Emerging Treatments | Cardiovascular

Session Focus

Zemansky opened on the central tension: cardiovascular medicine is arguably one of the great success stories of modern medicine, yet cardiovascular disease remains a leading cause of death worldwide. The panel addressed where the greatest unmet need now sits, what changed most over the past decade, and how residual risk should be phenotyped.

Where the Unmet Need Sits

Emily Lau MD argued the field has done relatively well on established cardiovascular disease and that the opportunity now lies upstream, in prevention.

Her specific case concerns women. Accumulating evidence identifies multiple points decades before overt disease that represent prevention opportunities: menarche, pregnancy as a major cardiovascular stress test, and menopause as an important inflection point in risk.

What the field has not done is marry preventive strategies to those transition points. In her view that is the biggest opportunity of the coming decade.

Jorge Plutzky MD agreed on moving earlier, identifying those at risk before an event. Imaging is used considerably more than before and carries some imprecision, but can put people on a track toward more aggressive treatment.

He coupled that to a problem the field has not solved: recurrent disease in people with established events. That raises the question of why, and one answer is an unmet target not yet approached, which is where new risk factors and markers like lipoprotein(a) and inflammation come in, along with what he called recent bumps in the road. The alternative explanation is primordial: treatment simply started too late to stop progression even after a first event.

Christian Ruff MD split unmet need into two camps.

Implementation. The field already has terrific therapies and is very ineffective at delivering them to patients, particularly in primary care. He sees substantial opportunity there that would translate into better outcomes for the bulk of patients.

Phenotyping risk. This matters most when extending therapies into the primary prevention population, because treating everybody is difficult. The harder version is phenotyping residual risk in patients with known disease who remain at high risk of recurrent events.

His formulation of precision medicine in this context: everyone gets foundational therapy, and the art lies in identifying which patients are particularly active in a given pathway, so one group receives a specific therapy and another twenty percent receives something else, according to metabolic, atherosclerotic or inflammatory phenotype.

What Changed Most in a Decade

Ruff named two developments.

The first is that lowering atherogenic lipoproteins as aggressively and as early as possible is now a foundational advance, supported by statins, ezetimibe, PCSK9 inhibitors and extending through recent trial data. The key shift is not waiting until overt disease develops.

The second is the cardiometabolic incretins. His reasoning is about treatment philosophy: the field has tended to treat one driver at a time, whether lipids or blood pressure. A therapy addressing inflammation, blood pressure, adiposity and lipids simultaneously is a far more effective population strategy, treating the patient as a constellation of risk and likely serving as the most potent disease modifier.

Plutzky set LDL lowering aside as an established triumph, noting that some countries make statins available over the counter, which itself signals the safety and efficacy profile.

His emphasis was on GLP-1s, framed through thirty years as a preventive cardiologist. A key underlying theme among patients in his waiting room was excess adiposity and obesity, whether referred for hypertriglyceridemia or for diabetes and prediabetes. The accompanying frustration was the inability to improve cardiovascular outcomes by treating diabetes.

He called GLP-1 access offering cardiovascular event reduction independent of diabetes a seismic change with broad ramifications at both societal and medical levels. It answered the long-standing question of why treating obesity had not reduced cardiovascular events, paralleling the earlier resolution of the same question for diabetes.

Lau added two reframings she considers central.

An integrated view of cardiometabolic health rather than individual risk factors, spanning the metabolic, inflammatory and thrombosis axes, with therapy targeted according to phenotype.

A life course approach. Cardiovascular prevention needs to begin in adolescence. She noted that roughly twenty years ago the field did not understand the intimate relationship between a woman’s reproductive milestones and cardiovascular risk, and now has convincing epidemiologic and early genetic data identifying those transitions as points where risk emerges and inflects.

Her summary of the next decade: moving away from looking at LDL cholesterol and blood pressure in isolation toward an integrated picture across an entire lifetime.

Key Takeaways

1. The opportunity has moved upstream. The field treats established disease well and intervenes far too late.

2. Reproductive milestones are cardiovascular inflection points, recognized only in roughly the last twenty years.

3. Recurrent events in treated patients signal either an unaddressed target or treatment that began too late.

4. Implementation is a distinct unmet need. Existing therapies are delivered ineffectively, particularly in primary care.

5. Incretins shifted the model from treating one driver to treating a constellation of risk at once.

6. GLP-1s answered why treating obesity had not reduced cardiovascular events, paralleling the earlier diabetes question.

7. Precision in cardiology means phenotyping residual risk on top of foundational therapy given to everyone.