Medical Therapy of Thoracic Aortic Aneurysms

Danyi, Peter; Elefteriades, John A.; Jovin, Ion S.

doi:10.1161/circulationaha.110.006486

Cited by 75 publications

(58 citation statements)

References 84 publications

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“…Abdominal aortic aneurysm is a common and lethal vascular disorder as about 6 -9% of the elderly population have an AAA (6,40). Although small aneurysms can be managed conservatively with imaging and controlling of risk factors such as smoking and hypertension, patients continue to experience significant morbidity and mortality from ruptured aneurysms (4,6).…”

Section: Discussionmentioning

confidence: 99%

“…AAA has remained an unresolved clinical problem because ␤-blockers (1, 2), statin therapy (3), and angiotensin-converting enzyme inhibitors have been ineffective in controlling AAA expansion, and AAA remains as the 13th leading cause of death in Western countries (4 -6). Surgical and mechanical interventions are the only effective treatments to prevent AAA rupture, but that is only recommended in severe AAA cases where the inherent risk of surgery is less than the risk of aortic rupture (1,6). The 10-year survival for patients deemed unfit for surgical repair is less than 25% (7).…”

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confidence: 99%

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Loss of Timp3 Gene Leads to Abdominal Aortic Aneurysm Formation in Response to Angiotensin II

Basu

Fan

Kandalam

et al. 2012

Journal of Biological Chemistry

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Background: TIMP3 is ECM-bound and is implicated in patients with abdominal aortic aneurysm (AAA). Results: Timp3 deficiency triggers AAA in response to Ang II. Additional deletion of Mmp2 exacerbated AAA with enhanced inflammation. Broad spectrum MMP inhibition prevented AAA in both genotypes. Conclusion: TIMP3 is protective against Ang II-mediated adverse remodeling. Significance: Replenishment of TIMP3 in aneurysmal aorta could prevent aneurysm expansion and rupture.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Loss of Timp3 Gene Leads to Abdominal Aortic Aneurysm Formation in Response to Angiotensin II

Basu

Fan

Kandalam

et al. 2012

Journal of Biological Chemistry

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“…Progressively expanding ATAA mandates surgical intervention to prevent vessel dissection or free rupture 1. ATAA is age related and is frequently encountered in patients with hypertension, hypercholesterolemia, or diabetes mellitus 2. It is also diagnosed in young patients with genetic disorders associated with intrinsic structural abnormalities such as Marfan syndrome and bicuspid aortic valve and as a result of aortic inflammatory diseases 3, 4, 5.…”

mentioning

confidence: 99%

Local Application of Leptin Antagonist Attenuates Angiotensin II–Induced Ascending Aortic Aneurysm and Cardiac Remodeling

Ben‐Zvi

Savion

Kolodgie

et al. 2016

JAHA

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BackgroundAscending thoracic aortic aneurysm (ATAA) is driven by angiotensin II (AngII) and contributes to the development of left ventricular (LV) remodeling through aortoventricular coupling. We previously showed that locally available leptin augments AngII‐induced abdominal aortic aneurysms in apolipoprotein E–deficient mice. We hypothesized that locally synthesized leptin mediates AngII‐induced ATAA.Methods and ResultsFollowing demonstration of leptin synthesis in samples of human ATAA associated with different etiologies, we modeled in situ leptin expression in apolipoprotein E–deficient mice by applying exogenous leptin on the surface of the ascending aorta. This treatment resulted in local aortic stiffening and dilation, LV hypertrophy, and thickening of aortic/mitral valve leaflets. Similar results were obtained in an AngII‐infusion ATAA mouse model. To test the dependence of AngII‐induced aortic and LV remodeling on leptin activity, a leptin antagonist was applied to the ascending aorta in AngII‐infused mice. Locally applied single low‐dose leptin antagonist moderated AngII‐induced ascending aortic dilation and protected mice from ATAA rupture. Furthermore, LV hypertrophy was attenuated and thickening of aortic valve leaflets was moderated. Last, analysis of human aortic valve stenosis leaflets revealed de novo leptin synthesis, whereas exogenous leptin stimulated proliferation and promoted mineralization of human valve interstitial cells in culture.ConclusionsAngII‐induced ATAA is mediated by locally synthesized leptin. Aortoventricular hemodynamic coupling drives LV hypertrophy and promotes early aortic valve lesions, possibly mediated by valvular in situ leptin synthesis. Clinical implementation of local leptin antagonist therapy may attenuate AngII‐induced ATAA and moderate related LV hypertrophy and pre–aortic valve stenosis lesions.Clinical Trial Registration URL: https://www.clinicaltrials.gov/. Unique identifier: NCT00449306.

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“…Препаратами первой линии при формировании аневризмы являются бета-бло-каторы [10]. Они уменьшают механическое повреж-дение стенки аорты, благодаря снижению артери-ального давления и силы сердечных сокращений.…”

Section: рис 2 сколиоз при синдроме марфанаunclassified

Involvement of cardiovascular system in hereditary disorders of connective tissue

Zhuravlyova¹,

Romanenko²

2016

Shidnoevr. z. vnutr. simejnoi med.

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Medical Therapy of Thoracic Aortic Aneurysms

Cited by 75 publications

References 84 publications

Loss of Timp3 Gene Leads to Abdominal Aortic Aneurysm Formation in Response to Angiotensin II

Loss of Timp3 Gene Leads to Abdominal Aortic Aneurysm Formation in Response to Angiotensin II

Local Application of Leptin Antagonist Attenuates Angiotensin II–Induced Ascending Aortic Aneurysm and Cardiac Remodeling

Involvement of cardiovascular system in hereditary disorders of connective tissue

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