January 31st, 2012
Consensus Document Provides Roadmap to Uptake of TAVR in U.S.
Larry Husten, PHD
Following the recent FDA approval of transcatheter aortic valve replacement (TAVR), the ACC, AATS, SCAI, and STS — in conjunction with several other medical organizations — have released a critical consensus document to guide use of the new landmark procedure.
“We have tried to collate the evidence into a coherent road map for judicious use, rational dispersion, and careful post-marketing scrutiny of this promising technology,” said Sanjay Kaul, vice chair of the writing committee, in a press release. “It is now the collective responsibility of all the stakeholders to optimize its full potential for improving the duration as well as the quality of survival in patients with severe symptomatic aortic valvular stenosis.”
Here are some of the key recommendations identified by the committee:
–Careful patient selection
–Team-based approach given the complexity of procedure coupled with the high-risk profile of suitable patients, many of whom have extensive comorbid conditions that require ongoing management
–Specialized heart centers and physician expertise in treating valve disorders; this includes use of proctors as needed to serve on the heart care team during the first few cases, as well as proper facilities (hybrid operating rooms or modified cath labs)
–TAVR screening tests to inform treatment decisions
–Enhanced patient and family education in the risk and benefits of this procedure
–Ongoing evaluation and participation in national TAVR registry to assess real world outcomes
The document also emphasizes the groups for whom TAVR is not recommended, including adults with:
–An acceptable surgical risk for conventional surgical AVR
–Known bicuspid aortic valve
–Severe mitral annular calcification or severe MR
–Moderate AS
–Other (e.g., severe AR and subaortic stenosis)
(CardioExchange Interventional Cardiology co-moderators Rick Lange and David Hillis pose questions to writing committee member Steven R. Baily here. Take a look, then share your own insights.)
January 31st, 2012
Robert Harrington Leaving Duke for Stanford University
Larry Husten, PHD
Robert Harrington will be leaving his position as the director of the Duke Clinical Research Institute, a position he has held since 2006, to become the new chair of the department of medicine at Stanford University. Harrington was also the Richard S. Stack MD Distinguished Professor at Duke University School of Medicine.
The news was publicly announced by Philip Pizzo, the dean of the Stanford University School of Medicine, in The Dean’s Newsletter.
January 31st, 2012
Appropriate Use Criteria for Revascularization Updated
Larry Husten, PHD
The ACC, AHA, and other organizations have released updated appropriate use criteria for coronary revascularization. The 2012 Appropriate Use Criteria for Coronary Revascularization Focused Update incorporates data from the SYNTAX trial on the indications for PCI and CABG in patients with symptomatic, multivessel disease, as well as data from the CathPCI registry.
Here are some of the key ratings:
- PCI for low-burden left main disease alone or with blockages in other arteries with a low disease burden: uncertain
- PCI for intermediate- or high-burden left main disease: inappropriate
- PCI for low-burden three-vessel disease: appropriate
- PCI for intermediate- or high-burden three-vessel disease: uncertain
- CABG remains appropriate for patients with two-vessel disease including the proximal LAD and three-vessel and left main disease.
January 30th, 2012
Very Large Observational Study Finds Significant Mortality Advantage for CABG Over PCI in High-Risk Patients
Larry Husten, PHD
Although PCI has a small, early mortality benefit compared to CABG in high-risk patients, after the first year a striking survival advantage for CABG develops, according to results of the ASCERT study, presented on Monday at the annual meeting of the Society of Thoracic Surgeons (STS).
Fred Edwards presented the high-risk subset of ASCERT (ACCF-STS Database Collaboration on the Comparative Effectiveness of Revascularization Strategies), an NHLBI-funded study based on linked data from the STS, the ACC, and CMS. (The full results of ASCERT will be presented in March at the ACC scientific sessions.) The study population included patients 65 or older with 2- or 3-vessel disease who underwent CABG or PCI from 2004 through 2007. Some 189,793 patients were followed in the study; 103,549 underwent PCI and 86,244 underwent CABG.
At 4 years, there was a 22% risk reduction in adjusted mortality in the CABG group compared to the PCI group (RR, 0.78; CI, 0.74-0.82). A similar pattern was observed in patients regardless of age, sex, diabetes status, and ejection fraction.
“Previous observational studies have shown a long-term survival advantage for CABG over PCI. These partial ASCERT results confirm that in important high-risk clinical subsets the CABG survival advantage can also be seen in a large nationwide population,” said Edwards in an STS press release.
January 30th, 2012
Selections from Richard Lehman’s Weekly Review: Week of January 30th
Richard Lehman, BM, BCh, MRCGP
CardioExchange is pleased to reprint selections 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.
Week of January 30th
NEJM 26 Jan 2012 Vol 366
321 Here is a classic paper which describes the lifetime risks of cardiovascular disease: though the very fact of its being a printed article places absurd limits on its usefulness. A meta-analysis like this, covering more than a quarter of a million people from the age of 45 till death, needs a whole website with full databases and several banks of Powerpoint slides. Traditional publishing is rubbish when it comes to a topic like this: and you don’t even get open access to these printed titbits. Suffice to say that wherever you live and whatever your ancestry, your CV risk is a simple function of four factors: blood pressure, smoking, cholesterol, and diabetes. These are all continuous variables, and we are looking at 18 cohorts studies involving 257,384 individuals. And here is an 8-page article: what a way to carry on in the year 2012!
Lancet 28 Jan 2012 Vol 379
322 I’ve already commented on this meta-analysis by Carl Heneghan et al of individual patient data relating to self-monitoring of anticoagulation, which has major implications for clinical practice. Come on, primary care academia: there is more low-hanging fruit like this if only you would get on and pick it.
Arch Intern Med 23 Jan 2012 Vol 172
98 Ever since immediate percutaneous coronary intervention was shown to be superior to thrombolysis for high-risk ST-elevation myocardial infarction, health systems have been pouring huge resources into providing 24-hour immediate PCI facilities, but with inevitably mixed success. Outcomes researchers in the USA have come up with some pretty dire statistics for time to transfer from hospitals without PCI capacity to hospitals with, and in this editorial Rita Redberg grasps the nettle and urges a more realistic approach: “For low and intermediate risk patients, there is no mortality advantage to primary PCI (pPCI) over thrombolytic therapy. Even for high-risk patients with STEMI, the mortality benefit of pPCI is frequently lost due to routine delays of 1-3 hours by transfer. It is time to reconsider transferring patients with STEMI for pPCI. Timely reperfusion by thrombolytics, not late pPCI via transfer, will save lives.” Discuss.
101 Popular myth tells us that exercise combats depression by producing endorphins – or is it serotonin? – and for all I know popular myth may be right. There’s no doubt that exercise has other benefits too, so it’s nice to know from this systematic review that the antidepressant effect of exercise in chronic illness is supported by evidence from a large number of trials in a large range of conditions.
144 I would like to claim that the population benefits of taking statins are not outweighed by any potential for irreversible harm, and that now they are so cheap there is no reason why anyone should be advised against taking a statin if they wish to reduce their cardiovascular risk. There is no threshold effect, after all. But now there is a nagging worry that statins may induce diabetes, confirmed here by data from the Women’s Health Initiative, which included over 150,000 postmenopausal women without diabetes at baseline. This needs a lot more investigation: there is a lot of scope in such studies for residual confounders, including confounding by indication; and we need to know more about the potential reversibility of statin-induced hyperglycaemia.
January 27th, 2012
Plaque Rupture with Thrombosis, After Shooting Hoops
Indu Poornima, MD and James Fang, MD
A 22-year-old white man presented to the ER with acute non-ST-segment-elevation MI, after playing basketball. He had experienced chest pain on and off for more than 10 hours before presentation. His initial EKG showed T-wave inversions in leads III and avF (see image), and his troponin T level was 1.2 ng/mL. The patient’s initial pain resolved with nitroglycerin, and he was transferred to a tertiary-care teaching hospital.
Click to enlarge
On arrival, he reported no pain but continued to exhibit the T-wave inversions in the inferior leads. Two-dimensional echocardiography, performed at bedside, showed normal wall motion and an LV ejection fraction of 55%. The patient was monitored in the CCU. He was started on aspirin and IV heparin.
One hour after admission the patient developed 18 beats of nonsustained ventricular tachycardia but remained asymptomatic. His troponin T level increased to 1.5 ng/mL, and he was taken to the catheterization lab, where he was found to have a proximal left-anterior descending plaque rupture with thrombus. He had distal TIMI 3 blood flow with an abrupt cutoff at the apical LAD that suggested an embolic process. Given the good distal flow, he was managed conservatively and started on prasugrel and integrilin, in addition to the heparin and aspirin. He was also given 80-mg atorvastatin (on admission, his LDL level was 76 mg/dL and his HDL level was 38 mg/dL). This regimen was continued for 2 days, during which the patient remained asymptomatic.
The patient was discharged on aspirin, prasugrel, and atorvastatin. His hypercoagulability workup was negative. He had no family history of premature coronary artery disease or sudden death, and no prior use of cocaine. However, he had recently started using supplements called Jack3d and Phenorex, which contain high doses of caffeine and a stimulant.
Questions:
1. Why would this healthy 22-year-old have developed plaque rupture and thrombosis?
2. What would be your long-term management strategy for this patient?
Response:
February 6, 2012
Myocardial infarction in people age 40 or younger has multiple etiologies, although accelerated atherosclerotic coronary artery disease remains the most common cause. This premature disease is often associated with lipid abnormalities such as familial hyperlipidemias and other lipoprotein disorders. For example, in Southeast Asian populations, abnormalities in lipoprotein(a) are common.
History alone is notoriously misleading in this clinical setting, so toxicology testing should be used to screen for use of cocaine, amphetamines, and other illicit drugs. Embolic disorders (e.g., myxoma and endocarditis) and coronary vasospasm should also be considered. Endothelial dysfunction could be addressed with brachial reactivity and/or ST-segment Holter monitoring for transient ST-segment elevation. I would not consider acetylcholine or ergonovine testing because of the potential risk during the peri-infarct period.
Other rare causes are divided into vasculopathies (e.g., vasculitis) and thrombophilias (e.g., antiphospholipid syndrome). Rarely, true connective tissue disorders (e.g., pseudoxanthoma elasticum) or metabolic disorders (e.g., involving homogentisic acid) may present with myocardial infarction.
In this case, it appears that most of these etiologies have been considered, although the specifics are not described. The use of supplements is notable and should be explored further.
I’d consider a coronary calcium score to assess whether a diffuse coronary vasculopathy is present, as well as a referral to a vascular medicine specialist to consider unusual vasculopathies.
The long-term management strategy should remain vigilant for the rare, potential etiologies described above, and the patient should continue to take aspirin and a statin. I would also consider the long-term use of dual antiplatelet therapy, despite the absence of any compelling data to support such an approach, because at his age the patient is at very low risk for bleeding.
Update:
February 13, 2012
The patient tested negative for other illicit drugs such as cocaine. His echocardiogram was negative for all other embolic causes. Erythrocyte sedimentation rate (ESR) was used to identify active vasculitis, and the result was negative. Specific testing for vasospasm was not planned, as this was not evident on the coronary angiogram. The plaque rupture was identified by the interventional cardiologist using intravascular ultrasound.
The patient has been seen in 3-week follow-up since hospital discharge. His workup included lipoprotein(a), ESR, gene mutations for prothrombin variants, antiphospholipid antibodies, and lupus anticoagulant — all were negative. Detailed lipoprotein analysis with a VAP test was normal.
The patient has been avoiding the use of supplements and continues to take aspirin, prasugrel, and atorvastatin. Follow-up echo continues to show normal LV function. He is scheduled for a symptom-limited stress test in 4 to 6 weeks, to determine whether he can return to sporting activities.
The plan is to continue dual antiplatelet therapy for 1 year, when the patient (who does not fall under any current guidelines) will be reevaluated. The appropriateness of high-dose atorvastatin in this setting is debatable, as several commenters here have noted. However, the fact that the patient’s initial event was plaque rupture, followed by acute thrombosis, led to this decision. He is also scheduled for a CT scan to detect coronary calcium, although I agree with Dr. Powell that the finding of an absence of calcification would not be very helpful in a 22-year-old.
January 26th, 2012
Follow the Fellows: Turning Points
William Kent Cornwell, MD, Kathryn Jesseca Lindley, MD, Aaron C. Earles, DO and Erica Sarah Spatz, MD, MHS
For our ongoing series at CardioExchange, “Follow the Fellows,” we have invited physicians from various cardiology fellowship programs to document their course through their training. In this post, the fellows describe the challenging moment that brought them to select cardiology as their specialty. You can read their earlier posts here, here, and here.
A Special Niche in Cardiology
by Kate Lindley, MD
I started residency with the intention of staying in general internal medicine. I liked the idea of preventive care and developing long-term relationships with my patients. I liked to see variety. I wanted a mixture of both inpatient and outpatient medicine. I was hopeful that medicine would be able to provide that to me.
My first night of call as an intern was in the CCU. I had never done an ICU rotation in medical school, I didn’t know the medical record system at my new institution, and I didn’t even know how to replete magnesium or potassium levels. Terrified may be the best word to describe me.
My first admission that night was a little old lady, probably 80 years old, who presented to the ER with chest pain — and an unknown coagulopathy. She had a “new” left bundle branch block (of course there were no previous EKGs in the system), and so she went to the cath lab for evaluation. Her coronary arteries were clean. That night, she developed a retroperitoneal bleed as a complication of her procedure. I spent hours holding pressure on her groin, and we transfused 28 units of blood products. She was intubated for respiratory failure. She ultimately went to surgery for vascular repair and, after a difficult course, was extubated and transferred to the floor. The next morning after rounds, I went home, exhausted, thinking, “I’m not sure if I’m ready for this! These people are sick!”
It was not the complication of a cardiac procedure that made the impression on me but, rather, my affinity for critical care medicine that I continued to discover throughout that month. Cardiac patients often come critically ill into the hospital, and in many cases, we have feasible therapies to offer them, and they actually recover and go home. Each year, my CCU month was without a doubt my favorite rotation, and I think this was ultimately what led me down the path towards cardiology.
The field offers me the opportunity to develop long-term relationships with patients and practice prevention (both primary and secondary), but also offers the chance to care for critically ill patients and actually see some good outcomes. I’m hopeful to find a balance between inpatient and outpatient medicine, and a mix of both procedures and prevention. It’s a tall order, but I’m confident that cardiology offers that niche.
Learning Not to Worry About the Hours
by Aaron Earles, DO, MS
Residency is filled with challenging moments. Most physicians while in residency encounter several cases that change our perspectives not just in medicine, but life as well.
My internal medicine training took place in rural Mississippi, where heart disease, diabetes, and obesity are common. I was fortunate enough to get exposure to cardiology early in my IM training, which definitely helped my decision to pursue the specialty. During my first year of residency, I had a good friend whose father came into the ER with a STEMI. The cardiologist I was rotating with asked if I would go to the catheterization suite and assist on the case. My friend’s father had a successful PCI and made a full recovery. Seldom in medicine do you see an almost instant improvement with treatment, but in cardiology it frequently is the case.
Intensive care rotations also proved to have daily challenging moments. Every day, I would need to call a cardiologist for assistance in cases ranging from rapid atrial fibrillation to WPW management. I learned tons of information from cardiologist during my ICU rotations.
On the flip side, seeing the long hours that cardiologists have to work weighed heavily on my choice. Those of you who have been on STEMI call know how unpredictable the work schedule can be. I can honestly say my love for cardiology outweighed the dread of those long hours. I have found in my first year of fellowship that the hours don’t seem as bad if you truly love the field you have chosen.
During my residency, I almost decided to practice internal medicine and not to pursue a subspecialty. You may hear many negative comments from specialists about why you should choose primary care as opposed to a subspecialty. My advice to residents in training who are trying to decide on a career path: select a field of medicine that you truly loved during your residency. If I had not chosen cardiology, I know that in 10 to 15 years I would have looked back and regretted not doing a fellowship.
Fellowship is rough, especially in the first year. I have been on call for every holiday this year except for Independence Day and Christmas. It is also tough to make the transition from a resident in IM to a fellow in a subspecialty. With great responsibility come great sacrifice and even greater rewards. If you honestly love helping people, then any field in medicine can be rewarding. If I had it to do over again, I would again choose cardiology.
The Field with the Most Data, But –
by Erica Spatz, MD, MHS
Our strength is our weakness. No, I’m not talking about how to answer that dreaded question on interviews. I’m referring to the field of cardiology. One of its strengths is the incredible rate at which new studies are conducted. No other specialty parallels cardiology in the amount of data constantly informing our practice. But, are we asking the right questions? Are we interpreting the findings of these studies correctly? How, and for whom, are these data applied, and at what expense? For me, the weakness of cardiology is the sometimes indiscriminate, sometimes self-serving motivation with which data are applied or not applied.
Residency seemed to magnify my ambivalence about the rapidity with which new cardiology data became available. I, like so many other wannabe cardiologists, imbibed each new study as it came out. I put to heart the acronym du jour, and with any luck, I got the study name correct, applied it to the correct patient population, and gave the proper amount of enthusiasm or skepticism to the findings and whether they should be adopted. Truthfully, while exciting, the whole exercise was stressful.
As a resident, I was riveted by studies like AFFIRM, COURAGE, and COMET. Sadly, however, I remember such details as who said what about the study, more than which patient prompted the discussion about the study. On January 19, 2005, as a second-year resident, I was rounding with my team on a patient with nonischemic cardiomyopathy. While discussing the evolution of indications for primary prevention of sudden death, leading up to the MADIT-II trial which demonstrated ICD placement to be superior to standard medical therapy for patients with ischemic cardiomyopathy (and thus not our patient), I was abruptly interrupted by my co-resident, also interested in cardiology. In a matter-of-fact way, he let me know that I was wrong…. Without a doubt, he assured me, the indications were for people with nonischemic heart disease as well. I cowered; now I wasn’t sure about the data. I no longer liked this game and suggested we readdress it the following day. As it so happened, I went home that night and opened my New England Journal of Medicine only to find the SCD-HeFT trial published that very same day.
I don’t remember what happened to the patient. Did she get an ICD? How did she do? I do not know. What has lingered after all these years, however, is that these wonderful, exciting cardiology studies are all-too-often utilized for the benefit of the physician and not of the patient. The good news is that once you recognize how often studies are misquoted, misinterpreted, or misapplied…you don’t have to beat yourself up about not remembering the acronym. On the flip side, however, only if we get the data right, can we hope to improve outcomes for the patient.
The Opportunity to Help Patients with Advanced Disease
by Bill Cornwell, MD
In residency, I spent a great deal of time deciding between pulmonology/critical care and cardiology as a subspecialty. Several moments throughout my training influenced my final decision. The first was in January of my intern year when my team admitted a middle-aged man with end-stage heart failure for an LVAD. In retrospect, this doesn’t sound like anything extraordinary (for anyone on a CCU or heart failure service, it likely seems like a typical case). However, this was my first time managing such a patient and witnessing firsthand the opportunities we have to intervene with critically ill patients with advanced disease.
Another “moment” during residency came with publication of the PARTNER trial in the New England Journal of Medicine, showing that cardiologists could intervene on patients with aortic stenosis who were poor surgical candidates. Who would have thought, even a few years ago, that such interventions would be possible? A third “moment” came when I reviewed a surface echo and cardiac MRI on a patient admitted for dyspnea, and we diagnosed noncompaction.
Outsiders often label cardiologists as plumbers (the interventionalists) and electricians (the electrophysiologists) — but the truth is, cardiology is a world in and of itself, with a broad spectrum of interesting diseases, and continues to evolve, offering new treatment options over time. Cardiology, more so than other subspecialties, incorporates the latest technological advancements into clinical assessments and treatment decisions. Considering the high prevalence of heart disease, society will always need cardiologists to care for sick patients, and cardiologists will have opportunities to make a significant and lasting impact on individual patients and on the field as a whole.
January 26th, 2012
NHLBI Launches Two Large Cardiac Arrest Treatment Trials
Larry Husten, PHD
The NHLBI today announced the launch of two large clinical trials evaluating treatments for out-of-hospital cardiac arrest.
The Continuous Chest Compressions (CCC) trial will randomize 23,600 people with out-of-hospital cardiac arrest to either standard CPR or continuous chest compressions, both delivered by paramedics or fire fighters. In recent years, studies published in the New England Journal of Medicine, JAMA, and the Lancet have provided evidence that continuous chest compressions may be preferable to traditional CPR. Graham Nichol is the principal investigator.
“The CCC trial will help to determine if continuous compressions is equal to or better than standard professional CPR when paramedics, who are better able to provide assisted breathing than bystanders, intervene,” said Nichol, in an NHLBI press release.
The Amiodarone, Lidocaine, or Neither [Placebo] for Out-Of-Hospital Cardiac Arrest Due to Ventricular Fibrillation or Tachycardia study (ALPS) will randomize 3000 people with shock-resistant VF to amiodarone, lidocaine, or placebo. Although amiodarone and lidocaine are often given when shock treatment fails in VF patients, a beneficial effect of the drugs has never been demonstrated in this setting. Peter Kudenchuk is the principal investigator.
Both trials are part of the NIH-supported Resuscitation Outcomes Consortium (ROC), which the NIH describes as “the first large-scale clinical research network in the world designed to study, improve, and standardize how EMS teams deliver very early, pre-hospital interventions to improve patient survival after cardiac arrest or trauma.”
January 26th, 2012
Big Drop in MI Incidence and Fatality in England
Larry Husten, PHD
Since 2002, the incidence of acute MI in England has dropped by one-half and the case fatality rate by one-third, according to a new study published in BMJ. The overall decline in deaths from MI is about equally due to improvements in the prevention of MI and the treatment of MI.
Kate Smolina and colleagues analyzed data from 861,134 acute MIs in England from 2002 through 2010. Over the course of the study period, the MI event rate declined:
- in men by 33%, from 230 to 154 per 100,000, for an average annual decline of 4.8%
- in women by 31%, from 95.4 to 66.0 per 100,000, for an average annual decline of 4.5%
Similarly, the case fatality rate also declined:
- in men by 24%, from 42.0% to 32.1%, for an average annual decline of 3.6%
- in women by 29%, from 42.2% to 29.9%, for an average annual decline of 4.2%
The authors report that for middle-aged people, the decline in event rate played a bigger role in the changes, but for younger and older people, the case fatality played a bigger role.
In an accompanying editorial, Hugh Tunstall-Pedoe writes that the progress made in England and other western countries has not been replicated elsewhere:
As the world population ages and becomes more industrialised and urbanised, the decline in coronary mortality is predominantly in rich nations, while rates increase in dozens of others. Can these countries learn from us, or must they repeat our mistakes?
January 26th, 2012
Sizing Up Clinical Trials — Quickly and Intuitively
John E Brush, MD
A pharmaceutical sales rep comes to your office bringing lunch. He shows you a graphic stating that Multaq (dronedarone) reduced the primary endpoint in the ATHENA trial by 24%. The fine print shows an impressive P value: <0.0001. You come away satisfied that this drug looks good. You may not realize it, but you also feel a sense of obligation to the rep for the lunch.
Nevertheless, you go to the New England Journal of Medicine paper to look into this for yourself. There you find that the primary endpoint — first hospitalization due to a cardiovascular event, or death — occurred in 31.9% of the treatment group and 39.4% of the placebo group. That represents a 19% relative reduction (apparently, the 24% figure was initially reported at a national meeting but is not reflected in the published data). The difference between the treatment groups was mainly due to the reduction in the rate of hospitalizations. A 7.5% absolute risk reduction for the combined endpoint is starting to look less impressive.
The inverse of this absolute risk reduction, the number needed to treat (NNT), is 13. The drug was discontinued because of adverse events in 12.7% of the treatment group and 8.1% of the placebo group, yielding a number needed to harm (at least enough to discontinue the drug) of 22. The average follow-up was 21 months, and the drug costs $276 per month.
You think to yourself, “I would need to treat 13 patients over an average of 21 months, at a total cost of more than $80,000 to prevent one hospitalization due to a cardiovascular event or one death. If I treat an additional 9 patients, I would cause enough harm to cause one patient to discontinue the drug.” Hmmm, not so good after all.
Psychologists, such as Gerd Gigerenzer and colleagues, tell us that we can be fooled by the relative risk reduction, which exaggerates the observed difference between treatment groups. Our example bears that out. The simple statement using the NNT is much more intuitive.
In his recent book Thinking, Fast and Slow, Daniel Kahneman summarizes years of research on how we use intuition to make decisions. According to Kahneman and others, we have two modes of thinking: a fast, intuitive mode, called System 1 thinking, and a slower, analytical mode called System 2 thinking.
System 1 — intuitive and almost automatic — looks for quick, easy answers and is a sucker for a story. System 2 — deliberate and analytical — is consciously effortful and plodding. System 1 sees the forest; System 2 sees the trees. System 1, intuitive as it is, misses details. But slow System 2 can’t handle uncertainty. We need System 1 to quickly size up situations and to integrate complex but incomplete data. Despite its proneness to specific errors, System 1’s gut reaction is often right on.
System 1 can be set up to fail or succeed. Kahneman gives this example: If you tell a person that a bat and a ball cost $1.10 in total and the bat costs $1.00 more than the ball, and then ask how much the ball costs, System 1 wants to quickly answer, “10 cents.” But with a little extra time and thought, System 2 comes up with the correct answer of 5 cents. The original question is a setup for a System 1 failure. But if you frame the question differently — by stating that the bat and ball cost $1.10 and the bat costs $1.05 — System 1 won’t get fooled.
By using NNTs, we can set up System 1 to succeed, as we try to integrate the results of complex clinical trials into our everyday practice. Kaul and Diamond suggest that a good NNT is less than 50, and the number needed to harm (NNH) should be much greater than the NNT. Of course, you should also consider the cost and clinical impact of the treatment in question.
The NNT for post-MI aspirin is only 14. For heparin to treat unstable angina, it’s 40. The NNT for clopidogrel is 48, for prasugrel 46, for warfarin 48, for glycoprotein IIb/IIIa antagonists 77, and for TAVR 5 (with an NNH of 7 for vascular complications and 26 for stroke). The NNT and NNH summarize the evidence in a format that our System 1 thinking can easily handle.
So the next time a sales rep shows you a new study, turn down the lunch and ask to see the absolute risk reduction. Divide that number into 100 to calculate the NNT. Then turn that number into a simple declarative sentence that allows your intuition to better appreciate the true value of the new drug or intervention.
How often do you focus on the NNT when you assess clinical trials?
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