Up to 80% of individuals with ARVD present have symptoms like syncope and dyspnea.The remainder frequently present with palpitations or other symptoms due to right ventricular outflow tract (RVOT) tachycardia (a type of monomorphic ventricular tachycardia).

Symptoms are usually exercise-related. In populations where hypertrophic cardiomyopathy is screened out prior to involvement in competitive athletics, it is a common cause of sudden cardiac death.

The first clinical signs of ARVD are usually during adolescence. However, signs of ARVD have been demonstrated in infants.

Arrhythmogenic right ventricular dysplasia (ARVD) is an inherited heart disease.

ARVD is caused by genetic defects of the parts of heart muscle (also called "myocardium" or "cardiac muscle") known as desmosomes, areas on the surface of heart muscle cells which link the cells together. The desmosomes are composed of several proteins, and many of those proteins can have harmful mutations.

The disease is a type of nonischemic cardiomyopathy that involves primarily the right ventricle. It is characterized by hypokinetic areas involving the free wall of the right ventricle, with fibrofatty replacement of the right ventricular myocardium, with associated arrhythmias originating in the right ventricle.

ARVD can be found in association with diffuse palmoplantar keratoderma, and woolly hair, in an autosomal recessive condition called Naxos disease, because this genetic abnormality can also affect the integrity of the superficial layers of the skin most exposed to pressure stress.

ARVC/D is an important cause of ventricular arrhythmias in children and young adults. It is seen predominantly in males, and 30–50% of cases have a familial distribution.

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.

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.

An enlargement of the aorta may occur; an increased risk of abnormality is seen in babies of women taking lithium during the first trimester of pregnancy (though some have questioned this) and in those with Wolff-Parkinson-White syndrome.

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.

While Ebstein's anomaly is defined as the congenital displacement of the tricuspid valve towards the apex of the right ventricle, it is often associated with other abnormalities.

There are various symptoms that can be seen:

- Chest pains

- Shortness of breath

- Pressure on the chest

- Rapid heartbeats

- Heart palpitations

- Irregular heartbeat

- Dizziness

- Loss of appetite

- Swelling in legs, ankles, or feet

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 (also known as "Boxer arrhythmogenic right ventricular cardiomyopathy") is a disease of the myocardium primarily affecting Boxer dogs. It is characterized by the development of ventricular tachyarrhythmias, resulting in syncope and sudden cardiac death. Myocardial failure and congestive heart failure are uncommon manifestations of the disease.

No specific set of criteria has been developed for diagnosis of pacemaker syndrome. Most of the signs and symptoms of pacemaker syndrome are nonspecific, and many are prevalent in the elderly population at baseline. In the lab, pacemaker interrogation plays a crucial role in determining if the pacemaker mode had any contribution to symptoms.

Symptoms commonly documented in patients history, classified according to cause:

- Neurological - Dizziness, near syncope, and confusion.

- Heart failure - Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and edema.

- Hypotension - Seizure, mental status change, diaphoresis, and signs of orthostatic hypotension and shock.

- Low cardiac output - Fatigue, weakness, dyspnea on exertion, lethargy, and lightheadedness.

- Hemodynamic - Pulsation in the neck and abdomen, choking sensation, jaw pain, right upper quadrant (RUQ) pain, chest colds, and headache.

- Heart rate related - Palpitations associated with arrhythmias

In particular, the examiner should look for the following in the physical examination, as these are frequent findings at the time of admission:

- Vital signs may reveal hypotension, tachycardia, tachypnea, or low oxygen saturation.

- Pulse amplitude may vary, and blood pressure may fluctuate.

- Look for neck vein distension and cannon waves in the neck veins.

- Lungs may exhibit crackles.

- Cardiac examination may reveal regurgitant murmurs and variability of heart sounds.

- Liver may be pulsatile, and the RUQ may be tender to palpation. Ascites may be present in severe cases.

- The lower extremities may be edematous.

- Neurologic examination may reveal confusion, dizziness, or altered mental status.

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.

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.

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.

Major symptoms of Lutembacher's syndrome as a result of ASD and MS can range from heart failure to pulmonary congestion.

- Right ventricular overload and Right-sided heart failure: Both are caused by a large ASD and MS (moderate to severe).

- Palpitations: This is caused by blood flowing from left atrium to the right atrium causing a higher left atrial pressure and leading to mitral stenosis. Both atria will be dilated (stretched or open)leading to future atrial arrhythmias or atrial fibrillation (Riaz).

- Pulmonary congestion: When blood or fluid pools within the lungs; this is usually a symptom of mitral stenosis and a small ASD.

- Loud mitral S1 and wide fixed split of pulmonary S2: The loud sound of the mitral S1 and the wide fixed split of pulmonary S2 is a symptoms of mitral stenosis. The sounds often are caused by a reduced pressure gradient in the mitral area that was caused from decompression of the left atrium from the ASD and a displacement (moving from normal position) of the left ventricular lower portion of the heart to the a large right ventricle. The second heart sound (S2) split is caused by the increase right heart blood flow through the ASD causing a late closing of the pulmonary component of the S2 as well as decreased left ventricular and aortic blood flow.

- III/IV mid diastolic murmur, early systolic murmur: This heart murmur is caused by an increase blood flow through the tricuspid valve due to ASD; it is heard best in the left lower sternal area or the bottom of the heart (apex).

Many people with long QT syndrome have no signs or symptoms.

Some people may experience the following symptoms:

- Fainting (or syncope). This may occur when the patient is emotionally or physically stressed. It is unusual in QT syndrome to have any signs before the person actually faints.

- Seizures

- Sudden death. If there is sudden death, and doctors suspect long QT syndrome as the cause, they may recommend that the family members of the deceased get tested for the disease.

Ventricular septal defect is usually symptomless at birth. It usually manifests a few weeks after birth.

VSD is an acyanotic congenital heart defect, aka a left-to-right shunt, so there are no signs of cyanosis in the early stage. However, uncorrected VSD can increase pulmonary resistance leading to the reversal of the shunt and corresponding cyanosis.

- Pansystolic (Holosystolic) murmur along lower left sternal border (depending upon the size of the defect) +/- palpable thrill (palpable turbulence of blood flow). Heart sounds are normal. Larger VSDs may cause a parasternal heave, a displaced apex beat (the palpable heartbeat moves laterally over time, as the heart enlarges). An infant with a large VSD will fail to thrive and become sweaty and tachypnoeic (breathe faster) with feeds.

The restrictive VSDs (smaller defects) are associated with a louder murmur and more palpable thrill (grade IV murmur). Larger defects may eventually be associated with pulmonary hypertension due to the increased blood flow. Over time this may lead to an Eisenmenger's syndrome the original VSD operating with a left-to-right shunt, now becomes a right-to-left shunt because of the increased pressures in the pulmonary vascular bed.

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)

As Lutembacher's syndrome is known for ASD and MS, most of the symptoms experienced will be associated with ASD and MS. For most people, they will remain asymptomatic (experience no symptoms) but when symptoms are shown, they are due mainly to ASD and will vary depending on the size of the hole in the atria. If the patient has a large ASD, pulmonary congestion (blood or fluid buildup in the lungs) will happen later but if the patient has a small ASD, symptoms will appear early in the disorder. In general, unless the ASD and mitral stenosis causing Lutembacher's syndrome is severe, symptoms may not appear until the second and third decade of the patient's life. As many of the symptoms are asymptomic and may not appear until later in life, the duration or frequency of the symptoms varies. For symptoms such as palipitations, ventricular overload, heart failure, and pulmonary congenstion, these symptoms may be sudden and not that frequent as they are very severe symptoms. For symptoms such as loud mitral S1, pulmonary S2, mid-diastolic murmur, fatigue, reduced exercise tolerance, weight gain, ankle edema, and right upper quadrant pain, and ascities, these symptoms may be less frequent and severe; their duration may be only a few seconds, minutes, or even months.

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.

Right ventricular hypertrophy (RVH) is a form of ventricular hypertrophy affecting the right ventricle.

Blood travels through the right ventricle to the lungs via the pulmonary arteries. If conditions occur which decrease pulmonary circulation, meaning blood does not flow well from the heart to the lungs, extra stress can be placed on the right ventricle. This can lead to right ventricular hypertrophy.

It can affect electrocardiography (ECG) findings. An ECG with right ventricular hypertrophy may or may not show a right axis deviation on the graph.

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.

Common symptoms include:

- tachycardia (a heart rate exceeding the normal resting rate)

- respiratory problems

- dyspnea (shortness of breath)

- continuous "machine-like" (also described as "rolling-thunder" and "to-and-fro") heart murmur (usually from aorta to pulmonary artery, with higher flow during systole and lower flow during diastole)

- cardiomegaly (enlarged heart, reflecting ventricular dilation and volume overload)

- left subclavicular thrill

- bounding pulse

- widened pulse pressure

- increased cardiac output

- increased systolic pressure

- poor growth

- differential cyanosis, i.e. cyanosis of the lower extremities but not of the upper body.

Patients typically present in good health, with normal respirations and heart rate. If the PDA is moderate or large, widened pulse pressure and bounding peripheral pulses are frequently present, reflecting increased left ventricular stroke volume and diastolic run-off of blood into the (initially lower-resistance) pulmonary vascular bed. Prominent suprasternal and carotid pulsations may be noted secondary to increased left ventricular stroke volume.

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

Hypertrophy of the ventricle can be measured with a number of techniques.

Electrocardiogram (EKG), a non-invasive assessment of the electrical system of the heart, can be useful in determining the degree of hypertrophy, as well as subsequent dysfunction it may precipitate. Specifically, increase in Q wave size, abnormalities in the P wave as well as giant inverted T waves are indicative of significant concentric hypertrophy. Specific changes in repolarization and depolarization events are indicative of different underlying causes of hypertrophy and can assist in appropriate management of the condition. Changes are common in both eccentric and concentric hypertrophy, though are substantially different from one another. In either condition fewer than 10% of patients with significant hypertrophy display a normal EKG.

Transthoracic echocardiography, a similarly non invasive assessment of cardiac morphology, is also important in determining both the degree of hypertrophy, underlying pathologies (such as aortic coarction), and degree of cardiac dysfunction. Important considerations in echocardiography of the hypertrophied heart include lateral and septal wall thickness, degree of outflow tract obstruction, and systolic anterior wall motion (SAM) of the mitral valve, which can exacerbate outflow obstruction.

It is not uncommon to undergo cardiopulmonary exercise testing (CPET), which measures the heart's response to exercise, to assess the functional impairment caused by hypertrophy and to prognosticate outcomes.