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Journal articles on the topic 'Cire inguinale'
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Kim, Kyoung Soo, Hari Madhuri Doss, Hee-Jin Kim, and Hyung-In Yang. "Taurine Stimulates Thermoregulatory Genes in Brown Fat Tissue and Muscle without an Influence on Inguinal White Fat Tissue in a High-Fat Diet-Induced Obese Mouse Model." Foods 9, no. 6 (May 26, 2020): 688. http://dx.doi.org/10.3390/foods9060688.
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This study was conducted to investigate if taurine supplementation stimulates the induction of thermogenic genes in fat tissues and muscles and decipher the mechanism by which taurine exerts its anti-obesity effect in a mildly obese ICR (CD-1®) mouse model. Three groups of ICR mice were fed a normal chow diet, a high-fat diet (HFD), or HFD supplemented with 2% taurine in drinking water for 28 weeks. The expression profiles of various genes were analyzed by real time PCR in interscapular brown adipose tissue (BAT), inguinal white adipose tissue (iWAT), and the quadriceps muscles of the experimental groups. Genes that are known to regulate thermogenesis like PGC-1α, UCP-1, Cox7a1, Cox8b, CIDE-A, and β1-, β2-, and β3-adrenergic receptors (β-ARs) were found to be differentially expressed in the three tissues. These genes were expressed at a very low level in iWAT as compared to BAT and muscle. Whereas, HFD increased the expression of these genes. Taurine supplementation stimulated the expression of UCP-1, Cox7a1, and Cox8b in BAT and only Cox7a1 in muscle, while there was a decrease in iWAT. In contrast, fat deposition-related genes, monoamine oxidases (MAO)-A, and -B, and lipin-1, were decreased by taurine supplementation only in iWAT and not in BAT or muscle. In conclusion, the potential anti-obesity effects of taurine may be partly due to upregulated thermogenesis in BAT, energy metabolism of muscle, and downregulated fat deposition in iWAT.
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Muto, Yuki, Akiomi Yoshihisa, Yukiko Sugawara, Satoshi Abe, Masayoshi Oikawa, ATSUSHI KOBAYASHI, Hiroyuki Kunii, et al. "Abstract 10514: Inguinal Fat Tissue Biopsy to Identify Transthyretin Amyloidosis in Patients Undergoing Transcatheter Aortic Valve Implantation." Circulation 144, Suppl_1 (November 16, 2021). http://dx.doi.org/10.1161/circ.144.suppl_1.10514.
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Background: Several studies have recently reported that transthyretin (ATTR) amyloidosis is present in patients with aortic stenosis (AS). This study aimed to 1) examine the utility of inguinal fat tissue biopsy in AS patients who underwent transcatheter aortic valve implantation (TAVI) to detect ATTR amyloidosis, 2) compare clinical characteristics between AS patients with ATTR (ATTR group) and those without ATTR (non-ATTR group). Methods and Results: We prospectively analyzed consecutive 56 patients who underwent transfemoral TAVI from December 2018 to December 2020 in our hospital. To screen ATTR in these patients, we performed inguinal fat tissue biopsy from cut down or puncture site during TAVI. Of 56 AS patients, 5 (8.9%) patients were diagnosed as ATTR by inguinal fat biopsy. Compared with non-ATTR group, ATTR group presented higher levels of B-type natriuretic peptide (BNP, 566.4 vs. 242.5 ng/ml, P=0.0045), higher levels of troponin I (0.053 vs. 0.024 ng/ml, P=0.003), lower left ventricular ejection fraction (LVEF, 49.3 vs. 60.3%, P=0.0035), larger left ventricular mass index (150.2 vs. 115.5 g/m 2 , P=0.019), larger aortic valve area (0.84 vs. 0.63 cm 2 , P=0.029) and lower peak velocity of aortic valve (3.8 vs. 4.4 m/s, P=0.041). In contrast, age, sex, STS score, clinical frailty scale, prevalence of diabetes, chronic kidney disease and AF, levels of albumin, and eGFR were comparable between the two groups. Electrocardiogram and other echocardiographic parameters including interventricular septal wall thickness, posterior wall thickness, stroke volume index and E/A ratio did not differ between the two groups. Although TAVI was successfully completed in all patients, the incidence of life-threatening bleeding and 30-day readmission was higher in ATTR group than in non-ATTR group (40.0 vs. 5.9%, P=0.011 and 20.0 vs. 0.0%, P=0.001). There was no difference in occurrence of myocardial infarction, stroke, acute kidney injury, major vascular complication, pacemaker implantation and 30-day mortality. Conclusions: In AS patients, especially in those with increased BNP and troponin I levels and low-flow low-gradient pattern, ATTR should be considered. In this population, inguinal fat tissue biopsy is a novel and safe approach to identify ATTR.
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Hu, Ruoci, Jooman Park, Shaolei Xiong, Pingwen Xu, and Yuwei Jiang. "Abstract 4145171: The CCL22/CCR4 Axis Promotes Beige Adipocyte Formation." Circulation 150, Suppl_1 (November 12, 2024). http://dx.doi.org/10.1161/circ.150.suppl_1.4145171.
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Introduction: Beige adipocytes hold therapeutic promise for obese and diabetic patients. Beige adipocytes can be generated from tissue-residing beige progenitors (APCs) in response to cold temperatures preferably around lymph nodes (LN), suggesting that there are unique LN-derived signals controlling beige adipocyte generation. Methods: CCR4 KO mice (spCas9 mice were injected with AAV8-CCR4-sgRNA into biolateral inguinal adipose tissue) were generated on a C57BL/6 background. Stromal vascular cells were isolated and differentiated into beige adipocytes for in vitro studies. Flow cytometer analysis were conducted for sorting and identifying immune cells. Results: Here, we show that local LN removal greatly impairs cold-induced beiging, and this impairment can be restored by injecting M2 macrophages or macrophage-derived chemokine C-C motif ligand 22 (CCL22) into iWAT. Mechanistically, cold exposure increases the level of CCL22, which binds to its receptor C-C chemokine motif receptor 4 (CCR4), and then promotes beiging. Furthermore, CCL22 levels are inversely correlated with body weight and fat mass, and elevated CCL22 levels prevent diet-induced obesity along with increased energy expenditure in mice and humans. Conclusion: The results suggest that beige adipogenesis around the inguinal LNs of white adipose tissues depends on the CCL22-CCR4 signaling. Our findings underline the potential of targeting the CCL22-CCR4 axis to counter obesity and its associated health complications.
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Sharma, Swapna, Abiah Pritchard, Michael Young, and Stanislav Henkin. "Abstract 13946: Subclinical Atherosclerosis and Peri-Operative Cardiac Events in Patients Undergoing Peripheral Bypass Surgery." Circulation 144, Suppl_1 (November 16, 2021). http://dx.doi.org/10.1161/circ.144.suppl_1.13946.
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Introduction: Coronary artery disease (CAD) is associated with a higher risk of peri-operative adverse events after vascular surgery. Subclinical CAD, defined as presence of coronary calcium, has not been established as a risk factor for adverse events after vascular surgery. Hypothesis: We sought to describe the epidemiology and peri-operative outcomes in patients with subclinical coronary atherosclerosis (SCA) undergoing supra- and infra-inguinal peripheral bypass. Methods: Using the Vascular Quality Initiative, we identified patients at a single institution undergoing supra- and infra-inguinal peripheral bypass surgery (2009-2020). Retrospective chart review was performed to identify chest computed tomography (CT) within one year prior to revascularization; imaging was reviewed for presence of coronary calcifications, a marker of SCA. Individuals were stratified by: no atherosclerosis, SCA, and CAD. Comorbidities and peri-operative outcomes were compared among groups with the chi-square or ANOVA, as appropriate. Results: Of 1018 patients undergoing peripheral bypass surgery, 199 (20%) had a CT available. SCA was noted in 96 patients (48%) while 72 (36%) had known CAD. Patients with SCA had similar comorbidities to patients with CAD (Table) but were less likely to be on a pre-operative beta-blocker or P2Y12 inhibitor. The incidence of postoperative myocardial infarction and congestive heart failure was similar in patients with SCA (13% and 9%, respectively) as those with CAD (10%, 6% respectively), compared to those without atherosclerosis (3% and 0, respectively). Conclusions: SCA is common in patients undergoing peripheral bypass surgery and is associated with a risk of peri-operative myocardial infarction or congestive heart failure similar to occult CAD. Aggressive secondary prevention measures should be considered in patients with polyvascular disease, including subclinical CAD.
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Quintero Bisono, Janina, Bistees George, and Kori Ormachea. "Abstract 15479: High Output Cardiac Failure Associated With Arteriovenous Fistula." Circulation 148, Suppl_1 (November 7, 2023). http://dx.doi.org/10.1161/circ.148.suppl_1.15479.
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Introduction: High output heart failure (HOHF) secondary to arteriovenous fistula (AVF) is known. However, having a high index of suspicion for the latter when encountering diuretic resistance in patients with a remote history of hemodialysis is key. Case A 68-year-old female with a history of kidney transplant in 2012 with no recent dialysis, hypertension, hyperlipidemia, pulmonary hypertension, heart failure with reduced ejection fraction, and atrial fibrillation presented with decompensated heart failure and acute kidney injury (AKI). Physical exam was remarkable for anasarca, and no apparent fistulas were noted. She was started on milrinone and furosemide drips. Clinical decision making Initial transthoracic echocardiogram (TTE) revealed an ejection fraction (EF) of 20%, which declined from 35%, along with new mitral and tricuspid regurgitation. Her hospitalization was complicated by altered mental status, worsening AKI requiring hemodialysis, atrial fibrillation with rapid ventricular response, and resistance to multiple diuretics and after-load reduction combinations. Diuretics and inotropic support were discontinued due to worsening clinical status. Given concerns for valvular disease, a transesophageal echocardiogram was obtained, confirming moderate to severe mitral and tricuspid valve regurgitation, bi-atrial enlargement, and reduced biventricular function. However, the patient was not clinically optimized for Mitra-clip. Further hemodynamics and volume status assessment with RHC revealed a mean PAP 44, PCWP 26, and CO 11 L/min. RHC results raised suspicion for HOHF. Interestingly, the patient was noted to have a right inguinal surgical scar with a palpable thrill, and an arteriovenous graft duplex revealed high volume flow. The patient underwent ligation of the right inguinal fistula. Repeat TTE two weeks post AVF ligation showed EF of 40% and improved functional mitral and tricuspid valve regurgitation. The patient ultimately was taken off hemodialysis and had clinically improved heart failure. GDMT was optimized, and outpatient evaluation for mitral valve intervention was scheduled. Conclusion Longstanding AVF can cause HOHF. Early index of suspicion is warranted for AVF ligation as it results in rapid EF recovery.
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Ravi, Srekar, George Bcharah, Christine Firth, Austin Saugstad, Mayowa Osundiji, Yuxiang Wang, Chadi Ayoub, and Fadi Shamoun. "Abstract 4146529: Impact of Connective Tissue Features on Vascular Outcomes in Fibromuscular Dysplasia." Circulation 150, Suppl_1 (November 12, 2024). http://dx.doi.org/10.1161/circ.150.suppl_1.4146529.
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Introduction/Background: Fibromuscular Dysplasia (FMD) is a non-atherosclerotic vascular disease that primarily affects medium-sized arteries and is characterized by abnormal cell development in the artery walls. Recent studies have suggested that various connective tissue features may be prevalent in patients with FMD, however the clinical significance of these findings on the disease course are uncertain. Research Questions/Hypothesis: We hypothesized that the presence of connective tissue features in patients with FMD might indicate a more severe disease course, potentially associated with increased severity of vascular complications. Goals/Aims: To evaluate the association between connective tissue features and the severity of vascular complications in FMD patients on outcomes including dissections and stroke. Methods/Approach: This cross-sectional study involved 2,454 patients diagnosed with FMD at a tertiary referral center. Patients were classified into two groups based on the presence (n=324) or absence (n=2130) of connective tissue features (pectus deformity of any kind, scoliosis, pneumothorax, inguinal hernia, uterine rupture, bowel perforation, Achilles tendon rupture). We evaluated the incidence of dissections and ischemic or hemorrhagic strokes using odds ratios and chi-squared tests. Results/Data: The cohort consisted of 2,454 participants with an average age of 64.8 years, of whom 89.1% were female and 92.4% identified as White. When comparing groups with and without connective tissue features, there were no significant differences in the prevalence of aneurysms at any site. Among the subgroup of FMD patients with connective tissue features (n=234), prevalent conditions included pectus (12.35%), scoliosis (47.22%), pneumothorax (16.67%), inguinal hernia (13.58%), uterine rupture (16.36%), bowel perforation (6.48%), and Achilles tendon rupture (1.85%). Vascular outcome analysis showed significant differences: the odds of experiencing a stroke were higher in patients with these features (odds ratio: 1.60; P-value: <0.01), whereas the odds of experiencing dissections were lower (odds ratio: 0.77; P-value: 0.03). Conclusion: The presence of connective tissue features in patients with FMD is associated with 60% higher odds of experiencing a stroke, equivalent to a 1.6-fold increase, compared to those without these features. This association may represent a novel finding in the literature, warranting further investigation.
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Ahiskalioglu, Elif O., Erkan C. Celik, Binali Firinci, Miraç S. Ozkal, Ibrahim H. Tor, Irem Ates, Ozgur Ozmen, and Ali Ahiskalioglu. "Eficacia del bloqueo del plano de la fascia transversal en la reparación de la herniotomía inguinal pediátrica: estudio controlado aleatorizado." Cirugía y Cirujanos, November 20, 2024. http://dx.doi.org/10.24875/ciru.24000008.
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Turan, Umit, and Ahmet Baris-Dirim. "Predicción de la proporción de aspartato aminotransferasa a alanina aminotransferasa (De Ritis) para detectar necrosis intestinal en pacientes con hernia inguinal incarcerada." Cirugía y Cirujanos 91, no. 4 (August 30, 2023). http://dx.doi.org/10.24875/ciru.22000273.
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Solís-De la Cruz, J. Ramón, Gustavo Leal-Mérida, and Enrique O. Guadarrama-Díaz. "Comparación de las características epidemiológicas, clínicas y quirúrgicas de pacientes con y sin recidiva de hernias inguinales operados en el Centro Médico Naval." Cirugía y Cirujanos 90, no. 6 (November 2, 2022). http://dx.doi.org/10.24875/ciru.21000500.
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Wilson, Robin, Lakshmi Arivazhagan, Henry Ruiz, Jay Pendse, Laura Frye, Kaamashri Mangar, Ravichandran Ramasamy, and Ann Marie SCHMIDT. "Abstract 17023: Adipose Tissue Specific Temporal Deletion of Ager Induces Weight Loss in Diet Induced Obese Mice and Improves Glucose Homeostasis." Circulation 142, Suppl_3 (November 17, 2020). http://dx.doi.org/10.1161/circ.142.suppl_3.17023.
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Introduction: The incidence of obesity and its comorbidities is increasing at an alarming rate in US and around the globe. Our previous studies showed that the receptor for advanced glycation end products (RAGE) and its ligands contribute to the pathogenesis of obesity and insulin resistance (IR), as global Ager (gene encoding RAGE) and adipocyte-specific Ager- deleted mice fed a high fat diet (HFD) showed protection from weight gain and IR. However, the role of Ager deletion in mice with established obesity, switched to low fat diet has not been tested. We hypothesize that temporal adipocyte-specific deletion of Ager in obese mice could enhance weight loss and improves glucose homeostasis. Methods: Mice with conditional adipocyte-specific Ager deletion were generated by breeding Ager flox/flox mice with AdipoQ ERT2 Cre recombinase mice resulting in Ager flox/flox / AdipoQ ERT2 Cre (+) and Cre (-) animals. Mice were fed HFD (60% kcal/fat) for 20 weeks starting at 8 weeks of age to establish obesity and were then treated with tamoxifen (TAM) (75 mg/kg per day x 3 alternative days) to induce deletion of Ager . After 4 weeks of TAM treatment, mice were switched to standard chow for 7 weeks and body weight was monitored regularly. Fasting glucose, insulin and glucose tolerance was measured. Results: After 7 weeks of switching to standard chow following TAM, Cre (+) lost significantly more body weight whereas Cre (-) mice showed no significant weight loss over 7 weeks. Furthermore, Cre (+) mice exhibited significantly higher food intake, lower fasting glucose, lower epididymal and inguinal white adipose tissue weights, and improved glucose and insulin tolerance compared to Cre (-) mice. Conclusions: Temporal adipocyte-specific deletion of Ager in mice with established obesity promotes weight loss and improves glucose homeostasis. RAGE may act as a novel therapeutic target in obesity.
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Takeshita, Kyosuke, Maimaiti Yisireyili, and Toyoaki Murohara. "Abstract 17008: Dipeptidyl peptidase-4 Inhibitor Ameliorates Stress-induced Glucose Metabolism Disorder and Prothrombotic State." Circulation 132, suppl_3 (November 10, 2015). http://dx.doi.org/10.1161/circ.132.suppl_3.17008.
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Introduction: Psychological stress evokes lipolytic release of free fatty acid (FFA) and low-grade inflammation in visceral adipose tissue, mediated by increased adipokine secretion, and contributes to glucose metabolism disorder and prothrombotic state via production of coagulation factors (plasminogen activation inhibitor-1 [PAI-1] and tissue factor [TF]) in white adipose tissue (WAT). Hypothesis: As accumulating evidence suggests anti-inflammatory potential of dipeptidyl peptidase-4 (DPP4) inhibitors, we investigated the effects of alogliptin on stress-induced adipose tissue inflammation, insulin resistance and prothrombotic state. Methods: Mice were subjected to 2-week intermittent restraint stress and orally treated with vehicle, 15 or 45 mg/kg/day alogliptin. Plasma lipids, expression of GLP-1, DPP4 activity, 8OHdG (an oxidant stress marker), monocyte/macrophage markers (CD11b, CD68, and F4/80), proinflammatory cytokines (monocyte chemoattractant protein-1, tumor necrosis factor-α, and interleukin-6), adiponectin, and coagulation factors (PAI-1 and TF) in blood and inguinal WAT was determined using immunohistochemistry, enzyme-linked immunosorbent assay, and RT-PCR, respectively. Glucose metabolism was assessed by glucose tolerance tests (GTTs) and insulin tolerance tests (ITT), and expression of insulin receptor substrate-1 (IRS-1) and glucose transporter 4 (GLUT4) in WAT. Results: The stress procedure increased FFA release, 8OHdG-positive cells and monocyte accumulation in WAT, proinflammatory cytokine, and reduced adiponectin and GLP-1, followed by DPP4 activation in plasma. The stress-induced adipose inflammation increased PAI-1 and TF, and worsened insulin sensitivity and decreased IRS-1 and GLUT4 in WAT. The alogliptin administration suppressed stress-induced FFA release, oxidant stress production, adipose inflammation, procoagulant state in a dose dependent manner, and restored glucose metabolism in GTT and ITT. Conclusions: The results indicate that alogliptin improves stress-induced prothrombotic state, and glucose metabolism disorder. Our results suggests that alogliptin exerts additive benefits for cardiovascular complication in diabetes patients with mental stress.
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Chen, Phetcharat, Christina Park, Eltayeb Karrar, Chaoyung Wang, and James Liao. "Abstract 19727: ROCK2 Mediates Browning of White Fat and Protects Against Obesity." Circulation 130, suppl_2 (November 25, 2014). http://dx.doi.org/10.1161/circ.130.suppl_2.19727.
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Background: The Rho-activated kinases (ROCK1 and ROCK2) are serine threonine kinases that are ubiquitously expressed with higher levels of ROCK2 compared to ROCK1 in adipocytes. Recent studies suggest that ROCK2 may be an important regulator of energy metabolism and obesity. However, its role in adipocyte development and function is unknown. Methods and Result: To determine the role of ROCK2 in adipocyte development and obesity, we generated adipocyte-specific deletion (ROCK2 adipoQ-/- ) and overexpression (CA-ROCK adipoQ+/+ ) of ROCK2 in mice. Compared to control mice, CA-ROCK adipoQ+/+ mice exhibited increased browning of inguinal white adipose tissue (iWAT). Indeed, immunohistochemical staining of iWAT in CA-ROCK adipoQ+/+ mice showed that UCP1 was upregulated. Furthermore, CA-ROCK adipoQ+/+ mice on high fat diet were resistant to weight gain and obesity for up to 18 weeks. This is in contrast to ROCK2 adipoQ-/- mice, which developed more weight gain or obesity than control mice. To determine the physiological effects of ROCK2 on browning of iWAT, control and ROCK2 adipoQ-/- mice were exposed to 4°C for 1 week. In control mice, cold exposure increased ROCK2 activity and lead to browning of iWAT. However, the iWAT in ROCK2 adipoQ-/- mice failed to undergo browning. Analysis of gene expression in iWAT demonstrated increased UCP1 and mitochondria proteins in control but not ROCK2 adipoQ-/- mice. Thermal imaging revealed that ROCK2 adipoQ-/- mice were unable to maintain basal body temperature after prolonged cold exposure. In contrast, the heat map of the CA-ROCK adipoQ+/+ mice showed an elevation of body temperature, particularly in areas of iWAT as compared to that of control littermates. Conclusions: ROCK2 mediates the “browning” of white adipocytes and prevents the development of obesity through increased thermogenesis. These findings suggest that the activation of ROCK2 in adipocytes may have therapeutic benefits in preventing diet-induced obesity.
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Rockson, Stanley G. "Abstract 11422: Aligned Nanofibrillar Collagen Scaffold Guide Therapeutic Lymphangiogenic Repair in Secondary Lymphedema." Circulation 132, suppl_3 (November 10, 2015). http://dx.doi.org/10.1161/circ.132.suppl_3.11422.
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Background: As a mechanical adjunct to therapeutic lymphatic repair in acquired lymphedema, we have investigated the applicability of guided lymphatic regeneration, through the introduction of a biological scaffold consisting of aligned collagen fibrils. These fibrils provide for cell attachment, alignment, and migration. Methods: We refined a large animal model using minipigs (n=16). We resected the inguinal and popliteal lymphatic system and irradiated the groin area to reproduce the conditions encountered in human cancer-related lymphedema. We assessed the status of lymphedema by detecting interstitial fluid accumulation through bioimpedance, the number of major lymphatic collectors by contrast-enhanced CT, and presence of lymphatic dermal backflow by contrast-enhanced MRI. Results: Three months after lymphatic resection and irradiation, animal subjects were randomized to: (1) scaffolds only, (2) scaffolds impregnated with VEGF-C, and (3) VEGF-C-scaffolds with additional transplantation of autologous lymph node fragments. The control group (4) did not receive any treatment. Seven animals out of 16 developed chronic lymphedema by the pre-defined bioimpedance threshold. The number of lymphatic collectors, as determined by CT, correlated with bioimpedance data. In group 1, there was slight improvement of bioimpedance ratios. In groups 2 and 4 (control), lymphedema persisted. In group 3 lymphedema was reversed in all subjects at post-Rx time-point 6 months. Macroscopic analysis of collectors in the implantation area after intradermal injection of blue dye showed newly developed lymphatic collectors aligned in the direction of the implanted collagen scaffolds. Conclusions: In this porcine acquired lymphedema model, implantation of aligned nanofibrillar collagen scaffolds facilitates the ingrowth of lymphatics across the treatment field. Moreover, simultaneous transplantation of autologous lymph node fragments improves lymphatic regeneration. The biocompatibility of these surgical approaches suggests their potential as an effective treatment option for the human disease.
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Khetarpal, Sumeet, Haobo LI, Claire Castro, Nicholas A. Houstis, James Rhee, Hans-Georg Sprenger, Melanie Mittenbuhler, et al. "Abstract 16612: Cardiomyocyte PGC-1α Prevents Cardiac Atrophy and Failure in Response to Endurance Exercise Training." Circulation 148, Suppl_1 (November 7, 2023). http://dx.doi.org/10.1161/circ.148.suppl_1.16612.
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Introduction: Aerobic exercise promotes physiologic hypertrophy of the heart in healthy individuals. In skeletal muscle and heart, a key orchestrator of the adaptation to exercise is the transcriptional regulator PGC-1α. PGC-1α may mediate cardiac adaptation to physiological stress through myriad mechanisms. The role of cardiac PGC-1α to the systemic training response is poorly understood. Methods: We generated PGC-1α cardiomyocyte-specific knockout (KO) mice to study its role in endurance exercise. We also silenced Ppargc1a expression in a cell model of physiologic cardiomyocyte hypertrophy. Results: Sedentary KO mice demonstrated normal cardiac function and minimal differences in acute exercise tolerance. However, KO mice demonstrated a lack of ability to augment exercise capacity after 6 weeks of wheel running (work achieved 32.9 J in WT [39% increase] vs 23.1 J in KOs [no change vs baseline], p<0.001, unpaired t-test). This was despite comparable voluntary wheel distance run during training (2.93-3.67 km/day for both over 5 weeks, p=0.58). Unexpectedly, after 6 weeks of training, KO mice developed a dilated cardiomyopathy and exercise-related dysfunction (contractile reserve [ΔFS stress-rest ] +6.0 in WT vs -6.4% in KO, p<0.05, unpaired t-test). They also demonstrated features of cardiac cachexia as measured by 27% and 19% reductions in inguinal adipose and gastrocnemius mass, respectively (P<0.05, unpaired t-test). RNA sequencing of the hearts from these mice demonstrated activation of pathological ( Nppa , Nppb , Myh7/Myh6 ), fibrotic and atrophic secreted factors ( Gdf15 , Fstl3 ). Silencing Ppargc1a in rat cardiomyocytes after IGF1 treatment failed to induce physiologic hypertrophy and activated fibrotic programs and conferred atrophy. Conclusions: Our studies posit cardiomyocyte PGC-1α as a key mediator of the adaptive response to exercise training and unveil its central role in protecting from exercise-related cardiac atrophy and fibrosis.
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Osawa, Takumi, Kazuko Tajiri, and Masaki Ieda. "Abstract 11622: A Case of Successful Malignant Lymphoma Treatment Following Transcatheter Aortic Valve Replacement." Circulation 146, Suppl_1 (November 8, 2022). http://dx.doi.org/10.1161/circ.146.suppl_1.11622.
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Doxorubicin, an anthracycline drug, is a key drug in the treatment for diffuse large B-cell lymphoma (DLBCL). It is contraindicated in patients with serious heart diseases due to the cardiotoxicity. Transcatheter aortic valve replacement (TAVR) has been an established treatment for patients with severe aortic stenosis (AS) at high or prohibitive risk for surgical aortic valve replacement (SAVR). A 67-year-old woman was referred to our department with severe AS. Two months ago, the patient presented with bilateral cervical and inguinal lymphadenopathy. A biopsy of the lymph nodes revealed the primary diffuse large B-cell lymphoma (DLBCL). The patient had been diagnosed with stage IVA non-Hodgkin lymphoma according to the Ann Arbor staging system. The echocardiogram demonstrated a left ventricular ejection fraction of 67% and severe bicuspid AS with a peak velocity of 4.1 m/sec, mean pressure gradient of 44.1 mmHg, and aortic valve area of 0.58 cm 2 . She was initially treated with chemotherapy without anthracycline due to the high risk of anthracycline cardiotoxicity. However, anthracyclines were thought to be essential for controlling DLBCL. She was referred to our department and evaluated from the heart-team, which considered the following characteristics: severe impairment of mobility and frailty with a Society of Thoracic Surgeons (STS) score of 5.99%. Due to the high surgical risk for SAVR, we decided to perform TAVR. The procedure was completed without complications during the perioperative period. Ten days after TAVR, the patient received the therapy of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone), which resulted in complete remission without cardiac symptoms. Before the advent of TAVR, it was difficult for patients with both severe AS and cancer to receive surgery and/or cardiotoxic treatment. In patients with cancer, AS may interfere with optimal antineoplastic therapy (ie, high-risk oncological surgery and/or cardiotoxic anticancer drugs). TAVR does not need cardiac arrest, extracorporeal circulation, and thoracotomy. TAVR could increase therapeutic options in cancer patients with severe AS who are at high surgical risk.
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Kuganathan, Ann, Marcos Leal, Vincent Lu, Bo Gao, Jeffrey Dickhout, and Joan C. Krepinsky. "Abstract 14157: Effects of Follistatin on the Regulation of Vascular Function by Perivascular Adipose Tissue in a Model of Essential Hypertension." Circulation 146, Suppl_1 (November 8, 2022). http://dx.doi.org/10.1161/circ.146.suppl_1.14157.
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Introduction: We previously showed that follistatin (FST), a potent activin inhibitor, lowers BP in the spontaneously hypertensive rat (SHR), a model of essential HTN. This was associated with improved vessel structure (reduced collagen) and function (reduced hypercontractility and improved endothelium-dependent relaxation). FST also reduced vascular oxidative stress (ROS). Perivascular adipose tissue (PVAT) is known to regulate vascular tone. FST induces browning and thus increased thermogenic activity of peripheral adipose tissue. Transition from white to brown adipose tissue is associated with decreased risk of CVD. Here, we assess FST effects on PVAT and its regulation of SHR vascular function. Methods: SHR were treated with FST from 12-20 weeks of age. Normotensive WKY rats served as controls. Mesenteric resistance arteries were isolated with or without intact PVAT. Vessel function was assessed using wire myography. In separate studies, white mesenteric and brown aortic PVAT, or peripheral fat depots, were isolated from WKY rats. These were introduced to WKY mesenteric vessels to study PVAT-isolated function. Results: Intact PVAT augmented constriction to KCl in SHR, but not WKY arteries, an effect prevented by FST. Improvement in endothelium-dependent vasodilation in FST-treated SHR was PVAT-dependent. SHR PVAT had increased adipocyte size and ROS (by DHE), both reversed by FST. Isolated PVAT from WKY incubated with pyocyanin (30’) to induce ROS augmented the KCl response, suggesting that FST inhibition of PVAT oxidative stress in HTN restores beneficial vascular effects. Incubation of WKY vessels with brown PVAT inhibited constriction to KCl more effectively than did white PVAT. Interestingly, peripheral white adipose (inguinal) did not have any anticontractile effect. Brown adipose (interscapular) effects were intermediate. Conclusions: Improvement in anticontractile effects of PVAT by FST in resistance vessels is associated with reduced PVAT oxidative stress. Brown PVAT is more effective than white PVAT in inhibiting vessel contraction, and unlike white PVAT, peripheral white adipose does not have anticontractile effects. Future work will assess effects of FST on PVAT browning, and whether browning itself can improve BP.
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Ozcan, Mualla, Aynaz Lotfinaghsh, Carla Valenzuela Ripoll, Ahmed Diab, Zhen Guo, Wentong Jia, Anahita Ataran, et al. "Abstract 4145510: SLIT2 is a novel driver of doxorubicin cardiotoxicity through adipose-cardiac crosstalk." Circulation 150, Suppl_1 (November 12, 2024). http://dx.doi.org/10.1161/circ.150.suppl_1.4145510.
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Background: Dox cardiomyopathy remains a clinically significant problem. Alternate-day fasting has been shown to exacerbate Dox cardiomyopathy and cachexia. We sought to identify common disease mechanisms by comparing proteomics in mice vs. humans with Dox cardiomyopathy. Methods: Chow-fed C57BL/6 male mice (n=50) were treated with Dox (5 mg/kg intraperitoneal x 3 doses). One day after the last dose, mice were randomized to ad-lib feeding or ADF (24 hours of fasting followed by 24 hours of refeeding) for two weeks, followed by echocardiography, and body composition analysis. For aptamer-based human proteomics, we utilized banked blood from patients with Dox cardiomyopathy (n=47) and other cardiomyopathy (n=2167) from the Penn Heart Failure Study. For 2 group comparisons in mice and humans, we used Student’s t-test and false-discovery rate adjusted for covariates, respectively. For 3-group analyses, one-way ANOVA with Sidak’s correction for multiple comparisons was utilized. Results: Alternate-day fasting (ADF) decreased left ventricular (LV) ejection fraction (p=0.047, 95% CI of difference: -5.61 to -0.04) and LV mass (p=0.012, 95% CI of difference: -10.10 to -1.39) and increased end-diastolic volume/body weight (p=0.035, 9.5% relative reduction) in mice treated with Dox. Dox+ADF also increased adiposity (p=0.005, 95% CI of difference: 6.266 to 29.52) and brown adipose mass (p<0.001, 95% CI: 1.231 to 3.206). Aptamer-based plasma proteomics showed that Dox+ADF upregulated SLIT2, which was the most significant and pronounced protein identifying human Dox cardiomyopathy (vs other cardiomyopathies, p<0.0001, 95% CI of difference: 20307 to 25447). Furthermore, Dox+ADF stimulated SLIT2 and its target UCP1 in inguinal adipose tissue, while UCP1 knockout attenuates Dox cardiotoxicity. Further studies showed that SLIT2 was both necessary and sufficient for Dox cardiotoxicity. Conclusion: These findings suggest that adipose-cardiac crosstalk mediated by SLIT2 is a novel mechanism of Dox cardiomyopathy.
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Conklin, Daniel J., Abhinav Agarwal, Srinivas Sithu, Iris Zeller, Petra Haberzettl, Timothy E. O'Toole, Aruni Bhatnagar, and Sanjay Srivastava. "Abstract 15705: Chronic Inhaled Acrolein Depresses Circulating Endothelial Progenitor Cells and Promotes Atherosclerosis." Circulation 132, suppl_3 (November 10, 2015). http://dx.doi.org/10.1161/circ.132.suppl_3.15705.
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We have previously shown that acute exposure to air pollutants including particulate matter or the volatile acrolein leads to reversible suppression of circulating angiogenic cells in humans and mice. Exposure to tobacco smoke, which contains both particles and aldehydes such as acrolein, also suppresses EPC number and function in association with an increase in cardiovascular disease risk. To assess whether acrolein alone worsened vascular pathogenesis, we exposed mice to acrolein (1 ppm * 6h/day) in a murine model of hind limb ischemia. Mice were exposed to acrolein for 4 days prior to permanent right femoral artery and vein ligation and bisection (distal to inguinal ligament) with continued exposure to filtered air (control) or acrolein for another 2 weeks. Blood flow recovery in the ischemic hind limb was measured via Laser Doppler Perfusion Imaging (LDPI) and normalized as a percentage of flow in the non-ischemic limb. Although acute exposure to acrolein reduced the number of circulating angiogenic cells it had only a modest effect blood flow recovery after 7 days (% Recovery: air, 86.2±21.4; acrolein, 68.3±21.6, n=8,8, p=0.12). Hence to determine whether chronic acrolein exposure worsened chronic vascular injury, we exposed C57BL/6J mice to 1 ppm acrolein for 12 weeks. This long-term exposure significantly depressed (by 51%) circulating levels of Flk-1+/Sca-1+ cells (as % of lymphocytic counts: air 0.15±0.09; acrolein 0.07±0.05; p<0.02). To tested if cell changes were associated with changes in atherogenesis, apoE-null mice on normal chow or high-fat diet were exposed to chronic acrolein (1 ppm; 12 week). Acrolein accelerated aortic atherosclerosis by 1.6-fold (p<0.001) but it did not affect coincident dyslipidemia (total cholesterol: air, 1224±189; acrolein, 1076±195 mg/dL) compared with air-exposed, HFD-fed mice. These results suggest that that chronic low level acrolein exposure suppresses circulating angiogenic cells and accelerates atherogenesis; hence the atherogenic effect of exposure to traffic pollutants, indoor smoke or cigarette smoke may be in part attributable to acrolein. These findings could inform exposure risk assessments and the development of new policies for regulating pollutant exposure and tobacco product use.
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Krayem, Hussein, Rafae Shaikh, MACK HENDRIX, Jose Huizar, Alex Tan, Kenneth Ellenbogen, and KAROLY KASZALA. "Abstract 4141627: Not The Corona You Wish For After a Successful Atrial Fibrillation Ablation!" Circulation 150, Suppl_1 (November 12, 2024). http://dx.doi.org/10.1161/circ.150.suppl_1.4141627.
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Background: Corona mortis artery or ring of death, is a common variant (25-30%) vascular anastomosis between the obturator artery and inferior epigastric or external iliac artery. However, injury to this vessel during EP procedures has not been described. We present a case of an inguinal hematoma secondary to arteriovenous fistula(AVF) and pseudoaneurysm of the corona mortis artery due to puncture injury during atrial fibrillation(AF) ablation. Case: A 71-year-old male underwent pulmonary vein isolation for persistent AF. The right femoral vein was accessed using ultrasound guidance and 3 sheaths were placed after which intravenous heparin was administered. At the end of the case, protamine was given for heparin and a figure of 8 suture was placed after sheath removal. Six hours post procedure, a soft 2.5 cm right groin hematoma was noted, that was treated conservatively with manual pressure and pressure dressing overnight. The patient was discharged home next day but returned one week later with continued groin pain and swelling. Examination revealed a moderate groin hematoma, ecchymosis and a loud right femoral bruit. Duplex ultrasound demonstrated a fistula between the right external iliac artery and vein with potential pseudoaneurysm at the fistula site. CT angiogram of the abdomen and pelvis showed a pseudoaneurysm of a distal branch of the external iliac artery arising from the inferior epigastric artery and an AVF (Fig 1a). Selective arteriogram was performed via left groin access, which confirmed the above findings as a result of injury to the corona mortis (Fig 1b). Coil embolectomy of the right inferior epigastric artery and the obturator branch up to the respective origins was performed with resolution of the fistula (Fig 1c). The patient was discharged home and oral anticoagulation therapy was restarted 24 hours later. He recovered well with no further sequelae. Discussion: The corona mortis artery is a common vascular variant which may be a source of bleeding complications during groin injury or during vascular groin access. Familiarity with this variant allows its consideration in the differential diagnosis of post procedural groin hematoma which ensures rapid diagnosis and appropriate management.
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Hussain, Tasmeen, Emily Chu, Hoda Sayegh, Stefan Torelli, Emily Keamy-Minor, and Ronald Witteles. "Abstract 4145488: Unique Presentation of Acute Massive Pulmonary Embolism as Complete Heart Block." Circulation 150, Suppl_1 (November 12, 2024). http://dx.doi.org/10.1161/circ.150.suppl_1.4145488.
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Description of Case: An 81-year-old man with left bundle branch block (LBBB) and recent inguinal hernia repair presented with 2 weeks of dizziness and shortness of breath. On presentation, sinus tachycardia was noted with a heart rate of 100 bpm. While in the emergency department, he acutely developed complete heart block, initially with a right bundle branch block (RBBB) pattern escape at a rate of 53 bpm. Gradually, the escape slowed to 20 bpm with vomiting and hypotension so an emergent transvenous pacer was placed; he was paced at VVI 80 bpm with improvement in status. Transthoracic echocardiogram exhibited McConnell’s sign (Figure 1) with severe RV enlargement, severely reduced RV systolic function and normal LV systolic function. Arterial line tracings fluctuated with inspiration/expiration consistent with a pulsus paradoxus pattern (Figure 2) without evidence of pericardial effusion. CT angiography of the chest showed emboli in the bilateral main pulmonary arteries. For treatment, the patient was started on a therapeutic heparin drip, transitioned later to therapeutic apixaban. He did continue to require intermittent pacing and so underwent dual-chamber permanent pacemaker placement on hospital day 3. Discussion: EKG findings in patients with pulmonary emboli can be variable. In one prospective cohort study of 246 consecutive patients suspected to have pulmonary embolism (PE), only tachycardia (p = 0.008) and incomplete right bundle branch block (p = 0.002) amongst 28 total EKG findings evaluated were associated with confirmed pulmonary embolism by imaging. Interestingly, new RBBB may be a sensitive and specific marker for massive PE. In 50 patients with proven pulmonary embolism, all 16 cases with new RBBB on EKG were noted to have massive trunk obstruction (no patients with peripheral PEs had new RBBB). In the several case reports we found of patients with prior/observed LBBB and PEs who subsequently developed CHB, PEs were notably large, described as either bilateral or saddle-shaped, suggesting an association of acquired RBBB with significant PE burden. The cause of new complete heart block should always be acutely sought; in patients with baseline LBBB, a new RBBB leading to complete heart block can occur with massive/submassive PE. Rapid identification and treatment are needed to limit mortality in this often hemodynamically unstable entity.
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QIAN, YANYU, Ruifan Wu, Jooman Park, and Yuwei Jiang. "Abstract 4143504: Genetically Prolonged Beige Fat In Male Mice Confers Long-lasting Metabolic Health." Circulation 150, Suppl_1 (November 12, 2024). http://dx.doi.org/10.1161/circ.150.suppl_1.4143504.
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Background: Beige adipocytes, express UCP1 and have thermogenic capability, making them a promising target for obesity treatments. However, beige adipocytes quickly transition into white adipocytes upon removal of stimuli. Our research identifies the cyclin-dependent kinase inhibitor 2A ( Cdkn2a ) as a crucial regulator of this transition. Ablation of Cdkn2a prolongs beige adipocyte lifespan, enhances energy expenditure, and improves glucose tolerance by inhibiting BECN1-mediated autophagy. These findings offer a potential therapeutic strategy to maintain beige adipocytes and combat obesity and related diseases. Methods: We used Ucp1-Cre ERT2 mice with a Rosa26R RFP indelible labeling reporter and Cdkn2a floxed mice. All mice were maintained on a mixed C57BL6/J-129SV background. To induce Cre recombination, mice received tamoxifen for 2 days. For in vitro induction, cells were treated with 2 µM 4-hydroxy-tamoxifen. In our in vitro study, we isolated stromal vascular fraction (SVF) cells from the inguinal white adipose tissue (IGW) or brown adipose tissue (BAT) of 6-week-old male mice for seeding. For the in vivo study, we used cold exposure, metabolic cages, and glucose tolerance tests. Results: Cdkn2a plays a pivotal role in the beige-to-white transition. Its absence prolongs the lifespan of beige adipocytes and in male mice, confers long-term metabolic protection against diet-induced obesity, along with enhanced energy expenditure and improved glucose tolerance. Mechanistically, Cdkn2a promotes the expression and activity of beclin 1 (BECN1) by directly binding to its mRNA and its negative regulator BCL2 like 1 (BCL2L1), activating autophagy and accelerating the beige-to-white transition. Reactivating autophagy by pharmacological or genetic methods abolishes beige adipocyte maintenance induced by Cdkn2a ablation. Furthermore, hyperactive BECN1 alone accelerates the beige-to-white transition in mice and human. Hence, blocking Cdkn2a -mediated BECN1 activity holds therapeutic potential in treating obesity and related metabolic diseases. Conclusion: Cdkn2a depletion extends beige adipocyte lifespan, providing long-term metabolic benefits against diet-induced obesity in male mice. Cdkn2a boosts BECN1 expression, triggering the beige-to-white transition by directly interacting with BECN1 mRNA and its negative regulator BCL2L1, activating autophagy. Targeting Cdkn2a -mediated BECN1 activity holds promise as a therapeutic approach for treating obesity.
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Goel, Mehak, Tariq Hamid, Mohamed Ameen Ismahil, Guihua Zhou, Kenneth Brittian, Heather Clair, Shangzhi Guo, and Sumanth D. Prabhu. "Abstract 17284: Selective Macrophage Ablation Attenuates Diet-Induced Obesity and Insulin Resistance and Reverses Diabetic Cardiomyopathy." Circulation 124, suppl_21 (November 22, 2011). http://dx.doi.org/10.1161/circ.124.suppl_21.a17284.
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Although activated macrophages infiltrate the heart and adipose tissue in type 2 diabetes (T2D), the role of these cells in the genesis of cardiomyopathic phenotype is unknown. We tested the hypothesis that activated resident macrophages are fundamental mediators of diet-induced diabetic cardiomyopathy. Transgenic mice expressing an AP20187-inducible Fas-dependent suicide gene in macrophages and dendritic cells (MAFIA mice) were fed a high fat diet (HFD, 45% kcal fat) or control diet (CD, 10% kcal fat) for 28 weeks to induce T2D, and subsequently given either vehicle or AP20187 (0.5mg/kg IP every 10 d) for one month to induce macrophage apoptosis and depletion. HFD-fed mice exhibited a significant (p < 0.05) 43% increase in body weight when compared to CD fed mice (43±5 vs 35±1 g) and developed hyperglycemia (199±44 vs 121±10 mg/dL), hyperinsulinemia (1.27±0.6 vs 0.43±0.14 µg/L) and decreased insulin sensitivity indicating T2D. Echocardiography revealed concentric LV hypertrophy in HFD-fed mice with increased wall thickness (anterior wall 1.2±0.1 vs 0.9±0.1 mm), decreased LV end-diastolic diameter (LVEDD 3.9±0.2 vs 4.2±0.4 mm), and unchanged LV ejection fraction. AP20187 treatment significantly reduced the caloric intake (0.3±0.08 vs 0.4±0.05 kcal/g/day) and body weight of HFD-fed mice (36±2 vs 47±5 g), attenuated hyperglycemia (108±8 vs 195±14 mg/dL) and hyperinsulinemia (0.6±0.2 vs 1.9±0.5 µg/L), and improved insulin sensitivity when compared to vehicle treated HFD-fed mice. Importantly, the improvements in metabolic parameters were accompanied by reversal of LV remodeling with decreased wall thickness (anterior wall 0.8±0.1 vs 1.3±0.1 mm) and increased LVEDD (4.6±0.5 vs 3.9±0.2 mm). White adipose tissue weights in AP20187-treated HFD-fed mice were also significantly decreased when compared to vehicle treated HFD-fed mice [epididymal (0.6±0.2 vs 1.4±0.3 g); inguinal (0.6±0.2 vs 1.1±0.3 g); retroperitoneal (0.8±0.5 vs 1.4±0.4 g). We conclude that resident activated macrophages play central and causative roles in the development of diet-induced T2D and diabetic cardiomyopathy. Targeting systemic macrophage activation may represent a therapeutic approach to reverse pathological cardiac remodeling associated with T2D and obesity.
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Ho, David, Lin Yan, Xin Zhao, Shumin Gao, Kousaku Iwatsubo, Yoshihiro Ishikawa, Dorothy E. Vatner, and Stephen F. Vatner. "Abstract 18237: Inhibition of Adenylyl Cyclase Type 5 Protects Against Obesity and Diabetes." Circulation 124, suppl_21 (November 22, 2011). http://dx.doi.org/10.1161/circ.124.suppl_21.a18237.
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Adenylyl cyclase type 5 (AC5) is one of 9 major isoforms of AC. Mice with AC5 gene disruption (knockout, KO) live one third longer than wild type (WT) littermates. Like caloric restriction, the most commonly studied model of longevity, the AC5KO mice weigh 12% less than WT (p<0.05) and have less body fat, i.e., adiposity index, calculated by dividing the sum weights of the three major fat pads (inguinal, retroperitoneal, gonadal) by the body weight, was 50% lower than WT (p<0.05). The first goal of this study was to determine if AC5KO mice are protected, not only against obesity, but also diabetes. Insulin sensitivity, assessed by blood glucose measurement following insulin injection, was improved by 24% compared to WT. Glucose tolerance was also improved, p<0.05. A major limitation of studies in genetically altered mouse models, is that it is difficult to translate these results to the bedside, since it is not possible to knock out a gene in patients. Accordingly, we identified a pharmacological inhibitor of AC5, vidaribine, and examined the extent to which it ameliorated obesity and diabetes. First we demonstrated its selectivity for AC5; the inhibitor reduced inotropic responses to isoproterenol more than WT only in AC5 cardiac transgenic mice, but not in AC6 cardiac transgenic mice. To induce obesity, WT mice were fed a high fat diet feeding for 2 months, increasing body weight by 51% over mice fed a standard diet. WT mice with high fat diet and AC5 inhibitor on board for an additional 3 months, compared with WT mice on vehicle and high fat diet, increased body weight and adiposity index less, p<0.05, by 20% and 28%, respectively, while insulin resistance was reduced by 76% and glucose tolerance was improved by 66% (p<0.05). In AC5KO mice on the high fat diet insulin resistance was also reduced and glucose tolerance was also improved compared to WT on the high fat diet, similar to that observed with the AC5 inhibitor on the high fat diet. Thus, inhibition of AC5 provides a novel target for obesity and diabetes; the effective pharmacological inhibitor of AC5 enhances its clinical relevance.
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Song, Bong Gun, Shin Yi Jang, Yong Hwan Park, Sang Yeub Lee, Yeon Hyeon Choe, Young Soo Do, Dong Ik Kim, Young Wook Kim, Jidong Sung, and Duk-Kyung Kim. "Abstract 3428: Presence Of Renal Simple Cysts Is Associated With Increased Risk For Abdominal Aortic Aneurysm." Circulation 116, suppl_16 (October 16, 2007). http://dx.doi.org/10.1161/circ.116.suppl_16.ii_774-c.
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Background : An increased prevalence of abdominal aortic aneurysm (AAA) has been demonstrated in patients with emphysema or inguinal hernia. Therefore, it has been suggested that the cause of AAA is a degenerative disorder of the connective tissue that can not always be explained by means of atherosclerosis. We hypothesized that the presence of renal simple cysts, another possible manifestation of connective tissue weakness, is associated with the increased risk for AAA. We compared incidence of renal simple cyst between the group of patients with AAA and healthy control group. Methods : We reviewed 279 patients with AAA and 1397 healthy control group who underwent abdominal computed tomography as a routine health screening from 1994 to 2006 in Samsung Medical Center. AAA was defined as an aortic diameter equal to or greater than 40 mm. Comparisons between groups were made for established risk factors for AAA. Results : AAA group has significantly more diabetes, smoking, history of anti-hyperlipidemic medication, hypertension, metabolic syndrome, higher systolic blood pressure than control group (all p values <0.0001). In the univariate analysis, prevalence of renal cysts ( p< 0.0001), bilateral renal involvement of cysts ( p< 0.0001), number of renal cysts ( p< 0.0001), and sum of sizes of renal cysts ( p< 0.0001) were significantly higher in AAA group as compared with control group. In the multivariate analysis, a person with renal cyst was more likely (OR: 4.379, CI: 3.402–5.636) to have AAA after adjustment for age, gender, smoking, hypertension, diabetes, HDL and LDL cholesterol. This relationship was similar for bilateral renal involvement of cysts, number of renal cysts, and sum of sizes of renal cysts. Neither a diameter nor an expansion rate of AAA was associated with the size of renal cysts. Conclusion: Patients with AAA have increased burden of renal simple cysts compared to healthy control group. The structural weakness predisposing for renal simple cysts may be associated with the initiation of AAA formation. Prospective study is needed to determine whether the presence of renal cysts can be considered as a risk factor of AAA.