• D H Spodick.
• Am. J. Med. 1986 Oct 1; 81 (4): 661-8.

AbstractBecause a prospective controlled investigation showed a highly significant association of the onset of acute myocardial infarction with signs of preceding respiratory infection, the clinical, laboratory, experimental, and epidemiologic evidence more directly supporting this association was analyzed. Inflammation--specifically of infectious, usually viral, origin--has been shown by several lines of evidence to be capable of precipitating or mimicking clinical myocardial infarction. Myocardial biopsy is producing rapidly increasing confirmation that myocarditis can perfectly mimic clinical acute myocardial infarction. Coronary arteritis, with implications for vasospasm and thrombosis, is being increasingly demonstrated when deliberately sought in necropsy and biopsy material. Effects of blood-borne infectious agents, particularly viremia, on platelets in vivo and in vitro--aggregation and lysis with release of vasoactive substances--have even more serious potential for coronary thrombosis and vasospasm. It is not clear whether such mechanisms operate entirely independently or are more potent in high-risk patients, particularly in view of the demonstrable hypercoagulable state in many patients with coronary disease. Because of the great importance of confirming precipitating mechanisms for acute myocardial infarction (as well as its frequent mimic, myocarditis), intensive investigation of the relation between infection and infarction has important preventive and therapeutic implications.

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