Symptoms and signs, if confirmed by objective diagnostic tools, serve as warning on impeding CHF. Initial clinical evaluation should include periodic observations, palpation and auscultation [9]. Interpretation of dyspnea, edematous ankle, and tiredness can be difficult among the elderly, women and obese persons. Different modes  of observations should be employed, with or without effort, in diurnal or nocturnal activity. Fatigue per se is likewise difficult to quantify and may be due to several factors such as skeletal muscle dysfunction, low cardiac output, and peripheral hypoperfusion. Elevated venous pressure, peripheral edema, and liver enlargement are indicative of systemic vein congestion. 

CHF is ischemic or non-ischemic based on history of myocardial infarction (MI) or on the presence of coronary artery disease as determined by angiography or functional testing. Identifying etiology may be difficult since there are CHF patients without CAD but having typical angina or regional wall motion abnormalities, in contrast to severe CAD patients without angina or history of MI. Noninvasive functional testing or coronary angiography is recommended for patients with systolic dysfunction taking into consideration clinical presentation and risk factors involved [5].

Electrocardiogram

A normal ECG is not conclusive in the diagnosis of congestive heart failure.  Changing ECG profiles are commonly observed in suspected HF cases. While an abnormal electrocardiogram (ECG) is not predictive of the presence of CHF, normal ECG may indicate that LV dysfunction is not the cause of heart failure. Therefore, ECG of patients with CHF requires careful evaluation. Myocardial infarction as the etiology of cardiac dysfunction may be interpreted from the appearance of pathological Q-waves.  Cardiac dyssynchrony may be considered for treatment with a QRS width of .120 ms  [9].

Chest X-ray

Chest X-ray is useful in detecting cardiomegaly and pulmonary congestion as part of the initial diagnosis of CHF; however, it should be evaluated in consonance with the typical signs and symptoms of CHF and with abnormal ECG [9].

Haematology and biochemistry

Clinical laboratory examination includes: CBC, Hb, WBC, platelets, S-creatinine, S-electrolytes, S-glucose, SGOT, SGPT, and urinalysis. Thyroid function may be needed. In exacerbated disease, acute myocardial infarction is ruled out by myocardial specific enzyme determination [9].

Natriuretic peptides

Plasma concentrations of natriuretic peptides or their precursors, BNP and NT-proBNP, have prognostic value in the diagnosis of heart failure. However, the role of these peptides in following up the outcome of treatment remains to be ascertained. While a 'normal' value may accompany cardiac disease, low to normal concentration of these peptides in an untreated patient is not necessarily indicative of heart failure. Elevated concentrations of these peptides are linked to CHF, indicating diastolic dysfunction and presence of cardiac abnormalities, such as valvular heart disease, left ventricular hypertrophy, pulmonary embolism, acute or chronic ischemia or hypertension. The practical value of these peptides is in screening for significant cardiac disease in primary and secondary health care centers. A normal result can save expenses on unnecessary cardiological examinations in specialized diagnostic facilities [9].    

PET (Positron Emission Tomography)

PET imaging has high predictive value in the assessment of metabolism-perfusion, allowing quantification of myocardial perfusion and metabolism, and is more efficient than SPECT or DSE (Dobutamine Stress Echocardiography) [1].

SPECT (Single-photon Emission Computed Tomography) 

SPECT has been the mainstay of noninvasive imaging. Hibernating myocardium and myocardial perfusion can be studied using tracers at the level of the cell membrane and mitochondria. Beta-oxidation and mitochondrial function can be assessed with low-dose dobutamine, although this has not been sufficiently evaluated clinically. The drawbacks of PET and SPECT are radiation hazard and low spatial resolution [1].

Echocardiography

Echocardiography is widely used as a first line diagnostic tool. Although low dose DSE detects hibernating myocardium, myocardial contrast echocardiography (MCE) can show evidence of new wall motion abnormalities at higher stress levels or a biphasic response indicating the presence of inducible myocardial ischemia. MCE is more accurate in detecting regional wall motion abnormalities and inducible myocardial ischemia during vasodilator stress. It is the method of choice versus DSE and SPECT for measuring myocardial blood flow in hibernating myocardium. Furthermore, echocardiography can detect and quantify myocardial infarct scars and augments the reliability of late gadolinium enhancement cardiovascular magnetic resonance (LGE CMR) in assessing patients with ICM. Disadvantages of the technic are inadequate endocardial border definition and poor acoustic windows [1].

Computed tomography

Computed tomography (CT)  is effective for examining coronary arteries but limited in usefulness in chronic CAD patients with high calcium burden.  LV function, scar formation, and perfusion can be studied with CT scan. Dual combinations of cardiac PET-CT and SPECT-CT systems allow simultaneous evaluation of coronary artery anatomy, ischemia and hibernating myocardium. Its main drawback is high ionizing radiation [1].

Treatment of CHF patients with left ventricular dysfunction involves several strategies such as counseling, pharmacological and non-pharmacological management, use of mechanical aids, and surgical intervention [9].

Non-pharmacological management 

• General advice and measures.

The family and caregivers should be adequately informed on the proper healthcare of a CHF patient. Monitoring of the patient's weight should be done on a regular basis, preferably after morning toilet. An unexpected weight gain of 0.2 kg in 3 days indicate the need to adjust dietary sodium intake of the patient, more so in advanced cases than in mild CHF. Self-management of diuretic dose should be encouraged.

Drugs to be avoided or used with caution when prescribed in combination with other treatment modalities for heart failure, are: corticosteroids; non-steroidal anti-inflammatory drugs; tricyclic anti-depressants; Class I anti-arrhythmic agents; lithium; and calcium antagonists (verapamil, diltiazem, short-acting dihydropyridine derivatives).

Patients with acute heart failure or those undergoing destabilization of CHF are required to rest or stay in bed. Ambulatory patients may be allowed to perform routine daily activities or recreational activities that do not precipitate symptoms. Programmed non-strenuous exercise under a qualified physical therapist may be recommended for stable patients in NYHA class II-III. 

Pharmacological therapy

• ACE-inhibitors

Patients with reduced LV systolic function (i.e., subnormal ejection fraction of 40-45%), with or without symptoms, are initially treated with angiotensin-converting enzyme inhibitors.  Prescription should conform with the recommendation on effective dose from large, controlled trials in heart failure and not on empirical observations alone. 

• Diuretics

Diuretics are required to offset fluid overload, manifested by pulmonary congestion or peripheral edema. These facilitate rapid relief of dyspnea and increased tolerance for exercise.

• Beta-adrenoceptor antagonists

Beta-blockers are recommended for the following subgroups of patients: all HF patients (in NYHA class II–IV) with ischemic or non-ischemic cardiomyopathies and reduced LVEF on standard treatment with diuretics, and ACE-inhibitors. This treatment regimen has benefited patients with reference to gender, age, functional class, LVEF, ischemic and non-ischemic categories. It has lessened progression of illness towards heart failure and shortened hospitalization stay of cardiovascular and HF patients. 

• Aldosterone receptor antagonists

Patients with advanced heart failure (NYHA-III-IV) with systolic dysfunction may be treated with aldosterone antagonists with ACE-inhibitors, beta-blockers and diuretics. This treatment regimen has improved survival and the clinical course of illness of patients after myocardial infarcts with left ventricular dysfunction and signs of heart failure and diabetes.  

• Angiotensin receptor antagonists

Angiotensin II receptor blockers (ARBs) can replace ACE-inhibitors in symptomatic patients who are intolerant to the latter. ARBs and ACE-inhibitors have comparable therapeutic effects in acute myocardial infarction with signs of heart failure or left ventricular dysfunction. Their impacts on mortality are similar.

• Cardiac glycosides

Cardiac glycosides are prescribed for patients with atrial fibrillation, with or without LV dysfunction. Ventricular function is slowed down and symptoms of heart failure are alleviated.  

• Vasodilator agents (nitrates/hydralazine)

These are used in conjunction with other drugs for angina and hypertension: Hydralazine-isosorbide dinitrate (for patients with intolerance for ACE-inhibitors and ARBs) and nitrates (for the relief of angina and dyspnea). 

• Calcium antagonists are not recommended for the treatment of heart failure caused by systolic dysfunction (e.g., diltiazem- and verapamil-type calcium antagonists, and newer drugs, felodipine, and amlodipine). These are not to be used with beta-blockers.

• Nesiritide, a recombinant human brain or B-type natriuretic peptide (BNP), relieves dyspnea and causes vasodilatation, administered intravenously to patients with acute heart failure. 

• Positive inotropic agents

These are administered intravenously in patients with severe heart failure and with signs of both pulmonary congestion and peripheral hypoperfusion. Prolonged use is not recommended in CHF. Complications may occur and expected outcome of treatment is uncertain. Some calcium sensitizers (e.g. levosimendan) may relieve symptoms and are safe to use.

• Anti-coagulants

Anticoagulation is prescibed in CHF associated with atrial fibrillaton, a mobile left ventricle thrombus or a previous thromboembolic episode. It remains inconclusive whether anti-thrombotic therapy can impact on mortality and morbidity in patients with heart failure. Aspirin or oral anti-coagulants may be given as secondary prophylaxis after myocardial infarction. However, aspirin is not advisable in patients with recurrent hospitalization and worsening heart failure. Anti-coagulant therapy should be undertaken under close supervision by a physician because of possible hemorrhagic diathesis.

• Antiarrhythmic agents

These drugs, as with beta blockers, are not recommended in CHF. The prescription is for atrial fibrillation (rarely flutter) and non-sustained, or sustained ventricular tachycardia. 

Class I antiarrhythmics - not recommended as they may trigger fatal ventricular arrhythmias and hemodynamic instability.

Class II antiarrhythmics - may be used alone or in combination with amiodarone or nonpharmacological therapy in the management of sustained or non-sustained ventricular tachy-arrhythmias. Beta-blockers may avert sudden death in heart failure.

Class III antiarrhythmics - such as amiodarone, is prescribed for most supraventricular and ventricular arrhythmias. It stabilizes sinus rhythm in patients with heart failure and atrial fibrillation even with enlarged left atria. Electrical cardioversion is enhanced and no negative inotropic side effects have been observed. Routine administration of amiodarone in patients with heart failure is not recommended.

• Oxygen- indicated for the treatment of acute heart failure but not in CHF.

Devices and surgery

• Revascularization (catheter interventions and/or surgery)

Limited qualitative studies on heart failure of ischemic etiology endorse revascularization for symptomatic treatment. However, while waiting  for the results of randomized trials, surgical or percutaneous revascularization is not routinely recommended for patients with heart failure and coronary disease. 

• Other forms of surgery (mitral valve repair)

Mitral valve surgery has been efficacious in patients with severe left ventricular systolic dysfunction and severe mitral valve insufficiency following ventricular insufficiency. The procedure is also appropriate for secondary mitral valve insufficiency due to left ventricular dilatation.

• Bi-ventricular (multi-site) pacing

Patients with HF have used pacemakers for bradycardia. However, ventricular dyssynchrony and exacerbation of symptoms may result when pacing only the right ventricle in patients with systolic dysfunction.

• Implantable cardioverter defibrillator (ICD) - for arrythmias
• Heart transplantation ventricular assist device

Heart transplantation is the accepted final mode of treatment for terminal cases of heart failure. In the hands of experts this option has significantly increased survival and capacity to engage in exercise and daily activities, as well as the general quality of life.

• Artificial heart is an important alternative for patients dying of end-stage biventricular heart failure.

Heart failure is a paramount concern of health authorities worldwide. Two thirds of HF cases are linked to coronary artery disease with uncontrolled ischemic crisis. Ischemia in ICM precedes heart failure and sudden death. Thus, timely intervention in ICM has improved chances of survival of patients with CAD and heart failure [8].

Quality of life is an important consideration since the goal of treatment is not only to prolong life but also to restore the patient's ability to resume and appreciate normal daily activity. Treatment modalities that are currently available provide a wide range of options to suit individual needs and resources. The most important prognostic indicator in HF hinges on the differential diagnosis of left ventricular dysfunction [5]. 

In patients with normal ejection fraction, prognosis in CAD depends on the severity of ischemia  and reduction in ischemia with treatment, with or without hibernating myocardium. However, this has not been demonstrated in patients with subnormal ejection fraction [1].

While surgical ventricular remodeling has a place in the treatment of ischemic cardiomyopathy, it is not well accepted in the case of non-ischemic cardiomyopathy (Batista procedure) with high rates of failure [6].

Coronary artery disease occurs in two forms, i.e., arteriosclerosis  (thickening and loss of plasticity of the coronary artery) and the presence of cholesterol and lipoid deposits (atheroma) in the artery, resulting in reduced blood flow (ischemia). Severe extensive CAD and left ventricular dysfunction and dilatation are the main causes of ischemic cardiomyopathy. 

Although the patient's age, response to exercise and presence of co-existing diseases influence the outcome of treatment, the most important determinant is the extent of restoration of myocardial viability and ventricular remodeling. Patients with viable myocardium but without revascularization are still at high risk for heart failure.

Myocardial ischemia and LV dysfunction are independent variables in HF which influence the decision whether or not to perform revascularization vis-a-vis the response of the patient to pharmacologic intervention. Recent studies suggest that sudden death may occur in both ischemic and non-ischemic HF patients, indicating the importance of differentiating between these two etiologies [5]. Myocardial ischemia, with or without infarction from CAD, is the main cause of ventricular dysfunction in ICM. On the other hand, there are many other potential causes of non‐ischemic cardiomyopathy (NICM) including infection, genetics, immunological aberrations, hemodynamic pathology, or toxic injury [6].

CAD is the leading cause of deaths from heart failure in Europe. Almost 2 million deaths are reported each year. ICM, with reduction in ventricular systolic function (ejection fraction of ≤35%-40%), is responsible for 19% of cardiac mortality rates during a follow-up period of 22 months [3].

ICM is the result of deficiency of oxygen in the heart due to obstruction of the main coronary arteries by infarction, leading to loss of cardiac muscle cells and scarring, and left ventricular dysfunction. In addition, contraction of the epicardial branches of the coronary circulation and disruption of the network of capillaries contribute further to ischemia and tissue injury. These pathological processes occur in large and small vessels of the coronary arterial circulation accounting for a range of clinical disease entities, from acute myocardial infarction to chronic ischemic cardiomyopathy. This may become, after long years of damage of viable tissue, a dilated congestive ischemic myopathy with multiple localized myocardial injuries and anatomical changes in the ventricular wall [7].

Contractile function of the myocardium may be abolished by necrosis or in a viable myocardium, with severe contractile impairment causing myocardial hibernation or stunning. Stunning is caused by a temporary ischemic or reperfusion injury of the heart, lasting for hours or days. So long as reperfusion recovers, contractile activity can be restored. Hibernation also involves contractile dysfunction in chronic ischemic heart disease. In contrast to myocardium stunning where contractile function can be restored spontaneously, coronary revascularization (CR) is required in hibernation to restore ventricular function [3].

Treatment of underlying conditions such as hypertension and coronary artery disease, especially the latter, is the key to the prevention of heart failure. CAD causes myocardial ischemia and left ventricular systolic dysfunction, which are the hallmarks of ischemic cardiomyopathy, leading to heart failure. Next to myocardial dysfunction, high priority should be given to addressing the underlying causes of ventricular dysfunction such as ischemia, alcohol, thyroid disease, drugs. Preventing or mitigating left ventricular dysfunction means to avert the risk of developing heart failure and sudden death.   

Thus, prevention of heart failure is the goal of treatment. Risk factors which predispose to ICM should be avoided or treated according to the case, but the benefits should outweigh the risks [6]. 

Ischemic cardiomyopathy is a potentially fatal disease, characterized by defects in coronary circulation, myocardium, and left ventricular function. High precision imaging studies have made possible accurate diagnosis and successful management of ICM, increasing patients chances for survival [3]. Basically, the pathogenesis of ICM is attributed to poorly contracting ischemic myocardium with coronary artery disease, with or without infarcts [4]. ICM, if left untreated, leads to heart failure and sudden death.

Occlusion of coronary arteries impedes blood flow and oxygen supply to the heart, including the myocardium, eventually, diminishing the heart's capacity to pump blood. Loss of muscle tissue and scarring weaken the left ventricle, resulting in reduction of ventricular systolic function. Thus, ventricular dysfunction is the consequence of coronary arteriosclerosis and myocardial ischemia and infarction. 

Ischemia is a predictor of heart failure in ICM. However, there are other underlying causes of HF such as hypertension and valvular disease. Whereas, advances in chemotherapy have prolonged many lives the real challenge lies in determining the best treatment strategy in ICM. For the past several years, ischemic heart disease has been a frequent cause of heart failure, more than hypertension and valvular disease. 

Congestive heart failure is a major public health concern in developed countries. It follows that prevention should focus on eliminating the underlying conditions that lead to ICM and heart failure. A number of options are available, i.e., pharmacological, non-pharmacological, and if all these fail, surgery. Heart transplantation is the accepted last resort for end stage heart failure.

Ischemic cardiomyopathy simply means that blood supply to the heart is reduced due to damage sustained by the myocardium from a co-existing coronary artery disease. Occlusion of the coronary arteries by cholesterol plaques diminishes the flow of blood to the heart. Consequently, myocardial ischemia and coronary artery infarction lead to reduction in the pumping capacity of the left ventricle. If left undiagnosed and untreated, the result is heart failure and sudden death.

Ischemic cardiomyopathy open link is a leading cause of morbidity in the United States, affecting 1:100 persons, especially middle-aged and older men. Risk factors that are associated with ICM are: high-cholesterol diet; obesity; diabetes; hypertension; sedentary lifestyle; smoking; and history of cardiovascular diseases.

Symptoms associated with ICM are: fatigue (especially in women); heartburn or feeling of indigestion; dyspnea; feeling of tightness or heavy pressure on the chest; angina; pain spreading to the neck, jaw, back, shoulder, or arm; dizziness or light-headedness; nausea; vomiting; cold sweats; and palpitations.

Symptoms of heart failure are: dyspnea following activity or after lying down; abrupt awakening from sleep due to dyspnea; cough; anorexia; edema of ankles and feet (adults); abdominal distention (adults); fatigue; weakness; faintness; irregular or rapid pulse; and palpitations.

Signs and tests include: hepatomegaly; "crackles" in the lungs (heard with a stethoscope); extra heart sounds; and elevated pressure in the neck vein. 

Heart failure is considered when the pumping function of the heart is found to be below the normal ejection fraction by a level  of 55-65%. Ischemic heart disease can lead to heart failure when the ejection fraction is normal or near normal, accompanied by the aforementioned signs and symptoms. The heart in this case is unusually relaxed and the condition is called "diastolic heart failure" or "heart failure with preserved ejection fraction". 

Tests used to measure ejection fraction include high precision imaging studies (e.g., Echocardiogram, Gated SPECT, MRI); ventriculogram (by cardiac catheterization); and biopsy. Laboratory tests include: CBC; blood chemistry; cardiac biochemical markers (CK-MB, troponin); and coronary risk profile (including blood lipids).  

The primary purpose of treatment is to minimize the risks and ameliorate conditions that predispose to heart failure. Advanced cases require hospitalization. For instance, cardiac catheterization may be done via coronary artery bypass (CABG) surgery or a balloon procedure (angioplasty) to improve blood flow to the myocardium.

The overall management of cardiomyopathies is based on a holistic approach using both pharmacological and non-pharmacological methods. These include: vasodilators (isosorbide dinitrate or hydralazine); ACE-nhibitors (captopril, enalapril, lisinopril, and ramipril); digitalis glycosides; angiotensin receptor blockers (ARBs) such as losartan and candesartan; diuretics, including thiazide, loop diuretics, and potassium-sparing diuretics; and beta-blockers (carvedilol and metoprolol).

Heart devices that can be used by patients are: implantable cardioverter-defibrillator; single or dual chamber pacemaker; left ventricular assist device (LVAD); and biventricular pacemaker. 

Preventive measures:

• Taking medications as prescribed  
• Maintaining a low-salt diet (for adults).
• Moderation in fluid intake  
• Avoiding over exertion in daily activities and exercise.
• Refraining from alcoholic drinks and smoking.
• Minimizing or controlling stress 
• Consulting a doctor for treatment of infection and other illnesses 
• Consulting a doctor for monitoring progress of treatment [7]
• Adopting a healthy lifestyle 

1. Schuster A, Morton G, Chiribiri A, Perera D, Vanoverschelde  J, Nagel E. Imaging in the management of ischemic cardiomyopathy: special focus on magnetic resonance. J Am Coll Cardiol. 2012;59:359-370.
2. Beltrami CA, Finato N, Rocco M, et all. Structural basis of end-stage failure in ischemic cardiomyopathy in humans. Circulation. 1994;89:151-163.
3. Candell-Riera J, Romero-Farina G, Aguade-Bruix S, Castell-Conesa J. Ischemic cardiomyopathy: a clinical nuclear cardiology perspective. Rev. Esp. Cardiol. 2009;62:903-917. 
4. Malcolm J, Arnold O. Overview of Cardiomyopathies. MSD Manual Professional Edition; 2013. 
5. Felker GM, Shaw LK, O’Connor CM. A standardized definition of ischemic cardiomyopathy for use in clinical research. J Am Coll Cardiol. 2002;39:210–218.
6. Wu AH. Management of patients with non-ischaemic cardiomyopathy. Heart. 2007;93:403–408.
7. Anversa P, Sonnenblick EH. Ischemic cardiomyopathy: pathophysiologic mechanisms. Prog Cardiovasc Dis. 1990;33:49-70.
8. Swedberg K, Cleland J, Dargie H, et all. Task Force for the Diagnosis, Treatment of Chronic Heart Failure of the European Society of Cardiology. Guidelines for the diagnosis and treatment of chronic heart failure: executive summary. Eur Heart J. 2005;26:1115–1140.
9. Velazquez EJ, Williams JB, Yow E, et all. Long-term survival of patients with ischemic cardiomyopathy treated by coronary artery bypass grafting versus medical therapy. Ann Thorac Surg. 2012;93:523–530