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.

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.

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

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.

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.

Non-compaction cardiomyopathy (NCC), also called spongiform cardiomyopathy, is a rare congenital cardiomyopathy that affects both children and adults. It results from the failure of myocardial development during embryogenesis.

During development, the majority of the heart muscle is a sponge-like meshwork of interwoven myocardial fibers. As normal development progresses, these trabeculated structures undergo significant compaction that transforms them from spongy to solid. This process is particularly apparent in the ventricles, and particularly so in the left ventricle. Noncompaction cardiomyopathy results when there is failure of this process of compaction. Because the consequence of non-compaction is particularly evident in the left ventricle, the condition is also called left ventricular noncompaction. Other hypotheses and models have been proposed, none of which is as widely accepted as the noncompaction model.

Symptoms range greatly in severity. Most are a result of a poor pumping performance by the heart. The disease can be associated with other problems with the heart and the body.

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.

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.

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

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.

Diastolic heart failure and diastolic dysfunction refer to the decline in performance of one (usually the left ventricle) or both (left and right) ventricles during diastole. Diastole is the cardiac cycle phase during which the heart is relaxing and filling with incoming blood that is being returned from the body through the inferior (IVC) and superior (SVC) venae cavae to the right atrium and from lungs through pulmonary veins to the left atrium. In diastolic failure, if the patient has symptoms, there is a pathologic cause inducing them. Diastolic dysfunction can be found when doing a Doppler echocardiography in an apparently healthy patient, mainly in an elderly person.

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.

Cardiomegaly is a condition affecting the cardiovascular system, specifically the heart. This condition is strongly associated with congestive heart failure. Within the heart, the working fibers of the myocardial tissue increase in size. As the heart works harder the actin and myosin filaments experience less overlap which increases the size of the myocardial fibers. If there is less overlap of the protein filaments actin and myosin within the sarcomeres of muscle fibers, they will not be able to effectively pull on one another. If the heart tissue (walls of left and right ventricle) gets too big and stretches too far, then those filaments cannot effectively pull on one another to shorten the muscle fibers, thus impacting the heart's sliding filament mechanism. If fibers cannot shorten properly, and the heart cannot contract properly, then blood cannot be effectively pumped to the lungs to be re-oxygenated and to the body to deliver oxygen to the working tissues of the body.

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)

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.

Symptoms usually include one or more of the following: orthopnea (difficulty breathing while lying flat), dyspnea (shortness of breath on exertion), pitting edema (swelling), cough, frequent night-time urination, excessive weight gain during the last month of pregnancy (1-2+ kg/week; two to four or more pounds per week), palpitations (sensation of racing heart-rate, skipping beats, long pauses between beats, or fluttering), and chest pain.

The shortness of breath is often described by PPCM patients as the inability to take a deep or full breath or to get enough air into the lungs. Also, patients often describe the need to prop themselves up overnight by using two or more pillows in order to breathe better. These symptoms, swelling, and/or cough may be indications of pulmonary edema (fluid in the lungs) resulting from acute heart failure and PPCM.

Unfortunately, patients and clinicians sometimes dismiss early symptoms because they appear to be typical of normal pregnancy. Yet, early detection and treatment are critically important to the patient with PPCM. Delays in diagnosis and treatment of PPCM are associated with increased morbidity and mortality.

It is important to note that occasionally patients present with other signs or symptoms. This is demonstrated by one report of a woman with liver failure five weeks postpartum who was being considered for liver transplant. An echocardiogram was performed and revealed PPCM and heart failure as the cause of her severe liver failure. Conventional heart failure medications were administered. She survived and completely recovered from both the liver failure and PPCM.

It is also quite common for women to present with evidence of having an embolus (clot) passing from the heart to a vital organ, causing such complications as stroke, loss of circulation to a limb, even coronary artery occlusion (blockage) with typical myocardial infarction (heart attack).

For these reasons, it is paramount that clinicians hold a high suspicion of PPCM in any peri- or postpartum patient where unusual or unexplained symptoms or presentations occur.

Among the causes of LBBB are:

- Aortic stenosis

- Dilated cardiomyopathy

- Acute myocardial infarction

- Extensive coronary artery disease

- Primary disease of the cardiac electrical conduction system

- Long standing hypertension leading to aortic root dilatation and subsequent aortic regurgitation

- Lyme disease

- Side effect of some cardiac surgeries (e.g., aortic root reconstruction)

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.

Left bundle branch block (LBBB) is a cardiac conduction abnormality seen on the electrocardiogram (ECG). In this condition, activation of the left ventricle of the heart is delayed, which causes the left ventricle to contract later than the right ventricle.

The symptoms associated with MI are dependent on which phase of the disease process the individual is in. Individuals with acute MI are typically severely symptomatic and will have the signs and symptoms of acute decompensated congestive heart failure (i.e. shortness of breath, pulmonary edema, orthopnea, and paroxysmal nocturnal dyspnea), as well as symptoms of cardiogenic shock (i.e., shortness of breath at rest). Cardiovascular collapse with shock (cardiogenic shock) may be seen in individuals with acute MI due to papillary muscle rupture, rupture of a chorda tendinea or infective endocarditis of the mitral valve.

Individuals with chronic compensated MI may be asymptomatic for long periods of time, with a normal exercise tolerance and no evidence of heart failure. Over time, however, there may be decompensation and patients can develop volume overload (congestive heart failure). Symptoms of entry into a decompensated phase may include fatigue, shortness of breath particularly on exertion, and leg swelling. Also there may be development of an irregular heart rhythm known as atrial fibrillation.

Findings on clinical examination depend on the severity and duration of MI. The mitral component of the first heart sound is usually soft and with a laterally displaced apex beat, often with heave. The first heart sound is followed by a high-pitched holosystolic murmur at the apex, radiating to the back or clavicular area. Its duration is, as the name suggests, the whole of systole. The loudness of the murmur does not correlate well with the severity of regurgitation. It may be followed by a loud, palpable P, heard best when lying on the left side. A third heart sound is commonly heard.

In acute cases, the murmur and tachycardia may be the only distinctive signs.

Patients with mitral valve prolapse may have a holosystolic murmur or often a mid-to-late systolic click and a late systolic murmur. Cases with a late systolic regurgitant murmur may still be associated with significant hemodynamic consequences.

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.

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.