The echocardiogram is commonly used to confirm the diagnosis of MI. Color doppler flow on the transthoracic echocardiogram (TTE) will reveal a jet of blood flowing from the left ventricle into the left atrium during ventricular systole. Also, it may detect a dilated left atrium and ventricle and decreased left ventricular function.

Because of inability to obtain accurate images of the left atrium and the pulmonary veins with a transthoracic echocardiogram, a transesophageal echocardiogram may be necessary in some cases to determine the severity of MI.

Another method of measuring the severity of mitral stenosis is the simultaneous left and right heart chamber catheterization. The right heart catheterization (commonly known as Swan-Ganz catheterization) gives the physician the mean pulmonary capillary wedge pressure, which is a reflection of the left atrial pressure. The left heart catheterization, on the other hand, gives the pressure in the left ventricle. By simultaneously taking these pressures, it is possible to determine the gradient between the left atrium and left ventricle during ventricular diastole, which is a marker for the severity of mitral stenosis. This method of evaluating mitral stenosis tends to overestimate the degree of mitral stenosis, however, because of the time lag in the pressure tracings seen on the right-heart catheterization and the slow Y descent seen on the wedge tracings. If a trans-septal puncture is made during right heart catheterization, however, the pressure gradient can accurately quantify the severity of mitral stenosis.

Chest X-ray may also assist in diagnosis, showing left atrial enlargement.

Electrocardiography may show "P mitrale", that is, broad, notched P waves in several or many leads with a prominent late negative component to the P wave in lead V, and may also be seen in mitral regurgitation, and, potentially, any cause of overload of the left atrium. Thus, "P-sinistrocardiale" may be a more appropriate term.

The chest X-ray in individuals with chronic MI is characterized by enlargement of the left atrium and the left ventricle. The pulmonary vascular markings are typically normal, since pulmonary venous pressures are usually not significantly elevated.

A chest x-ray will be given to determine the size of the heart and the blood vessels supplying blood to the lungs.

A color flow and doppler imaging is used to help confirm the presence as well as evaluate the severity of ASD and MS.

Individuals with MVP are at higher risk of bacterial infection of the heart, called infective endocarditis. This risk is approximately three- to eightfold the risk of infective endocarditis in the general population. Until 2007, the American Heart Association recommended prescribing antibiotics before invasive procedures, including those in dental surgery. Thereafter, they concluded that "prophylaxis for dental procedures should be recommended only for patients with underlying cardiac conditions associated with the highest risk of adverse outcome from infective endocarditis."

Many organisms responsible for endocarditis are slow-growing and may not be easily identified on routine blood cultures (these fastidious organisms require special culture media to grow). These include the HACEK organisms, which are part of the normal oropharyngeal flora and are responsible for perhaps 5 to 10% of infective endocarditis affecting native valves. It is important when considering endocarditis to keep these organisms in mind.

Generally, MVP is benign. However, MVP patients with a murmur, not just an isolated click, have an increased mortality rate of 15-20%. The major predictors of mortality are the severity of mitral regurgitation and the ejection fraction.

A less invasive method for detecting a PFO or other ASDs than transesophagal ultrasound is transcranial Doppler with bubble contrast. This method reveals the cerebral impact of the ASD or PFO.

In the diagnosis of tricuspid insufficiency a chest x-ray will demonstrate right heart enlargement. An echocardiogram will assess the chambers of the heart, as well as, right ventricular pressure. Cardiac magnetic resonance may also be used as a diagnostic tool, and finally, cardiac catheterization may determine the extent of the regurgitation.

Once someone is found to have an atrial septal defect, a determination of whether it should be corrected is typically made. If the atrial septal defect is causing the right ventricle to enlarge a secundum atrial septal defect should generally be closed. If the ASD is not causing problems the defect may simply checked every two or three years. Methods of closure of an ASD include surgical closure and percutaneous closure.

Drug therapy can be used to minimize risk of thromboembolism and stroke in PFO. Anticoagulants, such as warfarin, are commonly used to reduce blood clotting, whereas antiplatelet agents, such as aspirin, are used to reduce platelet aggregation and thrombosis.

A VSD can be detected by cardiac auscultation. Classically, a VSD causes a pathognomonic holo- or pansystolic murmur. Auscultation is generally considered sufficient for detecting a significant VSD. The murmur depends on the abnormal flow of blood from the left ventricle, through the VSD, to the right ventricle. If there is not much difference in pressure between the left and right ventricles, then the flow of blood through the VSD will not be very great and the VSD may be silent. This situation occurs a) in the fetus (when the right and left ventricular pressures are essentially equal), b) for a short time after birth (before the right ventricular pressure has decreased), and c) as a late complication of unrepaired VSD. Confirmation of cardiac auscultation can be obtained by non-invasive cardiac ultrasound (echocardiography). To more accurately measure ventricular pressures, cardiac catheterization, can be performed.

AVSDs can be detected by cardiac auscultation; they cause atypical murmurs and loud heart tones. Confirmation of findings from cardiac auscultation can be obtained with a cardiac ultrasound (echocardiography - less invasive) and cardiac catheterization (more invasive).

Tentative diagnosis can also be made in utero via fetal echocardiogram. An AVSD diagnosis made before birth is a marker for Down syndrome, although other signs and further testing are required before any definitive confirmation of either can be made.

Although there are several classifications for VSD, the most accepted and unified classification is that of Congenital Heart Surgery Nomenclature and Database Project.

The classification is based on the location of the VSD on the right ventricular surface of the inter ventricular septum and is as follows:

Canadian genetic testing guidelines and recommendations for individuals diagnosed with HCM are as follows:

- The main purpose of genetic testing is for screening family members.

- According to the results, at-risk relatives may be encouraged to undergo extensive testing.

- Genetic testing is not meant for confirming a diagnosis.

- If the diagnosed individual has no relatives that are at risk, then genetic testing is not required.

- Genetic testing is not intended for risk assessment or treatment decisions.

- Evidence only supports clinical testing in predicting the progression and risk of developing complications of HCM.

For individuals "suspected" of having HCM:

- Genetic testing is not recommended for determining other causes of left ventricular hypertrophy (such as "athlete's heart", hypertension, and cardiac amyloidosis).

- HCM may be differentiated from other hypertrophy-causing conditions using clinical history and clinical testing.

In terms of treatment for tricuspid insufficiency prosthetic valve substitutes can be used, though artificial prostheses may cause thrombo‐embolic phenomena(bioprostheses may have a degeneration problem). Some evidence suggests that there are no significant differences between a mechanical or biological tricuspid valve in a recipient.

Generally, surgical treatment of tricuspid regurgitation is not indicated when it has arisen as a result of right ventricular dilatation. In such instances of secondary tricuspid regurgitation, the mainstay of therapy is medical. When left-sided heart failure is the cause, the individual is instructed to decrease intake of salt. Medications in this case may include diuretics and angiotensin-converting enzyme inhibitors.

Hypoplastic left heart syndrome can be diagnosed prenatally or after birth via echocardiography. Typical findings include a small left ventricle and aorta, abnormalities of the mitral and aortic valves, retrograde flow in the transverse arch of the aorta, and left-to-right flow between the atria. It is often recognized during the second trimester of pregnancy, between 18 and 24 weeks' gestation.

LAE is suggested by an electrocardiogram (ECG) that has a pronounced notch in the P wave. However, if atrial fibrillation is present, a P wave would not be present. In any case, LAE can be diagnosed and measured using an echocardiogram (ECHO).

Characterizing the size of the left atrium according to its volume is preferred over a single linear dimension since enlargement can be different for different directions. For example, because of the smaller distance in the thoracic cavity between the sternum and spine, compared to the other directions, less room exists for enlargement of the left atrium along the anteroposterior axis. By approximating the shape of the left atrium as an ellipsoid, its volume can be calculated from measurements of its dimensions along three perpendicular directions.

Indexing the left atrial volume to body surface area (volume/BSA) is recommended by the American Society of Echocardiography and the European Association of Echocardiography. The values for volume/BSA in the following table are the best validated, and are the same for both men and women.

l-TGA can sometimes be diagnosed in utero with an ultrasound after 18 weeks gestation. However, many cases of simple l-TGA are "accidentally" diagnosed in adulthood, during diagnosis or treatment of other conditions.

A doctor will listen to the heart with stethoscope. A "tumor plop" (a sound related to movement of the tumor), abnormal heart sounds, or a murmur similar to the mid-diastolic rumble of mitral stenosis may be heard. These sounds may change when the patient changes position.

Right atrial myxomas rarely produce symptoms until they have grown to be at least 13 cm (about 5 inches) wide.

Tests may include:

- Echocardiogram and Doppler study

- Chest x-ray

- CT scan of chest

- Heart MRI

- Left heart angiography

- Right heart angiography

- ECG—may show atrial fibrillation

Blood tests:

A FBC may show anemia and increased WBCs (white blood cells). The erythrocyte sedimentation rate (ESR) is usually increased.

Diastolic dysfunction must be differentiated from diastolic heart failure. Diastolic dysfunction can be found in elderly and apparently quite healthy patients. If diastolic dysfunction describes an abnormal mechanical property, diastolic heart failure describes a clinical syndrome. Mathematics describing the relationship between the ratio of Systole to Diastole in accepted terms of End Systolic Volume to End Diastolic Volume implies many mathematical solutions to forward and backward heart failure.

Criteria for diagnosis of diastolic dysfunction or diastolic heart failure remain imprecise. This has made it difficult to conduct valid clinical trials of treatments for diastolic heart failure. The problem is compounded by the fact that systolic and diastolic heart failure commonly coexist when patients present with many ischemic and nonischemic etiologies of heart failure. Narrowly defined, diastolic failure has often been defined as "heart failure with normal systolic function" (i.e. left ventricular ejection fraction of 60% or more). Chagasic heart disease may represent an optimal academic model of diastolic heart failure that spares systolic function.

A patient is said to have diastolic dysfunction if he has signs and symptoms of heart failure but the left ventricular ejection fraction is normal. A second approach is to use an elevated BNP level in the presence of normal ejection fraction to diagnose diastolic heart failure. Concordance of both volumetric and biochemical measurements and markers lends to even stronger terminology regarding scientific/mathematical expression of diastolic heart failure. These are both probably too broad a definition for diastolic heart failure, and this group of patients is more precisely described as having heart failure with normal systolic function. Echocardiography can be used to diagnose diastolic dysfunction but is a limited modality unless it is supplemented by stress imaging. MUGA imaging is an earlier mathematical attempt to distinguish systolic from diastolic heart failure.

No one single echocardiographic parameter can confirm a diagnosis of diastolic heart failure. Multiple echocardiographic parameters have been proposed as sufficiently sensitive and specific, including mitral inflow velocity patterns, pulmonary vein flow patterns, E:A reversal, tissue Doppler measurements, and M-mode echo measurements (i.e. of left atrial size). Algorithms have also been developed which combine multiple echocardiographic parameters to diagnose diastolic heart failure.

There are four basic Echocardiographic patterns of diastolic heart failure, which are graded I to IV:

- The mildest form is called an "abnormal relaxation pattern", or grade I diastolic dysfunction. On the mitral inflow Doppler echocardiogram, there is reversal of the normal E/A ratio. This pattern may develop normally with age in some patients, and many grade I patients will not have any clinical signs or symptoms of heart failure.

- Grade II diastolic dysfunction is called "pseudonormal filling dynamics". This is considered moderate diastolic dysfunction and is associated with elevated left atrial filling pressures. These patients more commonly have symptoms of heart failure, and many have left atrial enlargement due to the elevated pressures in the left heart.

Grade III and IV diastolic dysfunction are called "restrictive filling dynamics". These are both severe forms of diastolic dysfunction, and patients tend to have advanced heart failure symptoms:

- Class III diastolic dysfunction patients will demonstrate reversal of their diastolic abnormalities on echocardiogram when they perform the Valsalva maneuver. This is referred to as "reversible restrictive diastolic dysfunction".

- Class IV diastolic dysfunction patients will not demonstrate reversibility of their echocardiogram abnormalities, and are therefore said to suffer from "fixed restrictive diastolic dysfunction".

The presence of either class III and IV diastolic dysfunction is associated with a significantly worse prognosis. These patients will have left atrial enlargement, and many will have a reduced left ventricular ejection fraction that indicates a combination of systolic and diastolic dysfunction.

Imaged volumetric definition of systolic heart performance is commonly accepted as ejection fraction. Volumetric definition of the heart in systole was first described by Adolph Fick as cardiac output. Fick may be readily and inexpensively inverted to cardiac input and injection fraction to mathematically describe diastole. Decline of injection fraction paired with decline of E/A ratio seems a stronger argument in support of a mathematical definition of diastolic heart failure.

Another parameter to assess diastolic function is the , which is the ratio of mitral peak velocity of early filling (E) to early diastolic mitral annular velocity (E'). Diastolic dysfunction is assumed when the E/E' ratio exceed 15.

Hypoplastic right heart syndrome is less common than hypoplastic left heart syndrome which occurs in 4 out of every 10,000 births. [3].

This rare anomaly requires prenatal diagnosis since it needs immediate and emergency treatment. Pregnant women whose pregnancy is complicated with this anomaly should be referred to a level 3 hospital with pediatric cardiology and pediatric cardiothoracic surgical team.[3]

It can be associated with aortic stenosis.

Surgical operations to assist with hypoplastic left heart are complex and need to be individualized for each patient. A cardiologist must assess all medical and surgical options on a case-by-case basis.

Currently, infants undergo either the staged reconstructive surgery (Norwood or Sano procedure within a few days of birth, Glenn or "Hemi-Fontan procedure" at 3 to 6 months of age, and the Fontan procedure at 1 1/2 to 5 years of age) or cardiac transplantation. Current expectations are that 70% of those with HLHS will reach adulthood. Many studies show that the higher the volume (number of surgeries performed) at a hospital, the lower the mortality (death) rate. Factors that increase an infant's risk include lower birth weight, additional congenital anomalies, a genetic syndrome or those with a highly restrictive atrial septum.) For patients without these additional risk factors, 5 year survival now approaches 80%. Further, studies show that about 50% of those children who survived surgery in the early development of staged reconstruction have developmental delay or need special education; about 25% of these surgical survivors have severe disabilities. There is growing evidence that while the incidence of developmental and behavioral disabilities continues to be higher than that in the general population, children operated upon in the more current era have shown significantly better neurological outcomes. An alternative to the traditional Norwood is the Hybrid procedure.

Some physicians offer "compassionate care", instead of the surgeries, which results in the child's death, usually within 2 weeks of birth. Compassionate care is overseen by a physician, and may be carried out either in the hospital or at home. However, due to the vast improvement of surgical intervention, with many hospitals achieving over 90% survival, there is debate on whether or not "compassionate care" should still be offered to families. A study in 2003 concluded that a selection of physicians who are experts in the care of children with HLHS were evenly split when asked what they would do if their own children were born with HLHS, with 1/3 stating that they would choose surgery, 1/3 stating that they would choose palliative (compassionate) treatment without surgery, and 1/3 stating that they are uncertain which choice they would make.

The three-stage procedure is a palliative procedure (not a cure), as the child's circulation is made to work with only two of the heart's four chambers.

With a series of operations or even a heart transplant, a newborn can be treated but not be cured. Young individuals who have undergone reconstructive surgery must refer to a cardiologist who is experienced in congenital heart diseases, "Children with HLHS are at an increased level for developing endocarditis." Kids that have been diagnosed with HRHS must limit the physical activity they participate in to their own endurance level.

Although HCM may be asymptomatic, affected individuals may present with symptoms ranging from mild to critical heart failure and sudden cardiac death at any point from early childhood to seniority. HCM is the leading cause of sudden cardiac death in young athletes in the United States, and the most common genetic cardiovascular disorder. One study found that the incidence of sudden cardiac death in young competitive athletes declined in the Veneto region of Italy by 89% since the 1982 introduction of routine cardiac screening for athletes, from an unusually high starting rate. As of 2010, however, studies have shown that the incidence of sudden cardiac death, among all people with HCM, has declined to one percent or less. Screen-positive individuals who are diagnosed with cardiac disease are usually told to avoid competitive athletics.

HCM can be detected with an echocardiogram (ECHO) with 80%+ accuracy, which can be preceded by screening with an electrocardiogram (ECG) to test for heart abnormalities. Cardiac magnetic resonance imaging (CMR), considered the gold standard for determining the physical properties of the left ventricular wall, can serve as an alternative screening tool when an echocardiogram provides inconclusive results. For example, the identification of segmental lateral ventricular hypertrophy cannot be accomplished with echocardiography alone. Also, left ventricular hypertrophy may be absent in children under thirteen years of age. This undermines the results of pre-adolescents’ echocardiograms. Researchers, however, have studied asymptomatic carriers of an HCM-causing mutation through the use of CMR and have been able to identify crypts in the interventricular septal tissue in these people. It has been proposed that the formation of these crypts is an indication of myocyte disarray and altered vessel walls that may later result in the clinical expression of HCM. A possible explanation for this is that the typical gathering of family history only focuses on whether sudden death occurred or not. It fails to acknowledge the age at which relatives suffered sudden cardiac death, as well as the frequency of the cardiac events. Furthermore, given the several factors necessary to be considered at risk for sudden cardiac death, while most of the factors do not have strong predictive value individually, there exists ambiguity regarding when to implement special treatment.