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December 19th, 2013

Early Doses of Warfarin Paradoxically Associated with Higher Stroke Risk

Patients with atrial fibrillation seem to be at increased risk for ischemic stroke when starting warfarin prophylaxis, according to a case-control study in the European Heart Journal.

The study was undertaken after trials of both apixaban and rivaroxaban noted increased stroke risks among patients transitioning to open-label warfarin. This study was funded by the makers of apixaban.

Using a U.K. database, researchers examined a cohort of some 70,000 patients with AF; they matched 5500 cases of ischemic stroke with 55,000 controls. AF patients initiating warfarin therapy had a 71% increased risk for ischemic stroke within the first 30 days of therapy, compared with those on no anticoagulants. The risk was highest in the first week. However, the warfarin group had half the stroke risk after 30 days.

The authors say the observed “paradoxical procoagulant effect” may be due to warfarin’s effect in blocking some endogenous anticoagulants.

December 18th, 2013

New Trial Confirms Role for Dabigatran in Venous Thromboembolism

A new study helps support a role for  the new oral anticoagulant dabigatran (Pradaxa, Boehringer Ingelheim) in patients with venous thrombosis (VTE).  The RE-COVER II trial, published online in Circulation, confirms the finding of the earlier and highly similar RE-COVER trial, published in the New England Journal of Medicine in 2009, that dabigatran is as safe and effective as warfarin for the treatment of deep vein thrombosis (DVT) and pulmonary embolism (PE). Dabigatran is currently approved only for stroke prevention in patients with non-valvular atrial fibrillation.

In RE-COVER II, 2589 patients with acute VTE were  randomized to dabigatran or warfarin following standard heparin treatment for 5 to 11 days. At 6 months, the rate of recurrent VTE and related deaths was 2.3% in the dabigatran group versus 2.2% in the warfarin group (HR 1.08, CI 0.64 – 1.80; p<0.001 for noninferiority). There were no significant differences in the incidence of deaths, adverse events, and acute coronary syndromes.

Major bleeding, the primary safety endpoint, occurred in 1.2% of the dabigatran group and 1.7% of the warfarin group (HR 0.69. CI 0.36 – 1.32). There was a significant reduction in total bleeds: 15.6% versus 22.1% (HR 0.67, CI 0.56 – 0.81).

A pooled analysis of both RE-COVER trials turned up similar hazard ratios: recurrent VTE: 1.09 (CI 0.76 – 1.57), major bleeding: 0.73 (CI 0.48 – 1.11), and total bleeds: 0.70 (CI 0.61 – 0.79).

The findings are broadly consistent with the VTE trials for the other new oral anticoagulants — apixaban, rivaroxaban, and edoxaban — according to the authors. In all the trials, the newer agents were noninferior to warfarin in efficacy and had lower bleeding rates.

In an accompanying editorial, Peter Verhamme and Henri Bounameaux write that RE-COVER II is the last of the phase III trials studying the newer anticoagulants in the acute treatment of VTE. They agree with the study authors that all the drugs have now shown noninferiority to warfarin along with less bleeding.

One clinically important issue is that apixaban and rivaroxaban were studied using a single-drug approach, making these drugs preferable in patients for whom outpatient treatment is possible. The new agents, they write, “offer patients, physicians and healthcare systems an effective, safer, and more convenient treatment for acute VTE.”

 

December 18th, 2013

Behind the Curtain: Study Reveals Big Role of Medical Communication Companies

Everyone knows that medical information flows out of medical centers and schools; research institutions and the NIH; pharmaceutical companies; journals; and medical societies. But one important information source — medical communication companies (MCCs) — “are among the most significant but least analyzed health care stakeholders,” according to Sheila Rothman and colleagues. In a new report in JAMA, they set out to explore the important but poorly understood role of MCCs.

Until recently, little has been known about these companies. But in recent years, either as a result of legal settlements with the government or public pressure, 14 pharmaceutical and device companies have published their grant awards on the internet. In 2010, the authors report, the 14 companies gave over $170 million to MCCs, “more funds than any other recipient, including academic medical centers, professional associations, and research organizations.” Almost all the MCCs were for-profit companies. The top recipient of industry funds was Medscape/WebMD, which received more than $20 million, representing 12% of all awards to the MCCs.

One major source of concern involves online CME activities produced by the companies. This, write the authors, “allows them the opportunity to collect personal data and create digital profiles. Although MCCs did not elicit users’ explicit consent, they interpreted participating in a CME course and navigating the website as an implicit agreement to share information with third parties. It is possible that physicians using MCC websites do not appreciate the full extent of MCC-industry financial ties or are aware of data sharing practices.”

“Physicians who interact with MCCs should be aware that all require personal data from the physician and that some share these data with unnamed third parties,” the authors conclude.

In an accompanying editorial, Lisa Schwartz and Steven Woloshin write:

Medical communication companies’ reliance on industry funding highlights the importance of keeping promotion separate from education. All companies will feel unconscious (and perhaps explicit) pressure to present their clients’ products in the best light. Bias can easily occur in the selection and training of speakers, in their presentations, on the websites, and even in test questions.

Despite new efforts aimed to prevent some of the worst abuses of CME, the editorialists discuss persistent concerns:

Continuing medical education that is tainted by promotion is marketing masked as education. It can lead to inappropriate prescribing that can harm patients and waste money. To remove promotion from CME, some have called for eliminating all industry funding.

GlaxoSmithKline Announcement

GlaxoSmithKline made an important announcement that, although not directly related to the JAMA study, touches on many of the same general issues. ProPublica reporter Charles Ornstein writes:

In a major departure from industry practice, GlaxoSmithKline, the sixth-largest global drug maker, announced Tuesday that it will no longer hire doctors to promote its drugs.

The company also will stop tying compensation for sales representatives to the number of prescriptions written for drugs they market. The changes will be made worldwide over the next two years.

December 18th, 2013

Missing High Blood Pressure Guideline Turns Up in JAMA

After  years of delay and many twists and turns, the hypertension guideline originally commissioned by the NIH has now finally been published in JAMA. The evidence-based document contains a major revision of hypertension treatment targets and includes new and somewhat simplified recommendations for drug treatment.

The previous U.S. hypertension guideline was published more than a decade ago. After many delays, the new guideline was ready for publication earlier this year, but then the NIH decided to get out of the guidelines business. The American Heart Association and the American College of Cardiology assumed responsibility for the development and publication of cardiovascular guidelines and last month published four new cardiovascular guidelines, with the notable exception of the hypertension guideline. As an accompanying JAMA editorial explains:  “Rather than submit the hypertension guideline for review by these organizations, the panel members submitted the guideline to JAMA, where it underwent both internal and external peer review.”

The big headline of the new guideline is an important change in treatment targets. The previous guideline recommended that all adults have a target systolic blood pressure below 140 mm Hg. For people with diabetes or kidney disease,/ the target was even lower, <130 mm Hg. In the new guideline, the target remains the same for adults under 60 but eliminates the lower target for people with diabetes and renal disease. Most importantly, however, for people 60 and over the new guideline establishes a more conservative, easier-to-achieve target of 150 mm Hg or lower.

The authors write that they have not established a new definition of hypertension: “the panel believes that the 140/90 mm Hg definition from JNC 7 remains reasonable.” Lower is still better, at least when it occurs naturally: “The relationship between naturally occurring BP and risk is linear down to very low BP.” The change in target is based, instead, on the lack of evidence showing that drug treatment to the lower levels is better.

For nonblack adults, the guideline recommends starting drug treatment with an ACE inhibitor, an ARB, a calcium-channel blocker, or a thiazide-type diuretic. For blacks, the guideline recommends starting with a calcium-channel blocker or a thiazide-type diuretic.  People with chronic kidney disease should receive an ACE inhibitor or an ARB. (Although once a cornerstone of antihypertensive therapy, beta-blockers are no longer recommended for initial treatment.)

If goal blood pressure is not achieved after a month, then the guideline recommends increasing the drug dose or adding a second drug. Blood pressure should be monitored until the treatment goal is reached. A third drug can be added if necessary, but an ACE inhibitor and an ARB should not be used together.

One important difference between the hypertension guideline and the AHA/ACC guidelines released last month is the approach to risk assessment. Where the AHA/ACC recommendations were based on an assessment of total cardiovascular risk, the hypertension guideline is more narrowly focused on blood pressure. Also, as noted in another accompanying editorial, following the new hypertension guideline will lead to less treatment for elderly people, while the AHA/ACC guidelines lead to more treatment in these patients. “Such divergent philosophies may cause confusion among clinicians and patients alike,” write Eric Peterson, J. Michael Gaziano, and Philip Greenland.

The guideline offers a frank admission that many of the recommendations are based on expert opinion and not clinical trial evidence.

December 18th, 2013

Doc, Do I Really Need a New Battery?

and

A 45-year-old man with nonischemic cardiomyopathy, diagnosed 8 years ago, presents for annual follow-up. A transthoracic echocardiogram (TTE), taken 3 years ago, showed an LV ejection fraction of 25%. Since then, the patient has improved a great deal and now has barely any signs or symptoms of heart failure. Repeat TTE right before the current visit showed an LVEF of 50% and no significant abnormal findings.

An electrophysiologist who saw the patient a week before his current visit noted that his implantable cardioverter-defibrillator (ICD), which was placed 6 years ago but has never fired, is near the end of its life and needs a new battery. The battery replacement is scheduled for 1 month from now, but the patient is unsure whether to bother getting a new battery. He notes that his heart function is close to normal and wants to know if he should still take his heart failure medications (metoprolol, lisinopril, and spironolactone).

What would you advise this patient ­— and why?

1. Replace the ICD battery; keep taking the heart failure medications.

2. Do not replace the battery; keep taking the heart failure medications.

3. Do not replace the battery; discontinue the heart failure medications.

4. Another option

 

RESPONSE: December 22, 2013
James Fang, MD
I recommend option 1: Replace the ICD battery and keep taking the heart failure medications. Although the improvement in ventricular function is dramatic, an LVEF of 50% is, in fact, not normal. Moreover, the case makes no mention of ventricular remodeling — is the ventricle still dilated?

It is important to distinguish true myocardial recovery (true normalization of cardiac function after a reversible insult) from myocardial disease that is in remission. When there is remission, as in this case, myocardial dysfunction is still demonstrable (lack of inotropic or chronotropic reserve, elevated biomarkers, remodeling, abnormal ECG findings), and patients may still experience clinical events, including heart failure–related hospitalization and mortality. MRI imaging can also be helpful, in that persistent myocardial fibrosis strongly indicates a disease in remission. Nevertheless, in the case of true recovery (as evident from a completely normal ECG, echocardiogram, biomarkers, and so on), a trial of medication withdrawal with appropriate surveillance may be considered.

 

FOLLOW-UP: December 30, 2013

Tariq Ahmad, MD, MPH

We discussed the various options with the patient. He ultimately chose option 2: Do not replace the battery; keep taking the heart failure medications. He reported feeling “100%,” going to the gym regularly, and working full time as a computer analyst — all without incident. He agreed to follow up in a year to have a repeat echocardiogram and laboratory testing.

On his return clinic visit, approximately 1 year from the discussion, his echocardiogram parameters were unchanged and his N-terminal pro-BNP level was within normal limits. He had not experienced any signs or symptoms of cardiac arrhythmia or heart failure and wanted to continue to stave off a battery upgrade. He said he didn’t mind continuing the medications, noting “If it isn’t broken, don’t try to fix it.”

December 16th, 2013

Case Closed: Multivitamins Should Not be Used

The editorialists are fed up: “Enough is enough.” Writing about three new papers in the Annals of Internal Medicine that find no benefits for the use of multivitamins — only the latest in a long line of negative findings — Eliseo Guallar and colleagues write:

…we believe that the case is closed — supplementing the diet of well-nourished adults with (most) mineral or vitamin supplements has no clear benefit and might even be harmful. These vitamins should not be used for chronic disease prevention. Enough is enough.”

In the first paper, Stephen Fortmann and colleagues performed an updated systematic evidence review of vitamin and mineral supplements for the U.S. Preventive Services Task Force (USPSTF). They found “no evidence of an effect of nutritional doses on CVD, cancer, or mortality in healthy individuals without known nutritional deficiencies for most supplements we examined.” However, they were unable to rule out a benefit for vitamin D, and they called for improved studies to better assess both potential harms and potential benefits.

In the second paper, investigators from the Physicians Health Study II randomized nearly 6,000 physicians 65 years of age or older to  a multivitamin or a placebo. Over 12 years the physicians underwent as many as four assessments of global cognition, verbal memory, and category fluency. There were no significant differences between the groups in any of the test scores at any time.

In the third paper, Gervasio Lamas and his fellow investigators in the NIH’s Trial to Assess Chelation Therapy (TACT) randomized 1,708 patients who had had a heart attack to a multivitamin supplement or placebo. They found no significant difference in outcomes between the two groups after 4.6 years of followup. The results were less robust because the nonadherence rate was much higher than anticipated.

It should be noted that patients in TACT were also randomized to chelation therapy or placebo. Last year the results of that arm of the trial sparked an enormous controversy by suggesting that chelation therapy might be beneficial. Last month the TACT investigators reported that all the benefits observed in the main trial occurred in the large subgroup of patients who also had diabetes. At the American Heart Association meeting last month they also presented results showing that, although multivitamins did not have an independent effect, when added to chelation there was an additional 10% reduction in events. These findings have not yet been published.

 

December 16th, 2013

Three Cases of Sudden Cardiac Death Linked to Lyme Carditis

Three cases of sudden cardiac death associated with Lyme carditis were reported in 2012 and 2013 and are described in MMWR. Only four such deaths have previously been reported.

The three patients, aged 26 to 38, lived in states with a high incidence of Lyme disease. None had rash; two had pre-existing heart conditions. Postmortem investigation by state health departments and the CDC found Borrelia burgdorferi in heart tissue and evidence of Lyme carditis in all three patients.

“Physicians and health-care providers should ask patients with suspected Lyme disease about cardiac symptoms, and conversely, ask patients with acute, unexplained cardiac symptoms about possible tick exposure and symptoms of Lyme disease,” the authors recommend.

December 16th, 2013

Selections from Richard Lehman’s Literature Review: December 16th

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.

NEJM  12 Dec 2013  Vol 369

A Pharmacogenetic vs. a Clinical Algorithm for Warfarin Dosing (pg. 2283):  This week most of the NEJM is taken up with trials of genotyping to guide starting doses of vitamin K antagonists. Fair enough: this is a common clinical problem, and warfarin initiation is an important test case for genotyping as the gateway to personalised therapeutics. Dosing people with warfarin is currently a matter of trial and error: you grope your way forward, using lots of blood tests, and some patients end up on a dose of 1mg daily, others on a dose of 11mg, all for the same target INR. We know that a lot of this variation is governed by variants in the gene loci CYP2C9 and VKORC1. Now if genotyping can’t help in a situation as extreme as this, what use is it ever going to be as a guide to drug treatment? Here is the first trial of three: in 1015 patients during the first four weeks of newly started warfarin therapy, genotyping made absolutely no difference in achieving and maintaining the target INR.

A Randomized Trial of Genotype-Guided Dosing of Warfarin (pg. 2294): The next trial, from Europe, was smaller in size but longer in duration, and used a different genotyping platform. In 455 patients with atrial fibrillation being started on warfarin, slightly more of those in the genotyping group achieved their target INR at 12 weeks. The important outcomes—episodes of bleeding or thrombosis—were not measured in these trials.

A Randomized Trial of Genotype-Guided Dosing of Acenocoumarol and Phenprocoumon (pg. 2304): Finally, a similar trial was conducted in European countries where weirder coumarol anticoagulants are fashionable—acenocoumarol and phenprocoumon. These 548 patients fared exactly as well whether their dosing was guided by clinical factors or by genotyping. The journal runs two commentaries on these studies, one of which observes that, “The public’s expectations for pharmacogenetics may arguably be declining.” This is so true. Ever since I got my bus pass, I have used a lot of public transport, and never once have I overheard an upbeat conversation about pharmacogenetics. Neither of the articles can quite bring itself to make the final diagnosis. Yes, genotyping for vitamin K antagonist dosing may have appeared to stop breathing: yes, there is a dilated look about its pupils; no, we can’t feel a pulse; but it can’t be time to give up yet. Actually guys, if you don’t mind, I’m off for some coffee; and while I’m there I’ll fill out the death certificate.

JAMA  11 Dec 2013   Vol 310

Statin Therapy for Primary Prevention of Cardiovascular Disease (pg. 2451): Statins! For everybody who wants them, say I. You probably disagree, so read this clinical evidence synopsis about statin therapy for primary prevention of cardiovascular disease. We can agree that more evidence is needed: so once again, young research fellows, get digging in those large databases. I think the biggest question is whether the increase in “diabetes” with statins has any long term significance or is merely an artefact of the way we arbitrarily define “diabetes.”

Lancet  14 Dec 2013  Vol 382

Cangrelor: A New CHAMPION for PCI? (pg. 1981): When the Medicines Company ran its initial CHAMPION trials of cangrelor, a fast-acting intravenous platelet inhibitor, they failed to show benefit. Then earlier this year, the NEJM published the CHAMPION-PHOENIX trial which purported to show that “Cangrelor significantly reduced the rate of ischemic events, including stent thrombosis, during PCI, with no significant increase in severe bleeding.” But in fact it showed no such thing, because 63% of patients had received oral clopidogrel as well, as the NEJM editorial points out. Now the Lancet sees fit to publish a Medicines Company funded pooled patient data analysis from all the company’s CHAMPION trials with the conclusion that “Compared with control (clopidogrel or placebo), cangrelor reduced PCI periprocedural thrombotic complications, at the expense of increased bleeding.” So the bleeding bit is contradictory. But let’s leave the last word to the Lancet editorial entitled “Cangrelor: a new CHAMPION for percutaneous coronary intervention”, which ends “its favourable pharmacodynamic profile and effectiveness in reducing periprocedural events makes cangrelor a useful and welcome agent for interventional cardiologists and their patients.” The author then goes on to declare “I have worked as a consultant for AstraZeneca, Eli Lilly, and Sanofi, and my institution has received grant support from AstraZeneca and Boston Scientific.” So that’s all right then; his ringing endorsement of this product can’t be biased. Except that last year the Medicines Company and AstraZeneca joined forces to promote each other’s antiplatelet drugs, as reported in Forbes Weekly. How can the Lancet ignore conflicts of interest on such a scale?

 

 

December 16th, 2013

Possible New Lease on Life for Vorapaxar and Rivaroxaban for ACS

Early next year an FDA panel will review a new drug from Merck and a new indication for Xarelto (rivaroxaban), Johnson & Johnson’s highly successful new oral anticoagulant. Both drugs have had a rocky road getting to this stage and their success is by no means assured, but the announcement of the meeting of the FDA’s Cardiovascular and Renal Drugs Advisory Committee suggests that the companies have made progress resolving earlier problems.

Merck’s new drug application (NDA) for vorapaxar (Zontivity is the proposed trade name) will be discussed on January 15 for the proposed indication of reduction of atherothrombotic events in patients with a history of myocardial infarction (MI). (Here’s the notice in the Federal Register.) Merck will also try to demonstrate that the drug reduces the rate of a combined endpoint of cardiovascular death, MI, stroke, and urgent coronary revascularization.

The background story of vorapaxar is quite interesting. The once highly-promising novel antiplatelet drug, a thrombin receptor antagonist, was widely thought to have no future after unacceptably high serious bleeding rates were found in two large clinical trials studying the drug in a wide variety of acute and chronic cardiovascular patients. But hopes for the drug resurfaced last year based on new data from a prespecified analysis of the TRA 2P-TIMI 50 trial published in the Lancet. The new proposed indication is considerably narrower than the company had originally hoped.

In the full trial, which randomized 26,449 patients with a history of MI, ischemic stroke, or peripheral arterial disease to either vorapaxar or placebo in addition to standard therapy, the rate of CV death, MI, or stroke was significantly reduced by vorapaxar, but there was also a doubling of the very serious complication of intracranial bleeding. But the substudy published in the Lancet focused on the subgroup of 17,779  patients with a history of MI. After 2.5 years of followup, the rate of CV death, MI, or stroke was significantly reduced in the vorapaxar group compared to the placebo group, though vorapaxar was also associated with an increased risk of bleeding, though not, importantly, intracranial bleeding.

In general, a substudy does not provide sufficient evidence to support an NDA for a novel drug. But, the study authors pointed out, the substudy was larger than is usually found in the entire population of most clinical trials. It seems likely that the FDA reviewers and the advisory committee members will spend some time considering this issue.

On January 16 the panel will discuss the supplemental NDA for Johnson & Johnson’s Xarelto (rivaroxaban) to reduce the risk of thrombotic cardiovascular events in patients in the first 90 days after suffering acute coronary syndrome (ACS). Earlier this year the FDA turned this supplemental NDA down for the second time.

The ACS indication has proved tantalizingly elusive, the one major blank space in a large trophy case of successful indications garnered by the drug. The proposed indication is based on the ATLAS ACS 2-TIMI 51 trial, which was widely praised when results were first unveiled in 2011. The FDA then granted priority review for the indication. But momentum ground to a halt when FDA reviewers raised questions about the ATLAS trial, largely centering on significant amounts of missing data from the trial. The FDA advisory panel, highlighted by vocal criticisms from Steve Nissen and Sanjay Kaul, resulted in a vote against the ACS indication, leading to the first complete response letter.

Johnson & Johnson has revealed neither the contents of the most recent complete response letter nor the substance of its answer to the FDA.

 

December 16th, 2013

Examining the Value of My Medical Training

Earlier this month, I completed the Clinical Knowledge portion of Step 2 of the United States Medical Licensing Examination (USMLE). The nine-hour slog of confirming when a squatting child has tetralogy of Fallot, diagnosing African American women with sarcoidosis, and never selecting “urine metanephrines” as an answer choice (even in the world of artificial scenarios I was denied seeing a patient with a pheochromocytoma) has made me reflect about the training I am receiving. As the practice of medicine in the United States changes rapidly, medical students like me feel a great tension between the model of the all-knowing, all-doing independent physician of the past and the highly segmented, team-based model of the future.

The Step exams emblemize the problem. As a test taker, I must identify the correct growth medium for fungal cultures, distinguish among the various dysmorphic facies of children born with chromosomal abnormalities, know how to triage care for a woman whose Pap smear shows atypical squamous cells of unknown significance, pinpoint the location of a seizure that has an aura with a smell of burnt rubber, and prescribe all-trans retinoic acid for the variant of acute myelogenous leukemia with a translocation between chromosomes 15 and 17. Useful information to someone, to be sure, but I am not surprised that the National Board of Medical Examiners (NBME) found a significant gap between what we learn in medical school and the everyday practice of medicine.

Researchers have tried to discern whether these exams (or any other metric) can predict performance in residency, though mostly in small, single-center studies. Residency program directors have probably initiated the most work on this topic — see this useful compilation and analysis done at Ohio State University and, fittingly, published in the Journal of the American Academy of Dermatology. Dermatology is arguably the most competitive residency to enter: A very high Step 1 score can be the ticket to an average salary of more than $300,000, great hours, and the highest level of job satisfaction in any medical specialty. The conclusion of the research was that high scores on previous tests predicted high scores on future tests but bore little relation to supervisors’ ratings of performance.

In a recent viewpoint article for JAMA’s themed issue on medical education, members of the NBME discuss how to make the USMLE more useful in assessing competency in clinical practice. One of their stated goals is greater emphasis on the basic sciences because students “fail to recognize” its value. Recognizing the value of basic science is undoubtedly a worthy goal that I support, but will increasing medical students’ knowledge of it improve the quality of healthcare delivery?

I sometimes wonder if it would be more valuable for medical students to memorize clinical practice guidelines. Maybe then children would receive more than 46.5% of indicated care in the ambulatory setting, we might reverse the decade-long slide away from guideline-recommended care for chronic back pain, and more than 62% of adults would receive appropriate prescriptions; in the process, we could prevent 67,996 deaths a year from heart failure. A recent effort by students to learn and implement quality-improvement initiatives and, thereby, increase adherence to screening guidelines for diabetes, dyslipidemia, HIV, and cervical cancer was probably a more worthy endeavor than if they had organized a journal club to discuss a review article on IVIG for autoimmune and inflammatory disease.

In the future, my greater basic science education may add to my core knowledge and intrinsic value as a physician. But for now, the popular advice is not to hire more physicians with all their refined qualifications, as discussed in an article in Medical Economics:

If you are having trouble finding physicians to join your practice, dismayed by their demands or expectations at interviews, or concerned about their high cost or need to be a partner, hiring a physician assistant (PA) or nurse practitioner (NP) may be your answer.

It’s actually pretty good advice. After all, NPs who work in the UK’s National Health Service have more satisfied patients than doctors do, with no difference in health outcomes. Nurse endoscopists in the U.S. are as accurate and safe at flexible sigmoidoscopy as experienced gastroenterologists. Certified registered nurse anesthetists (CRNAs) can perform the same set of anesthesia services, including open heart surgeries and organ transplants, as anesthesiologists, and can work unsupervised without increases in patient complications or deaths. Minnesotans who go to retail clinics receive the same level of care as at a physician’s office or an urgent care center, and at lower cost.

My school, in keeping with current trends and feedback from students, is cutting the pre-hospital rotation component of our curriculum from 2 years to 1.5 years. The goal is to give us more time to explore electives and make a better decision about what specialty to enter. That’s a good idea, but it also means that the lecture-based, basic-sciences portion of my education is a mere 6 months longer than what the PA curriculum sets aside for the same material. My friends who have graduated from PA programs are now expected to operate on the level of a resident and, on some surgery floors, to effectively manage all post-op patient care, while being paid well and working just 40 hours a week. I take comfort in knowing that, several years from now, my extra 6 months studying the basic sciences will blossom into the proper credentials to enter a subspecialty.

In the absence of evidence, economic factors will continue to force change. PAs and NPs represent about 30% of the current primary care workforce in the U.S., and that number is constantly increasing. Primary care PAs represent about 31% of all PAs in the U.S., and like their PCP counterparts, their median compensation of $85,000 ranks lowest among specialties. The incentive is, as with physicians, toward specialty care.

The nimbleness of the PA profession is an incredible advantage. It has few traditions and taboos, so PAs can go anywhere that has a demand and, probably, administer about the same amount of recommended care as doctors do at a lower cost. It would not be surprising if someday a study shows that PAs who had worked in a cardiology practice and had taken classes in reading ECGs and echocardiograms could obtain patient outcomes as good as the cardiologists did in this Duke study.

Imagine a more hypothetical scenario, one in which you create a healthcare system in a society that doesn’t have one. Would you decide that the proper way to train a highly specialized physician, such as a cardiothoracic surgeon, is with four years of medical school, five to seven years of general surgery, and two to three years of a fellowship? Or would you cut out all the parts involving hernia repairs, cholecystectomies, and lipoma resections? Does performing interventional radiology require four years of a radiology residency? It appears that the interventional radiologists themselves are questioning that assumption with a new pilot program.

I support the NBME’s decision to stake the value of future doctors on the basic sciences — it is a forward-thinking approach. Currently, though, we cannot accurately calculate the added value of my ability to detect a rare condition, given my additional scientific training. It would be even more difficult to calculate the risk for serious complications from a delay in diagnosis and treatment because I did not detect an underlying condition until it manifested in an obvious way — or until it was too late. I am optimistic that the day will come when the NBME can make these types of calculations. When it does, I’ll be ready for their metanephrines.

Offer your thoughts on these reflections from Nicholas. Is the training we give to medical students changing adequately to meet the new realities of healthcare delivery?