The diagnosis of constrictive pericarditis is often difficult to make. In particular, restrictive cardiomyopathy has many similar clinical features to constrictive pericarditis, and differentiating them in a particular individual is often a diagnostic dilemma.

- Chest X-Ray - pericardial calcification (common but not specific), pleural effusions are common findings.

- Echocardiography - the principal echographic finding is changes in cardiac chamber volume.

- CT and MRI - useful in select cases.

- BNP blood test - tests for the existence of the cardiac hormone brain natriuretic peptide, which is only present in RCMP but not in CP

- Conventional cardiac catheterization

- Physical examination -can reveal clinical features including Kussmaul's sign and a pericardial knock.

For acute pericarditis to formally be diagnosed, two or more of the following criteria must be present: chest pain consistent with a diagnosis of acute pericarditis (sharp chest pain worsened by breathing in or a cough), a pericardial friction rub, a pericardial effusion, and changes on electrocardiogram (ECG) consistent with acute pericarditis.

A complete blood count may show an elevated white count and a serum C-reactive protein may be elevated. Acute pericarditis is associated with a modest increase in serum creatine kinase MB (CK-MB). and cardiac troponin I (cTnI), both of which are also markers for injury to the muscular layer of the heart. Therefore, it is imperative to also rule out acute myocardial infarction in the face of these biomarkers. The elevation of these substances may occur when inflammation of the heart's muscular layer in addition to acute pericarditis. Also, ST elevation on EKG (see below) is more common in those patients with a cTnI > 1.5 µg/L. Coronary angiography in those patients should indicate normal vascular perfusion. Troponin levels increase in 35-50% of people with pericarditis.

Electrocardiogram (ECG) changes in acute pericarditis mainly indicates inflammation of the epicardium (the layer directly surrounding the heart), since the fibrous pericardium is electrically inert. For example, in uremia, there is no inflammation in the epicardium, only fibrin deposition, and therefore the EKG in uremic pericarditis will be normal. Typical EKG changes in acute pericarditis includes

- stage 1 -- diffuse, positive, ST elevations with reciprocal ST depression in aVR and V1. Elevation of PR segment in aVR and depression of PR in other leads especially left heart V5, V6 leads indicates atrial injury.

- stage 2 -- normalization of ST and PR deviations

- stage 3 -- diffuse T wave inversions (may not be present in all patients)

- stage 4 -- EKG becomes normal OR T waves may be indefinitely inverted

The two most common clinical conditions where ECG findings may mimic pericarditis are acute myocardial infarction (AMI) and generalized early repolarization. As opposed to pericarditis, AMI usually causes localized convex ST-elevation usually associated with reciprocal ST-depression which may also be frequently accompanied by Q-waves, T-wave inversions (while ST is still elevated unlike pericarditis), arrhythmias and conduction abnormalities. In AMI, PR-depressions are rarely present. Early repolarization usually occurs in young males (age <40 years) and ECG changes are characterized by terminal R-S slurring, temporal stability of ST-deviations and J-height/ T-amplitude ratio in V5 and V6 of <25% as opposed to pericarditis where terminal R-S slurring is very uncommon and J-height/ T-amplitude ratio is ≥ 25%. Very rarely, ECG changes in hypothermia may mimic pericarditis, however differentiation can be helpful by a detailed history and presence of an Osborne wave in hypothermia.

Another important diagnostic electrocardiographic sign in acute pericarditis is the Spodick sign. It signifies to the PR-depressions in a usual (but not always) association with downsloping TP segment in patients with acute pericarditis and is present in up to 80% of the patients affected with acute pericarditis. The sign is often best visualized in lead II and lateral precordial leads. In addition, Spodick’s sign may also serve as an important distinguishing electrocardiographic tool between the acute pericarditis and acute coronary syndrome. The presence of a classical Spodick’s sign is often a giveaway to the diagnosis.

Rarely, electrical alternans may be seen, depending on the size of the effusion.

A chest x-ray is usually normal in acute pericarditis, but can reveal the presence of an enlarged heart if a pericardial effusion is present and is greater than 200 mL in volume. Conversely, patients with unexplained new onset cardiomegaly should always be worked up for acute pericarditis.

An echocardiogram is typically normal in acute pericarditis but can reveal pericardial effusion, the presence of which supports the diagnosis, although its absence does not exclude the diagnosis.

The definitive treatment for constrictive pericarditis is pericardial stripping, which is a surgical procedure where the entire pericardium is peeled away from the heart. This procedure has significant risk involved, with mortality rates of 6% or higher in major referral centers.

A poor outcome is almost always the result after a pericardiectomy is performed for constrictive pericarditis whose origin was radiation-induced, further some patients may develop heart failure post-operatively.

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

Patients with uncomplicated acute pericarditis can generally be treated and followed up in an outpatient clinic. However, those with high risk factors for developing complications (see above) will need to be admitted to an inpatient service, most likely an ICU setting. High risk patients include the following:

- subacute onset

- high fever (> 100.4 F/38 C) and leukocytosis

- development of cardiac tamponade

- large pericardial effusion (echo-free space > 20 mm) resistant to NSAID treatment

- immunocompromised

- history of oral anticoagulation therapy

- acute trauma

- failure to respond to seven days of NSAID treatment

Pericardiocentesis is a procedure whereby the fluid in a pericardial effusion is removed through a needle. It is performed under the following conditions:

- presence of moderate or severe cardiac tamponade

- diagnostic purpose for suspected purulent, tuberculosis, or neoplastic pericarditis

- persistent symptomatic pericardial effusion

NSAIDs in "viral" or "idiopathic" pericarditis. In patients with underlying causes other than viral, the specific etiology should be treated. With idiopathic or viral pericarditis, NSAID is the mainstay treatment. Goal of therapy is to reduce pain and inflammation. The course of the disease may not be affected. The preferred NSAID is ibuprofen because of rare side effects, better effect on coronary flow, and larger dose range. Depending on severity, dosing is between 300–800 mg every 6–8 hours for days or weeks as needed. An alternative protocol is aspirin 800 mg every 6–8 hours. Dose tapering of NSAIDs may be needed. In pericarditis following acute myocardial infarction, NSAIDs other than aspirin should be avoided since they can impair scar formation. As with all NSAID use, GI protection should be engaged. Failure to respond to NSAIDs within one week (indicated by persistence of fever, worsening of condition, new pericardial effusion, or continuing chest pain) likely indicates that a cause other than viral or idiopathic is in process.

Colchicine, which has been essential to treat recurrent pericarditis, has been supported for routine use in acute pericarditis by recent prospective studies. Colchicine can be given 0.6 mg twice a day (0.6 mg daily for patients <70 kg) for 3 months following an acute attack. It should be considered in all patients with acute pericarditis, preferably in combination with a short-course of NSAIDs. For patients with a first episode of acute idiopathic or viral pericarditis, they should be treated with an NSAID plus colchicine 1–2 mg on first day followed by 0.5 daily or twice daily for three months. It should be avoided or used with caution in patients with severe renal insufficiency, hepatobiliary dysfunction, blood dyscrasias, and gastrointestinal motility disorders.

Corticosteroids are usually used in those cases that are clearly refractory to NSAIDs and colchicine and a specific cause has not been found. Systemic corticosteroids are usually reserved for those with autoimmune disease.

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)

Electrocardiography test can determine if a heart condition contributes to the symptoms.

Blood tests can detect bacterial or viral infections, pneumonia, rheumatic fever, a pulmonary embolism, or lupus.

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.

Initial diagnosis can be challenging, as there are a number of differential diagnoses, including tension pneumothorax, and acute heart failure. In a trauma patient presenting with PEA (pulseless electrical activity) in the absence of hypovolemia and tension pneumothorax, the most likely diagnosis is cardiac tamponade.

Signs of classical cardiac tamponade include three signs, known as Beck's triad. Low blood pressure occurs because of decreased stroke volume, jugular-venous distension due to impaired venous return to the heart, and muffled heart sounds due to fluid buildup inside the pericardium.

Other signs of tamponade include pulsus paradoxus (a drop of at least 10 mmHg in arterial blood pressure with inspiration), and ST segment changes on the electrocardiogram, which may also show low voltage QRS complexes, as well as general signs and symptoms of shock (such as fast heart rate, shortness of breath and decreasing level of consciousness). However, some of these signs may not be present in certain cases. A fast heart rate, although expected, may be absent in people with uremia and hypothyroidism.

In addition to the diagnostic complications afforded by the wide-ranging differential diagnosis for chest pain, diagnosis can be additionally complicated by the fact that patients will often be weak or faint at presentation. For instance, a fast rate of breathing and difficulty breathing on exertion that progresses to air hunger at rest can be a key diagnostic symptom, but it may not be possible to obtain such information from patients who are unconscious or who have convulsions at presentation.

Tamponade can often be diagnosed radiographically. Echocardiography, which is the diagnostic test of choice, often demonstrates an enlarged pericardium or collapsed ventricles. A large cardiac tamponade will show as an enlarged globular-shaped heart on chest x-ray. During inspiration, the negative pressure in the thoracic cavity will cause increased pressure into the right ventricle. This increased pressure in the right ventricle will cause the interventricular septum to bulge towards the left ventricle, leading to decreased filling of the left ventricle. At the same time, right ventricle volume is markedly diminished and sometimes it can collapse.

Dressler syndrome is best treated with high dose aspirin. In some resistant cases, corticosteroids can be used but are not preferred (avoided) in first month due to the high frequency of impaired ventricular healing leading to increased rate of ventricular rupture. NSAIDs though once used to treat Dressler syndrome, are less advocated and should be avoided in patients with ischemic heart disease. One NSAID in particular, indomethacin, can inhibit new collagen deposition thus impairing the healing process for the infarcted region. NSAIDS should only be used in cases refractory to aspirin. Heparin in Dressler syndrome should be avoided because it can lead to hemorrhage into the pericardial sac leading to tamponade. The only time heparin could be used with pericarditis is with coexisting acute MI in order to prevent further thrombus formation.

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

Tuberculous pericarditis is a form of pericarditis.

Pericarditis caused by tuberculosis is difficult to diagnose, because definitive diagnosis requires culturing "Mycobacterium tuberculosis" from aspirated pericardial fluid or pericardial , which requires high technical skill and is often not diagnostic (the yield from culture is low even with optimum specimens). The Tygerberg scoring system helps the clinician to decide whether pericarditis is due to tuberculosis or whether it is due to another cause: night sweats (1 point), weight loss (1 point), fever (2 point), serum globulin > 40g/l (3 points), blood total leucocyte count <10 x 10/l (3 points); a total score of 6 or more is highly suggestive of tuberculous pericarditis. Pericardial fluid with an interferon-γ level greater than 50/ml is highly specific for tuberculous pericarditis.

There are no randomized trials which evaluate the length of anti-tuberculosis treatment required for tuberculous pericarditis. There is a small but not conclusive benefit for treatment with a schedule of steroids with anti-tuberculosis drugs. Open surgical drainage of fluid though effective in preventing cardiac tamponade was associated with more deaths.

Initial treatment given will usually be supportive in nature, for example administration of oxygen, and monitoring. There is little care that can be provided pre-hospital other than general treatment for shock. Some teams have performed an emergency thoracotomy to release clotting in the pericardium caused by a penetrating chest injury.

Prompt diagnosis and treatment is the key to survival with tamponade. Some pre-hospital providers will have facilities to provide pericardiocentesis, which can be life-saving. If the patient has already suffered a cardiac arrest, pericardiocentesis alone cannot ensure survival, and so rapid evacuation to a hospital is usually the more appropriate course of action.

Dressler syndrome needs to be differentiated from pulmonary embolism, another identifiable cause of pleuritic (and non-pleuritic) chest pain in people who have been hospitalized and/or undergone surgical procedures within the preceding weeks.

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.

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.

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.

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.

It may be:

- "transudative" (congestive heart failure, myxoedema, nephrotic syndrome),

- "exudative" (tuberculosis, spread from empyema)

- "hemorrhagic" (trauma, rupture of aneurysms, malignant effusion).

- "malignant" (due to fluid accumulation caused by metastasis)

The most common causes of pericardial effusion have changed over time and vary depending on geography and the population in question. When pericardial effusion is suspected, echocardiography usually confirms the diagnosis and allows assessment for signs of hemodynamic instability. Cross-sectional imaging with computed tomography (CT) can help to localize and quantify (as in a loculated effusion) or assess for pericardial pathology (pericardial thickening, constrictive pericarditis).

Treatment depends on the underlying cause and the severity of the heart impairment. Pericardial effusion due to a viral infection usually goes away within a few weeks without the treatment. Some pericardial effusions remain small and never need treatment. If the pericardial effusion is due to a condition such as lupus, treatment with anti-inflammatory medications may help. If the effusion is compromising heart function and causing cardiac tamponade, it will need to be drained, most commonly by a needle inserted through the chest wall and into the pericardial space called pericardiocentesis. A drainage tube is often left in place for several days. In some cases, surgical drainage may be required by cutting through the pericardium creating a pericardial window.

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

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

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.

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.