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LETTER TO EDITOR |
Department of Surgery, Queen’s Hospital, Burton on Trent, Staffordshire, UK.
The Wessex Cardiothoracic Centre, Southampton General Hospital, Southampton, UK
Department of Paediatric, Southampton General Hospital, Southampton, UK
Chemical Pathology Department, Mail point 6, Level D South Academic Block, Southampton General Hospital, Southampton SO16 6YD, UK, Tel: 44 23 8079 3465, Fax: 44 23 8079 6339, Email: elziber{at}yahoo.com
We read with interest the paper by Shin et al in which they stated that the causes of mitral regurgitation were degenerative in 238 (54%), rheumatic in 134 (31%), and others in 65 (15%). Their study extended from January 1994 to January 2002 and included 437 patients with mitral regurgitation1. The presence of metabolic syndrome in addition to the risk factors mentioned by Shin et al may accelerate the process of mitral regurgitation especially ischemic mitral regurgitation (IMR). The clustering of insulin resistance, dysglycemia, dyslipidemia, hypertension and central obesity represent the major features of metabolic syndrome. These clusters of factors may share common etiology and each of which is a risk factor for cardiovascular disease. The metabolic syndrome appears to affect 10% to 25% of adult populations worldwide. Several studies have described the association between metabolic syndrome, diabetes and cardiovascular disease2,3.
A search of the midline for the last 35 years has shown that there are 777 papers addressing the link between metabolic syndrome and ischemic heart disease (IHD) and none linked metabolic syndrome to ischemic mitral regurgitation (IMR), a serious clinical problem facing both the cardiologists and cardiac surgeons. Ischemic mitral regurgitation is caused by a prior myocardial infarction which causes the ventricular remodeling that leads to mitral regurgitation4. The myocardial ischemia can result in altered ventricular geometry with mitral valve annular dilatation. The inferioposterior wall bulges outward, displacing the attached papillary muscles apically and outward. The leaflets, tethered at both end, cannot close effectively and are restrained within the left ventricle; this effect is compounded by a decrease in the ventricular force to close the leaflet thus causing IMR4. Furthermore, the incidence of IMR is estimated to be around 5% to 8% in patients with ischemic heart disease undergoing coronary artery bypass grafting (CABG) and in 30% of patients following myocardial infarction. It is associated with higher cardiovascular mortality within 5 years if left uncorrected 5,6.
Patients with metabolic syndrome represent a high-risk group for coronary heart disease as well as for type II diabetes. Because the prevalence of these two conditions is likely to increase with increasing prevalence of metabolic syndrome, it is reasonable to propose that metabolic syndrome may be blamed for the increase of the incidence of IMR. Moreover, this hypothesis may also contribute to explain the increase in the burden of metabolic syndrome may affect not only diabetologist and cardiologists but will extend to affect cardiac surgeons.
REFERENCES
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