The influence of anticoagulant therapy on the incidence of thromboembolism, hemorrhage and cardiac rupture in acute myocardial infarction

Capeci, Nicholas E.; Levy, Robert L.

doi:10.1016/0002-9343(59)90329-8

Cited by 22 publications

(4 citation statements)

References 13 publications

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“…For example, Lee and O'Neal (1956), in a survey of 500 necropsies, found that the incidence of thrombi within the heart, pulmonary embolism, and systemic arterial embolism was the same in necropsy cases examined before and after the introduction of anticoagulant therapy. In a more recent study (comparing 50 treated and 50 nontreated cases) Capeci and Levy (1959) reported similar findings.…”

Section: Literaturesupporting

confidence: 57%

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Anticoagulants in Acute Myocardial Infarction

1973

JAMA

199

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Section: Literaturesupporting

confidence: 57%

“…Lee and O'Neal (1956) and Capeci and Levy (1959) also found a greater frequency of these complications in those who had been given anticoagulants. Aarseth and Lange (1958), from a study of 89 cases of haemopericardium.…”

Section: Literaturementioning

confidence: 88%

Anticoagulants in Acute Myocardial Infarction

1973

JAMA

199

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“…These series showed a threefold increase in FWR or hemopericardium in patients treated with either heparin or warfarin while simultaneously showing an overall decrease in mortality from AMI. [36][37][38][39] Whereas these data suggested that impeding the clotting cascade may increase the risk of FWR, more recent data regarding the association of FWR and thrombolytic use has provided conflicting evidence. The United States National Registry of Myocardial Infarction (NRMI) showed a decrease in overall AMI mortality from 12.9% to 5.9% after thrombolytic use became widespread, while there was no change in FWR incidence (<1.0% in both the thrombolytic and nonthrombolytic groups).…”

Section: Natural Historymentioning

confidence: 99%

Free-Wall Rupture of the Myocardium Following Infarction: A Changing Clinical Portrait in the Reperfusion Era: A Case Report

et al. 2006

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Free wall rupture of the myocardium is an important complication and major cause of death following acute transmural (ST segment elevation) myocardial infarction. Pathologic changes on a cellular level may combine with mechanical stressors to weaken the myocardium postinfarction. Risk factors for myocardial rupture include advanced age, female gender, prior hyper-tension, first myocardial infarction, late presentation, lack of collateral blood flow, and persisting chest pain and ST segment elevations. Thrombolytic therapy does not increase risk of rupture when given early in myocardial infarction, but late thrombolytic therapy may heighten risk. Primary percutaneous coronary intervention for acute myocardial infarction has reduced the incidence of myocardial rupture compared to thrombolytic therapy. This advantage likely can be ascribed to higher rates of immediate reperfusion with catheter techniques, as well as to the avoidance of thrombolytic-mediated hemorrhagic transformation of the infarction zone. Careful regulation of blood pressure and pulse using nitrates and beta-adrenergic blockers may mitigate the tendency toward myocardial rupture. Early and accurate diagnosis based on clinical and echocardiographic evidence can lead to successful surgical treatment.

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“…Wessler et al (1952) reported 11 male and 9 female cases and exhaustively reviewed the literature; they list many other surveys, some from large general hospitals, some from mental institutions, and some from coroners' material; they conclude that the sex incidence is equal in spite of the higher rates of classical myocardial infarction in men. Recently there have been further publications mainly connected with anticoagulant therapy (Maher et al, 1956;Aarseth andLange, 1958: Capeci andLevy, 1959). There is disagreement about the effects of anticoagulants, but it is generally accepted that the number of cases is increasing, probably owing to such therapy (Kohn, 1959;Sigler, 1960).…”

mentioning

confidence: 99%