Focus Session
SCMR 22nd Annual Scientific Sessions
Alessia Pepe, MD, PhD
Cardiologist
Fondazione G. Monasterio CNR Regione Toscana
Cinzia Nugara, MD
Cardiologist
Università degli Studi di Palermo, Policlinico “Paolo Giaccone” and IRCSS centro neurolesi
Antonella Meloni, PhD
Biomedical Engineer
Fondazione G. Monasterio CNR Regione Toscana
Maria Vaccaro, MD
Cardiologist
Università degli Studi di Catania, Policlinico Vittorio Emanuele
Chrysanthos Grigoratos, MD
Cardiologist
Fondazione G. Monasterio CNR Regione Toscana
Giancarlo Todiere, MD
Cardiologist
Fondazione G. Monasterio CNR Regione Toscana
Andrea Barison, MD
Cardiologist
Fondazione G. Monasterio CNR Regione Toscana
Daniele De Marchi, MRT
Radiology Technician
Fondazione G. Monasterio CNR Regione Toscana
Giuseppina Novo, MD
Associate Professor
Università degli Studi di Palermo, Policlinico “Paolo Giaccone”
Giovanni Aquaro, MD
Cardiologist
Fondazione G. Monasterio CNR Regione Toscana
Background: Dipyridamole stress CMR provides detailed information on the key phases (perfusion and wall motion) of the ischemic cascade. Although the diagnostic value of stress CMR has been assessed, further studies are needed to evaluate its prognostic role at long-term, specifically using dipyridamole where no data are available to our knowledge. So, the aim of this study was to determine the long-term prognostic value of dipyridamole stress-CMR in patients with known or suspected coronary artery disease (CAD).
Methods:
Two hundred and forty-six consecutive patients (61 females, main age 61.96±10.05 years) who underwent dipyridamole stress-CMR in a high volume CMR Laboratory were considered. Abnormal wall motion at rest and after dipyridamole, perfusion at stress and at rest, and late gadolinium enhancement (LGE) were analysed.
End-points were "major non-fatal cardiac events" (ventricular arrhythmias, coronary syndromes, heart failure hospitalization ) and cardiac death.
Results:
The Table shows the baseline data for all patients.
An abnormal stress CMR was found in 65 (26.4%) patients; 39 patients had a reversible stress perfusion defect in at least one myocardial segment and 26 a reversible stress perfusion defect plus worsening of stress wall motion in comparison with rest.
During a median follow up of 60.59 months (IQ range 41.98 months), 69 patients (28.0%) experienced major nonfatal cardiac events. LGE, reversible perfusion deficit, age, diabetes and family history were univariate prognosticators. In the multivariate analysis the independent predictive factors were reversible perfusion deficit (hazard ratio-HR=2.21, P=0.001) and diabetes (HR=2.21, P=0.003).
Ten patients died during follow-up and reversible motion abnormality and LGE were univariate prognosticators. At multivariate analysis, LGE remained a significant prognosticator (HR=10.83, P=0.026), after adjusting for age and diabetes.
When the composite end-point (cardiac events + death) was considered, both myocardial fibrosis and reversible perfusion deficit resulted to be significant univariate prognosticators, in addition to age, diabetes and family history. At multivariate analysis the independent predictive factors were reversible perfusion deficit (HR=2.26, P<0.0001) and diabetes (HR=2.59, P<0.0001) (Figure 1).
Conclusion:
Reversible perfusion deficit and diabetes identify patients at high risk of fatal and non fatal cardiac events. LGE is a strong predictor for death in patients with known or suspected CAD.