Heart Failure

Heart failure is a progressive clinical syndrome that occurs when the heart is unable to pump sufficient blood to meet the body's metabolic needs.
It can result from any disorder that damages the pericardium, heart valves, myocardium, or ventricle function.
The primary manifestations of heart failure are dyspnea, fatigue, and fluid retention.
Outdated term "congestive heart failure" is inaccurate because patients may present without congestion.

Coronary artery disease is the most common cause of systolic heart failure, accounting for nearly 70% of cases.
Ischemic heart disease and hypertension contribute to the development of heart failure.
Systolic dysfunction (decreased contractility) can result from:
- Reduction in muscle mass (e.g., myocardial infarction)
- Dilated cardiomyopathies
- Ventricular hypertrophy:
  - Pressure overload (e.g., systemic or pulmonary hypertension, aortic or pulmonic valve stenosis)
  - Volume overload (e.g., valvular regurgitation, shunts, high-output states)
Diastolic dysfunction (restricted ventricular filling) can result from:
- Increased ventricular stiffness
- Ventricular hypertrophy, hypertrophic cardiomyopathy
- Infiltrative myocardial diseases (e.g., amyloidosis, sarcoidosis, endomyocardial fibrosis)
- Myocardial ischemia and infarction
- Mitral or tricuspid valve stenosis
- Pericardial disease (e.g., pericarditis, pericardial tamponade)

Heart's decrease in pumping capacity results in compensatory responses to maintain cardiac output (CO).
Responses are intended to be short-term after acute reductions in blood pressure or renal perfusion.
Persistent decline in CO in heart failure results in long-term activation of compensatory responses, leading to functional, structural, biochemical, and molecular changes.
Compensatory mechanisms include:
- Tachycardia and increased contractility
- Fluid retention and increased preload
- Vasoconstriction and increased afterload
- Ventricular hypertrophy and remodeling

Ventricular hypertrophy is a term used to describe an increase in ventricular muscle mass.
Cardiac or ventricular remodeling is a broader term that describes changes in both myocardial cells and extracellular matrix, resulting in changes in the size, shape, structure, and function of the heart.
Ventricular hypertrophy and remodeling can occur in association with any condition that causes myocardial injury, including MI, cardiomyopathy, hypertension, and valvular heart disease.

Initiating event leads to decreased CO.
Becomes a progressive systemic disease mediated by neurohormones and autocrine/paracrine factors.
Not a full explanation: drug therapies that target neurohormonal imbalances slow progression but do not stop disease progression.

Neurohormones: angiotensin II, norepinephrine, aldosterone, natriuretic peptides (ANP, BNP, CNP), and arginine vasopressin.
Autocrine/paracrine factors: proinflammatory cytokines (TNF-α, IL-6, IL-1β), endothelin peptides, and other circulating mediators.

Previously compensated patients may develop worsening symptoms that require hospitalization.
Factors that exacerbate or may precipitate heart failure:
- Noncompliance with medications and dietary recommendations.
- Cardiac events: MI, ischemia, coronary artery disease, atrial fibrillation.
- Non-cardiac events: pulmonary infection, anemia.
- Inadequate or inappropriate medications.
Most causes are preventable.