Although Prinzmetal's angina has been documented in between 2% to 10% of angina patients, it can be overlooked by cardiologists who stop testing protocol after ruling out typical angina. Rarely, an ECG can capture diffuse ST elevations.

Patients who develop cardiac chest pain are generally treated empirically as an "acute coronary syndrome", and are generally tested for cardiac enzymes such as creatine kinase isoenzymes or troponin I or T. These may or may not show a degree of positivity, as coronary spasm too can cause myocardial damage or may leave the arteries undamaged. Echocardiography or thallium scintigraphy is often performed.

The gold standard is coronary angiography with injection of provocative agents into the coronary artery. Rarely, an active spasm can be documented angiographically (e.g. if the patient receives an angiogram with intent of performing a primary coronary intervention with angioplasty). Depending on the local protocol, provocation testing may involve substances such as ergonovine, methylergonovine or acetylcholine and hyperventilation. Exaggerated spasm is diagnostic of Prinzmetal angina.

There are various risk assessment systems for determining the risk of coronary artery disease, with various emphasis on different variables above. A notable example is Framingham Score, used in the Framingham Heart Study. It is mainly based on age, gender, diabetes, total cholesterol, HDL cholesterol, tobacco smoking and systolic blood pressure.

Angina should be suspected in people presenting tight, dull, or heavy chest discomfort that is:

1. Retrosternal or left-sided, radiating to the left arm, neck, jaw, or back.

2. Associated with exertion or emotional stress and relieved within several minutes by rest.

3. Precipitated by cold weather or a meal.

Some people present with atypical symptoms, including breathlessness, nausea, or epigastric discomfort or burning. These atypical symptoms are particularly likely in older people, women, and those with diabetes.

Anginal pain is not usually sharp or stabbing or influenced by respiration. Antacids and simple analgesics do not usually relieve the pain. If chest discomfort (of whatever site) is precipitated by exertion, relieved by rest, and relieved by glyceryl trinitrate, the likelihood of angina is increased.

In angina patients momentarily not feeling any chest pain, an electrocardiogram (ECG) is typically normal unless there have been other cardiac problems in the past. During periods of pain, depression, or elevation of the ST segment may be observed. To elicit these changes, an exercise ECG test ("treadmill test") may be performed, during which the patient exercises to his/her maximum ability before fatigue, breathlessness, or pain intervenes; if characteristic ECG changes are documented (typically more than 1 mm of flat or downsloping ST depression), the test is considered diagnostic for angina. Even constant monitoring of the blood pressure and the pulse rate can lead to some conclusion regarding angina. The exercise test is also useful in looking for other markers of myocardial ischemia: blood pressure response (or lack thereof, in particular, a drop in systolic blood pressure), dysrhythmia and chronotropic response. Other alternatives to a standard exercise test include a thallium scintigram or sestamibi scintigram (in patients unable to exercise enough for the purposes of the treadmill tests, e.g., due to asthma or arthritis or in whom the ECG is too abnormal at rest) or Stress Echocardiography.

In patients in whom such noninvasive testing is diagnostic, a coronary angiogram is typically performed to identify the nature of the coronary lesion, and whether this would be a candidate for angioplasty, coronary artery bypass graft (CABG), treatment only with medication, or other treatments. In hospitalized patients with unstable angina (or the newer term of "high-risk acute coronary syndromes"), those with resting ischaemic ECG changes or those with raised cardiac enzymes such as troponin may undergo coronary angiography directly.

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.

Hospital admission for people with the following symptoms is recommended, as they may have unstable angina: pain at rest (which may occur at night), pain on minimal exertion, angina that seems to progress rapidly despite increasing medical treatment. All people with suspected angina should be urgently referred to a chest pain evaluation service, for confirmation of the diagnosis and assessment of the severity of coronary heart disease.

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 "stable" angina, chest pain with typical features occurring at predictable levels of exertion, various forms of cardiac stress tests may be used to induce both symptoms and detect changes by way of electrocardiography (using an ECG), echocardiography (using ultrasound of the heart) or scintigraphy (using uptake of radionuclide by the heart muscle). If part of the heart seems to receive an insufficient blood supply, coronary angiography may be used to identify stenosis of the coronary arteries and suitability for angioplasty or bypass surgery.

Stable coronary artery disease (SCAD) is also often called stable ischemic heart disease (SIHD). A 2015 monograph explains that "Regardless of the nomenclature, stable angina is the chief manifestation of SIHD or SCAD." There are U.S. and European clinical practice guidelines for SIHD/SCAD.

Prinzmetal's angina typically responds to nitrates and calcium channel blockers.

Use of a beta blocker such as propranolol is contraindicated in Prinzmetal's angina. Prazosin has also been found to be of value in some patients. Coronary revascularization is only useful when the patient shows concomitant coronary atherosclerosis on coronary angiogram.

Hemopericardium can be diagnosed using echocardiography, a cardiac ultrasound. Chest X-rays are also often taken when hemopericardium is suspected and would reveal an enlarged heart. Other observable signs include rapid heart rate, jugular venous distension, low blood pressure, and pulsus paradoxus.

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 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

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 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.

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.

Symptoms of hemopericardium often include difficulty breathing, abnormally rapid breathing, and fatigue, each of which can be a sign of a serious medical condition not limited to hemopericardium. In many cases, patients also report feeling chest pressure and have an abnormally elevated heart rate.

An implantable cardioverter defibrillator (ICD) is a battery powered device that monitors electrical activity in the heart and when an arrhythmia or asystole is detected is able to deliver an electrical shock to terminate the abnormal rhythm. ICDs are used to prevent sudden cardiac death (SCD) in those that have survived a prior episode of sudden cardiac arrest (SCA) due to ventricular fibrillation or ventricular tachycardia (secondary prevention). ICDs are also used prophylactically to prevent sudden cardiac death in certain high risk patient populations (primary prevention).

Numerous studies have been conducted on the use of ICDs for the secondary prevention of SCD. These studies have shown improved survival with ICDs compared to the use of anti-arrhythmic drugs. ICD therapy is associated with a 50% relative risk reduction in death caused by an arrhythmia and a 25% relative risk reduction in all cause mortality.

Primary prevention of SCD with ICD therapy for high risk patient populations has similarly shown improved survival rates in a number of large studies. The high risk patient populations in these studies were defined as those with severe ischemic cardiomyopathy (determined by a reduced left ventricular ejection fraction (LVEF)). The LVEF criteria used in these trials ranged from less than or equal to 30% in MADIT-II to less than or equal to 40% in MUSTT.

Coronary arteriovenous fistula between coronary artery and another cardiac chamber, like, the coronary sinus, right atrium, or right ventricle may cause steal syndrome under conditions like myocardial infarction and possible angina or ventricular arrhythmias, if the shunt is large in magnitude.

It can also be associated with new patterns of blood vessel growth.

The hemodynamic sequelae of AI are dependent on the rate of onset of AI. Therefore, can be acute or chronic as follows:

- Acute aortic insufficiency In acute AI, as may be seen with acute perforation of the aortic valve due to endocarditis, there will be a sudden increase in the volume of blood in the left ventricle. The ventricle is unable to deal with the sudden change in volume. The filling pressure of the left ventricle will increase. This causes pressure in the left atrium to rise, and the individual will develop pulmonary edema. Severe acute aortic insufficiency is considered a medical emergency. There is a high mortality rate if the individual does not undergo immediate surgery for aortic valve replacement.

- Chronic aortic insufficiency If the individual survives the initial hemodynamic derailment that acute AI presents as, the left ventricle adapts by eccentric hypertrophy and dilatation of the left ventricle, and the volume overload is compensated for. The left ventricular filling pressures will revert to normal and the individual will no longer have overt heart failure. In this compensated phase, the individual may be totally asymptomatic and may have normal exercise tolerance. Eventually (typically after a latency period) the left ventricle will become decompensated, and filling pressures will increase.Some individuals enter this decompensated phase asymptomatically, treatment for AI involves aortic valve replacement prior to this decompensation phase.

The risk of death in individuals with aortic insufficiency, dilated ventricle, normal ejection fraction who are asymptomatic is about 0.2 percent per year. Risk increases if the ejection fraction decreases or if the individual develops symptoms.

Individuals with chronic (severe) aortic regurgitation follow a course that once symptoms appear, surgical intervention is needed. AI is fatal in 10 to 20% of individuals who do not undergo surgery for this condition. Left ventricle dysfunction determines to an extent the outlook for severity of aortic regurgitation cases.

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.

Previously, diagnosis was usually done through autopsy. Advances in imaging technologies allow for early detection and thus ample treatment and monitoring of the affected patient. A short-axis ultrasound of the aortic valve allows for the best view of the aortic valve, and gives a clear indication of the adduction pattern of the aortic valves.

If an “X” shape is seen, then the patient can be diagnosed with having a quadricuspid aortic valve. A transthoracic echocardiogram (TTE) indicates if there is an aortic regurgitation, but a 3-D transesophageal echocardiogram can give a better view of the aortic valve.

Multidetector coronary CT angiography has been indicated as a single competent diagnostic imaging tool capable of delineating valvular anatomy, severity of regurgitation, and high risk coronary problems. The typical method of treatment is through surgery such as aortic valve reconstruction surgery (AVRS) and aortic valve replacement, usually with a synthetic valve.

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.

It is associated with dipyridamole. Hence, dipyridamole is a pharmacological success diagnostically, but a therapeutic failure because of the coronary steal phenomenon.

Coronary steal is also the mechanism in most drug-based cardiac stress tests; When a patient is incapable of doing physical activity they are given a vasodilator that produces a "cardiac steal syndrome" as a diagnostic procedure. The test result is positive if the patient's symptoms reappear or if ECG alterations are seen.

It is also associated with the administration of Isoflurane, which is an inhaled anesthetic. Hydralazine can potentially cause this condition as well, as it is a direct arteriolar vasodilator.

It has been associated with nitroprusside.

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.

Studies have shown that patients with Pacemaker syndrome and/or with sick sinus syndrome are at higher risk of developing fatal complications that calls for the patients to be carefully monitored in the ICU. Complications include atrial fibrillation, thrombo-embolic events, and heart failure.