Abstract
BackgroundMicrovascular dysfunction in the setting of ST-segment myocardial infarction (STEMI) is thought to be related to stress-related metabolic changes, including acute glucose intolerance. The aim of this study was to assess the relationship between admission glucose levels and microvascular function in non-diabetic STEMI patients.Methods92 consecutive patients with a first anterior-wall STEMI treated with primary percutaneous coronary intervention (PPCI) were enrolled. Blood glucose levels were determined immediately prior to PPCI. After successful PPCI, at 1‑week and 6‑month follow-up, Doppler flow was measured in culprit and reference coronary arteries to calculate coronary flow velocity reserve (CFVR), baseline (BMR) and hyperaemic (HMR) microvascular resistance.ResultsThe median admission glucose was 8.3 (7.2–9.6) mmol/l respectively 149.4 mg/dl [129.6–172.8] and was significantly associated with peak troponin T (standardised beta coefficient [std beta] = 0.281; p = 0.043). Multivariate analysis revealed that increasing glucose levels were significantly associated with a decrease in reference vessel CFVR (std beta = −0.313; p = 0.002), dictated by an increase in rest average peak velocity (APV) (std beta = 0.216; p = 0.033), due to a decreasing BMR (std beta = −0.225; p = 0.038) in the acute setting after PPCI. These associations disappeared at follow-up. These associations were not found for the infarct-related artery.ConclusionElevated admission glucose levels are associated with impaired microvascular function assessed directly after PPCI in first anterior-wall STEMI. This influence of glucose levels is an acute phenomenon and contributes to microvascular dysfunction through alterations in resting flow and baseline microvascular resistance.
Highlights
It is well recognised that even after rapid and successful revascularisation of ST-segment elevation myocardial infarction (STEMI), myocardial tissue perfusion remains compromised in 30–40% of patients despite restored epicardial patency [1, 2]
Elevated admission glucose levels are associated with impaired microvascular function assessed directly after primary percutaneous coronary intervention (PPCI) in first anterior-wall STEMI
Major stress-related metabolic changes occur in the first hours after ST-segment elevation myocardial infarction (STEMI), leading to glucose intolerance in some patients Elevated glucose levels and glucose intolerance are associated with an increased risk of mortality, heart failure and cardiogenic shock and no-reflow phenomenon in the culprit vessel Elevated admission glucose levels in the setting of STEMI are associated with impaired microvascular function in non-culprit vessels at baseline Larger STEMI’s with higher Troponin T levels are associated with higher glucose levels, which may be associated with microvascular dysfunction in non-culprit vessels
Summary
It is well recognised that even after rapid and successful revascularisation of ST-segment elevation myocardial infarction (STEMI), myocardial tissue perfusion remains compromised in 30–40% of patients despite restored epicardial patency [1, 2] This phenomenon is attributed to microvascular dysfunction in the setting of acute STEMI [3], which is observed in both the perfusion territory of the culprit artery, and in non-ischaemic regions remote from the infarcted myocardial tissue [4]. In patients with STEMI, hyperglycaemia is associated with the no-reflow phenomenon in the culprit vessel, postulated to be a proxy of microvascular dysfunction [10] It suggests that the acute metabolic changes in STEMI may contribute to microvascular dysfunction in this setting through alterations in glucose homeostasis. After successful PPCI, at 1-week and 6-month followup, Doppler flow was measured in culprit and reference coronary arteries to calculate coronary flow velocity reserve (CFVR), baseline (BMR) and hyperaemic (HMR) microvascular resistance
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