Ask the Doctors May 2015 Issue

Ask The Doctors: May 2015

I’ve read quite a bit in Heart Advisor about atrial fibrillation, but not much about ventricular fibrillation (VF). As a heart attack survivor, I’m curious about all types of arrhythmias. What should I know about VF?

VF is a chaotic rhythm of the heart, in which the ventricles quiver, but do not pump blood. As a result, VF is lethal unless an electrical shock or “defibrillation” is performed. While VF is not common, it is also not rare. In the U.S., about 325,000 people experience sudden cardiac death per year, and evidence suggests that the predominant arrhythmia involved is VF. The most frequent cause of VF is abrupt blockage in a coronary vessel, as occurs during some heart attacks. Certain types of structural heart disease, like hypertrophic cardiomyopathy, as well as inborn electrical disorders of the heart such as long QT syndrome, can also result in VF. Often, the heart starts off with a fast rhythm originating in the ventricles, known as ventricular tachycardia (VT), which then degenerates into VF. The only effective means of treating VF is defibrillation, generally by external pads or paddles, or via implantable cardioverter-defibrillator. The shock rids the heart of disorderly wave patterns, allowing the natural pacemaker to take control of cardiac function.

I take a proton pump inhibitor (PPI) for my acid reflux (GERD), but I was also recently put on warfarin after receiving a new heart valve. I’ve heard that PPIs can interact with warfarin and other drugs. Any advice?

PPIs such as omeprazole (Prilosec®) are, to a minor degree, broken down by the same liver enzyme which metabolizes warfarin. So, by competing for this enzyme, PPIs can slow warfarin’s breakdown. However, the contribution is small. Your physician may choose to follow your prothrombin time (PT) or International Normalized Ratio (INR) more closely for a little while after the surgery, to make sure your dose of warfarin does not need to be reduced. Another “blood-thinning” or antithrombotic medication which can interact with PPIs is clopidogrel, which is often prescribed after coronary artery stent placement. Clopidogrel is a “pro-drug,” meaning that it needs to be converted to its active form by an enzyme in the liver. Otherwise, it cannot perform its key function of inhibiting platelets, cell fragments which naturally serve to help stop bleeding, but can also trigger clots to form inside metal stents. It turns out that clopidogrel needs to be activated by the same enzyme which metabolizes omeprazole and, to a lesser extent, other PPIs. Hence, the potential exists for omeprazole to slow the activation of clopidogrel, leading to more clots in stents and more heart attacks.

Although the data from numerous studies are conflicting, the only randomized trial which treated patients with either clopidogrel plus omeprazole, or clopidogrel plus placebo, found that the group receiving omeprazole had fewer gastrointestinal bleeds, but no increase in cardiovascular events, such as heart attacks. Given the evidence, and the wish to maximize patient safety, the FDA has recommended that patients requiring both clopidogrel and a PPI be preferentially prescribed one of the four other PPIs rather than omeprazole or esomeprazole (Nexium®).

You should also be aware of the many drug-drug interactions which can occur with warfarin. Some medications, such as fluconazole, amiodarone, trimethoprim/sulfamethoxazole (Bactrim®) and metronidazole will strengthen warfarin’s effect, increasing the chance of dangerous bleeding. Drugs like aspirin, NSAIDs, and clopidogrel will increase the risk of bleeding while taking warfarin. Your doctor and pharmacist should be aware of all drugs you take, so that potential interactions can be flagged before medication is prescribed or dispensed.

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