February 25th, 2014
FDA Approves New Catheter for Treatment of Atrial Fibrillation
Larry Husten, PHD
The FDA has granted marketing approval for the Thermocool Smarttouch ablation catheter for use in patients with drug-resistant paroxysmal atrial fibrillation (AF), sustained monomorphic ischemic ventricular tachycardia, and type I atrial flutter. The device is manufactured by Biosense Webster, a Johnson & Johnson company.
The device, according to the company, “is the first therapeutic catheter approved in the U.S. that enables direct and real-time measurement of contact force during catheter ablation procedures.”
The new catheter was evaluated in the SMART-AF Trial, which was presented last May at the Heart Rhythm Society meeting (webcast of presentation). At 1 year, there was a 74% overall success rate in patients treated with the catheter. There were, however, four cases of tamponade among the 160 patients who underwent ablation.
“The Thermcool Smarttouch catheter is an important new device that will benefit the electrophysiology community, as it will enable us to more precisely control the amount of contact force applied to the heart wall when creating lesions during catheter ablation,” said Andrea Natale, the Primary Investigator of the trial, in a press release. “Data from the SMART-AF Trial demonstrated that consistent and stable application of contact force has a significant impact on patient outcomes. The use of contact force-sensing technology has emerged as a critical tool in delivering optimal outcomes in the treatment of patients with atrial fibrillation and represents a major advancement for the clinical community.”
February 24th, 2014
Vitamin Supplements Come Up Short Once Again
Larry Husten, PHD
Once again, the U.S. Preventive Services Task Force (USPSTF) has concluded that there is no good evidence to support the routine use of multivitamins or most individual or combination vitamins by healthy adults to prevent cardiovascular disease or cancer.
The USPSTF also recommended against the use of two specific vitamins — beta-carotene and vitamin E. Beta-carotene has been linked to a significant increase in the risk for lung cancer among smokers, while “a large and consistent body of evidence has demonstrated that vitamin E supplementation has no effect on cardiovascular disease, cancer, or all-cause mortality.”
For other vitamins or multivitamins, the task force found few significant harms, though they said the evidence was insufficient to allow definitive assessments of the risks and benefits.
The recommendation statement, published in Annals of Internal Medicine, updates the USPSTF’s previous 2003 recommendations and incorporates new evidence about vitamin D, calcium, selenium, and folic acid. An initial draft of the recommendation statement was published last December. The USPSTF statement is broadly consistent with similar statements from the National Institutes of Health, the Academy of Nutrition and Dietetics, the American Cancer Society, the American Institute for Cancer Research, the American Heart Association, and the American Academy of Family Physicians, all of which found no evidence that vitamins could help prevent cardiovascular disease or cancer.
The USPSTF states that vitamins and minerals are essential to overall health and notes that “a diet rich in fruits, vegetables, whole grains, fat-free and low-fat dairy products, and seafood has been associated with a reduced risk for cardiovascular disease and cancer.” The group also acknowledges that some people with well-defined conditions may benefit from specific nutrients. Folic acid, for instance, when taken by pregnant women can help prevent neural tube defects, and vitamin D may be beneficial in older people to prevent damage from falling.
Nearly half (40%) of U.S. adults take at least one dietary supplement, and nearly a third (32%) take a multivitamin supplement. In 2010, people in the U.S. spent more than $28 billion on dietary supplements.
February 24th, 2014
What Is “Non-Valvular” Atrial Fibrillation?
Shengshou Hu, M.D.
CardioExchange welcomes this guest post from Dr. Westby Fisher, an electrophysiologist practicing at NorthShore University HealthSystem in Evanston, Illinois, and a Clinical Associate Professor of Medicine at the University of Chicago’s Pritzker School of Medicine. This piece originally appeared on his blog, Dr. Wes.
With the recent heavy marketing of the relatively new novel oral anticoagulants dabigatran, rivaroxaban, and apixaban, a new marketing phrase has been born: “non-valvular” atrial fibrillation.
What, exactly, is “non-valvular” atrial fibrillation?
Is it atrial fibrillation without any valvular heart disease like a teeny, tiny bit of functional mitral insufficiency? Or should doctors “ignore” the degree of mitral insufficiency when prescribing these medications? What about mitral-valve-prolapse patients with severe prolapse?
Is it atrial fibrillation without the presence of any prosthetic heart valve? What about a valve ring placed when a mitral valve is surgically “repaired?”
Is it atrial fibrillation without any rheumatic heart disease? What about mild mitral stenosis compared to moderate or severe mitral stenosis? If there’s a difference, what valve area should we use to judge safety of prescribing the novel oral antiocoagulants?
Or is it some combination of one or more of these above patient groups?
For doctors who manage patients with atrial fibrillation and are considering if they should offer a novel oral anticoagulant to a patient in lieu of warfarin, this issue is not a trivial question.
To answer some of these questions, we should turn to the RE-LY, Rocket AF, and Atristotle Trials. But these trials offer only minimal guidance to today’s practicing physicians.
For instance, in the RE-LY trial, only patients without “history of heart valve disorder (i.e., prosthetic valve or hemodynamically relevant valve disease)” were studied. What, exactly, do they mean by “hemodynamically relevant heart valve disease?” Does any valve qualify or just the mitral valve?
The Rocket AF trial describes their “non-valvular” heart disease patients a bit better as those with (1) hemodynamically significant mitral valve stenosis or (2) a prosthetic heart valve (annuloplasty with or without prosthetic ring, commissurotomy and/or valvuloplasty WERE permitted.) But were mild mitral stenosis patients included? What, exactly, defined “hemodynamically-significant” mitral stenosis patients?
The Aristotle trial defined their excluded valvular heart disease as patients with “moderate or severe mitral stenosis, or conditions other than atrial fibrillation that required anticoagulation (e.g., a prosthetic heart valve).” The reader must assume that surgically-repaired mitral valves were okay, but were they included or excluded from this trial – we’re not sure.
For doctors on the front line of medicine who might want to prescribe these new drugs to their patients, the term “non-valvular atrial fibrillation” seems to mean different things to different people.
Common sense would dictate that any patient with mitral stenosis (of any severity, in my opinion — be it rheumatic or post-surgical) or patients with prior placement of a prosthetic heart valve (either bioprosthetic or mechanical) should not be considered for these agents. But this is just my wild-ass guess. After all, there is no clear consensus on what really defines “non-valvular” atrial fibrillation, especially when we examine the evidence-based data available to doctors on this issue.
But beyond this, as researchers test new therapies, we should be careful not to coin confusing new marketing terms to describe a complicated constellation of patients. Otherwise, we might risk injuring those we really are trying to help.
February 24th, 2014
Meta-Analysis Links Vegetarian Diet and Lower Blood Pressure
Larry Husten, PHD
A new meta-analysis provides the strongest evidence yet that a vegetarian diet is strongly associated with lower blood pressure. Although various health benefits of a vegetarian diet have often been proposed, a rigorous examination of the effect on blood pressure has not been previously performed.
In a paper published in JAMA Internal Medicine, Japanese researchers analyzed data from seven clinical trials, including 311 participants, and 32 observational studies, including 21,604 participants. In the clinical trials the vegetarian diet was associated with a 4.8 mm Hg drop in the systolic blood pressure and a 2.2 mm Hg drop in the diastolic blood pressure. In the observational studies, the reductions were 6.9 mm Hg and 4.7 mm Hg.
The authors noted that the magnitude of the blood pressure-lowering effect was about half the size of typical antihypertensive drugs and roughly equivalent to commonly recommended lifestyle modifications such as a low-salt diet or weight reduction. Based on previous research the blood pressure reductions would be expected to lead to a 7% reduction in overall mortality, a 9% reduction in coronary heart disease, and a 14% reduction in stroke.
The authors speculated about possible explanations for the relationship between the vegetarian diet and blood pressure:
- Vegetarians are less likely to be obese and more likely to have a lower body mass index than nonvegetarians.
- Vegetarian diets are high in potassium.
- Some but not all studies have found that vegetarian diets contain less sodium.
- Vegetarians may drink less alcohol.
February 24th, 2014
Selections from Richard Lehman’s Literature Review: February 24th
Richard Lehman, BM, BCh, MRCGP
CardioExchange is pleased to reprint this selection from Dr. Richard Lehman’s weekly journal review blog at BMJ.com. Selected summaries are relevant to our audience, but we encourage members to engage with the entire blog.
JAMA 19 Feb 2014 Vol 311
Radiofrequency Ablation vs Antiarrhythmic Drugs as First-Line Treatment of Paroxysmal Atrial Fibrillation (pg. 692): As a would be designer of decision aids, I am always on the look out for situations of clinical equipoise. Take atrial fibrillation. The classic choices are between rate control or rhythm control, between various beta-blockers, or amiodarone or digoxin, or elective cardioversion; and between aspirin and warfarin or one of the fixed dose new anticoagulants. All very entertaining and ever changing. Now a trial comes along comparing drug therapy with radiofrequency ablation as first-line treatment for paroxysmal AF. The two work equally badly: recurrences are common. So is this a case of clinical equipoise? I don’t think so, because in this trial the rate of serious complications in the radiofrequency ablation group was 9%: an alarming 6% of the group had cardiac tamponade. Give me those pills please doc.
Lancet 22 Feb 2014 Vol 383
18F-fluoride positron emission tomography for identification of ruptured and high-risk coronary atherosclerotic plaques (pg. 705): The Holy Grail of cardiac imaging would be a technique for spotting the atheromatous plaques most likely to rupture as opposed to those merely causing the most stenosis. It’s just possible that it has now been found, but it’s far from clear to a mere onlooker what the clinical consequences might be. A team from Edinburgh used the radioactive tracer 18F-sodium fluoride to identify the kind of plaque that is most likely to cause trouble. In a complex exploratory study, they took newly harvested plaque from people who had just had carotid endarterectomy and showed that marked 18F-NaF uptake occurred at the site of all carotid plaque ruptures and was associated with histological evidence of active calcification, macrophage infiltration, apoptosis, and necrosis. Concurrently they used the tracer in 40 patients with recent myocardial infarction and in 40 with stable angina, and located its presence using PET-CT imaging of the coronary arteries. They also used intra-coronary ultrasound on these patients to pick up calcification and necrosis. In this way they were able to establish that the areas of highest 18F-NaF uptake are in plaques which show the most dangerous characteristics. This is clever stuff, and is bound to lead to a wave of new studies using this relatively cheap isotope and PET-CT hardware wherever it may be available. Perhaps the insights this generates will one day permeate into the world of real-life patient management: in the mean time it is nice to see some good old British investigational science of world class.
Symplicity HTN-1 and Symplicity HTN-3:
How I was misled by The Lancet last week:
In last week’s Lancet, three articles celebrated the success of renal denervation for “treatment-resistant” hypertension. There was a report of the Symplicity HTN-1 trial emphasizing huge sustained reductions in BP, though there was no control arm and very incomplete follow-up, as I noted. There was a laudatory editorial and a profile of the chief investigator, Henry Krum, pointing out that Australia was a good place to do clinical trials because of its permissive regulatory environment.
But it had escaped my attention that the Symplicity-1 trial had already been superseded by Symplicity-HTN-3. This well-powered randomized trial using a sham control failed to meet its primary end point, a 10mmHg reduction in systolic BP. This had been announced by Medtronic on 9 Jan. And in fact Darrel Francis and colleagues in the renal denervation field had already pointed out the inherent flaws in the design and execution of Symplicity HTN-1 in a paper just published in the International Journal of Cardiology, another Elsevier journal.
This had managed to get under my radar, which isn’t too surprising; but it is quite worrying that it managed to get under The Lancet‘s.
February 21st, 2014
Unpacking a Systematic Review of TAVR Research
Philip Green, MD and Kumar Dharmarajan, MD MBA
The Annals of Internal Medicine recently published an article by Caroline A. Kim and colleagues, titled “Functional Status and Quality of Life After Transcatheter Aortic Valve Replacement: A Systematic Review.” We believe that this paper warrants careful analysis.
Kim et al. reviewed 62 studies, involving more than 11,000 patients who underwent TAVR; all the studies included some measure of functional status or quality of life. Despite heterogeneity in design, quality, and results among the studies, a clear message emerged: Overall, TAVR is associated with statistically significant, though at times clinically modest, improvements in symptoms, functional status, and quality of life 6 to 23 months after the procedure. Two aspects of the review by Kim and colleagues merit further examination.
First, the authors state that function and symptoms do not improve for a substantial minority of TAVR recipients. This conclusion must be interpreted carefully. Although therapeutic failures do occur after TAVR, many patients who report no symptom improvement are actually doing quite well. Often patients with the worst baseline functional status have the highest mortality rate after TAVR, but they also often experience the greatest improvements in function and quality of life. The opposite is frequently true for patients whose symptoms were already mild before TAVR and who, therefore, do not feel much better after the procedure. For patients with mild preprocedural symptoms, we must ensure that their aortic stenosis is truly severe and that they do not have other life-limiting conditions, to maximize the likelihood that TAVR will confer a meaningful survival benefit. To that end, researchers must better characterize the heterogeneity in symptom response so that we can better predict improvements in function and symptoms for individual patients. This goal may be more important than understanding the overall expected benefit across broad study cohorts.
Second, as the authors note, survival bias may have influenced the study findings. Specifically, patients with the worst functional status and symptom scores might have been the most likely to die and, therefore, the least likely to be represented in analyses of outcomes 6, 12, or 24 months after the procedure. We therefore need to integrate survival, functional status, and symptoms into a single, validated outcome measure. Suzanne Arnold and colleagues have proposed combining both mortality and quality-of-life measures into a composite endpoint on the basis of empirical data in the PARTNER trial. Arnold argues that the most appropriate definition of a poor outcome 6 months after TAVR involves consideration of (1) death, (2) a Kansas City Cardiomyopathy Questionnaire summary score <45 (corresponding to class IV heart failure), and (3) a KCCQ summary score decrease of ≥10 points. In essence, patients who have died, have class IV heart failure, or have significantly worse symptoms post-TAVR have failed to achieve a therapeutic endpoint. The exact parameters of such a definition can be debated, of course, but we nonetheless see a need for an integrated endpoint that includes survival and quality of life, to help us better identify which patients benefit most from TAVR.
JOIN THE DISCUSSION
Do you agree with the analysis of Dr. Green and Dr. Dharmarajan?
February 19th, 2014
Victor Dzau Leaving Duke to Head the Institute of Medicine
Larry Husten, PHD
Cardiologist Victor Dzau will leave his positions as the chancellor for health affairs at Duke University and the CEO of the Duke University Health System to become the next president of the Institute of Medicine. He will replace Harvey Fineberg, who has been the IOM president for the last 12 years.
“I am humbled and honored to be selected to lead the IOM at a time of unprecedented opportunities and challenges in health, health care, and biomedical sciences,” said Dzau in a statement from the IOM. “Harvey Fineberg has been an exceptional leader of the IOM, and I am committed to building on his outstanding work and advancing the impact of the IOM on the nation and globally.”
Before moving to Duke almost a decade ago, Dzau was the chair of the department of medicine and director of research at Brigham and Women’s Hospital and the Hersey Professor of the Theory and Practice of Physic (Medicine) at Harvard Medical School. Prior to that, he had been the chair of the department of medicine at Stanford University. In his career as a researcher, Dzau played a key role in understanding the renin-angiotensin-aldosterone system.
Robert Califf, director of the Duke Translational Medicine Institute, sent the following comment:
This appointment is a real honor for Victor and for Duke. During his tenure, the instituiton has grown into an academic health and science system, made numerous scientific contributions and thrived financially.
Dzau was first elected to the IOM in 1998. He will begin his 6-year term as president on July 1.
February 18th, 2014
Trial Offers Little Support for Early Use of Radiofrequency Ablation in Atrial Fibrillation
Larry Husten, PHD
A new trial offers little support for early use of radiofrequency ablation (RFA) to treat atrial fibrillation (AF). Current guidelines state that RFA may be indicated in patients with symptomatic paroxysmal AF after antiarrhythmic drug therapy has failed. Although earlier hopes have been dashed that RFA would prove to be a cure for AF, some experts have held out hope that RFA therapy would be better than drug therapy as initial treatment.
Some 127 patients with paroxysmal AF were randomized to antiarrhythmic therapy or RFA as initial treatment in the RAAFT-2 trial, published in JAMA. After 2 years, a documented symptomatic or asymptomatic atrial arrhythmia had occurred in 72.1% of patients in the drug group compared with 54.5% in the RFA group (HR 0.56, CI 0.35-0.90, p=0.02). But the difference in symptomatic arrhythmias alone was much smaller: 59% in the drug group compared with 47% in the RFA group (p=0.03). There were four cases of cardiac tamponade in the RFA group, a serious complication. After 1 year, there was a small improvement in quality of life in the overall patient population, but there was no significant difference between the groups. During the second year of follow-up, 43% of patients in the drug group crossed over and received RFA.
The authors note that although there were no deaths or strokes during the trial, the high rate of cardiac tamponade — despite the fact that all of the participating hospitals were highly experienced in RFA — was an indication that RFA “carries considerable risks that need to be discussed with the patient when offering it as a therapeutic alternative to patients who have not yet taken antiarrhythmic drugs.”
In an accompanying editorial, Hugh Calkins writes that RAAFT-2, along with other studies, “make it clear that symptomatic and asymptomatic recurrences of AF are not uncommon following AF ablation and that the efficacy of this procedure, even in optimal candidates, is modest.” The overall findings serve as “a powerful endorsement” of the current guidelines, which recommend RFA only after drug therapy has failed. However, he states, “patient preference and operator experience are important to consider.”
RAAFT-2 was sponsored by Biosense Webster. Other manufacturers of RFA devices for AF include Medtronic, Boston Scientific, and St. Jude Medical.
February 17th, 2014
Selections from Richard Lehman’s Literature Review: February 17th
Richard Lehman, BM, BCh, MRCGP
CardioExchange is pleased to reprint this selection from Dr. Richard Lehman’s weekly journal review blog at BMJ.com. Selected summaries are relevant to our audience, but we encourage members to engage with the entire blog.
JAMA Internal Medicine
Rates of Complications and Mortality in Older Patients With Diabetes Mellitus (pg. 251): Goodness, it’s taken a long time for the diabetes community to come to terms with the obvious. A study of people over 60 with diabetes finds that the main ill effects of their condition in old age are coronary artery disease and hypoglycaemia. In people who develop diabetes after the age of 60, microvascular disease is so uncommon it is hardly a consideration: whereas the commonest treatments given to lower sugar frequently cause hypoglycaemia and have little or no effect on coronary disease. Step back, guys: treating type 2 diabetes is a whole different ball game in a 65 year old as compared with a 35 year old. One size does not fit all ages. In fact, each patient of any age needs to be treated in accordance with his or her own goals and informed preferences. People with diabetes have for so long been misinformed about the benefits and harms of treatment that I suspect we often keep them on drugs out of sheer embarrassment at admitting we didn’t know what we were doing. And it’s still going on: we “put people on” drugs like incretin mimetics when we haven’t a clue what they do to long-term outcomes, and then congratulate ourselves just because their HbA1c has gone down.
Hospital Variation in the Use of Noninvasive Cardiac Imaging and Its Association With Downstream Testing, Interventions, and Outcomes (online): Another week, another great paper from a Yale medical student. If this is beginning to sound like advertising, I don’t care: I wish every medical school had a Harlan Krumholz and Joe Ross who would encourage attached students to produce work of such quality. This time the student’s name is Kyan Safavi, and he did a massive survey of data about variation in non-invasive cardiac imaging for suspected ischaemia across US hospitals. “Hospitals with higher imaging rates did not have substantially different rates of therapeutic interventions or lower readmission rates for AMI but were more likely to admit patients and perform angiography.” So non-invasive imaging leads to invasive imaging without showing any clear benefit in patient outcomes. Those Americans, eh? But I bet you would find exactly the same variation in the UK, especially between district general and teaching hospitals.
The Lancet
Percutaneous Renal Denervation in Patients with Treatment-Resistant Hypertension (pg. 622) In this paper, the abstract conclusion (called Interpretation) can afford to be laconic: “Changes in blood pressure after renal denervation persist long term in patients with treatment-resistant hypertension, with good safety.” This is indeed true of the 88 out of 153 patients who had full follow-up data at 36 months in this Medtronic-funded Symplicity HTN-1 trial. These were people whose blood pressure remained high despite treatment with an average of five different agents. And the drop in BP following percutaneous radiofrequency ablation of the renal nerve supply was little short of spectacular: a mean fall of 32 mm Hg in systolic and 14.4 mm diastolic. So something really big is happening here, and you could say that this is the kind of intervention which did not get a randomized trial because it didn’t need one. What it did need, however, was tighter follow-up. I know this is something Medtronic are keen to carry out in the future, and to be fair they didn’t design this trial themselves: it was instigated by a company they bought up half way through. But it was a missed opportunity to do better from the outset in the evaluation of a treatment which looks to have immense potential.
February 17th, 2014
Another Satellite of JUPITER: Lipoprotein(a)
Amit Khera, MD
CardioExchange’s Harlan M. Krumholz interviews Amit V. Khera, lead author of an analysis of lipoprotein(a) concentrations and residual vascular risk among participants in the placebo-controlled JUPITER trial of rosuvastatin. The study is published in Circulation.
Krumholz: How did you get interested in lipoprotein(a)?
Khera: Relatively few circulating biomarkers, when measured in patients on moderate- to high-intensity statin therapy, retain their ability to predict future events. My interest in lipoprotein(a) assessment relates to:
- A large body of epidemiologic studies from general populations linking elevated Lp(a) levels with future risk for cardiovascular events
- Multiple putative mechanisms by which Lp(a) may be linked to events, including a prothrombotic role, carrier of oxidized phospholipids, and increasing expression of endothelial adhesion molecules.
- Lp(a) levels are highly stable over time, with more than 50% of variation genetically determined. Furthermore, people born with genetic polymorphisms that correlate with higher Lp(a) levels are at increased risk for disease, thus supporting a causal role for the molecule in atherothrombosis.
Data regarding Lp(a) in the context of potent statin therapy and low-achieved LDL-cholesterol levels is both limited and conflicting, serving as the primary motivation for this analysis.
Krumholz: What should clinicians remember about Lp(a), beyond its being an LDL-like particle with apolipoprotein B covalently linked to apolipoprotein(a)?
Khera: Lipoprotein(a) is linked to both atherosclerotic events and valvular calcification in a relationship that is likely causal in nature. It retains its predictive value beyond standard risk factors, although incremental value is modest. Lp(a) was discovered more than 50 years ago, but we still have a lot to learn about which mechanism of its link to disease is most important and whether we can manipulate its metabolism in risk reduction.
Krumholz: How did the “little a” nomenclature evolve?
Khera: Apo(a), discovered in the 1960s, is a protein byproduct of the LPA gene in humans. The genetic locus is among the most highly polymorphic across the entire human genome, specifically with regard to the number of kringle IV repeats. This apo(a) protein is then covalently linked to apolipoprotein B, thus known as “little a.”
Krumholz: No guideline recommends measurement of this lipid. Do you routinely measure it in your patients? If so, when and why?
Khera: The role of lipoprotein(a) assessment in clinical practice is currently uncertain. In a 2010 consensus statement, the European Atherosclerosis Society suggested measurement of Lp(a) in high-risk patients. A 2011 expert panel convened by the National Lipid Association suggests that measurement is reasonable in selected intermediate- to high-risk patients, such as those with a family history of premature cardiovascular disease.
In my own practice, I have measured Lp(a) using validated assays in a small subgroup of patients with cardiovascular or valvular disease burden otherwise unexplained by conventional risk factors. If Lp(a) is elevated, current evidence would support aggressive risk-factor modification with statins and antiplatelet therapy to achieve global cardiovascular risk reduction. Niacin is known to decrease Lp(a), but its use in patients with elevated values for risk reduction does not have a strong evidence base at this time. I counsel patients that knowledge of their values may become increasingly relevant in the coming years, as we have multiple novel agents that decrease Lp(a) values in development, and I ultimately hope for targeted therapy of Lp(a) metabolism. Patients with extreme values may benefit from lipoprotein apheresis.
Krumholz: What is the main message from your findings?
Khera: In JUPITER, a primary-prevention trial involving patients with low-to-normal LDL-cholesterol but elevated C-reactive protein, lipoprotein(a) values were measured at both baseline and while participants were on potent rosuvastatin therapy. Lp(a) values were highly stable over time and largely independent of other risk factors. Statin therapy had minimal effect on Lp(a) concentrations despite a marked reduction in LDL-cholesterol. Black participants had a more than twofold higher Lp(a) concentration than whites. Both baseline and on-statin values of Lp(a) were linked to increased risk for cardiovascular events. Notably, this finding is in contrast to those from a limited number of smaller studies indicating that Lp(a) may not predict future events once low LDL-cholesterol levels are achieved. Our study, which showed that Lp(a) remains a significant risk factor despite a median on-treatment LDL-cholesterol level of 54 mg/dL, supports ongoing efforts to target Lp(a) metabolism in risk reduction.
JOIN THE DISCUSSION
Share your thoughts on Dr. Khera’s analysis of the lipoprotein(a) findings from JUPITER.
NEJM Journal Watch — Recent Cardiology Articles- New Recommendations for Lipid Management in Patients with Acute Coronary Syndromes
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- Beta-Blocker Use After Takotsubo Syndrome
- CTA-Guided Care in Stable Angina: Long-Term Results
- Patients Need Standardized Education for Accurate Home Blood Pressure Monitoring