Changes in the Hemostatic Mechanism After Myocardial Infarction

Goldenfarb, Paul B.; Cathey, Mary H.; Zucker, Stanley; Wilber, Patricia; Corrigan, James J.

doi:10.1161/01.cir.43.4.538

Cited by 24 publications

(5 citation statements)

References 21 publications

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“…Changes of blood coagulation, fibrinolysis, platelet number and function have long been recorded in postoperative patients (Dawbarn et al 1928;Payling Wright 1942;Wood et al 1972) but it is uncertain if these changes are more marked or occur more frequently in patients who develop postoperative thrombosis than in patients who do not. Similar changes have also been described after myocardial infarction (Goldenfarb et al 1971). Recently, a few studies have related changes in platelet function, fibrinolytic activity and blood viscosity to the development of postoperative thrombosis detected with 1 25 I-fibrinogen scanning.…”

Section: Blood Testssupporting

confidence: 81%

Diagnosis of Thrombosis Evaluation of 125I-fibrinogen Scanning and Blood Tests

1974

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Section: Blood Testssupporting

confidence: 81%

Diagnosis of Thrombosis Evaluation of 125I-fibrinogen Scanning and Blood Tests

1974

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“…R en a u d et al [21] found increase susceptibility to thrombin-induced aggregation among sub jects with suspected coronary artery disease, but normal responses when tested with ADP or collagen. G o ld en fa rb et al [3] found increased ADP-induced platelet aggregation among patients surviving myocardial infarction. Salky and D u g d a le [23] found normal platelet aggregation among patients with ischemic heart disease when tested with ADP, but increased aggregability when tested with collagen.…”

Section: Exercise Testmentioning

confidence: 97%

Effects of Exercise-Induced Stress on Platelet Aggregation

Levites¹,

Haft²

1975

Cardiology

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In order to determine if the stress of a standard exercise test wil affect the propensity for platelets to aggregate, platelet aggregometer studies were performed before and after a double two-step Master’s test in 19 patients with angina and in 19 normal controls. The response of platelet-rich plasma to 0.1, 1 and 10 µMof ADP and 1 and 10 µMof epinephrine were tested in a Chrono-Log aggregometer. Prior to exercise there was no significant difference between the number of patients and controls responding with irreversible aggregation to any of the five tests. Immediately following exercise, no significant differences in the number of irreversible aggregation responses were seen in the control group. In the group with coronary artery disease, the incidence of irreversible responses was significantly higher after exercise on test with 1 µM ADP (p < 0.05), 1 µM epinephrine (p = 0.02), and 10 µM epinephrine (p < 0.05). It is concluded that exercise increases significantly the tendency of platelets to aggregate among patients with coronary artery disease. It is possible that this effect may play a role in myocardial infarction induced during stress.

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“…It has been reported that circulating platelet aggregates occur more frequently in patients with transmural myocardial infarction than in patients with subendocardial infarction; 108 ' 274 this is somewhat unexpected because the former condition is more frequently associated with coronary artery thrombosis, and it has been suggested that subendocardial infarction might be asso- 227 Goldenfarbetal. 103 Sano et al 270 Steele et al 304 Salky and Dugdale 267 Frishman et al 97 Yamazaki et al 346 Gormsen et al 104 Zahavi 348 Knudsen et al 162 No 342 Gjesdal 102 Guyton and Willerson 108 Rohrer et al 257 Lowe et al 176 Schwartz et al 274 Amodeo et al 4 Salem et al 264 No ciated with occlusion of the distal coronary vasculature with platelets or platelet-fibrin microthrombi.…”

Section: Referencementioning

confidence: 99%

Platelet Consumption in Cardiovascular Disease

Ag¹,

Ac²,

Genton³

1982

Semin Thromb Hemost

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Many tests have been devised to investigate the role of platelets in arterial or venous thromboembolism. The mechanisms of platelet reactivity that the tests have measured have been variable and the early studies have been of little value in determining the contribution of platelet consumption in thromboembolic diseases. More recently, tests of in vivo platelet release and of platelet survival and turnover have been introduced and thought to be of great potential in the investigation of thromboembolic disorders. However, the data published thus far using more tests are far from conclusive that platelet activation and consumption occurs in thromboembolic disorders associated with arteriosclerosis. It may be that they are neither sensitive nor specific enough to detect minor changes in platelet activation. There is, however, some consistency that in conditions involving the larger vessels, prosthetic surfaces, or in association with active and recurrent venous thromboembolism, platelet release and platelet consumption measured by platelet survival time may occur. In particular, the abnormal results are consistently found in acute and recurrent venous thromboembolism, cardiac valve replacement with the older prosthetic devices, and arteriosclerosis of the larger arteries with clinical episodes of thromboembolism. However, in coronary artery disease, cerebrovascular disease, and peripheral vascular disease, the data are inconclusive, probably because the tests lack sensitivity. In addition, the value of the tests in the management of patients with thromboembolic disorders appears to be limited.

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Changes in the Hemostatic Mechanism After Myocardial Infarction

Cited by 24 publications

References 21 publications

Diagnosis of Thrombosis Evaluation of 125I-fibrinogen Scanning and Blood Tests

Diagnosis of Thrombosis Evaluation of 125I-fibrinogen Scanning and Blood Tests

Effects of Exercise-Induced Stress on Platelet Aggregation

Platelet Consumption in Cardiovascular Disease

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