Month: March 2026

A Plan to Tackle CAD Mortality by 2050

Posted on by Viktor Zarev

Coronary artery disease is the leading cause of cardiovascular death throughout the world, and a Lancet commission just released a new statement about what it will take to significantly reduce CAD deaths by 2050.

  • The commission’s original recommendation was to reclassify coronary disease as atherosclerotic coronary artery disease (ACAD). 
  • Now the field is moving away from a traditional focus on the late-stage CAD symptoms and acute cardiac events towards the disease process itself.

Based on four core pillars, the statement tackles the epidemiology of ACAD, current management strategies, gaps in our scientific knowledge, and a look at the incentives that drive our system.

For epidemiology, the authors clarified that although U.S. ACAD outcomes have substantially improved since 1960, with mortality being cut in half, we still have work to do…

  • There will be over 450k ACAD deaths in the year 2050.
  • A quarter of all Americans are expected to have an ACAD event at some point.
  •  Over 1 million of those Americans will have a heart attack each year.

When it comes to applying what we already know, the statement argues that we need more…

  • Smoking cessation, lipid-lowering and blood pressure-lowering therapies.
  • Glucose-lowering agents, revascularization procedures, and cardiac rehabilitation.
  • And finally a recognition that high-sugar foods and beverages need to be limited.

While we know a lot about tackling CAD, there are also some knowledge gaps to consider–

  • For starters, a long-term connection between lower noncalcified plaque and improved CV outcomes has yet to be made.
  • Polygenic risk scores and early-detection imaging still need validation.

And of course, no U.S. healthcare discussion would be complete without mentioning incentives.

  • For example, the current payment models don’t incentivize population-level strategies. 
  • Despite two decades of value-based initiatives, the authors also contend there is no clear evidence that these programs improve care quality or outcomes.

So what to do with this statement? The Lancet’s commission argues that if these pillars are all considered, implemented, and addressed it could help reduce ACAD deaths by >350k per year by 2050.

The Takeaway

Every month we seem to get foreboding forecasts that tell a grim tale about America’s CVD burden. This statement is different, since it outlines the real steps needed to get more serious about population-level prevention while finding a way to make it attractive to a profit-driven healthcare system.

What Can Fat Around the Heart Tell Us?

Posted on by Viktor Zarev

We all know by now that too much body fat isn’t good for your heart, and new research suggests that the fat directly around your heart could play a role in your risk of coronary artery disease (CAD).

  • Fat around the heart is also known as epicardial adipose tissue (EAT).
  • While studies have looked at overall body fat burden as a clinical risk factor, none have tried to quantify the risk of a fatty heart until the PARADIGM registry.

Drawing data from PARADIGM, researchers followed 773 patients for eight years after they underwent serial CCTA imaging and categorized them into three EAT volume categories: low (≤ 77 cm3), moderate (77-113 cm3), and high (> 113 cm3).

  • Nearly all patients (83.7%) saw their plaque volume progress, while a third of them developed new plaque after starting a zero.
  • Progression of total plaque volume (including calcified and non-calcified) was consistently greater for the highest EAT volume category. 
  • Additionally, plaque progression rates (78.9% vs. 83.9% vs. 88.5%) increased across all three EAT categories.

There’s a serious caveat to these results though, since researchers determined that EAT volume measured with CCTA was not independently associated with major adverse cardiovascular events.

  • Only when the fat volume readings were considered alongside a patient’s plaque progression data did it influence 10-year MACE risk predictions.
  • However, high EAT volume was independently associated with CAD presence and progression.

So what does this mean for paying attention to fat around the heart?

  • For one, it can still be a useful non-invasive biomarker for following statin and GLP-1 therapy impacts on the heart, since both can reduce EAT.
  • Moreover, enlarged fat cells release proinflammatory cytokines that could contribute to localized inflammation of the heart tissue, ultimately contributing to heart disease.
  • EAT could also eventually find a place among other CAD risk factors like cholesterol, Lp(a), and CAC.

The Takeaway

Fat around the heart isn’t random nor harmless, and while this study does suggest keeping an eye on it can provide some useful information, it’s still unclear how we’ll use that data for clinical decisions.

The CV Risks of Premature Menopause

Posted on by Viktor Zarev

Keeping a close eye on women’s reproductive health could give insights into their future cardiovascular risk after a new JAMA study found that women who experience premature menopause face higher lifetime risk of coronary heart disease (CHD).

  • The average age for menopause for most women is 51, with premature menopause occurring in women under 40.
  • Current cardiovascular risk assessment doesn’t really incorporate reproductive history factors despite early estrogen loss influencing ASCVD progression.
  • It also hasn’t been clear how premature menopause impacts women of different racial/ethnic backgrounds.

To answer these questions, researchers followed 10k postmenopausal women (65% White, 35% Black) free of baseline coronary heart disease from 1964-2018, finding that lifetime risk calculations revealed concerning patterns…

  • Premature menopause increased lifetime CHD risk by 40% between the two groups with a hazard ratio of 1.41 for Black women and 1.39 for White women.
  • However, PM occurred over three-fold more frequently in Black women (15.5%) versus White women (4.8%), leading to higher absolute CHD burden despite similar risk.

These results suggest that premature menopause is an important risk-enhancing factor for women, so adding it into the consideration is important, but it also serves as a stress test for a woman’s body.

  • That’s because menopause at any age changes a woman’s body in drastic ways, with lipids and BP often increasing, while energy and muscle mass decrease.
  • This ultimately leads to a less active lifestyle and the compounding of cardiovascular risk factors like increased body fat, hypertension, and hormonal changes.

The Takeaway

As the research on women’s cardiovascular health expands, one thing becomes increasingly clear – cardiologists cannot evaluate and treat the female heart the same as the male. Special considerations are needed for women whose bodies drastically change from fertility, to pregnancy, to eventually menopause.

Ultraprocessed Foods are Bad for Everyone and Worse for Some

Posted on by Viktor Zarev

We already know that what you put in your body is directly related to your overall health, including cardiovascular risk, but a new JACC study suggests your ethnic background could impact just how much damage ultraprocessed foods do to your body.

  • There still isn’t 100% consensus on what an “ultraprocessed” food is, but industrial products like frozen pizza, energy drinks, soda, and cereals tend to fit the bill.
  • That’s because they’re engineered to maximize the reward pathway effects in our brains while providing energy-dense, high-sugar, high-sodium, and low-fiber nutrition.
  • Prior studies have already linked ultraprocessed food diets to higher ASCVD risk, but research was mostly on white participants or homogeneous non-U.S. populations.

Bringing plenty of new data to the table, the MESA analysis followed 6.5k diverse adults ( 39% white, 27% Black, 22% Hispanic, 12% Chinese) without baseline clinical disease consuming an average of 4.38 daily ultraprocessed food servings, finding some substantial risk associations…

  • Each additional daily serving of ultraprocessed food led to a 5.1% relative CVD risk increase for a composite of nonfatal MI, cardiac arrest, CHD death, and stroke death.
  • People in the highest category of ultraprocessed consumption had a 66% higher CVD risk than those in the lowest, with risk increasing steadily across the middle categories.
  • It’s worth noting these results remained consistent when calculating ultraprocessed food as a percentage of total daily calorie intake.

There were also some finer details worth considering, with the ethnic background of a person greatly impacting CVD risk.

  • For example, Black participants experienced a severe risk interaction with 12.3% CVD risk increase per 10% ultraprocessed percentage increase. 
  • Meanwhile this risk increase was only 7.9% in non-Black participants.
  • Curiously, researchers didn’t find an interaction between ultraprocessed food consumption and sex or income.

Whether or not this increased risk is due to genetic factors or biological differences is unclear, since the study simply examined data rather than analyzing the relationship between food consumption and population risk across each ethnic category.

The Takeaway

More and more data and studies keep confirming that ubiquitous ultraprocessed foods are driving CVD risk and ultimately burden. This study now confirms that the burden is unequal, and while it’s still unknown why, it’s all the more reason to take a stand against industrial food.

Where We’ve Been, and Where We’re Going in CV Health

Posted on by Viktor Zarev

JACC released its inaugural Cardiovascular Statistics 2026 report covering a wide spectrum of major CV risk factors and conditions, and despite the medical advancements in the last ten years, it’s clear we still have a lot of work left to do.

  • The report covers five risk factors and six conditions that account for most cardiovascular deaths and disability.
  • It is meant to serve as a comprehensive snapshot of CV health in the U.S. to inform patients, clinicians, researchers, policymakers, and the public.

As part of its process, JACC synthesized data from multiple national sources and evaluated trends in disease epidemiology, quality of care, and morbidity and mortality across risk factors and conditions.

When it came to CV risk factors, the report focused on each one’s prevalence from 2009-2023 and found that…

  • Half of all Americans have hypertension.
  • Diabetes rose steadily, with only half of diabetics achieving glycemic control.
  • Obesity reached epidemic proportions (>40% of adults).
  • The majority of high-risk adults do not achieve LDL guideline targets.
  • Smoking declined substantially in the past 15 years (-5.8%).

For cardiovascular conditions, JACC focused on the trend and impact for six of the most common diseases and found…

  • Coronary artery disease prevalence declined for 25 years, then began rising in 2019, though CAD mortality decreased by 50% in the same period.
  • Acute MI hospitalizations went from 3 per 1,000 in 2004 to 2.3 per 1,000 by 2010, remaining stable since.
  • Approximately 6.7M U.S. adults have HF, and HF-related mortality has risen since 2011.
  • Lower extremity PAD is common, underdiagnosed, affecting 1 in 14 adults.
  • Stroke affects nearly 7.8M U.S. adults, and accounted for ~160k deaths in 2023.

So what to do with this behemoth amount of data?

  • Prevalence data can help the broader CV societies and policymakers prioritize public health initiatives.
  • The report could also help unite the American healthcare system across these broad cardiovascular problems due to how interconnected the risks and conditions are.

The Takeaway
You can’t fix what you don’t know about, so the Cardiovascular Statistics 2026 report’s biggest benefit is its wealth of information, and as JACC’s Editor-in-Chief, Harlan M. Krumholz, MD, wrote, “The data tell a story—but what we do next will define its course.”

IVI or Angiography for Complex PCI Guidance?

Posted on by Viktor Zarev

New follow-up data from the RENOVATE-COMPLEX-PCI trial suggests that intravascular imaging continues to provide better clinical outcomes for patients with complex coronary lesions five years after their PCI procedure.

  • Intravascular imaging (IVI) refers to catheter-based invasive technologies used to visualize the inside of coronary arteries in real-time.
  • The two IVI modalities are intravascular ultrasound and optical coherence tomography, providing cross-sectional images of the vessel wall to guide stent placement.

The RENOVATE-COMPLEX-PCI trial originally randomized 1.6k patients with complex coronary lesions to receive either IVI or angiography guided PCI and found that IVI led to a 36% relative reduction in composite target lesion failure (TLF) compared to angiography after a two year follow-up.

  • More specifically, target-vessel MI or cardiac death was reduced by 37%, and cardiac death alone decreased by 53%.

For this latest analysis, researchers followed up after five years and found that…

  • The primary TLF endpoint was still significantly lower when intravascular imaging was used to guide PCI (10.5% vs. 14.9%).
  • Meanwhile, the composite of cardiac death or target-vessel MI occurred in 7.6% of the imaging group and 10.7% of the angiography group. 

Landmark analysis of the data also revealed that most of IVI’s advantages occurred within the first two years following PCI, with no significant difference between the two groups in the years after.

However, due to cost and education, IVI has yet to be widely adopted in the United States despite guidelines giving the methodology a class 1A indication for guiding PCI in chronic and acute coronary syndromes.

  • For example, the median cost of hospitalization for single-vessel PCI using IVUS or OCT was approximately $23k from 2016-2018, compared to $19k without these imaging technologies.
  • That said, RENOVATE-COMPLEX-PCI’s evidence stands out, since prior studies of IVI PCI did not always show significant decreases in mortality and target vessel MI.

The Takeaway

While the initial two year results of RENOVATE-COMPLEX-PCI were strong, the five year results now provide a robust argument for making intravascular imaging the go-to when it comes to PCI guidance. The even better news is that outcomes like these may be enough to overcome the initial cost of implementing IVI.

Barostim Boosts QoL and LVEF, but Mortality Benefit Still Unknown

Posted on by Viktor Zarev

Strong results from two separate studies on CVRx’s Barostim baroreflex activation therapy suggest the technology might offer symptomatic relief even though its mortality benefit is still up in the air.

  • Abnormal baroreflex signaling causes neurohormonal issues that drive heart failure progression, so Barostim is intended to help reverse this while combined with GDMT.
  • The FDA approved Barostim in 2019 based on the BeAT-HF trial which showed improved quality of life and exercise capacity, but long-term outcomes remained uncertain.
  • Barostim is very unique among cardiac therapies, since it’s an implantable neuromodulator that treats HF by stimulating carotid artery baroreceptors.

The first of two Barostim studies discussed at THT 2026, the REBALANCE registry enrolled 435 patients with a low average baseline LVEF, mostly NYHA class III symptoms, and high average NT-proBNP levels to evaluate the nerve therapy’s functional improvements.

  • Following the therapy, the average LVEF increased significantly from 26.8% at baseline to 29.9% at 6 months, 30.8% at 1 year, and 33.7% at 2 years.
  • Meanwhile 49.8% of patients achieved a clinically meaningful ≥5% LVEF rise.
  • NYHA functional class improved significantly with 34% advancing at least one class at 6 months.

In parallel, the separate COSMOS database analysis of 1.5k patients showed year-over-year reductions in HF hospital burdens.

  • This manifested as a 14.4% drop in all-cause hospitalizations, 29.1% decrease in HF-related hospitalizations, and 26.8% lower HF-related ED visits.
  • An 18.3% increase in all-cause ED visits also occurred but was attributed to the generally poor health of the cohort.

Despite these demonstrated functional and hospitalization benefits, the studies still can’t tell us how much long-term survival is improved by giving patients Barostim.

  • Since Barostim is like an add-on therapy that improves symptoms and isn’t intended to directly treat HF, rather manage symptoms, we’ll need more years of data to find out.

The Takeaway

The good news about Barostim? It’s safe and effective for improving an HF patient’s quality of life while reducing burden on the healthcare system. The bad news? It’s still too early to know if this therapy extends lifespan in the patients who receive it.

What NT-proBNP Can Tell Us About TEER Outcomes

Posted on by Viktor Zarev

New research presented at THT 2026 suggests that the NT-proBNP biomarker could give us a glimpse into which patients with severe tricuspid regurgitation (TR) will benefit the most from transcatheter edge-to-edge repair (TEER).

  • NT-proBNP (N-terminal pro-B-type natriuretic peptide) is a key blood biomarker used to diagnose, rule out, and manage heart failure by measuring cardiac stress.
  • TEER for severe TR is proven to improve symptoms and reduce heart failure hospitalizations, but predicting treatment success has been difficult.

Using data from the EuroTR registry, researchers evaluated 2.2k patients undergoing TEER, and organized them into three NT-proBNP categories (≤1,674, 1,675-3,743, >3,743 pg/mL) to compare baseline levels plus 30-day trajectory changes, finding that…

  • Higher baseline NT-proBNP was associated with a greater 2-year composite mortality or first HF hospitalization risk (aHR: 1.62).
  • Patients in the highest NT-proBNP category showed less functional improvement and less procedural success (81.4% in the highest vs. 86.3% in the lowest).

The 30-day NT-proBNP levels also predicted outcomes in patients who started at high baseline and saw their levels increase more than 30%. 

  • Patients like these faced a 36% event-free survival rate versus 76% in the low NT-proBNP group.

While the study demonstrated NT-proBNP’s prognostic value, it also raised questions about the study population, since the extremely elevated baseline NT-proBNP levels suggest patients might not have been on optimal GDMT prior to TEER.

  • Only 26% of patients received SGLT2is despite guidelines, while 43.9% were on MRAs and 57.4% were on RASis.

The Takeaway

When it comes to a complex procedure like transcatheter edge-to-edge repair for severe TR, being able to predict a patient’s response to treatment is invaluable. This study suggests that NT-proBNP could help do that, so long as physicians know a patient’s GDMT history.

Two Cardiac Troponins Don’t Tell the Same Story

Posted on by Viktor Zarev

There might be a bigger difference between the types of cardiac troponin assays, after a recent JACC analysis found that the type of troponin could help us better understand the kind of damage occurring after a heart attack.

  • Cardiac troponin I and troponin T are currently used interchangeably in clinical practice with guidelines assuming they reflect identical myocardial damage. 
  • Currently, most practices measure one type or the other but not both.
  • Early studies have suggested that the cTnI/cTnT ratio may differ between acute necrotic versus chronic or non-necrotic myocardial injury, but that was uncertain till now.

As part of a multicohort validation, researchers examined 9.7k patients who were marked as having no known, chronic, or acute cardiac disease, and then measured their hs-cTnI and hs-cTnT concentrations to see what cTnI/cTnT ratio could tell them about the injury type.

  • The cTnI/cTnT ratio proved highest in acute cardiac disease (2.06).
  • This was approximately 4-fold greater than the ratio found in patients with chronic disease (0.66) and no known cardiac disease (0.50).
  • Incorporating the cTnI/cTnT ratio alongside individual troponin values made it easier to tell between type 1 and type 2 acute myocardial infarction (AUC: 0.73 vs 0.70).

Experimental cardiomyocyte models were also used to replicate the clinical findings, with researchers discovering that mild nonlethal injury produced cTnT-dominant release, while lethal injury led to cTnI-dominant release.

Given that current practice assumes cTnI and cTnT reflect identical pathophysiology, these findings could challenge single-troponin measurement strategies and guideline recommendations that treat the biomarkers as interchangeable.

  • The good news is that implementing this information would require minimal additional cost, since physicians can measure both troponins rather than choosing one.
  • The ratio’s ability to distinguish type 1 from type 2 MI could also help guide decision-making about invasive coronary angiography versus medical management.

The Takeaway

It seems like a method for better classifying and triaging cardiac damage was under our noses the whole time. On the bright side, thanks to this study, physicians will no longer have to scratch their heads on which assay to use, since the answer is both.

Get twice-weekly insights on the biggest stories shaping cardiology.