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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.
male > females
>45 years for males
>55 years for females
positive family history: a history of a first-degree male relative (i.e. brother, father, son) with MI <55 years of age or a first-degree female relative (i.e. mother, sister, daughter) with MI <65 years of age
classically presents with pressure-like central precordial/epigastric discomfort with several associated factors suggestive of an ischemic etiology:
radiation to bilateral arms, radiation to the right shoulder, radiation to the left arm
concomitant diaphoresis, vomiting, and/or dyspnea
classically decreased likelihood of ischemic chest pain when described as stabbing or sharp or pain which is exacerbated by inspiration, palpation, or positional change 15
ischemia in the absence of chest pain can occur in those with poor visceral sensation (diabetics, post-cardiothoracic surgery)
may present with an "anginal equivalent" such as dyspnea, nausea, or pre-syncope
The mainstay of laboratory diagnosis revolves around the measurement of a cardiac troponin level; elevation above the 99th percentile (defining myocardial injury) with a dynamic rise and/or fall (implying an acute change) associated with clinical evidence of acute myocardial ischemia defines an acute myocardial infarction 16. Creatine kinase (specifically, CK-MB) was of historical use in this context.
proximal left anterior descending artery occlusion
produces an "extensive anterior MI" pattern, with ST-segment elevation in precordial leads V1-6 and limb leads I and aVL
reciprocal ST-segment depression in lead III
mid-left anterior descending artery occlusion
produces an "apical MI" pattern, with ST-segment elevation in precordial leads V3-6 and most of the limb leads
elevation in lead II > III
leads III and aVL both elevated (usually show reciprocity)
reciprocal ST-segment depression in lead aVR
proximal right coronary artery occlusion
usually produces an "inferior MI" pattern, with ST-segment elevation in limb leads II, III, and aVF
reciprocal ST-segment depression in lead I and aVL
associated right ventricular MI denoted by elevation of the ST segment in III>II and V1>V2
associated posterior MI pattern has tall right (V1-3) precordial R waves with horizontal ST depression and tall, upright T waves
left circumflex artery occlusion
usually produces a "high lateral wall MI" pattern, with ST-segment elevation in limb leads I and aVL
reciprocal ST-segment depression in lead III
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:
ischemic imbalance (i.e. myocardial oxygen supply/demand imbalance)
in critically ill patients or the setting of major (non-cardiac) surgery
iatrogenic, e.g. during revascularization procedures
The most commonly used method of classification is as follows:
type I: spontaneous MI related to ischemia from a primary coronary event (e.g., plaque rupture, thrombotic occlusion)
type III: MI resulting in sudden cardiac death
type IVa: is an MI associated with percutaneous coronary intervention
type IVb: associated with in-stent thrombosis
type V: MI associated with coronary artery bypass surgery
typically supplies the anterior wall of the left ventricle, the anterior two-thirds of the interventricular septum (via septal branches) and the anterolateral wall of the left ventricle (via diagonal branches)
supplies the lateral and posterior aspect of the left ventricle; in 10% of patients, this artery is dominant, meaning that it supplies the inferior heart and posterior interventricular septum
For a more in-depth discussion of coronary dominance, see the article coronary arterial dominance.
Given various advances in cardiac imaging such as:
dual source (effectively halving the rotation time of the tube)
increasing detector area (256-row and 320-row single-source CT systems), allowing the entire heart to be scanned in 1 rotation (at significantly lower radiation doses - as low as 1 mSv in prospective ECG-triggered scanning) 6
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.
CT coronary angiogram
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.
"Triple rule-out” coronary CT angiography
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 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 predict 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:
delayed enhancement (7-15 minutes post-CT contrast dose) 4
delayed peak enhancement occurs slightly later compared to normal myocardium:12.8 vs 11.6 seconds 8
peak enhancement is lowest in infarcts (26 HU) vs ischemia (36 HU) vs normal myocardium (58 HU) 8
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 infarction. 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 artifacts 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 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:
new regional wall motion abnormalities
correspond to vascular territory affected
adjacent segmental hyperkinesis
previously infarcted myocardium will also demonstrate wall motion abnormalities but is characteristically thin (<7 mm or <30% the thickness of adjacent myocardium) and displays increased relative echogenicity
decreased systolic wall thickening
normal wall thickening is >40%
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