Enoxaparin may have resulted in increased bleeding complications and use of blood products in patients with renal insufficiency. Prospective studies need to be conducted to define the drug's role and dosage adjustments in these patients.

Patients with cardiac disease, specifically ischemic heart disease and heart failure, have a higher frequency of major depressive disorder than patients without cardiac disease. The pathophysiologic reason for this is not completely understood. Previous depression, other debilitating illnesses, and type A personality are risk factors for the development of depression in cardiac patients. Depression has been shown to lower the threshold for ventricular arrhythmias. Therefore, treatment of depression potentially may prolong life in these patients. Antidepressant options that have been evaluated include several of the tricyclic antidepressants, trazodone, bupropion, and several of the selective serotonin reuptake inhibitors. Individual antidepressant drugs vary in their pharmacologic activity and side-effect profiles. Although clinical data are limited, it is important to individualize therapy in order to minimize cardiac adverse effects. Clinicians are encouraged to evaluate patients with cardiac disease for major depressive disorder and to consider antidepressant drug therapy for these patients when appropriate.

No abstract

The use of diuretics for the treatment of sodium retention in congestive heart failure was evaluated. Particular focus was given to the altered renal response to diuretics in patients with heart failure and adverse responses to diuretic therapy. Highlighted information included historical aspects of the development of diuretics, mechanisms of sodium retention, the physiologic and clinical response to diuretics, and the altered pharmacokinetics and pharmacodynamics of diuretics in congestive heart failure. Despite more than 60 years of empiric diuretic use in heart failure, the actual database regarding the long-term efficacy, adverse effects, and altered mortality outcome in heart failure is relatively small. Existent pharmacokinetic and pharmacodynamic data are typically not collected within the context of heart failure efficacy trials. In addition to altered electrolyte transport and total-body electrolyte depletion, diuretics may be associated with adverse neurohormonal activation. Thus, guidelines for acute and long-term therapy with diuretics in heart failure remain somewhat empiric. Diuretics will remain a mainstay for the treatment of edema in congestive heart failure but must be accompanied by moderate sodium restriction. However, large clinical trials of diuretics would be necessary to demonstrate that improved clinical efficacy with edema reduction is not offset by adverse effects, which include electrolyte depletion, ventricular arrhythmias, and subsequent increased mortality.