casibom deneme bonusu Betturkey giriş casibom CHRONIC HEART FAILURE – Ferozsons Laboratories Limited




Heart failure (HF) is a major public health problem, with a prevalence of more than 5.8 million in the United States and more than 23 million worldwide.(1,2) Every year in the USA, more than 550,000 individuals are diagnosed with HF for the first time, and there is a lifetime risk of one in five of developing this syndrome.(1,3)

Pakistan prevalence of CHF is 14.75-22.87 %.(4) The situation in Pakistan is no better as a study shows increasing numbers as well as increasing hospitalizations due to heart failure.(5)


Compensatory mechanisms exist on every level of organization, from subcellular all the way through organ-to-organ interactions. Only when this network of adaptations becomes overwhelmed does heart failure ensue. (6-10)

Most important among the adaptations are the following:(11)

  • The Frank-Starling mechanism, in which an increased preload helps to sustain cardiac performance
  • Alterations in myocyte regeneration and death
  • Myocardial hypertrophy with or without cardiac chamber dilatation, in which the mass of contractile tissue is augmented
  • Activation of neurohumoral systems

The release of norepinephrine by adrenergic cardiac nerves augments myocardial contractility and includes activation of the renin-angiotensin-aldosterone system [RAAS], the sympathetic nervous system [SNS], and other neurohumoral adjustments that act to maintain arterial pressure and perfusion of vital organs.

The primary myocardial response to chronic increased wall stress is myocyte hypertrophy, death / apoptosis, and regeneration.(12) 

The reduction of cardiac output following myocardial injury sets into motion a cascade of hemodynamic and neurohormonal derangements that provoke activation of neuroendocrine systems, most notably the above-mentioned adrenergic systems and RAAS.(13)

The release of epinephrine and norepinephrine, along with the vasoactive substances endothelin-1 (ET-1) and vasopressin, causes vasoconstriction, which increases calcium afterload and, via an increase in cyclic adenosine monophosphate (cAMP), causes an increase in cytosolic calcium entry. The increased calcium entry into the myocytes augments myocardial contractility and impairs myocardial relaxation (lusitropy).

The calcium overload may induce arrhythmias and lead to sudden death. The increase in afterload and myocardial contractility (known as inotropy) and the impairment in myocardial lusitropy lead to an increase in myocardial energy expenditure and a further decrease in cardiac output. The increase in myocardial energy expenditure leads to myocardial cell death / apoptosis, which results in heart failure and further reduction in cardiac output, perpetuating a cycle of further increased neurohumoral stimulation and further adverse hemodynamic and myocardial responses.

In addition, the activation of the RAAS leads to salt and water retention, resulting in increased preload and further increases in myocardial energy expenditure. Increases in renin, mediated by decreased stretch of the glomerular afferent arteriole, reduce delivery of chloride to the macula densa and increase beta1-adrenergic activity as a response to decreased cardiac output. This results in an increase in angiotensin II (Ang II) levels and, in turn, aldosterone levels, causing stimulation of the release of aldosterone. Ang II, along with ET-1, is crucial in maintaining effective intravascular homeostasis mediated by vasoconstriction and aldosterone-induced salt and water retention.

ANG II: Ang II mediates myocardial cellular hypertrophy and may promote progressive loss of myocardial function. The neurohumoral factors above lead to myocyte hypertrophy and interstitial fibrosis, resulting in increased myocardial volume and increased myocardial mass, as well as myocyte loss. As a result, the cardiac architecture changes, which, in turn, leads to further increase in myocardial volume and mass.

MYOCYTES AND MYOCARDIAL REMODELING: Progenitor cells become progressively less effective as the underlying pathologic process worsens and myocardial failure accelerates. These features, namely, the increased myocardial volume and mass, along with a net loss of myocytes, are the hallmark of myocardial remodeling. This remodeling process leads to early adaptive mechanisms, such as augmentation of stroke volume (Frank-Starling mechanism) and decreased wall stress (Laplace's law), and, later, to maladaptive mechanisms such as increased myocardial oxygen demand, myocardial ischemia, impaired contractility, and arrhythmogenesis.

As heart failure advances, there is a relative decline in the counter regulatory effects of endogenous vasodilators, including nitric oxide (NO), prostaglandins (PGs), bradykinin (BK), atrial natriuretic peptide (ANP), and B-type natriuretic peptide (BNP). This decline occurs simultaneously with the increase in vasoconstrictor substances from the RAAS and the adrenergic system, which fosters further increases in vasoconstriction and thus preload and afterload. This results in cellular proliferation, adverse myocardial remodeling, and antinatriuresis, with total body fluid excess and worsening of heart failure symptoms.

SYSTOLIC AND DIASTOLIC FAILURE: Systolic and diastolic heart failure each result in a decrease in stroke volume.(14,15) This leads to activation of peripheral and central baroreflexes and chemoreflexes that are capable of eliciting marked increases in sympathetic nerve traffic.

ANP AND BNP: ANP and BNP are endogenously generated peptides activated in response to atrial and ventricular volume / pressure expansion. ANP and BNP are released from the atria and ventricles, respectively, and both promote vasodilation and natriuresis. Their hemodynamic effects are mediated by decreases in ventricular filling pressures, owing to reductions in cardiac preload and afterload. ANP and BNP are elevated in chronic heart failure.

OTHER VASOACTIVE SYSTEMS: Other vasoactive systems that play a role in the pathogenesis of heart failure include the ET receptor system, the adenosine receptor system, vasopressin, and tumor necrosis factor-alpha (TNF-alpha).(16) ET, a substance produced by the vascular endothelium, may contribute to the regulation of myocardial function, vascular tone, and peripheral resistance in heart failure. Elevated levels of ET-1 closely correlate with the severity of heart failure. ET-1 is a potent vasoconstrictor and has exaggerated vasoconstrictor effects in the renal vasculature, reducing renal plasma blood flow, glomerular filtration rate (GFR), and sodium excretion.
TNF-alpha has been implicated in response to various infectious and inflammatory conditions. Elevations in TNF-alpha levels have been consistently observed in heart failure and seem to correlate with the degree of myocardial dysfunction.

HEART FAILURE WITH NORMAL EJECTION FRACTION: In diastolic heart failure (heart failure with normal ejection fraction [HFNEF]), altered relaxation and increased stiffness of the ventricle (due to delayed calcium uptake by the myocyte sarcoplasmic reticulum and delayed calcium efflux from the myocyte) occur in response to an increase in ventricular afterload (pressure overload). The impaired relaxation of the ventricle then leads to impaired diastolic filling of the left ventricle (LV).

LV CHAMBER STIFFNESS: An increase in LV chamber stiffness occurs secondary to any one of, or any combination of, the following 3 mechanisms:

  • Rise in filling pressure
  • Shift to a steeper ventricular pressure-volume curve
  • Decrease in ventricular distensibility

A rise in filling pressure is the movement of the ventricle up along its pressure-volume curve to a steeper portion, as may occur in conditions such as volume overload secondary to acute valvular regurgitation or acute LV failure due to myocarditis.

A shift to a steeper ventricular pressure-volume curve results, most commonly, not only from increased ventricular mass and wall thickness (as observed in aortic stenosis and long-standing hypertension) but also from infiltrative disorders (e.g. amyloidosis), endomyocardial fibrosis, and myocardial ischemia.

Parallel upward displacement of the diastolic pressure-volume curve is generally referred to as a decrease in ventricular distensibility. This is usually caused by extrinsic compression of the ventricles.

CONCENTRIC LV HYPERTROPHY: Pressure overload that leads to concentric LV hypertrophy (LVH), as occurs in aortic stenosis, hypertension, and hypertrophic cardiomyopathy, shifts the diastolic pressure-volume curve to the left along its volume axis. As a result, ventricular diastolic pressure is abnormally elevated, although chamber stiffness may or may not be altered.

ARRHYTHMIAS: While life-threatening rhythms are more common in ischemic cardiomyopathy, arrhythmia imparts a significant burden in all forms of heart failure. In fact, some arrhythmias even perpetuate heart failure. The most significant of all rhythms associated with heart failure are the life-threatening ventricular arrhythmias. Structural substrates for ventricular arrhythmias that are common in heart failure, regardless of the underlying cause, include ventricular dilatation, myocardial hypertrophy, and myocardial fibrosis.
At the cellular level, myocytes may be exposed to increased stretch, wall tension, catecholamines, ischemia, and electrolyte imbalance. The combination of these factors contributes to an increased incidence of arrhythmogenic sudden cardiac death in patients with heart failure.


Symptoms of Heart Failure (HF) 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 exertion. Fluid retention in HF is initiated by the fall in cardiac output, leading to alterations in renal function, due in part to activation of the sodium retaining, renin angiotensin aldosterone and sympathetic nervous systems.

Important information concerning the acuity of HF is suggested by the presenting symptoms:

  • Acute and subacute presentations (days to weeks) are characterized primarily by shortness of breath, at rest and / or with exertion. Also common are orthopnea, paroxysmal nocturnal dyspnea, and, with right HF, right upper quadrant discomfort due to acute hepatic congestion, which can be confused with acute cholecystitis. Patients with atrial and / or ventricular tachyarrhythmias may complain of palpitations with or without lightheadedness. Patients with acute decompensated HF require prompt diagnosis and management.
  • 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 poor perfusion of the splanchnic circulation, bowel edema, and nausea induced by hepatic congestion. Over time, pulmonary venous capacitance accommodates to the chronic state of volume overload, leading to less or no fluid accumulation in the alveoli, despite the increase in total lung water. These patients present with excessive fatigue and low output symptoms.

Other clinical features such as older age, history of coronary artery disease or myocardial infarction, and use of a loop diuretic are associated with increased likelihood of HF.(17,18)


The New York Heart Association (NYHA) classification of heart failure is widely used in practice to quantify clinical assessment of heart failure. Breathlessness, a cardinal symptom of LV failure, may manifest with progressively increasing severity as the following:

  • Exertional dyspnea
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
  • Dyspnea at rest
  • Acute pulmonary edema

Other cardiac symptoms of heart failure include chest pain / pressure and palpitations. Common non-cardiac signs and symptoms of heart failure include anorexia, nausea, weight loss, bloating, fatigue, weakness, oliguria, nocturia, and cerebral symptoms of varying severity, ranging from anxiety to memory impairment and confusion.

EXERTIONAL DYSPNEA: The principal difference between exertional dyspnea in patients who are healthy and exertional dyspnea in patients with heart failure is the degree of activity necessary to induce the symptom.

ORTHOPNEA: Orthopnea is an early symptom of heart failure and may be defined as dyspnea that develops in the recumbent position and is relieved with elevation of the head with pillows.

PAROXYSMAL NOCTURNAL DYSPNEA: Paroxysmal nocturnal dyspnea usually occurs at night and is defined as the sudden awakening of the patient, after a couple of hours of sleep, with a feeling of severe anxiety, breathlessness, and suffocation.
In contrast to orthopnea, which may be relieved by immediately sitting up in bed, paroxysmal nocturnal dyspnea may require 30 minutes or longer in this position for relief. Episodes may be so frightening that the patient may be afraid to resume sleeping, even after the symptoms have subsided.

DYSPNEA AT REST: Dyspnea at rest in heart failure is the result of the following mechanisms:

  • Decreased pulmonary function secondary to decreased compliance and increased airway resistance
  • Increased ventilatory drive secondary to hypoxemia due to increased pulmonary capillary wedge pressure (PCWP); ventilation / perfusion (V/Q) mismatching due to increased PCWP and low cardiac output; and increased carbon dioxide production
  • Respiratory muscle dysfunction, with decreased respiratory muscle strength, decreased endurance, and ischemia

PULMONARY EDEMA: Acute pulmonary edema is defined as the sudden increase in PCWP (usually more than 25 mm Hg) as a result of acute and fulminant left ventricular failure. The patient appears extremely ill, poorly perfused, restless, sweaty, tachypneic, tachycardic, hypoxic, and coughing, with an increased work of breathing and using respiratory accessory muscles and with frothy sputum that on occasion is blood tinged.

CHEST PAIN / PRESSURE AND PALPITATIONS: Chest pain / pressure may occur as a result of either primary myocardial ischemia from coronary disease or secondary myocardial ischemia from increased filling pressure, poor cardiac output (and therefore poor coronary diastolic filling), or hypotension and hypoxemia.(19)
Palpitations are the sensation a patient has when the heart is racing. It can be secondary to sinus tachycardia due to decompensated heart failure, or more commonly, it is due to atrial or ventricular tachyarrhythmias.

FATIGUE AND WEAKNESS: Fatigue and weakness are often accompanied by a feeling of heaviness in the limbs and are generally related to poor perfusion of the skeletal muscles in patients with a lowered cardiac output. Although they are generally a constant feature of advanced heart failure, episodic fatigue and weakness are also common in earlier stages.

NOCTURIA AND OLIGURIA: Nocturia may occur relatively early in the course of heart failure. Recumbency reduces the deficit in cardiac output in relation to oxygen demand, renal vasoconstriction diminishes, and urine formation increases. Oliguria is a late finding in heart failure and is found in patients with markedly reduced cardiac output from severely reduced LV function.
CEREBRAL SYMPTOMS: The following may occur in elderly patients with advanced heart failure, particularly in those with cerebrovascular atherosclerosis

  • Confusion
  • Memory impairment
  • Anxiety
  • Headaches
  • Insomnia
  • Bad dreams or nightmares
  • Rarely, psychosis with disorientation, delirium, or hallucinations

The American College of Cardiology / American Heart Association (ACC/AHA),(20) Heart Failure Society of America (HFSA),(21,22)  and European Society of Cardiology (ESC)(23) recommend the following basic laboratory tests and studies in the initial evaluation of patients with suspected heart failure:

  • Complete blood count (CBC), which may indicate anemia or infection as potential causes of heart failure. Leukocytosis may signal underlying infection
  • Urinalysis (UA), which may reveal proteinuria, which is associated with cardiovascular disease
  • Serum electrolyte levels (including calcium and magnesium), which may be abnormal owing to causes such as fluid retention or renal dysfunction
  • Blood urea nitrogen (BUN) and creatinine levels, which may indicate decreased renal blood flow
  • Fasting blood glucose levels, because elevated levels indicate a significantly increased risk for heart failure (diabetic and non-diabetic patients)
  • Liver function tests (LFTs), which may show elevated liver enzyme levels and indicate liver dysfunction due to heart failure
  • B-type natriuretic peptide (BNP) and N-terminal pro-B-type (NT-proBNP) natriuretic peptide levels, which are increased in heart failure; these measurements are closely correlated with the NYHA heart failure classification
  • Electrocardiogram (ECG) (12-lead), which may reveal arrhythmias, ischemia / infarction, and coronary artery disease as possible causes of heart failure

The ACC / AHA recommendations also include obtaining a lipid profile and thyroid stimulating hormone (TSH) level.(20) These tests reveal potential cardiovascular or thyroid disease as causes of heart failure. If the clinical presentation also suggests an acute coronary syndrome, the ESC recommends obtaining levels of troponin I or T(23) ; increased troponin levels indicate injury to the myocytes and the severity of heart failure.

Other studies may be indicated in selected patients,(20) such as the following:

  • Screening for hemochromatosis, in which iron overload affects cardiac function
  • Screening for sleep-disturbed breathing, which affects neurohormonal activation
  • Screening for human immunodeficiency virus (HIV), which may result in heart failure from possible direct infectious effects, from disease treatment effects causing CAD, or from other causes
  • Testing for rheumatologic diseases, amyloidosis, or pheochromocytoma, all of which may cause cardiomyopathy
  • Serum and urine electrophoresis for light-chain disease
  • Genetic testing for at-risk patients with a first-degree relative who has been diagnosed with a cardiomyopathy leading to heart failure, which may aid in detecting early disease onset and guide treatment(21,22)
  • Holter monitoring, which may reveal arrhythmias or abnormal electrical activity (e.g. in patients with heart failure and a history of MI who are being considered for electrophysiologic study to document ventricular tachycardia [VT] inducibility)(21,23)

The ESC indicates that pulmonary function testing is generally not helpful in the diagnosis of heart failure. However, it may demonstrate or exclude respiratory causes of dyspnea and help assess any pulmonary causes of dyspnea.(23)

Following tests are also recommended:

  • Assessment of Hypoxemia
  • Arterial and venous blood gases: Although arterial blood gas (ABG) measurement is more accurate than pulse oximetry for measuring oxygen saturation, it is unclear if ABG results add any clinical utility to pulse oximetry.
  • Pulse oximetry: Pulse oximetry is highly accurate at assessing the presence of hypoxemia and, therefore, the severity of acute heart failure presentations. Patients with mild to moderate acute heart failure may show modest reductions in oxygen saturation, whereas patients with severe heart failure may have severe oxygen desaturation, even at rest. Pulse oximetry is also useful for monitoring the patient's response to supplemental oxygen and other therapies.

Electrocardiography may suggest an acute tachyarrhythmia or bradyarrhythmia as the cause of heart failure. It may also aid in the diagnosis of acute myocardial ischemia or infarction as the cause of heart failure or may suggest the likelihood of prior MI or the presence of coronary artery disease as the cause of heart failure.(20,21)

Chest radiographs are used in cases of heart failure to assess heart size, pulmonary congestion, pulmonary or thoracic causes of dyspnea, and the proper positioning of any implanted cardiac devices. Posterior-anterior and lateral views are recommended.(20, 21, 23)


TWO-DIMENSIONAL (2-D) ECHOCARDIOGRAPHY: is recommended in the initial evaluation of patients with known or suspected heart failure.(20,21,23)  Ventricular function may be evaluated, and primary and secondary valvular abnormalities may be accurately assessed.(24-28)

DOPPLER ECHOCARDIOGRAPHY: along with 2-D echocardiography, may play a valuable role in determining diastolic function and in establishing the diagnosis of diastolic heart failure.

Doppler and 2-D echocardiography may also be used to determine both systolic and diastolic LV performance, cardiac output (ejection fraction), and pulmonary artery and ventricular filling pressures. In addition, echocardiography may be used to identify clinically important valvular disease.

TRANSESOPHAGEAL ECHOCARDIOGRAPHY: also has the potential to be a noninvasive alternative to pulmonary artery catherization for hemodynamic monitoring, as it also allows measurement of central venous, pulmonary arterial, and pulmonary capillary wedge pressures, as well as pulmonary and systemic vascular resistance, and stroke volume and cardiac output.(29)

STRESS ECHOCARDIOGRAPHY: This imaging modality may be used to detect ventricular dysfunction caused by ischemia, evaluate myocardial viability in the presence of marked hypokinesis or akinesis, identify myocardial stunning and hibernation, and relate heart failure symptoms to valvular abnormalities.(23)

Computed tomography (CT) or magnetic resonance imaging (MRI)

Computed tomography (CT) or magnetic resonance imaging (MRI) may be useful in evaluating chamber size and ventricular mass, cardiac function, and wall motion; delineating congenital and valvular abnormalities; and demonstrating the presence of pericardial disease.(20) However, cardiac CT is usually not required in the routine diagnosis and management of heart failure, and echocardiography and MRI may provide similar information without exposing the patient to ionizing radiation.

Nuclear Imaging

RADIONUCLIDE MULTIPLE-GATED ACQUISITION SCANNING: Radionuclide multiple-gated acquisition (MUGA) scan is a reliable imaging technique for evaluation of LV and RV function and wall motion abnormalities. Because of its reliability, LV ejection fraction (LVEF), as determined by MUGA scanning, is often used for serial assessment of postchemotherapy LV function.(30)

ELECTROCARDIOGRAM-GATED MYOCARDIAL PERFUSION IMAGING: ECG-gated single-photon emission CT (SPECT) images allow for assessment of global LVEF, regional wall motion, and regional wall thickening at rest in patients with documented stress-induced wall motion and perfusion abnormalities.

According to the American College of Cardiology / American Heart Association (ACC / AHA),(20) Heart Failure Society of America (HFSA),(21) and European Society of Cardiology (ESC),(23) cardiac catheterization and coronary angiography should be considered for patients with heart failure in the following situations:

  • When symptoms worsen without a clear cause in patients with heart failure, no angina, and known coronary artery disease
  • In heart failure caused by systolic dysfunction in association with angina or regional wall-motion abnormalities and / or scintigraphic evidence of reversible myocardial ischemia when revascularization is being considered
  • When pretest probability of underlying ischemic cardiomyopathy is high and surgical coronary procedures are being considered
  • Before cardiac transplantation or left ventricular assist device placement
  • In cases of heart failure secondary to post-infarction ventricular aneurysm or other mechanical complications of myocardial infarction.

Endomyocardial biopsy is indicated only when a specific diagnosis is suspected that would influence therapy in patients presenting with heart failure. The Heart Failure Society of America (HFSA) suggests that endomyocardial biopsy be considered in patients with rapidly progressive clinical heart failure or ventricular dysfunction, despite appropriate medical therapy, as well as in patients suspected of having myocardial infiltrative processes (e.g. sarcoidosis, amyloidosis) or in patients with malignant arrhythmias out of proportion to their LV dysfunction (e.g. sarcoidosis, giant cell myocarditis).(21)

The European Society of Cardiology (ESC) indicates the 6-minute walk test is a good indicator of functional status and prognosis in patients with heart failure.(23) 

Cardiopulmonary stress testing (maximal exercise stress testing with measurement of respiratory gas exchange) can help assess a patient’s chance of survival within the next year, as well as determine the need for referral for either cardiac transplantation or implantation of mechanical circulatory support.


Many of the symptoms and signs of heart failure (HF) are nonspecific, so other potential causes should be considered. Patients with HF may present with a syndrome of decreased exercise tolerance, fluid retention, or both.(31)


Drugs that can exacerbate heart failure should be avoided, such as nonsteroidal anti-inflammatory drugs (NSAIDs), calcium channel blockers (CCBs), and most antiarrhythmic drugs (except class III). NSAIDs can cause sodium retention and peripheral vasoconstriction, and they can attenuate the efficacy and enhance the toxicity of diuretics and ACEIs. CCBs can worsen heart failure and may increase the risk of cardiovascular events; only the vasoselective CCBs have been shown not to adversely affect survival. Antiarrhythmic agents can have cardio-depressant effects and may promote arrhythmia; only amiodarone and dofetilide have been shown not to adversely affect survival.



  • Cessation of smoking.
  • Restriction of or abstinence from alcohol consumption
  • Avoidance of illicit drug use (e.g. cocaine).
  • Dietary sodium restriction to 2-3 g/day is recommended.
  • Fluid restriction to 2 L/day is recommended for patients with evidence of hyponatremia (Na < 130 mEq/dL) and for those whose fluid status is difficult to control despite sodium restriction and the use of high-dose diuretics. Caloric supplementation is recommended for patients with evidence of cardiac cachexia.
  • Avoidance of obesity.
  • Daily weight monitoring is recommended to detect fluid accumulation before it becomes symptomatic.


The 2013 American College of Cardiology / American Heart Association (ACC / AHA) updated guidelines,(32) 2010 Heart Failure Society of America (HFSA) guidelines,(21) and the 2008 European Society of Cardiology (ESC)(23) guidelines, with varying levels of evidence, recommend the following:

  • Diuretics (to reduce edema by reduction of blood volume and venous pressures) and salt restriction (to reduce fluid retention) in patients with current or previous heart failure symptoms and reduced left ventricular ejection fraction (LVEF) for symptomatic relief
  • Angiotensin-converting enzyme inhibitors (ACEIs) for neurohormonal modification, vasodilatation, improvement in LVEF, and survival benefit
  • Angiotensin receptor blockers (ARBs) for neurohormonal modification, vasodilatation, improvement in LVEF, and survival benefit
  • Hydralazine and nitrates to improve symptoms, ventricular function, exercise capacity, and survival in patients who cannot tolerate an ACEI / ARB or as an add-on therapy to ACEI / ARB and beta-blockers in the black population for survival benefit
  • Beta-adrenergic blockers for neurohormonal modification, improvement in symptoms and LVEF, survival benefit, arrhythmia prevention, and control of ventricular rate
  • Aldosterone antagonists, as an adjunct to other drugs for additive diuresis, heart failure symptom control, improved heart rate variability, decreased ventricular arrhythmias, reduction in cardiac workload, improved LVEF, and increase in survival
  • Digoxin, which can lead to a small increase in cardiac output, improvement in heart failure symptoms, and decreased rate of heart failure hospitalizations
  • Anticoagulants to decrease the risk of thromboembolism
  • Inotropic agents to restore organ perfusion and reduce congestion

CABG and percutaneous coronary intervention (PCI) are revascularization procedures that should be considered in selected patients with heart failure and CAD. The choice between CABG and PCI depends on the following factors:

  • Patient comorbidities
  • Procedural risk
  • Coronary anatomy
  • Likely extent of viable myocardium in the area to be revascularized
  • Ischemic symptoms
  • LV function
  • Presence of hemodynamically significant valvular disease

In patients who are at low risk for CAD, findings from noninvasive tests such as exercise ECG, stress echocardiography, and stress nuclear perfusion imaging should determine whether subsequent angiography is indicated.(20,21,23)


Valvular heart disease may be the underlying etiology or an important aggravating factor in heart failure.(20,21,23) The ACC / AHA recommends that valve repair or replacement in patients with hemodynamically significant valvular stenosis or regurgitation and asymptomatic heart failure should be based on contemporary guidelines. In addition, the ACC / AHA indicates that such surgery should be considered for patients with severe aortic or mitral valve stenosis or regurgitation, even when ventricular function is impaired.


Heart failure is a common indication for aortic valve replacement (AVR), but one must be cautious in patients with a low LVEF and possible aortic stenosis. Assessment of contractile reserve with dobutamine has been demonstrated as a reliable method to determine which patients with low EF and aortic stenosis may benefit from AVR.(33)


Mitral valve surgery in patients with heart failure has gained favor, because it abolishes the regurgitant lesion and decreases symptoms. The pathophysiologic rationales for repair or replacement are to reverse the cycle of excessive ventricular volume, to allow for ventricular unloading, and to promote myocardial remodeling.


After a transmural MI occurs, the ventricle pathologically remodels from its normal elliptical shape to a spherical shape. This change in geometry is in part responsible for the constellation of symptoms associated with HF and decreased survival.

Several ventricular restoration techniques exist. All aim to correct the above-described pathologic alteration in geometry. Most approaches involve incising and excluding nonviable myocardium with either patch or primary reconstruction to decrease ventricular volume.

In some cases of extreme cardiopulmonary failure, the only recourse is complete support with extracorporeal membrane oxygenation (ECMO). ECMO provides both oxygenation and circulation of blood, allowing the lungs and heart time to recover. Unlike cardiopulmonary bypass, whose duration of use is measured in hours, ECMO can be used for 3-10 days.

Ventricular assist devices (VADs) are invaluable tools in the treatment of heart failure. A number of these devices are available to support the acutely or chronically decompensated heart. Depending on the particular device used, the right ventricle and left ventricle can be assisted with a left ventricular assist device (LVAD), a right VAD (RVAD), or a biventricular assist device (BiVAD). An alternative term for a VAD is a ventricular assist system (VAS).

Selected patients with severe heart failure, debilitating refractory angina, ventricular arrhythmia, or congenital heart disease that cannot be controlled despite pharmacologic, medical device, or alternative surgical therapy should be evaluated for heart transplantation.(21)  The patient must be well informed, motivated, and emotionally stable; have a good social support network; and be capable of complying with intensive medical treatment.(23)

The creation of a suitable total artificial heart (TAH) for orthotopic implantation has been the subject of intense investigation for decades.(34) In 1969, Dr. Denton Cooley implanted the Liotta TAH (which is no longer made) into a high-risk patient after failing to wean the patient off cardiopulmonary bypass after LV aneurysm repair. The patient was sustained until, after 3 days, a donor heart became available, but the patient subsequently died of pneumonia and multiple organ failure.(35)


The goals of therapy of heart failure with reduced ejection fraction (HFrEF) are to reduce morbidity (i.e. reducing symptoms, improving health related quality of life and functional status, decreasing the rate of hospitalization), and to reduce mortality.


Treatment for CHF is based on guidelines from the prestigious societies mentioned below. Please click on below link (mentioned next to societies name) to view the guidelines:

  • 2013 American College of Cardiology Foundation / American Heart Association guideline
  • The Canadian Cardiovascular Society guidelines
  • The 2012 European Society of Cardiology guidelines
  • The 2010 Heart Failure Society of America guidelines
  • The 2010 National Institute for Health and Care Excellence chronic HF guideline


The best way to prevent heart failure is to have a heart-healthy lifestyle and control existing health problems like high blood pressure and diabetes.

Patient should be suggested on following:

  • Not to smoke. Also avoid secondhand smoke.
  • Eat heart-healthy foods. Eat fruits, vegetables, fish, lean meats, and whole grains. Choose foods that are low in saturated fat and avoid trans-fat. Limit sodium, alcohol, and sugar.
  • Get regular exercise. Try to do activities that raise your heart rate. Aim for at least 2½ hours of moderate exercise a week.
  • Stay at a healthy weight. Lose weight if you need to.
    Manage other health problems that can raise your risk of heart disease and heart failure. These include high blood pressure, high cholesterol, and diabetes. You can use heart-healthy lifestyle changes along with medicines to manage these conditions.
  • Appropriate preventative care includes pneumococcal vaccination and annual influenza vaccination.(36,37)


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