January 26th, 2015
Califf to Leave Duke to Become FDA Deputy Commissioner
Larry Husten, PHD
The FDA announced today that Duke University cardiologist Robert Califf will be the next FDA Deputy Commissioner for Medical Products and Tobacco. The agency said that Califf will be responsible for the Center for Drug Evaluation and Research, the Center for Biologics Evaluation and Research, the Center for Devices and Radiological Health and the Center for Tobacco Products.”
Califf replaces Steven Spielberg, who resigned last week due to an unspecified “family medical issue.” Califf will be the third person to hold the position, which was created by FDA commissioner Margaret Hamburg as “part of a broader set of changes” emerging from an FDA reorganization, according to FDA maven Alexander Gaffney.
Califf is now the vice chancellor of clinical and translational research at Duke University, where he has held a number of leadership positions. Califf initially gained national attention in the 1980s as one of the pioneers of clinical trials involving thrombolysis for acute myocardial infarction, which at the time was one of the hottest areas of medicine. Along with co-principal investigator Eric Topol, Califf led the TAMI group, which eventually evolved into the first GUSTO study, an enormously influential trial at the time. The trial helped struggling Genentech establish one of the first major biotechnology drugs, tPA (alteplase). The GUSTO trial also led directly to Califf’s founding of the Duke Clinical Research Institute (DCRI), which is the world’s largest academic research organization, employing over 1,000 people. Most recently Califf was in the limelight as a co-principal investigator of the IMPROVE-IT trial.
In 2009 there was widespread speculation that Califf was under consideration for the top position of FDA commissioner. Some are now speculating that Commissioner Hamburg may be seeking to put Califf in position to possibly take over her job when she retires.
Further reading:
- FDA announcement
- FierceBiotech
- David Kroll in Forbes
- Wall Street Journal
- Regulatory Affairs Professionals Society
January 26th, 2015
Measuring FFR During Cardiac Cath: Time to Go with the Flow?
John Ryan, MD
Anecdotally, we’ve noticed that the use of fractional flow reserve (FFR) during cardiac catheterization seems to be increasing, in both community and academic centers. We pose these questions to our fellow members on CardioExchange:
- Do you feel that FFR is being overused, underused, or neither?
- Should some sort of objective assessment be mandatory in outpatient PCI?
- Do results with FFR vary among providers?
- Does the use of FFR improve care?
Share your reactions with the CardioExchange community.
January 26th, 2015
Selections from Richard Lehman’s Literature Review: January 26th
Richard Lehman, BM, BCh, MRCGP
CardioExchange is pleased to reprint this selection from Dr. Richard Lehman’s weekly journal review blog at BMJ.com. Selected summaries are relevant to our audience, but we encourage members to engage with the entire blog.
JAMA Intern Med Jan 2015 Vol 175
Dietary Sodium Content, Mortality, and Risk for Cardiovascular Events in Older Adults: I have been contemplating writing a blog on salt for the UK Cochrane Collaboration to mark the appearance of the latest Cochrane review of reduced dietary salt for the prevention of cardiovascular disease.
The review concludes that current evidence does not confirm clinically important effects of dietary advice and salt substitution on cardiovascular mortality in normotensive or hypertensive populations. In August, the NEJM published the PURE studies which showed that an estimated sodium intake between 3 g per day and 6 g per day was associated with a lower risk of death and cardiovascular events than was either a higher or lower estimated level of intake. This latest paper in JAMA Intern Med is a cohort study of people aged 71-80 and concludes that in older adults, food frequency questionnaire-assessed sodium intake was not associated with 10-year mortality, incident CVD, or incident HF. So the Salt Reduction Emperor turns out to have few clothes on, if any. But rather than tackle the blushful dictator full-on, we should perhaps allow him the favour of a curtain to hide behind whilst he adjusts his underwear. There are some residual uncertainties, of course we should encourage people to prepare fresh food, more potassium is good too, and so on. It will all take an awfully long time, and I imagine that “healthy eating” guides will still repeat rubbish about vitamins, minerals, antioxidants, and reducing salt for as long as I live. “It is difficult to get a man to understand something when his salary depends on not understanding it” as Upton Sinclair once said. The irony is that the word salary comes from the allowance of salt which was an essential of health in the Roman army.
Lancet 24 Jan 2015 Vol 385
Zotarolimus-Eluting Durable-Polymer-Coated Stent vs. a Biolimus-Eluting Biodegradable-Polymer-Coated Stent in Unselected Patients Undergoing PCI: “Zotarolimus-eluting durable-polymer-coated stent versus a biolimus-eluting biodegradable-polymer-coated stent in unselected patients undergoing percutaneous coronary intervention (SORT OUT VI): a randomised non-inferiority trial.” Hey, I hear you say, you told us about this Lancet paper a few weeks ago. Nope, that was “Ultrathin strut biodegradable polymer sirolimus eluting stent versus durable polymer everolimus-eluting stent for percutaneous coronary revascularisation (BIOSCIENCE): a randomised, single-blind, non-inferiority trial.” You clearly aren’t paying attention.
Central Arteriovenous Anastomosis for the Treatment of Patients with Uncontrolled Hypertension: Resistant hypertension is a slippery thing. You may remember that there was a renal nerve ablation device that showed spectacular reductions in an open label study. Then Medtronic bought it up and ran a proper double blinded randomized trial which showed it was little better than a sham procedure. A device company called ROX medical has now come up with a cunning little device which creates a small anastomosis between the iliac artery and vein. In an open label trial, 20% of participants were rewarded with a swollen leg, so that may be a glitch that needs sorting. Some huge reductions in BP were observed, averaging 26.9/13.5mm Hg SBP/DBP. Long-term results including adverse effects like device migration, high output heart failure etc? We have no idea. We’ll need a sham-controlled RCT of long duration.
BMJ 24 Jan 2015 Vol 350
High Sensitivity Cardiac Troponin and the Under-Diagnosis of MI in Women: There has been a lot of publicity for this cohort study of 1126 patients presenting with “suspected acute coronary syndrome” to the Edinburgh Royal Infirmary over a three month period. The use of high sensitivity troponin testing made little difference to the diagnosis rate in men but doubled the number of women diagnosed with myocardial infarction. This is an important and well reported study and I think it calls for an immediate change in practice followed by a series of further studies. I think we are still some way short of knowing how best to diagnose and treat MI in women.
Diagnostic Accuracy of Single Baseline Measurement of Elecsys Troponin T High-Sensitive Assay for Diagnosis of Acute MI in the ED: Using high sensitivity troponin testing appropriately can also help in the early rule-out of MI in patients presenting with suggestive symptoms, according to a systematic review and meta-analysis of studies using a different diagnostic product—the Elecsys Troponin T high-sensitive assay.” The results indicate that a single baseline measurement of the Elecsys Troponin T high-sensitive assay could be used to rule out acute myocardial infarction if lower cut-off values such as 3 ng/L or 5 ng/L are used.” But pay attention to all the basic principles of using diagnostic tests—the pre-test probability in each individual, the likelihood ratio, and the importance of timing.
January 22nd, 2015
New Device to Lower Resistant Hypertension Shows Early Promise
Larry Husten, PHD
A novel implantable device appears to show early promise in the treatment of resistant hypertension. The “Coupler” device from ROX Medical is about the size of a paper clip and is delivered via a catheter to the upper thigh, where it creates an anastomosis between the distal external iliac vein and artery, thereby mechanically lowering blood pressure.
In a paper published in the Lancet, European investigators report the results of an open-label trial in in which 83 patients with persistent high blood pressure despite taking multiple antihypertensive drugs were randomized to implantation of the Coupler device or current treatment. After six months there were large and highly significant reductions in blood pressure in the treatment group but not in the control group: systolic BP measured in the office decreased by 26.9 mm Hg in the treatment group versus 3.7 mm Hg in the control group; systolic blood pressure measured by a 24-hour ambulatory monitor decreased 13.5 mm Hg in the treatment group versus 0.5 mm Hg in the control group. The same pattern was evident in the group of 17 who had previously undergone renal denervation.
Twenty-nine percent of patients who received the device developed edema in the leg caused by venous stenosis, which was treated with venoplasty or stenting. Three patients in the control group and none in the treatment group were admitted to the hospital for a hypertensive crisis.
In their discussion the investigators pointed out that, unlike renal denervation as it has been performed in the past, “technical success with the arteriovenous coupler is documented during the procedure and is associated with an immediate fall in blood pressure. This difference eliminates the placebo effect and isolates the sham effect to an interaction between a patient’s knowledge of treatment allocation with longer-term clinical behaviors.” In a press statement, Melvin Lobo, the study principal investigator, said:
This is an entirely new and highly promising concept in high blood pressure treatment. Existing drugs focus on hormonal or neurological regulation of blood pressure, and newer treatments such as renal denervation are uniquely centered on the renal nervous system. The Coupler effectively targets the mechanical aspects of how blood circulation works — so it’s a totally new approach to controlling blood pressure. The Coupler also highlights the importance of arterial stiffness as a major cause of resistant high blood pressure and it targets this issue both safely and successfully. Once the Coupler is placed, the results are also immediate, which again is unique to this treatment.”
Hypertension experts Franz Messerli and Sripal Bangalore offered the following comment:
This is an exceedingly provocative study identifying a novel mechanism to treat hypertension. By creating an arterio-venous anastomosis with an arterio-venous coupler, the investigators create an additional big branch in a stiff arterial tree, thereby improving overall arterial compliance, restoring the Windkessel function and of course, lowering peripheral resistance and blood pressure. In contrast to renal denervation, this innovative technique is straightforward and easy to understand. However, as fascinating as such an approach of “letting off steam” in a high pressure system seems at a first glance, a few items will have to be scrutinized. Most important will be the long-term sequelae to the local venous system that now will have to bear the brunt of a potentially destructive hemodynamic burden. Could several small shunts possibly be better tolerated than a single large one? Are we setting the stage for a high-output heart failure situation? And of course after the sobering results of Symplicity HTN-3, we have become skeptical about interventional studies without a sham control. Finally, if this really were to work, shouldn’t there be little or no hypertension in our dialysis patients with arterio-venous fistula?”
January 22nd, 2015
How Accurately Do ICD-9 Codes Identify Strokes in Patients with Atrial Fibrillation?
Jonathan L. Thigpen, PharmD
The CardioExchange Editors interview Jonathan L. Thigpen about his research group’s assessment of the validity of ICD-9 codes in identifying strokes in patients with atrial fibrillation. The article is published in Circulation: Cardiovascular Quality and Outcomes.
CardioExchange Editors: Please describe what you studied and what you found.
Thigpen: We assessed the accuracy of International Classification of Disease, 9th edition (ICD-9) stroke codes in identifying valid stroke events in a cohort of atrial fibrillation (AF) patients. The initial electronic search yielded 1812 events across three stroke centers (Boston Medical Center, Geisinger Health System, and the University of Alabama). All ICD-9–identified stroke events were vetted through manual chart review with final adjudication by a stroke neurologist. AF was verified by electrocardiographic evidence at the stroke admission, 6 months before the admission, or 90 days after the admission.
In addition to assessing the accuracy of the stroke codes alone, we also assessed the combined accuracy of stroke and AF codes, as well as the accuracy of stroke codes in identifying stroke that was associated with AF. These additional steps offer insight about the accuracy and reliability of using only ICD-9 codes to create a “stroke plus AF” cohort. This effort is extremely important given the increasing reliance on ICD-9 codes to identify stroke events and covariates in research, especially research that uses administrative data.
The positive predictive value (PPV) of stroke codes alone was 94.2%. PPVs did not differ across clinical site or by type of event (ischemic vs. intracranial hemorrhage), but they did differ by event-coding position (primary vs. other; 97.2% vs. 83.7%) and by ischemic stroke code (433 vs. 434; 85.2% vs. 94.4%). When combined with validation of AF codes, the PPV of stroke codes dropped to 82.2%. After we excluded ischemic stroke that was caused by a different mechanism (e.g., a vascular procedure, tumor, sepsis), the PPV dropped further to 72.8%. As a separate exercise, manual review confirmed 33 (7.2%) ischemic strokes in 458 events coded as “without infarction.”
Editors: What are the implications for published papers that have used claims data?
Thigpen: Our results indicate that ICD-9 stroke codes alone have limited use in identifying acute strokes in patients with active AF. We suggest that, to limit potential bias, manual verification of stroke is needed to confirm stroke events in the setting of AF.
We recognize that a screening method with a PPV ≥85% (as has been previously suggested) may be adequate for research purposes and is likely to bias estimates very little. However, this thinking rationalizes inaccuracies, which may not be acceptable to some observers. Results derived from screening methods with PPVs <85% are likely to have minimal value. For example, a stroke research study implementing a screening method with a PPV of 80% would mean that 20% of the patients identified as having stroke were in fact false positives, likely leading to significant bias in results.
In any paper that uses ICD-9 screening methods, readers must critically assess the given PPV of the ICD-9 codes and identify the specific screening methods employed (i.e., only including strokes coded in the primary position). The latter is especially important considering that many studies do not report ICD-9 accuracies.
Editors: Do particular studies concern you? Might their results have been different with more-accurate data on outcomes?
Thigpen: Concerns should be raised about any study that withholds information regarding the accuracy of ICD-9 stroke codes used for case ascertainment. This is especially true if methods to increase accuracies of ICD-9 screening procedures are not implemented (our study reports several available methods, confirmed in previous literature). Without being given the ICD-9 accuracy data for a given study, readers must assume that there are false positives in the cohort, thereby leading to bias (the extent of the false positives and resulting bias may be hard to determine). In recognizing the varying accuracies of ICD-9 stroke codes, we suggest (as many researchers employ) additional screening methods (i.e., manual verification) to increase accuracy.
Increasing the accuracy of ICD-9 stroke codes in the setting of AF will have a variable effect on a study’s results depending on several factors, including (but not limited to) the degree of the increase in accuracy, how the codes were used (to identify patients vs. to ascertain outcomes), and the investigators’ initial conclusions.
Editors: Do you think that ICD-10 will be better?
Thigpen: We know little about the accuracy of ICD-10 stroke codes. Current evidence indicates that the accuracy is similar to that of ICD-9 codes, although ICD-10 codes are thought to be more specific and provide a more intuitive coding method. For example, ICD-10 codes specify the hemorrhage location and source in intracranial hemorrhage, distinguish between thrombotic and embolic ischemic stroke, and include codes for intraoperative and postprocedural strokes. However, we suggest that until ICD-10 stroke codes’ accuracies are further pinpointed and compared with those of ICD-9 stroke codes, manual review of events seems to be warranted.
JOIN THE DISCUSSION
Do Jonathan Thigpen’s findings affect your degree of trust in how well ICD-9 codes identify strokes in patients with atrial fibrillation?
January 21st, 2015
A Tragic Loss
Harlan M. Krumholz, MD, SM
The news of the death of Michael Davidson, a surgeon at Brigham and Women’s Hospital, allegedly at the hands of a patient’s relative, has shaken us all. The words of Betsy Nabel, on behalf of BWH, conveyed how much he was respected and loved. To his family, friends and colleagues, we send our sympathy. As a cardiovascular surgeon, he is part of our community, and we stand with you in shock at the loss – and the tragedy. And we hope that we can make progress toward a world where such senseless acts, here and elsewhere, are no more.
January 19th, 2015
Intense Exercise Doesn’t Eliminate the Hazard of Intense Sitting
Larry Husten, PHD
A large new analysis published in Annals of Internal Medicine supports earlier observations that the health hazards of sedentary behavior aren’t completely neutralized by exercise.
Researchers in Toronto scoured the literature to find studies that assessed the health effects of sedentary behavior adjusted for physical activity. They found 47 studies, including 13 that assessed all-cause mortality, 14 that assessed cardiovascular disease and diabetes, and 14 that assessed cancer. Sedentary behavior was defined as “waking behaviors characterized by little physical movement and low-energy expenditure,” including sitting and television watching.
Sedentary time was associated with a statistically significant independent increase in risk for all-cause, cardiovascular, and cancer mortality, as well as the incidence of cardiovascular disease, cancer, and type 2 diabetes. Increased sedentary time had the biggest effect on the risk for type 2 diabetes. The authors also reported that increased exercise blunted but did not completely eliminate the excess risk associated with sedentary behavior. Separating the effects of sedentary behavior and exercise is not just an academic distinction. The authors note that public health programs have mostly sought to encourage physical activity. “Health-promotion messaging advocating for a reduction in sedentary time is far less common and faces many challenges.”
In an accompanying editorial, Brigid Lynch and Neville Owen write that studies looking at sedentary behavior and exercise suffer from many shortcomings, but “the implications of these findings are far-reaching. Sedentary behavior is ubiquitous. Society is engineered, physically and socially, to be sitting-centric. In our workplaces, homes, common methods of transportation, and recreational venues, we are required or encouraged to sit. Now, mounting evidence shows that sedentary behavior contributes to all-cause, cardiovascular, and cancer death as well as the incidence of cardiovascular disease, cancer, and type 2 diabetes.”
Senior study author David Alter said that “exercising one hour per day should not give us the… peace of mind to remain seated for the remaining 23.” James Brown, a much earlier expert in the field, offered this succinct advice: Get Up Offa That Thing.
January 19th, 2015
Putting Your Heart Into Your Music: Beethoven’s Cardiac Arrhythmia
Edward J. Schloss, MD
The CardioExchange editors interview Dr. Zachary Goldberger about his collaborative study of the relationship between cardiac health and musical composition inspired by the work of Ludwig van Beethoven. The paper is published in Perspective in Biology and Medicine.
CardioExchange Editors: You just published a very interesting and unusual article, could you describe what you wrote about?
Goldberger: This paper was a collaboration between a cardiologist, a Beethoven scholar, and a medical historian, and explores the hypothesis that Beethoven suffered from cardiac arrhythmias. Musicologists, medical historians, and cardiologists have speculated that he had an arrhythmia, and that distinct rhythmic motifs in the opening of Piano Sonata in E-flat major (Opus 81a) were “transpositions” of premature ventricular beats. Our paper segues off this previous notion and attempts to amplify it by identifying other Beethoven works which include “arrhythmic” tempi. Was the composer mapping his own electrophysiologic dynamics onto musical scores? We reexamined Opus 81a to see why others felt that it was a direct arrhythmic transposition. Then we studied other works where “arrhythmia” may be manifest: we examined the 5th movement (Cavatina) of the String Quartet in B-flat major (Opus 130) composed in 1825, and Piano Sonata in A-flat major (Opus 110) composed in 1821.
CardioExchange Editors: How did you happen to think about this project? What was the spark of creativity that led to it?
Goldberger: Music was the “overture” to my career path into medicine. I grew up studying classical piano, and I had two albums of solo piano compositions published by the time I entered college at Brown. The second of these was entitled “Heartsongs: Musical Mappings of the Heartbeat.” This work was part of a collaboration between the Boston Museum of Science, investigators at Harvard Medical School, and Boston University. We were able to translate the cardiac interbeat interval fluctuations—derived from Holter monitoring in both healthy subjects and those with heart disease—into music. The intervals were translated into numerical sequences which were then mapped onto the musical scale. The rise and fall of the melody (of which I had no control) — not the rhythm—reflects these interbeat intervals.The variation in healthy hearts produced a very complex, variable melody line. Patients with severe cardiac disease (i.e., heart failure with reduced ejection fraction) yielded a melody line that was more monotonous in range and dynamics. A “heartsong” from a healthy subject (Heartsong 1), will therefore sound slightly different than one from a patient with heart failure (Heartsong 15).
This early connection between music and the heartbeat sparked my interest in medicine and influenced my decision to become a cardiologist. During my cardiology fellowship at the University of Michigan, I read the remarkable book History of the Disorders of Cardiac Rhythms by German electrophysiologist Berndt Lüderitz. In the preface, he mentions that Beethoven was thought to have an arrhythmia, as described above. I looked further and found that a few others had mentioned this hypothesis as well. But it wasn’t entirely clear where the notion originally came from, even after corresponding with these individuals. I looked briefly at Beethoven’s letters written around the time of the sonata as well as the report of his autopsy, but neither provided any definite evidence. Of critical importance was the fact that the ECG was not introduced into practice until more than century after Beethoven’s death.
After my cardiology fellowship, I entered the Robert Wood Johnson Clinical Scholars Program at Michigan where I met Dr. Joel Howell, an internist, medical historian, and a classical music enthusiast. I asked his opinion about the hypothesis that Beethoven may have had a cardiac arrhythmia. He introduced me to Dr. Steven Whiting, a professor and Beethoven scholar at the UM School of Music. The three of us met in his office, listened to music for a few hours, and we were off.
CardioExchange Editors: You mentioned that Mahler also may have been influenced by arrhythmias, can you explain more about that?
Goldberger: This merits some clarification. Mahler likely suffered from rheumatic heart disease with mitral valve pathology. This diagnosis was discovered incidentally by the physician who was tending to his wife in 1907 after the death of their daughter. He examined the composer and heard a murmur, later confirmed by the famed Viennese cardiologist Friedrich Kovacs. Indeed, while mitral stenosis (and possible concomitant regurgitation) may lead to atrial fibrillation, its relevance to Mahler’s compositions requires more investigation. As other have asked, does the opening of his 9th symphony actually have features reminiscent of rumbles and snaps? At the very least, perhaps posing this question and related ones will enhance the “auscultatory awareness” of our trainees.
CardioExchange Editors: Do you think that adequate treatment of Beethoven would have robbed the world of some masterpieces?
Goldberger: Absolutely not. Part of Beethoven’s genius, his sublimity, was to overcome adversity and transcend limitations with his art. We want to emphasize that this paper presents a speculation and may offer a new dimension by which one can attend to Beethoven, as well as other works of music. We are listening to his music with a stethoscope. We invite the reader-listener to approach these works with open minds and open ears, and formulate their own opinions. Most important is simply to listen to the music, which speaks for itself and for all of us in ways that need no translation (nor an ECG).
January 19th, 2015
Optimum Salt Intake in Elderly Remains Elusive
Larry Husten, PHD
A new study offers fresh evidence that current salt recommendations should be taken with, well, a grain of salt. Current guidelines now recommend that everyone should have sodium intake levels below 2300 mg per day. For many people at higher risk, including everyone over 50 years of age, sodium intake should be below 1500 mg/d. (The American Heart Association promotes the more rigorous goal of 1500 mg/d for everyone.) But a 2013 report from the Institute of Medicine, along with findings from the PURE study published last year, have raised concerns that the lower target level in particular is neither practical nor beneficial.
The new study, published in JAMA Internal Medicine, looks at the growing and important elderly patient population. The researchers analyzed 10-year followup data from 2,642 adults between 71 and 80 years of age who participated in an observational study and who had their sodium intake assessed based on a food frequency questionnaire filled out in the second year. Median sodium levels were 2850 for men and 2320 for women.
No significant relationship was found between sodium intake and mortality or the development of cardiovascular disease or heart failure. There were trends in favor of moderate sodium intake (1,500 to 2,300 mg/d) compared with very low (<1,500 mg/d) or high (>2,300 mg/d) intake. Overall mortality was 33.8% in the very-low group, 30.7% in the moderate group, and 35.2% in the high group. Similar patterns were observed for cardiovascular disease and heart failure, but at no point did these differences achieve statistical significance.
The authors acknowledged that their study was imperfect, mentioning the well-known limitations of observational studies and the use of a self-reported questionnaire to measure salt intake. But they also pointed out the limitations of the evidence base for the current recommendations.
Considering the special case of older adults, in whom comorbidities, inadequate caloric intake, and medication interactions are additional concerns with very low sodium intake, the effect of sodium restriction should probably be tested explicitly in this population before implementing a generalized recommendation for very low (<1500 mg/d) sodium intake target.”
Until “stronger evidence, preferably from rigorous controlled trials,” is obtained, they recommend that “a more conservative approach to sodium restriction (e.g., targeting “<2300 mg/d) might be appropriate for older adults.”
January 18th, 2015
“I’m Just Not a Pill Person”: Emotional Underpinnings of Nonadherence
The CardioExchange Editors interview Lisa Rosenbaum about her recent commentary on patients’ emotional responses to taking medications as a factor in nonadherence to therapy for heart disease. The article is published in the New England Journal of Medicine.
CardioExchange Editors: In the current model of healthcare delivery, care is fragmented into 15–20 minute clinic visits. Can the insight and education you propose be provided in this model?
Lisa Rosenbaum: Unfortunately I think the answer is “No.” I think some of the challenges that seem specific to medication adherence are really just reflections of the more deeply embedded systemic challenges — namely, not having enough time with patients to really understand where they are coming from, and being beholden to certain quality metrics, which clearly help us keep up with a certain standard of care, but which also consume our attention and force us to deal with medications in a more perfunctory way. For some patients, this is fine; indeed, the straight march from guidelines to prescription to checking off the box can be comforting and expected. For others, however, there are emotional barriers, which are tough enough to overcome when we actually know they exist, but tougher still when we and our patients are not aware of them. My sense is that patients themselves are often unaware of what it is about medications for heart disease that puts them off, which is why it helps to have time to talk it out, and also why it’s often expressed under the generic guise of “not being a pill person.”
Given these constraints, what I really wish, though I fear it’s impossible, is that we could go back to the days where we had 15 minutes just to talk to patients about how they are doing. Face to face. In the office. No computers. That wouldn’t solve this problem, but it would begin to provide a foundation for conversations about people’s feelings about medications.
Editors: As you state, comments such as “I’ve never been a pill person,” and “I don’t like taking them, period” are common among patients. How can this attitude be changed and — well, should it be changed?
Rosenbaum: The “should it be changed” question is worthy of a book, so for the sake of argument, let’s just say the answer is yes. The question then is: how? As above, I think having more time with patients is necessary, but certainly not sufficient. The “good news” about the structural constraints that hamper free communication is that I’m not sure how relevant they are to the ultimate answer. Meaning, I think that the only real solution, almost by definition, has to come from patients rather than us. I thought about this a lot during the interviews I conducted — ok, great to know how people feel. But so what? During that time, I read the book Influence by Robert Cialdini, which describes in great and engaging detail much of the psychology research around social norm-setting. The bottom line is that much of our willingness to do anything is based upon our sense that others are doing it. That it’s cool. And so the question becomes, stated entirely informally: how could we make taking medications for heart disease feel more cool? Again, worthy of a book. But I definitely think there is something to be said for the idea of getting people together to support one another, emphasizing shared health over shared illness, and perhaps broadcasting medication-taking successes like one shares marathon-training stats. That said, there is no one-size-fits-all solution for general nonadherence to meds; solutions targeted at the emotions will need to be diverse. But I think any emotion-directed intervention will be more successful if it involves patients helping one another.
Editors: Why do you think many people are so interested in “natural” remedies, but so averse to taking evidence-based medicines — especially if they consider toxins such as tobacco and cocaine to be “natural”? How do you discuss this with patients?
Rosenbaum: This has baffled me for a long time. While I do not have an answer, I do know that my instinct —throwing more evidence and information at patients who feel this way — usually backfires. This gets back to the cool thing. It’s cool to walk down the street drinking a kale smoothie. It’s not cool to take a statin. If appealing to evidence is not effective than what is? My mentors and other creative investigators like Brendan Nyhan, who conducts some really amazing research on getting parents to vaccinate their children, are doing some remarkable work in this space. Not about the definition of “natural,” per se. But about how to get around some of our emotional quirks to help people adopt more healthy behaviors, like taking meds. I’m counting on that type of work to take us from believing the evidence ourselves to having an evidence-based approach for helping patients believe it.
Editors: Last year, a team led by Darrel Francis published results of their study on “medication disutility” in Circulation. What’s your response to this paper?
Rosenbaum: I think their fundamental point — that we can’t just assume disutility to be zero, and that therefore our cost-effectiveness analyses are likely flawed — is essential. For bringing some rigor to, and essentially providing a metric for, a concept that is often ignored, the paper is a tremendous contribution; in our world, having metrics and statistics really helps to get doctors thinking. A critical question is how to figure out who is “at risk” for nonadherence. While we know all kinds of factors that are associated with nonadherence, we really do not have a hard and fast way of identifying patients who might benefit from a targeted intervention to discourage nonadherence. So the disutility metric offers a path toward “at-risk” identification, which would be an invaluable tool. The study also seemed to confirm, albeit using a different methodology, what we already know: people do not like taking medications!
Perhaps this gets back to the philosophical question I can’t answer: if we do identify someone at risk for nonadherence, should we intervene? Assuming we should, then the disutility metric could be a useful gauge. But fundamentally, I think for some patients it’s simply not worth taking the pill, and we need to be ok with that. What worries me about a blanket acceptance of this decision is an underlying question: are there some reasons for not wanting to take meds that are more ok than others? Maybe someone’s aversion to taking a medication stems from hearing things about it that are not true. Is that a feeling we should try to change? Does it differ from the feeling of a person who completely understands the evidence-based 10 years of potential life gain but just can’t stand the thought of statin therapy? It’s so complicated!
Through grant support, I have had the luxury of time with patients in the last few years. And for that reason it’s easy for me to appreciate the value of this dynamic and what an informed choice really means. But I am certain if I had only 15 minutes with a patient I would “lapse” and just go back to my old way of handing them a prescription and saying “Take this so you don’t have another heart attack and live as long as possible…”
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