Pathology

The underlying pathology in MI is atherosclerosis, an inflammatory process located within the arterial wall in the form of atheromatous plaques (Fig 27.1). These cause narrowing of the arterial lumen, resulting in reduced coronary perfusion, the clinical manifestation of which is chest pain (angina pectoris). If an unstable plaque ruptures, the released contents precipitate the formation of a clot. This process, known as thrombosis, may result in sudden complete occlusion of the affected artery and infarction of the area of myocardium it supplies.

Definitions

Diagnosis

The essential components of diagnosis are the history, the characteristic ECG changes and the detection in blood of biochemical markers of myocardial injury. Patients experiencing MI classically complain of severe crushing central chest pain. However, such a characteristic history is not always obtained, and a minority of patients may even have a ‘silent’ MI. When present, the characteristic ECG changes (Fig 27.2) are specific to MI, but they are equivocal or absent in up to 30% of patients. It is in this group of patients that cardiac markers are most useful.

Cardiac biomarkers

When myocardial cells die, they break up and release their contents. This is the basis for the role of cardiac biomarkers in MI diagnosis. Historically, various ‘cardiac enzymes’ have been used (Fig 27.3); however, at present, cardiac troponins are used in the diagnosis of MI. Troponin is a complex contractile protein comprising of three subunits: C, T and I. Troponin T and I are cardiospecific (therefore used in MI diagnosis; Tables 27.2 and 27.3), whereas C is also present in skeletal muscle. Troponins rise within a few hours on onset of symptoms and remain elevated for 1–2 weeks. This property enables early as well as late diagnosis. The diagnostic sensitivity of troponin reaches 100% 12 hours after onset of symptoms, i.e. MI can be excluded with confidence with a negative (undetectable) troponin if the blood sample is collected 12 hours or more after the onset of chest pain. Point-of-care devices are also available, which allow on-site measurement of troponin, but these tests are still relatively expensive.

Crucially, any elevation of troponin i.e. detectable levels in the blood, especially with the newer ultra-sensitive assays, implies a greater risk of morbidity and mortality from a cardiac event over the next 30–60 days. Therefore its application has extended from just the diagnosis of MI to risk stratification and therapy modification in ACS. It is also worth noting that though troponins are considered very specific markers of ACS, they can also increase in other cardiovascular pathologies such as myocarditis, pulmonary embolism and stroke and non-cardiac conditions such as severe sepsis.