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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.
Yahoo
24-03-2025
- Health
- Yahoo
Opinion: Marijuana's newfound health problems
Were the 24 states that legalized recreational marijuana during the last decade or so too hasty? Did they fail to consider the long-term consequences and the changing nature of the drug? Just as importantly, should such a decision have been left up to voters in the first place? Those questions may seem unfair. There were voices in the past warning about adding a new mind-altering substance to the list of legal substances, but hindsight is always clearer than foresight. Now, however, with evidence mounting, it's clearly time to revisit the issue. It may be unrealistic to expect the states that legalized recreational use to completely reverse course, but it should not be unrealistic to demand some changes. Public health experts are raising alarms. The latest concern comes from two studies that show regular cannabis users are much more likely to suffer heart attacks than people who don't use the drug. This was true even among relatively young and otherwise healthy adults. A report on said one study was published in JACC Advances and the other will be presented at the American College of Cardiology's Annual Scientific Session. The first studied 4.6 million people retroactively, while the other was an analysis of 12 studies previously published. The first concluded that marijuana use is on the rise in the U.S., but particularly in places where it is now legal. Users younger than 50 were found to be more than six times more likely to suffer a heart attack than non-users. The second study found a 50% increased risk. This comes on the heels of a New York Times report in January that cited a survey showing almost 18 million Americans today report using marijuana either daily or almost daily, which it said is 'more than the number drinking alcohol that often.' A Times report last October said, 'A growing number are enduring addiction, psychosis and other harms.' This is because the marijuana products being sold are far more potent than in years past. Years ago, the typical THC level of marijuana (tetrahydrocannabinol, the compound that makes users high) equaled less than 5%. Today, the Times said, 'Cannabis vapes, infused pre-rolled joints and high-intensity THC beverages now line dispensary shelves. And many businesses sell concentrates, some promoting nearly 100% THC, in the form of waxes, liquids and crystalline 'diamonds' — products that have gone from niche to mainstream.' Growers are looking for ways to breed more potent plants and products. Sellers say this is where the money is. Writing for Harvard Public Health, Master of Public Health student John Wilson said 'marijuana's evolution has outpaced our regulatory systems.' People often claim marijuana reduces anxiety, but regularly smoking or otherwise ingesting high-potency varieties of the drug has the opposite effect. 'It's the public health equivalent of throwing water on a grease fire — good intentions gone horribly wrong,' he wrote. 'This misalignment leaves consumers, especially young adults, vulnerable to its unintended consequences. 'And yet, marketing strategies, particularly on social media, glamorize these high-strength options, targeting younger consumers.' The Times found most of the 20 largest brands making unproven claims about health benefits, 'potentially violating federal and state regulations.' The Biden White House started the process of rescheduling marijuana from a Schedule I drug, with strict rules against research, to Schedule III. That would allow for more research and federal regulation. As a Schedule I drug, marijuana remains illegal on the federal level, despite being legal in several states. It's unclear whether the Trump administration is committed to carrying out this rescheduling, but Health Secretary Robert F. Kennedy Jr. has sent some positive signals. Wilson suggests standardized labeling that clearly posts the potency of the drug. The label should also spell out potential risks and side effects, similar to what exists now on tobacco cigarettes. The National Cannabis Industry Association has already proposed something similar, clearly because it would be in its own interests. Also, the federal government should set limits on the potency of marijuana offered for sale. The beauty of democracy is that laws can change and adapt as new information is presented. Last year, voters in Florida, North Dakota and South Dakota defeated ballot measures to legalize adult-use marijuana. Clearly, unregulated market forces, including competition from the still-illegal sellers of the drug, have led to a destructive cycle. The Wild West days of mostly unregulated legal marijuana use must come to an end before more credible studies linking it to a variety of health problems begin to pile up.
Yahoo
21-03-2025
- Health
- Yahoo
Despite some health benefits, could cannabis break your heart?
While marijuana is becoming more available nationwide as medicine and for recreational use, two new studies build on growing evidence that cannabis users are more apt to have heart attacks than those who do not use the drug. And it's true even among young, healthy adults. Cannabis users who are not yet 50 are six times as likely to have heart attacks as those who don't use the drug, per a retrospective study involving 4.6 million people that was published in JACC Advances, one of the American College of Cardiology's journals. And a review of 12 previous studies — the largest to look at the issue of heart attacks and cannabis use — found 50% increased risk among cannabis users. The findings are being presented at the American College of Cardiology's Annual Scientific Session next week in Chicago. reported that marijuana is legal for recreational use in 24 states and for medical use in 39 states. 'Asking about cannabis use should be part of clinicians' workup to understand patients' overall cardiovascular risk, similar to asking about smoking cigarettes,' said Dr. Ibrahim Kamel, clinical instructor at the Boston University Chobanian & Avedisian School of Medicine and internal medicine resident at St. Elizabeth Medical Center in Boston, who led the study. 'At a policy level, a fair warning should be made so that the people who are consuming cannabis know that there are risks.' The retrospective study took data from TriNetX, a global health research network that lets researchers use electronic medical records. Over follow-up averaging more than three years, the researchers found that cannabis users had: More than a sixfold increased risk of heart attack Fourfold increased risk of ischemic stroke Twofold increased risk of heart failure Threefold increased risk of cardiovascular death, heart attack or stroke Those participants were all younger than 50 and didn't have any significant cardiovascular problems when the study began, 'with blood pressure and low-density lipoprotein (LDL) cholesterol levels within a healthy range and no diabetes, tobacco use or prior coronary artery disease,' according to a news release on the study. In the other study, which reviewed an international collection of previous research involving more than 75 million people, mostly conducted in the U.S., seven found a link between cannabis use and having a heart attack, four didn't, and one suggested less risk. When all the study data was pooled, a link between cannabis use and heart attack was significant. Users were 1.5 times as apt to have a heart attack compared to those not currently using. Not all of those studies included age, but among those that did, 41 years old was average, suggesting 'a relatively young population,' the researchers said. Dr. Sameer Amin, cardiologist and chief medical officer at L.A. Care Health Plan, who was not part of the research, told Healthline that more research is needed. But 'based on early information showing an association of cannabis with an increased risk of worse cardiovascular outcomes, there appears to be an emerging concern.' Why cannabis might increase risk of heart attack isn't known, the researchers theorize it could impact heart rhythm, increase oxygen demand in the heart and make it harder for blood vessels to relax and expand, thus changing blood flow. The release noted that one study found the risk of heart attack peaked an hour after marijuana consumption. Because of the data, the researchers couldn't eliminate the possibility of confounders that could also influence the results, such as the amount and duration of cannabis use or use of tobacco and other drugs. 'We should have some caution in interpreting the findings in that cannabis consumption is usually associated with other substances such as cocaine or other illicit drugs that are not accounted for,' Kamel said. 'Patients should be forthcoming with their doctors and remember that we are their No. 1 advocate and having the full story matters.' The researchers said they're hoping to do more studies on the issue. They note an earlier study presented at the American College of Cardiology's Annual Scientific Session in 2023 found daily marijuana use increased risk of developing coronary artery disease.
Fox News
18-03-2025
- Health
- Fox News
Cannabis use endangers heart health for certain group
While marijuana has been legalized in many states, research has shown that it could have detrimental health impacts for some — including a higher risk of heart attacks. Two recent studies have linked cannabis use to cardiac events, particularly among young, healthier people, according to a release from the American College of Cardiology (ACC). One study included more than 4.6 million people. The other was a large review that looked at 12 previous studies including more than 75 million people, which is said to be the largest combined study examining the relationship between cannabis and heart attacks. The findings will be presented at the ACC's Annual Scientific Session March 29-31 in Chicago and will also be published in the journal JACC Advances. Healthy cannabis users who were younger than age 50 were more than six times as likely to experience a heart attack compared to those who did not use the substance, the researchers found. They were also four times as likely to have a stroke, twice as likely to experience heart failure and three times as likely to die from a cardiac event. This risk was shown to peak as soon as one hour after cannabis use in one of the studies. All participants had no previous heart conditions, were not tobacco users, had healthy blood pressure and cholesterol levels, and had no history of diabetes. "We do know that smoking cigarettes increases the risk of a cardiac event, and it's reasonable to assume that smoking marijuana presents a similar risk." The study did not identify exactly how marijuana compromises heart health, but the researchers presented some possibilities. Those included that it could "affect heart rhythm regulation, heighten oxygen demand in the heart muscle, and contribute to endothelial dysfunction, which makes it harder for the blood vessels to relax and expand, and can interrupt blood flow," the release stated. "Asking about cannabis use should be part of clinicians' workup to understand patients' overall cardiovascular risk, similar to asking about smoking cigarettes," said lead author Ibrahim Kamel, MD, clinical instructor at the Boston University Chobanian & Avedisian School of Medicine and internal medicine resident at St. Elizabeth Medical Center in Boston, in the release. "At a policy level, a fair warning should be made so that the people who are consuming cannabis know that there are risks." The study did have some limitations, the researchers noted. There were some inconsistencies in the data regarding the duration and amount of cannabis use or the use of tobacco or other drugs, the release stated. "We should have some caution in interpreting the findings in that cannabis consumption is usually associated with other substances, such as cocaine or other illicit drugs, that are not accounted for," Kamel said. "Patients should be forthcoming with their doctors and remember that we are their No. 1 advocate and having the full story matters." The researchers called for additional studies to confirm the findings and identify the highest-risk groups. Dr. Jasdeep Dalawari, an Illinois-based interventional cardiologist and regional chief medical officer at VitalSolution, an Ingenovis Health company, was not involved in the study but reiterated its limitations as a retrospective study. "A randomized control trial is ideal, but difficult with this topic," he told Fox News Digital. "It raises questions as to the safety of marijuana as it becomes more ubiquitous." "At a policy level, a fair warning should be made so that the people who are consuming cannabis know that there are risks." While Dalawari said this study is "interesting and concerning," he also called for more data on the topic. "I advise all my patients to quit smoking all substances, because we do know that smoking cigarettes increases the risk of a cardiac event, and it's reasonable to assume that smoking marijuana presents a similar risk," he said. For more Health articles, visit "It would be interesting to know if this study addresses the risks of ingesting versus smoking. Nevertheless, I would advise patients to limit cannabis use until definitive studies are published." Fox News Digital reached out to the researchers for comment.
