Coronary microvascular obstruction
Microvascular obstruction (MVO), also known as no reflow phenomenon, is an established complication encountered in coronary angioplasty for prolonged acute myocardial infarction.
The phenomenon results from obstruction of the myocardial microcirculation, which is composed of vessels less than 200 μm in diameter 1-2.
There are four mechanisms in the pathogenesis of coronary microvascular obstruction 1-8:
- depends on duration and extent of ischaemia
- characterised by:
- severe capillary damage
- endothelial protrusions
- blebs that block the capillary lumen
- endothelial gaps with extravascular erythrocytes
- myocardial cell swelling, which is due to sodium and calcium overload, compresses the capillaries and small arterioles resulting to decreased flow through these dysfunctional vessels
- obliteration of the vessel lumen is due to neutrophil-platelet aggregates and release of vasoconstrictors and inflammatory mediators (i.e. endothelin-1 and thomboxane-A2)
- in the mitochondria of cardiomyocytes, reperfusion results to reactive oxygen species that aggravate microvascular function
- reperfusion also increase infarct size due to mitrochondrial swelling and cell rupture as well as favour intra-myocardial haemorrhage.
- distal embolisation of atherosclerotic plaque and thrombus material results to mechanical obstruction of the microcirculation
individual susceptibility of the microcirculation to injury
- due to genetic factors and pre-existing coronary microvascular dysfunction
- factors modulating individual susceptibility to coronary microvascular obstruction include:
- genetic variability
- acute hyperglicaemia
- lack of pre-conditioning
Cardiovascular magnetic resonance (CMR) is very useful in the detection, diagnosis, and quantification of microvascular obstruction as well as following its subsequent effects on myocardial infarct evolution and healing.
On late gadolinium-enhancement (LGE), areas of microvascular obstruction are seen as central foci of low signal or hypoenhancement (so-called “dark zones”) within an avidly enhancing site of myocardial infarction. These dark zones of no reflow tend to fill in (brightens) on delayed sequences due to the penetration of gadolinium into the damaged capillaries.
Treatment and prognosis
Microvascular obstruction is recognized as a poor prognostic indicator and marker of subsequent adverse left ventricular remodeling 6. With microvascular obstruction, perfusion of the ischaemic myocardium is either unrestored or incompletely restored in up to 30% of patients despite recanalisation of the epicardial coronary circulation 5.
Conditions that may mimic the appearance of microvascular obstruction include 7:
- focal myocardial haemorrhage
- manifests as a central dark zone on T2 or T2* weighted MRI sequences due to the paramagnetic properties of haemoglobin breakdown products, especially during the subacute phase of the heamorrhage
- microvascular obstruction without haemorrhage may also be seen as myocardial low-signal areas on T2 weighted sequences but does not typically demonstrate low signal on T2* weighted sequences
- left ventricular thrombus
- seen as low signal foci within the cavity abutting the wall of the myocardium
- low signal foci due to microvascular obstruction are confined within the myocardium
- calcified myocardial infarcts
- may appear as focal low signal areas within a region of myocardium showing avid enhancement on late gadolinium-enhancement
- timing of the study, history of previous myocardial infarct and evidence of left ventricular remodeling are helpful clues in differentiating a calcified myocardial infarct from microvascular obstruction
- myocardial thinning is typically observed in chronic infarcts with calcifications in contrast to acute myocardial infarcts with microvascular obstruction, wherein myocardial thickness is usually preserved
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