Impaired subendocardial perfusion in patients with metabolic syndrome. (1st November 2021)

• Record Type: Journal Article
• Authors: Fantin, Francesco; Giani, Anna; Gasparini, Ludovico; Rossi, Andrea P; Zoico, Elena; Mazzali, Gloria; Zamboni, Mauro
• Is Part Of: Diabetes & vascular disease research. Volume 18:Number 6(2021)
• Publication Date: 2021-11-01
• Subjects: Arterial stiffness -- cardiovascular risk factors -- metabolic syndrome -- SEVR -- subendocardial perfusion; Diabetic angiopathies -- Periodicals; 616.462005
• DOI: 10.1177/14791641211047135
• Languages: English
• ISSNs: 1479-1641

Abstract

Background: Metabolic Syndrome (MS) is associated to vascular damage, increased arterial stiffness, and impaired myocardial perfusion. Subendocardial viability ratio (SEVR) is a noninvasive estimation of myocardial workload, oxygen supply, and perfusion. The aim of the study was to describe the relation between arterial stiffness, SEVR, and cardio-metabolic risk factors. Methods: A cohort of 55 patients, aged 59.9 ± 10.8 years, was studied; 28 subjects (50.9%) had metabolic syndrome. All patients underwent a clinical evaluation and blood venous sampling, to assess glico-lipid profile. Applanation tonometry was performed, to obtain pulse wave analysis and SEVR values. Results: In the overall study population, SEVR showed negative associations with mean (r = −0.301; p = 0.026) and systolic (borderline relation, r = −0.257; p = 0.058) arterial pressure. Metabolic syndrome patients presented lower level of SEVR ( p = 0.012), even after adjusting for age, sex, and mean arterial pressure ( p = 0.040). Subdividing the study population by the number of metabolic syndrome components, SEVR significantly decreased as the number of Metabolic Syndrome components increased ( p for trend 0.005). In a logistic backward regression analysis, both metabolic syndrome and mean arterial pressure resulted significant predictors of SEVR, accounting for 18% of variance. Conclusion: The reduced SEVR in metabolic syndrome patients could be an important pathophysiological determinant of the increased cardiovascular risk.