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Jean Wassenaar, MD PhD @jeanwassenaar.bsky.social · Sep 5

In summary, both obese HFpEF 🐁 and 🚶‍♂️show evidence of adipocyte browning and ⬆️ fibrosis from ⬇️ collagen turnover. I’ll be staying tuned to see how these changes are altered by treatment with GLP1 agonists! 🧵: 8/8

Jean Wassenaar, MD PhD @jeanwassenaar.bsky.social · Sep 5

Obese HFpEF 🐁 also had ⬇️expression of endothelial markers; but this was not translated in human subjects 🚶‍♂️. 🧵: 7/8

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Jean Wassenaar, MD PhD @jeanwassenaar.bsky.social · Sep 5

Obese HFpEF 🐁 also show more fibrosis in their adipose tissue, but paradoxically there is ⬇️ expression of collagen, suggesting ⬇️ collagen turnover as the cause. Similarly, collagen mRNA levels were ⬇️ in HFpEF patients 🚶‍♂️ compared to obese controls. 🧵: 6/8

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Jean Wassenaar, MD PhD @jeanwassenaar.bsky.social · Sep 5

The adipose tissue of these 🐁 also shows evidence of browning – with smaller, more loculated adipocytes, and increased expression of Ucp1, Cidea, and Eva. Evidence of browning is also seen in fat pad biopsies of patients in acute HFpEF. 🧵: 5/8

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Jean Wassenaar, MD PhD @jeanwassenaar.bsky.social · Sep 5

Interestingly, the obese-HFpEF mice have ⬇️ body weight, driven by ⬇️ body fat% compared to obese non-HFpEF mice. But they have evidence of ⬆️ free water, suggestive of a congested state. 🧵: 4:8

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Jean Wassenaar, MD PhD @jeanwassenaar.bsky.social · Sep 5

Histologically, the hearts demonstrate cardiomyocyte hypertrophy and fibrosis. 🧵: 3/8

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Jean Wassenaar, MD PhD @jeanwassenaar.bsky.social · Sep 5

The 🐁 model combines obesity (induced through 20 weeks of high fat diet) with 4 weeks of the SAUNA model (1% salt water, uni-nephrectomy, and aldosterone infusion), leading to pulmonary congestion, cardiac hypertrophy, and diastolic dysfunction. 🧵: 2/8

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Jean Wassenaar, MD PhD @jeanwassenaar.bsky.social · Sep 5

Obesity is a major risk factor for HFpEF. Join me in learning about a new HFpEF model that Valero-Munoz et al developed to study how adipose tissue changes in a 🐁 model and human patients🚶‍♂️in this month's #JACCBTS @jaccjournals.bsky.social . 🧵: 1/8

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Reposted by Jean Wassenaar, MD PhD

Kathryn Lindley @drklindley.bsky.social · Jul 24

Jonesborough nurse’s heart attack-pregnancy journey leads to Vanderbilt Women’s Heart Center news.vumc.org/2025/07/21/p...

#teamwork #cardioobstetrics
@scadalliance.bsky.social

Jonesborough nurse's heart attack-pregnancy journey leads to Vanderbilt Women's Heart Center

Patient's medical journey highlights the need for women to be vigilant about heart health when pregnant or thinking about becoming pregnant.

news.vumc.org

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Jean Wassenaar, MD PhD @jeanwassenaar.bsky.social · Jul 15

In summary, targeting FXI using a gene silencing approach allows for long term inhibition of FXI activity, which leads to ⬇️ venous and arterial thrombosis without affecting bleeding time. I can’t wait to see the translation of these results in upcoming clinical trials! 🧵: 8/8

Jean Wassenaar, MD PhD @jeanwassenaar.bsky.social · Jul 15

However, compared to enoxaparin, RBD4059 did not significant increase bleeding time in a tail bleeding model 🩸. 🧵: 7/8

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Jean Wassenaar, MD PhD @jeanwassenaar.bsky.social · Jul 15

Similar results were seen in the carotid artery thrombosis model. 🧵: 6/8

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Jean Wassenaar, MD PhD @jeanwassenaar.bsky.social · Jul 15

Using a jugular venous thrombosis model (A) the authors show that both the 3mg/kg and 9mg/kg dose of RBD4059 is as effective in restoring blood flow as Enoxaparin, the positive control. 🧵: 5/8

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Jean Wassenaar, MD PhD @jeanwassenaar.bsky.social · Jul 15

Using a gene silencing approach, a single dose of RBD4059 led to ⬇️ in FXI activity and ⬆️ APTT for weeks, potentially allowing for intermittent dosing in patients 🎉! (🧵: 4/8)

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Jean Wassenaar, MD PhD @jeanwassenaar.bsky.social · Jul 15

The authors created a small interfering RNA (siRNA) that would silence FXI mRNA and conjugated it to a ligand (GalNAc) that would target it towards hepatocytes, where the majority of coagulation proteins are made. 🧵: 3/8

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Jean Wassenaar, MD PhD @jeanwassenaar.bsky.social · Jul 15

Why target FXI?, because recent studies show that the intrinsic pathway, which FXI is a part of, is more responsible for intravascular thrombosis. Thus, targeting FXI would have less effect on hemostasis (📷: EMJ Cardiol. 2024;12[Suppl 2]:2-13). 🧵: 2/8

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Jean Wassenaar, MD PhD @jeanwassenaar.bsky.social · Jul 15

Balancing the risk for clotting and bleeding is constant challenge for cardiologists, so I was very excited to see in this month’s #JACCBTS work on targeting different parts of the coagulation cascade (Factor 11, FXI) to reduce bleeding risk while lowering risk for thrombosis. 🧵: 1/8

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Reposted by Jean Wassenaar, MD PhD

JACC Journals @jaccjournals.bsky.social · Apr 30

This #FINEHEART pooled analysis, published in #JACC, demonstrated that finerenone significantly reduced the risk of new-onset atrial fibrillation/atrial flutter across the CKM spectrum. www.jacc.org/doi/10.1016/... #AFib

Finerenone Reduces New-Onset Atrial Fibrillation Across the Spectrum of Cardio-Kidney-Metabolic Syndrome: The FINE-HEART Pooled Analysis

www.jacc.org

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Reposted by Jean Wassenaar, MD PhD

Jeff Hsu, MD, PhD @jeffhsumd.bsky.social · Apr 30

🚨Last day to secure Advanced Registration rates for ACC Care of the Athletic Heart!

Virtual seats still available for the Hybrid meeting

To learn the latest in #SportsCardio from the experts who authored the recently updated guidelines, register today

acc.org/Education-and-…

Flyer advertising the ACC Care of the Athletic Heart meeting, taking place from June 12-14 in Washington DC and available virtually

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Jean Wassenaar, MD PhD @jeanwassenaar.bsky.social · May 1

Follow @michaelraddatz.bsky.social @jeffhsumd.bsky.social and @vascularimmuno.bsky.social and I for more updates on great science from #JACCBTS (🧵: 10/10)

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Jean Wassenaar, MD PhD @jeanwassenaar.bsky.social · May 1

To summarize, the authors found that congestive hepatopathy is histologically and pathophysiologically distinct from other causes of cirrhosis and that a mouse model of pIVCL may recapitulate some of its key features. (🧵: 9/10)

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Jean Wassenaar, MD PhD @jeanwassenaar.bsky.social · May 1

CK7+ cells in HF patients co-stain with hepatocyte lineage marker HFN4A and LCN2, suggesting they derive from hepatocytes, which was not found in other causes of cirrhosis such as PBC, PSC, MASH, HBV, or alcohol, suggesting a distinct pathophysiological difference in congestive hepatopathy (🧵: 9/10)

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Jean Wassenaar, MD PhD @jeanwassenaar.bsky.social · May 1

Similarly, IF of IVC ligated mice (pIVCL) show expansion of CK7 producing cells bordering CD68+ macrophage aggregates. (🧵: 8/10)

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Jean Wassenaar, MD PhD @jeanwassenaar.bsky.social · May 1

🚶‍♂️➡️ 🐁: The authors then show that the mouse model of partial IVC ligation recapitulated histological features of human congestive hepatopathy (🧵: 7/10)

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Jean Wassenaar, MD PhD @jeanwassenaar.bsky.social · May 1

Immunofluorescence demonstrated that CK7 is expressed in the liver parenchyma next to CD68+ macrophages and expansion of recruited monocyte derived macrophages (MARCO-) in heart failure patients. (🧵: 6/10)

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