Key result
Endothelial and microvascular dysfunction frequently affect non-culprit arteries in patients with STEMI, potentially altering hyperemic physiological indices and highlighting the need for further validation of resting indices.
Why the study?
Non-culprit artery physiology in STEMI is complex, and microvascular and endothelial dysfunction may affect prognosis and interfere with physiological stenosis assessment.
This review highlights the complex physiology of non-culprit arteries in STEMI patients, emphasizing the prognostic implications of microvascular and endothelial dysfunction and the challenges in assessing stenosis severity.
Alerts clinicians to microvascular dysfunction complicating non-culprit assessment in AMI; extends revascularization strategy research beyond angiography.
Approximately 30-50% of patients with ST-segment elevation acute myocardial infarction have multivessel disease. The physiology of the non-culprit artery (NCA) is complex and represents a challenge to physicians as, while these plaques are presumably stable, clinical data show that they frequently lead to major adverse cardiovascular events. In addition the presence of microvascular and endothelial dysfunction may have prognostic implications and interfere with current physiological indices for stenosis severity assessment. In this review we aim to summarize current methods to study the microcirculation, discuss the evidence available regarding the endothelium and the microvascular compartment of the NCA; the best strategies to perform a complete revascularization based on proven ischemia; real limitations associated to hyperemic stenosis indices; and the potential role of novel resting-indices in this specific acute context.
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Díez‐Delhoyo et al. (2019) conducted a review in ST-segment elevation acute myocardial infarction with multivessel disease. Physiological assessment of non-culprit coronary arteries was evaluated. Endothelial and microvascular dysfunction frequently affect non-culprit arteries in patients with STEMI, potentially altering hyperemic physiological indices and highlighting the need for further validation of resting indices.
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