Latest news with #Cardiology
Yahoo
16-07-2025
- Business
- Yahoo
NextGen Healthcare Chosen by Phoenix Heart to Optimize Financial Outcomes and Enhance Patient Experience
Large Arizona Cardiology Group to Boost Clinical, Operational, and Financial Efficiency with Specialty-Specific HealthTech REMOTE-FIRST COMPANY/PHOENIX, July 16, 2025--(BUSINESS WIRE)--NextGen Healthcare, a leading provider of innovative, cloud-based healthcare technology solutions, has been selected by Phoenix Heart to improve workflows, deliver meaningful financial and operational analytics, and enable a better experience for patients, providers and staff. The NextGen Cardiology Suite, a specialty package that overlays the NextGen® Enterprise EHR (electronic health record), will reduce friction by supporting specialty-specific workflows. Voted the state's #1 cardiology group for eight consecutive years in the annual The Best in Arizona Business poll, Phoenix Heart offers heart, vein, and vascular care across eight locations in the greater Phoenix region. Until now, staff at Phoenix Heart have relied on tedious manual processes to complete mission-critical workflows. NextGen® Enterprise PM (practice management), NextGen® Financial Analytics and NextGen® Operational Analytics will be integrated to simplify workflows while offering transparency, predictive analytics, and actionable insights. "NextGen Healthcare understands our needs and shares our commitment to making healthcare as seamless as possible for providers, staff, and the communities we serve," said Elizabeth Saylor, chief executive officer, Phoenix Heart. "We're excited to work together to improve clinical, operational, and financial processes and continue raising the bar in cardiovascular care." NextGen® Patient Engage powered by Luma will boost staff efficiency by equipping patients to complete pre-visit intake at their own convenience from their personal devices. The Instant Medical History enhancement will capture discrete data from patients during remote check-in and seamlessly deliver that information to the appropriate places in the system. NextGen® Automated Document Sharing will also automate outbound faxes and expedite the delivery of documents into patient portals—minimizing work for staff and making it easier for patients to quickly access information. "Phoenix Heart has been leading the way in cardiovascular care in Arizona for over four decades," said Srinivas (Sri) Velamoor, president and chief operating officer, NextGen Healthcare. "We are privileged to support Phoenix Heart with the next stage of their growth journey and elevate the provider, staff, and patient experiences with specialty-specific solutions that reduce burdens and make healthcare delivery more intuitive." To learn more about how NextGen Healthcare helps cardiology practices achieve their goals, visit About Phoenix Heart Voted No. 1 in cardiology groups by Ranking Arizona magazine's Best in AZ Businesses readers' poll, Phoenix Heart is the leading cardiology group in the greater Phoenix area. Phoenix Heart has eight offices, conveniently located in Glendale, Scottsdale, Avondale, Anthem, Black Canyon City, Buckeye, Cottonwood, and Laveen Village. Since its inception in 1981, Phoenix Heart has set the gold standard for cardiological care in Arizona and beyond. The cardiologists that make up the medical team at Phoenix Heart represent an incredibly diverse and elite background of training, skills, and specialties. They're committed to improving and enriching the lives and health of every patient they see and are consistently at the forefront of adopting the newest and best technologies to advance the health of their patients. About NextGen Healthcare NextGen Healthcare, Inc. is a leading provider of innovative healthcare technology and data solutions. We are reimagining ambulatory healthcare with award-winning EHR, practice management and surround solutions that enable providers to deliver whole-person health and value-based care. Our highly integrated, intelligent, and interoperable solutions increase clinical quality and productivity, enrich the patient experience and drive superior financial performance. We are on a relentless quest to achieve better healthcare outcomes for all. Learn more at and follow us on Facebook, X, LinkedIn, YouTube, and Instagram. View source version on Contacts Anjali Bright(731) 234-6422Abright@ Sign in to access your portfolio
Globe and Mail
24-06-2025
- Business
- Globe and Mail
BSX Raises 2025 Financial Outlook: What's Backing It?
Boston Scientific BSX has raised its full-year 2025 guidance following robust first-quarter results and continued momentum across key growth areas. The company now anticipates net sales to grow approximately 15-17% on a reported basis (earlier 12.5-14.5%) and nearly 12-14% on an organic basis (earlier 10-12%). Full-year adjusted earnings per share are expected to be in the range of $2.87-$2.94 (previously $2.80-$2.87). On the flip side, the company expects a $200 million tariff impact in 2025, mainly in the second half. In the first quarter, the company delivered organic sales growth of 18%, exceeding the guided range of 14-16%. Adjusted EPS was $0.75, marking a 34% year-over-year increase and surpassing the forecasted $0.66-$0.68 range. This growth reflects the durability of BSX's category leadership strategy, which is powered through meaningful innovation and clinical evidence generation. Boston Scientific's Cardiology segment sales surged 31%, driven by robust growth in products such as WATCHMAN, AGENT drug-coated balloon (DCB) and FARAPULSE. WATCHMAN gained market share through rising concomitant procedures. In addition, its Electrophysiology ('EP') business experienced robust growth, with sales up 145% year over year. This has positioned BSX as the second-largest player globally, largely due to the rapid adoption of pulsed field ablation (PFA) with FARAPULSE. Geographically, sales in the United States rose 31%, while Asia-Pacific and EMEA regions delivered 11% and 8% sales growth, respectively. Asia-Pacific growth was led by double-digit growth in Japan and high single-digit growth in China (despite volume-based procurement headwinds). BSX also plans to successfully offset the tariff impact through full-year organic sales guidance raise, targeted discretionary spending reductions and a $0.01FX benefit. Boston Scientific's Competitors Edwards Lifesciences EW reiterated its 2025 sales growth forecast of 8-10% but raised the sales dollar guidance range by $100 million, reaching $5.7-$6.1 billion. The revision was made to account for the recent movement in foreign exchange rates. Edwards continues to expect 2025 adjusted EPS to be in the range of $2.40-$2.50 despite headwinds from tariffs. This growth trajectory is driven by the continued global adoption of SAPIEN 3 Ultra RESILIA, PASCAL and EVOQUE systems. Stryker SYK raised its sales guidance for 2025, led by strong first-quarter performance, continued capital demand and robust commercial execution. The company now expects total revenues to grow in the range of 8.5-9.5% on an organic basis (previously 8-9%). However, SYK lowered its EPS guidance to $13.20-$13.45 from $13.45-$13.70, reflecting headwinds from the Inari Medical acquisition and a $200 million impact from announced tariffs. BSX Stock Price Performance, Valuation and Estimate Trend Shares of Boston Scientific have gained 33.4% in the past year compared with the industry's growth of 8.8%. The S&P 500 composite has grown 9.3% in the same period. Image Source: Zacks Investment Research From a valuation standpoint, BSX trades at a forward 12-month price-to-earnings ratio (P/E) of 33.19X, above the industry's 20.83X. The Zacks Consensus Estimate for BSX's earnings has been on the rise over the past 60 days. BSX stock currently carries a Zacks Rank #3 (Hold). You can see the complete list of today's Zacks #1 Rank (Strong Buy) stocks here. Zacks Names #1 Semiconductor Stock It's only 1/9,000th the size of NVIDIA which skyrocketed more than +800% since we recommended it. NVIDIA is still strong, but our new top chip stock has much more room to boom. With strong earnings growth and an expanding customer base, it's positioned to feed the rampant demand for Artificial Intelligence, Machine Learning, and Internet of Things. Global semiconductor manufacturing is projected to explode from $452 billion in 2021 to $803 billion by 2028. See This Stock Now for Free >> Want the latest recommendations from Zacks Investment Research? Today, you can download 7 Best Stocks for the Next 30 Days. Click to get this free report Boston Scientific Corporation (BSX): Free Stock Analysis Report Stryker Corporation (SYK): Free Stock Analysis Report Edwards Lifesciences Corporation (EW): Free Stock Analysis Report
Zawya
06-06-2025
- Health
- Zawya
Liberia: Ambassador Yin Chengwu Attends Handover Ceremony of Cardiology Department Project Under Paired Hospital Cooperation Mechanism
On June 3, Chinese Ambassador to Liberia Yin Chengwu attended the handover ceremony of the Cardiology Department project under the China-Liberia Paired Hospital Cooperation Mechanism. Also present were Liberian Health Minister Hon. Dr. Louise M. Kpoto, JFK Medical Center Chief Executive Officer Dr. Linda Birch, representatives from Heilongjiang Provincial Hospital, members of the 17th Chinese Medical Team to Liberia, and representatives from JFK Medical Center, totaling about 100 attendees. Minister Dr. Louise Kpoto and CEO Dr. Linda Birch expressed gratitude to the Chinese government for its long-term and strong support to Liberia's health sector. They stated that this project, as Liberia's first dedicated cardiology diagnosis and treatment department, would surely provide higher quality medical services to the people. Ambassador Yin pointed out that the Cardiology Department project is a powerful testament to the friendship between the two peoples, a concrete manifestation of China's policy towards Africa characterized by "sincerity, real results, amity and good faith", and a positive outcome of implementing the consensus reached by the leaders of the two countries at the Forum on China-Africa Cooperation (FOCAC) Beijing Summit. China, ambassador Yin affirmed, will continue to support the development of Liberia's health sector and promote Liberia's ARREST Agenda for Inclusive Development. Distributed by APO Group on behalf of Embassy of the People's Republic of China in the Republic of Liberia.
Yahoo
01-06-2025
- Health
- Yahoo
Adding This Leafy Green to Lunch Lowers Systolic Levels Fast, According to Cardiologists
Adding This Leafy Green to Lunch Lowers Systolic Levels Fast, According to Cardiologists originally appeared on Parade. A small tweak to your lunch routine may do wonders for your heart health thanks to its impact on your systolic blood pressure.A study published in Nutrients reported that dark, leafy greens like arugula, cabbage, chard, kale and spinach that are high in vitamins, minerals are amazing for your blood pressure. But there's one that cardiologists love the most when it comes to nutritional value and cardiovascular health benefits, particularly on systolic blood pressure.A quick refresher on blood pressure readings in case you need it: Your systolic pressure is the upper number on your blood pressure reading, which the American Heart Association explains is the measurement of the pressure of your blood pushing against your arterial walls when your heart beats. The bottom number is your diastolic blood pressure, which is the pressure your blood puts on the walls of your arteries when your heart is at rest in between out the best leafy green to toss in your lunch bag for a seriously big boost to your precious ticker.🩺SIGN UP for tips to stay healthy & fit with the top moves, clean eats, health trends & more delivered right to your inbox twice a week💊 Shoutout to our boy Popeye: It's spinach! "Spinach may help lower systolic blood pressure, largely due to its rich content of dietary nitrates," Dr. Deepak Talreja, MD, cardiologist and clinical chief of cardiology at Sentara Health, tells Parade. "When we eat nitrate-rich foods like spinach, the body converts nitrates to nitric oxide, a molecule that relaxes and dilates blood vessels."When your blood vessels are dilated and relaxed, Dr. Talreja explains, your blood flow improves and your vascular resistance, which is the resistance against blood flowing through your veins and arteries."This can lead to a modest reduction in systolic blood pressure," he also points out that multiple studies support the impact of spinach on systolic blood pressure, singling out one in particular. "A randomized crossover trial published inHypertension found that a diet high in nitrate-rich vegetables such as spinach significantly reduced both systolic and diastolic blood pressure in hypertensive patients, particularly when consumed regularly," he says. "The effect may be seen within hours of consumption and can persist with daily intake." That said, if you're on medication for any cardiovascular issue, spinach isn't a substitute for that! But in most cases, it absolutely can be a huge boon to your health. "Regularly incorporating fresh spinach into meals—whether in salads, smoothies or sautés—can be a simple, natural way to support healthier blood pressure and overall cardiovascular wellbeing," Dr. Talreja says. "While spinach alone won't replace medications or other proven treatments, it can be part of a broader dietary strategy aligned with the DASH (Dietary Approaches to Stop Hypertension) and Mediterranean diets—both of which are associated with lower cardiovascular risk."Related: Whether You're Dealing With High Blood Pressure or Want to Avoid It in the Future, Here Are the 25 Best Foods to Eat There are so many—there's a reason it's most cardiologists' favorite food for protecting your arteries. According to Dr. Talreja, these are the main other ways spinach can contribute to your cardiovascular health. "Spinach is high in potassium, which helps counterbalance sodium in the diet and supports healthy blood pressure regulation," Dr. Talreja says. Related: The One Habit That Can Lower Your Blood Pressure Overnight, According to a Cardiologist "Adequate magnesium intake is associated with improved endothelial function and reduced risk of arrhythmias," he tells us. (Endothelial function means how well the thin inner lining of cells in your blood vessels work.) Antioxidants are so good for you in so many ways. Dr. Talreja says that spinach is particularly high in vitamin C, vitamin E and beta-carotene, all of which can reduce oxidative stress. Oxidative stress, in turn, can contribute to atherosclerosis (arteries clogged with cholesterol, fats and other substances) and vascular inflammation (damaged blood vessels).Related: "Folate is a B-vitamin helps lower homocysteine levels, which are linked to endothelial dysfunction and cardiovascular risk," Dr. Talreja explains. Dr. Talreja says this means it's great for weight control, blood sugar regulation and lipid management. You'll feel fuller longer when you eat it, which can also help prevent you from succumbing to cravings for less healthy snacks. Up Next:"Understanding Blood Pressure Readings." American Heart Association. Kapil, et. al. "Dietary nitrate provides sustained blood pressure lowering in hypertensive patients: a randomized, phase 2, double-blind, placebo-controlled study." Hypertension. Dr. Deepak Talreja, MD Adding This Leafy Green to Lunch Lowers Systolic Levels Fast, According to Cardiologists first appeared on Parade on May 31, 2025 This story was originally reported by Parade on May 31, 2025, where it first appeared.
Medscape
09-05-2025
- Health
- Medscape
May 09 2025 This Week in Cardiology
Please note that the text below is not a full transcript and has not been copyedited. For more insight and commentary on these stories, subscribe to the This Week in Cardiology podcast , download the Medscape app or subscribe on Apple Podcasts, Spotify, or your preferred podcast provider. This podcast is intended for healthcare professionals only. In This Week's Podcast For the week ending May 9, 2025, John Mandrola, MD, comments on the following topics: the controversial KETO-CTA study, tough decisions in subclinical AF, and potentially huge benefit for GLP-1 receptor agonists. Meta-analysis The journal JACC Advances published a study looking at plaque progression in people eating a ketogenic diet (KD). It stirred all sorts of controversy on social media. I will review it this week. A few background comments. An obstacle to the broad clinical implementation of carbohydrate-restricted diets (CRDs) and KD are lipid changes that occur in a minority of patients upon carbohydrate restriction. Bad lipid changes. As in large increases in LDL cholesterol (LDL-C) and associated apolipoprotein B (ApoB). While there are many factors contributing to increases in LDL-C and ApoB in the KD, "leanness" seems important. Get this: The authors cite a meta-analysis of 41 studies that reports that mean baseline BMI had a strong inverse association with LDL cholesterol change [whereas saturated fat amount was not significantly associated with LDL-C change. For trials with mean baseline BMI <25, LDL cholesterol increased by 41 mg/dL (95% CI, 19.6-63.3) on the low carbohydrate diet (LCD). By contrast, for trials with a mean of BMI 25 to less than 35, LDL cholesterol did not change, and for trials with a mean BMI ≥35, LDL cholesterol decreased by 7 mg/dL (95% CI, –12.1 to –1.3). I did not know that lipid changes with CHD was modified by BMI. These observations have given rise to the characterization of the lean mass hyper-responder (LMHR) phenotype. From the authors: the aim of the study was "to examine the association between plaque progression and its predicting factors." I know; it is a bit confusing. 100 people who were on a KD (for years actually), and had a "keto-induced" LDL-C ≥190 mg/dl and HDL ≥60 mg/dl and TG ≤ 80 mg/dl were followed for 1 year using coronary artery calcium (CAC) scan and coronary computed tomography angiography (CCTA). I say "keto-induced" because the LDL-C had to be less than 160 before adapting the KD. Entry criteria also included an increase in ≥ 50% in the LDL-C. Plaque progression predictors were assessed with linear regression and Bayes Factors. Study subjects had to have normal glucose and A1c and normal CRP. Patients on the KD had a normal BMI at 22 and very high LDL of 254, HDL 89 and triglycerides of 67. Pause there: average LDL 254, so many were higher. These were 55-year-old mostly men who were adherent to KD as documented with beta-hydroxybutyrate (BHB) measures. Over the year, there was no substantial changes in ApoB or BMI. The study was actually pre-registered, and the primary endpoint was originally the change in noncalcified plaque burden. They did not formally present this endpoint. Instead, they gave the median change in percent atheroma volume, which they said was 0.8%. Who knows what this means? They tells us that this value is comparable with those observed in other cohorts. The thing is…the primary endpoint of change in noncalcified plaque volume (NCPV) was presented in a figure which you could look at and see that most individuals have an increase in NCPV. This lack of data on the PEP caused a stir online and the lead author offered the data in a video on Twitter/X. The numerical pooled NCPV change value was an in increase of 18.8 mm³. If this means nothing to you, don't worry. I will come back to it. Weird though that we had to get the primary endpoint in a Twitter video. The main thrust of the paper were the correlations. Neither the change in ApoB throughout the study nor the ApoB at the beginning of the study were associated with the change in NCPV. There was also no correlation between LDL-C and NCPV. What was correlated? The baseline CAC was positively associated with a change in NCPV. So also were baseline plaque measures. Simplifying: if there was plaque or CAC at baseline, there was a positive correlation with NCPV. The authors make the case that while both LDL-C and ApoB are independent risk factors for atherosclerosis, the absolute risk associated with elevated LDL-C and ApoB is context-dependent and may not apply to this lean mass hyper-responder (LMHR) group. Thus, they write, "these data are consistent with the observation that high LDL-C and ApoB among a metabolically healthy population have different cardiovascular risk implications than high LDL-C among those with metabolic dysfunction." Gosh, that is a big conclusion because these people had total cholesterol of 350 and LDL-C of 255. The authors make the case that the lean mass hyper-responders are different from the person with abnormal lipids from metabolic syndrome: Difference 1 : LDL-C and ApoB elevations are dynamic and result from the metabolic response of carb restriction and this is not a genetic defect. Difference 2 : LMHR are normal weight and metabolically healthy; they don't have obesity, diabetes, or insulin resistance. Difference 3 : The high LDL-C and ApoB in this phenotype emerge as part of a lipid triad, also inclusive of high HDL-C and low triglycerides, representing a metabolic signature of a distinct physiological state. Difference 4: The degree of this phenotype appears inversely related to BMI ("leanness"), consistent with the idea that it is a metabolic response to carbohydrate restriction that is accentuated in leaner, more metabolically healthy persons. The authors really are not shy in their conclusions. And I call them Whoppers No. 1, No. 2, and No. 3: Whopper 1: The LMHR population constitutes a unique and important natural experiment evaluating the lipid heart hypothesis in an unprecedented manner. Whopper 2: Our data are consistent with the notion that elevated ApoB, even at extreme levels, does not drive atherosclerosis in a dose-dependent manner in this population of metabolically healthy individuals. They qualify this conclusion by saying that LHMR may still have risk. For instance, they noted that PAV increase comparable to what has been observed in other studies on populations with lower LDL-C across the cardiovascular disease risk spectrum. They offer no citation here. Whopper 3: Quote: "These insights can facilitate personalized treatment and risk mitigation strategies based on modern, cost-effective cardiac imaging." For instance, they say, despite profound elevations in LDL-C and ApoB, based on their data, LMHR subjects with CAC = 0 at baseline (n = 57) constitute a low-risk group for percent atheroma volume (PAV) progression, even as compared to other cohorts with far lower LDL-C and ApoB. By contrast, LMHR subjects with elevated baseline CAC, possibly from a history of metabolic damage and dysfunction prior to adopting a CRD, appear to constitute a relatively higher risk group for PAV progression even where LDL-C and ApoB are equal to their CAC = 0 counterparts. Before closing they coin the phrase " plaque begets plaque. " I see why this paper generated angst online. The idea of the study is reasonable; what's unreasonable are the conclusions. First, if you look at the primary endpoint of change in noncalcified plaque volume, it went up. A lot. 18.8 mm3. That was 2.5x higher than they predicted in their study protocol. So, if you believe that the delta of NCPV is a great surrogate, it looks quite ominous. Second, imaging tests are almost always a terrible surrogate measure. Images are images. To assess risk, you need to measure events. Heart attacks. Stroke. CV death. I realize this is a small uncontrolled study, and it's fine to look at these things (in fact, I am curious), but you cannot claim clinical importance just because you weaved a nice story about high LDL-C in LMHR being different from high LDL-C in metabolic syndrome patients. Third, there is like 50 years of data supporting LDL-C being causal for atherosclerosis. Like every Bradford Hill criteria is met. So…. If you are going to claim an exception, you need more rigorous evidence than this. The priors here — the priors being that these LMHR are an exception — have to be extremely pessimistic, so you'd need really strong data to change your posterior view. This study surely was not strong evidence. Fourth, assuming you believe the plaque images are precise and reproducible and clinically relevant, this study really suffers from a lack of control. All they had to do is recruit a group of people eating a Mediterranean diet. Let's see what happens to them relative to the Keto people. Fifth, the authors don't tell us how many people they screened to find these 100 people. I get the sense they are highly selected bunch. Finally, the question of heart health from a specific diet is going to be really hard to sort out. Nutritional studies always are. An RCT in a prison might work, but cardiac event rates in young people—even with KD-induced LDL will be infrequent. What's more, the LMHR will surely do other things that affect heart disease, like exercise, not smoking etc. If the authors are wrong, and actually eating a diet that causes crazy high LDL levels and maintaining a lean body mass is actually harmful , then, given the popularity of carbohydrate-restricted diets, this could be a public health disaster. As for diet, I do think Americans eat too many carbs, but the KD seems extreme. Why not just eat a balanced diet, like they do in Sicily? JAMA Network Open has published an interesting modeling study from a Finnish group on the matter of net benefit of oral anticoagulation (OAC) in subclinical device-detected atrial fibrillation (AF). The background here is known to anyone practicing cardiology. It's perhaps the most common question I receive: John, Mrs Smith had 4 hours of AF on her pacemaker. Her CHA 2 DS 2 VASc score is 4; should we anticoagulate? And if we don't anticoagulate, how much AF does she have to have before we do? The short answer is that I have no idea. Your comeback is…come on Mandrola, we have two trials. And it is true. We have the NOAH trial. Edoxaban vs placebo in 2500 patients with a median duration of AF 2.8 hours. The primary outcome of CV death, stroke, and systemic embolism (SE) was 19% lower in the edoxaban group. The confidence intervals (CI) were wide, and the difference did not reach significance. Major bleeding was 31% higher and this did reach statistical significance. We also have the ARTESIA trial. Apixaban vs acetylsalicylic acid (ASA) in 4000 patients with median duration AF 1.5 hours. The primary outcome of stroke and SE was 37% lower with apixaban and this did meet statistical significance. Major bleeding however was 80% higher and this met statistical significance. Some have said NOAH was negative and ARTESIA was positive. Perhaps, technically, this is true. But I think they both show the same thing. OAC reduces stroke and increases bleeding. It leaves us with the question of net benefit. I've heard Jeff Healey, the PI of ARTESIA, rightly say that we should favor OAC because strokes are worse than bleeds. This is certainly true. The tension in subclinical AF is that the yearly stroke rates were low—in the 1% range. Far lower than what would be predicted in the CHA 2 DS 2 VASc assessment for clinical AF. And if that is true, even if OAC reduces the relative risk, the absolute risk reduction is tiny, in the order of 4 per 1000, with a number needed to treat (NNT) of 250. Therefore, any increase in bleeding may mitigate the net benefit. Led by senior author Konsta Teppo, the group set out to estimate the "net benefit" of OAC in SCAF. They used modeling. It's technical. A Medscape colleague, nephrologist F. Perry Wilson, covered this paper, and he wrote: The study was done using a computer. I know — all studies are done with computers. But here I mean literally. The authors used a decision analytical model run with 10,000 patients with subclinical AF on OAC and 10,000 without OAC. They then used a "Markov decision model" to estimate net outcomes of NOACs. You all know that doctors who ablate AF and put in pacers and defibrillators don't know much about Markov modeling. I was going to ask Professor Teppo. He would have told me. But to make life easier, I just asked Claude. Who said: A Markov model consists of multiple health states individuals can move between based on specific transition probabilities. Think of it as a simulation where: Patients exist in various health states (e.g., well, post-stroke, bleeding event, death) In each cycle (1 month in this study), patients can transition between states with certain probabilities The model tracks what happens to a cohort of simulated patients over time The model was constructed in multiple steps: Base Case Patient: The researchers created a model patient, aged 77 years (matching the average age in the clinical trials), and applied the untreated stroke and bleeding rates from the NOAH-AFNET 6 and ARTESIA trials. Health States: The model included states for: Being Well with subclinical AF Ischemic stroke (with varying severities) Major bleeding events (hemorrhagic stroke, other intracranial bleeding, extracranial bleeding) Development of clinical AF Death Transition Probabilities: The pooled point risk estimates from the meta-analysis combining the two trials were used as the effect sizes for anticoagulation on stroke (32% decrease) and major bleeding (62% increase). The model assigned an 80% weight to nonintracranial bleedings for the increase in bleedings caused by the DOACs. The numbers come from the McIntyre et al meta-analysis of NOAH and ARTESIA in Circulation . Event Severity: Probabilities for the severity of stroke and bleeding events in the anticoagulation and non-anticoagulation groups of the model were approximated from previous observations in patients with and without anticoagulation. Quality of Life Weights: The net benefit outcome was assessed in terms of QALYs (Quality-Adjusted Life Years), where clinical events reduced patients' quality of life based on the type and severity of the event according to previously published quality of life data. Time Horizon: The simulation was run for a 10-year period with 10,000 samples in both decision groups (with and without the DOACs). The main outcome measure for net benefit was the cumulative quality-adjusted life-years (QALYs) during the simulation. This included things like severity of ischemic strokes, hemorrhagic strokes, other intracranial bleeds, and extracranial bleeds, as well as the number of deaths during a 10-year simulation. It's really neat way to look at net benefit. As I said, I don't know anything more than what I read about Markov modeling, but the thing that strikes me, and perhaps you too, is that there are a lot of degrees of freedom of choices. That said, here is what the model shows: Over the 10-year period, you would have 1076 strokes in nontreated subclinical AF vs 843 with treatment. The delta of 233 strokes saved seems like a lot but it's only 2.3% per year. There would be 1213 major bleeds without OAC vs 1664 with OAC. The 453 more bleeds that would be 4.5% per year. Deaths were nearly the same. 55 fewer in the anticoagulation (AC) arm but it's only 0.6% delta per year. OK, what about the primary endpoint of quality-adjusted life years. It was, drumroll… Per patient, the differences listed led to 1 additional quality-adjusted week of life (0.024 QALYs) with DOAC treatment during the 10-year simulation. When the 95% CIs of treatment effect sizes were considered in probabilistic sensitivity analysis, there was a 66% probability that DOAC treatment leads to more QALYs than withholding treatment. The authors did an exploratory analysis looking at higher risk patients and as you would expect, in patients with CHADSVASC score >4, the increase QALY with DOAC was now a month, not a week. But they note caution because this estimate came from subgroup analyses in the two trials, neither of which met statistical significance for interaction. The authors concluded that "initiating DOACs in patients with device-detected subclinical AF was associated with a minimal increase in QALYs. However, the benefits were uncertain, and the effect size of the overall net benefit does not appear to be clinically meaningful." I loved this paper and the authors' discussion. The modeling and estimates make intuitive sense, right? The trials find extremely low rates of stroke with SCAF. The average age of patients was 77. Older patients have many competing risks. Andrew Foy has a nice model thinking about domains acting on treatment effect. They are overlapping circles where you have the risk of the primary outcome vs competing risk, and the treatment benefit and treatment harm. Treating subclinical AF is a perfect example of these four domains coming together to almost cancel themselves out. The Markov model basically quantifies this to 1-week extra of good quality of life. Perhaps a few weeks longer if the patient has extremely high stroke risk. The clear conclusion I make from this paper is that subclinical AF is a different entity than clinical AF of old. I co-authored a paper on that in Stroke . The Finnish group has shown very little net benefit in treating SCAF. This contrasts with the famous Singer et al net benefit paper in Annals of Internal Medicine in 2010, where they showed clear net benefit of warfarin in patients in the ATRIA cohort. Here, even with an annual stroke rate of only 2%, warfarin provided a large net benefit. In clinical AF, stroke reduction for anticoagulation was larger than the bleeding increase. But subclinical AF has a different meaning. Yes, it is electrically the same; the atria is fibrillating. But, and this is my opinion, I am beginning to think that a certain degree of short duration occurs in older people as a matter of normal life. We know that PACs and PVCs increase with age, why not short duration AF? For now, the only solution to the matter is to do what David Sackett described when he coined the term evidence-based medicine. That is, we align care with patient preferences. With our patients we discuss the uncertainty, seek their preferences, and treat accordingly. There can be no algorithm, no guideline. This problem does not fit into those colored boxes in guidelines, and the top people who write guidelines should resist the urge to help us clinicians. If a patient fears stroke and is willing to deal with the disutility of taking a daily pill (that is, the cost and taking it every day), then use OAC. If a patient fears bleeding, then hold off and monitor more. I know, this is a cardiology podcast, but here me out. There is a connection. Plus, the science of this study is striking. In Kentucky, one of the least healthy states in the US, obesity is essentially the norm. I estimate that more than half the patients I see in clinic have some degree of metabolic syndrome—overweight or obese, insulin resistant, type 2 diabetes (T2D). Many of these patients also have fatty liver disease, which used to be called non-alcoholic steatohepatitis, or NASH. But it is now called MASH, or metabolic-associated steatohepatitis. It's a bad condition, and I think it flies under the radar of most of us cardiologists—because we see these patients for hypertension or AF or ischemic heart disease. My friend Claude says that 9-15 million adults in the US have MASH. And it's getting worse. The prevalence of MASH in the US is predicted to increase 63% from 16.5 million cases in 2015 to 27 million cases in 2030. And in patients with T2D and obesity, the prevalence of MASH is as high as 16%, so almost 1 in 5 patients. NEJM recently published the results of the ESSENCE trial of 1197 patients with documented inflammation on liver biopsy of semaglutide vs placebo. This is a two-part trial. Part 1 looks at histology. And it has resolution of steatohepatitis without worsening of liver fibrosis and reduction in liver fibrosis without worsening of steatohepatitis as the primary endpoints. ESSENCE trial is ongoing, and Part 2 will measure clinical outcomes. NEJM published the PART 1 and it is shocking. Patients were young, age 56, and more than half were females. The mean BMI was 34-35. The primary endpoints were twofold: Resolution of steatohepatitis without worsening of fibrosis occurred in 63% vs 34% in the semaglutide vs placebo groups. That is an absolute treatment difference of 29 percentage points, which was highly significant. The second primary endpoint, a reduction in liver fibrosis without worsening of steatohepatitis, was reported in 37% vs 22% in the semaglutide vs placebo arms. That is absolute treatment diff of 14.4 percentage points, also highly significant. All secondary outcomes favored semaglutide. I mention this study because a) oodles of our patients have MASH, whether we know it or not, b) MASH is on the rise, and c) MASH portends a poor prognosis; it is the leading cause of liver transplant, but perhaps most relevant to cardiologists is that most patients with MASH die of cardiovascular (CV) complications. The GLP-1 agonist drug in ESSENCE basically shredded evidence of liver disease, at least histologically, and I suspect the follow-on outcomes portion of ESSENCE will be stopped early for benefit. There is an approved medication for MASH, called resmetirom, but this is a thyroid hormone receptor-beta (THR-β) selective agonist that specifically targets the liver. Other than mild lipid-lowering effects, it has no known CV benefits. This is unlike GLP-1 agonists which have RCT-proven benefits in CV disease and diabetes. I am not yet prescribing GLP-1, but like the SGLT2 inhibitors, I think GLP-1 agonists will soon be a drug that cardiologist will want to prescribe. I realize that some listeners may say we should be treating obesity and obesity-related diseases with weight loss and diet and exercise. The GLP-1 benefit seen in ESSENCE was likely due to weight loss. My answer to that is it doesn't matter why the GLP-1 drugs work. When trials show that something works, an evidenced-based practitioner should embrace it. What's more, clinical medicine is pragmatic. It's pretty obvious that lifestyle interventions have a low success rate. So, if the GLP-1 agonists work, we should prescribe them. And, finally, there is a big difference in using GLP-1 agonists in an adult with diabetes, heart disease, and liver inflammation vs an adolescent who is overweight. The former person is in real trouble. The net benefit calculus favors treatment. The younger person should be counseled aggressively to change lifestyle. In other words, treatment is different from prevention. CABG Still Superior to Stents Despite FAME 3 Endpoint Swap A few weeks ago, I discussed the FAME-3 trial 5-year results. I turned this into a column that is up now. The short story is that FAME-3 was designed as a one-year non-inferiority trial comparing fractional flow reserve (FFR)-guided PCI to coronary artery bypass grafting (CABG) in patients with multivessel disease. Why someone would want to compare revascularization strategies at one year is mysterious, but that is what they did. And CABG was much better. FFR-PCI did not even reach non-inferiority in a four-point composite endpoint of death, myocardial infarction, stroke, and unplanned revascularization. My column pushes back against the claims in 3 and 5-year results that FFR-PCI is now equivalent to CABG. The claims stem from use of a different endpoint. Take a look at my column and see what you think.
