Heart failure is a common and complex clinical syndrome that results from any functional or structural heart disorder, impairing ventricular filling or ejection of blood to the systemic circulation to meet the body's needs. Heart failure can be caused by diseases of the endocardium, myocardium, pericardium, heart valves, vessels or metabolic disorders. Most patients with Heart failure have symptoms due to impaired left ventricular myocardial function. Patients usually present with dyspnea and fatigue limiting exercise tolerance, fluid retention characterized by pulmonary and peripheral edema.
Heart failure due to left ventricular dysfunction is categorized according to left ventricular ejection fraction (LVEF) into heart failure with reduced ejection fraction (LVEF 40% or less), known as HFrEF and heart failure with preserved ejection fraction (LVEF greater than 40%); known as HFpEF.
Heart failure is caused by several disorders, including diseases affecting the pericardium, myocardium, endocardium, cardiac valves, vasculature, or metabolism.
The most common causes of systolic dysfunction (HFrEF) are idiopathic dilated cardiomyopathy (DCM), coronary heart disease (ischemic), hypertension, and valvular disease. For diastolic dysfunction (HFpEF), similar conditions have been described as common causes, adding hypertrophic obstructive cardiomyopathy, and restrictive cardiomyopathy.
Approximately 5.1 million people in the United States have clinically manifest heart failure, and the prevalence continues to increase. Heart failure incidence has remained stable over the past decades, with more than 650,000 new cases heart failure cases diagnosed annually, especially for individuals greater than 65 years of age. Because prevalence is greater in this age group, heart failure is expected to worsen in the future.Epidemiological differences have been noted. Black men have the highest incidence rate (1000 person-years) for heart failure and the greatest five-year mortality rate when compared to whites. White women represent the lowest incidence. Heart failure in non-Hispanic black males and females has a prevalence of 4.5% and 3.8%, respectively, versus 2.7% and 1.8% in non-Hispanic white males and females, respectively. Although survival has improved, the absolute mortality rates for patients with heart failure remain approximately 50% within five years of diagnosis.
By 2013, heart failure costs in the United States exceeded $30 billion.
The adaptive mechanisms that may be adequate to maintain the overall contractile performance of the heart at relatively normal levels become maladaptive when trying to sustain adequate cardiac performance. The primary myocardial response to chronically increased wall stress is myocyte hypertrophy, death due to apoptosis, and regeneration. This process eventually leads to remodeling, usually the eccentric type, and reduced cardiac output, causing a cascade of the neurohumoral and vascular mechanism.
Decreased carotid baroreceptor stimulation and renal perfusion will activate the sympathetic nervous system and Renin-Angiotensin-Aldosterone system.
Sympathetic nervous system activation will cause increased heart rate and inotropy, leading to myocardial toxicity. Renin-Angiotensin-Aldosterone system activation leads to vasoconstriction, increasing afterload (angiotensin II) and hemodynamic alterations, increasing preload (aldosterone).
All of these mechanisms will cause negative remodeling and worsen the left ventricular function, causing symptoms of heart failure.
Symptoms of heart failure include those due to excess fluid accumulation (dyspnea, orthopnea, edema, pain from hepatic congestion, and abdominal distention from ascites) and those due to a reduction in cardiac output (fatigue, weakness) that is most pronounced with physical exertion.
Acute and subacute presentations (days to weeks) are characterized by shortness of breath at rest and/or with exertion, orthopnea, paroxysmal nocturnal dyspnea, and right upper quadrant discomfort due to acute hepatic congestion (right heart failure). Palpitations, with or without lightheadedness can occur if patient develops atrial or ventricular tachyarrhythmias
Chronic presentations (months) differ in that fatigue, anorexia, abdominal distension, and peripheral edema may be more pronounced than dyspnea. The anorexia is secondary to several factors including a poor perfusion of the splanchnic circulation, bowel edema, and nausea induced by hepatic congestion.
Diuretics, beta-blockers, angiotensin converting enzyme inhibitors, angiotensin receptor blockers, angiotensin receptor neprilysin inhibitor, hydralazine plus nitrate, digoxin, and aldosterone antagonists can produce an improvement in symptoms
Prolongation of patient survival has been documented with beta blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor neprilysin inhibitor, hydralazine plus nitrate, and aldosterone antagonists. More limited evidence of survival benefit is available for diuretic therapy. Replace an angiotensin converting enzyme inhibitors or angiotensin receptor blockers by angiotensin receptor neprilysin inhibitor in chronic symptomatic patients with CHF NYHA class II-III with an adequate blood pressure who are tolerating an optimal dose of these medications. Angiotensin receptor neprilysin inhibitor should not be given within 36 hrs of angiotensin converting enzyme inhibitors dose.
In African-Americans, hydralazine plus oral nitrate is indicated in patients with persistent NYHA class III to IV HF and LVEF less than 40%, despite optimal medical therapy (beta-blocker, angiotensin converting enzyme inhibitors, ARB, aldosterone antagonist (if indicated), and diuretics.
Device therapy: implantable cardioverter-defibrillator (ICD) is used for primary or secondary prevention of sudden cardiac death. Cardiac resynchronization therapy with biventricular pacing can improve symptoms and survival in selected patients who are in sinus rhythm and have a reduced left ventricular ejection fraction and a prolonged QRS duration. Most patients who satisfy criteria for cardiac resynchronization therapy implantation are also candidates for an implantable cardioverter-defibrillator and receive a combined device.
A ventricular assist device (bridge to transplant or as a destination therapy) or cardiac transplant are reserved for those with severe disease despite all other measures.
To reduce heart failure hospitalizations, it is reasonable (class IIa) to use Ivabradine in patients with NYHA II-III with guideline-directed medical therapy (including a beta-blocker) and heart rate of more than 70 bpm.
Heart failure disease management is a complex condition that requires a multidisciplinary framework for the care of patients, including discharge planning, patient education, and frequent outpatient assessment.
Heart failure is a serious disorder that is best managed by an interprofessional team that includes the primary care physician, emergency department physician, cardiologist, radiologist, cardiac nurses, internist, and a cardiac surgeon. It is imperative to treat the cause of heart failure. Healthcare workers who look after these patients must be familiar with current guidelines on treatment. The risk factors for heart disease must be modified and the pharmacist should educate the patient on the importance of medication compliance. When the condition is not managed appropriately, it is associated with high morbidity and mortality, including a poor quality of life.