Knöchelödeme nicht alle Dihydropyridin-Kalziumantagonisten sind gleich beschaffen

Pedal oedema is a common dose dependent adverse effect of dihydropyridine calcium antagonists. Pathogenetic mechanisms leading to pedal oedema are related to a calcium antagonist induced paresis of the precapillary sphincter resulting in intracapillary hypertension. Intracapillary hypertension increases capillary permeability and facilitates oedema formation. Longstanding pedal oedema can lead to hyperpigmentation and dyspigmentation. Calcium antagonist induced pedal oedema is more common in women than in men and increases with age. Recent studies have documented that not all dihydropyridine calcium antagonists are created equal with regard to pedal oedema. For a given fall in blood pressure, lercanidipine and lacidipine are associated with lesser pedal oedema than is amlodipine. The pedal oedema associated with calcium antagonist does not respond well to diuretic therapy since it is not directly caused by sodium retention. The addition of a blocker of the renin angiotensin system (ACE inhibitor, angiotensin receptor blocker, direct renin inhibitor) by opening the post capillary sphincter diminishes intracapillary pressure and therefore has a mitigating effect on the calcium antagonist induced pedal oedema.