Impaired Peripheral Microvascular Function and Risk of Major Adverse Cardiovascular Events in Patients With Coronary Artery Disease

Author:

Young An12,Garcia Mariana12,Sullivan Samaah M.1,Liu Chang1,Moazzami Kasra12,Ko Yi-An3ORCID,Shah Amit J.124ORCID,Kim Jeong Hwan2ORCID,Pearce Brad1,Uphoff Irina1ORCID,Bremner J. Douglas54ORCID,Raggi Paolo6ORCID,Quyyumi Arshed2ORCID,Vaccarino Viola12ORCID

Affiliation:

1. Department of Epidemiology (A.Y., MG., S.M.S., C.L., K.M., A.J.S., B.P., I.U., V.V.), Rollins School of Public Health, Emory University, Atlanta, GA.

2. Emory Clinical Cardiovascular Research Institute, Division of Cardiology (A.Y., M.G., K.M., A.J.S., J.H.K., A.Q., V.V.), Emory University School of Medicine, Atlanta, GA.

3. Biostatistics and Bioinformatics (Y.-A.K.), Rollins School of Public Health, Emory University, Atlanta, GA.

4. Atlanta VA Medical Center (A.J.S., J.D.B.).

5. Psychiatry and Behavioral Sciences (J.D.B.), Emory University School of Medicine, Atlanta, GA.

6. Mazankowski Alberta Heart Institute, University of Alberta, Canada (P.R.).

Abstract

Objective: In patients with stable coronary artery disease (CAD), the risk of major adverse cardiovascular events (MACE) remains elevated despite treatment. The role of microvascular dysfunction on MACE beyond traditional risk indicators and inflammation is not well established. We examined whether peripheral microvascular dysfunction is associated with MACE in patients with CAD. Approach and Results: Microvascular function was measured with the Reactive Hyperemia Index (RHI) using digital peripheral arterial tonometry in 546 patients with CAD, who were followed 7 years for incident MACE. The primary end point included cardiovascular death or myocardial infarction; the secondary end point included cardiovascular death, myocardial infarction, or heart failure hospitalization. Hazard models for competing risk were used to estimate the association between RHI and MACE adjusting for age, sex, race, traditional risk factors, medications, and CAD severity. We also examined the association of baseline interleukin-6, C-reactive protein, monocyte chemoattractant protein-1, and matrix metallopeptidase-9 with RHI. Mean age was 62±9 years. Mean RHI was 2.1±0.63. After adjustment, for each 1-SD decrease in RHI, there was a 40% increase in the primary end point (hazard ratio, 1.4 [95% CI, 1.1–1.9], P =0.01) and a similar increase in the secondary end point (HR, 1.3 [95% CI, 1.1–1.7], P =0.006). Inflammatory biomarker levels were associated with greater RHI impairment ( P <0.05) but did not affect the relationship between RHI and MACE. Conclusions: Peripheral microvascular dysfunction is associated with increased risk of MACE in patients with stable CAD, implicating the role of microvascular disease in the pathogenesis of adverse outcomes in patients with CAD.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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