ST elevation myocardial infarction causes: Difference between revisions
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Revision as of 21:14, 7 October 2012
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ST Elevation Myocardial Infarction Microchapters |
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Differentiating ST elevation myocardial infarction from other Diseases |
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Risk calculators and risk factors for ST elevation myocardial infarction causes |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
ST elevation myocardial infarction can be physiologically induced via exertional strain. A discussion regarding the risk factors and triggers can be found in other chapters.
Causes
Heart attack rates are higher in association with intense exertion, be it psychological stress or physical exertion, especially if the exertion is more intense than the individual usually performs.[1] The period of intense exercise and subsequent recovery is associated with about a 6-fold higher myocardial infarction rate (compared with other more relaxed time frames) for people who are physically very fit.[1] For those in poor physical condition, the rate differential is over 35-fold higher.[1] One observed mechanism for this phenomenon is the increased arterial pulse pressure stretching and relaxation of arteries with each heart beat, which, as has been observed with intravascular ultrasound, increases mechanical "shear stress" on atheromas and the likelihood of plaque rupture.[1]
Acute severe infection, such as pneumonia, can trigger myocardial infarction. A more controversial link is that between Chlamydophila pneumoniae infection and atherosclerosis.[2] While this intracellular organism has been demonstrated in atherosclerotic plaques, evidence is inconclusive as to whether it can be considered a causative factor.[2] Treatment with antibiotics in patients with proven atherosclerosis has not demonstrated a decreased risk of heart attacks or other coronary vascular diseases.[3]c
There is an association of an increased incidence of a heart attack in the morning hours, more specifically around 9 a.m.[4][5][6] Some investigators have noticed that the ability of platelets to aggregate varies according to a circadian rhythm, although they have not proven causation.[7]
References
- ↑ 1.0 1.1 1.2 1.3 Wilson PW, D'Agostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB. (1998). "Prediction of coronary heart disease using risk factor categories" (PDF). Circulation. 97 (18): 1837–47. doi:10.1161/01.CIR.97.18.1837. PMID 9603539.
- ↑ 2.0 2.1 Saikku P, Leinonen M, Tenkanen L, Linnanmaki E, Ekman MR, Manninen V, Manttari M, Frick MH, Huttunen JK. (1992). "Chronic Chlamydia pneumoniae infection as a risk factor for coronary heart disease in the Helsinki Heart Study". Ann Intern Med. 116 (4): 273–8. PMID 1733381.
- ↑ Andraws R, Berger JS, Brown DL. (2005). "Effects of antibiotic therapy on outcomes of patients with coronary artery disease: a meta-analysis of randomized controlled trials". JAMA. 293 (21): 2641–7. doi:10.1001/jama.293.21.2641. PMID 15928286.
- ↑ Muller JE, Stone PH, Turi ZG; et al. (1985). "Circadian variation in the frequency of onset of acute myocardial infarction". N. Engl. J. Med. 313 (21): 1315–22. doi:10.1056/NEJM198511213132103. PMID 2865677.
- ↑ Beamer AD, Lee TH, Cook EF; et al. (1987). "Diagnostic implications for myocardial ischemia of the circadian variation of the onset of chest pain". Am. J. Cardiol. 60 (13): 998–1002. doi:10.1016/0002-9149(87)90340-7. PMID 3673917.
- ↑ Cannon CP, McCabe CH, Stone PH; McCabe; Stone; Schactman; Thompson; Theroux; Gibson; Feldman; Kleiman; et al. (1997). "Circadian variation in the onset of unstable angina and non-Q-wave acute myocardial infarction (the TIMI III Registry and TIMI IIIB)". Am. J. Cardiol. 79 (3): 253–8. doi:10.1016/S0002-9149(97)00743-1. PMID 9036740.
- ↑ Tofler GH, Brezinski D, Schafer AI; et al. (1987). "Concurrent morning increase in platelet aggregability and the risk of myocardial infarction and sudden cardiac death". N. Engl. J. Med. 316 (24): 1514–8. doi:10.1056/NEJM198706113162405. PMID 3587281.