Myocardial infarction

Myocardial infarction (MI) results from interruption of myocardial blood flow and resultant ischaemia

Epidemiology 

• responsible for 20% of deaths¹
• male > females
• age (> 45 for males) (> 55 for females)
• cardiovascular risk factors
  • smoking
  • hypertension
  • LDL cholesterol
  • hyperlipidaemia
  • diabetes
  • obesity

Clinical presenation

• chest pain / tightness
• may radiate down left arm or into jaw
• "silent" ischaemia can occur in those with poor visceral sensation (diabetics, post cardiothoracic surgery)

Pathology and relevant anatomy

Rupture of coronary atherosclerotic plaque resulting in occlusion (local thrombosis / dissection)

The heart is supplied by 3 main coronary arteries. Thus,  hypoperfusion patterns usually follow a territorial pattern

• 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. In10% of patients, this artery is dominant, meaning that it supplies the inferior heart and posterior interventricular septum

Diagnosis

The mainstay of diagnosis revolves around cardiac enzymes (troponin and creatinine kinase MB) and  electrocardiogram findings.

Occasionally, secondary tests such as nuclear medicine (hot sestamibi) and echocardiography (localised hypokinesis) are used to aid in the diagnosis.

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 1mSv 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, CT has the added advantage of being able to diagnose other causes of chest pain (eg. pulmonary embolus, pneumonia, aortic dissection). 

Radiographic features

Plain film

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

CT imaging

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

CT perfusion

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 (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 (26HU) versus ischaemia (36HU) versus normal myocardium (58HU).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 homogenous enhancement of the myocardium. Secondly, streak artefact (consider saline chaser) from 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

Angiography

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.

MRI / PET

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