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All About Heart Failure

All About Heart Failure

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Published by Sherwan R Shal
Review Heart Failure
Review Heart Failure

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Published by: Sherwan R Shal on Dec 06, 2009
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Heart Failure
Robert Hobbs Andrew Boyle
CHAPTER SECTION LINKS
 
 
Definition and causes 
 
Prevalence and risk factors 
 
Pathophysiology and natural history 
 
Signs and symptoms 
 
Diagnosis 
 
Treatment 
 
Prevention and screening 
 
Considerations in special populations 
 
Summary 
 
References ShareThis 
Definition and causes
Heart failure is a clinical syndrome characterized by systemic perfusion inadequate to meet thebody's metabolic demands as a result of impaired cardiac pump function. This may be furthersubdivided into systolic or diastolic heart failure. In systolic heart failure, there is reducedcardiac contractility, whereas in diastolic heart failure there is impaired cardiac relaxation andabnormal ventricular filling (Fig. 1
 
).Figure 1: Click to Enlarge The most common cause of heart failure is left ventricular systolic dysfunction (about 60% of patients). In this category, most cases are a result of end-stage coronary artery disease, eitherwith a history of myocardial infarction(s) or chronically underperfused, yet viable, myocardium.In many patients, both processes are present simultaneously (Fig. 2A
 
). Other common causes of left ventricular systolic dysfunction include idiopathic dilated cardiomyopathy, valvular heart
 
disease, hypertensive heart disease, toxin-induced cardiomyopathies (e.g., doxorubicin,herceptin, alcohol), and congenital heart disease (seeFig. 2B
 
).Figure 2: Click to Enlarge Right ventricular systolic dysfunction is usually a consequence of left ventricular systolicdysfunction. It may also develop as a result of right ventricular infarction, pulmonaryhypertension, chronic severe tricuspid regurgitation, or arrhythmogenic right ventriculardysplasia. 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 left ventricular dysfunction (impaired relaxation) usually is related to chronichypertension or ischemic heart disease. Other causes include restrictive, infiltrative, andhypertrophic cardiomyopathies. Inadequate filling of the right ventricle may result frompericardial constriction or cardiac tamponade.Back to Top 
Prevalence and risk factors
Heart failure is a common syndrome, especially in older adults. Although more patients surviveacute myocardial infarction because of reperfusion therapy, most have at least some residual leftventricular systolic dysfunction, which may lead to heart failure. Currently, 5 million Americansare afflicted with heart failure, approximately 2% of the population.
 1 
Patients with heart failureaccount for about 1 million hospital admissions annually, with another 2 million patients havingheart failure as a secondary diagnosis. One third of these patients are readmitted within 90 daysfor recurrent decompensation.Patients at high risk for developing heart failure are those with hypertension, coronary arterydisease, diabetes mellitus, familial history of cardiomyopathy, use of cardiotoxins, and obesity.Back to Top 
Pathophysiology and natural history
Although much progress has been made in the treatment of heart failure, there is a high overallannual mortality (5% to 20%), particularly in patients with New York Heart Association(NYHA) Class IV symptoms.
 2 
Many patients succumb to progressive pump failure andcongestion, although one half die from sudden cardiac death. Some patients die from end-organfailure resulting from inadequate systemic organ perfusion, particularly to the kidneys. Indicators
 
of poor cardiac prognosis include renal dysfunction, cachexia, valvular regurgitation, ventriculararrhythmias, higher NYHA heart failure class, lower left ventricular ejection fraction, highcatecholamine and B-type natriuretic peptide levels, low serum sodium level,hypocholesterolemia, and marked left ventricular dilation. Patients with combined systolic anddiastolic left ventricular dysfunction also have a worse prognosis than patients with either inisolation.
 3 
In left ventricular systolic dysfunction, regardless of the cause, cardiac output is low andpulmonary pressures are high, leading to pulmonary congestion. Initially, as a direct result of inadequate cardiac output and systemic perfusion, the body activates several neurohormonalpathways to increase circulating blood volume. The sympathetic nervous system increases heartrate and contractility, both of which increase cardiac output. Circulating catecholamines alsocause arteriolar vasoconstriction in nonessential vascular beds and stimulate secretion of reninfrom the juxtaglomerular apparatus of the kidney.Unfortunately, catecholamines aggravate ischemia, potentiate arrhythmias, promote cardiacremodeling, and are directly toxic to myocytes. Stimulation of the renin-angiotensin system as aresult of increased sympathetic stimulation and decreased renal perfusion results in furtherarteriolar vasoconstriction, sodium and water retention, and release of aldosterone. An increasedaldosterone level, in turn, leads to sodium and water retention, endothelial dysfunction, andorgan fibrosis.In heart failure, baroreceptor and osmotic stimuli lead to vasopressin release from thehypothalamus, causing reabsorption of water in the renal collecting duct. Endothelin levels areelevated in heart failure and correlate with the severity of disease and prognosis. Endothelin is anendogenous vasoconstrictor and growth factor. Levels of the proinflammatory cytokines also areelevated in heart failure, and contribute to cardiac cachexia and apoptosis. Although theseneurohormonal pathways initially are compensatory and beneficial, eventually they aredeleterious, 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.They have a beneficial influence in heart failure, including systemic and pulmonary vasodilation,enhanced sodium and water excretion, and suppression of other neurohormones.With continuous neurohormonal stimulation, the left ventricle undergoes remodeling consistingof left ventricular dilation and hypertrophy, such that stroke volume is increased without anactual increase in ejection fraction. This is achieved by myocyte hypertrophy and elongation.Left ventricular chamber dilation causes increased wall tension, worsens subendocardialmyocardial perfusion, and may provoke ischemia in patients with coronary atherosclerosis.Furthermore, left ventricular chamber dilation may cause separation of the mitral leaflets andmitral regurgitation, leading to pulmonary congestion. Enhanced neurohormonal stimulation of the myocardium also causes apoptosis or programmed cell death, worsening of ventricularcontractility, and death.

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