Myocardial infarction (MI), colloquially known as a heart attack, an acute coronary syndrome, results from interruption of myocardial blood flow and resultant ischemia and is a leading cause of death worldwide. 

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Coronary artery disease with rupture of an atherosclerotic plaque resulting in occlusion (local thrombosis/dissection) is the proximate cause of type I myocardial infarctions. Other causes include 12:

The most commonly used method of classification is as follows:

The heart is supplied by three main coronary arteries. Thus, hypoperfusion patterns usually follow a territorial pattern:

For a more in-depth discussion of coronary dominance, see the article coronary arterial dominance.

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Secondary tests such as nuclear medicine (hot sestamibi) and echocardiography (localized hypokinesis) are used to aid in the diagnosis of some patients.

Given various advances in cardiac imaging such as:

CT scanning has the potential to play a central role in the investigation of chest pain. Apart from being able to detect large territory infarcts on coronary CT angiography (CTA), CT has the added advantage of being able to diagnose other causes of chest pain (e.g. pulmonary embolism, aortic dissection, pneumonia), in a protocol known as “triple rule-out” CTA.

Useful in excluding other causes of chest pain, e.g. pneumonia. Less useful in the direct diagnosis of myocardial infarction. The cardiomediastinal contours are usually normal. One may occasionally see signs of heart failure.

Most of the studies evaluating the usefulness of CT imaging have used 64 multislice CT scanning with ECG gating to assess the lumen of coronary arteries. Using this technique, a sensitivity of 92% and specificity of 76% was achieved, even in patients who were initially ECG- and troponin-negative 2.

Some institutions are using this protocol that examines not only coronary artery disease, but also aortic dissection, pulmonary embolism, and other chest diseases. While there is a consensus about this protocol offering advantages in evaluating emergency department patients presenting with symptoms consistent with an acute coronary syndrome, there is an ongoing debate about proper indications. It should not be used routinely and lacks demonstration of increasing efficiency of resource use 10,11.

See triple-rule-out CT.

In patients who have established coronary artery narrowing, CT perfusion can be used to predict the significance of the luminal narrowing as well as predicting post-infarction myocardial viability/salvageability 3-4.

An acute myocardial infarct would manifest with a reduced first-pass effect (hypodense myocardium). A CT thoracic aortogram is, in effect, a cardiac first-pass perfusion study (albeit, without the ECG gating) and has the potential to detect large territory myocardial infarcts. Despite these described findings, the role of CT perfusion in assessing acute myocardial infarction has not been well-established. 

An established myocardial infarct would manifest with:

Infarct scars can mimic acute myocardial infarcts as they demonstrate a similar enhancement pattern; however, old infarcts are often associated with myocardial thinning and contour abnormality (bulges away from ventricle), useful distinguishing features. Subendocardial fat may be present in some cases.

One study has assessed the utility of a non-ECG-gated 16-slice CT pulmonary angiogram in detecting myocardial infarct. This method suffers from a few problems. First, the relatively early (cf. with CT aortogram/coronary angiogram) phase results in non-homogeneous enhancement of the myocardium. Second, streak artifact (consider saline chaser) from the undiluted contrast in the superior vena cava/right atrium caused "pseudo-areas" of reduced myocardial attenuation. Third, movement artifact from the beating heart caused areas of increased/decreased attenuation. Despite these problems, this study published optimistic figures of 66.6% sensitivity and 91.4% specificity 5. 

Approaches using dual-energy CT to visualize late myocardial enhancement as a marker for scars showed only a limited diagnostic value compared to MRI 7.

Digital subtraction angiography will show luminal arterial compromise. Primary percutaneous coronary intervention (primary PCI) with angioplasty and stenting is the gold standard for the treatment of ST-elevation myocardial infarction. Patients with non-ST-elevation myocardial infarction also commonly undergo coronary angiography as inpatients.

Recent advances in MRI have made it possible to assess myocardial infarction in patients with acute chest pain as well as those with subacute or chronic disease. Using different MR signals and techniques provides valuable information on assessing the scar tissue as well as salvageable myocardium.

In the acute phase of infarction, myocardial edema can be seen as T2-weighted high signal regions. It has been shown that these regions are salvageable. These segments of the myocardium are called "myocardium at risk".

Perfusion MRI at rest and during a vasodilator stress administration using a ‘first-pass' technique shows a signal increase in normal myocardium. Enhancement is limited in the ischemic myocardium.

Myocardial scar tissue can be identified using late gadolinium enhancement (LGE) images and is useful in differentiating infarction (subendocardial or transmural) from non-infarcted myocardium or other non-ischemic cardiomyopathies and infiltrative diseases 13.

In those who have had a myocardial infarct, PET/MRI can be used to identify patients with potentially viable/salvageable myocardium that may be a candidate for revascularization therapy (stunned myocardium or hibernating myocardium).

The first manifestation of the ischemic cascade detectable by echocardiography is diastolic dysfunction, preceding derangement of systolic function. Other features suggestive of myocardial ischemia in an appropriate clinical context include: