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.

A coronary angiography is performed only after a stress test or ECG shows a sign of coronary ischemia or CAD. This test is very important in finding where the blockages are in the arteries.

This test helps determine if an angioplasty or bypass surgery is needed.

During this test the doctor makes a small incision in the patient's groin (femoral) or wrist (radial) and inserts a catheter. The catheter has a very small video camera on the end of it so that the doctor can find the arteries.

Once he has found the arteries, he injects a dye in them so that he/she can detect any blockages in the arteries. The dye is able to be seen on a special x-ray machine.

The test takes one to two hours.

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.

A stress test, is just that, a test to put stress on the heart through exercise. A doctor will put a patient through a series of exercises to measure the tolerance for stress on the heart. This test uses an ECG to detect the electrical impulses of the heart during physical exertion.

During this test a patient is put on a treadmill or a stationary bike. The incline or resistance of the bike are steadily increased until the patient reaches the target heart rate for the patient's age and weight.

An exercise stress test is not always accurate in determining if one has a blockage in the arteries. Women and those who are young may show abnormalities on their test even though no signs of coronary ischemia or CAD are present.

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.

The survival of PVF largely depends on the promptness of defibrillation. The success rate of prompt defibrillation during monitoring is currently higher than 95%. It is estimated that the success rate decreases by 10% for each additional minute of delay.

After return of heart function, there has been a moderately higher risk of death in the hospital when compared to MI patients without PVF. Whether this still holds true with the recent changes in treatment strategies of earlier hospital admission and immediate angioplasty with thrombus removal is unknown. PVF does not affect the long-term prognosis.

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.

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.

Restoring adequate blood flow to the heart muscle in people with heart failure and significant coronary artery disease is strongly associated with improved survival, some research showing up to 75% survival rates over 5 years. A stem cell study indicated that using autologous cardiac stem cells as a regenerative approach for the human heart (after a heart attack) has great potential.

American Heart Association practice guidelines indicate (ICD) implantable cardioverter-defibrillator use in those with ischemic cardiomyopathy (40 days post-MI) that are (NYHA) New York Heart Association functional class I. LVEF of >30% is often used to differentiate primary from ischemic cardiomyopathy, and a prognostic indicator. At the same time, people who undergo ventricular restoration on top of coronary artery bypass show improved postoperative ejection fraction as compared to those treated with only coronary artery bypass surgery. Severe cases are treated with heart transplantation.

Due to the acute hemodynamic deterioration associated with myocardial rupture, the diagnosis is generally made based on physical examination, changes in the vital signs, and clinical suspicion. The diagnosis can be confirmed with echocardiography. The diagnosis is ultimately made at autopsy.

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 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.

Myocardial infarctions are generally clinically classified into ST elevation MI (STEMI) and non-ST elevation MI (NSTEMI). These are based on changes to an ECG. STEMIs make up about 25 – 40% of myocardial infarctions. A more explicit classification system, based on international consensus in 2012, also exists. This classifies myocardial infarctions into five types:

1. Spontaneous MI related to plaque erosion and/or rupture, fissuring, or dissection

2. MI related to ischemia, such as from increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anemia, arrhythmias, high blood pressure or low blood pressure

3. Sudden unexpected cardiac death, including cardiac arrest, where symptoms may suggest MI, an ECG may be taken with suggestive changes, or a blood clot is found in a coronary artery by angiography and/or at autopsy, but where blood samples could not be obtained, or at a time before the appearance of cardiac biomarkers in the blood

4. Associated with coronary angioplasty or stents

- Associated with percutaneous coronary intervention (PCI)

- Associated with stent thrombosis as documented by angiography or at autopsy

5. Associated with CABG

The prognosis of myocardial rupture is dependent on a number of factors, including which portion of the myocardium is involved in the rupture. In one case series, if myocardial rupture involved the free wall of the left ventricle, the mortality rate was 100.0%. The chances of survival rise dramatically if the patient: 1. has a witnessed initial event; 2. seeks early medical attention; 3. has an accurate diagnosis by the emergentologist; and 4. happens to be at a facility that has a cardiac surgery service (by whom a quick repair of the rupture can be attempted). Even if the individual survives the initial hemodynamic sequelae of the rupture, the 30‑day mortality is still significantly higher than if rupture did not occur.

Unstable angina is characterized by at least one of the following:

1. Occurs at rest or minimal exertion and usually lasts more than 20 minutes (if nitroglycerin is not administered)

2. Being severe (at least Canadian Cardiovascular Society Classification 3) and of new onset (i.e. within 1 month)

3. Occurs with a crescendo pattern (brought on by less activity, more severe, more prolonged or increased frequency than previously).

Fifty percent of people with unstable angina will have evidence of necrosis of the heart's muscular cells based on elevated cardiac serum markers such as creatine kinase isoenzyme (CK)-MB and troponin T or I, and thus have a diagnosis of non-ST elevation myocardial infarction.

Echocardiography is the main diagnostic tool for LVT. A distinct mass is visible in the left ventricle. Computed Tomography and Magnetic Resonance Imaging are effective, but less common ways to detect LVT, due to their costs and risks. It is possible to assess whether a thrombus will become an embolus through echocardiography. Mobility and protrusion of the thrombus are two characteristics associated with increased embolic potential.

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.

The prevalence of LVT with AMI is 5-15%. The rates of AMI associated with LVT is declining due to the use of better therapies and percutaneous coronary intervention used to treat myocardial infarction. LVT formation has been found to be higher in anterior wall AMI than other types of AMI.

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.

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.

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.

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.

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.