Educate the patient. One way to do this is to provide adequate patient education, stressing the importance of taking the medication exactly as prescribed and, when necessary, showing patients how to divide pills until the target dose is reached.
Respond to adverse effects. Closely monitoring for adverse effects is crucial, as well. The development of symptomatic bradycardia, second or third degree atrioventricular block, or a heart rate <50 BPM suggests that the dosage be reduced or the medication withheld, with this caveat: There is increasing recognition that heart rate and BP readings change throughout the day, and a decision to adjust or to halt beta-blocker therapy should not be based on a single measure.
That said, physicians should watch for clinical evidence of hypoperfusion, such as postural dizziness or decreasing urine output, when systolic BP approaches 80 to 90 mm Hg in patients with heart failure. In such cases, adjusting the dose, increasing the interval between doses, or even discontinuing beta-blocker therapy may be necessary.
Are beta-blockers contraindicated for these heart failure patients?
Because of the bradyarrhythmic and hypotensive effects of beta-blockers, the major heart failure trials excluded patients with a heart rate of <50 to 68 beats per minute (BPM) or systolic blood pressure <80 to 100 mm Hg (the ranges cited reflect the variation in cut points from one study to another).1-3,6 And in clinical practice, physicians often withhold beta-blocker therapy from heart failure patients who also have chronic obstructive pulmonary disease (COPD) or asthma, hypotension, or metabolic risk factors for diabetes.4 Some avoid prescribing beta-blockers because they believe that the drugs adversely affect patients’ quality of life, despite evidence to the contrary.3,23-25 In all these cases, there is little justification for doing so.
COPD and asthma. Although beta-blockers can worsen and precipitate bronchospasm, recent evidence suggests that patients with COPD and asthma can tolerate them.26-28 In fact, there is reason to believe that bronchospasm is aggravated by excessive stimulation and sensitization of the beta-2 receptors, and that blocking them may even be of therapeutic value.29 Nonetheless, the danger of worsening bronchospasm with a nonselective beta-blocker such as carvedilol remains—particularly for patients with asthma, who tend to have a higher degree of bronchial sensitivity and reactivity. So, while beta-blockers are not contraindicated for patients with COPD, their use in this patient population requires caution.30,31
Metabolic risk factors. Caution is also needed for patients with metabolic risk factors. Although beta-blockers have been found to increase the risk of diabetes, raise triglycerides, and lower high-density lipoprotein cholesterol,32-34 the benefits for patients with heart failure outweigh the risk. Physicians must remember that the mortality rate of heart failure, as well as the rate of progression, is higher than that of metabolic abnormalities, asymptomatic bradycardia, hypotension, or bronchospasm, which are relatively benign. In view of evidence that beta-blockers reduce both mortality and hospitalization rates associated with heart failure, the best approach is to continue beta-blocker therapy and seek control of risk factors and adverse effects.
CORRESPONDENCE HT Ong FRCP, FACC, FESC, HT Ong Heart Clinic, 251C Burma Road, Penang 103250, Malaysia; ongheanteik@gmail.com
