Late thrombolysis: controlled clinical trial overdue.
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Biomedical subjects
Publications and source records attributed to D H Spodick.
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Because 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.
Following exercise testing, a 71-year-old man developed atrial tachycardia with a unusual form of conduction disturbance: 4:2 atrioventricular (A-V) block. This pattern of A-V block is explainable by two different mechanisms of concealed conduction: two different levels of block in the A-V nodal region and dual A-V nodal pathways with concealed retrograde conduction of P waves. These concepts can also explain a variety of other unusual conduction disturbances.
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Exercise testing is contraindicated during active pericarditis because of the possibility of myocarditis. In a patient suspected of having ischemic heart disease, a pericardial rub appeared for the first time following a maximal exercise test, during which the elevated J-points descended to baseline. In two normal volunteer subjects with early repolarization during a maximal exercise test, the elevated J-points behaved similarly. We conclude that, contrary to previous belief, electrocardiographic exercise responses cannot distinguish between pericarditis and early repolarization.
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