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Glycolipid dysregulation mediated Left ventricular diastolic dysfunction in coronary microvascular disease pathogenesis
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Abstract
Background: Ischemic heart disease (IHD) from coronary microvascular disease (CMVD) is key in non-obstructive coronary heart disease, and left ventricular diastolic dysfunction (LVDD) may link to CMVD via glycolipid dysregulation.
Objective: To explore LVDD-CMVD association and mediation by glycolipid dysregulation.
Methods: This study enrolled patients with chest pain and no obstructive coronary artery disease to explore glycolipid dysregulation -mediated LVDD triggers CMVD. Logistics regression model and linear correlation analysis were constructed to explore the associations between LVDD and CMVD. Restricted cubic splines were applied to further the associations of LVDD with CMVD. Given glycolipid dysregulation as intermediary factor, we investigate the mediating effects of LVDD on CMVD.
Results: 376 patients were eventually recruited and 222 patients were diagnosed with CMVD. In the multivariable-adjusted model, LVDD and glycolipid dysregulation including the triglyceride-glucose (TyG), triglyceride/high-density lipoprotein cholesterol (TG/HDL-C) and triglyceride/high-density lipoprotein (TG/HDL)were positively related to CMVD (Odds Ratio (OR)=2.18, 95% CI=1.03-4.60; OR=1.10, 95% CI=0.83-1.45; OR=0.82, 95% CI=0.58-1.14, respectively). Mediation analysis indicated that TyG mediated 4% of the association of LVDD with CMVD.
Conclusion: LVDD positively associates with CMVD, with TyG mediating this link, highlighting glycolipid dysregulation’s role in CMVD pathogenesis.
Title: Glycolipid dysregulation mediated Left ventricular diastolic dysfunction in coronary microvascular disease pathogenesis
Description:
Abstract
Background: Ischemic heart disease (IHD) from coronary microvascular disease (CMVD) is key in non-obstructive coronary heart disease, and left ventricular diastolic dysfunction (LVDD) may link to CMVD via glycolipid dysregulation.
Objective: To explore LVDD-CMVD association and mediation by glycolipid dysregulation.
Methods: This study enrolled patients with chest pain and no obstructive coronary artery disease to explore glycolipid dysregulation -mediated LVDD triggers CMVD.
Logistics regression model and linear correlation analysis were constructed to explore the associations between LVDD and CMVD.
Restricted cubic splines were applied to further the associations of LVDD with CMVD.
Given glycolipid dysregulation as intermediary factor, we investigate the mediating effects of LVDD on CMVD.
Results: 376 patients were eventually recruited and 222 patients were diagnosed with CMVD.
In the multivariable-adjusted model, LVDD and glycolipid dysregulation including the triglyceride-glucose (TyG), triglyceride/high-density lipoprotein cholesterol (TG/HDL-C) and triglyceride/high-density lipoprotein (TG/HDL)were positively related to CMVD (Odds Ratio (OR)=2.
18, 95% CI=1.
03-4.
60; OR=1.
10, 95% CI=0.
83-1.
45; OR=0.
82, 95% CI=0.
58-1.
14, respectively).
Mediation analysis indicated that TyG mediated 4% of the association of LVDD with CMVD.
Conclusion: LVDD positively associates with CMVD, with TyG mediating this link, highlighting glycolipid dysregulation’s role in CMVD pathogenesis.
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