PREVENT equation accurately estimated 10-year CVD risk and those with calcium buildup
Research Highlights:
Embargoed until 4 a.m. CT/5 a.m. ET Wednesday, May 21, 2025
( NewMediaWire ) - May 21, 2025 - DALLAS — The PREVENTTM risk calculator helped to identify people with plaque buildup in the arteries of the heart, in addition to predicting their risk of a future heart attack, according to new research published today in the Journal of the American Heart Association, an open access, peer-reviewed journal of the American Heart Association.
In addition, when combining PREVENT and a coronary calcium score, risk prediction was further improved, with patients with the highest risk of heart attack matched the group of participants who had a heart attack during the follow-up period.
'These findings are important because when we can better predict a patient's risk of heart attack, we can also tailor care and determine who may benefit from treatment to prevent a heart attack, such as cholesterol-lowering medications,' said corresponding author Morgan Grams, M.D., Ph.D., the Susan and Morris Mark Professor of Medicine and Population Health at New York University's Grossman School of Medicine in New York City.
The PREVENT (Predicting Risk of cardiovascular disease EVENTs) risk calculator, released by the American Heart Association in 2023, can estimate 10-year and 30-year risk for heart attack, stroke, heart failure or all three in adults as young as age 30. PREVENT factors in age, blood pressure, cholesterol, body mass index, Type 2 diabetes status, social determinants of health, smoking and kidney function to estimate future risk of heart attack, stroke or heart failure.
One tool for screening heart health is coronary computed tomography angiography (CCTA), a non-invasive imaging test that visualizes plaque buildup in the heart's arteries. From the CCTA, patients are given a coronary artery calcium (CAC) score, which helps to inform decisions about heart disease prevention and treatment, including when it may be appropriate to prescribe cholesterol-lowering medications.
In this study, researchers investigated whether the PREVENT score matched the level of calcium buildup according to the CAC score. In addition, they used the PREVENT risk assessment and coronary artery calcium scores, separately and in combination, to predict future heart attack risk and assessed the accuracy of each with the participants who had a heart attack during the follow-up period.
They reviewed electronic health records for nearly 7,000 adults who had had CCTA screening at NYU Langone Health in New York City between 2010 and 2024.
The analysis found that for all participants:
'The findings illustrate that PREVENT is accurate in identifying people who may have subclinical risk for cardiovascular disease, meaning blocked arteries before symptoms develop,' said Grams. 'This study used a real-world set of patients, so our findings are important in shaping future guidelines on the use of the PREVENT calculator and coronary computed tomography angiography.'
Study co-author and American Heart Association volunteer expert Sadiya Khan, M.D., MSc., FAHA, said the CAC score can help classify risk for heart disease by analyzing calcium buildup.
'CT scans to evaluate for coronary calcium and extent of coronary artery calcium buildup may be useful when patients are uncertain if they want to start lipid-lowering therapy or if lipid-lowering therapy should be intensified. We have so many tools in our armamentarium for reducing risk of heart attack, we want to be able to optimize treatments for patients, and especially those with higher risk,' said Khan, who chaired the writing group for the Association's 2023 Scientific Statement announcing PREVENT, Novel Prediction Equations for Absolute Risk Assessment of Total Cardiovascular Disease Incorporating Cardiovascular-Kidney-Metabolic Health.
Study details, background and design:
The study had several limitations, including that patients were screened at a single institution and the majority of participants were noted as white, so the findings may not be generalizable to other people. The analysis only included people who had undergone coronary calcium screening, and electronic health records were the sole source of data. In addition, the follow-up time was short at 1.2 years, and the presence of non-calcified plaque in the heart's arteries was not assessed. Finally, the study may overestimate the prevalence of coronary artery calcium in low-risk people since participants in this study were referred for CCTA/CAC score by a health care professional, which means they may have more heart disease risk factors than the general population.
Co-authors, disclosures and funding sources are listed in the manuscript.
Studies published in the American Heart Association's scientific journals are peer-reviewed. The statements and conclusions in each manuscript are solely those of the study authors and do not necessarily reflect the Association's policy or position. The Association makes no representation or guarantee as to their accuracy or reliability. The Association receives more than 85% of its revenue from sources other than corporations. These sources include contributions from individuals, foundations and estates, as well as investment earnings and revenue from the sale of our educational materials. Corporations (including pharmaceutical, device manufacturers and other companies) also make donations to the Association. The Association has strict policies to prevent any donations from influencing its science content. Overall financial information is available here.
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About the American Heart Association
The American Heart Association is a relentless force for a world of longer, healthier lives. Dedicated to ensuring equitable health in all communities, the organization has been a leading source of health information for more than one hundred years. Supported by more than 35 million volunteers globally, we fund groundbreaking research, advocate for the public's health, and provide critical resources to save and improve lives affected by cardiovascular disease and stroke. By driving breakthroughs and implementing proven solutions in science, policy, and care, we work tirelessly to advance health and transform lives every day. Connect with us on heart.org, Facebook, X or by calling 1-800-AHA-USA1.
For Media Inquiries and AHA/ASA Expert Perspective: 214-706-1173
Bridgette McNeill: [email protected]
For Public Inquiries: 1-800-AHA-USA1 (242-8721)
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Typical angina had all three; atypical angina had 2 of 3, noncardiac had one, and there was also a group with dyspnea only. There were five groups of patients: 25% no symptoms 10% dyspnea only 6% noncardiac 37% atypical chest pain 22% typical angina Now pause. The authors had total plaque volume and FFR-CT on each of these patients. Then they just did correlations. And they found, with these correlations: Only typical angina had a positive correlation with plaque atheroma. Typical angina also correlated strongly with negative values of FFR-CT. The authors also noted, surprisingly, that atypical chest pain, noncardiac chest pain, and dyspnea each correlated with higher FFR-CT, greater than 0.8 suggestive of normal flow. The authors and imaging proponents seem excited about this. In a Medscape news article, one of the authors says: 'Even having no symptoms was not a reliable indicator of cardiovascular health in these patients. 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The primary endpoint of the registry is the reclassification rate between the management plan based on coronary CTA alone vs CTA plus FFR-CT. Two teams came up with the original plan based only on CTA. A site team and a blinded core team from Duke. The primary endpoint was the reclassification of the treatment plan from the CT-FFR results. The primary results were that it changed management in about two-thirds of the cases. It was hard for me to see a pattern in the reclassification. The authors tell us later that the majority of subjects were safely deferred to medical management alone, and only a minority required 'further testing.' A second finding was that rate of no significant disease at angiography was significantly lower in patients who had a positive FFR < 0.8 (about 15%) vs > 0.8 (44%). Odds ratio for no significant disease was 0.19 for a positive FFR (that is < 0.8) A third finding was that 19 MACE events happened in the 90 days after the study, 10 of them were death, and all happened in the FFR < 0.8 category — 19 vs 0. The authors concluded that FFR-CT was great. It guided management, helped predict no disease, and even had a strong association with MACE events. They noted this: 'FFR-CT led to a recommendation of invasive coronary angiography (ICA) in only 40% of subjects in a cohort with an anatomic obstructive disease rate of 72%, and subjects referred for ICA downstream were significantly more likely to have obstructive disease at ICA if they had a positive FFR-CT.' And this: 'Importantly, a negative FFR-CT was associated with an excellent short-term prognosis, as none of the 1600 subjects with negative FFR-CT experienced death, MI, or unplanned hospitalization for ACS and urgent revascularization.' A colleague in imaging advises me that this was one of the major studies cited to establish FFR-CT. My gosh, this is terrible. What a mess. First of all, the study was sponsored by HeartFlow. It was a late-breaker at ESC in 2018. I must have had jet lag because I missed it. Much of my criticism follows a Twitter thread from my friend Venk Murthy at University of Michigan. A primary endpoint in change in management in a voluntary registry sponsored by the company is about as weak an endpoint as you can get. Why isn't this a measurement of clinical psychology? What if you chose, say, in a non-industry-funded study, a doctor team skeptical of FFR-CT. I bet few would be swayed by the CT-FFR results. Another problem was that most of the FFR-CT values were abnormal in the left anterior descending artery (LAD) and were between 0.7-0.85. We know this from the IQR values. But now I will cite a study from Christopher Cook in Darrell Francis' group published in JAMA Cardiology 2017. What this London group found is that when doing a systematic review of all studies measuring the diagnostic accuracy of FFR-CT, they found that values just under the cutoff of 0.8 (that is, between 0.7 and 0.8) had the lowest accuracy — only 46% accurate. Pause there. That's like a coin flip. Cook et al report that if you want accuracy from FFR-CT, say 82% overall accuracy threshold, you needed values lower than 0.63 or above 0.83. And if you wanted more stringent 95% and 98% diagnostic accuracy thresholds from FFR-CT, you needed values lower than 0.53 or above 0.93, and lower than 0.47 or above 0.99, respectively. A third issue is that most of the patients (77%) were nontypical angina — either atypical or non-cardiac pain. But we know from the Manesh Patel seminal NEJM paper from 2010 that when patients with atypical symptoms go to cath, the chance of obstructive disease is low — regardless of the results of stress testing. In fact, a positive stress test only changed the likelihood of having CAD from 35% to 41%; hence, my stance that if every stress imaging machine broke, CV outcomes would hardly change. The point in citing this seminal paper is that most patients in the ADVANCE registry study — the 77% with atypical symptoms — should not have had a change in management. A fourth issue is that the MACE events are 100% noise — 19 vs 0. And 10 deaths in the first 90 days. I can't even believe they mentioned MACE events. The CI for the odds ratio goes from 1.2 to 326. The P-value, however, was calculated to be significant at .039, which is crazy. So, in sum, this is one of the weakest, late-breaking, practicing-changing trials I have seen. It's a psychology experiment and we have no idea a) which treatment strategy was best, and b) what meaning is there in changing a treatment strategy without knowing which one is correct. If we wanted to know about FFR-CT, it's simple: you randomize people to care with the HeartFlow FFR-CT vs those without. Then you measure outcomes — MI, CV deaths, even urgent revascularization. But this was not done. Instead, FDA approves the HeartFlow, proponents and key opinion leaders speak highly of it, these studies are not highly criticized, and CT scans get $1500 added to them. HeartFlow was approved de novo in 2014 but received a 2019 clearance for 'virtual modeling.' When I asked my AI friend Claude to explain the difference between the two designations — 2014 and 2019 — one of the 'significant' points was a business model expansion wherein the original FFR-CT was a one-time diagnostic test, but the 'planner (the virtual modeling) creates additional revenue opportunities for each patient who needs intervention.' And then this: the 2019 decision Expands HeartFlow's market from diagnosis into treatment planning. My AI program Claude must not know I am a critical appraiser because it then wrote: Physicians can now use HeartFlow for the entire patient journey: diagnosis → treatment planning → post-intervention assessment. This creates much stronger physician adoption and stickiness. And it makes the cost–benefit analysis more favorable since one CT scan can support multiple clinical decisions. The 2019 Planner approval was huge for HeartFlow because it transformed them from a diagnostic company into a comprehensive coronary care platform. Instead of just answering "Does this patient need a catheterization?", they can now answer: "Exactly how should we treat this patient's disease?" This is why HeartFlow's valuation and market penetration accelerated significantly after 2019. They weren't just competing with stress tests anymore; they were competing with the entire invasive workup process. I had no idea this stuff was happening. What a tragic waste of money. This may be one of the lowest value medical interventions I have seen. And you think I am wrong to be hopeful about FDA new leadership. Regulators should have required an RCT. Since they did not require and RCT, physicians should. Companies are not nefarious. They simply jump over the bar we hold for them. In this case the bar was ridiculously low. Speaking about lax FDA regulation, JACC has published a sobering research letter on the transcatheter tricuspid valve replacement called the EVOQUE valve. This one is also really scary. On this I hardly need commentary; I can just tell you the data. First author was Lior Lupu. FDA approved the valve in February 2024. This was based on the pivotal TRISCEND II trial, which was driven quality-of-life measures, not hard outcomes, and was not blinded. Thus, placebo effects were surely present. The group of authors from Washington, DC used the MAUDE database at FDA, which stands for Manufacturer and User Facility Device Experience. It contains information about device malfunctions, injuries, and deaths associated with medical devices that have been reported by manufacturers, healthcare facilities, and users. The main weakness of MAUDE is that there is no denominator and it's voluntary. In the year since approval, the research team found 150 reports on EVOQUE that describe 158 events. 1. Bradycardia or high degree atrioventricular (AV) block was most common (n = 70 or 44%) and there were 2 deaths. 66 of the 70 required pacemakers. Most were detected at the implant however a third were seen later between days 3 and 90. 2. Device malposition, migration, or embolization occurred in 33 patients (20.9%), causing 6 deaths. Most events were diagnosed within 3 months: 76% intraprocedurally, 14% within 2 days, and 7% between 3 days and 3 months. Management included transcatheter valve-in-valve implantation in 10 cases (eg, SAPIEN-in-Evoque), with 2 requiring a second valve for optimization. Two patients underwent transcatheter treatment for paravalvular leak, while 16 required surgery. 3. EVOQUE leaflet thickening or thrombus was identified in 20 patients (12.7%), with clinical or hemodynamic consequences reported in 16 of the 20. Cases were detected within the first month (56.3%), between months 2 and 6 (25.1%), and after 1 year (18.8%). Management included thrombolysis (n = 4), transcatheter valve-in-valve implantation (n = 2; 1 also had device migration), and surgery (1 patient with severe postprocedural thrombosis with hemodynamic instability). 4. Cardiac tamponade was reported in 8 patients (5.1%), with 5 patients undergoing surgery and 4 deaths. 5. Venous injury or bleeding occurred in 8 patients (5.1%), with 2 deaths. 6. Five cases of ventricular tachycardia, fibrillation, or cardiac arrest were reported: 2 intraprocedurally and 3 postprocedurally (days 0, 4, and 7). 7. Mechanical failure of the delivery catheter was reported in 4 patients (2.5%), all due to nose cone separation. The authors write that while bradycardia, tamponade, valve injury, and valve thrombosis had been reported in the trial, valve malposition, migration, or embolization — the second most frequently reported adverse event in this research letter — were not reported in the trial. So, they were new discoveries. Also, additionally, 3 cases of ventricular arrhythmia or cardiac arrest were reported within the first postprocedural week without a definite etiology. Nose cone separation wherein the nose can go missing into the PA also occurred. Like I said, I hardly need comment because the list of complications is so sobering. Of course, MAUDE has no denominator, but on the other hand it is also voluntary, so this is likely underreporting. I would note that only 237 patients received a valve in the TRISCEND II pivotal trial. There were substantial complications noted. To me, this was quite lax regulation. First, there should have been a trial with a sham procedure. Quality-of-life metrics are meaningless when one group gets a procedure and the other group gets bland white tablets. Second, there should have been more patients in the trial. And third, the approval should have been contingent on a required database, such as that with TAVR. This report is really scary given the number of deaths. In fact, mortality from tricuspid valve surgery is the main reason transcatheter techniques were designed. In the transcript, I highlighted in orange font the number of deaths. I counted 14 deaths and 5 cases of ventricular tachycardia/cardiac arrest. Proponents may cite the learning curve, but I doubt it because I read that the company did a slow rollout where centers who were part of the trial were first. And you wonder why I am a medical conservative and slow adopter.
