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Biomedical subjects

A S Jaffe

Publications and source records attributed to A S Jaffe.

At least 109 records · Page 6Linked to original sources
PubMed1987

Relationship between elevated plasma levels of crosslinked fibrin degradation products (XL-FDP) and the clinical presentation of patients with myocardial infarction.

To assess whether the intense thrombotic state known to occur early after the onset of acute myocardial infarction is further exacerbated by impaired intrinsic fibrinolysis, we compared the intensity of fibrinolysis as measured by the level of crosslinked fibrin degradation products (XL-FDP) in plasma with the intensity of thrombosis as assessed by fibrinopeptide A (FPA) in 98 patients with transmural and 14 patients with non-Q wave infarction. Patients without complications of infarction such as shock, mural thrombi, or malignant arrhythmias requiring countershock generally had normal plasma levels of XL-FDP, less than or equal to 300 ng/ml (81% of those presenting less than 8 hours after onset and 66% of those presenting greater than 8 hours after onset) on admission despite elevated FPA indicative of ongoing thrombosis. In contrast, patients with complications generally had elevated levels of XL-FDP greater than 300 ng/ml (80% of those presenting early and 62.5% of those presenting late) and 50% of these patients had marked elevations to greater than 1000 ng/ml. FPA was markedly elevated in patients with complications whether they presented early or late after onset of infarction. Our direct measurements at the time of infarction support previous data indicating that intrinsic fibrinolysis is impaired in patients with acute infarction, despite marked thrombin activity, when complications are not present. However, when complications are present initially, a more exuberant fibrinolytic response is observed perhaps due to thrombosis associated with the complications themselves.

Female↗
PubMed1987

Sustained fibrinolysis after administration of t-PA despite its short half-life in the circulation.

To characterize the duration of the fibrinolytic response to tissue-type plasminogen activator (t-PA) and streptokinase (SK) in patients with acute myocardial infarction we serially assayed crosslinked fibrin degradation products (XL-FDP) and B beta 15-42 fibrinopeptide. Use of specific monoclonal antibodies permitted quantification and differentiation of fibrin from fibrinogen degradation products. Marked elevations of XL-FDP occurred within 1 hour after administration of t-PA (n = 13) or SK (n = 35) to greater than 1000 ng/ml in 79% of the patients. All patients given t-PA exhibited elevations of XL-FDP greater than 1000 ng/ml, most exhibited values greater than 5000 ng/ml (79% of patients). In contrast 6 of the patients given SK failed to exhibit XL-FDP greater than 1000 ng/ml. XL-FDP greater than 5000 ng/ml occurred in only 14%. The difference in the response to t-PA compared to SK was particularly striking 7 hours or more after administration of activator at which time XL-FDP were markedly elevated in patients given t-PA (5821 +/- 1683 ng/ml) compared with decreasing values in patients given SK (2924 +/- 1186 ng/ml) (p less than 0.01). Levels of B beta 15-42 were significantly higher after t-PA compared with SK beginning 3 hours after treatment, consistent with a greater intensity of fibrinolytic response to t-PA. Marked elevations of this short lived degradation product of fibrin (t 1/2 = 10-20 minutes) in the samples drawn late after administration of t-PA (44.3 +/- 12.8 nM) but not after SK (11.7 +/- 4.5 nM) confirmed prolonged fibrinolytic activity of plasmin after t-PA.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Burden↗
PubMed1987

Enhancement of metabolism of jeopardized myocardium by nifedipine.

To define effects of nifedipine on regional metabolism in jeopardized myocardium we quantified accumulation of carbon-11 labeled palmitate ([11C]palmitate) in patients with acute myocardial infarction by positron emission tomography in a randomized, double-blind, placebo controlled study. Tomographic studies were performed prior to treatment as soon as possible after hospital admission. Subsequent studies were performed seven days later. Twenty-two patients with acute myocardial infarction were randomized to treatment with nifedipine (n = 13) or placebo (n = 9). The dosage of active medication was guided by a "third party observer" to avoid iatrogenic hypotension. Treatment was initiated within 9.6 +/- 1 hours after the onset of symptoms of infarction. The extent of the zone of abnormal accumulation of [11C]palmitate was similar in pre-treatment positron emission tomograms from patients subsequently given nifedipine compared with those given placebo. In subsequent positron emission tomography studies, patients treated with nifedipine exhibited improved metabolism of [11C]palmitate (by 16 +/- 10%, SE, P less than 0.05) compared with no change in patients given placebo. Neither enzymatic estimates of infarct size nor scintigraphic estimates of left ventricular ejection fraction differed in the two groups. Patients given nifedipine and manifesting substantial improvement in accumulation of [11C]palmitate had a high incidence of chest pain and recurrent infarction compared with those given placebo in whom no improvement was evident. These observations suggest that some regions of myocardium were benefited transiently by nifedipine but that they remained at high risk for recurrent injury. Thus, patients benefited transiently by drugs early after the onset of infarction may require aggressive intervention such as angioplasty or early coronary bypass surgery. Accordingly, they should be evaluated angiographically early for identification of lesions with unusually high risk.

Blood Pressure↗
PubMed1987

Effects of gender and race on prognosis after myocardial infarction: adverse prognosis for women, particularly black women.

Controversy has arisen concerning whether gender influences the prognosis after myocardial infarction. Although some studies have shown there to be no difference between the sexes, most have indicated a worse prognosis for women, attributing this to differences in baseline characteristics. It has been further suggested that black women have a particularly poor prognosis after infarction. To determine the contribution of gender and race to the course of infarction, 816 patients with confirmed myocardial infarction who were enrolled in the Multicenter Investigation of the Limitation of Infarct Size (MILIS) were analyzed. Of those patients, 226 were women and 590 were men, 142 were black and 674 were white. The cumulative mortality rate at 48 months was 36% for women versus 21% for men (p less than 0.001, mean follow-up 32 months). The cumulative mortality rate by race was 34% for blacks versus 24% for whites (p less than 0.005). Both women and blacks exhibited more baseline characteristics predictive of mortality than did their male or white counterparts. It was possible to account for the greater mortality rate of blacks by identifiable baseline variables; however, even after adjustment, the mortality rate for women remained significantly higher (p less than 0.002). The poorer prognosis for women was influenced by a particularly high mortality rate among black women (48%); the mortality rate for white women was 32%, for black men 23% and for white men 21%. The mortality for black women was significantly greater than that of the other subgroups. Thus, findings in the MILIS population indicate that the prognosis after myocardial infarction is worse for women, particularly black women.

Black People↗
PubMed1987

Paradoxic elevation of fibrinopeptide A after streptokinase: evidence for continued thrombosis despite intense fibrinolysis.

Elevated levels of fibrinopeptide A, a marker of thrombin activity associated with acute myocardial infarction, have been found to decrease after administration of streptokinase when reperfusion occurs. In contrast, in patients without reperfusion and those with reocclusion after streptokinase therapy, fibrinopeptide A remains elevated. In the present study early serial measurements of fibrinopeptide A were used to further characterize this paradoxic increase in thrombin activity after streptokinase and to characterize its response to heparin. In 19 patients with acute myocardial infarction fibrinopeptide A was elevated to 82.3 +/- 43.5 ng/ml (mean +/- SE) before therapy. Thirty minutes after the initiation of streptokinase, fibrinopeptide A increased to 300.1 +/- 117.4 ng/ml (p less than 0.01), consistent with extensive thrombin activity. Fibrinopeptide A remained elevated until 15 minutes after a heparin bolus injection when levels decreased to 15% of the poststreptokinase value (49.2 +/- 13.3 ng/ml) (p less than 0.001). These data document a prompt paradoxic increase in thrombin activity after administration of streptokinase that may be responsible for failure of therapy in some patients.

Cardiomyopathies↗
PubMed1987

Prognostic implications of an early peak in plasma MB creatine kinase in patients with acute myocardial infarction.

To determine the prognostic implications of an early peak in plasma MB creatine kinase (MB CK) in patients with acute myocardial infarction who were not treated with an acute intervention, 342 patients with myocardial infarction confirmed by MB CK were retrospectively studied. The patients were classified into those with an early peak MB CK (less than or equal to 15 hours after the onset of symptoms, n = 84) and those with a late peak MB CK (greater than 15 hours after the onset of symptoms, n = 258). Patients with an early peak MB CK were slightly older, were more frequently female and had a higher incidence of prior myocardial infarction, congestive heart failure and arrhythmias compared with patients with a late peak MB CK. Patients with an early peak MB CK more frequently presented with ST segment depression (23 versus 11%, p less than 0.01), with anterior location of ischemia or infarction (71 versus 52%, p less than 0.01) and with a lower mean left ventricular ejection fraction (41.4 versus 47.4%, p less than 0.01). Despite more extensive left ventricular dysfunction at initial presentation, patients with an early peak MB CK had a smaller mean MB CK infarct size index (12.6 versus 18.9 g-Eq/m2, p less than 0.01), with no difference in the incidence of in-hospital complications, including death. The early left ventricular dysfunction improved in the patients with an early peak MB CK, evidenced by a 4.5% increase in ejection fraction from admission to 10 days after infarction, whereas the ejection fraction did not improve in patients with a late peak MB CK. However, the patients with an early peaking MB CK had myocardium in jeopardy as reflected by a higher incidence of ST segment depression and a decrement in the global left ventricular ejection fraction with exercise. The 4 year life table estimate for the rate of recurrent myocardial infarction after hospital discharge was higher in patients with an early peak MB CK (33 versus 22%, p less than 0.05), with an even more striking difference in the 4 year estimate for the rate of fatal recurrent infarction (20 versus 8%, p less than 0.001). The 4 year mortality estimate was markedly higher in hospital survivors with an early peak MB CK than in those with a late peak (47 versus 19%, p less than 0.0001) and, even after adjustment for differences in baseline characteristics, the residual excess mortality in those with an early peak was still significant (p less than 0.02).(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1987

Demographic correlates of fatigue in a university family health centre.

To delineate the demographic correlates of the fatigued patient, 297 patients attending a family practice centre were investigated. Women were more frequently tired than were men; patients with less than a college education were over-represented, and employed persons were more robust than the unemployed. Fatigue was also associated with lack of exercise, nightly wakening and the presence of children less than six years old in the household. There were no significant relationships between fatigue and age, smoking or 'reducing' diets. The results of the study shed new light on the correlates of fatigue and confirmed some long-standing beliefs.

Academic Medical Centers↗
PubMed1987

Coronary thrombolysis: practical considerations.

The decision to administer thrombolytic agents to patients with acute myocardial infarction requires consideration of both the potential risks and benefits of treatment. In patients treated very early (1 to 2 hours) after the onset of infarction, benefit has been established. In those presenting later, factors such as age, location of infarction, the interval from the onset of symptoms to treatment, and any risks of therapy need to be weighed. This article will review the selection of patients for treatment, the state of the art for its implementation, and for the use of adjunctive therapies.

Anistreplase↗
PubMed1987

Conversion of MM creatine kinase isoforms in human plasma by carboxypeptidase N.

This study was undertaken to identify the carboxypeptidase(s) (CPase) in plasma mediating sequential conversion of the tissue isoform of the MM isoenzyme of creatine kinase (MM3 CK) to MM2 and MM1 isoforms and to elucidate relationships between CPase activity measured in plasma and observed rates of isoform conversion in vitro. Purified MM3 was incubated at 37 degrees C in plasma from normal subjects and patients with acute myocardial infarction. Isoforms were quantified by chromatofocusing. Preincubation with antiserum to CPase N prevented conversion of added MM3 to MM2 and MM1. Isoform conversion rates in the absence of antibody were proportional to plasma CPase N activity assayed spectrophotometrically by hydrolysis of furylacryloyl-L-alanyl-L-lysine substrate (r = 0.89, n = 8). Plasma CPase N activity varied by nearly 300% among individuals, but average activity was similar in samples from normal subjects (267 +/- 45 [SD] U/L, n = 18), those from outpatients with angina (289 +/- 43 U/L, n = 9), and those obtained at hospital admission from patients with acute infarction (Q wave: 279 +/- 70 U/L, n = 16; non-Q wave: 272 +/- 61 U/L, n = 14) or unstable angina (280 +/- 71 U/L, n = 11). In patients with Q wave infarction, CPase N activity increased by 43% +/- 25% between 48 hours and 72 hours (P less than 0.005 compared with admission) with a concomitant change in the rate of conversion of isoforms. Thus, the rate of conversion of isoforms in individual subjects can be estimated by assay of CPase N activity in plasma.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Mercaptopropionic Acid↗
PubMed1986

Implications for acute intervention related to time of hospital arrival in acute myocardial infarction.

The time from onset of symptoms to arrival in the hospital emergency room (ER) was studied in 778 patients randomized into a study of acute myocardial infarction (AMI) size limitation. Patients at relatively high risk of death after AMI (including those with preexisting diabetes mellitus, systemic hypertension or congestive heart failure), women and older patients arrived significantly later in the ER than did patients without these characteristics. A significantly higher mortality rate was observed in patients who arrived late, i.e., those who arrived more than 2 hours after the onset of chest pain, even though patients with hemodynamic compromise (bradycardia, hypotension) tended to arrive earlier. The difference in long-term mortality between those who arrived early (within 2 hours of onset of chest pain) and those who arrived late was accounted for by the baseline differences between these 2 groups. These baseline differences may influence the effects of early interventions in AMI. In addition, these findings have implications for education of high-risk patients who could benefit the most from aggressive early intervention.

Age Factors↗
PubMed1986

A simplified method to predict occurrence of complete heart block during acute myocardial infarction.

Data were analyzed from 698 patients with proved acute myocardial infarction (AMI) to develop a method to predict the occurrence of complete heart block (CHB). The presence of electrocardiographic abnormalities of atrioventricular or intraventricular conduction during hospitalization was determined for each patient. The electrocardiographic risk factors considered were: first-degree atrioventricular block, Mobitz type I atrioventricular block, Mobitz type II atrioventricular block, left anterior hemiblock, left posterior hemiblock, right bundle branch block and left bundle branch block. A CHB risk score was developed that consisted of the sum of each patient's individual risk factors. CHB risk scores of 0, 1, 2 or 3 or more were associated with incidences of CHB of 1.2, 7.8, 25.0 and 36.4%, respectively. When applied to an independent AMI data base, as well as to the summed results of 6 previously reported series that identified predictors of CHB during AMI, a similar incremental risk of CHB as predicted by the risk score method was demonstrated.

Electrocardiography↗
PubMed1986

Sudden death and its relation to QT-interval prolongation after acute myocardial infarction: two-year follow-up.

Risk of sudden death was assessed in 533 patients who survived 10 days after acute myocardial infarction (AMI) and were followed for up to 24 months (mean 18) in the Multicenter Investigation of the Limitation of Infarct Size. Analysis of clinical and laboratory variables measured before hospital discharge revealed that the QT interval, either corrected (QTc) or uncorrected for heart rate, did not contribute significantly to prediction of subsequent sudden death or total mortality. In this population, frequent ventricular premature complexes (more than 10 per hour) on ambulatory electrocardiographic monitoring and left ventricular (LV) dysfunction (radionuclide LV ejection fraction of 0.40 or less) identify patients at high risk of sudden death. In patients with these adverse clinical findings, the QTc was 0.468 +/- 0.044 second among those who died suddenly and 0.446 +/- 0.032 second in survivors, and was not statistically significant as an additional predictor of sudden death. Consideration of the use of type I antiarrhythmic agents, digoxin, presence of U waves and correction for intraventricular conduction delay did not alter these findings. Although QT-interval prolongation occurs in some patients after acute myocardial infarction, reduced LV ejection fraction and frequent ventricular premature complexes are the most important factors for predicting subsequent sudden death in this patient population.

Adrenergic beta-Antagonists↗
PubMed1986

Digoxin therapy and mortality after myocardial infarction. Experience in the MILIS Study.

Recent studies have led to controversy about whether long-term digoxin therapy after confirmed or suspected myocardial infarction increases mortality. We analyzed the mortality experience in 903 patients enrolled in the Multicenter Investigation of Limitation of Infarct Size (MILIS). As in previous studies, the decision to treat or not to treat with digoxin was made by the patient's personal physician on the basis of the usual clinical indications. Cumulative mortality was 28 percent for the 281 digoxin-treated patients as compared with 11 percent for the 622 patients who did not receive digoxin (P less than 0.001; follow-up interval, six days to 36 months; mean, 25.1 months). However, patients treated with digoxin had more base-line characteristics predictive of mortality than did their counterparts. Adjustment for these differences with two separate applications of the Cox method yielded P values of 0.14 and 0.34 for tests of difference in mortality, providing no evidence for a significant excess mortality associated with digoxin. Thus, the findings in the MILIS population do not support the assertion that digoxin therapy is excessively hazardous after infarction, but the existence of an undetected harmful effect can only be excluded with a randomized study. Until the results of such a study are available, we recommend careful consideration of whether any treatment of ventricular dysfunction is actually needed, consideration of alternatives to digoxin therapy, and restriction of digoxin use to the subgroup of patients (with severe chronic congestive failure and a dilated left ventricle) previously shown to have a beneficial clinical response.

Clinical Trials as Topic↗
PubMed1986

Paucity of subtle myocardial injury after angioplasty delineated with MB CK.

To determine the extent to which PTCA elicits subtle myocardial ischemic injury, 28 patients were studied prospectively. The presence of myocardial injury was assessed by analysis of frequent (q4 hours) serial samples of MB CK, a sensitive and specific marker of myocardial injury. Immediately prior to angioplasty, baseline 12-lead ECGs and blood samples for evaluation of total CK and MB CK were obtained. Additional ECGs were obtained immediately after the procedure and on the following morning, and serial samples for total and MB CK were obtained at 4-hour intervals for 24 hours. Patients requiring cardiac surgery within 24 hours after PTCA were excluded. Samples (n = 203) were assayed by the glass bead method. Total CK rose by more than 20 IU/L in only five patients, four of whom had received intramuscular premedication. Mean MB CK was 3.4 +/- 6.1 IU/L at 12 hours and 4.1 +/- 4.7 IU/L at 24 hours compared to 3.1 +/- 1.7 IU/L prior to angioplasty. Only one patient with obvious infarction had a value for MB CK above the normal range. Thus, uncomplicated PTCA is not accompanied by objectively detectable subtle myocardial injury.

Angioplasty, Balloon↗