# Impact of Coronary Microvascular Dysfunction on Left Ventricular Function After Percutaneous Coronary Intervention: Assessment With Combined Dipyridamole‐Exercise Stress and Myocardial Strain/Work

**Authors:** Wanyu Zhao, Xiaoli Dong, Xiangyu Ji, Jiong Tang, Lin Ding, Yunfei Zhou, Shuanglan Yu, Jian Li, Haibo Li, Chunfang Yang, Qiuzhe Guo, Zhiling Luo, Yan Shen

PMC · DOI: 10.1111/echo.70419 · 2026-03-18

## TL;DR

This study shows that impaired coronary microvascular function after heart procedures leads to worse heart function and quality of life.

## Contribution

The study introduces a combined stress echocardiography and strain/work analysis method to assess post-PCI left ventricular function.

## Key findings

- Lower coronary flow velocity reserve (CFVR) was linked to reduced global longitudinal strain and work efficiency.
- CMD after PCI correlated with worse 1-year quality of life scores on the Seattle Angina Questionnaire.
- Peak exercise global constructive work and recovery wasted work were independent predictors of CMD.

## Abstract

Coronary microvascular dysfunction (CMD) persists after percutaneous coronary intervention (PCI) in individuals with coronary artery disease (CAD). This study assessed CMD using combined dipyridamole‐exercise stress echocardiography (DExE) and myocardial strain/work to evaluate the impact on left ventricular (LV) function.

This prospective study enrolled CAD individuals who underwent left anterior descending artery PCI and DExE assessment at 3 months post‐PCI to evaluate myocardial strain/work parameters at rest and stress. The primary endpoint was adverse clinical events, and the secondary endpoint was Seattle Angina Questionnaire (SAQ) health status at 1‐year.

The cohort comprised 84 individuals (54 ± 10 years, 17.9% female). Participants were stratified into two groups by coronary flow velocity reserve (CFVR): CFVR ≥ 2.5 group (n = 63) and CFVR < 2.5 group (n = 21). Compared with the CFVR ≥ 2.5 group, the CFVR < 2.5 group showed impaired LV functional reserve, with lower global longitudinal strain (GLS), global work index (GWI), and global work efficiency (GWE) at peak exercise and recovery, lower peak exercise global constructive work (GCW), higher recovery global wasted work (GWW), and smaller absolute changes ΔE—R (difference before vs. after exercise stress) in GLS, GWI, and GCW (all p < 0.05). In multivariable analysis, peak exercise GCW, recovery GWW, and ΔGCW (E − R) were independent predictors of CMD. At 1 year, no adverse clinical events occurred, and the CFVR ≥ 2.5 group had higher SAQ physical limitation (92.86 ± 11.38 vs. 82.14 ± 17.93), quality of life (95.63 ± 10.57 vs. 83.33 ± 19.90), and summary score (94.05 ± 8.51 vs. 85.71 ± 15.71) than the CFVR < 2.5 group (all p < 0.05).

Combined DExE with myocardial strain/work analysis effectively evaluates LV function in CMD. Decreased CFVR post‐PCI is associated with impaired LV function and worse 1‐year quality of life outcomes, underscoring the need for close cardiac function monitoring in post‐PCI CMD individuals.

URL: https://www.chictr.org.cn/; Unique identifier: ChiCTR2500103229.

Decreased coronary flow velocity reserve (CFVR) was correlated with left ventricular (LV) dysfunction after percutaneous coronary intervention (PCI), as assessed via dipyridamole‐exercise stress echocardiography (DExE). This dysfunction was characterized by lower myocardial strain/work index and worse 1‐year Seattle Angina Questionnaire (SAQ) scores.

## Linked entities

- **Diseases:** coronary artery disease (MONDO:0005010)

## Full-text entities

- **Genes:** ACE (angiotensin I converting enzyme) [NCBI Gene 1636] {aka ACE1, CD143, DCP, DCP1}, AP2B1 (adaptor related protein complex 2 subunit beta 1) [NCBI Gene 163] {aka ADTB2, AP105B, AP2-BETA, CLAPB1}
- **Diseases:** LAD (MESH:D020759), CFVR (MESH:D003323), stenosis (MESH:D003251), intracardiac shunt (MESH:C562451), stable angina (MESH:D060050), -elevation (MESH:D006937), dyspnea (MESH:D004417), epicardial ischemia (MESH:D007511), cardiomyopathy (MESH:D009202), microvascular angina (MESH:D017566), EAE (MESH:D004675), CAD (MESH:D003324), NSTEMI (MESH:D000072657), ACS-UA (MESH:D054058), stroke (MESH:D020521), unstable angina (MESH:D000789), nausea (MESH:D009325), dizziness (MESH:D004244), spasm (MESH:D013035), cardiac dysfunction (MESH:D006331), Diseases (MESH:D004194), myocardial mechanical abnormalities (MESH:D041781), cardiac death (MESH:D003643), coronary steal phenomenon (MESH:D013349), heart failure (MESH:D006333), fever (MESH:D005334), ischemic lesions (MESH:D017202), valvular disease (MESH:D006349), LV dysfunction (MESH:D018487), inflammation (MESH:D007249), thrombosis (MESH:D013927), arrhythmias (MESH:D001145), hyperemia (MESH:D006940), endothelial dysfunction (MESH:D014652), atrial fibrillation (MESH:D001281), MI (MESH:D009203), ischemic (MESH:D002545), chest tightness (MESH:D002637), Angina (MESH:D000787), motion abnormalities (MESH:D009041), coronary artery stenosis (MESH:D023921), myocardial strain (MESH:D013180), atrial or ventricular premature beats (MESH:D018879), CMD (MESH:D003327)
- **Chemicals:** aminophylline (MESH:D000628), CFVR (-), oxygen (MESH:D010100), Dipyridamole (MESH:D004176)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Mutations:** A4C

## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12998498/full.md

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Source: https://tomesphere.com/paper/PMC12998498