Month: October 2025

The Top Trends of TCT 2025

Posted on by Viktor Zarev

This year marked the 37th Annual Transcatheter Cardiovascular Therapeutics conference, and while the core of the conference is still catheter-based heart therapies, this year’s research studies and device demonstrations made it clearer than ever that cardiac medtech continues to push the boundaries of what can be done with a catheter.

Structural Heart is King – The biggest research and booth presence at this year’s TCT came from valve replacement technologies, underscoring just how much the field of transcatheter valve replacements has grown, with TAVR now being just one of many valve replacement procedures available through the minimally invasive method. 

Coronary Therapies are a Close Second – Though a lot of the excitement is around valve replacements, innovations in percutaneous coronary intervention, coronary revascularization, and intravascular lithotripsy all featured heavily, showing just how central coronary artery disease is to interventional cardiology.

Imaging Solutions For Less Catheterization – With the increases in catheter-based heart procedures, many companies are now developing “wire-free” ways to help cardiologists plan interventions, reducing the paradox of needing a catheter to figure out if you need a catheter.

Improving the Cath Lab – In the same vein, once care teams are in the cath lab, companies like Egg Medical and Rampart both showed several ways to improve physical safety by blocking radiation exposure through adjustable patient tables and ultra-lightweight lead vests.

AI at TCT Focused on Planning over Diagnosis – Early on in 2025, cardiology conferences like ACC and HRS were full of news and studies about cardiology AI technology changing the way we diagnose heart disease, yet the exhibitors and research at TCT 2025 took a more procedural approach to AI for transcatheter therapies, with the majority of use-cases focusing on planning TAVR or PCI.

Genetic Risk Scores Improve CAD Detection

Posted on by Viktor Zarev

Coronary artery disease risk assessment might soon rely on genetic testing, following a UK Biobank analysis that suggests adding a CAD multi-gene risk score to conventional biomarkers significantly improves disease prediction and patient identification.

  • Traditional CAD risk assessment uses biomarkers that fluctuate over time, while genetic scores capture inherited disease risk since birth.
  • Currently, there are over one million genetic mutations that can lead to inherited CAD risk.

Examining genetic profiles, researchers followed 353k UK Biobank participants without baseline CAD for 11 years on average, and compared the predictive effects of adding a polygenic risk score (PRS) to a combo of three CV biomarkers (LDL-C, Lp(a), hs-CRP), finding substantial improvements…

  • The predictive model’s discrimination significantly improved when CAD PRS was added to biomarkers (C-index: 0.739 vs. 0.754).
  • The improvement was also similar when apoB replaced LDL-C (C-index: 0.740 vs. 0.754).
  • Patients in the highest category for all three biomarkers showed 2x CAD risk (aHR: 2.15), but those also in the highest CAD PRS category faced nearly 4x higher risk (aHR: 3.71).
  • CAD PRS alone showed stronger association than any single biomarker, with the highest PRS group facing 78% higher risk.
  • Risk stratification also remained consistent across patient sex, suggesting universal applicability.

Since genetic risk is determined at birth and remains constant, using polygenic risk scores for CAD could enable early identification of high-risk patients before biomarker abnormalities even develop.

  • Some institutions already use PRS in clinical risk assessment, but insurance coverage remains limited with tests costing $200-$250.
  • It’s also worth noting that high genetic risk doesn’t doom a patient, since knowing earlier can enable preventive interventions before disease manifests.

The Takeaway

This study, like other genetic cardiology studies, reminds us that some people are at higher risk of heart disease no matter how they live their lives. The good news is, we have the technology to find out who these people are and with a disease like CAD, catching it sooner always leads to better outcomes.

Intensive BP Lowering Doesn’t Hurt Patient QoL

Posted on by Viktor Zarev

Intensive blood pressure lowering might enhance patient wellbeing, after the deeper analysis of the ESPRIT trial demonstrated that lowering systolic BP to <120 mmHg leads to modest but significant improvements in health-related quality of life.

  • Intensive BP-lowering treatment targeting has proven CV benefits, but many worry that aggressive targets might lead to excessive medical burden and adverse events.
  • Previous trials (ACCORD, SPRINT) found no significant QoL differences between intensive and standard treatment, but lacked follow-up duration alongside high missing data rates.
  • BP related quality of life is often measured using the EQ-5D-5L questionnaire which evaluates mobility, self-care, usual activities, pain/discomfort, and anxiety/depression.

To fill in these gaps, the ESPRIT QoL analysis examined 5.4k intensive treatment and 5.4k standard treatment participants over a 3.4-year follow-up, using the EQ-5D-5L questionnaire to evaluate the differences between patient QoL and found that…

  • EQ-5D scores increased by 0.56 points with intensive treatment versus decreased by 0.50 points with standard treatment, suggesting better QoL for the intensive group.
  • Intensive treatment led to a 16% higher likelihood of meaningful improvement, while standard treatment led to worsening quality of life.
  • No significant differences were found across the five EQ-5D domains between treatment groups.

Considering the widespread clinical hesitation about intensive BP targets due to quality-of-life concerns, these findings provide real world patient-centered evidence supporting more aggressive treatment in high-risk hypertensive populations.

  • For example, the study’s robust sample size (>10,000 participants) provides the evidence previously lacking from earlier trials that faced limited follow-up and completeness.
  • Moreover, patient-reported outcomes increasingly drive treatment decisions, making this QoL data essential for decision-making about BP targets.

The Takeaway

The results of ESPRIT’s quality-of-life analysis could help dispel concerns that intensive blood pressure control impairs patient wellbeing through excessive treatment burden. On the contrary, it appears that intensive treatment actually improves health-related quality of life while reducing cardiovascular events.

Don’t Blame Your Heart for Heart Failure

Posted on by Viktor Zarev

Perhaps the biggest cardiology story of the year, an entire issue of JACC now hypothesizes that heart failure with preserved ejection fraction (HFpEF) might actually be caused by visceral fat tissue that triggers cardiac weakening through adipokine signaling.

  • HFpEF has traditionally been seen as a heterogeneous disorder related to comorbidities like obesity, hypertension, and diabetes, with an unclear cause of pathophysiology.
  • Obesity is present in over 95% of HFpEF patients and tracks with disease severity, yet it has been viewed as a contributing factor rather than the cause.
  • Adipokines are substances that are released by fat tissue and act as hormones to regulate body functions like appetite, metabolism, and inflammation.

The new unifying adiposity framework now proposes that visceral fat expansion causes secretion of an altered adipokine profile that leads to systemic inflammation alongside cardiac hypertrophy and fibrosis. The hypothesis organizes adipokines into three functional domains…

  • Domain I adipokines are cardioprotective molecules suppressed by excess body fat, representing a critical protective pathway that becomes disabled.
  • Domain II adipokines are also cardioprotective molecules but they are increased by the body as a compensatory response to body fat level.
  • Domain III adipokines, which are heightened during high body fat and drive the inflammation, hypertrophy, and fibrosis effects directly causing HFpEF

Taking the hypothesis a step further, this means that HFpEF is the result of high body fat imbalances that promote the Domain III adipokines while suppressing Domain I adipokines  with Domain II.

Although we have yet to see a definitive adipokine study, the authors put together several converging lines of evidence supporting adipose tissue as the primary pathogenic driver of HFpEF. Some examples include…

  • Obesity and calorie excess are the drivers of experimental HFpEF models, with visceral fat changes visible years before HF diagnosis specifically predicting HFpEF (but not HFrEF).
  • Striking parallels exist between obesity and HFpEF in molecular, pathophysiological, and clinical features, with adipokine levels correlating with disease severity in both.
  • Experimental interventions targeting only adipose tissue to modify specific adipokine secretion cause distant cardiac effects, changing cardiomyopathy progression.

The Takeaway

This unifying hypothesis fundamentally reframes HFpEF from a multi-cause cardiac disorder with obesity as one comorbidity to an adipose-driven endocrine disease. If future studies validate this hypothesis, it could transform HFpEF treatment and the conversation around how to prevent our hearts from failing.

MedAxiom Report: Cardiologist Compensation Soars, Patient Access Struggles

Posted on by Viktor Zarev

Good news and bad news from MedAxiom’s latest cardiology compensation survey. The good news? Cardiologist median compensation reached new record highs last year. The bad news? Patient access deteriorated while the number of patients physicians had to manage swelled.

  • The 2025 MedAxiom Cardiovascular Provider Compensation and Production Survey represents the cardiovascular industry’s most comprehensive compensation dataset.
  • It can also help signal fundamental shifts in how cardiovascular care is valued and delivered.

The 2025 survey findings aggregated data across cardiology, cardiac surgery, and vascular surgery specialties, examining compensation trends, workforce deployment patterns, and productivity metrics and found that…

  • Full-time cardiologist median compensation reached $695k despite slight wRVU production declines.
  • When filtering by employment type, integrated practice cardiologists surpassed $700k compared to private practice physicians at $588k — the largest gap in over five years.
  • Cardiac surgeons saw only modest compensation increases while vascular surgeons maintained near-peak compensation despite both showing productivity drops.

Even with those pay raises, patient access hasn’t improved, rather going in the other direction…

  • Patient access showed significant strain with panel sizes reaching nearly 2,000 per physician FTE. 
  • Meanwhile, new patient office visits declined for the first time in years to just 15.4% of total visits.
  • Catheterization and PCI volumes per 1,000 active cardiology patients continued downward trends, reflecting shifts toward more advanced imaging guidance.

Given mounting access challenges despite workforce expansion, the survey once again confirmed that advanced practice providers are central to maintaining care capacity.

  • Cardiology programs increased APP-to-physician ratios to 0.75, while cardiac and vascular surgery programs saw declining APP support per surgeon.
  • Cardiology APPs demonstrated 8% productivity growth, with private practice APPs significantly outperforming integrated peers.
  • The declining physician FTEs per 1,000 active patients alongside rising APP utilization represents a fundamental care delivery transformation rather than adaptation.

The Takeaway

MedAxiom’s 2025 compensation survey captures cardiovascular care at a turning point because while provider compensation reaches historic highs, access metrics reveal capacity shortcomings that compensation probably won’t solve. Whether or not more APPs or more physicians is the right answer remains to be seen.

Specialist Care Can Improve HF Outcomes Across the Board

Posted on by Viktor Zarev

A recent study out of the U.K. suggests that multidisciplinary team management could significantly reduce death or rehospitalization risk for HF patients across the LVEF spectrum.

  • Specialist heart failure care involves management by specialist nurses under direct cardiologist supervision.
  • This approach is traditionally reserved primarily for HFrEF patients who have the most proven guideline-directed medical therapies available.
  • However, recent studies demonstrating SGLT2i and finerenone efficacy in HFmrEF/HFpEF has expanded the therapeutic options for specialist care beyond HFrEF.

Based in a single U.K. county, the Buckinghamshire analysis examined 2.1k patients hospitalized for acute heart failure who received either specialist care or standard care over a 618-day follow-up and found some striking outcome differences…

  • Specialist care reduced the composite risk of death or HF rehospitalization across all LVEF categories: HFrEF (HR 0.58), HFmrEF (HR 0.49), and HFpEF (HR 0.76).
  • Despite clear benefits, only 61% of discharge survivors received specialist outpatient care, with disparities between HFrEF (79%), HFmrEF (77%), and HFpEF (53%) patients.
  • Overall outcomes were concerning: 63% died and 21% were rehospitalized for acute HF over follow-up, with 68% experiencing either endpoint.

Given the expanding HF population and increasing treatment complexity, the specialist nursing capacity, both in the U.K. and U.S. could be inadequate for population needs, especially since other specialist care implementation barriers persist.

  • Among those with specialist care arranged, 38% missed their first appointment, highlighting implementation challenges beyond care availability.
  • The population distribution (55% HFpEF, 36% HFrEF, 9% HFmrEF) suggests that current HFrEF-focused services also miss the majority of HF patients who could benefit from specialist care.

So where do we go from here? Currently, the British Society for Heart Failure argues that at least four specialist nurses per 100k people are needed to address growing treatment complexity and aging demographics.

  • Further restructuring of HF care teams and understanding that all types of HF patients benefit from specialist care will also be necessary to move the needle on practice opinions.

The Takeaway

Heart failure comes in many forms in many different types of patients, but that doesn’t mean that only one subset of the disease should receive multidisciplinary care. This small, but important study raises the point that both having enough care providers and the right approach will be critical to improving HF care in the long run.

Screening For Lp(a) is Still Too Uncommon

Posted on by Viktor Zarev

A recent JACC analysis of the Epic Cosmos database suggests lipoprotein(a) screening is still one of cardiology’s most neglected risk assessment tools, representing a serious gap in the way we evaluate patients’ CVD risk.

  • Lipoprotein(a) is a fat molecule that significantly increases CVD risk, with roughly 20% of individuals having elevated levels above 50 mg/dL.
  • Despite its well-established relationship with MACE, Lp(a) testing remains widely underutilized in clinics with limited data available until now.
  • Currently statins and ezetimibe are the main drugs for lowering Lp(a) levels, but there’s a field of promising Lp(a) therapies on the horizon.

To learn more about Lp(a) testing trends, researchers searched for Lp(a) screening patterns in the Epic Cosmos database from 2015-2024 across more than 300M patients and found both progress and persistent gaps…

  • Total distinct patients tested increased dramatically from 14.5k in 2015 to 309k in 2024 (a 21x increase).
  • However, annual testing rates rose from just 0.03% in 2015 to only 0.24% in 2024, so only 728k total patients (0.2% of the U.S. population) were tested the entire decade.
  • Testing was mostly in adults aged 50-65 years (34.8%), with similar rates between males (51.8%) and females (48.2%).

Despite the growth in the raw number of patients tested, the persistently low testing rate means that the vast majority of at-risk patients fly under the radar despite growing awareness of Lp(a)’s risk implications, but there are two important details to highlight.

  • Testing rates varied from state to state, with California (11.6%), Ohio (8.6%), and Texas (7.6%) accounting for the highest testing volumes.
  • During the study, Lp(a) testing methods shifted from mass-based assays (mg/dL) to the recommended molar assays (nmol/L), which reached 64.2% of tests by 2024.

The Takeaway

Even with a 21x increase over the past decade, Lp(a) testing in the U.S. is still seriously underutilized at just 0.2% of the population annually and far below what would be needed to identify the potential 20% of people with elevated levels. While some aspects of Lp(a) screening have improved, it may be that we need a true Lp(a) treatment to emerge before screening becomes a priority.

Secondary Cardiomyopathy Isn’t so Secondary After All

Posted on by Viktor Zarev

Secondary cardiomyopathies might not be caused by environmental factors after all, after a massive four-biobank study found that their development is a lot more dependent on which combination of genetic risks you already have.

  • Secondary cardiomyopathies including peripartum (PPCM), alcohol-induced (ACM), and cancer therapy-related (CCM) have traditionally been viewed as caused by environmental conditions.
  • While rare single gene mutations linked to dilated cardiomyopathy (DCM) were known to be higher in these populations, the role of mult-gene expression was unclear until now.

The multi-biobank genetic analysis examined nearly 1.3M individuals identifying 3.4k people with secondary cardiomyopathies (70 PPCM, 2,281 ACM, 1,063 CCM). Upon looking at the combination of genes these patients had, researchers found some stunning gene architectures.

  • People with the combination of genes that lead to DCM were also at far greater risk for all secondary cardiomyopathy types: PPCM (OR: 1.82 per SD), ACM (OR: 1.56), and CCM (OR: 1.64).
  • In medically reviewed cases, monogenic variants were present in only 7 of 113 individuals, while 66 had high polygenic scores making them 3x more likely to develop CM.
  • Most people with cardiomyopathy didn’t have prior risk factors, suggesting genetics rather than environmental exposure drives disease development.
  • Researchers also found that while some people developed cardiomyopathy due to a single genetic mutation, far more developed CM due to multi-gene mutations.

Even with well-established environmental triggers like pregnancy, alcohol, and chemotherapy, the genetic data suggests these exposures act as magnifiers in people who are already genetically susceptible rather than primary causes.

  • The shared genetic architecture between secondary cardiomyopathies and DCM implies these conditions may represent the same underlying disease process triggered by distinct environmental stressors.
  • This reframes “secondary” cardiomyopathies as primarily genetic conditions with environmental magnifiers, rather than environmental conditions with genetic contributions.

The Takeaway

This landmark genetic study fundamentally challenges how we understand secondary cardiomyopathies, revealing that most cases reflect underlying genetic predisposition triggered by environmental factors rather than direct environmental causes. Future prevention strategies should focus on population-level genetic screening to identify at-risk individuals, potentially preventing thousands of cases currently classified as unavoidable environmental complications.

Where HF is Headed – Takeaways from HFSA 2025

Posted on by Viktor Zarev

Cardiac Wire attended its first ever Heart Failure Society of America meeting this year, exploring everything from the latest pharmaceutical advancements to the complex relationship between cardio-renal health and beyond. Here are some of the big takeaways from HFSA 2025.

Heart Failure Comes in Many Forms: While the gold-standard for diagnosing heart failure is still tied to left ventricular ejection fraction, what causes decreased LVEF varies greatly from congenital defects, to cardiometabolic causes, and even gene over-expression. This was reflected in the studies presented by researchers and the solutions offered by companies.

Pharma Has a Strong HF Priority: Among the booths and studies at HFSA, both the research and floor space were dominated by pharma companies, underscoring how many of the treatments for HF focus on either biochemically reducing symptoms, improving quality of life, or addressing the root cause of HF.

Patient Monitoring is Central to HF Treatment: Whether it’s getting the dose right, or making sure a patient’s heart function is steady, one thing was clear from this year’s studies: data drives the decisions clinicians make on the individual level. Stats like serum potassium or arterial pressure vary from patient to patient, so no two HF treatments are really the same.

Transplants are Still Inevitable: Even with all the discussion around how to best treat heart failure, there still isn’t a cure in sight, meaning that the final option for many patients with failing hearts is a transplant.

Many HF Forms Are Still Preventable: Though it may seem like a discouraging takeaway, the lack of a definitive cure for HF highlights just how important prevention is, with the HFSA now moving in the direction of prioritizing prevention rather than just treating it when it happens.


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