Anticoagulants in congestive heart failure.

Abstract

Kinsey and White (1940) found clinical evidence of pulmonary infarction in 14 % of patients surviving episodes of cardiac failure and in 29% of those dying in heart failure but not submitted to necropsy. Where necropsy was carried out the incidence of pulmonary infarction was found to be nearly 50%. Wishart and Chapman (1948) found clinical or necropsy evidence of pulmonary embolism in only 6.5 % of patients with congestive heart failure given bishydroxycoumarin (dicoumarol) prophylactically. Subsequent trials have shown an incidence of thromboembolic complications ranging from 2% to 7% in congestive-failure patients given anticoagulants, as compared with 8 % to 33 % of controls

The Diagnostic and Therapeutic Value of Spironolactone in Patients with Systemic Hypertension

“…The increase in serum urea concentration in group 1 and 2 during spironolactone therapy was ac companied by an increase in the daily urinary urea excretion and was unassoci ated with any change in the serum creatinine concentration, suggesting that the spironolactone had resulted in an increase in endogenous protein catab olism. This observation is similar to that reported in patients with congestive cardiac failure during treatment with diuretics [18].…”

Metabolism of Digoxin in Relation to Therapy in the Elderly

“…Since the relationship of glomerular filtration rate to blood urea is not linear, and is affected by the urea production rate, which may be reduced in old age as a consequence of reduced lean body mass and reduced protein intake, or conversely increased by the presence of severe congestive failure [Domenet and Evans, 1969], the blood urea is a poor guide to digoxin ex cretion. Serum creatinine levels may be more helpful, but again may be below the upper limit of normal of 1.6 mg/100 ml in the presence of greatly reduced creatinine clearance.…”