Abstract
Background: Cardiovascular magnetic resonance (CMR) with late gadolinium enhancement (LGE) has emerged as a potential marker for risk of adverse events in patients with hypertrophic cardiomyopathy (HCM). However, previous studies have been limited to small cohorts with short follow-up periods and therefore the clinical significance of LGE in HCM remains uncertain.
Methods: Cine and contrast-enhanced CMR were performed on 594 HCM patients (49±16 years; 65% males). CMR scans were analyzed at a single data coordinating center. Mean follow-up was 3.5 ± 1.4 years.
Results: LGE was identified in 235 (40%) patients, occupying 10 ± 11% of LV myocardial volume. There was no statistically significant relationship between presence of LGE and a number of clinical end-points including all HCM-related adverse disease events (OR 1.64, 95% CI 0.99-2.70, p>0.05), progression to NYHA class III or IV or death from heart failure or stroke (OR 1.42, 95%CI 0.78-2.51, p=0.24), or sudden death (OR 1.89, 95% CI 0.78-4.55, p=0.16). However, when LGE was present a significant linear relation was evident between the extent of LGE and risk of progressive heart failure symptoms/cardiovascular death (OR 1.17/5% LGE, 95% CI 1.04-1.32; p<0.01) and sudden death (OR 1.20/5% LGE, 95%CI 1.04-1.40 p=0.016). HCM patients with extensive LGE ≥15% were at more than 3-fold higher risk of sudden death compared to patients with <15% or no LGE (OR 3.52, 95%CI 1.23-10.08, p=0.019). Multivariable analysis confirmed that extent of LGE was independently associated with an increased risk of sudden death (adj. OR 1.25/5% increase, p=0.02), even after controlling for traditional sudden death risk factors. The absence of LGE trended towards a low likelihood of experiencing HCM-related adverse events (adj. OR 0.59, 95% CI 0.34-0.99, p=0.052).
Conclusion: In patients with HCM, the amount of LGE (but not presence) was associated with an increased risk of HCM-related adverse events, including sudden death. Extensive LGE may represent a risk marker with the potential to arbitrate ambiguous decisions regarding ICD therapy. The absence of LGE is consistent with lower risk status and can be used to reassure patients.
Methods: Cine and contrast-enhanced CMR were performed on 594 HCM patients (49±16 years; 65% males). CMR scans were analyzed at a single data coordinating center. Mean follow-up was 3.5 ± 1.4 years.
Results: LGE was identified in 235 (40%) patients, occupying 10 ± 11% of LV myocardial volume. There was no statistically significant relationship between presence of LGE and a number of clinical end-points including all HCM-related adverse disease events (OR 1.64, 95% CI 0.99-2.70, p>0.05), progression to NYHA class III or IV or death from heart failure or stroke (OR 1.42, 95%CI 0.78-2.51, p=0.24), or sudden death (OR 1.89, 95% CI 0.78-4.55, p=0.16). However, when LGE was present a significant linear relation was evident between the extent of LGE and risk of progressive heart failure symptoms/cardiovascular death (OR 1.17/5% LGE, 95% CI 1.04-1.32; p<0.01) and sudden death (OR 1.20/5% LGE, 95%CI 1.04-1.40 p=0.016). HCM patients with extensive LGE ≥15% were at more than 3-fold higher risk of sudden death compared to patients with <15% or no LGE (OR 3.52, 95%CI 1.23-10.08, p=0.019). Multivariable analysis confirmed that extent of LGE was independently associated with an increased risk of sudden death (adj. OR 1.25/5% increase, p=0.02), even after controlling for traditional sudden death risk factors. The absence of LGE trended towards a low likelihood of experiencing HCM-related adverse events (adj. OR 0.59, 95% CI 0.34-0.99, p=0.052).
Conclusion: In patients with HCM, the amount of LGE (but not presence) was associated with an increased risk of HCM-related adverse events, including sudden death. Extensive LGE may represent a risk marker with the potential to arbitrate ambiguous decisions regarding ICD therapy. The absence of LGE is consistent with lower risk status and can be used to reassure patients.
Original language | English |
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Pages (from-to) | E1570 |
Number of pages | 1 |
Journal | Journal of the American College of Cardiology |
Volume | 59 |
Issue number | 13 Supplement |
Early online date | 25 Mar 2012 |
DOIs | |
Publication status | Published - 27 Mar 2012 |