Key result
Late gadolinium enhancement extent ≥ 45% of left ventricular mass independently predicted all-cause mortality and new-onset heart failure (HR 5.25) in patients with stable coronary artery disease.
Why the study?
Does the extent of late gadolinium enhancement (LGE) by CMR predict adverse cardiac outcomes beyond conventional risk factors, including LVEF, in patients with stable coronary artery disease?
Observational (n=376)
No
Does the extent of late gadolinium enhancement (LGE) by CMR predict adverse cardiac outcomes beyond conventional risk factors, including LVEF, in patients with stable coronary artery disease?
Late gadolinium enhancement assessed by CMR is a robust independent predictor of mortality and heart failure in stable CAD patients, providing complementary prognostic value to left ventricular ejection fraction.
Answers are grounded in this paper and cite their sources.
May refine risk stratification beyond LVEF in stable CAD; extends observational data but leaves adoption open pending trials.
BACKGROUND: Late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR) predicts adverse prognosis in patients with stable coronary artery disease (CAD). However, the interaction with conventional risk factors remains uncertain. Our aim was to assess whether the extent of LGE is an independent predictor of adverse cardiac outcome beyond conventional risk factors, including left ventricle ejection fraction (LVEF). METHODS: We enrolled 376 patients (88% males, 64 ± 11 years) with stable CAD, who underwent LGE assessment and a detailed conventional evaluation (clinical and pharmacological history, risk factors, ECG, Echocardiography). During a follow-up of 38 ± 21 months, 56 events occurred (32 deaths, 24 hospitalizations for heart failure). RESULTS: LGE and LVEF showed the strongest univariate associations with end-points (HR: 13.61 [95%C.I.: 7.32-25.31] for LGE ≥ 45% of LV mass; and 12.34 [6.80-22.38] for LVEF ≤ 30%; p < 0.0001). Multivariate analysis identified baseline LVEF, loop diuretic therapy, moderate-severe mitral regurgitation and pulmonary hypertension as significant predictors among conventional risk factors. According to a step-wise approach, LGE showed strong association with prognosis as well (5.25 [2.64-10.43]; p < 0.0001). LGE significantly improved the model predictability (chi-square 239 vs 221, F-test p < 0.0001) with an additive effect on the prognostic power of LVEF, which however retained its prognostic power (4.89 [2.50-09.56]; p < 0.0001). Patients with LGE ≥ 45% and/or LVEF ≤ 30% had much worse prognosis compared to patients without risk factors (annual event rates of 43% vs 3%; p < 0.0001). Interestingly LGE was a significant predictor when all cause mortality was analyzed as the only endpoint. CONCLUSIONS: This study demonstrates that LGE assessed by CMR is a robust independent non-invasive marker of prognosis in stable CAD patients. LGE can integrate the available metrics to substantially improve risk stratification.
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Catalano et al. (2012) conducted an observational in stable coronary artery disease (n=376). Late gadolinium enhancement (LGE) ≥ 45% of LV mass vs. LGE < 45% of LV mass was evaluated on Composite of all-cause mortality and new onset heart failure requiring hospitalization (HR 5.25, 95% CI 2.64-10.43, p=<0.0001). Late gadolinium enhancement extent ≥ 45% of left ventricular mass independently predicted all-cause mortality and new-onset heart failure (HR 5.25) in patients with stable coronary artery disease.
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