https://orcid.org/0000-0001-9433-6119
-
Views
-
Cite
Cite
Ruben Coronel, Joris R. de Groot, Jan J. Piek, Transient ST-segment elevation and coronary flow, European Heart Journal, Volume 40, Issue 29, 1 August 2019, Pages 2463–2464, https://doi.org/10.1093/eurheartj/ehz331
Close - Share Icon Share
Extract
This commentary refers to ‘Timing of revascularization in patients with transient ST-segment elevation myocardial infarction: a randomized clinical trial’, by J.S. Lemkes et al., 2019;40:283–291.
Lemkes et al.1 investigated whether patients with acute myocardial ischaemia and transient ST-segment elevation may benefit from deferred reperfusion. Bergmark and Faxon2 state that electrocardiogram findings and clinical symptoms are good predictors of coronary flow. This implies that ST-normalization is a measure of reperfusion. However, not all ST-normalization is caused by reperfusion.
During acute regional myocardial ischaemia, potassium is released into the extracellular space and the resting membrane potential becomes less negative. As a result, a diastolic, intracellular ‘injury’ current flows from the depolarized region towards a normal region and causes TQ-depression in the ischaemic tissue. On the body surface, this shows as ST-segment elevation. Two mechanisms for ST-normalization during continued coronary occlusion exist.
First, extracellular potassium accumulation at the margin of the ischaemic tissue is much less than in the centre of the ischaemic tissue. It even shows a temporary decrease because potassium is lost from the extracellular space (of the ∼1 cm) wide border zone into the normal zone. This is accompanied by a normalization of TQ-depression (ST-elevation, Figure 1).3 A small ischaemic zone contains a relatively large border zone and, therefore, is characterized by transient ST-elevation.
