Faculty Peer Reviewed
No matter how hard I try I just can’t get the picture of Kevin Ware fracturing his leg last Easter Sunday out of my head. Not only did it ruin my appetite for a perfectly cooked crown roast, but it has had me asking “How?”. How could this happen, how could a young, fit, elite college athlete suffer such a horrible injury after what appeared to be an routine jump for a pass block. A quick Google search for “How the heck did Kevin Ware’s leg break?” turns up some interesting thoughts and diagnoses. Bone cyst is a common one, as is severe osteoporosis (but this is the NCAA not the AARP), Paget’s disease, stress fracture (leading contender) and my personal favorite – overuse of anabolic steroids (see our feature later this week). In the end, what it seems to boil down to is bad luck and mechanism. A careful slow motion replay of the incident reveals the he did in fact land with incredible lateral force, and with his height and weight it was just too much for the bone to withstand. The rest is history and by the time we hit the presses Louisville, bolstered by Ware’s courage on and off the court may well be national champs.
Getting down to business, I am happy to announce that the Mediterranean diet finally has a randomized trial that it can feature prominently on its curriculum vitae. In this week’s edition of the New England Journal of Medicine a group of Spanish investigators give us the much anticipated results of the PREDIMED trial. Over 7000 patients deemed at high cardiovascular risk were enrolled and randomized to the Mediterranean + EVOO, Mediterranean + mixed nuts, or control advice to reduce dietary fat. Both Mediterranean diets, after premature termination at a median of 4.8 years*, came in with a 30% relative risk reduction for the primary endpoint of MI, stroke or death from a cardiovascular cause. This is exciting. Rarely do we see such reductions in risk from our most potent medications, and now we have a landmark randomized trial to add to the ever growing observational and cohort data. Diet really does work. Now, lest I get carried away, let me direct you to the astute accompanying editorial by Appel and Van Horn. They point out that this is more a test of adding EVOO and/or mixed nuts rather than a pure test of the Mediterranean diet. Don’t be fooled, these folks were consuming up to a liter of EVOO a week (22% daily energy!) and an ounce or more of nuts daily. This would be difficult for a wealthy vegan triathlete, let alone the average Joe with diabetes and hypertension. If you have been to your local Trader Joe’s lately you know how expensive these supplemental foods can be. Regardless, we should be emphatically stressing dietary modifications and hope that our patients can meet us half-way. I’d take a 15% relative risk reduction any day. By the way, Brazil nuts are delicious and much higher than almonds in Omega-3 fatty acids.
Now that my cupboards are filled with imported cans of olive oil and satchels of nuts, can I rest assured that I will live as long as an Okinawan (50 centenarians per 100,000!), or will my efforts be stymied by my new friend, androgenetic alopecia (a.k.a male pattern baldness)? Fortunately, Yamada et al. from the University of Tokyo must have read my and Matt Lauer’s mind, and this week in BMJ Open they present a comprehensive meta-analysis of observational studies looking for an association between baldness and coronary disease. The analysis included nearly 37,000 balding men from six observational studies. And the winner (more like loser) is…severe vertex baldness, coming in at a respectable relative risk of 1.5 for coronary disease. The authors do admit flaws in the data including recall bias for onset of balding, incomplete data for treatment of CV risk factors, and different definitions for baldness. Flaws aside, we are brought back to the question of How? In their analysis, Yamada and colleagues discuss the probable mechanisms for this potential association. Among the most intriguing are insulin resistance, inflammation of the follicular and vessel walls from high circulating cytokines, and activation of the dihydrotestosterone receptor leading to atherosclerotic change. In the end, with prevention and treatment of concrete cardiovascular risk factors like truncal obesity, hypertension and smoking, baldness may be relegated to the archives of clinical associations along with the earlobe crease (http://www.clinicalcorrelations.org/?s=earlobe) and hand lines.
Finally, I wouldn’t be able to call myself a neo-gastroenterologist without mentioning aspirin and bleeding risk. In the most recent Alimentary Pharmacology and Therapeutics, Lanas et al. present us with an easy to use “aspirin CV/GI risk calculator”. We have all been there, whether in primary care or the endoscopy suite, faced with the elephant in the room, and asked ourselves, our students, our nurses, the desk clerk, our friends, our relatives, anyone who will listen! “Should I start this patient on aspirin?”, fearful that an acute GI bleed will be the outcome. The problem with this fun to use calculator lies not in the CV risk portion that is driven predominantly by the time tested Framingham model, but in the bleeding risk portion that is based in several key assumptions about bleeding propensity and prevention with PPI and is based largely in systematic review. Shortcomings aside, this tool can be added to our bedside arsenal when we determine whether to start primary prevention ASA in high risk patients, yet should not serve as the sole determinant. We can also expect that with advancements in endoscopic therapies, increasing H. pylori eradication efforts and widespread use of acid suppression, bleeding risk may become less and less of a factor in the coming years.
From all of us here at Clinical Correlations, we hope to see you back real soon, and Kevin Ware if you are out there…Got Milk?
*Premature study termination can result in a significant loss of power and/or generate false-positive results. Data derived from prematurely terminated studies should be taken with a grain of salt, unless you adhere to the DASH diet, then half a grain.
Dr. Robert Gianotti is Associate Editor, Clinical Correlations
Peer reviewed by Neil Shapiro, Editor-In-Chief, Clinical Correlations
1. Estruch RE et al. Primary prevention of cardiovascular disease with a Mediterranean diet. NEJM 2013; 368: 1279-90. http://www.ncbi.nlm.nih.gov/pubmed/23432189
2. Appel LJ and Van Horn L. Did the PREDIMED trial test a Mediterranean diet? NEJM 2013; 368: 1353-54. http://www.nejm.org/doi/pdf/10.1056/NEJMe1301582
3. Yamada T et al. Male pattern baldness and its association with coronary heart disease: a meta-analysis. BMJ Open 2013; 3: e002537. http://www.bmjopen.bmj.com/content/3/4/e002537
4. Lanas A et al. The aspirin cardiovascular/gastrointestinal risk calculator – a tool to aid clinicians in practice. AP&T 2013;37:738-48. http://www.medscape.com/viewarticle/780923