Symptoms are a good indicator of the severity of dilated cardiomyopathy. The following are the symptoms with which the patient may present and based on how severe the symptoms are, it suggests how advanced the diseased condition may be. The following are the symptoms with which a patient may present: fatigue, orthopnea, dyspnea on exertion, paroxysmal nocturnal dyspnea, increasing edema, weight gain, or an increase in the abdominal girth. Vital signs must be assessed with special attention to the following: tachypnea, tachycardia and hypertension. Other findings which are of importance include: cyanosis, clubbing, jugular venous distension, pulmonary edema, S 3 gallop, enlarged liver and peripheral edema.

On examination of the heart, the following findings must be paid attention to: cardiomegaly, murmurs, S 2 at the base S 3, and S 4, tachycardia, irregularly regular rhythm and gallops [3]. Symptoms of left- and right-sided congestive failure develop gradually in most patients. Some patients have left ventricular dilatation for months or even years before becoming symptomatic. Vague chest pain may be occasionally present, but typical angina pectoris is rare and suggests presence of concomitant coronary heart disease. Syncope may occur due to arrhythmias and systemic embolism (often emanating from a ventricular thrombus).

TThe workup must include the following: a complete blood count, metabolic panel, thyroid function tests, cardiac biomarkers, B-type natriuretic peptide assay, chest radiography, echocardiography, cardiac magnetic resonance imaging (MRI), electrocardiography (ECG) [1].

The chest X-ray demonstrates enlargement of the cardiac silhouette due to left ventricular dilatation, although generalized cardiomegaly is seen easily too. The lung fields may demonstrate evidence of pulmonary venous hypertension and interstitial or alveolar edema. The electrocardiogram often shows sinus tachycardia, atrial fibrillation, premature ventricular complexes, nonspecific ST-T-wave abnormalities, Q waves, left ventricular hypertrophy, ventricular arrhythmias, and conduction defects. Echocardiography and radionuclide ventriculography may show dilatation, with thinned walls and systolic dysfunction [6].

The detection of elevated circulating levels of brain natriuretic peptide may help clarify which patients with dyspnea of uncertain etiology actually have heart failure rather than pulmonary disease as the cause of their symptoms, and identifies patients at increased risk of sudden death. Cardiac catheterization and coronary angiography are often performed to exclude ischemic heart disease, and bedside hemodynamic monitoring is helpful in managing acutely decompensated patients. Angiography reveals a dilated, diffusely hypokinetic left ventricle, with mild grade mitral regurgitation. Transvenous endomyocardial biopsy is usually not necessary in idiopathic or familial dilated cardiomyopathy. However, it may be helpful in the recognition of secondary cardiomyopathies, like acute myocarditis and amyloidosis [3].

Treatment and management of dilated cardiomyopathy is usually the same as that of congestive heart failure. Some therapeutic interventions treat symptoms whereas others treat factors that affect survival. The drug classes used include the following: Angiotensin-converting enzyme (ACE) inhibitors, vasodilators, angiotensin II receptor blockers (ARBs), aldosterone antagonists, diuretics, antiarrhythmics, beta-blockers, human B-type natriuretic peptide, cardiac glycosides, and inotropic agents. Anticoagulants may be used in certain cases [7]. Surgical options include the following: cardiac resynchroniztion, ventricular restoration surgery, left ventricular assist devices, automatic implantable cardioverter defibrillators and heart transplantation [7].

Most patients pursue an inexorably downhill course, and the majority, particularly those >55 years, die within 3 years of the onset of symptoms. African Americans are more likely to suffer progressive heart failure and death than Caucasians. Spontaneous stabilization occurs in about a quarter of patients. Death is due to either CHF or ventricular tachy- or bradyarrhythmia; sudden death is a constant threat. Systemic embolization is a possible complication and should be considered for chronic anticoagulation. Standard therapy of heart failure is following a salt restricted diet. Angiotensin-converting enzyme (ACE) inhibitors, diuretics, and digitalis produce symptomatic improvement [8]. An angiotensin II receptor blocker may be substituted in ACE-intolerant patients. Most patients should be treated with a β-adrenergic blocker. Spironolactone should be added for most patients with recent or current advanced heart failure [9].

Some patients with dilated cardiomyopathy who have biopsy evidence of myocardial inflammation have been treated with immunosuppressive therapy, but long-term evidence of efficacy is lacking. Alcohol should be avoided because of its cardiac toxic effects, as should calcium channel blockers and non-steroidal anti-inflammatory drugs. Anti-arrhythmic agents are best avoided for fear of pro-arrhythmia, unless they are needed to treat symptomatic or serious arrhythmias. For one in three patients with an intraventricular conduction delay, biventricular pacing improves symptoms, reduces hospitalizations and mortality. Insertion of an implantable cardioverter-defibrillator is useful in patients with symptomatic ventricular arrhythmias [10]. In patients with advanced disease who are refractory to medical therapy, cardiac transplantation should be considered.

Although a few cases of dilated cardiomyopathy are reversible with treatment of the underlying disease, many progress to heart failure. Continued decompensation might necessitate heart transplantation. The prognosis depends on many factors with etiology of the disease being the primary factor. Other factors which play an important role are the patient's age, sex, ability to follow medical advice, access to optimal medical therapy, and presence of severe congestive heart failure (CHF). The Framingham heart study found that approximately 50% of patients diagnosed with CHF died within 5 years [5]. Patients with severe heart failure have a mortality rate of more than 50% yearly. Patients having mild heart failure benefit tremendously with optimal medical therapy.

DCM is one of the cardiomyopathies that affect mainly the myocardium. Various cardiomyopathies have differing causes and may affect the heart in many ways. In DCM, a portion of the myocardium is enlarged, often without any obvious cause. Obesity increases the risk of developing heart failure, and so does sleep apnea. Probably 20% to 40% of affected individuals have familial forms of the disorder, with possible mutations and chromosomal aberrations in more than 30 genes yet identified [2]. The disease is genetically heterogeneous, but most commonly autosomal dominant in transmission, but autosomal recessive, mitochondrial (especially in children), and X-linked inheritance is found as well [2].

DCM may occur secondary to other cardiovascular disease, ischemia, hypertension, valvular disease and tachycardia. Whipple disease and Lyme disease are probable infectious causes. Viral, bacterial, fungal, rickettsial, metazoal and protozoal infections can also cause DCM. Endocrine diseases such as hyperthyroidism and hypothyroidism or diabetes mellitus, are also a contributing factors. The other causes of DCM include nutritional imbalances such as beriberi and protein deficiency, collagen vascular disease, sarcoidosis, physical agents such as electric shock, ionizing radiation and extreme temperatures. A primary cardiac tumor (myxoma) and transplant rejection are also causes for DCM. Toxins are a significant cause. Almost one third of the cases may occur from severe ethanol abuse. However, often in dilated cardiomyopathy, the cause remains unexplained. Some idiopathic cases may be occurring from failure to identify known causes such as infections or toxins or familial forms.

It is difficult to assess the prevalence of cardiomyopathy. Dilated cardiomyopathy may be the late sequel of acute viral myocarditis, mediated via immunologic mechanisms. Although it may occur in any patient population, it is most commonly a disease of middle aged men and is more common in African Americans than in whites [3]. The most common ages of developing DCM is between the ages of 20 and 60 years. Dilated cardiomyopathy also occurs in children. The prevalence of this condition is increasing. Patients with the condition often go undiagnosed and may present directly with sudden cardiac arrest. The estimated prevalence of idiopathic dilated cardiomyopathy is 0.4 per 1,000 of population. In the future, as more causes are elucidated and more patients diagnosed with genetic or familial cardiomyopathy, the number of cases with idiopathic disease, a diagnosis of exclusion, are bound to decrease.

DCM is primarily a failure of systolic function with inadequate contractility (pump failure). Left ventricular hypertrophy is calculated as the ratio of LV mass to cavity size; this ratio is decreased in persons with dilated cardiomyopathies [1]. Dilated cardiomyopathies may have both systolic and diastolic dysfunction. The decrease in systolic function is the primary abnormality which leads to an increase in end-diastolic and end-systolic volumes.

Continuous and progressive dilatation may cause significant regurgitation at the mitral and tricuspid orifices, which may further diminish the cardiac output and increase end-systolic volumes and ventricular wall stress. This further leads to dilatation and myocardial dysfunction [4]. Thus, the affected myocardium is unable to generate the pressures required to maintain cardiac output. As a result the ventricles become stretched and overloaded. The poor cardiac output can be explained by applying the Frank-Starling Law. The law states that the myocardial force increases at end-diastole compared to the end-systole as the muscle length increases, thereby generating a greater force as the muscle is stretched. Overstretching produces failure of myocardial contractile unit. These compensatory mechanisms are dysfunctional in persons with dilated cardiomyopathies, compared to patients with normal LV function. These compensatory methods lead to further damage to myocaridum, cardiac dysfunction, and geometric remodelling [1][4].

Decreased cardiac output leads to reductions in organ perfusion which results in neurohormonal activation, and stimulation of adrenergic nervous system and the renin-angiotensin-aldosterone system (RAAS). Additional factors important to compensatory neurohormonal activation include the release of arginine vasopressin and the secretion of natriuretic peptides [4]. These compensatory responses worsen the cardiomyopathy gradually.

It is a well-known fact that following a healthy lifestyle is one of the best ways to reduce the effects of heart related complaints. One must refrain from smoking; alcohol must be moderated [11]. Complete alcohol abstinence is ideal. One must refrain from using cocaine or other illegal drugs and must follow a healthy diet. Caffeine intake should be limited. It is also important to maintain a healthy weight, follow a recommended exercise regimen and get enough sleep and rest. At times, people who have cardiomyopathy but no signs or symptoms may not need treatment because sometimes dilated cardiomyopathy that comes up suddenly may even go on its own.

Dilated cardiomyopathy abbreviated as DCM is a progressive condition of the heart muscle which is characterized by dilation of one or both ventricles along with contractile dysfunction and normal left ventricular thickness [1]. Because of this, the enlarged heart cannot pump blood efficiently. Hence, this decreased function of the heart can affect the lungs, liver and other body systems. Statistics show that DCM is the third most common cause of heart failure as well as the most frequent cause for a cardiac transplantation. About one in three cases of congestive heart failure (CHF) is due to dilated cardiomyopathy, with the remainder the consequence of coronary artery disease [1] [2].

Dilated cardiomyopathy (DCM) is a heart condition in which there is enlargement of one of the chambers of the heart. This, results in the heart being over worked which is why a person comes up with symptoms of breathlessness, increase in weight and edema along with others. It is more common in males and a higher incidence is found among African-American people. However, DCM can be found amongst people in their 20’s or amongst children as well.

Mostly DCM is secondary to other heart diseases. At times viral and bacterial infections can also contribute to the same. The main goals of treating cardiomyopathy include controlling the signs and symptoms, manage other conditions which contribute to the disease, reduce complications of a sudden cardiac arrest. ACE inhibitors are usually prescribed to lower the blood pressure. It is important to maintain lifestyle changes which reduce the severity of the symptoms and thus the outcome of the disease. A healthy diet is a part of a healthy lifestyle. A healthy diet includes fruits, vegetables and grains. It is important to aim for a healthy weight.

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