PVCs: Modifiable Risk Factor for Heart Failure . . . Maybe

John Mandrola


August 13, 2015

A colleague recently asked me how I would approach an asymptomatic young patient with thousands of premature ventricular complexes (PVCs). She said, "I used to think I knew how to treat PVCs, but after reading a recent study in the Journal of the American College of Cardiology[1] about the dangers of PVCs, I am confused."

PVCs are a common and vexing problem. PVCs cause symptoms, but more important, the aberrations induce fear in both patient and doctor. Fear is bad. In the US healthcare culture, fear sets the stage for overtreatment.

The established approach to patients with ventricular ectopy turns on associated disease. What company do the PVCs keep? Old teaching had it that PVCs in the setting of a normal heart were benign and PVCs in the setting of heart disease were mere markers of the disease. Seeing PVCs as nonmodifiable stems from the well-known failure of antiarrhythmic drugs to modify outcomes in patients with MI and heart failure.

Times may be changing. Drugs are out; ablation is in. New revelations, specifically, the improvement of LVEF after successful ablation of high-burden PVCs,[2,3] raises the possibility that the aberrant beats may be both a marker of early cardiomyopathy and a modifiable factor in heart failure. Maybe.

A study published in the Journal of the American College of Cardiology tempts us to think anew about ventricular ectopy. But let's think slowly.

The Study

Dr Jonathon Dukes (University of California, San Francisco) and colleagues used a subset of the Cardiovascular Health Study (CHS) to investigate PVC frequency as a predictor of decreased left ventricular ejection fraction, incident heart failure, and death.

For this analysis, 842 subjects (age >65) had both 24-hour Holter monitor recordings and serial echocardiograms. All subjects had normal EFs at the beginning of the study. This allowed researchers to look at the association of ventricular arrhythmia with future heart failure or death over the decade-long follow-up.

PVC percentage associated with a decrease in LVEF, incident CHF, and mortality. The associations met statistical significance, but the adjusted hazard ratios were modest: 1.13 for decreased EF, 1.06 for incident CHF, and 1.04 for mortality. The sensitivity of PVC burden as a predictor of CHF was low (many patients without PVCs developed CHF), but the specificity was over 90%. When dividing PVC burden into quartiles from low to high frequency, the researchers found subjects in the highest burden (compared with lowest burden) had more than a threefold greater risk of lower EF. CHF risk attributable to PVCs was estimated at 8%—similar to traditional risk factors such as high body-mass index (BMI), hypertension, and diabetes.

In the discussion section, the authors speculate that PVCs might be an important cause of occult cardiomyopathy. They tell us that other population-based studies,[4,5] have found similar relationships between ventricular ectopy and future risk. They urge us to think of PVCs as a risk factor (like hypertension or obesity) that we might be able to modify to help prevent future heart failure—which is a big deal given that CHF currently afflicts millions of Americans.


In a related editorial,[6] Drs Pasquale Santangeli and Francis Marchlinksi (University of Pennsylvania, Philadelphia) cite Friedrich Nietzsche in their lead and urge the EP community not to dismiss these findings because of the poor results of drug-induced PVC suppression.

They argue that advanced diagnostic tests, such as cardiac MRI and detailed electroanatomic mapping, may allow for tailoring of therapy in individual patients. Some patients, for instance, may have a focal area of scar that is amenable to ablation. They cite intriguing work from their lab[7] showing that some areas of abnormal electrograms seen during an ablation procedure may not show up as scar on MRI scans. This observation suggests the possibility of diffuse microscopic fibrotic process, poor cell-to-cell coupling, and/or myocyte disarray in patients with cardiomyopathy and ventricular ectopy. (I've seen this in an endurance athlete. MRI, echo, and cath were normal, but there was a large area of abnormal electrograms in the perivalvular right ventricle.)

You can tell these two experienced ablationists are not intimidated with placing catheters and burns in the human ventricle: "Clearly, the time to reexplore this important issue has arrived, particularly in light of the effectiveness and low-risk nature of ventricular premature depolarization elimination with catheter-ablation techniques," they write.


Consider first why ventricular ectopy bothers us? It's because we know it's not normal. It's better not to have PVCs, just as it's better not to have AF.

The challenge of treating patients with PVCs is balancing the risk of the treatment against the disease. We learned that lesson the hard way with antiarrhythmic drugs.

I am all for busting dogma, but we must think slowly. This observational study and its persuasive editorial from leaders in the field tempt us to overreach.

The bias of ablation is strong. Most electrophysiologists see ablation as better than drugs because of the beautiful cases. Miserable patients with thousands of PVCs cured with a single lesion; heart failure averted by an ablation of an aberrant focus; ICD patients freed from shocks. The joy of cure powers our spirit but clouds our mind. It's easy to forget those who had complications—the dissected aorta, the inadvertent coronary injury or AV block, the perforation requiring surgery, or the stroke.

Yes, ablation works in selected patients, in symptomatic patients, in patients with objective evidence of harm from the arrhythmia. And, yes, some patients with ectopy have something going on at the cardiac myocyte level.

In light of massive gains in EP technology, ventricular ectopy warrants further study. I love the suggestion from Santangeli and Marchlinksi that we should compare those patients who have high PVC burden and no cardiomyopathy with those who have lesser PVC burden and muscle disease. There is much to learn about what determines why some patients live in harmony for decades with their funny-looking ECGs while other develop dangerous heart disease.

Until we learn more, and until all operators move catheters with the skill of Santangeli and Marchlinksi, it seems best to rely on three basic rules of doctoring.

The first rule is that if a patient tells you she is well, our chief job is not messing that up. Staying true to the do-no-harm rule is easier when we see the person before us rather than aberrations on an ECG.

A second rule: it does no good to create fear. I believe we can be vigilant without inducing fear. We can follow patients with PVCs without shackling them to a disease.

Then there is Voltaire's rule: "The art of medicine consists of amusing the patient while nature cures the disease."We increase the odds of nature helping us when we prescribe that patients go to sleep on time, eat healthy foods, and exercise regularly. Time and healthy behaviors make for strong comparators.



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