Myocardial infarction (MI), an acute coronary syndrome, results from interruption of myocardial blood flow and resultant ischaemia, and are a leading cause of death worldwide.
- male > females
- > 45 for males
- > 55 for females
- cardiovascular risk factors: smoking, hypertension, LDL cholesterol, hyperlipidaemia, diabetes, obesity
- chest pain/tightness, which may radiate down left arm or into the jaw
- "silent" ischaemia can occur in those with poor visceral sensation (diabetics, post-cardiothoracic surgery)
- ischaemic imbalance (i.e. myocardial oxygen supply/demand imbalance)
- in critically-ill patients or in the setting of major (non-cardiac) surgery
- iatrogenic, e.g. during revascularisation procedures
One method of classification is as:
- type I: spontaneous MI related to ischaemia from a primary coronary event (e.g., plaque rupture, thrombotic occlusion)
- type II: secondary to ischaemia from a supply-and-demand mismatch.
- 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.
- right coronary artery: supplies the thin (3 mm) walled right ventricle; this artery is dominant in 70% of patients, meaning that this artery supplies the inferior heart and posterior interventricular septum via the posterior descending artery
- left anterior descending artery: supplies the anterior part of the left ventricle and the anterior aspect of the interventricular septum
- circumflex artery: 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.
The mainstay of diagnosis revolves around cardiac enzymes (troponin and creatine kinase MB) and electrocardiogram findings.
Secondary tests such as nuclear medicine (hot sestamibi) and echocardiography (localised hypokinesis) are used to aid in the diagnosis in some patients.
Given various advances in cardiac imaging such as:
- ECG gating
- 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 the central role in the investigation of chest pain. Apart from the 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 called 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 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 for not only coronary artery disease, but also aortic dissection, pulmonary embolism, and other chest diseases. While there is a consensus about its 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 or 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:
- delayed enhancement (7-15 minutes post CT contrast dose) 4
- delayed peak enhancement occurs slightly later compared to normal myocardium 12.8 versus 11.6 seconds 8
- peak enhancement is lowest in infarcts (26 HU) versus ischaemia (36 HU) versus 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.
One study has assessed the utility of non-ECG-gated 16 slice CT pulmonary angiogram in detecting myocardial infarct. This method suffers from a few problems. Firstly, the relatively early (cf with CT aortogram/coronary angiogram) phase results in non-homogeneous enhancement of the myocardium. Secondly, streak artefact (consider saline chaser) from the undiluted contrast in the SVC / right atrium caused "pseudoareas" of reduced myocardial attenuation. Thirdly, movement artefact 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 in comparison to MRI 7.
Digital subtraction angiography will show luminal arterial compromise. Acute intervention with angioplasty and stent is the gold standard for treatment of ST elevation myocardial infarct.
Recent advances in MR has made it possible to assess myocardial infarction in patients with acute chest pain as well as those in 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 myocardium are called "myocardium at risk."
Perfusion MRI at rest and during a vasodilator stress administration using a ‘first-pass' technique shows signal increase in normal myocardium. Enhancement is limited in ischemic myocardium.
The scar tissue can also be identified using late gadolinium enhancement (LGE) images. LGE images are T1 weighted inversion recovery images obtained 10 minutes after gadolinium injection. The inversion time is set to null myocardial signal which gives a better visualization of abnormally enhancing tissue (scar). The patter of LGE is useful in differentiating infarction (sub-endocardial or transmural) from non-ischemic dilated cardiomyopathy (mid-wall or sub-epicardial) and infiltrative diseases (scattered or sub-epicardial) 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 revascularisation therapy (stunned myocardium or hibernating myocardium).
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