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Journal of Postgraduate Medicine, Vol. 55, No. 4, October-December, 2009, pp. 314-315 Commentary Towards assessment of the mechanisms related to myocardial infarction in young individuals Chrysohoou C, Stefanadis C 1st Cardiology Clinic, University of Athens, Greece Correspondence Address: 1st Cardiology Clinic, University of Athens, Greece, chrysohoou@usa.net Code Number: jp0999 PMID: 20083888 DOI: 10.4103/0022-3859.58945 In this issue, Cengel and Tanindi [1] review the literature for the large spectrum of clinical conditions which result in myocardial infarction in young adults. The authors refer to several pathogenetic conditions from congenital heart anomalies, to connective tissue disorders, irradiation, drug use and hypercoagulability states. Finally, they conclude that in the routine management of young patients with an acute coronary syndrome, the physician should first exclude the existence of atherosclerosis. Acute myocardial infarction (AMI) in individuals below the age of 40, is commonly characterized by evidence of multiple cardiovascular risk factors (above all smoking, dyslipidemia, and family history of coronary artery disease) and variable prognosis in short- and medium-term follow-up from 14 to 30%. [2] The relative high rates of long-term mortality in young patients with AMI have been attributed to the high incidence of cardiovascular risk factors, the delayed presentation and the late or even absent initiation of revascularization due to underdiagnosis. Misdiagnosis of AMI in young individuals is a common clinical condition, as AMI can be misdiagnosed as myocarditis, and vice versa. The diagnosis of acute myocarditis is based on clinical presentation, physical examination, laboratory testing, course of electrocardiographic changes and lack of epicardial coronary disease revealed by cardiac angiography. Interestingly, the prevalence of coronary arteries being normal in AMI is remarkably high in younger individuals and it has been reported in 16-35% of patients below 30 years of age; which is rather contrary with the one observed in patients above 50 years old. [2] The only available method for definitive diagnosis of myocarditis is endomyocardial biopsy, which shows sensitivity from 43-64% and an overall complication rate of 6%. Cardiac magnetic resonance imaging (MRI) can noninvasively detect myocardial edema and myocyte damage. In patients with myocarditis, MRI shows a characteristic pattern of contrast enhancement, which originates primarily from the epicardium, sparing the supendocardium layer. [3] AMI in young patients is likely to result from multiple pathogenetic mechanisms, such as rupture of a vulnerable plaque or erosion of the endothelial layer, hypercoagulable states, coronary artery spasm and inflammation, with atherosclerosis remaining the main cause. [2] Among classic risk factors, smoking has been recognized as the stronger factor for the occurrence of acute coronary syndrome in men and women under the age of 40. [4] Smoking affects all phases of atherosclerosis since it potentiates thrombosis, causes endothelial dysfunction, induces coronary vasoconstriction even in patients with normal coronary vessels and has pro-inflammatory effects. Young heavy smokers with angiographically normal coronary arteries have an abnormal coronary vasoconstriction induced by acetylcholine, which means that nitric oxide (NO) is probably decreased locally. Since NO is inactivated by superoxide anions, which are scavenged by extracellular superoxide dismutase (EC-SOD), and smokers have lower EC-SOD levels, it is reasonable to suggest that smoking might increase the coronary tone via oxidative stress-related pathway. Decreased plasma EC-SOD level has also been implicated in male smokers with vasospastic angina and slow coronary flow. Smoking might be playing a triggering role in those patients with slow coronary flow. [5] Therefore, it is plausible to speculate that in young survivors of AMI where conventional cardiovascular risk factors and extensive atheromatosis are less prevalent, the atherothrombotic properties of smoking are more "deleterious" contributing to the adverse cardiac outcome. Numerous studies have shown significant benefits after smoking cessation, leading to a 36% decrease in mortality. Unfortunately, in the literature the percentage of quitters among coronary patients ranges from 28-60%. [2] The clustering of risk factors which usually begin in childhood, track into adulthood and have been linked to acceleration of atherosclerotic lesions in coronary arteries of young individuals. Autopsy studies in youth from the Bogalusa Heart Study [6] showed a strong association between the extent of atherosclerotic lesions in the aorta and coronary arteries with Low Density Lipoprotein cholesterol levels, triglyceride levels, smoking status, blood pressure and body mass index and this association was more striking when there was an aggregation of the risk factors. Myocardial infarctions caused by coagulation disorders constitute 5% of all cases. An imbalance between coagulation and fibrinolysis may increase the risk of thrombus forming in the unchanged artery. Blood platelets play an important role in the development of thrombosis and several polymorphisms of platelet receptors, fibrinogen coding genes, coagulation factors' mutations, have been illustrated, although the underlying mechanisms are multi-factorial and unclear. An open question, however, is the quantitative estimation of the independent contribution of genetic factors opposed to environmental factors on cardiovascular risk. Previous epidemiologic data support the hypothesis of a genetic component conditioning the development of coronary heart disease. It has been suggested that genetic factors are more likely to affect the young rather than older individuals and they may contribute to the different mechanisms leading to atherosclerotic lesions. References
Copyright 2009 - Journal of Postgraduate Medicine |
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