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Prognostic value of perfusion cardiovascular magnetic resonance with adenosine triphosphate stress in stable coronary artery disease.

ABSTRACT:

Background

Adenosine triphosphate (ATP) has been predominantly used in the Asia-Pacific region for stress perfusion cardiovascular magnetic resonance (CMR). We evaluated the prognosis of patients stressed using ATP, for which there are no current data.

Methods

We performed a retrospective longitudinal study from January 2016 to December 2020 and included 208 subjects with suspected obstructive coronary artery disease (CAD) who underwent ATP stress perfusion CMR. An inducible stress perfusion defect was defined as a subendocardial dark rim involving ≥ 1.5 segments that persisted for ≥ 6 beats during stress but not at rest. The primary outcome measure was a composite of major adverse cardiovascular events (MACE) including (1) cardiac death, (2) nonfatal myocardial infarction, (3) cardiac hospitalization, (4) late coronary revascularization. We compared outcomes in patients with and without perfusion defect using Kaplan-Meier and log rank tests. Significant predictors of MACE were identified using multivariable Cox regression analysis.

Results

Median follow-up was 3.3 years. Patients with no stress perfusion defect had a lower incidence of MACE (p < 0.001), including lower cardiac hospitalization (p = 0.004), late coronary revascularization (p = 0.001) and cardiac death (p = 0.003). Significant independent predictors for MACE were stress induced perfusion defect (p < 0.001, hazard ratio [HR] = 3.63), lower left ventricular ejection fractino (LVEF) (p < 0.001, HR = 0.96) and infarct detected by late gadolinium enhancement (LGE) (p = 0.001, HR = 2.92).

Conclusion

Perfusion defects on ATP stress are predictive of MACE which is driven primarily by cardiac hospitalization, late coronary revascularization and cardiac death. Significant independent predictors of MACE were stress induced perfusion defect, lower LVEF and infarct detected by LGE.

SUBMITTER: Ng MY

PROVIDER: S-EPMC8223349 | biostudies-literature |

REPOSITORIES: biostudies-literature

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