before hospital discharge revealed that frequent ventricular premature beats (VPBs) (greater than or equal to 10/hour) on ambulatory electrocardiographic monitoring and left ventricular (LV) dysfunction (radionuclide LV ejection fraction less than or equal to 0.40) were independently significant markers of risk for subsequent sudden death believed to be the result of a primary ventricular arrhythmia. The incidence of sudden death was 18% in patients with both LV dysfunction and frequent VPBs (11 times that of patients with neither of these findings). Seventy-nine percent of all sudden deaths occurred within 7 months after the index MI. In 280 survivors reclassified 6 months after MI with regard to the presence or absence of frequent VPBs and LV dysfunction, these risk factors could not be associated with sudden coronary death over a further follow-up period of up to 18 months; the overall incidence of sudden cardiac death was low (1.4%) after 6 months. Thus, the presence of frequent VPBs in association with LV dysfunction early after MI identifies patients at high risk for sudden death over the next 7 months.

Aged↗
PubMed1984

Plasma MB creatine kinase after vigorous exercise in professional athletes.

Plasma MB creatine kinase (CK) activity was quantitatively evaluated by several independent methods in 9 young professional athletes after vigorous exercise in competitive football games. Seven of the 9 had elevated total plasma CK activity. None had clinical findings of myocardial injury. However, 4 of the 7 with total CK elevations also had elevated MB-CK. MB-CK elevations occurred in players with the highest elevations of total CK activity. It is known that well-trained athletes liberate less conventionally measured muscle enzyme into the blood after exertion than do untrained individuals. These results indicate that a substantial fraction of professional athletes who engage in unusually vigorous exercise have elevations of plasma MB-CK that should not be interpreted as necessarily indicative of myocardial ischemic injury.

Creatine Kinase↗
PubMed1984

Significance of elevated MB creatine kinase in patients after cardiac catheterization.

To clarify the etiology of elevations in plasma MB creatine kinase (CK) in patients after cardiac catheterization, we studied 32 consecutive patients undergoing cardiac catheterization and coronary arteriography. Total CK and MB CK were within the normal range in all patients prior to catheterization. Total CK activity rose from a mean of 61.46 +/- 33.8 IU/1 (SD) to 141 +/- 105 in the first sample after catheterization (p less than .005) and 121.6 +/- 92.4 in the second catheterization sample (p less than .0005). The MB CK activity also rose from a mean of 3.2 +/- 1.6 IU/1 prior to catheterization to a maximum value of 5.0 +/- 2.9. The mean increase in MB CK, though statistically significant (p less than .005), was only 1.8 IU/1. Only one patient's value for MB CK rose to outside of the normal range (greater than 12) likely due to cardiac injury. Thus, our data document that marked elevations in MB CK after cardiac catheterization are unusual. They likely represent cardiac muscle injury rather than MB CK released due to skeletal muscle injury induced by the catheterization itself.

Adult↗
PubMed1984

Increased congestive heart failure after myocardial infarction of modest extent in patients with diabetes mellitus.

To elucidate the factors involved in the reduced survival rate of diabetic patients after acute myocardial infarction (AMI), we prospectively evaluated 100 patients with well-documented diabetes and 426 control patients. We characterized infarct size and analyzed the incidence and severity of congestive heart failure (CHF) and subsequent death with respect to infarct size. The extent of the index infarct was less in diabetic compared to nondiabetic patients, 16.2 +/- 2.2 CK-gm-eq/m2 compared with 19.2 +/- 0.9 (p less than 0.02). However, CHF was more prevalent in diabetic patients (31.2% of the diabetic patients compared to 15.7%). The difference was most prominent in diabetic patients who had sustained prior infarction (50% compared to 16%), but was evident also in diabetic patients with initial infarction (26% compared to 16%). The mortality rate was greater in diabetic patients (p less than 0.04). When diabetic and nondiabetic patients were stratified with respect to the presence or absence of CHF, survival curves were comparable. The increased incidence of CHF despite a smaller infarct size suggests that additional factors must contribute to myocardial dysfunction and the resultant excess in mortality.

Diabetes Complications↗