Plaque rupture and consequent thromboses probably do not cause acute coronary syndromes.
The objective of this communication is to provide evidence that the spasm of resistance vessel (S-RV) concept of ischemic heart disease (IHD) and other ischemic disorders provides a more consistent set of explanations for acute coronary syndromes than the accepted mechanism of plaque rupture and consequent thromboses. The concept avers that S-RV directly induces symptoms in the various syndromes of IHD, including acute coronary syndromes. The S-RV concept is considered to be an alternate paradigm to explain IHD, and interest only develops in such models when there is significant doubt about the validity of the accepted paradigm. This report is an update of a study reported in this Journal in 1999 and has 2 changes; evidence will be evaluated by formal verification/falsification (pass/fail) methods - the method used to evaluate paradigms, and this report focuses on the mechanism of acute coronary syndromes because of the importance of these syndromes. It is well accepted that acute coronary syndromes are due directly to plaque rupture/thromboses, and there is considerable evidence to support this obvious mechanism. In spite of the obviousness of this mechanism, the S-RV concept asserts that S-RV is a more rational mechanism to explain acute coronary syndromes. Consistent with this position, the results of the study favor the S-RV concept. The standard position was given 8 passes, 2 passes with associated possible limited failures, and 2 possible failures. In contrast, the S-RV concept was given 12 passes, and no failures. Hopefully, the results of this study, and other available information about the S-RV concept, will prompt interest in the concept - such as independent testing of its premises.
Richard Hellstrom
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Department of Pathology, College of Medicine, SUNY Upstate Medical University, Syracuse, New York 13210, USA. hellstrr@mail.upstate.edu
D000208:Acute Disease; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D001161:Arteriosclerosis / Q000150:complications / Q000503:physiopathology; D003327:Coronary Disease / Q000209:etiology* / Q000503:physiopathology; D003329:Coronary Vasospasm / Q000150:complications / Q000503:physiopathology; D006801:Humans; D008955:Models, Cardiovascular; D009203:Myocardial Infarction / Q000188:drug therapy; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D012422:Rupture, Spontaneous; D013577:Syndrome; D015912:Thrombolytic Therapy; D013927:Thrombosis / Q000150:complications / Q000503:physiopathology; D014655:Vascular Resistance
D000924:Anticholesteremic Agents; D010975:Platelet Aggregation Inhibitors