[Hypokalemia, hypomagnesemia and ventricular arrhythmia during diuretic treatment of arterial hypertension].

Diuretics have been used for 25 years in the treatment of arterial hypertension, where they have proved effective and well tolerated. However, recent therapeutic trials have failed to demonstrate a significant reduction of coronary disease mortality in moderately hypertensive patients under antihypertensive therapy. These disappointing results have led to a reappraisal of the cardiovascular risk inherent in antihypertensive treatments and notably diuretics. Thiazides and the so-called heigh-ceiling diuretics increase urinary potassium excretion, thereby reducing serum potassium levels by 0.3 to 0.6 mmol/l on average. Kalaemia falls below 3.0 mmol/l in 1 to 7 percent of the patients. The long-term consequences of hypokalaemia are imperfectly known. Several authors have used continuous or exertion electrocardiographic recordings to evaluate the risk of ventricular arrhythmia induced by hypokalaemia, but their results are conflicting and inconclusive. The risk of ventricular arrhythmia is perhaps not negligible when hypokalaemia occurs in certain patients with coronary disease or left ventricular hypertrophy who are under digitalis therapy. Diuretics also reduce serum levels of magnesium. The consequences of isolated hypomagnesaemia are obscure. The risk of hyperexcitability seems to be increased when hypokalaemia is associated with digitalis toxicity. The fall in serum concentrations of potassium and magnesium is dose-dependent, and it occurs mainly with the excessive doses formerly prescribed. The dose-response curve of antihypertensive agents is relatively flat, which suggests that diuretics should be used in lower dosage.