LONDON – Persistent mechanical dyssynchrony in patients with heart failure with reduced ejection fraction and a narrow QRS width appears to be a new marker of heightened risk.
That’s the key take-away message of an update of the EchoCRT trial presented by Dr. John Gorcsan III at the annual congress of the European Society of Cardiology.
Dr. John Gorcsan III
EchoCRT was a large, multicenter randomized trial of cardiac resynchronization therapy (CRT) in patients with severely symptomatic heart failure with a QRS width of less than 130 ms, a left ventricular ejection fraction of 35% or less, and echocardiographic evidence of dyssynchrony. It was a negative study, with no improvement in rates of death or heart failure hospitalizations noted with CRT turned on versus off (N Engl J Med. 2013 Oct 10;369[15]:1395-405).
However, this still left open the question of the clinical significance of mechanical dyssynchrony in such patients. Dr. Gorcsan and coinvestigators conducted a secondary subgroup analysis of 614 EchoCRT participants with baseline and 6-month echocardiograms in order to provide the answer.
“Our hypothesis was that persistent or worsening dyssynchrony is associated with unfavorable outcomes,” explained Dr. Gorcsan, professor of medicine and director of echocardiography at the University of Pittsburgh.
This indeed turned out to be the case. Three-quarters of patients experienced persistent or worsening dyssynchrony as measured by tissue Doppler or speckle-tracking radial strain delay during 6 months of follow-up, and they were 1.54-fold more likely to experience the combined primary endpoint of death or heart failure hospitalization, compared with the 25% of patients who experienced improvement in their dyssynchrony.
Moreover, even after statistical adjustment for potential confounders including baseline QRS width, ejection fraction, and left ventricular end-diastolic diameter, persistent or worsening dyssynchrony at 6 months remained associated with a 1.57-fold increased likelihood of heart failure hospitalization.
CRT being turned on or off had no impact on whether a patient’s dyssynchrony improved or not during follow-up.
“We hypothesize that a reason for improvement in dyssynchrony may be in part due to favorable left ventricular reverse remodeling – 97% of patients were on a beta-blocker and 95% were on an ACE inhibitor or angiotensin receptor blocker – but the precise mechanism remains uncertain,” Dr. Gorcsan observed.
Simultaneous with Dr. Gorcsan’s presentation, the clinical update of the EchoCRT trial was published online (Eur Heart J. 2015 Aug 30. doi: 10.1093/eurheartj/ehv418).
Dr. Scott D. Solomon
In an accompanying editorial, Dr. Amil M. Shah and Dr. Scott D. Solomon of Brigham and Women’s Hospital, Boston, said the new EchoCRT findings suggest mechanical dyssynchrony is a risk factor – a marker of progressive contractile dysfunction – but not a viable treatment target. That’s worth bearing in mind because mechanical dyssynchrony is now under consideration as a potential therapeutic target in patients with heart failure with preserved ejection fraction and other populations with conditions other than those addressed in EchoCRT (Eur Heart J. 2015 Aug 30. doi: 10.1093/eurheartj/ehv458).
The EchoCRT trial was sponsored by Biotronik. Dr. Gorcsan reported receiving research grants from Biotronik, GE, Medtronic, and St. Jude.