Fifteen year mortality in Coronary Drug Project patients: long-term benefit with niacin.

The Coronary Drug Project was conducted between 1966 and 1975 to assess the long-term efficacy and safety of five lipid-influencing drugs in 8,341 men aged 30 to 64 years with electrocardiogram-documented previous myocardial infarction. The two estrogen regimens and dextrothyroxine were discontinued early because of adverse effects. No evidence of efficacy was found for the clofibrate treatment. Niacin treatment showed modest benefit in decreasing definite nonfatal recurrent myocardial infarction but did not decrease total mortality. With a mean follow-up of 15 years, nearly 9 years after termination of the trial, mortality from all causes in each of the drug groups, except for niacin, was similar to that in the placebo group. Mortality in the niacin group was 11% lower than in the placebo group (52.0 versus 58.2%; p = 0.0004). This late benefit of niacin, occurring after discontinuation of the drug, may be a result of a translation into a mortality benefit over subsequent years of the early favorable effect of niacin in decreasing nonfatal reinfarction or a result of the cholesterol-lowering effect of niacin, or both.

Clinical trials on the efficacy of pharmacologic intervention reducing mortality from cardiovascular diseases.

Results of recent clinical trials on secondary prevention of ischemic heart disease indicate that judicious, long-term administration of adrenergic beta blockers and platelet-active drugs such as aspirin and Persantine (dipyridamole) would seem to yield protection against mortality associated with acute myocardial infarction, including sudden death. These drugs are beneficial also in prevention of recurrent myocardial infarction, especially among patients with unstable angina. These drugs should be considered as soon as the diagnosis of myocardial infarction or unstable angina is confirmed clinically. In terms of primary prevention of ischemic heart disease and cerebrovascular disease (stroke), the results of the Hypertension Detection and Follow-Up Program provide an excellent set of data on the efficacy of rigorous treatment of hypertension, especially those with mild hypertension. To be effective, treatment must start before there is evidence of target end organ damage, such as left ventricular hypertrophy. Recent data from the Australian Therapeutic Trial in Mild Hypertension also confirms these findings.

Iatrogenic hyperthyroidism secondary to dextrothyroxine administration.

Two patients are reported who presented with clinical hyperthyroidism, increased serum thyroid function studies, and depressed radioactive iodine uptake, secondary to chronic ingestion of D-T4. Symptoms abated, and function studies returned to normal, following discontinuation of D-T4. This uncommon effect of D-T4 may be more prevalent than is generally realized and must be recognized as another potential cause of low radioiodine uptake in patients with clinical hyperthyroidism.

Elevated triiodothyronine and dextrothyroxine levels: a potential cause of iatrogenic hyperthyroidism.

A woman in whom the use of dextrothyroxine was associated with clinical hyperthyroidism is described. She had a markedly elevated T3 level while receiving the drug, apparently resulting from conversion of the dextrothyroxine to triiodothyronine. The T3 levels fell to normal after withdrawal. Patients receiving dextrothyroxine should be examined for possible elevation of T4 and T3 thyrotoxicosis.