October 12th, 2012
PCI Public Reporting Programs: Incentivizing Better Decisions?
Joseph S. Ross, MD, MHS
Public reporting of health care quality and outcomes has become the norm. Fifteen years ago the idea that nearly all health plans, hospitals, and physicians would be subject to reporting programs would have been considered implausible.
However, despite its growing prevalence and the specter of quality evaluation being used as part of reimbursement decisions, the science of public reporting remains in its infancy.
For surgery, research has strongly suggested that public reporting leads to improved surgeon and hospital outcomes. The most likely explanation is that providers respond to objective feedback, motivating quality-improvement efforts to maintain or develop a “high-quality” reputation.
But skeptics of public reporting programs have raised concerns, centrally that physicians and hospitals caring for the sickest patients will be disincentivized to provide care for the highest-risk patients, potentially leading clinicians to avoid offering care.
Surgeons have generally disagreed, but some early studies have supported these concerns.
This month’s JAMA provides some much needed evidence to inform this discussion, as Joynt and colleagues used CMS administrative claims data to examine whether several state public reporting programs of PCI outcomes (Massachusetts, New York, and Pennsylvania) were associated with differentially lower rates of PCI and mortality for acute MI patients.
In essence, use of PCI was lower in these three states compared to seven control states in the same region of the U.S. However, there was no difference in overall acute MI mortality between states with and without public reporting.
The reduction in rates seems largely attributable to lower PCI use among STEMI patients, patients in cardiogenic shock, and patients 75 years of age or over; PCI use was no different among NSTEMI patients.
And there was no differential increase in CABG surgery rates with states that had PCI public reporting programs, so higher-risk patients did not migrate to a higher-risk surgery (although there is a question of whether this finding held true for Massachusetts or only New York and Pennsylvania).
Nevertheless, there was no difference in 30-day mortality rates for acute MI patients in states with and without PCI public reporting programs.
So what does this pattern of care imply about the care decisions being made in states with PCI public reporting programs?
Are physicians in these states simply doing a better job of risk-assessment and avoiding PCIs for patients where outcomes were futile?
Or, are they doing a better job of judging appropriateness and the likelihood of patient benefit from the procedure?
Or, have the concerns of public reporting skeptics been realized, such that physicians and hospitals are avoiding offering care for the sickest patients because of concerns about their publicly reported outcomes?
What do you think these new data mean for practice?
If public reporting programs are the new norm, are they driving efforts to genuinely improve quality or merely incentivizing ways to game the numbers, perhaps by not offering care to the highest-risk patients?
And if you are in a state that publicly reports PCI outcomes, can you share any stories of your experiences?
October 10th, 2012
Chocolate and Nobel Prizes Linked
Larry Husten, PHD
You don’t have to be a genius to like chocolate, but geniuses are more likely to eat lots of chocolate, at least according to a new paper published in the august New England Journal of Medicine. Franz Messerli reports a highly significant correlation between a nation’s per capita chocolate consumption and the rate at which its citizens win Nobel Prizes.
Building on research raising the possibility that the flavanols in chocolate may enhance cognitive performance, Messerli “wondered whether there would be a correlation between a country’s level of chocolate consumption and its population’s cognitive function.” Using a country’s success in winning Nobel Prizes as a surrogate for “the proportion with superior cognitive function” in that country, he analyzed the relationship between the number of Nobel laureates and the yearly chocolate consumption per capita in a given country.
Messerli reported “a close, significant linear correlation (r=0.791, p<0.0001) between chocolate consumption per capita and the number of Nobel laureates per 10 million persons in a total of 23 countries.” The relationship was even stronger when Sweden, the home of the Nobel Prize, was removed from the calculations, as it appeared to have won more Nobel prizes than expected based on its chocolate consumption. Switzerland, on the other hand, “was the top performer in terms of both the number of Nobel laureates and chocolate consumption.” (It should perhaps be noted at this point that Messerli, a hypertension expert who lives in New York City, was born in Switzerland and reports in his disclosure statement that he consumes chocolate daily, “mostly but not exclusively in the form of Lindt’s dark varieties.”)
Messerli duly points out that correlation does not prove causation, but, he writes, “since chocolate consumption has been documented to improve cognitive function, it seems most likely that in a dose-dependent way, chocolate intake provides the abundant fertile ground needed for the sprouting of Nobel laureates. Obviously, these findings are hypothesis-generating only and will have to be tested in a prospective, randomized trial.”
Regarding Sweden’s status as an outlier, Messerli writes that “one cannot quite escape the notion that either the Nobel Committee in Stockholm has some inherent patriotic bias when assessing the candidates for these awards or, perhaps, that the Swedes are particularly sensitive to chocolate, and even minuscule amounts greatly enhance their cognition.” Messerli also raises the possibility that reverse causation may explain the main finding, “that is, that enhanced cognitive performance could stimulate countrywide chocolate consumption.”
October 10th, 2012
Danish Study Gives a Boost to Hormone Replacement Therapy ‘Timing Hypothesis’
Larry Husten, PHD
Hormone replacement therapy (HRT) suffered a sharp blow a decade ago when the Women’s Health Initiative failed to show any cardiovascular benefit in women taking HRT. Despite the setback, many researchers theorized that HRT might still be beneficial in women who start HRT close to menopause. Now a study from Denmark published in BMJ lends strong support to the “timing hypothesis.”
Louise Lind Schierbeck and colleagues analyzed data from 1006 recently postmenopausal or perimenopausal women who were randomized to HRT or no treatment.
After 10 years, there were 16 primary endpoint events (the composite of death, admission to the hospital for heart failure, or MI) in the HRT group compared with 33 in the control group (hazard ratio 0.48, CI 0.26-0.87, p=0.015).
- Mortality: 15 versus 26, HR 0.57, 0.30-1.08, p=0.084
- Heart failure: 1 versus 7, HR 0.14, 0.02-1.16, p=0.07
- MI: 1 versus 4, HR 0.25, 0.03-2.21, p=0.21.
There was no significant difference between the groups in the rate of any cancer or of breast cancer. Women who were under 50 years of age at the start of the trial appeared to enjoy the greatest benefit from HRT.
The authors concluded:
Our findings suggest that initiation of hormone replacement therapy in women early after menopause significantly reduces the risk of the combined endpoint of mortality, myocardial infarction, or heart failure. Importantly, early initiation and prolonged hormone replacement therapy did not result in an increased risk of breast cancer or stroke.
Andrew Kaunitz told Physician’s First Watch that, when “taken together with findings from a subanalysis of younger women from the WHI, these data should reassure clinicians and women that use of hormone therapy in recently menopausal women is safe.”
October 9th, 2012
PCI Utilization Lower in States with Public Reporting of Outcomes
Larry Husten, PHD
In patients with acute MI, utilization of percutaneous coronary intervention (PCI) is lower in states that publicly report outcomes data, according to a new study published in JAMA. Despite the difference in utilization, however, there was no difference in mortality between reporting and nonreporting states.
Karen Joynt and colleagues used Medicare data to analyze PCI utilization and mortality in acute MI patients in three states with public reporting of PCI outcomes (New York, Massachusetts, and Pennsylvania) and other states in the same region without public reporting. The differences in utilization were greatest in patients at highest risk, who presented with ST-segment elevation MI (STEMI), cardiogenic shock, or cardiac arrest.
- Overall unadjusted PCI rate: 37.7% for reporting states versus 42.7% for nonreporting states
- Risk-adjust odds ratio: 0.82, CI 0.71-0.93, p=0.003)
Overall mortality did not differ between the reporting and nonreporting states (12.8% and 12.1%, respectively; adjusted OR 1.08 (CI 0.96-1.20], p=0.20), although there was a significant mortality difference in the STEMI subgroup (13.5% vs. 11.0%; OR 1.35, CI 1.10-1.66, p=0.004).
In Massachusetts, where outcomes reporting was initiated during the course of the study period, PCI utilization was at first no different from the other nonreporting states, but was significantly lower than nonreporting states after the change.
The authors offer two potential explanations for the findings:
…the foregone procedures were futile or unnecessary, and public reporting focused clinicians on ensuring that only the most appropriate procedures were performed. Alternatively, public reporting may have led clinicians to avoid PCI in eligible patients because of concern over the risk of poor outcomes.
The mortality findings, they write, suggest “that the foregone procedures might have been a mix of appropriate and inappropriate PCIs.”
In an accompanying editorial, Mauro Mosucci writes that the mortality finding may be due to “a conscious or unconscious ‘futility assessment'” in states with public reporting,” leading to “avoidance of PCI for patients who are less likely to benefit.” Alternatively, “public reporting might have resulted in a drive toward improved quality of care and improved outcomes in patients receiving PCI, offsetting the adverse effect of not performing PCI in high-risk patients.” Mosucci also points out that the data may be skewed because public reporting might result in “gaming” the coding of cases.
In his Voices blog, Joe Ross wonders what’s really behind the lower rates of PCI use. Read his theories, and share your comments or questions, here.
October 9th, 2012
Erasmus Medical Center Releases Final Report on Cardiovascular Research Scandal
Larry Husten, PHD
After an extensive investigation, a large medical center in the Netherlands has confirmed earlier charges of research misconduct against a prominent cardiovascular researcher. On Tuesday, Erasmus Medical Center in Rotterdam released a final report on the scientific integrity of trials conducted by Don Poldermans, a well-known and highly prolific Dutch cardiovascular researcher. The final report contains numerous allegations of scientific misconduct related to several clinical trials run by Poldermans at Erasmus MC.
Poldermans admits responsibility for some instances of misconduct but also vigorously denies the most serious charges involving scientific fraud. He provided CardioExchange with detailed written responses to the charges and also presented a spirited defense during an exclusive interview conducted in August during the ESC meeting in Munich.
In a statement to the press, Erasmus MC said that the new report confirms the earlier suspicions raised in the case, which ignited a firestorm of controversy in the Netherlands last winter. The press statement mentions”serious shortcomings” in obtaining informed consent for patients enrolled in studies and the submissions of “unreliable data” based on “scientifically inaccurate data collection.” Poldermans and Erasmus MC are in full agreement, however, that the misconduct “did not lead to health damage to patients.”
In a statement prepared for CardioExchange in response to the report, Poldermans apologizes for his “administrative carelessness” and accepts full responsibility for the missing consent forms. He accepts the “extreme consequence” — his dismissal from Erasmus MC — over this issue, but emphasizes that no harm occurred to any of the patients and, further, that no additional or unnecessary treatments or diagnostic procedures took place. He vigorously denies any larger scientific misconduct or fraud.
The committee report — and Poldermans defense — are often highly technical, and the report is based on incomplete and inconsistent information obtained by the investigating committee at Erasmus MC. One problem is missing data. Investigators scrutinizing Polderman’s work have been unable to find the case files and other documentation for some patients in the trials. Consequently, the report raises concerns about possible data fabrication. Poldermans strongly denies this suggestion and states that he properly stored all the files at Erasmus MC. His defense is that some records were damaged by water and some records disappeared when the hospital itself threw out boxes of documents stored in the archives.
Poldermans had been a professor of medicine and the head of perioperative cardiac care at Erasmus MC. He was widely published and active in the field, serving as a member of the European Society of Cardiology committee for practice guidelines and as the chairperson of the ESC guidelines on preoperative cardiac risk assessment and perioperative cardiac management in noncardiac surgery. He was also the lead author of the influential 1999 New England Journal of Medicine DECREASE study on the use of bisoprolol during vascular surgery. Poldermans now works as a vascular medicine physician at a nonteaching hospital in the Netherlands.
CardioExchange will publish a follow-up story in the near future based on an interview with Poldermans conducted in Munich during the ESC.
Related Links:
October 9th, 2012
Observational Study Links Common Household Chemical to Cardiovascular Disease
Larry Husten, PHD
High levels of a man-made chemical widely used in common household products and detectable in more than 98% of people may increase the risk for cardiovascular (CV) disease and peripheral arterial disease (PAD), according to a study published in the Archives of Internal Medicine. (The study was published online in September and will appear in this week’s print edition of Archives.)
Anoop Shankar and colleagues measured serum levels of perfluorooctanoic acid (PFOA) in 1216 people participating in the National Health and Nutritional Examination Survey (NHANES) and found a strong correlation between PAD and CV disease and PFOA levels. After adjustment for other risk factors, people in the highest quartile of PFOA levels had about double the risk for CV disease and PAD:
- Odds ratio for the top quartile of PFOA: CV disease 2.01 (1.12-3.60), PAD 2.78 (1.03-3.08), CVD or PAD 2.28 (1.40-3.71)
The authors cite several studies that support the plausibility of a harmful effect of PFOA. They duly note the risk of “residual confounding and reverse causality,” but write that if their findings are replicated “the population-attributable risk of PFOA exposure on CVD risk could potentially be high.”
In an invited commentary, Debabrata Mukherjee acknowledges the limitations of the study but writes that, given the biological plausibility in the relationship, “it would make sense to limit or to eliminate the use of PFOA and its congeners in industry through legislation and regulation while improving water purification and treatment techniques to try and remove this potentially toxic chemical from our water supply.” But, he warns concerns about PFOA “should not dissuade us from aggressively managing known existing risk factors for CVD such as dyslipidemia, smoking, hypertension, diabetes, obesity, and lack of regular physical activity.”
October 8th, 2012
Selections from Richard Lehman’s Literature Review: October 8th
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.
JAMA 3 Oct 2012 Vol 308
Beta-Blockers: No Cardioprotective Effect for Certain Patients (pg. 1340): This week’s most fascinating and practice-changing paper must be this large observational study of beta-adrenergic blocking drugs and clinical outcomes in three classes of patients: those with a remote history of myocardial infarction, those with stable coronary artery disease (CAD) and those with risk factors for CAD. The primary outcome was a composite of cardiovascular death, nonfatal MI, and nonfatal stroke. The result of this propensity-matched analysis was even more startling than the authors let on in their abstract: not only was there no significant benefit to patients with past MI, there was statistically significant harm to those with CV risk factors but no known CAD (see Figure 1: HR 1.18 (95%CI 1.02-1.36). When I first started doctoring, ß-blockers (a brand new British invention) were considered a panacea for everything cardiovascular, except heart failure. Now it seems they are useless for most things cardiovascular, except heart failure.
NEJM 4 Oct 2012 Vol 367
Intra-Aortic Balloon Support for MI with Cardiogenic Shock (pg. 1287): Cardiogenic shock is the kind of situation where people want to rush in and do things. It is not for me to criticize such people, as I am rarely faced with patients suddenly on the cusp of death; but reading the literature, it does strike me that their intentions are often better than their results. Case-hardened, cash-starved British cardiologists often refer to intravenous inotropes as “embalming fluid,” but they still sometimes use them: intra-aortic balloon support, on the other hand, has never really caught on over here. Nor should it, according to this admirable German trial which randomized 600 patients in cardiogenic shock following myocardial infarction to receive intra-aortic balloon counterpulsation or none, prior to intended revascularization. The 30-day mortality in both groups was the same, at 40%. The study had more than 240 primary end-points—an insurance policy gone mad—but it still could not prove that the procedure has any real value. These balloons should be filled with helium and sold at street corners.
Prasugrel vs. Clopidogrel for Acute Coronary Syndromes without Revascularization (pg. 1297): More disappointment comes in this long-awaited trial of prasugrel versus clopidogrel for acute coronary syndromes without revascularization. Since a substantial proportion of people lack the ability to convert clopidogrel to its active metabolite, the newer drug prasugrel (which doesn’t need this conversion) should be much the better platelet inhibitor. But this just doesn’t seem to happen in real life. Eli Lilly and Daiichi Sankyo spent tens of millions of dollars recruiting 9326 patients at 966 sites in 52 countries and following them up for two and a half years—all to prove that their new drug is no better than the old one which costs twenty times less. Much as we would welcome a better drug for cardiovascular protection, this is good news for cash-strapped health systems.
C-Reactive Protein, Fibrinogen, and CVD Prediction (pg. 1310): Erasmus of Rotterdam visited Cambridge in England in the 1510s and was struck by its polyphonic music (which he couldn’t follow) and its futile scholastic learning, both of which he went on to ridicule in Encomium Moriae (literally Praise of Fools, but also containing a friendly pun on the name of his friend Thomas More). How little has changed in 500 years. The Cambridge (UK) authors of this study demonstrate that if you add high-sensitivity C-reactive protein to the risk score of a European population of mean age 60, you can reclassify enough intermediate risk individuals to make them worthy of a statin and so prevent one cardiovascular event (non-fatal or otherwise) in 10 years for every 400-500 people screened. That’s assuming you follow the current rules and don’t just lower the general threshold for statin prescribing to age 50, or something like that. You cannot help feeling sorry for the Emerging Risk Factors Collaboration which did this study: for all its clinical relevance it might as well be the St Thomas Aquinas Institute for Angel-Counting. But there are still a lot of great choirs to be heard in Cambridge, and someone could write a motet for them about it: O sensitivissimum protein C-reactivum, imple in cordibus servorum tuorum etc.
Lancet 6 Oct 2012 Vol 380
A Comparison of Thrombectomy Devices for Acute Ischemic Stroke: Britain’s premier medical journal gets more bizarre with each issue. Thrombectomy devices for acute stroke have yet to earn any place at all in mainstream clinical practice, but the Lancet gives all its research space this week to commercial studies comparing one device with two others. I would like to like the Lancet, but it’s very difficult.
October 8th, 2012
Triple Antithrombotic Therapy: What — and When — Is the Bleeding Risk?
Morten Lamberts, MD and John Ryan, MD
In a national registry study, researchers in Denmark studied the effect of multiple antithrombotic drugs — including triple therapy with warfarin, aspirin, and clopidogrel — in patients with atrial fibrillation and coronary artery disease (indicated by hospitalization for PCI or MI).
Among more than11,000 patients, 30-day bleeding rates were:
- Warfarin + ASA + clopidogrel (triple therapy): 22.6 per 100 patient-years
- Warfarin + single antiplatelet: 20.3 per 100 patient-years
- ASA + clopidogrel: 14.3 per 100 patient-years.
The increased bleeding risk observed with triple therapy persisted for up to 1 year after the initiation of therapy.
CardioExchange’s John Ryan sat down with lead investigator Morten Lamberts, MD, to ask some questions about this study and its implications.
Ryan: Dr Lamberts, congratulations on this wonderful paper. Can you give our readers an idea of why you believed it was important to do this study?
Lamberts: Thank you very much. In everyday practice, we face the problem of bleeding complications when balancing the addition of antiplatelet(s) on top of oral anticoagulation therapy in AF patients who suffer MI or undergo PCI. We know that antiplatelet therapy is indicated for CAD and oral anticoagulant therapy for AF, and current guidelines support an additive approach, although no firm evidence of the safety of triple therapy (ASA, clopidogrel, oral anticoagulant) exists. Our perception that short-term triple treatment is safe is based on expert opinion, which, if unfounded, could potentially put patients at even greater hazard.
Ryan: The mean CHADS2 score in this study was 1.5 (SD, 1.5). I think it is important for people to recognize that these results were obtained in a well-treated cohort that is not necessarily at high risk for bleeding. Similarly, from what I understand, you did not observe any significant differences in risk between various subgroups. Can you expand on that for our readers?
Lamberts: We looked at several clinically relevant subgroups for any differences in our main finding of early serious bleeding with triple therapy use. Regardless of sex, age, CHADS2 score (≥2 or ≤1), or MI or PCI status at inclusion, the relative risk for bleeding events was increased, particularly within the first 90 days after the index MI or PCI.
Ryan: At inclusion, 13% of patients were on triple therapy, whereas by day 180, only 8% were. Do you have a sense as to why treatment was altered in almost 40% of patients? And also, which agent was typically stopped when physicians took people off triple therapy?
Lamberts: We defined antithrombotic treatment from ongoing medication, which allowed us to continually update exposure status based on actual redeemed prescriptions; thus, patients could change exposure status during the 1-year follow-up period. Current guidelines arbitrarily recommend triple therapy for 1 to 12 months, based on the severity of CAD presentation, type of stent implanted, and presumed bleeding risk. We also know from several studies that antithrombotic treatment in real-life patients after MI or PCI is fairly consistent and adheres to recommendations, but antithrombotic treatment in AF patients is highly variable. In this light I am not surprised that the proportion of triple therapy users declined. We did not specifically look at which agent was stopped, but it seems to be the case that if an oral anticoagulant is prescribed, this treatment is continued.
Ryan: It is noteworthy that the combined endpoint of cardiovascular death, MI, and ischemic stroke was similar in patients on triple therapy and in those on warfarin plus a single antiplatelet agent. Did this surprise you, and what recommendations can you make based on that data?
Lamberts: Although the study was designed to evaluate safety issues, it somewhat surprised us that we could not find a benefit for the combined thrombosis outcome with triple therapy. With regard to recommendations, I think we need further evaluation of specific treatments and more details on outcomes (i.e., ischemic stroke, death, stent thrombosis, and recurrent MI), before the data can support advice against use of triple therapy. Nevertheless, I believe these data raise important questions for patients with dual indications for antithrombotic therapy. When the patient is already anticoagulated, do we really need two drugs to inhibit platelet aggregation? And, are there differences between the available antiplatelet agents?
Ryan: So, let me pose a case: If I have a 71 year old man with AF and diabetes mellitus who needs PCI for critical LAD disease, should I be thinking about placing a bare-metal stent so I can discontinue his triple therapy as soon as possible?
Lamberts: This is a very difficult case; interventionalists especially know this problem well. I believe that in this setting, a BMS should be preferred, which also accords with current American and European guidelines. The reasoning, as you say, is that the risk for stent thrombosis is lower with a BMS compared with a drug-eluting stent; consequently, an earlier removal of an antiplatelet agent is possible. Although our study suggests that even 30 days of triple therapy is associated with increased bleeding risk, at this point, we cannot firmly say that an oral anticoagulant and a single antiplatelet are sufficient to protect from recurrent coronary events in the initial vulnerable period. Until solid evidence is available, treating physicians must assess bleeding and thrombosis risks individually. They should also be aware that our data suggests that triple therapy does not have a safe therapeutic window.
October 5th, 2012
A Plea For Open Science And Data Sharing
Harlan M. Krumholz, MD, SM
I am still out pushing the cause of open science and data sharing. Something we can do better through the scientific community. It starts with the will – and a focus on societal good. The ‘how’ is challenging – but the problems can be solved.
Earlier this week I gave a talk at an Institute of Medicine workshop on this topic. I told the group:
Let’s be clear about what is needed. We need to have studies published and summary results reported on clinicaltrials.gov – but that is not enough. We need to have individual patient-level data broadly available for investigators – not parsed out to selected individuals – but available broadly and freely.
I invite CardioExchange members to read the whole talk— don’t worry, it’s brief– and start a discussion here about this important subject.
October 4th, 2012
U.K. Study Casts Doubts on Value of Type 2 Diabetes Screening
Larry Husten, PHD
The dramatic growth in type 2 diabetes has resulted in increased interest in screening programs. Now a new study published in the Lancet raises concerns that screening programs may not result in long-term improvement in outcomes.
In the ADDITION-Cambridge study, investigators in the U.K. randomized general practices to either screening or no screening. The practices allocated to screening were further divided to either intensive cardiovascular risk reduction or standard care. The study population included more than 20,000 adults 40-69 years of age at high risk for undiagnosed diabetes.
Some 3% of patients in the screening groups received a diagnosis of diabetes. After a median follow-up of 9.6 years, there were no significant differences between the screening and control groups.
Rate per 1000 person-years and hazard ratios for the no-screening and the screening group:
- Mortality: 9.89 versus 10.50, 1.06 (CI 0.90-1.25)
- CV mortality: 3.25 versus 3.30, 1.02 (0.75-1.38)
The authors proposed several explanations for the lack of benefit associated withs screening, including ad-hoc screening outside the practice setting in the unscreened group, patients who did not follow the screening program, and concurrent gains in identifying and managing other cardiovascular risk factors during the study period. In addition, the patient population in the study may have been a relatively healthy population with a lower prevalence of undiagnosed diabetes.
The authors concluded that “if population-based screening for diabetes is to be implemented, it should be undertaken alongside assessment and management of risk factors for diabetes and cardiovascular disease and population level preventive strategies targeting underlying determinants of these diseases.”
In a Lancet press release, senior author Simon Griffin said that “the benefits of screening might be smaller than expected and restricted to individuals with detectable disease. However, benefits to the population could be increased by including the detection and management of cardiovascular risk factors alongside the assessment of diabetes risk, performing repeated rounds of screening, and improving strategies to maximize the uptake of screening.”
In an accompanying comment, Michael Engelgau and Edward Gregg write that prevention programs should screen not just for diabetes but for high-risk individuals as well, though they note that this strategy “assumes that effective prevention programs are available to high-risk cases.” Further, the value of screening depends “on more than just mortality as an outcome,” and will need to include morbidity, quality of life, and costs.
