Myocardial necrosis
Myocardial necrosis refers to the cell death of cardiomyocytes related to irreversible myocardial injury.
Terminology
Myocardial necrosis is frequently used synonymously with myocardial infarction, but can also occur in diverse other clinical scenarios e.g myocardial inflammation, sepsis, cardiac contusion and iatrogenic injury .
Clinical presentation
Many clinical scenarios leading to myocardial necrosis will lead to some form of cardiac symptoms such as chest pain and/or dyspnea. Depending on the etiology and extent there will be characteristic changes on the electrocardiogram.
Myocardial necrosis can be fast and reliably detected biochemically with serologic markers such as troponin I and troponin T, creatine kinase MB isoform .
Pathology
Myocardial necrosis happens with acute myocardial cell death or irreversible myocardial injury and leads to a leakage of intracellular components of the irreversibly damaged cardiomyocytes into the myocardial extracellular space , which will then increase if the extent of damage is high enough. The necrotic myocardial zone will subsequently undergo a healing or remodeling process, starting with an inflammatory response, where the necrotic tissue is degraded and resorbed and will eventually be replaced by myocardial scar tissue .
Etiology
Myocardial necrosis can have the following causes :
- primary myocardial ischemia / myocardial infarction
- atherosclerotic plaque rupture with thrombosis
- mismatch in myocardial oxygen supply and demand
- coronary vasospasm
- coronary embolism / microembolism / dissection
- sustained bradyarrhythmias/tachyarrhythmias
- hypovolemic shock
- respiratory failure / severe anemia
- left ventricular hypertrophy / hypertrophic cardiomyopathy
- severe hypertension
- non-ischemic myocardial injury
- heart failure
- myocardial inflammation/myocarditis
- cardiomyopathies/Tako-tsubo cardiomyopathy
- cardiac contusion
- iatrogenic (revascularization, cardiac surgery, ablation, pacing, cardioversion, defibrillation)
- rhabdomyolysis
- multifactorial and systemic causes
- sepsis / critical illness
- cardiotoxicity (drugs)
- infiltrative disease (cardiac amyloidosis, cardiac sarcoidosis)
- pulmonary embolism / pulmonary hypertension
- acute or chronic renal disease
- stroke / subarachnoid hemorrhage
Radiographic features
Due to the excellent sensitivity and fast availability of serologic biomarkers, imaging methods have no real role in the detection of myocardial necrosis but in the localization and in the search for the etiology for non-ischemic or indeterminate cases.
MRI
Myocardial necrosis can be displayed with inversion recovery gradient echo images as late gadolinium enhancement or in case of microvascular obstruction as void or lack of any enhancement . It can be also demonstrated with myocardial mapping techniques . The enhancement is due to an increase of extracellular volume as a result of leakage of intracellular components into the extracellular space and hence increased volume of distribution for gadolinium-based contrast agents. As another result of this process, there will be also signs of concomitant myocardial edema.
Signal characteristics
- T2/STIR: hyperintensity
- T2-mapping: increased T2 [ms]
- T1-mapping: increased T1 [ms]
- ECV: increased
- IRGRE/PSIR:
- typically subendocardial to transmural late gadolinium enhancement in case of an acute myocardial infarction
- no enhancement in the no-reflow zone in case of microvascular obstruction, which will also reflect necrosis
- focal subepicardial or patchy midwall enhancement in myocardial inflammation
Differential diagnosis
- myocardial edema (no late gadolinium enhancement)
- myocardial fibrosis (difficult to differentiate)
- myocardial scar tissue (will usually not have any associated myocardial edema, but differentiation is rather difficult)
See also
