Dilated cardiomyopathy develops insidiously, and may not initially cause symptoms significant enough to impact on quality of life. Nevertheless, many people experience significant symptoms. These might include:

- Shortness of breath

- Syncope (fainting)

- Angina, but only in the presence of ischemic heart disease

A person suffering from dilated cardiomyopathy may have an enlarged heart, with pulmonary edema and an elevated jugular venous pressure and a low pulse pressure. Signs of mitral and tricuspid regurgitation may be present.

The clinical course of HCM is variable. Many people with HCM are asymptomatic or mildly symptomatic, and many of those carrying disease genes for HCM do not have clinically detectable disease. The symptoms and signs of HCM include shortness of breath due to stiffening and decreased blood filling of the ventricles, exertional chest pain (sometimes known as angina) due to reduced blood flow to the coronary arteries, uncomfortable awareness of the heart beat (palpitations), as well as disruption of the electrical system running through the abnormal heart muscle, lightheadedness, weakness, fainting and sudden cardiac death.

Dyspnea is largely due to increased stiffness of the left ventricle (LV), which impairs filling of the ventricles, but also leads to elevated pressure in the left ventricle and left atrium, causing back pressure and interstitial congestion in the lungs. Symptoms are not closely related to the presence or severity of an outflow tract gradient. Often, symptoms mimic those of congestive heart failure (esp. activity intolerance and dyspnea), but treatment of each is different. Beta blockers are used in both cases, but treatment with diuretics, a mainstay of CHF treatment, will exacerbate symptoms in hypertrophic obstructive cardiomyopathy by decreasing ventricular preload volume and thereby increasing outflow resistance (less blood to push aside the thickened obstructing tissue).

Major risk factors for sudden death in individuals with HCM include prior history of cardiac arrest or ventricular fibrillation, spontaneous sustained ventricular tachycardia, family history of premature sudden death, unexplained syncope, LV thickness greater than or equal to 30 mm, abnormal exercise blood pressure and nonsustained ventricular tachycardia.

Subjects' symptoms from non-compaction cardiomyopathy range widely. It is possible to be diagnosed with the condition, yet not to have any of the symptoms associated with heart disease. Likewise it possible to have severe heart failure, which even though the condition is present from birth, may only manifest itself later in life. Differences in symptoms between adults and children are also prevalent with adults more likely to have heart failure and children from depression of systolic function.

Common symptoms associated with a reduced pumping performance of the heart include:

- Breathlessness

- Fatigue

- Swelling of the ankles

- Limited physical capacity and exercise intolerance

Two conditions though that are more prevalent in noncompaction cardiomyopathy are: tachyarrhythmia which can lead to sudden cardiac death and clotting of the blood in the heart.

Symptoms of cardiomyopathies may include fatigue, swelling of the lower extremities and shortness of breath. Further indications of the condtion may include:

- Arrhythmia

- Fainting

- Diziness

Cardiomyopathies can be classified using different criteria:

- Primary/intrinsic cardiomyopathies

- Genetic

- Hypertrophic cardiomyopathy

- Arrhythmogenic right ventricular cardiomyopathy (ARVC)

- LV non-compaction

- Ion Channelopathies

- Dilated cardiomyopathy (DCM)

- Restrictive cardiomyopathy (RCM)

- Acquired

- Stress cardiomyopathy

- Myocarditis

- Ischemic cardiomyopathy

- Secondary/extrinsic cardiomyopathies

- Metabolic/storage

- Fabry's disease

- hemochromatosis

- Endomyocardial

- Endomyocardial fibrosis

- Hypereosinophilic syndrome

- Endocrine

- diabetes mellitus

- hyperthyroidism

- acromegaly

- Cardiofacial

- Noonan syndrome

- Neuromuscular

- muscular dystrophy

- Friedreich's ataxia

- Other

- Obesity-associated cardiomyopathy

Dilated cardiomyopathy (DCM) is a condition in which the heart becomes enlarged and cannot pump blood effectively. Symptoms vary from none to feeling tired, leg swelling, and shortness of breath. It may also result in chest pain or fainting. Complications can include heart failure, heart valve disease, or an irregular heartbeat.

Causes include genetics, alcohol, cocaine, certain toxins, complications of pregnancy, and certain infections. Coronary artery disease and high blood pressure may play a role, but are not the primary cause. In many cases the cause remains unclear. It is a type of cardiomyopathy, a group of diseases that primarily affects the heart muscle. The diagnosis may be supported by an electrocardiogram, chest X-ray, or echocardiogram.

In those with heart failure treatment may include medications in the ACE inhibitor, beta blocker, and diuretic families. A low salt diet may also be helpful. In those with certain types of irregular heartbeat, blood thinners or an implantable cardioverter defibrillator may be recommended. If other measures are not effective a heart transplant may be an option in some.

About 1 per 2,500 people are affected. It occurs more frequently in men than women. Onset is most often in middle age. Five-year survival rate is about 50%. It can also occur in children and is the most common type of cardiomyopathy in this age group.

Hypertrophic cardiomyopathy (HCM) is a condition in which a portion of the heart becomes thickened without an obvious cause. This results in the heart being less able to pump blood effectively. Symptoms vary from none to feeling tired, leg swelling, and shortness of breath. It may also result in chest pain or fainting. Complications include heart failure, an irregular heartbeat, and sudden cardiac death.

HCM is most commonly inherited from a person's parents. It is often due to mutations in certain genes involved with making heart muscle proteins. Other causes may include Fabry disease, Friedreich's ataxia, and certain medications such as tacrolimus. It is type of cardiomyopathy, a group of diseases that primarily affects the heart muscle. Diagnosis often involves an electrocardiogram, echocardiogram, and stress testing. Genetic testing may also be done.

Treatment may include the use of beta blockers, diuretics, or disopyramide. An implantable cardiac defibrillator may be recommended in those with certain types of irregular heartbeat. Surgery, in the form of a septal myectomy or heart transplant, may be done in those who do not improve with other measures. With treatment, the risk of death from the disease is less than one percent a year.

HCM affects about one in 500 people. Rates in men and women are about equal. People of all ages may be affected. The first modern description of the disease was by Donald Teare in 1958.

Boxer cardiomyopathy is an adult-onset disease with three distinct clinical presentations:

The concealed form is characterized by an asymptomatic dog with premature ventricular contractions (PVCs).

The overt form is characterized by ventricular tachyarrhythmias and syncope. Dogs with overt disease may also have episodic weakness and exercise intolerance, but syncope is the predominant manifestation.

The third form, which is recognized much less frequently, is characterized by myocardial systolic dysfunction. This may result in left-sided, right-sided, or bi-ventricular congestive heart failure. It is not known if this form represents a separate clinical entity, or whether it is part of the continuum of disease.

In a study (2006) carried out on 53 patients with the condition in Mexico, 42 had been diagnosed with another form of heart disease and only in the most recent 11 cases that ventricular noncompation was diagnosed and this took several echocardiograms to confirm. The most common misdiagnoses were:

- dilated cardiomyopathy: 30 Cases

- congenital heart disease: 6 Cases

- ischemic heart disease: 2 Cases

- disease of the heart valves: 2 Cases

- dilated phase hypertensive cardiomyopathy: 1 Case

- restrictive cardiomyopathy: 1 Case

The high number of misdiagnoses can be attributed to non-compaction cardiomyopathy being first reported in 1990; diagnosis is therefore often overlooked or delayed. Advances in medical imaging equipment have made it easier to diagnose the condition, particularly with the wider use of MRIs.

Untreated hearts with RCM often develop the following characteristics:

- M or W configuration in an invasive hemodynamic pressure tracing of the RA

- Square root sign of part of the invasive hemodynamic pressure tracing Of The LV

- Biatrial enlargement

- Thickened LV walls (with normal chamber size)

- Thickened RV free wall (with normal chamber size)

- Elevated right atrial pressure (>12mmHg),

- Moderate pulmonary hypertension,

- Normal systolic function,

- Poor diastolic function, typically Grade III - IV Diastolic heart failure.

Those afflicted with RCM will experience decreased exercise tolerance, fatigue, jugular venous distention, peripheral edema, and ascites. Arrhythmias and conduction blocks are common.

All dogs with Boxer cardiomyopathy are at risk of sudden cardiac death. This includes asymptomatic dogs, meaning that sudden death may be the first sign of disease.

Sudden cardiac death is usually caused by the degeneration of ventricular tachycardia to ventricular fibrillation. Unless terminated promptly by defibrillation, death usually occurs within minutes.

Restrictive cardiomyopathy (RCM) is a form of cardiomyopathy in which the walls of the heart are rigid (but not thickened). Thus the heart is restricted from stretching and filling with blood properly. It is the least common of the three original subtypes of cardiomyopathy: hypertrophic, dilated, and restrictive.

It should not be confused with constrictive pericarditis, a disease which presents similarly but is very different in treatment and prognosis.

For many people cardiomegaly is asymptomatic. For others, if the enlarged heart begins to affect the body's ability to pump blood effectively, then symptoms associated with congestive heart failure may arise.

- Heart palpitations – irregular beating of the heart, usually associated with a valve issue inside the heart.

- Severe shortness of breath (especially when physically active) – irregularly unable to catch one's breath.

- Chest pain

- Fatigue

- Swelling in legs

- Increased abdominal girth

- Weight gain

- Edema – swelling

- Fainting

Signs and symptoms presented by the occurrence of alcoholic cardiomyopathy are the result of the heart failing and usually occur after the disease has progressed to an advanced stage. Therefore, the symptoms have a lot in common with other forms of cardiomyopathy. These symptoms can include the following:

- Ankle, feet, and leg swelling (edema)

- Overall swelling

- Loss of appetite

- Shortness of breath (dyspnea), especially with activity

- Breathing difficulty while lying down

- Fatigue, weakness, faintness

- Decreased alertness or concentration

- Cough containing mucus, or pink, frothy material

- Decreased urine output (oliguria)

- Need to urinate at night (nocturia)

- Heart palpitations (irregular heart beat)

- Rapid pulse (tachycardia)

Abnormal heart sounds, murmurs, ECG abnormalities, and enlarged heart on chest x-ray may lead to the diagnosis. Echocardiogram abnormalities and cardiac catheterization or angiogram to rule out coronary artery blockages, along with a history of alcohol abuse can confirm the diagnosis.

The onset of FAC caused by aggregation of the V122I mutation and wild-type TTR, and senile systemic amyloidosis caused by the exclusive aggregation of wild-type TTR, typically occur after age 60. Greater than 40% of these patients present with carpal tunnel syndrome before developing ATTR-CM. Cardiac involvement is often identified with the presence of conduction system disease (sinus node or atrioventricular node dysfunction) and/or congestive heart failure, including shortness of breath, peripheral edema, syncope, exertional dyspnea, generalized fatigue, or heart block. Unfortunately, echocardiographic findings are indistinguishable from those seen in AL amyloidosis, and include thickened ventricular walls (concentric hypertrophy, both right and left) with a normal-to-small left ventricular cavity, increased myocardial echogenicity, normal or mildly reduced ejection fraction (often with evidence of diastolic dysfunction and severe impairment of contraction along the longitudinal axis), and bi-atrial dilation with impaired atrial contraction. Unlike the situation in AL amyloidosis, the ECG voltage is often normal, although low voltage may be seen (despite increased wall thickness on echocardiography). Marked axis deviation, bundle branch block, and AV block are common, as is atrial fibrillation.

In individuals with eccentric hypertrophy there may be little or no indication that hypertrophy has occurred as it is generally a healthy response to increased demands on the heart. Conversely, concentric hypertrophy can make itself known in a variety of ways. Most commonly, chest pain, either with or without exertion is present, along with shortness of breath with exertion, general fatigue, syncope, and palpitations. Overt signs of heart failure, such as edema, or shortness of breath without exertion are uncommon.

Cardiomegaly is a medical condition in which the heart is enlarged. It is more commonly referred to as an enlarged heart. The causes of cardiomegaly may vary. Many times this condition results from high blood pressure (hypertension) or coronary artery disease. An enlarged heart may not pump blood effectively, resulting in congestive heart failure. Cardiomegaly may improve over time, but many people with an enlarged heart need lifelong treatment with medications. Having an immediate family member who has or had cardiomegaly may indicate that a person is more susceptible to getting this condition. Cardiomegaly is not a disease but rather a condition that can result from a host of other diseases such as obesity or coronary artery disease. Recent studies suggest that cardiomegaly is associated with a higher risk of sudden cardiac death (SCD).

Ventricular hypertrophy (VH) is thickening of the walls of a ventricle (lower chamber) of the heart. Although left ventricular hypertrophy (LVH) is more common, right ventricular hypertrophy (RVH), as well as concurrent hypertrophy of both ventricles can also occur.

Ventricular hypertrophy can result from a variety of conditions, both adaptive and maladaptive. For example, it occurs in what is regarded as a physiologic, adaptive process in pregnancy in response to increased blood volume; but can also occur as a consequence of ventricular remodeling following a heart attack. Importantly, pathologic and physiologic remodeling engage different cellular pathways in the heart and result in different gross cardiac phenotypes.

The symptoms and signs of hypertensive heart disease will depend on whether or not it is accompanied by heart failure. In the absence of heart failure, hypertension, with or without enlargement of the heart (left ventricular hypertrophy) is usually symptomless.

Symptoms, signs and consequences of Congestive heart failure can include:

- Fatigue

- Irregular pulse or palpitations

- Swelling of feet and ankles

- Weight gain

- Nausea

- Shortness of breath

- Difficulty sleeping flat in bed (orthopnea)

- Bloating and abdominal pain

- Greater need to urinate at night

- An enlarged heart (cardiomegaly)

- Left ventricular hypertrophy and left ventricular remodeling

- Diminished coronary flow reserve and silent myocardial ischemia

- Coronary heart disease and accelerated atherosclerosis

- Heart Failure With Normal Left Ventricular Ejection Fraction (HFNEF), often termed diastolic heart failure

- Atrial fibrillation, other cardiac arrhythmias, or sudden cardiac death

Heart failure can develop insidiously over time or patients can present acutely with acute heart failure or acute decompensated heart failure and pulmonary edema due to sudden failure of pump function of the heart. Sudden failure can be precipitated by a variety of causes, including myocardial ischemia, marked increases in blood pressure, or cardiac arrhythmias.

One particularity of diabetic cardiomyopathy is the long latent phase, during which the disease progresses but is completely asymptomatic. In most cases, diabetic cardiomyopathy is detected with concomitant hypertension or coronary artery disease. One of the earliest signs is mild left ventricular diastolic dysfunction with little effect on ventricular filling. Also, the diabetic patient may show subtle signs of diabetic cardiomyopathy related to decreased left ventricular compliance or left ventricular hypertrophy or a combination of both. A prominent “a” wave can also be noted in the jugular venous pulse, and the cardiac apical impulse may be overactive or sustained throughout systole. After the development of systolic dysfunction, left ventricular dilation and symptomatic heart failure, the jugular venous pressure may become elevated, the apical impulse would be displaced downward and to the left. Systolic mitral murmur is not uncommon in these cases. These changes are accompanied by a variety of electrocardiographic changes that

may be associated with diabetic cardiomyopathy in 60% of patients without structural heart disease, although usually not in the early asymptomatic phase. Later in the progression, a prolonged QT interval may be indicative of fibrosis. Given that diabetic cardiomyopathy’s definition excludes concomitant atherosclerosis or hypertension, there are no changes in perfusion or in atrial natriuretic peptide levels up until the very late stages of the disease, when the hypertrophy and fibrosis become very pronounced.

Signs and symptoms of ischemic cardiomyopathy include sudden fatigue, shortness of breath, dizziness and palpitations.

The typical presentation of takotsubo cardiomyopathy is a sudden onset of chest pain associated with ECG changes mimicking a myocardial infarction of the anterior wall. During the course of evaluation of the patient, a bulging out of the left ventricular apex with a hypercontractile base of the left ventricle is often noted. It is the hallmark bulging out of the apex of the heart with preserved function of the base that earned the syndrome its name "tako tsubo", or octopus pot in Japan, where it was first described.

Stress is the main factor in takotsubo cardiomyopathy, with more than 85% of cases set in motion by either a physically or emotionally stressful event that prefaces the start of symptoms. Examples of emotional stressors include grief from the death of a loved one, fear of public speaking, arguing with a spouse, relationship disagreements, betrayal, and financial problems. Acute asthma, surgery, chemotherapy, and stroke are examples of physical stressors. In a few cases, the stress may be a happy event, such as a wedding, winning a jackpot, a sporting triumph, or a birthday.

Takotsubo cardiomyopathy is more commonly seen in postmenopausal women. Often there is a history of a recent severe (usually negative, sometimes happy) emotional or physical stress.

Heart problems are very important in people with Human Immunodeficiency Virus (HIV) as Acquired ImmunoDeficiency Syndrome (AIDS) patients with left ventricular dysfunction have a median survival of 101 days as compared to 472 days in AIDS patients with healthy hearts. HIV is a major cause of cardiomyopathy (problems with the heart muscle that reduce the efficiency with which the heart pumps blood). The most common type of HIV induced cardiomyopathy is dilated cardiomyopathy also known as eccentric ventricular hypertrophy which leads to impaired contraction of the ventricles due to volume overload. The annual incidence of HIV associated dilated cardiomyopathy was 15.9/1000 before the introduction of highly active antiretroviral therapy (HAART). However, in 2014, a study found that 17.6% of HIV patients have dilated cardiomyopathy (176/1000) meaning the incidence has greatly increased.

Familial Amyloid Cardiomyopathy (FAC), or Transthyretin Amyloid Cardiomyopathy (ATTR-CM) results from the aggregation and deposition of mutant and wild-type transthyretin (TTR) protein in the heart. TTR amyloid fibrils infiltrate the myocardium, leading to diastolic dysfunction from restrictive cardiomyopathy, and eventual heart failure. Both mutant and wild-type transthyretin comprise the aggregates because the TTR blood protein is a tetramer composed of mutant and wild-type TTR subunits in heterozygotes. Several mutations in TTR are associated with FAC, including V122I, V20I, P24S, A45T, Gly47Val, Glu51Gly, I68L, Gln92Lys, and L111M. One common mutation (V122I), which is a substitution of isoleucine for valine at position 122, occurs with high frequency in African-Americans, with a prevalence of approximately 3.5%. FAC is clinically similar to senile systemic amyloidosis, in which cardiomyopathy results from the aggregation of wild-type transthyretin exclusively.