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• W2315690806 abstract "Arterial hypertension is one of the leading causes of cardiovascular morbidity and mortality [1–3]. Excess body weight and obesity are associated with increased risk of coronary heart disease (CHD). Hypertension occurs frequently in individuals with excess body weight. However, several studies have reported inconclusive results on a potential causual relationship between arterial hypertension and obesity in the development of CHD [4–8]. Hypertensive heart disease is characterized by a variety of pathologies including development of (a)symetrical left ventricular hypertrophy, interstitial and perivascular fibrosis with diastolic dysfunction, left ventricular enlargement with systolic dysfunction and potential dysrhythmias, endothelial dysfunction, stenosis of epicardial arteries and/or coronary microangiopathy [9–14]. All these mechanisms may reduce an adequate supply demand ratio of coronary blood flow to myocardial tissue, resulting in angina, dyspnoea and major cardiac events. In addition, hypertension has been recently referred as a prothrombotic state [15,16]. Hypertension treatment has had a positive impact on stroke rates, but rates of CHD in treated hypertensive individuals still remains high [17]. Furhtermore, hypertensive patients are at higher risk for adverse events following coronary interventions [18]. Thus, a potential interaction of hypertension with obesity and other cardiovascular risk factors is of major clinical significance. In this issue of the journal, Mahamat et al. [19] report on the joint impact of arterial hypertension and obesity on the incidence and prevalence of clinical events related to CHD. In the PRIME study, investigators studied a cohort of 9756 middle-aged men over 5 years from five different MONICA centres throughout Europe. At study entry, those individuals with a known history of CHD were excluded. Study cohort was subdivided according to body mass index (BMI) tertiles (< 25, > 27.6 kg/m2, or inbetween) and the presence or absence of arterial hypertension. Confounding factors such as age, centre, smoking, alcohol consumption, physical activity, cholesterol levels, triglycerides and diabetes were corrected by different statistical models. During follow-up, 321 events related to CHD were registered: 154 episodes with (stable) effort angina and 167 unstable angina, myocardial infarctions or coronary deaths. The definition of coronary events used in this study did not exactly match the definitions of stable angina and acute coronary syndromes (ACS) according to the current ESC/AHA guidelines [20]. If used accordingly, the troponin-based definition might have further increased episodes of ACS, along with a concomittant reduction of episodes with stable angina. This would also have had some impact on the statistical analysis and extrapolation of the study findings to current practice in cardiology. Nevertheless, important epidemiological findings could be observed in the PRIME study. The absolute incidence of effort angina increased with increasing BMI, whereas ACS did not. The statistical analysis of a relation between increased BMI, hypertension and CHD events is critically dependent on the selection and adjustment of potential confounding factors such as other cardiovascular risk factors. This was carefully evaluated in the PRIME study. The relative risk of CHD events increased with higher BMI tertiles, even after correction for age, physical activity, smoking habits and alcohol consumption. Addition of the classical risk factors diabetes, hypercholesterolemia, and hypertension resulted in a loss of statistical significance. This might be in part explained by the unbalanced ratio of dependent variables put into the multivariate analysis in relation to the relative small number of CHD events. To further investigate the interaction of BMI and hypertension, the study cohort was subdivided into normotensive and hypertensive individuals keeping the adjustment of confounding factors mentioned above. Here, only in the hypertensive individuals was a progressive increase in CHD events observed with increasing BMI, whereas no relation was found in normotensive subjects. These findings suggest that hypertension and increasing BMI jointly ‘prime’ development of CHD events. Several mechanisms may have lead to this epidemiological observation. Obesity comprises a variety of metabolic disorders, including insulin resistance, endothelial dysfunction, dyslipidemia and impaired glucose tolerance, along with repetitive episodes of hyperglycemia, imbalances in sodium turnover and altered sympathetic activity [21–23]. As these factors were not analysed, the present study cannot contribute any further mechanistic insights into potential pathophysiological mechanisms mediating the joint impact of obesity and hypertension on CHD events. With respect to arterial haemodynamics, systolic, diastolic and pulse pressure were similar between the three groups, independent of the BMI tertiles, which rules out major differences in vascular compliance or distensibility between the groups at baseline. It is an intriguing observation that the numbers of episodes with unstable angina (12/13/15) revealed an even distribution over all BMI tertiles, whereas the events with effort angina increased with increasing BMI. Although speculative, this suggests that hypertensive episodes in obese subjects might trigger destabilization of coronary plaques, which is related to increased shear forces at the endoluminal surface of the vascular wall [24]. What are the consequences for clinical routine and daily practice? The important message of the PRIME study is that individuals with obesity and arterial hypertension represent a high-risk group for developing coronary events within the near future. Thus, in case those subjects present themselves to their physicians for the first time, a careful and thorough diagnostic evaluation of such individuals with respect to potential CHD appears mandatory." @default.
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• W2315690806 date "2003-03-01" @default.
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• W2315690806 title "Obesity and hypertension in coronary heart disease" @default.
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