Blood tests routinely performed include electrolytes (sodium, potassium), measures of kidney function, liver function tests, thyroid function tests, a complete blood count, and often C-reactive protein if infection is suspected. An elevated B-type natriuretic peptide (BNP) is a specific test indicative of heart failure. Additionally, BNP can be used to differentiate between causes of dyspnea due to heart failure from other causes of dyspnea. If myocardial infarction is suspected, various cardiac markers may be used.

According to a meta-analysis comparing BNP and N-terminal pro-BNP (NTproBNP) in the diagnosis of heart failure, BNP is a better indicator for heart failure and left ventricular systolic dysfunction. In groups of symptomatic patients, a diagnostic odds ratio of 27 for BNP compares with a sensitivity of 85% and specificity of 84% in detecting heart failure.

An electrocardiogram (ECG/EKG) may be used to identify arrhythmias, ischemic heart disease, right and left ventricular hypertrophy, and presence of conduction delay or abnormalities (e.g. left bundle branch block). Although these findings are not specific to the diagnosis of heart failure a normal ECG virtually excludes left ventricular systolic dysfunction.

Noninvasive imaging plays an important role in the diagnosis and characterisation of myocardial infarction. Tests such as chest X-rays can be used to explore and exclude alternate causes of a person's symptoms. Tests such as stress echocardiography and myocardial perfusion imaging can confirm a diagnosis when a person's history, physical examination (including cardiac examination) ECG, and cardiac biomarkers suggest the likelihood of a problem.

Echocardiography, an ultrasound scan of the heart, is able to visualize the heart, its size, shape, and any abnormal motion of the heart walls as they beat that may indicate a myocardial infarction. The flow of blood can be imaged, and contrast dyes may be given to improve image. Other scans using radioactive contrast include SPECT CT-scans using thallium, sestamibi (MIBI scans) or tetrofosmin; or a PET scan using Fludeoxyglucose or rubidium-82. These nuclear medicine scans can visualize the perfusion of heart muscle. SPECT may also be used to determine viability of tissue, and whether areas of ischemia are inducible.

Medical societies and professional guidelines recommend that the physician confirm a person is at high risk for myocardial infarction before conducting imaging tests to make a diagnosis, as such tests are unlikely to change management and result in increased costs. Patients who have a normal ECG and who are able to exercise, for example, do not merit routine imaging.

There are a number of different biomarkers used to determine the presence of cardiac muscle damage. Troponins, measured through a blood test, are considered to be the best, and are preferred because they have greater sensitivity and specificity for measuring injury to the heart muscle than other tests. A rise in troponin occurs within 2–3 hours of injury to the heart muscle, and peaks within 1–2 days. The gross value of the troponin, as well as a change over time, are useful in measuring and diagnosing or excluding myocardial infarctions, and the diagnostic accuracy of troponin testing is improving over time. One high-sensitivity cardiac troponin is able to rule out a heart attack as long as the ECG is normal.

Other tests, such as CK-MB or myoglobin, are discouraged. CK-MB is not as specific as troponins for acute myocardial injury, and may be elevated with past cardiac surgery, inflammation or electrical cardioversion; it rises within 4–8 hours and returns to normal within 2–3 days. Copeptin may be useful to rule out MI rapidly when used along with troponin.

Cardiac arrest is synonymous with clinical death.

A cardiac arrest is usually diagnosed clinically by the absence of a pulse. In many cases lack of carotid pulse is the gold standard for diagnosing cardiac arrest, as lack of a pulse (particularly in the peripheral pulses) may result from other conditions (e.g. shock), or simply an error on the part of the rescuer. Nonetheless, studies have shown that rescuers often make a mistake when checking the carotid pulse in an emergency, whether they are healthcare professionals or lay persons.

Owing to the inaccuracy in this method of diagnosis, some bodies such as the European Resuscitation Council (ERC) have de-emphasised its importance. The Resuscitation Council (UK), in line with the ERC's recommendations and those of the American Heart Association,

have suggested that the technique should be used only by healthcare professionals with specific training and expertise, and even then that it should be viewed in conjunction with other indicators such as agonal respiration.

Various other methods for detecting circulation have been proposed. Guidelines following the 2000 International Liaison Committee on Resuscitation (ILCOR) recommendations were for rescuers to look for "signs of circulation", but not specifically the pulse. These signs included coughing, gasping, colour, twitching and movement. However, in face of evidence that these guidelines were ineffective, the current recommendation of ILCOR is that cardiac arrest should be diagnosed in all casualties who are unconscious and not breathing normally. Another method is to use molecular autopsy or postmortem molecular testing which uses a set of molecular techniques to find the ion channels that are cardiac defective.

Clinicians classify cardiac arrest into "shockable" versus "non–shockable", as determined by the ECG rhythm. This refers to whether a particular class of cardiac dysrhythmia is treatable using defibrillation. The two "shockable" rhythms are ventricular fibrillation and pulseless ventricular tachycardia while the two "non–shockable" rhythms are asystole and pulseless electrical activity.

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.

When cardiomyopathy is suspected as the cause of cardiogenic shock, a biopsy of heart muscle may be needed to make a definite diagnosis.

There are two main types of cardiomegaly:

Dilated cardiomyopathy is the most common type of cardiomegaly. In this condition, the walls of the left and/or right ventricles of the heart become thin and stretched. The result is an enlarged heart.

In the other types of cardiomegaly, the heart's large muscular left ventricle becomes abnormally thick. Hypertrophy is usually what causes left ventricular enlargement. Hypertrophic cardiomyopathy is typically an inherited condition.

There are many techniques and tests used to diagnose an enlarged heart. Below is a list of tests and how they test for cardiomegaly:

1. Chest X-Ray: X-ray images help see the condition of the lungs and heart. If the heart is enlarged on an X-ray, other tests will usually be needed to find the cause. A useful measurement on X-ray is the "cardio-thoracic ratio", which is the transverse diameter of the heart, compared with that of the thoracic cage." These diameters are taken from PA chest x-rays using the widest point of the chest and measuring as far as the lung pleura, not the lateral skin margins. If the cardiac thoracic ratio is greater than 50%, pathology is suspected, assuming the x-ray has been taken correctly. The measurement was first proposed in 1919 to screen military recruits. A newer approach to using these x-rays for evaluating heart health, takes the ratio of heart area to chest area and has been called the two-dimensional cardiothoracic ratio.

2. Electrocardiogram: This test records the electrical activity of the heart through electrodes attached to the person's skin. Impulses are recorded as waves and displayed on a monitor or printed on paper. This test helps diagnose heart rhythm problems and damage to a person's heart from a heart attack.

3. Echocardiogram: This test for diagnosing and monitoring an enlarged heart uses sound waves to produce a video image of the heart. With this test, the four chambers of the heart can be evaluated.

- The results of these tests can be used to see how efficiently the heart is pumping, determine which chambers of the heart are enlarged, look for evidence of previous heart attacks and determine if a person has congenital heart disease.

4. Stress test: A stress test, also called an exercise stress test, provides information about how well the heart works during physical activity.

- An exercise stress test usually involves walking on a treadmill or riding a stationary bike while the heart rhythm, blood pressure, and breathing are monitored.

5. Cardiac computerized tomography (CT) or magnetic resonance imaging (MRI). In a cardiac CT scan, one lies on a table inside a machine called a gantry. An X-ray tube inside the machine rotates around the body and collects images of the heart and chest.

- In a cardiac MRI, one lies on a table inside a long tube-like machine that uses a magnetic field and radio waves to produce signals that create images of the heart.

6. Blood tests: Blood tests may be ordered to check the levels of substances in the blood that may show a heart problem. Blood tests can also help rule out other conditions that may cause one's symptoms.

7. Cardiac catheterization and biopsy: In this procedure, a thin tube (catheter) is inserted in the groin and threaded through the blood vessels to the heart, where a small sample (biopsy) of the heart, if indicated, can be extracted for laboratory analysis.

The Swan-Ganz catheter or pulmonary artery catheter may assist in the diagnosis by providing information on the hemodynamics.

The cause of cardiomegaly is not well understood and many cases of cardiomegaly are idiopathic (having no known cause). Prevention of cardiomegaly starts with detection. If a person has a family history of cardiomegaly, one should let one's doctor know so that treatments can be implemented to help prevent worsening of the condition. In addition, prevention includes avoiding certain lifestyle risk factors such as tobacco use and controlling one's high cholesterol, high blood pressure, and diabetes. Non-lifestyle risk factors include family history of cardiomegaly, coronary artery disease (CAD), congenital heart failure, Atherosclerotic disease, valvular heart disease, exposure to cardiac toxins, sleep disordered breathing (such as sleep apnea), sustained cardiac arrhythmias, abnormal electrocardiograms, and cardiomegaly on chest X-ray. Lifestyle factors which can help prevent cardiomegaly include eating a healthy diet, controlling blood pressure, exercise, medications, and not abusing alcohol and cocaine. Current research and the evidence of previous cases link the following (below) as possible causes of cardiomegaly.

The most common causes of Cardiomegaly are congenital (patients are born with the condition based on a genetic inheritance), high blood pressure which can enlarge the left ventricle causing the heart muscle to weaken over time, and coronary artery disease that creates blockages in the heart's blood supply, which can bring on a cardiac infarction (heart attack) leading to tissue death which causes other areas of the heart to work harder, increasing the heart size.

Other possible causes include:

- Heart Valve Disease

- Cardiomyopathy (disease to the heart muscle)

- Pulmonary Hypertension

- Pericardial Effusion (fluid around the heart)

- Thyroid Disorders

- Hemochromatosis (excessive iron in the blood)

- Other rare diseases like Amyloidosis

- Viral infection of the heart

- Pregnancy, with enlarged heart developing around the time of delivery (peripartum cardiomyopathy)

- Kidney disease requiring dialysis

- Alcohol or cocaine abuse

- HIV infection

- Diabetes

The medical care of patients with hypertensive heart disease falls under 2 categories—

- Treatment of hypertension

- Prevention (and, if present, treatment) of heart failure or other cardiovascular disease

The following screening tool may be useful to patients and medical professionals in determining the need to take further action to diagnose symptoms:

A jugular venous distension is the most sensitive clinical sign for acute decompensation.

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.

According to JNC 7, BP goals should be as follows :

- Less than 140/90mm Hg in patients with uncomplicated hypertension

- Less than 130/85mm Hg in patients with diabetes and those with renal disease with less than 1g/24-hour proteinuria

- Less than 125/75mm Hg in patients with renal disease and more than 1 g/24-hour proteinuria

Certain scenarios will require emergent consultation with cardiothoracic surgery. Heart failure due to acute aortic regurgitation is a surgical emergency associated with high mortality. Heart failure may occur after rupture of ventricular aneurysm. These can form after myocardial infarction. If it ruptures on the free wall, it will cause cardiac tamponade. If it ruptures on the intraventricular septum, it can create a ventricular septal defect. Other causes of cardiac tamponade may also require surgical intervention, although emergent treatment at the bedside may be adequate. It should also be determined whether the patient had a history of a repaired congenital heart disease as they often have complex cardiac anatomy with artificial grafts and shunts that may sustain damage, leading to acute decompensated heart failure.

In some cases, doctors recommend surgery to treat the underlying problem that led to heart failure. Different procedures are available depending on the level of necessity and include coronary artery bypass surgery, heart valve repair or replacement, or heart transplantation. During these procedures, devices such as heart pumps, pacemakers, or defibrillators might be implanted. The treatment of heart disease is rapidly changing and thus new therapies for acute heart failure treatment are being introduced to save more lives from these massive attacks.

Bypass surgery is performed by removing a vein from the arm or leg, or an artery from the chest and replacing the blocked artery in the heart. This allows the blood to flow more freely through the heart. Valve repair is where the valve that is causing heart failure is modified by removing excess valve tissues that cause them to close too tightly. In some cases, annuloplasty is required to replace the ring around the valves. If the repair of the valve is not possible, it is replaced by an artificial heart valve. The final step is heart replacement. When severe heart failure is present and medicines or other heart procedures are not effective, the diseased heart needs to be replaced.

Another common procedure used to treat heart failure patients is an angioplasty. Is a procedure used to improve the symptoms of coronary artery disease (CAD), reduce the damage to the heart muscle after a heart attack, and reduce the risk of death in some patients. This procedure is performed by placing a balloon in the heart to open an artery that is blocked by atherosclerosis or a buildup of plaque on the artery walls. People who are experiencing heart failure because of CAD or recent heart attack can benefit from this procedure.

A pacemaker is a small device that's placed in the chest or abdomen to help control abnormal heart rhythms. They work by sending electric pulses to the heart to prompt it to beat at a rate that is considered to be normal and are used to treat patients with arrhythmias. They can be used to treat hearts that are classified as either a tachycardia that beats too fast, or a bradycardia that beats too slow.

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.

Ischemic cardiomyopathy can be diagnosed via magnetic resonance imaging (MRI) protocol, imaging both global and regional function. Also the Look-Locker technique is used to identify diffuse fibrosis; it is therefore important to be able to determine the extent of the ischemic scar. Some argue that only left main- or proximal-left anterior descending artery disease is relevant to the diagnostic criteria for ischemic cardiomyopathy. Myocardial imaging usually demonstrates left ventricular dilation, severe ventricular dysfunction, and multiple infarctions. Signs include congestive heart failure, angina edema, weight gain and fainting, among others.

Myocarditis refers to an underlying process that causes inflammation and injury of the heart. It does not refer to inflammation of the heart as a consequence of some other insult. Many secondary causes, such as a heart attack, can lead to inflammation of the myocardium and therefore the diagnosis of myocarditis cannot be made by evidence of inflammation of the myocardium alone.

Myocardial inflammation can be suspected on the basis of electrocardiographic (ECG) results, elevated C-reactive protein (CRP) and/or erythrocyte sedimentation rate (ESR), and increased IgM (serology) against viruses known to affect the myocardium. Markers of myocardial damage (troponin or creatine kinase cardiac isoenzymes) are elevated.

The ECG findings most commonly seen in myocarditis are diffuse T wave inversions; saddle-shaped ST-segment elevations may be present (these are also seen in pericarditis).

The gold standard is still biopsy of the myocardium, in general done in the setting of angiography. A small tissue sample of the endocardium and myocardium is taken, and investigated by a pathologist by light microscopy and—if necessary—immunochemistry and special staining methods. Histopathological features are myocardial interstitium with abundant edema and inflammatory infiltrate, rich in lymphocytes and macrophages. Focal destruction of myocytes explains the myocardial pump failure.

Cardiac magnetic resonance imaging (cMRI or CMR) has been shown to be very useful in diagnosing myocarditis by visualizing markers for inflammation of the myocardium.

Recently, consensus criteria for the diagnosis of myocarditis by CMR have been published.

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.

It is critical to diagnose CRS at an early stage in order to achieve optimal therapeutic efficacy. However, unlike markers of heart damage or stress such as troponin, creatine kinase, natriuretic peptides, reliable markers for acute kidney injury are lacking. Recently, research has found several biomarkers that can be used for early detection of acute kidney injury before serious loss of organ function may occur. Several of these biomarkers include neutrophil gelatinase-associated lipocalin (NGAL), N-acetyl-B-D-glucosaminidase (NAG), Cystatin C, and kidney injury molecule-1 (KIM-1) which have been shown to be involved in tubular damage. Other biomarkers that have been shown to be useful include BNP, IL-18, and fatty acid binding protein (FABP). However, there is great variability in the measurement of these biomarkers and their use in diagnosing CRS must be assessed.

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.

There are no specific diagnostic criteria for TIC, and it can be difficult to diagnose for a number of reasons. First, in patients presenting with both tachycardia and cardiomyopathy, it can be difficult to distinguish which is the causative agent. Additionally, it can occur in patients with or without underlying structural heart disease. Previously normal left ventricular ejection fraction or left ventricular systolic dysfunction out of proportion to a patient’s underlying cardiac disease can be important clues to possible TIC. The diagnosis of TIC is made after excluding other causes of cardiomyopathy and observing resolution of the left ventricular systolic dysfunction with treatment of the tachycardia.

Specific tests that can be used in the diagnosis and monitoring of TIC include:

- electrocardiography (EKG)

- Continuous cardiac rhythm monitoring (e.g. Holter monitor)

- echocardiography

- Radionuclide imaging

- Endomyocardial biopsy

- Cardiac magnetic resonance imaging (CMR)

- N-terminal pro-B-type natriuretic peptide (NT-pro BNP)

Cardiac rhythm monitors can be used to diagnose tachyarrhythmias. The most common modality used is an EKG. A continuous rhythm monitor such as a Holter monitor can be used to characterize the frequency of a tachyarrhythmia over a longer period of time. Additionally, some patients may not present to the clinical setting in an abnormal rhythm, and continuous rhythm monitor can be useful to determine if an arrhythmia is present over a longer duration of time.

To assess cardiac structure and function, echocardiography is the most commonly available and utilized modality. In addition to decreased left ventricular ejection fraction, studies indicate that patients with TIC may have a smaller left ventricular end-diastolic dimension compared to patients with idiopathic dilated cardiomyopathy. Radionuclide imaging can be used as a non-invasive test to detect myocardial ischemia. Cardiac MRI has also been used to evaluate patients with possible TIC. Late-gadolinium enhancement on cardiac MRI indicates the presence of fibrosis and scarring, and may be evidence of cardiomyopathy not due to tachycardia. A decline in serial NT-pro BNP with control of tachyarrhythmia indicates reversibility of the cardiomyopathy, which would also suggest TIC.

People with TIC display distinct changes in endomyocardial biopsies. TIC is associated with the infiltration of CD68 macrophages into the myocardium while CD3 T-cells are very rare. Furthermore, patients with TIC display significant fibrosis due to collagen deposition. The distribution of mitochondria has found to be altered as well, with an enrichment at the intercalated discs (EMID-sign).

TIC is likely underdiagnosed due to attribution of the tachyarrhythmia to the cardiomyopathy. Poor control of the tachyarrhythmia can result in worsening of heart failure symptoms and cardiomyopathy. Therefore, it is important to aggressively treat the tachyarrhythmia and monitor patients for resolution of left ventricular systolic dysfunction in cases of suspected TIC.

A complication that may occur in the acute setting soon after a myocardial infarction or in the weeks following is cardiogenic shock. Cardiogenic shock is defined as a hemodynamic state in which the heart cannot produce enough of a cardiac output to supply an adequate amount of oxygenated blood to the tissues of the body.

While the data on performing interventions on individuals with cardiogenic shock is sparse, trial data suggests a long-term mortality benefit in undergoing revascularization if the individual is less than 75 years old and if the onset of the acute myocardial infarction is less than 36 hours and the onset of cardiogenic shock is less than 18 hours. If the patient with cardiogenic shock is not going to be revascularized, aggressive hemodynamic support is warranted, with insertion of an intra-aortic balloon pump if not contraindicated. If diagnostic coronary angiography does not reveal a culprit blockage that is the cause of the cardiogenic shock, the prognosis is poor.