Transient ST-segment elevation and coronary flow

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. (A) Transient increase in extracellular potassium concentration, and the corresponding transient decrease of the TQ-potential. Reproduced with permission from Coronel et al.3 (B) Decrease of injury potential over time. Reproduced with permission from De Mello et al.4 Second, the ‘injury’ current critically depends on the electrical coupling between myocytes through gap junctions.4 The gap junctions start to close after about 30–40 min of ischaemia after which the current of ‘injury’ abates and the electrophysiological changes return to normal (‘healing over’).4 This phenomenon has been first described by Engelmann5 in 1877 and can take minutes to hours after the start of the injury (Figure 1). Thus, the contention that the degree of ST-segment elevation in combination with symptoms is a good predictor of TIMI-flow is not supported in all patients with transient ST-elevation. As expected, transient ST-elevation myocardial infarction is related to a small ischaemic zone size.1 Reperfusion can be derived from patency of the coronary artery during angiography, from coronary flow measurements, or from the occurrence of accelerated idioventricular rhythms or typical T-wave changes. Conflict of interest: none declared.