CardioSource WorldNews September 2015 - Page 26

CLINICAL NEWS American College of Cardiology Extended Learning known duration, anticoagulate with warfarin for at least 3 weeks prior to and 4 weeks after cardioversion. • With AF or atrial flutter for > 48 hours or unknown duration requiring immediate cardioversion, anticoagulate as soon as possible and continue for at least 4 weeks. • With AF or atrial flutter for < 48 hours and high stroke risk, IV heparin or LMWH or factor Xa or direct thrombin inhibitor is recommended before or immediately after cardioversion, followed by long-term anticoagulation. • Following cardioversion of AF, long-term anticoagulation should be based on thromboembolic risk. The third bullet point is new. It’s given a level of evidence C, meaning expert opinion, but Dr. Prystowsky asked what if the patient has had AF or atrial flutter less than 4 hours: do you still need to anticoagulate first? In the past, he said, many clinicians would have said no to this. “It becomes a problem for clinicians and, I hate to say it, it become a medico-legal problem, too,” he said. “I could understand if they said greater than 24 but less than 48 hours, but I don’t know of any data to suggest that if a patient has had AF for 4 hours, you’re putting someone at high risk of you don’t anticoagulated them first.” Considering the new guidelines, Dr. Prystowsky said the committee did a wonderful job of getting everyone up-to-date. “Clearly, in the anticoagulation area there are changes and they are going to affect clinical practice.” He added, “I say this as a person who spent years writing guidelines: they are guidelines—not the tablets from the mountain. As a clinician, and it is stated in the (guidelines) preface, you need to incorporate them into patient care the best way you can.” ■ REFERENCES 1. Anderson JL, Halperin JL, Albert NM, et al. J Am Coll Cardiol. 2013;61(18):1935-44. 2. January CT, Wann L, Alpert JS, et al. J Am Coll Cardiol. 2014;64:e1-e76. 3. Wyse DG, Waldo AL, DiMarco JP, et al. N Engl J Med. 2002;347:1825-33. 4. Ionescu-Ittu R, Abrahamowicz M, Jackevicius CA, et al. Arch Intern Med. 2012;172:997-1004. 5. Prystowsky EN, Padanilam BJ. J Am Coll Cardiol. 2013;62:540-2. Take-aways • Treatment of AF involves three major strategies, but the bottom line is stroke prevention. • In the most recent iteration of AF treatment guidelines, there are changes that are going to affect clinical practice, especially in the area of anticoagulation. • Clinicians should do more to identify asymptomatic AF and evaluate new strategies to fulfill the first commandment of therapy for patients with AF: preserve the brain. 24 CardioSource WorldNews PCSK9: New Kid in Town FDA approval now puts reimbursement in the spotlight T here is a new option for patients at high risk from high cholesterol. What we don’t know, yet, is whether these new drugs (another is in the wings) represent a true breakthrough—or whether we can even afford them. On July 21, 2015, the European Commission approved Amgen’s PCSK9 inhibitor, evolocumab, for the treatment of patients with uncontrolled cholesterol who require additional intensive LDL-C reduction. That makes Repatha (as it’s called) the first PCSK9 inhibitor to be approved by any regulatory agency in the world. A few days later, alirocumab (Praluent), from Regeneron Pharmaceuticals Inc. and Sanofi SA, was approved by the U.S. Food and Drug Administration. (The FDA press release is here: 1.usa.gov/1EdYLiD ) The FDA approved alirocumab for use in addition to diet and maximally-tolerated statin therapy in adult patients with heterozygous familial hypercholesterolemia or patients with clinical atherosclerotic cardiovascular disease such as heart attacks or strokes, who require additional lowering of LDL cholesterol. A little more than a month later, as this issue of CardioSource WorldNews was being finalized, the FDA agreed with their European counterparts: evolocumab injection was approved as an adjunct to diet and maximally-tolerated statin therapy for the treatment of adults with heterozygous familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease, who require additional lowering of LDL-C; and as an adjunct to diet and other LDL-lowering therapies for the treatment of patients with homozygous familial hypercholesterolemia, who require add