News Release

Myocardial fibrosis identified as new therapeutic target

Obstructive sleep apnoea patients with myocardial fibrosis had poor cardiovascular outcomes

Peer-Reviewed Publication

European Society of Cardiology

Florence, Italy - 13 May 2016: Myocardial fibrosis could be a future therapeutic target after researchers found it correlated with adverse cardiovascular outcomes in patients with obstructive sleep apnoea (OSA) referred for cardiac magnetic resonance (CMR). The study was presented today at EuroCMR 2016 by Dr Yaron Fridman, a cardiology fellow at the Heart and Vascular Institute, University of Pittsburgh Medical Center in Pittsburgh, Pennsylvania, US.1

Dr Fridman said: "Fibrosis in the heart disrupts its normal architecture and function ultimately leading to cardiovascular morbidity and mortality. Patients with cardiovascular disease are at two to three times higher risk of having OSA. We hypothesised that quantifying myocardial fibrosis in patients with OSA could help identify those at increased risk of adverse cardiovascular outcomes."

The study included 1 094 patients who had been referred for CMR because of known or suspected heart disease. Of these, 324 had OSA and 770 did not have OSA. Sixteen healthy patients were included as a control group. Increased myocardial fibrosis was defined as an extracellular volume fraction (measured by CMR) of 30% or greater.

The investigators found that 30% of patients with OSA had a high degree of myocardial fibrosis. This was higher than healthy controls but similar to patients referred to CMR with known or suspected heart disease. After a median follow up of 2.3 years, there was no difference in the rates of heart failure hospitalisation or death between the OSA and non-OSA groups. However, in patients with OSA, myocardial fibrosis was significantly associated with increased event rates, even after adjusting for age, kidney function, myocardial infarction size, and ejection fraction. In fact, each 5% increase in extracellular volume fraction was associated with a 1.6 times higher risk of heart failure hospitalisation or death.

Dr Fridman said: "Myocardial fibrosis was prevalent in patients with OSA. We found that we could quantify the amount of myocardial fibrosis and stratify patients' risk of poor outcomes. This is a powerful and robust way of identifying OSA patients who may be at higher risk for adverse cardiovascular events."

"The findings are particularly exciting because they identify a potential imaging biomarker for a pathological process occurring in the myocardium itself," continued Dr Fridman. "When there is myocardial fibrosis and the extracellular matrix is abnormal, the myocardium is less able to tolerate the vascular, ischaemic and haemodynamic insults seen in patients with OSA."

Dr Fridman said the findings point the way towards a personalised approach to treating cardiovascular disease based on the patient's amount of myocardial fibrosis. "We need to go beyond the traditional way of classifying and treating patients," he said. "For example, no two patients with OSA are alike, and yet we treat them the same. We assume that OSA always has the same effect on the heart, but that may not be true."

Dr Fridman continued: "Our research suggests that we should characterise patients with OSA, and other conditions, in more detail by assessing their amount of myocardial fibrosis. That may help us to be more precise in our treatment."

Dr Fridman concluded: "Large clinical trials are needed to determine if using anti-fibrotic medications in patients with myocardial fibrosis identified by CMR improves cardiovascular outcomes. Ultimately, this is about better defining each patient's true risk and providing tailored treatment."

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Authors: ESC Press Office
Tel: +33 (0) 4 92 94 86 27
Email: press@escardio.org

Notes to editor

SOURCES OF FUNDING:  Dr Schelbert was supported by a grant from The Pittsburgh Foundation, Grant M2009-0068, and an American Heart Association Scientist Development grant (09SDG2180083) including a T. Franklin Williams Scholarship Award; funding provided by: Atlantic Philanthropies, Inc., the John A. Hartford Foundation, the Association of Specialty Professors, and the AHA. Dr. Wong was supported by a grant K12 HS19461-01 from the AHRQ.  

DISCLOSURES: Dr Fridman has no disclosures. Dr Schelbert has accepted contrast material from Bracco Diagnostics for research purposes beyond the scope of this work.

Notes

1Dr Fridman will present the abstract 'Myocardial Fibrosis is Prevalent in Obstructive Sleep Apnea and Associated with Hospitalization for Heart Failure or Death' during the session BEST Oral Abstracts which takes place on 13 May from 9:45 to 10:45 in the Main Auditorium.

About EuroCMR

EuroCMR is the annual CMR conference of the European Association of Cardiovascular Imaging (EACVI). The EuroCMR meeting has become the largest and most important CMR meeting in Europe with an increasing number of attendees, faculty and exhibitors from all over the world. http://www.escardio.org/Congresses-&-Events/Upcoming-congresses/EuroCMR/EuroCMR

About the European Association of Cardiovascular Imaging

The European Association of Cardiovascular Imaging (formerly EAE) is a registered branch of the ESC. Its aim is to promote excellence in clinical diagnosis, research, technical development, and education in cardiovascular imaging in Europe. http://www.escardio.org/The-ESC/Communities/European-Association-of-Cardiovascular-Imaging-EACVI/Welcome-to-EACVI

About the European Society of Cardiology

The European Society of Cardiology (ESC) represents more than 95 000 cardiology professionals across Europe and the Mediterranean. Its mission is to reduce the burden of cardiovascular disease in Europe. http://www.escardio.org/

Information for journalists attending EuroCMR 2016

EuroCMR 2016 takes place 12 to 14 May in Florence, Italy, at the Palazzo dei Congressi.

The full scientific programme is available here

http://eurocmr2016.medconvent.at/scientific.html

Journalists wishing to attend EuroCMR should email eurocmr@medconvent.at


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