Beta-adrenergic blockers delay the clinical progression of systolic dysfunction HF and reduce mortality. This is a new therapeutic concept and runs counter to the long-held dogma that HF was considered an absolute contraindication for prescribing beta-adrenergic blockers because of their negative inotropic effects. The observation that prolonged activation of the sympathetic nervous system can accelerate the progression of HF led researchers to explore the potential value of beta-adrenergic blockers in patients with systolic dysfunction HF. Recent clinical trials of NYHA II and III HF patients have demonstrated improved symptoms, increased LV EF, prevention of HF progression, and further reduction in mortality of 30% to 65% when beta-blockers are added to standard HF therapy (ACE inhibitor, diuretic, and or digoxin).
There are three beta-blockers that have shown positive effects in HF patients: carvedilol, bisoprolol, and metoprolol CR/XL. These medications have some pharmacologic differences and it is unclear if they have equivalent efficacy. Metoprolol exhibits beta1 (heart chronotropic) selectivity, bisoprolol has both beta1 and beta2 (peripheral vasoconstrictor) blockade, and carvedilol has beta1 and beta2 blockade as well as some alpha-1 (peripheral vasodilator) blocking properties. Initial clinical trials have shown benefit for patients with stable moderate HF (NYHA II, III) who are already taking standard HF therapy. There is less evidence for clinical or mortality benefit for mild HF patients (NYHA I) or for those with severe disease (NYHA IV HF patients).
Beta-blockers are initiated at low doses with a slow titration necessary until the target doses are achieved. (For carvedilol there appears to be significant change in LVEF and reduced hospitalizations even at 6.25 mg twice daily.) Patients should not have marginal fluid balance or they may not tolerate the medication initially. Patients may experience worsening symptoms, dizziness and fatigue, and the physician should determine if this due to overdiuresis (hypotension and dizziness), under diuresis (worsening dyspnea or fatigue), or the medication. Many patients require even slower titration and some do not tolerate target doses due to adverse effects. Persistence and encouragement are important because initial adverse drug effects often resolve if the patient continues on the medication.
Carvedilol can be taken with food to blunt peak drug levels and improve tolerance. Metoprolol CR/XL, because of its continuous drug absorption, may be tolerated better, and high dosages of this drug formulation were achieved in the trials (mean dose in MERIT-HF was >150 mg/day). It is still unclear if lower doses of metoprolol CR/XL produce the same effects. With reassurance and persistence, most patients will have improved symptoms with further up-titration of the drug and will tolerate the medication; less than 5% of patients in the beta-blocker trials stopped the drug as a result of adverse effects.
The evidence is strong and consistent for NHYA II and III HF patients that "triple therapy" with diuretics, ACE inhibitors, and beta-blockers provides the best outcomes. If patients are still symptomatic on this therapy, then digoxin may be added to augment cardiac contractility.
Treatment of Isolated Diastolic Dysfunction Treatment of HF owing to diastolic dysfunction is largely empiric and directed toward reversing or optimally managing the presumed underlying causes shown in Table 1 . The methods for achieving and maintaining optimal fluid balance are similar to those described for systolic dysfunction. Rapid or overdiuresis should be avoided as small changes in intravascular volume may cause significant decreases in diastolic filling and cardiac output. Treatment of cardiac ischemia may improve diastolic function.
The ideal drug for isolated diastolic dysfunction would have potent "lusotropic" effectsódirect improvement of the relaxation phase of the LV. Although the ideal lusotropic drug does not exist, nitrates, beta-blockers, and non-dihydropyridine calcium channel blockers all have pharmacologic properties that may improve diastolic dysfunction. Unfortunately, there is little direct evidence for their effectiveness in treating diastolic dysfunction. Beta-blockers are particularly attractive in this regard because of their antiischemic and rate limiting properties, both of which may improve diastolic filling. ACE inhibitors are often appropriate but compared with treatment of systolic dysfunction there is no evidence for specific indications in diastolic dysfunction HF.
Conversion of atrial fibrillation to sinus rhythm will restore the atrial component of diastolic filling and may improve cardiac output. If conversion to sinus rhythm is not feasible, then ventricular rate control with a rate limiting calcium channel blocker or digoxin may allow more complete ventricular filling in diastole. Theoretically, digoxin would not be indicated for patients with diastolic dysfunction; however, a subgroup analysis of the recent DIG clinical trial showed surprising improvement in clinical outcomes for the small number of patients in the study who had normal LVEF . Until more evidence is available, however, digoxin should be reserved for diastolic dysfunction patients who have a separate indication such as atrial fibrillation.
Establishment of Patient Goals for Self-Care, Determine the Level of Ancillary Support Needed, and Utilize a Regular Follow-Up Schedule HF patients often have multiple comorbid conditions and complex medication regimens. Some may have an incomplete understanding of HF, the role of diet, and use of specific medications. Noncompliance with diet and medication account for 35% to 50% of the reasons for recurrent hospitalizations. For these reasons, an essential management task of the primary care physician is to assist the patient in acquiring self-care attitudes and knowledge of the disease.
Patient education and self-care are important components of maintaining clinical stability. One approach is to assign specific responsibilities to an interested and knowledgable support staff person who is then given the charge to contact the patients on a regular basis. Starting on a small scale with clear measurable outcomes and adding more patients as resources and priorities allow would be a first step introducing more consistent monitoring for HF patients.
Patients should receive education about the causes of HF, the reason(s) for the heartís reduced performance, how this leads to the development of specific symptoms, and the potential for disease progression. This can be followed by a discussion of how those specific symptoms are treated and how disease progression can be delayed or controlled. Patient should be queried about specific health-related goals. Patients need to hear that optimal care involves a partnership with the physician, and they need to fulfill their role in the partnership to achieve success. They have specific responsibilities in managing symptoms.
Heart Failure Patientís Responsibilities for Self-Care
1. Measure and record your weight daily. If weight increases > 2 to 3 pounds/day contact office and increase diuretic if directed to do so by your physician.
2. Regularly assess severity of shortness of breath and leg edema.
3. Follow low sodium diet.
4. Engage in regular activity or follow specific exercise prescription.
5. Take medications as prescribed.
6. Abstain from or limit alcohol use.
7. Take aceteminophen for pain rather than NSAIDs; call doctor if stronger medications are needed.
8. Keep follow-up appointments.
The patient should be instructed to weigh themselves daily and monitor volume status symptoms such as peripheral edema or dyspnea. Baseline weight is determined when the patient is at optimal fluid balance on a stable medical regimen. The patient should contact the office if they experience a weight gain of greater than 3 to 5 pounds in a week or if they have worsening peripheral edema or dyspnea. Reliable patients may be instructed to increase daily diuretic dose for 2 to 4 days when they see an increase in daily weights.
Patients should limit sodium intake to 2 to 3 g per day or less by avoiding salty tasting foods and not adding salt at the table as well as by reading nutritional labels to choose lower sodium food options. A 7-day diet record may be helpful in identifying high sodium foods for individual patients. A sudden increase in dietary sodium intake is a frequent cause of acute fluid overload, pulmonary congestion, and hospitalization.
To prevent progressive skeletal muscle deconditioning and reduced physical functioning, patients should be evaluated for low level exercise prescription. Exercise training is an effective intervention that reverses some of the exaggerated peripheral compensatory changes in patients with stable mild to moderate (NYHA I-III) systolic dysfunction HF. A series of randomized trials have shown improvements in a number of peripheral hemodynamic parameters with diminished symptoms and improved physical functioning. Most trials have used supervised aerobic exercise on treadmills or stationary cycles and have excluded patients with a history of ventricular tachyarrhythmias. The long-term effect of exercise training on HF mortality has not been studied.
Patients should also appreciate the importance of taking their medications as prescribed. In addition, they should be encouraged to abstain from alcohol and to use acetominophen rather than NSAIDs as over-the-counter medication for pain. If acetominophen does not adequately control the pain, then the patient should contact the office to discuss the use of other pain relieving medicines.
Follow-up should be regularly scheduled and not left to up to the patientís initiative. The frequency of follow-up depends upon the patientís symptom severity, hospitalization history, social support, plans for titration of new medications, and ability to comply with the medical regimen and self-care responsibilities.
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