Heart failure: 
An update on current care

■ Either diastolic or systolic dysfunction can precede or accompany clinical HF.

■ Effectiveness of ACE inhibitors for risk reduction and symptom relief is common to all drugs in that class.

■ Three specific beta-blockers have been shown to be effective in reducing mortality from heart failure: bisoprolol, carvedilol, metoprolol succinate.

■ ACE inhibitors and specific beta-blockers should be used at their earliest indication in patients at risk for development of HF.

■ Unless specifically contraindicated, patients with asymptomatic left ventricular hypertrophy, reduced EF, or HFREF should be on an ACE inhibitor and a beta-blocker, as both have been shown to reduce mortality.

■ ARBs are an acceptable alternative, especially if the patient develops cough, which is the most common side effect of ACE inhibitors.

■ Hydralazine/isosorbide dinitrate is indicated as adjunctive therapy for African American patients with persistent symptoms of HF.

■ Indications for device therapies, such as ICD, will broaden as medical technology improves.

WHO SHOULD READ THIS?


PAs who provide adult primary care or manage patients with heart failure (HF). These guidelines do not apply to solely right-sided heart failure or to the pediatric population.


WHY IS THIS IMPORTANT?


Heart failure is a leading cause of hospitalization and death in persons 65 years or older.¹ The prevalence of HF is 1% to 2% in industrialized countries, and the rate is increasing.^1-4


Three goals of management are to (1) delay onset of refractory, end-stage disease, (2) avoid acute decompensated heart failure, and (3) reduce the incidence of sudden cardiac death (SCD). The American Heart Association (AHA) and the Heart Failure Society of America (HFSA) have published guidelines for HF diagnosis and management.^5,6


WHAT IS IMPORTANT 
TO KNOW?


Clinically, HF represents cardiac pumping capacity that is inadequate to meet the body's metabolic demands. To achieve adequate peripheral perfusion, left ventricle systolic forces must be sufficient to move an adequate volume of blood against systemic BP. Left ventricular ejection fraction (LVEF) is one criterion used to assess HF. Heart failure with reduced ejection fraction (HFREF) represents impaired systolic function. Customarily, disease progression is demonstrated by increasing reductions in LVEF.


Heart failure also occurs with preserved LVEF (HFPEF). This less-studied type of HF represents diastolic dysfunction and accounts for 30% to 50% of patients meeting clinical criteria for heart failure.^2,4,7 Patients who are older, female, or have hypertension tend to have HFPEF, but no clinical or demographic characteristics are exclusive for either type of HF.^4,7 Clinical prognosis appears similar, but further research is needed.^2,4-7 Also, clinically evident HF is rarely uniphasic. The Seattle Heart Failure Model is useful for assessing prognosis.⁸


Coronary disease and long-standing hypertension are the most common causes of HF.² Other antecedents include cardiomyopathies, valvular disease, arrhythmias, and diabetes. Renal and other end-organ dysfunction promote disease development. AHA and HFSA guidelines recommend identifying patients with these conditions and aggressively treating modifiable risk factors.^3,5,6 


Inflammation, with cytokine activation, initiates HF development.⁹ Unfortunately, targeting this pathway has proven therapeutically unsuccessful.³ The renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system (SNS) compensate for early hemodynamic deficits, but they are detrimental over time.⁹ A pathologic phenotype emerges: Myocyte hypertrophy increases local ischemia; apoptosis and fibrosis enhance left ventricle dysfunction.^2,10 The RAAS and SNS are primary targets of medical therapy. ACE inhibitors prevent progression of HF. Angiotensin-receptor blockers (ARBs) are indicated when ACE inhibitors are not tolerated. Three beta-blockers have been shown to reduce HF mortality (bisoprolol, carvedilol, and metoprolol succinate). An ACE inhibitor plus one of those beta-blockers is recommended for asymptomatic patients with reduced LVEF and should be prescribed at their earliest indication.^3,5,6


The New York Heart Association functional classes of HF are widely used, despite known interobserver variability and inability to capture preclinical HF.^5,11 The AHA developed a four-stage approach that addresses these flaws and couples therapies with structural disease and symptoms (Table 1). 


Subjective evidence of HF includes dyspnea, fatigue, and exercise intolerance. Objective evidence includes fluid retention in the systemic or pulmonary circulation plus impaired LV dynamics. The classic finding of rales is often absent.³ Two commonly used diagnostic screening tools are the Boston and the Framingham criteria.¹² Several serum biomarkers have been studied.⁹ Two are notable here: brain natriuretic peptide (BNP) and N-terminal pro-BNP. Testing for these markers is recommended in an acute setting when the diagnosis is not confirmed by thorough clinical workup. Testing is not recommended as routine indicators of HF progression.⁵


NSAIDs, antiarrhythmic drugs, and calcium channel blockers may exacerbate HF or increase HF hospitalization and are therefore best avoided in patients with HFREF.^5,6