It is estimated that approximately 1 million patients are discharged from the hospital annually with a diagnosis of chronic heart failure (HF). As the population ages, the prevalence of HF will increase significantly. The number of patients admitted to the hospital with HF continues to grow at an unprecedented rate. Eighty percent of men and 70% of women younger than 65 years diagnosed with HF will die within 8 years. Long-term survival following the diagnosis of HF has been found to be better in women than in men. However, less than 15% of women diagnosed with HF survive more than 8 to 12 years. The mortality rate in this cohort is high, with one in five patients dying within 1 year.¹ Recognizing the devastating effects of various medications on the exacerbation of HF, this discussion focuses on best practices in the drug therapy management of patients with HF.

One third of all HF patients admitted to the hospital are readmitted for the same condition within 90 days. Analysis of the factors leading to this high readmission rate shows many preventable causes. Nearly 50% of readmissions are due to noncompliance either with a salt-restricted diet or with prescribed drug therapy. Sixteen percent of all hospital readmissions due to exacerbation of HF are associated with the use of inappropriate medications.²

These findings have led to the development of disease management programs based on clinical guidelines and standardized protocols designed to improve and optimize outcomes of both the in-patient and outpatient treatment of HF. These approaches use trained nurse clinicians and advanced nurse practitioners focusing on patient education during the in-patient stay. These programs also provide follow-up supervision
through telephone contact and outpatient monitoring. Close attention is paid to weight gain, adherence to a salt-free diet, appropriate adjustment of diuretic dosage, and potassium supplements. Moreover, the continuation of evidence-based care with angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARB), and beta-blockers is maintained.

Many patients with HF are elderly with multiple comorbid conditions and require long-term follow-up. The concomitant use of medications that have the potential to precipitate or exacerbate HF or to produce life-threatening arrhythmias must be closely monitored. Often, these drugs may have been prescribed by another physician for the treatment of a comorbid chronic condition such as diabetes mellitus or may be inadvertently consumed by the patient for the temporary relief of some type of ailment, for example, an over-the-counter nonsteroidal anti-inflammatory drug (NSAID) for arthritic pain.

The “2005 Guidelines for Diagnosis and Management of Chronic Heart Failure in the Adult”³ lists three classes of drugs that can exacerbate HF and that should be avoided in these patients. These include antiarrhythmic agents, calcium channel blockers, and NSAIDs.

Table 7-1 is a comprehensive list of medications that have the potential to precipitate or worsen HF. An extensive review of the literature has been conducted. Two excellent reports, by Amabile and Spencer⁴ and Feenstra et al.,⁵ have eloquently addressed the issue of medications that exacerbate HF.

In this discussion, agents traditionally used in the treatment of acute or chronic HF that may have potentially serious side effects have been excluded. Consideration of certain other medications is beyond the scope of this discussion, including chemotherapeutic agents such as the anthracyclines, cyclophosphamide, trastuzumab (Herceptin), and paclitaxel and the immunomodulating agents interferon-alpha and -gamma and interleukin-2. In addition, the adverse cardiovascular effects of anesthetic agents and the effects of recreational drugs are not addressed.

Drug-induced exacerbation of HF may occur for varying reasons. It may take place in patients with impaired left ventricular (LV) function due to increased cardiac afterload, as a result of increased systemic vascular resistance from vasoconstriction. It may also result from a rise in preload due to fluid retention and volume expansion and the depression of cardiac contractility caused by negative inotropy of drugs. However, other factors may also play an important role in producing adverse outcomes in HF. Some of these mechanisms are summarized in Table 7-2.