scholarly journals Comprehensive Cardiac Rehabilitation as a Therapeutic Strategy for Abdominal Aortic Aneurysm

2019 ◽  
Vol 1 (11) ◽  
pp. 474-480
Author(s):  
Atsuko Nakayama ◽  
Hiroyuki Morita ◽  
Issei Komuro
Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Atsuko Nakayama ◽  
Masatoshi Nagayama ◽  
Hiroyuki Morita ◽  
Issei Komuro

Introduction: The useful biomarkers of cardiac rehabilitation after post cardiovascular surgery are still unknown. This is the first report describing the markers of the effect of cardiac rehabilitation on prognosis after abdominal aortic aneurysm (AAA) surgery. Methods: We conducted an observed cohort study on 1330 patients receiving surgical repair of AAA in the multicenter in Tokyo from January 2003 to December 2014. The patients who had cardiac rehabilitation more than once a week for more than 3 months after surgery were classified into rehabilitation group. The patients in rehabilitation group underwent cardiopulmonary exercise testing (CPX) before and 3 months after surgery. Total 274 inspection items including blood culture, computerized tomography, carotid duplex, ankle-brachial index test, cardiac echography, respiratory function test and CPX were cyclopaedically analyzed. The results of blood culture in rehabilitation group were compared to those in non-rehabilitaion group before surgery, 14 days after and 30days after surgery. Results: The average age of patients was 73±8 years and the average follow-up period was 2.5±2.2 years. The 355 patients had cardiac rehabilitation after AAA repair, and the other 975 patients did not. Basal characteristics including age, gender, hypertension, dyslipidemia, diabetes, smoking and drugs were statistically similar in both groups. The predictors of the risk of major adverse cardiac events (MACE) after surgery were co-existence of coronary artery disease, non-intake of beta-blockers, non-intake of ARBs and nonparticipation in cardiac rehabilitation. The ROC curve analysis of the markers demonstrated no remarkable marker for the risk of MACE after surgery. But the level of CRP in rehabilitation group was lower 14 days and 30 days after surgery compared to which in non-rehabilitation group (4.5 ± 4.3 mg/dl vs. 5.9 ± 6.5 mg/dl, p<0.001 and 4.2 ± 4.5 mg/dl vs. 6.5 ± 6.0 mg/dl, p<0.001), although the level of CRP was similar in both groups before surgery. Conclusions: Cardiac rehabilitation in patients after AAA surgery improved the risk of MACE, and especially CRP may be useful as a convenient marker of effective rehabilitation for secondary prevention of arteriosclerosis.


2019 ◽  
Vol 34 (12) ◽  
pp. 2040-2040
Author(s):  
Atsuko Nakayama ◽  
Eisuke Amiya ◽  
Hiroyuki Morita ◽  
Kanako Hyodo ◽  
Naoko Takayama ◽  
...  

2019 ◽  
Vol 34 (12) ◽  
pp. 2031-2039 ◽  
Author(s):  
Atsuko Nakayama ◽  
Eisuke Amiya ◽  
Hiroyuki Morita ◽  
Kanako Hyodo ◽  
Naoko Takayama ◽  
...  

Author(s):  
Atsuko Nakayama ◽  
Hiroyuki Morita ◽  
Masatoshi Nagayama ◽  
Katsuyuki Hoshina ◽  
Yukari Uemura ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Koichi Yoshimura ◽  
Hiroki Aoki

Abdominal aortic aneurysm (AAA) is a common disease causing segmental expansion and rupture of the aorta with a high mortality rate. The lack of nonsurgical treatment represents a large and unmet need in terms of pharmacotherapy. Advances in AAA research revealed that activation of inflammatory signaling pathways through proinflammatory mediators shifts the balance of extracellular matrix (ECM) metabolism toward tissue degradation. This idea is supported by experimental evidence in animal models that pharmacologic intervention at each pathological step can prevent AAA development. Previously, we identified c-Jun N-terminal kinase (JNK), a pro-inflammatory signaling molecule, as a therapeutic target for AAA. Abnormal activation of JNK in AAA tissue regulates multiple pathological processes in a coordinated manner. Pharmacologic inhibition of JNK tips the ECM balance back towards repair rather than degradation. Interventions targeting signaling molecules such as JNK in order to manipulate multiple pathological processes may be an ideal therapeutic strategy for AAA. Furthermore, the development of biomarkers as well as appropriate drug delivery systems is essential to produce clinically practical pharmacotherapy for AAA.


2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Chanwoo Kim ◽  
Sandeep Kumar ◽  
Dong Ju Son ◽  
In-Hwan Jang ◽  
Hanjoong Jo

Abdominal aortic aneurysm (AAA) is characterized by weakening of the vessel wall, followed by progressive expansion of the diseased aortic segment. MicroRNAs (miRNAs) have emerged as key regulator of gene expression in the cardiovascular diseases and may play a key role in therapeutically targeting AAA development. Although,vascular wall degradation by matrix metalloproteases (MMPs) is the key mechanism in AAA development, their targeting through miRNAs have never been studied. We identified microRNA-712 (miR-712) as a novel Angiotensin II(AngII)-sensitive miRNA which is upregulated in the abdominal aortic endothelium of AngII-infused mice. Mechanistically, we identified that miR-712 directly regulates two key endogenous inhibitors of MMP: tissue inhibitor of metalloproteinase 3 (TIMP3) and reversion inducing cysteine-rich protein with kazal motifs (RECK). Furthermore, inhibition of miR-712 by subcutaneous injection of anti-miR-712 significantly decreased MMP activity in the AngII-infused abdominal aorta wall, prevented the dilatation of aortae and significantly reduced AAA incidence from 80% (8/10) to 20% (2/10), compared to its mismatched control in ApoE -/- mice. Interestingly, based on the seeding sequence, we identified miR-205 as the human homolog of miR-712. miR-205 was also upregulated by AngII treatment and like miR-712 regulated MMPs activity via TIMP3 and RECK. Moreover, inhibition of miR-205 dramatically inhibits AngII-induced AAA development. We also found that miR-205 was significantly upregulated in the aortic sections of AAA patients in comparison to the healthy controls. Our findings demonstrate that AngII-sensitive miRNAs, miR-712 and miR-205, regulate MMP activity through TIMP3 and RECK and play important role in the pathogenesis of AAA. These results suggest that targeting these miRNAs using their inhibitors may hold promise as a therapeutic strategy to prevent the development of AAA.


VASA ◽  
2005 ◽  
Vol 34 (4) ◽  
pp. 217-223 ◽  
Author(s):  
Diehm ◽  
Schmidli ◽  
Dai-Do ◽  
Baumgartner

Abdominal aortic aneurysm (AAA) is a potentially fatal condition with risk of rupture increasing as maximum AAA diameter increases. It is agreed upon that open surgical or endovascular treatment is indicated if maximum AAA diameter exceeds 5 to 5.5cm. Continuing aneurysmal degeneration of aortoiliac arteries accounts for significant morbidity, especially in patients undergoing endovascular AAA repair. Purpose of this review is to give an overview of the current evidence of medical treatment of AAA and describe prospects of potential pharmacological approaches towards prevention of aneurysmal degeneration of small AAAs and to highlight possible adjunctive medical treatment approaches after open surgical or endovascular AAA therapy.


VASA ◽  
2020 ◽  
pp. 1-9
Author(s):  
Milos Sladojevic ◽  
Petar Zlatanovic ◽  
Zeljka Stanojevic ◽  
Igor Koncar ◽  
Sasenka Vidicevic ◽  
...  

Summary: Background: Main objective of this study was to evaluate the influence of statins and/or acetylsalicylic acid on biochemical characteristics of abdominal aortic aneurysm (AAA) wall and intraluminal thrombus (ILT). Patients and methods: Fifty patients with asymptomatic infrarenal AAA were analyzed using magnetic resonance imaging on T1w sequence. Relative ILT signal intensity (SI) was determined as a ratio between ILT and psoas muscle SI. Samples containing the full ILT thickness and aneurysm wall were harvested from the anterior surface at the level of the maximal diameter. The concentration of enzymes such as matrix metalloproteinase (MMP) 9, MMP2 and neutrophil elastase (NE/ELA) were analyzed in ILT and AAA wall; while collagen type III, elastin and proteoglycan 4 were analyzed in harvested AAA wall. Oxidative stress in the AAA wall was assessed by catalase and malondialdehyde activity in tissue samples. Results: Relative ILT signal intensity (1.09 ± 0.41 vs 0.89 ± 0.21, p = 0.013) were higher in non-statin than in statin group. Patients who were taking aspirin had lower relative ILT area (0.89 ± 0.19 vs 1.13. ± 0.44, p = 0.016), and lower relative ILT signal intensity (0.85 [0.73–1.07] vs 1.01 [0.84–1.19], p = 0.021) compared to non-aspirin group. There were higher concentrations of elastin in AAA wall among patients taking both of aspirin and statins (1.21 [0.77–3.02] vs 0.78 (0.49–1.05) ng/ml, p = 0.044) than in patients who did not take both of these drugs. Conclusions: Relative ILT SI was lower in patients taking statin and aspirin. Combination of antiplatelet therapy and statins was associated with higher elastin concentrations in AAA wall.


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