Relation of plasma aldosterone concentration to diuretic treatment in patients with severe heart disease.

Abstract

suMMARY To assess the relation of hyperaldosteronism and potassium depletion to the intensity of diuretic therapy we have measured plasma aldosterone by radioimmunoassay and total exchangeable potassium by radioisotope dilution in 24 patients when they were stable at the end of their preparation for cardiac operation.Some patients required intensive frusemide therapy to reach an optimal state for operation and many showed hyperaldosteronism. Plasma aldosterone was significantly related to daily dose of frusemide (r=0O77).Depletion of total exchangeable potassium expressed in terms of predicted weight was significantly related to plasma aldosterone (r= -0 64). The reduction in total exchangeable potassium is interpreted as chiefly related to loss of lean tissue mass from the wasting that leads to cardiac cachexia, but evidence is presented on the basis of measurements of extracellular fluid volume as sulphate space (20 patients) of entry of sodium into the cells which may indicate a true cellular potassium loss.

A propensity-matched study of the effects of chronic diuretic therapy on mortality and hospitalization in older adults with heart failure

“…Drugs that reduce mortality and morbidity in heart failure do so by suppressing these hormones [18]. Poor outcomes associated with diuretic therapy observed in our analysis may in part be explained by the activation of neurohormones by diuretics [19][20][21][22]. In particular, diuretic associated activation of aldosterone is associated with stimulation of pro-inflammatory cytokines, myocardial fibrosis, disease progression and poor outcomes in heart failure [23][24][25][26].…”

Association of serum bicarbonate with long-term outcomes in patients hospitalized with heart failure

“…We speculate that patients with greater changes in HCO 3 levels had correspondingly greater activation of the RAAS. Since the magnitude of RAAS activation correlates with HF severity and prognosis, we suspect that this mechanism likely contributed to our observations [6][7][8][9].…”

Fiftieth anniversary of aldosterone: from discovery to cardiovascular therapy

“…Intensive diuretic therapy may provoke hyperaldosteronism, which exacerbates potassium loss [109]. Interestingly, diuretic therapy was not associated with kaliuresis in adrenalectomised patients, thereby suggesting that it is the hyperaldosterone response to diuretic therapy that induced the kaliuresis, and not the diuretic itself [110].…”