Author + information
- Karolina Zareba,
- Timothy Wong,
- Peter Kellman,
- Kayla Piehler,
- Kathie Lin,
- Kathy S. Puntil,
- Sanjeev Shroff and
- Erik Schelbert
Myocardial fibrosis expands the extracellular matrix (ECM) adversely affecting mechanical, electrical, and vasomotor function. We quantified ECM expansion, evaluated its association with mortality in the non-ischemic patient population, and assessed the impact of renin angiotensin aldosterone system (RAAS) inhibition on ECM expansion.
We studied 843 consecutive patients presenting for cardiovascular magnetic resonance (CMR) without evidence of coronary artery disease or amyloidosis. We computed extracellular volume fraction (ECV) from measures of hematocrit and pre- and post-contrast (0.2 mmol/kg gadoteridol bolus) T1 measures of myocardium and blood using modified Look-Locker inversion recovery (MOLLI) pulse sequences.
There were 37 deaths over a median follow-up of 1.3 (IQR 0.8-1.8) years. ECV ranged from 18 to 48%. In multivariable Cox regression models ECV was the strongest predictor of all-cause mortality (HR 1.56, 95%CI 1.29-1.88 per 3% increase), stratifying by gender and late gadolinium enhancement and further adjusting for ejection fraction, age, and diabetes. RAAS inhibition was associated with 0.7% lower ECV in multivariable linear regression models (t value 2.2, p=0.04) after extensive risk adjustment.
ECV predicts mortality in the non-ischemic patient population. ECV can detect the effects of RAAS inhibition on ameliorating ECM expansion. ECV may be a novel tool to stratify risk and monitor response to treatment.
Moderated Poster Contributions
Poster Sessions, Expo North
Saturday, March 09, 2013, 10:00 a.m.-10:45 a.m.
Session Title: Imaging: MRI II Clinical Outcomes and CMR
Abstract Category: 19. Imaging: MRI
Presentation Number: 1138M-315
- 2013 American College of Cardiology Foundation