Thrilled to share that our study is out now in @ESC_Journals #EJPC! We examined long-term outcomes after coronary angiography among >5,000 individuals with measured lipoprotein(a) [Lp(a)] — one of the most important yet under-recognized drivers of atherosclerotic disease 🫀

Happy to share our @MassGenBrigham Biobank descriptor paper in @NatureComms ! Huge thanks to all Biobank participants and to my incredible mentors & colleagues. Phenome-wide RVAS/GWAS summary statistics are available at https://t.co/T3hdFQfTH5 Paper:

HUGE congrats to @NiekMohamma (on right) for winning the Dutch Cardiovascular Network's prize for best 🇳🇱 publication of the year for his work in @JACCJournals #JACC on colchicine and longitudinal dynamics of clonal hematopoiesis 🩸🧬🔥 in LoDoCo2 ⭐️👏 https://t.co/9dTKXPXjPz

🚀 Open postdoc position! If you're a driven scientist with a strong interest in human genetics related to cardiovascular disease and want to advance genetic discoveries, therapeutic hypotheses, and precision medicine for CVD, I hope you apply! https://t.co/OmU66LmYdf

Exciting to see @Merck's enlicitide (oral PCSK9 inhibitor) continue to show very high LDL-C-lowering efficacy (~ -60%) now in multiple trials https://t.co/hFREwFEw2W @JAMA_current @AHAScience #AHA25 Enlicitide is an important pharmacologic success that has key innovations to

Most Lp(a) analyses have been in 1st events, but (1) Lp(a) trials CV outcomes trials are being done in pts with prior events or evidence of atherosclerosis, and (2) Lp(a) is being checked frequently in such individuals. Great work from @KelvinS_MD @CFAndersenMD @mchonig @aklfahed

Excited to share our work @ESC_Journals #EJPC led by @KelvinS_MD @CFAndersenMD w/ @aklfahed Lp(a) + post-cath outcomes in 5,118 🧑‍🤝‍🧑 undergoing cor angio 🫀 @MGHHeartHealth : Lp(a) >=175 nmol/L ➡️ ⬆️ subsequent MI, revasc, ISR, need for PCI after CABG https://t.co/hc0pdKOdky

Immensely grateful for months of collaboration with my wonderful co-first author @CFAndersenMD and for the unwavering mentorship of @aklfahed @mchonig. Also huge thanks to all co-authors, including @somijemmacho @RoukozAKaram @pnatarajanmd @patrick_ellinor and many others who

So, what does this mean for our current clinical care? 🔹 Lp(a) testing should be part of risk assessment for patients undergoing coronary angiography. 🔹 Elevated Lp(a) identifies a subgroup with substantial residual risk, even with contemporary lipid-lowering therapy. 🔹

Among patients who underwent bypass surgery after their index angiogram, those with very high Lp(a) were: ⏺️ >2x more likely to require PCI during follow-up (adjusted HR 2.20) ⏺️ Had numerically higher graft failure risk Suggesting a potential role of Lp(a) in graft failure and

Notably, Lp(a)-related risk was evident early (within 2.5 years; reflecting the approximate follow-up duration of major CVD outcome trials) and continued to diverge over nearly two decades of follow-up. This emphasizes that Lp(a) is not just a biomarker ➡️ it reflects a

But the story didn’t end at the angiogram. Very high Lp(a) was associated with higher risks of acute MI (HR 1.27), revascularization (HR 1.37), in-stent restenosis (HR 1.32), mortality (HR 1.22), and repeat angiogram (HR 1.27) after coronary angiography. Importantly, these

On angiography, Lp(a) showed a clear quantitative relationship with disease burden. Individuals with very high Lp(a) had higher odds of severe disease (adjusted OR ~1.5), more multivessel and left main involvement (>60% ⬆️ likelihood), and a ~14-point ⬆️ Gensini score compared

Our study cohort: • 5,118 adults with measured Lp(a) who underwent coronary angiography at @MGHHeartHealth (2000–2023) • Median follow-up: ~17 years • 19% had very high Lp(a) (>=175 nmol/L) ➡️ the threshold used in current Lp(a)-lowering trials • Lp(a) categories were highly

So, we asked: 1️⃣ Are higher Lp(a) levels associated with more severe/complex coronary atherosclerosis on angiography? 2️⃣ Do individuals with elevated Lp(a) have worse long-term outcomes after coronary angiography? 3️⃣ What about outcomes after CABG? (3/10)

Why Lp(a)? Lp(a) is a causal, genetically determined risk factor for CAD. It promotes inflammation, lipid deposition, calcification, and thrombosis. But, despite growing attention, we still know little about how elevated Lp(a) affects angiographic disease severity and long-term

When Bayesian statistics meets cardiology @tigerstatdoc @MGHHeartHealth #AHA25

Insightful session by the amazing @mchonig on pathways from pregnancy to cardiovascular pathology 🫀🤰🧬 We learned that adverse pregnancy outcomes were risk enhancers of future ASCVD risk, highlighting shared mechanisms and prevention opportunities! #AHA25

#GOFRESH RCT among Black adults with untreated SBP 120-150 mmHg, a 12-week home-delivered DASH-patterned grocery intervention (vs. stipend for self-shopping) 🥕achieved a mean SBP drop of –5.7 mmHg vs –2.3 mmHg (P=.009) 🥕 –2.4 mmHg diastolic, –545 mg/24h urine Na and –8.0

Exciting talk at #AHA25 on the GPM and EPI Mid-Career Research Award & Lecture, @pnatarajanmd convinced us how human genomics inform therapeutic discovery, causal inference, and risk prediction in CVD. It’s fascinating to see how these discoveries have changed clinical practices.