Belgian expert opinion: how to reduce the residual risk in atherogenic dyslipidaemic patients: place of fibrates.

in Acta Cardiologica (2008), 63(2), 235-48

The demographics of dyslipidaemia have changed towards a more complex atherogenic dyslipidaemia involving increased levels of LDL-C, in particular highly atherogenic small dense particles ... [more ▼]

The demographics of dyslipidaemia have changed towards a more complex atherogenic dyslipidaemia involving increased levels of LDL-C, in particular highly atherogenic small dense particles, hypertriglyceridaemia and low HDL, together with increased levels of markers of cardiovascular inflammation, thrombogenesis and endothelial dysfunction. Statins were shown to significantly lower cardiovascular morbidity and mortality, but there still remains a high residual risk in dyslipidaemic patients, in particular with metabolic syndrome, type 2 diabetes, or low HDL levels. Fibrates have been shown to reduce plasma triglycerides and increase HDL-C, while improving inflammation, thrombogenesis and endothelial dysfunction. Clinical trials with fibrates have demonstrated their potential to reduce cardiovascular morbidity and mortality too, often through other mechanisms than these of statins. Combination trials of statins with fibrates have shown a more complete improvement of lipid profile and risk markers than each class separately. In contrast with gemfibrozil, fenofibrate does not interact significantly with the pharmacokinetics of statins, and up to now its combination with statins has been shown to have a low risk of muscular side effects or liver toxicity. The ACCORD outcome trial is exploring the possible benefits of the combination of fenofibrate with statins on morbidity and mortality of patients with atherogenic dyslipidaemia. [less ▲]

The clinical signification of troponin T, troponin I, CK and CK-MB after coronary angioplsaty

in Acta Cardiologica (1998), 53

Hypertension and left ventricular hypertrophy

in Acta Cardiologica (1996), 51(2), 143-154

In response to high blood pressure, left ventricular hypertrophy develops. But in hypertension, the myocardial hypertrophied structure is abnormal. The prevalence of this hypertrophy is influenced by age ... [more ▼]

In response to high blood pressure, left ventricular hypertrophy develops. But in hypertension, the myocardial hypertrophied structure is abnormal. The prevalence of this hypertrophy is influenced by age, gender, weight, race, genetics and the severity of high blood pressure. By echocardiography, it has been possible to detect non invasively and more precisely this hypertrophy and its anatomical pattern which is not uniform. This cardiac response is influenced by hemodynamic but also by non hemodynamic factors, but the exact mechanisms are not yet well understood. The humoral and tropic factors particularly affect the cardiac remodeling. Left ventricular hypertrophy has been noted by itself to be an independent risk factor for sudden death, ventricular arrhythmias, myocardial ischemia, and heart failure. Very early hypertension, diastolic dysfunction is noted. The progression to systolic failure in moderate hypertension usually occurs over several decades. According to the worse prognosis of left ventricular hypertrophy, it has been suggested that the reversibility of this anatomical modification by antihypertensive treatment is beneficial. Preliminary data support this idea. [less ▲]

Hypertension and pregnancy

in Acta Cardiologica (1977), 32