Cardiomyopathy is a chronic disease of the heart muscle (myocardium), in which the muscle is abnormally enlarged, thickened, and/or stiffened. The weakened heart muscle loses the ability to pump blood effectively, resulting in irregular heartbeats (arrhythmias) and possibly even heart failure.
Often, the cause of the cardiomyopathy is unknown. In some people, however, doctors are able to identify some contributing factors. Possible causes of cardiomyopathy include:
- Genetic conditions
- Long-term high blood pressure
- Heart tissue damage from a previous heart attack
- Chronic rapid heart rate
- Heart valve problems
- Metabolic disorders, such as obesity, thyroid disease or diabetes
- Nutritional deficiencies of essential vitamins or minerals, such as thiamin (vitamin B-1)
- Pregnancy complications
- Drinking too much alcohol over many years
- Use of cocaine, amphetamines or anabolic steroids
- Use of some chemotherapy drugs and radiation to treat cancer
- Certain infections, which may injure the heart and trigger cardiomyopathy
- Iron buildup in your heart muscle (hemochromatosis)
- A condition that causes inflammation and can cause lumps of cells to grow in the heart and other organs (sarcoidosis)
- A disorder that causes the buildup of abnormal proteins (amyloidosis)
- Connective tissue disorders
Types of cardiomyopathy include:
- Dilated cardiomyopathy. This is the most common type of cardiomyopathy. In this disorder, the pumping ability of your heart’s main pumping chamber — the left ventricle — becomes less forceful. The left ventricle becomes enlarged (dilated) and can’t effectively pump blood out of the heart.
Although this type can affect people of all ages, it occurs most often in middle-aged people and is more likely to affect men. Some people with dilated cardiomyopathy have a family history of the condition. In others, dilated cardiomyopathy may occur as a result of certain conditions such as coronary heart disease, infection, chemotherapy, or drug or alcohol use. The cause may also be unknown (idiopathic).
- Hypertrophic cardiomyopathy. This type involves abnormal thickening of your heart muscle, particularly affecting the muscle of your heart’s main pumping chamber (left ventricle). The thickened heart muscle can make it harder for the heart to pump blood.
Hypertrophic cardiomyopathy can develop at any age, but the condition tends to be more severe if it becomes apparent during childhood. Most affected people have a family history of the disease, and some genetic mutations have been linked to hypertrophic cardiomyopathy.
- Restrictive cardiomyopathy. The heart muscle in people with restrictive cardiomyopathy becomes rigid and less elastic, meaning the heart can’t properly expand and fill with blood between heartbeats. While restrictive cardiomyopathy can occur at any age, it most often tends to affect older people. It’s the least common type of cardiomyopathy and can occur for no known reason (idiopathic).
The condition may also be caused by diseases elsewhere in the body that affect the heart, such as a disease in which iron builds up in the heart muscle (hemochromatosis), a disorder that causes the buildup of abnormal proteins (amyloidosis), a disease that causes inflammation and can cause lumps of cells to grow in the heart and other organs (sarcoidosis), connective tissue disorders, or a disorder that causes abnormal blood cells to damage the heart (eosinophilic heart disease).
- Arrhythmogenic right ventricular dysplasia. In this rare type of cardiomyopathy, the muscle in the lower right heart chamber (right ventricle) is replaced by scar tissue. This can lead to heart rhythm problems. This condition is often caused by genetic mutations.
- Other types of cardiomyopathy. Other types of cardiomyopathy (unclassified cardiomyopathies) exist, but they don’t fit within the other types of cardiomyopathy.
Macroscopic examination of heart reveals ventricular chamber dilation with thickened or normal thickness walls. Valvular changes are not typical, although dilation of valvular orifices may be present as secondary changes due to dilation of chambers. Coronary anatomy is most commonly normal, although the presence of nonocclusive atherosclerotic plaques may be present. Thrombi are found most frequently in ventricles and atrial appendages.
The most typical DCM pattern is the development of interstitial and perivascular fibrosis of varying degree. Myocardial necrosis predominantly is present at subendocardium. Our study group investigated noninvasively using the Shirani method. The degree of myocardial fibrosis in patients with IDC and ischemic dilatation cardiomyopathy. The percentage of volumic collagen fraction in the LV myocardium was significantly higher in DCM patients compared to those with ischemic cardiomyopathy. Increase of collagen fraction correlated with the degree of dilation of the left ventricle.
The most common clinical manifestations of DCM are congestive heart failure symptoms and thromboembolic complications. The disease commonly has a progressive course. The determination of time of manifestation is not easy, because the disease course for a long period is not symptomatic. Patients are admitted to hospital in cases with expressed heart failure symptoms. A careful history taking and physical examination with diagnostic studies are essential for differential diagnosis of DCM. More commonly, DCM manifests without any history and provoking factor. Cardiomegaly at radiological examination or on abnormal electrocardiography (ECG) may be the first findings in an asymptomatic patient. The left ventricle is dilated, and more spherical than usual with raised wall stress and depressed systolic function. As the disease progresses, definite symptoms of congestive heart failure present. Chest discomfort may occur in some cases; however this discomfort is not relieved by nitroglycerin. Physical examination may reveal gallop rhythm in decompensated patients. The jugular venous pulse is normal until right heart decompensation is present. The clinical course of DCM may be variable both with slow progression and rapidly progressive over several months. Cachexia and peripheral edema typically arise late in the course. Sudden death, presumably due to ventricular fibrillation may be the first manifestation. Some cases of DCM most probably develop due to viral myocarditis and these patients may have a history viral infection prior to deterioration of heart failure symptoms. An acute systemic febrile infectious disease (such as influenza) is followed by a latent period during which time the patient may be asymptomatic. It is reported also that in 20%-25% of patients with new-onset DCM may have cardiac recovery.
Several clinical, laboratory and instrumental factors may have prognostic significance in DCM patients. These factors are symptomatic ventricular arrhythmias, persistent gallop rhythm, persistent jugular venous distention, systemic hypotension, persistently elevated B-type natriuretic peptide, left bundle branch block, pulmonary capillary wedge pressure > 20 mmHg, cardiac index < 2.5 L/min per square meter, severely reduced ejection fraction, restrictive diastolic filling pattern, and severe mitral regurgitation.
In the early stages, people with cardiomyopathy may not have any signs and symptoms. But as the condition advances, signs and symptoms usually appear. Cardiomyopathy signs and symptoms may include:
- Breathlessness with exertion or even at rest
- Swelling of the legs, ankles and feet
- Bloating of the abdomen due to fluid buildup
- Cough while lying down
- Irregular heartbeats that feel rapid, pounding or fluttering
- Chest pain
- Dizziness, lightheadedness and fainting
Dilated cardiomyopathy is a heart muscle disorder defined by the presence of a dilated and poorly functioning left ventricle in the absence of abnormal loading conditions (hypertension, valve disease) or ischaemic heart disease sufficient to cause global systolic impairment. A large number of cardiac and systemic diseases can cause systolic impairment and left ventricular dilatation, but in the majority of patients no identifiable cause is found—hence the term “idiopathic” dilated cardiomyopathy (IDC). There are experimental and clinical data in animals and humans suggesting that genetic, viral, and immune factors contribute to the pathophysiology of IDC.
Treatment varies depending on how damaged your heart is due to cardiomyopathy and the resulting symptoms.
Some people may not require treatment until symptoms appear. Others who are beginning to struggle with breathlessness or chest pain may need to make some lifestyle adjustments or take medications.
You can’t reverse or cure cardiomyopathy, but you can control it with some of the following options:
- heart healthy lifestyle changes
- medications, including those used to treat high blood pressure, prevent water retention, keep the heart beating with a normal rhythm, prevent blood clots, and reduce inflammation
- surgically implanted devices, like pacemakers and defibrillators
- heart transplant, which is considered a last resort
The goal of treatment is to help your heart be as efficient as possible and to prevent further damage and loss of function.