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.

Studies have shown no benefit for the use of herbal medicine on all cause mortality in viral myocarditis.

In eosinophilic myocarditis, echocardiography typically gives non-specific and only occasional findings of endocardium thickening, left ventricular hypertrophy, left ventricle dilation, and involvement of the mitral and/or tricuspid valves. However, in acute necrotizing eosinophilic myocarditis, echocardiography usually gives diagnostically helpful evidence of a non-enlarged heart with a thickened and poorly contracting left ventricle. Gadolinium-based cardiac magnetic resonance imaging is the most useful non-invasive procedure for diagnosing eosinophilic myocarditis. It supports this diagnosis if it shows at least two of the following abnormalities: a) an increased signal in T2-weighted images; b) an increased global myocardial early enhancement ratio between myocardial and skeletal muscle in enhanced T1 images and c) one or more focal enhancements distributed in a non-vascular pattern in late enhanced T1-weighted images. Additionally, and unlike in other forms of myocarditis, eosinophilic myocarditis may also show enhanced gadolinium uptake in the sub-endocardium. However, the only definitive test for eosinophilic myocarditis in cardiac muscle biopsy showing the presence of eosinophilic infiltration. Since the disorder may be patchy, multiple tissue samples taken during the procedure improve the chances of uncovering the pathology but in any case negative results do not exclude the diagnosis.

Intensive cardiac care and immunosuppressives including corticosteroids are helpful in the acute stage of the disease. Chronic phase has, mainly debility control and supportive care options.

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.

Screening ECGs (either at rest or with exercise) are not recommended in those without symptoms who are at low risk. This includes those who are young without risk factors. In those at higher risk the evidence for screening with ECGs is inconclusive.

Additionally echocardiography, myocardial perfusion imaging, and cardiac stress testing is not recommended in those at low risk who do not have symptoms.

Some biomarkers may add to conventional cardiovascular risk factors in predicting the risk of future cardiovascular disease; however, the clinical value of some biomarkers is questionable.

The NIH recommends lipid testing in children beginning at the age of 2 if there is a family history of heart disease or lipid problems. It is hoped that early testing will improve lifestyle factors in those at risk such as diet and exercise.

Screening and selection for primary prevention interventions has traditionally been done through absolute risk using a variety of scores (ex. Framingham or Reynolds risk scores). This stratification has separated people who receive the lifestyle interventions (generally lower and intermediate risk) from the medication (higher risk). The number and variety of risk scores available for use has multiplied, but their efficacy according to a 2016 review was unclear due to lack of external validation or impact analysis. Risk stratification models often lack sensitivity for population groups and do not account for the large number of negative events among the intermediate and low risk groups. As a result, future preventative screening appears to shift toward applying prevention according to randomized trial results of each intervention rather than large-scale risk assessment.

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.

About 30% of people with viral pericarditis or pericarditis of an unknown cause have one or several recurrent episodes.

Depending on the time of presentation and duration, pericarditis is divided into "acute" and "chronic" forms. Acute pericarditis is more common than chronic pericarditis, and can occur as a complication of infections, immunologic conditions, or even as a result of a heart attack (myocardial infarction). Chronic pericarditis however is less common, a form of which is constrictive pericarditis. The following is the clinical classification of acute vs. chronic:

- "Clinically": Acute (6 months)

The prognosis of eosinophilic myocarditis is anywhere from rapidly fatal to extremely chronic or non-fatal. Progression at a moderate rate over many months to years is the most common prognosis. In addition to the speed of inflammation-based heart muscle injury, the prognosis of eosinophilc myocarditis may be dominated by that of its underlying cause. For example, an underlying malignant cause for the eosinophilia may be survival-limiting.

These depend on the amount of inflammation. These are covered in their relevant articles.

- Acute: Heart failure; pericardial effusion; etc.

- Chronic: Valve diseases as noted above; Reduced cardiac output; Exercise intolerance.

Mortality in HIV-infected patients with cardiomyopathy is increased independently of CD4 count, age, sex, and HIV risk group.

The therapy is similar to therapy for non-ischemic cardiomyopathy: after medical therapy is begun, serial echocardiographic studies should be performed at 4-months intervals. If function continues to worsen or the clinical course deteriorates, a biopsy should be considered.

HAART has reduced the incidence of myocarditis thus reducing the prevalence of HIV-associated cardiomyopathy by about 30% in developed countries. However, the prevalence in developing countries is 32% and increasing as HAART is scarce – not to mention the effects of other risk factors such as high cholesterol and lipid diet. IVIGs can also help patients with HIV-associated myocarditis as mentioned earlier.

Myopericarditis is a combination of both myocarditis and pericarditis appearing in a single individual, namely inflammation of both the pericardium and the heart muscle. It can involve the presence of fluid in the heart. Myopericarditis refers primarily to a pericarditis with lesser myocarditis, as opposed to a perimyocarditis, though the two terms are often used interchangeably. Both will be reflected on an ECG. Myo-pericarditis usually involves inflammation of the pericardium, or the sac covering the heart.

The ACAM2000 smallpox vaccine has been known to cause myopericarditis in some people.

Among the diagnostic procedures done to determine a cardiomyopathy are:

- Physical exam

- Family history

- Blood test

- EKG

- Echocardiogram

- Stress test

- Genetic testing

Idiopathic giant-cell myocarditis (IGCM) is a cardiovascular disease of the muscle of the heart (myocardium).

The condition is rare; however, it is often fatal and there is no proven cure because of the unknown nature of the disorder.

IGCM frequently leads to death with a high rate of about 70% in first year. A patient with IGCM typically presents with symptoms of heart failure, although some may present initially with ventricular arrhythmia or heart block. Median age from the time the disease is diagnosed to the time of death is approximately 6 months. 90% of patients are either deceased by the end of 1 year or have received a heart transplant. Diagnosis is made by endomyocardial biopsy during heart catheterization. Biopsy shows multinucleated giant cells and thus the name. While previously cases universally required heart transplantation, recent studies show that two thirds of patients can survive past one year with high doses of immunosuppressants such as prednisone and cyclosporine. The transplanted heart has a high chance of disease recurrence. Compared to lymphocytic (presumed viral) myocarditis, giant cell myocarditis is much more severe with much more rapid progression.

It is suggested to be caused by T-lymphocytes.

Carditis is the inflammation of the heart or its surroundings. The plural of carditis is carditides.

It is usually studied and treated by specifying it as:

- Pericarditis is the inflammation of the pericardium

- Myocarditis is the inflammation of the heart muscle

- Endocarditis is the inflammation of the endocardium

- Pancarditis is the inflammation of the entire heart: the epicardium, the myocardium and the endocardium

- Reflux carditis refers to a possible outcome of esophageal reflux (also known as GERD), and involves inflammation of the esophagus/stomach mucosa

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.

Zidovudine is an example of a nucleoside analogue and has been shown to cause: myocarditis and dilated cardiomyopathy as well as an increase in total cholesterol, triglycerides, LDL, HDL and insulin resistance. Protease inhibitors are another group of drugs (e.g. ritonavir) and some of them can cause a range of problems such as: lipodystrophy, atherosclerosis, increase total cholesterol, triglyceride, HDL, LDL, and insulin resistance. Amphotericin B can cause dilated cardiomyopathy, hypertension and bradycardia whereas, Ganciclovir can cause ventricular tachycardia. Interferon-alpha can cause arrhythmia and myocardial infarction/ischemia.

Insufficient physical activity (defined as less than 5 x 30 minutes of moderate activity per week, or less than 3 x 20 minutes of vigorous activity per week) is currently the fourth leading risk factor for mortality worldwide. In 2008, 31.3% of adults aged 15 or older (28.2% men and 34.4% women) were insufficiently physically active.

The risk of ischemic heart disease and diabetes mellitus is reduced by almost a third in adults who participate in 150 minutes of moderate physical activity each week (or equivalent). In addition, physical activity assists weight loss and improves blood glucose control, blood pressure, lipid profile and insulin sensitivity. These effects may, at least in part, explain its cardiovascular benefits.

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.

Generalized enlargement of the heart is seen upon normal chest X-ray. Pleural effusion may also be noticed, which is due to pulmonary venous hypertension.

The electrocardiogram often shows sinus tachycardia or atrial fibrillation, ventricular arrhythmias, left atrial enlargement, and sometimes intraventricular conduction defects and low voltage. When left bundle-branch block (LBBB) is accompanied by right axis deviation (RAD), the rare combination is considered to be highly suggestive of dilated or congestive cardiomyopathy. Echocardiogram shows left ventricular dilatation with normal or thinned walls and reduced ejection fraction. Cardiac catheterization and coronary angiography are often performed to exclude ischemic heart disease.

Genetic testing can be important, since one study has shown that gene mutations in the TTN gene (which codes for a protein called titin) are responsible for "approximately 25% of familial cases of idiopathic dilated cardiomyopathy and 18% of sporadic cases." The results of the genetic testing can help the doctors and patients understand the underlying cause of the dilated cardiomyopathy. Genetic test results can also help guide decisions on whether a patient's relatives should undergo genetic testing (to see if they have the same genetic mutation) and cardiac testing to screen for early findings of dilated cardiomyopathy.

Cardiac magnetic resonance imaging (cardiac MRI) may also provide helpful diagnostic information in patients with dilated cardiomyopathy.

Athlete's heart is not dangerous for athletes (though if a nonathlete has symptoms of bradycardia, cardiomegaly, and cardiac hypertrophy, another illness may be present). Athlete's heart is not the cause of sudden cardiac death during or shortly after a workout, which mainly occurs due to hypertrophic cardiomyopathy, a genetic disorder.

No treatment is required for people with athletic heart syndrome; it does not pose any physical threats to the athlete, and despite some theoretical concerns that the ventricular remodeling might conceivably predispose for serious arrhythmias, no evidence has been found of any increased risk of long-term events. Athletes should see a physician and receive a clearance to be sure their symptoms are due to athlete’s heart and not another heart disease, such as cardiomyopathy. If the athlete is uncomfortable with having athlete's heart or if a differential diagnosis is difficult, deconditioning from exercise for a period of three months allows the heart to return to its regular size. However, one long-term study of elite-trained athletes found that dilation of the left ventricle was only partially reversible after a long period of deconditioning. This deconditioning is often met with resistance to the accompanying lifestyle changes. The real risk attached to athlete's heart is if athletes or nonathletes simply assume they have the condition, instead of making sure they do not have a life-threatening heart illness.

Treatment may include suggestion of lifestyle changes to better manage the condition. Treatment depends on the type of cardiomyopathy and condition of disease, but may include medication (conservative treatment) or iatrogenic/implanted pacemakers for slow heart rates, defibrillators for those prone to fatal heart rhythms, ventricular assist devices (VADs) for severe heart failure, or ablation for recurring dysrhythmias that cannot be eliminated by medication or mechanical cardioversion. The goal of treatment is often symptom relief, and some patients may eventually require a heart transplant.

Because several well-known and high-profile cases of athletes experiencing sudden unexpected death due to cardiac arrest, such as Reggie White and Marc-Vivien Foé, a growing movement is making an effort to have both professional and school-based athletes screened for cardiac and other related conditions, usually through a careful medical and health history, a good family history, a comprehensive physical examination including auscultation of heart and lung sounds and recording of vital signs such as heart rate and blood pressure, and increasingly, for better efforts at detection, such as an electrocardiogram.

An electrocardiogram (ECG) is a relatively straightforward procedure to administer and interpret, compared to more invasive or sophisticated tests; it can reveal or hint at many circulatory disorders and arrhythmias. Part of the cost of an ECG may be covered by some insurance companies, though routine use of ECGs or other similar procedures such as echocardiography (ECHO) are still not considered routine in these contexts. Widespread routine ECGs for all potential athletes during initial screening and then during the yearly physical assessment could well be too expensive to implement on a wide scale, especially in the face of the potentially very large demand. In some places, a shortage of funds, portable ECG machines, or qualified personnel to administer and interpret them (medical technicians, paramedics, nurses trained in cardiac monitoring, advanced practice nurses or nurse practitioners, physician assistants, and physicians in internal or family medicine or in some area of cardiopulmonary medicine) exist.

If sudden cardiac death occurs, it is usually because of pathological hypertrophic enlargement of the heart that went undetected or was incorrectly attributed to the benign "athletic" cases. Among the many alternative causes are episodes of isolated arrhythmias which degenerated into lethal VF and asystole, and various unnoticed, possibly asymptomatic cardiac congenital defects of the vessels, chambers, or valves of the heart. Other causes include carditis, endocarditis, myocarditis, and pericarditis whose symptoms were slight or ignored, or were asymptomatic.

The normal treatments for episodes due to the pathological look-alikes are the same mainstays for any other episode of cardiac arrest: Cardiopulmonary resuscitation, defibrillation to restore normal sinus rhythm, and if initial defibrillation fails, administration of intravenous epinephrine or amiodarone. The goal is avoidance of infarction, heart failure, and/or lethal arrhythmias (ventricular tachycardia, ventricular fibrillation, asystole, or pulseless electrical activity), so ultimately to restore normal sinus rhythm.

In patients with advanced disease who are refractory to medical therapy, heart transplantation may be considered. For these people 1-year survival approaches 90% and over 50% survive greater than 20 years.