The central role of conventional 12-lead ECG for the assessment of microvascular obstruction after percutaneous myocardial revascularization

Abstract

Guidelines report that the optimal treatment for ST-elevation myocardial infarction (STEMI) is a primary percutaneous coronary intervention (PPCI) when performed timely by trained operators. Yet, the reopening of the infarct-related artery (IRA) is not always followed by myocardial reperfusion. This phenomenon is most commonly called “no-reflow”, is caused by microvascular obstruction (MVO) and is associated to a worse outcome. Electrocardiogram (ECG) is crucial for the diagnosis of STEMI, but is also useful for the assessment of MVO. In this review we summarize ECG-derived parameters associated to MVO and their prognostic relevance.

Introduction

The most effective treatment for ST segment elevation acute myocardial infarction (STEMI) includes timely myocardial revascularization by pharmacological (fibrinolysis) or mechanical (primary percutaneous coronary intervention, or PPCI) interventions, which allow salvage of myocardium at risk [1], [2]. Yet recanalization of the infarct-related artery (IRA) is not followed by myocardial reperfusion in a definite proportion of patients. This phenomenon, commonly known as “no-reflow”, is caused by microvascular obstruction (MVO) [3]. MVO has been documented in about 30%–50% of patients undergoing successful PPCI [4], [5], [6] and, occasionally, also during elective PCI, particularly when performed on vein grafts [7] or in the setting of unstable angina [8]. The pathogenesis of MVO is complex, and can be caused by a variable combination of: 1) ischemic injury, 2) reperfusion injury [9], and 3) distal embolization of debris from plaque and/or thrombus during PCI [10], [11]. Furthermore, individual predisposing factors are likely to play a relevant role in its occurrence [12]. In particular, patients with MVO present more frequently the 1976 T > C polymorphism of the adenosine 2A receptors gene [13] and a more compact fibrin network [14]. Moreover, several studies carried out in humans and in animal models [15], [16] suggest that acquired risk factors such as diabetes and hypercholesterolemia might predispose to MVO. Patients presenting MVO have a worse outcome, including a higher rate of death and re-infarction [12]. Accordingly, it is important to identify these patients as early as possible, as they might benefit from a more aggressive pharmacological treatment, although no therapy has hitherto been shown consistently effective in improving or preventing MVO [17]. Notably, MVO has been reported to spontaneously improve in a few days after revascularization in a proportion of STEMI patients, and this improvement is associated with a better left ventricular remodelling [17], [18], [19], [20].

MVO can be diagnosed by coronary angiography or by non invasive imaging techniques, including myocardial contrast echocardiography (MCE) and cardiovascular magnetic resonance (CMR). MCE uses ultrasound to visualize contrast microbubbles that freely flow within patent microcirculation and MVO is detected as lack of intramyocardial contrast opacification. CMR, using gadolinium to assess regional cardiac perfusion, diagnoses MVO as: 1) lack of gadolinium enhancement during first pass; and 2) lack of gadolinium enhancement within a necrotic region, identified by late gadolinium hyper-enhancement [21]. These techniques, however, are usually not readily available, require specific expertise and are very expensive [21], [22], [23], [24], [25].

Several studies have suggested that a simple serial electrocardiogram (ECG) analysis can be very helpful to identify patients with persistent MVO within STEMI patients treated by PPCI [26], [27], [28], [29]. Furthermore, some ECG abnormalities that suggest the presence of MVO have been shown to be helpful for risk stratification.

Fig. 1 shows the most important diagnostic features of patients presenting MVO detectable by invasive and non-invasive imaging techniques.

In this report we review the evidence for the accuracy of 12-lead ECG in the detection of MVO and its impact on patient’s management.