Premature Ventricular Contraction percentage predicts new Systolic Dysfunction and clinically diagnosed CHF and overall Mortality
Reporter: Aviva Lev-Ari, PhD, RN
Cardiovascular Health Study (CHS)
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To determine the extent to which known risk factors predict coronary heart disease and stroke in the elderly, to assess the precipitants of coronary heart disease and stroke in the elderly, and to identify the predictors of mortality and functional impairments in clinical coronary disease or stroke.
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https://clinicaltrials.gov/ct2/show/NCT00005133?term=Cardiovascular+Health+Study&rank=2
Although links between frequent PVCs and ongoing heart failure have been observed, the current analysis, based on a cohort from the Cardiovascular Health Study (CHS), provides “the first evidence that PVC percentage predicts new systolic dysfunction, as well as clinically diagnosed CHF and overall mortality,” say the authors in their report, published in the July 14, 2015 issue of the Journal of the American College of Cardiology. It also raises the issue of whether PVCs might sometimes be an appropriate target for treatments aimed at preventing heart failure.
The observational study can’t demonstrate causality, note the authors, led by Dr Jonathan W Dukes (University of California, San Francisco). But overall, the findings “suggest that PVCs might be an important cause of occult or ‘idiopathic’ cardiomyopathy and might be an important determinant of incident CHF among those with other established CHF risk factors.”
Ablate PVCs in HF, LVEF Can Improve
“There’s this general notion that PVCs are very benign, which is certainly what I was taught, even in my general cardiology fellowship, before the more recent data that came out of the electrophysiology labs,” senior author Dr Gregory M Marcus (UCSF) said in an interview with heartwire from Medscape.
In recent years, he said, it’s been appreciated that ablation of PVCs in patients with lots of them can improve quality of life by alleviating symptoms such as syncope. And there are series of patients with PVCs and primarily nonischemic cardiomyopathy in the EP literature suggesting that “if you ablate those PVCs, their heart failure improves and often their reduced ejection fraction normalizes,” according to Marcus. “Many of us have seen that and witnessed it firsthand in many of our own patients.”
Although the analysis tried to control for such factors, she said, the question remains “whether PVCs are causing deterioration in EF and HF or if they are simply a marker of underlying disease. If the former is true, then treating PVCs would help. But if the latter is true, then treating PVCs may not make a difference.”
Marcus acknowledges that PVCs may be simply a risk marker in people with sick hearts. “But even if that’s the case, I think it’s potentially a very useful marker.” He said he hopes the report will help “motivate future research in potentially two different directions. One, might ablation be an effective therapy to prevent heart failure in the right patients? Alternatively, could this be used to help predict heart failure and implement other strategies, such as beta-blockers, to prevent heart failure in those patients?”
CASTing a New Light on Treatment of PVCs
The Cardiac Arrhythmia Suppression Trial (CAST), Marcus noted, “taught us a lot of important lessons. More generally, it was a great example of the need to look at hard outcomes rather than secondary or surrogate outcomes.”
As cardiology textbooks have since noted, CAST randomized about 2300 patients who had asymptomatic or only mildly symptomatic PVCs after acute MI to receive one of three antiarrhythmic agents or placebo. The drugs, which included the class Ic agents encainide and flecainide, were mostly effective at suppressing PVCs. But over a mean 10 months of follow-up, patients who had received those drugs showed steep rise in rate of arrhythmic death (the primary end point) as well as nonfatal cardiac arrest, almost certainly due to proarrhythmic effects.
The widely learned lesson: post-MI suppression of PVCs, a surrogate for the pathology behind sudden cardiac death in ischemic heart disease, doesn’t lower its risk; in fact, treatment of surrogate markers can make things a lot worse. (Importantly, CAST was conducted in the early days of arrhythmia ablation and implantable defibrillators, which were not options for its patients.)
As a result, according to Marcus, class Ic agents are generally avoided in patients with structural heart disease. “I think that while the proarrhythmic effects of those drugs were known, they weren’t fully appreciated, and CAST taught us to be wary of them.”
The CHS is sponsored by the National Heart, Lung, and Blood Institute. Dukes and Marcus report that they have no relevant financial relationships; disclosures for the other authors are in the report. Santangeli and Marchlinski report that they have no relevant financial relationships. Al-Khatib says she has no relevant financial relationships with industry.
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