Dr. Jana Brguljan,
Hypertension is well known to be one of the most important risk factors affecting cardiovascular morbidity and mortality across the world. It is also well recognised that elevated blood pressure (BP) is a powerful predictor of outcome and the best thing that can be done is to start treating high BP on time to prevent target organ damage. In some cases, damage is already done and it is useful to know how we can improve CV risk prediction focusing on the intermediate endpoints such as left ventricular hypertrophy (LVH), microalbuminuria and renal function, arterial stiffness and carotid intima-media thickness. LVH presents the heart’s response to increased biomechanical stress such as hypertension, as pointed out by Prof.Manolis. Prevalence of LVH varies depending on different diagnostic tests like ECG (1-8%) and echocardiography (20-30% in mild and moderate and 50-60% in severe hypertension.) Magnetic resonance is also a useful tool to detect LVH, but for daily clinical practice we probably cannot afford its costs. Molecular diagnosis of LVH would be useful but there is no reliable marker for the moment. LVH also affects function of the left atrium and presents a risk factor for developing atrial fibrillation. According to the ESH/ESC 2007 guidelines, ACE inhibitors /calcium antagonists / angiotensin-receptor blockers are still drugs of choice. It was also shown that the higher the plasma aldosterone concentration, the lower LVMI. Microalbuminuria and impaired renal function are known to be powerful predictors of cardiovascular outcome and new onset type 2 diabetes. Prof.Scmieder suggested that endothelial dysfunction is the common denominator associated with these deleterious outcomes. Correct diagnosis of microalbuminuria is important and should be based upon morning urine sample. Diagnosis of renal impairment should result in the initiation of antihypertensive therapy. Blockade of the RAAS system may result in an initial decline in glomerular filtration rate. However a decline of 10-20% is not normally of prognostic significance. Arterial stiffness measured by carotid femoral pulse wave velocity represents one of the measures of target organ damage, listed in the 2007 ESH-ESC Guidelines for the management of hypertension. The question is whether arterial stiffness is a surrogate end-point and, if demonstrated, can it be directly applied to clinical practice? Prof. Laurent reported that aortic stiffness has predictive value for all-cause and CV mortality, and total CV events. A novel cut off value for pulse wave velocity of 10m/s will be suggested in future guidelines. The further question that needs to be answered is whether this novel marker adds further predictive information to established standard risk markers. The evidence suggest that aortic stiffness has predictive value independent of classical CV factors and this will be investigated in the SPARTE study which will start in France next year. Prof.Schmidt-Trucksaess pointed out that an increase of one standard deviation in mean common carotid intima media thickness resulted in a 22% increase for MI and 21% for stroke. Therefore it is an important marker for CV events, but it is important to note that the proper measurement procedure should be followed. This was an interesting session that considered the predictive validity of various intermediate endpoints. The presenters provided cogent and compelling arguments to support the validity of their respective endpoints. However, we need to make an effort to include them in our daily practice and see how universally applicable each of these measures will be in routine clinical practice and how cost effective they will be.
Improving risk prediction focusing on intermediate endpoints
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