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.

Diagnosis is typically made via echocardiography. Patients will demonstrate normal systolic function, diastolic dysfunction, and a restrictive filling pattern. 2-dimensional and Doppler studies are necessary to distinguish RCM from constrictive pericarditis. Cardiac MRI and transvenous endomyocardial biopsy may also be necessary in some cases. Reduced QRS voltage on EKG may be an indicator of amyloidosis-induced restrictive cardiomyopathy.

Determining the risk of an embolism causing a stroke is important for guiding the use of anticoagulants. The most accurate clinical prediction rules are:

- CHADS2

- CHA2DS2-VASc

Both the CHADS2 and the CHA2DS2-VASc score predict future stroke risk in people with a-fib with CHA2DS2-VASc being more accurate. Some that had a CHADS2 score of 0 had a CHA2DS2-VASc score of 3, with a 3.2% annual risk of stroke. Thus a CHA2DS2-VASc score of 0 is considered very low risk.

In general, the minimal evaluation of atrial fibrillation should be performed in all individuals with AF. The goal of this evaluation is to determine the general treatment regimen for the individual. If results of the general evaluation warrant it, further studies may then be performed.

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.

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.

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.

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.

Left atrial enlargement can be mild, moderate or severe depending on the extent of the underlying condition. Although other factors may contribute, left atrium size has been found to be a predictor of mortality due to both cardiovascular issues as well as all-cause mortality. Current research suggests that left atrium size as measured by an echo-cardiograph may have prognostic implications for preclinical cardiovascular disease. However, studies that have found LAE to be a predictor for mortality recognize the need for more standardized left atrium measurements than those found in an echo-cardiogram.

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.

HFpEF is typically diagnosed with echocardiography. Techniques such as catheterization are invasive procedures and thus reserved for patients with co-morbid conditions or those who are suspected to have HFpEF but lack clear non-invasive findings. Catheterization does represent are more definitive diagnostic assessment as pressure and volume measurements are taken simultaneously and directly. In either technique the heart is evaluated for left ventricular diastolic function. Important parameters include, rate of isovolumic relaxation, rate of ventricular filling, and stiffness.

Frequently patients are subjected to stress echocardiography, which involves the above assessment of diastolic function during exercise. This is undertaken because perturbations in diastole are exaggerated during the increased demands of exercise. Exercise requires increased left ventricular filling and subsequent output. Typically the heart responds by increasing heart rate and relaxation time. However, in patients with HFpEF both responses are diminished due to increased ventricular stiffness. Testing during this demanding state may reveal abnormalities that are not as discernible at rest.

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.

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.

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.

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.

Typical atrial flutter is recognized on an electrocardiogram by presence of characteristic "flutter waves" at a regular rate of 200 to 300 beats per minute. Flutter waves may not be evident on an ECG in atypical forms of atrial flutter. Individual flutter waves may be symmetrical, resembling p-waves, or may be asymmetrical with a "sawtooth" shape, rising gradually and falling abruptly or vice versa. If atrial flutter is suspected clinically but is not clearly evident on ECG, acquiring a Lewis lead ECG may be helpful in revealing flutter waves.

General ECG features include:

- Right axis deviation (>90 degrees)

- Tall R-waves in RV leads; deep S-waves in LV leads

- Slight increase in QRS duration

- ST-T changes directed opposite to QRS direction (i.e., wide QRS/T angle)

- May see incomplete RBBB pattern or qR pattern in V1

- Evidence of right atrial enlargement (RAE)

Specific ECG features (assumes normal calibration of 1 mV = 10 mm):

- Any one or more of the following (if QRS duration <0.12 sec):

- Right axis deviation (>90 degrees) in presence of disease capable of causing RVH

- R in aVR > 5 mm, or

- R in aVR > Q in aVR

- Any one of the following in lead V1:

- R/S ratio > 1 and negative T wave

- qR pattern

- R > 6 mm, or S 10 mm

Other chest lead criteria:

- R in V1 + S in V5 (or V6) 10 mm

- R/S ratio in V5 or V6 < 1

- R in V5 or V6 < 5 mm

- S in V5 or V6 > 7 mm

ST segment depression and T wave inversion in right precordial leads is usually seen in severe RVH such as in pulmonary stenosis and pulmonary hypertension.

Although a myxoma is not cancer, complications are common. Untreated, a myxoma can lead to an embolism (tumor cells breaking off and traveling with the bloodstream), which can block blood flow. Myxoma fragments can move to the brain, eye, or limbs.

If the tumor grows inside the heart, it can block blood flow through the mitral valve and cause symptoms of mitral stenosis or mitral regurgitation. This may require emergency surgery to prevent sudden death.

Echocardiography and Tissue Doppler echocardiography are both needed to fully diagnose the different types of ventricular dyssynchrony.

The criteria to diagnose a right bundle branch block on the electrocardiogram:

- The heart rhythm must originate above the ventricles (i.e. sinoatrial node, atria or atrioventricular node) to activate the conduction system at the correct point.

- The QRS duration must be more than 100 ms (incomplete block) or more than 120 ms (complete block)

- There should be a terminal R wave in lead V1 (e.g. R, rR', rsR', rSR' or qR)

- There should be a slurred S wave in leads I and V6.

The T wave should be deflected opposite the terminal deflection of the QRS complex. This is known as appropriate T wave discordance with bundle branch block. A concordant T wave may suggest ischemia or myocardial infarction.

A mnemonic to distinguish between ECG signatures of left bundle branch block (LBBB) and right, is WiLLiaM MaRRoW; i.e., with LBBB, there is a W in lead V1 and an M in lead V6, whereas, with RBBB, there is an M in V1 and a W in V6.

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.

Treatment of restrictive cardiomyopathy should focus on management of causative conditions (for example, using corticosteroids if the cause is sarcoidosis), and slowing the progression of cardiomyopathy. Salt-restriction, diuretics, angiotensin-converting enzyme inhibitors, and anticoagulation may be indicated for managing restrictive cardiomyopathy.

Calcium channel blockers are generally contraindicated due to their negative inotropic effect, particularly in cardiomyopathy caused by amyloidosis. Digoxin, calcium channel blocking drugs and beta-adrenergic blocking agents provide little benefit, except in the subgroup of restrictive cardiomyopathy with atrial fibrillation. Vasodilators are also typically ineffective because systolic function is usually preserved in cases of RCM.

Heart failure resulting from restrictive cardiomyopathy will usually eventually have to be treated by cardiac transplantation or left ventricular assist device.