The renin-angiotensin-aldosterone system as a potential target for therapy in patients with calcific aortic stenosis: a literature review

Kostyunin, A. E.; Овчаренко, Е. А.; Barbarash, O. L.

doi:10.18087/cardio.n328

Cited by 3 publications

(1 citation statement)

References 118 publications

(206 reference statements)

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“…The inflammatory infiltrate consists of macrophages, monocytes, mast cells, and T cells that play an important role in remodeling the leaflets [45][46][47]. Interestingly, ACE (angiotensin-converting enzyme) and chymase are overexpressed in calcific aortic valves [48]. Mast cells secrete chymase, while ACE is carried by LDL [49].…”

Section: Pathogenesis Of Aortic Stenosis: Lipids Inflammation and Min...mentioning

confidence: 99%

Lp(a) in the Pathogenesis of Aortic Stenosis and Approach to Therapy with Antisense Oligonucleotides or Short Interfering RNA

Di Costanzo,

Indolfi,

Franzone

et al. 2023

IJMS

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To date, no medical therapy can slow the progression of aortic stenosis. Fibrocalcific stenosis is the most frequent form in the general population and affects about 6% of the elderly population. Over the years, diagnosis has evolved thanks to echocardiography and computed tomography assessments. The application of artificial intelligence to electrocardiography could further implement early diagnosis. Patients with severe aortic stenosis, especially symptomatic patients, have valve repair as their only therapeutic option by surgical or percutaneous technique (TAVI). The discovery that the pathogenetic mechanism of aortic stenosis is similar to the atherosclerosis process has made it possible to evaluate the hypothesis of medical therapy for aortic stenosis. Several drugs have been tested to reduce low-density lipoprotein (LDL) and lipoprotein(a) (Lp(a)) levels, inflammation, and calcification. The Proprotein Convertase Subtilisin/Kexin type 9 inhibitors (PCSK9-i) could decrease the progression of aortic stenosis and the requirement for valve implantation. Great interest is related to circulating Lp(a) levels as causally linked to degenerative aortic stenosis. New therapies with ASO (antisense oligonucleotides) and siRNA (small interfering RNA) are currently being tested. Olpasiran and pelacarsen reduce circulating Lp(a) levels by 85–90%. Phase 3 studies are underway to evaluate the effect of these drugs on cardiovascular events (cardiovascular death, non-fatal myocardial injury, and non-fatal stroke) in patients with elevated Lp(a) and CVD (cardiovascular diseases). For instance, if a reduction in Lp(a) levels is associated with aortic stenosis prevention or progression, further prospective clinical trials are warranted to confirm this observation in this high-risk population.

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Section: Pathogenesis Of Aortic Stenosis: Lipids Inflammation and Min...mentioning

confidence: 99%

Lp(a) in the Pathogenesis of Aortic Stenosis and Approach to Therapy with Antisense Oligonucleotides or Short Interfering RNA

Di Costanzo,

Indolfi,

Franzone

et al. 2023

IJMS

View full text Add to dashboard Cite

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Role of Lipoprotein (A) in aortic valve stenosis: Novel disease mechanisms and emerging pharmacotherapeutic approaches

Khan,

Zahir,

Dominguez

et al. 2024

IJC Heart & Vasculature

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Structural valve degeneration: are there common mechanisms with atherosclerosis and calcific aortic stenosis?

Kostyunin

2022

RJTAO

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Current research shows that some of the pathogenetic processes behind structural destruction of bioprosthetic valves are largely similar to those involved in the development of atherosclerotic vascular lesions and native valve calcification. These processes include lipid and leukocyte infiltration, typical for both prosthetic and native tissues. They are accompanied by formation of foam cells, excessive production of matrix-degrading enzymes and increased oxidative stress. This fact suggests that some approaches to conservative treatment of atherosclerosis may be useful for prolonging the lifespan of bioprosthetic valves.

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The renin-angiotensin-aldosterone system as a potential target for therapy in patients with calcific aortic stenosis: a literature review

Cited by 3 publications

References 118 publications

Lp(a) in the Pathogenesis of Aortic Stenosis and Approach to Therapy with Antisense Oligonucleotides or Short Interfering RNA

Lp(a) in the Pathogenesis of Aortic Stenosis and Approach to Therapy with Antisense Oligonucleotides or Short Interfering RNA

Role of Lipoprotein (A) in aortic valve stenosis: Novel disease mechanisms and emerging pharmacotherapeutic approaches

Structural valve degeneration: are there common mechanisms with atherosclerosis and calcific aortic stenosis?

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