HEART FAILURE

Definition and etiology

Heart failure is a clinical syndrome characterized by systemic perfusion inadequate to meet the
body's metabolic demands as a result of impaired cardiac pump function. This may be further
subdivided into systolic or diastolic heart failure. In systolic heart failure, there is reduced
cardiac contractility, whereas in diastolic heart failure there is impaired cardiac relaxation and
abnormal ventricular filling

The most common cause of heart failure is left ventricular (LV) systolic dysfunction (about 60%
of patients). In this category, most cases are a result of end-stage coronary artery disease, either
with a history of myocardial infarction or with a chronically underperfused, yet viable,
myocardium. In many patients, both processes are present simultaneously (Fig. 2A). Other
common causes of LV systolic dysfunction include idiopathic dilated cardiomyopathy, valvular
heart disease, hypertensive heart disease, toxin-induced cardiomyopathies (e.g., doxorubicin,
herceptin, alcohol), and congenital heart disease (see Fig. 2B).

Right ventricular systolic dysfunction is usually a consequence of LV systolic dysfunction. It can

also develop as a result of right ventricular infarction, pulmonary hypertension, chronic severe
tricuspid regurgitation, or arrhythmogenic right ventricular dysplasia. A less-common cause of
heart failure is high-output failure caused by thyrotoxicosis, arteriovenous fistulae, Paget's
disease, pregnancy, or severe chronic anemia.
Diastolic LV dysfunction (impaired relaxation) usually is related to chronic hypertension or
ischemic heart disease. Other causes include restrictive, infiltrative, and hypertrophic
cardiomyopathies. Inadequate filling of the right ventricle can result from pericardial constriction
or cardiac tamponade.

Prevalence and risk factors

Heart failure is a common syndrome, especially in older adults. Although more patients survive
acute myocardial infarction because of reperfusion therapy, most have at least some residual LV
systolic dysfunction, which can lead to heart failure. Currently, 5 million Americans are afflicted
with heart failure, approximately 2% of the population. Patients with heart failure account for
about 1 million hospital admissions annually, and another 2 million patients have heart failure as
a secondary diagnosis. One third of these patients are readmitted within 90 days for recurrent
decompensation.
Patients at high risk for developing heart failure are those with hypertension, coronary artery
disease, diabetes mellitus, family history of cardiomyopathy, use of cardiotoxins, and obesity.

Pathophysiology and natural history

Although much progress has been made in the treatment of heart failure, there is a high overall
annual mortality (5%-20%), particularly in patients with New York Heart Association (NYHA)
Class IV symptoms. Many patients succumb to progressive pump failure and congestion,
although one half die from sudden cardiac death. Some patients die from end-organ failure
resulting from inadequate systemic organ perfusion, particularly to the kidneys. Indicators of
poor cardiac prognosis include renal dysfunction, cachexia, valvular regurgitation, ventricular
arrhythmias, higher NYHA heart failure class, lower LV ejection fraction (LVEF), high
catecholamine and B-type natriuretic peptide (BNP) levels, low serum sodium level,
hypocholesterolemia, and marked LV dilation. Patients with combined systolic and diastolic LV
dysfunction also have a worse prognosis than patients with either in isolation.
In LV systolic dysfunction, the body activates several neurohormonal pathways to increase
circulating blood volume. The sympathetic nervous system increases heart rate and contractility,
causes arteriolar vasoconstriction in nonessential vascular beds, and stimulates secretion of renin
from the juxtaglomerular apparatus of the kidney. Unfortunately, catecholamines aggravate
ischemia, potentiate arrhythmias, promote cardiac remodeling, and are directly toxic to
myocytes. Stimulation of the renin-angiotensin system as a result of increased sympathetic
stimulation and decreased renal perfusion results in further arteriolar vasoconstriction, sodium
and water retention, and release of aldosterone. An increased aldosterone level, in turn, leads to
sodium and water retention, endothelial dysfunction, and organ fibrosis.
In heart failure, baroreceptor and osmotic stimuli lead to vasopressin release from the
hypothalamus, causing reabsorption of water in the renal collecting duct. Although these
neurohormonal pathways initially are compensatory and beneficial, eventually they are
deleterious, and neurohormonal modulation is the basis for modern treatment of heart failure.
In contrast, natriuretic peptides are hormones released by secretory granules in cardiac myocytes
in response to myocardial stretching. They have a beneficial influence in heart failure, including
systemic and pulmonary vasodilation, possible enhancement of sodium and water excretion, and
suppression of other neurohormones.
With continuous neurohormonal stimulation, the left ventricle undergoes remodeling consisting
of LV dilation and hypertrophy, such that stroke volume is increased without an actual increase

in EF. This is achieved by myocyte hypertrophy and elongation. LV chamber dilation causes
increased wall tension, worsens subendocardial myocardial perfusion, and can provoke ischemia
in patients with coronary atherosclerosis. Furthermore, dilation of the LV chamber can cause
mitral annular dilatation and mitral regurgitation, leading to pulmonary congestion.
In diastolic dysfunction, the primary abnormality is impaired LV relaxation, causing high
diastolic pressures and poor filling of the ventricle. To increase diastolic filling, left atrial and
pulmonary capillary pressures increase and pulmonary edema ensues. As a result, patients are
often symptomatic with exertion when increased heart rate reduces LV filling time and
circulating catecholamines worsen diastolic dysfunction.
The American College of Cardiology (ACC) and American Heart Association (AHA) have
developed a classification of heart failure based on stages of the syndrome . Stage A includes
patients who are at risk for developing heart failure but who have no structural heart disease at
present. The management strategy in this group is prevention of heart failure. Stage B includes
patients with structural heart disease but no symptoms. The management goal is prevention of
LV remodeling leading to heart failure. Stage C includes patients with structural heart disease
with current or prior symptomatic heart failure. Diuretics, digoxin, and aldosterone antagonists
may be added to angiotensin-converting enzyme (ACE) inhibitors and beta blockers, depending
on the severity of symptoms. Cardiac resynchronization therapy also may be considered. Stage D
includes patients with severe refractory heart failure. Physicians should consider either end-oflife care or high-technology therapies such as cardiac transplantation or mechanical circulatory
support, based on individual cases.
Table . American College of CardiologyAmerican Heart Association Classification of
Chronic Heart Failure
Stage
Description
A: High risk for developing heart Hypertension, diabetes mellitus, CAD, family history of
failure
cardiomyopathy
B: Asymptomatic heart failure
Previous MI, LV dysfunction, valvular heart disease
Structural heart disease, dyspnea and fatigue, impaired
C: Symptomatic heart failure
exercise tolerance
D: Refractory end-stage heart
Marked symptoms at rest despite maximal medical therapy
failure
CAD, coronary artery disease; LV, left ventricular; MI, myocardial infarction.

Signs and symptoms

There is a wide spectrum of potential clinical manifestations of heart failure. Most patients have
signs and symptoms of fluid overload and pulmonary congestion, including dyspnea, orthopnea,
and paroxysmal nocturnal dyspnea. Patients with right ventricular failure have jugular venous
distention, peripheral edema, hepatosplenomegaly, and ascites. Others, however, do not have
congestive symptoms but have signs and symptoms of low cardiac output, including fatigue,
effort intolerance, cachexia, and renal hypoperfusion. The NYHA functional classification

scheme is used to assess the severity of functional limitations and correlates fairly well with
prognosis
Table . New York Heart Association (NYHA) Heart Failure Symptom Classification System
NYHA
Class
I
II
III
IV

Level of Impairment
No symptom limitation with ordinary physical activity
Ordinary physical activity somewhat limited by dyspnea (e.g., long-distance walking,
climbing two flights of stairs)
Exercise limited by dyspnea with moderate workload (e.g., short-distance walking,
climbing one flight of stairs)
Dyspnea at rest or with very little exertion

On physical examination, patients with decompensated heart failure may be tachycardic and
tachypneic, with bilateral inspiratory rales, jugular venous distention, and edema. They often are
pale and diaphoretic. The first heart sound usually is relatively soft if the patient is not
tachycardic. An S3 and often an S4 gallop will be present. Murmurs of mitral or tricuspid
regurgitation may be heard. Paradoxical splitting of S2 may be present because of delayed
mechanical or electrical activation of the left ventricle. Patients with compensated heart failure
will likely have clear lungs but a displaced cardiac apex. Patients with decompensated diastolic
dysfunction usually have a loud S4 (which may be palpable), rales, and often systemic
hypertension.

Diagnosis
The initial evaluation of new-onset heart failure should include an electrocardiogram, chest
radiograph, and BNP assay. EKG findings of LV hypertrophy, left bundle branch block,
intraventricular conduction delay, and nonspecific ST-segment and T wave changes support a
diagnosis of heart failure. Q waves in contiguous leads strongly implicate a previous myocardial
infarction and coronary atherosclerosis as the cause. Chest radiographic findings of heart failure
include cardiomegaly, pulmonary vascular redistribution, pulmonary venous congestion, Kerley
B lines, alveolar edema, and pleural effusions.
The single most useful diagnostic test is the echocardiogram, which can distinguish between
systolic and diastolic dysfunction. If systolic dysfunction is present, regional wall motion
abnormalities or LV aneurysm suggest an ischemic basis for heart failure, whereas global
dysfunction suggests a nonischemic cause. Echocardiography is helpful in determining other
causes, such as valvular heart disease, cardiac tamponade, or pericardial constriction, and
provides useful clues about infiltrative and restrictive cardiomyopathies. Echocardiography can
also provide meaningful prognostic information about diastolic function, severity of hypertrophy,
chamber size, and valvular abnormalities. In many cases, however, the exact cause of the heart
failure cannot be discerned from the echocardiogram.
Cardiac catheterization can detect coronary atherosclerosis as the cause of heart failure. Severe
coronary artery disease is so prevalent that coronary angiography routinely should be performed

to exclude this cause and, if found, should lead to an assessment of myocardial viability, with a
goal of revascularization. Coronary computed tomographic angiography (CTA) might also be a
suitable alternative to exclude coronary artery disease in select patients.
Magnetic resonance imaging (MRI) is useful in assessing for arrhythmogenic right ventricular
dysplasia, myocardial viability, and infiltrative cardiomyopathies.
Objective information about functional capacity can be obtained from metabolic
(cardiopulmonary) exercise testing. This test can distinguish ventilatory from cardiac limitations
in patients with exertional dyspnea. A peak oxygen consumption higher than 25 mL/kg/min is
normal for middle-age adults, but a value lower than 14 mL/kg/min indicates severe cardiac
limitation and poor prognosis.
A useful diagnostic test for the detection of heart failure is the BNP assay. BNP levels correlate
with severity of heart failure and decrease as a patient reaches a compensated state. This blood
test may be useful for distinguishing heart failure from pulmonary disease. Because smokers
often have both these clinical diagnoses, differentiating between them may be challenging.
The routine use of invasive hemodynamic monitoring to guide the management of
decompensated heart failure has not proved to be beneficial. However, invasive hemodynamic
monitoring may be warranted if unanticipated responses to therapies are observed or for
diagnostic purposes if the diagnosis is uncertain.