31 results on '"Delafontaine, Patrice"'
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2. The effects of a growth hormone-releasing hormone antagonist and a gastrin-releasing peptide antagonist on intimal hyperplasia of the carotid artery after balloon injury in a diabetic rat model.
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Moscona, John C., Peters, Matthew N., Schally, Andrew V., Srivastav, Sudesh, Delafontaine, Patrice, and Irimpen, Anand
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Introduction Arterial restenosis after angioplasty/stenting has hindered coronary artery disease treatment, especially in diabetics. We theorized that gastrin-releasing peptide (GRP) antagonists and growth hormone-releasing hormone (GHRH) antagonists might decrease neointimal hyperplasia and restenosis in diabetic rats after common carotid arterial balloon injury. Methods Two separate experiments were conducted to test the effects of a GRP antagonist (RC-3095) and a GHRH antagonist (MZ-4-71) on vascular smooth muscle (VSM) growth. In a preliminary in vitro experiment non-injured human aortic vascular smooth muscle (VSM) proliferation was compared between growth media and control. In a second in vivo experiment, intimal and medial area, intima/media ratio (IM) and percent stenosis were compared between injured carotid arteries in twelve Zucker type II obese rats treated with subcutaneously injected RC-3095, MZ-4-71, or control media. Results In the in vitro experiment, decreased VSM cell growth was observed in GRP antagonist (p < 0.05) and GHRH antagonist groups (p < 0.05) compared to the control group. In the in vivo experiment, the GRP antagonist group had a decreased IM ratio (1.63 ± 0.41, p < 0.05) and an increased area of stenosis (98.78% ± 1.48 p = NS) compared to control (2.38 ± 1.09) while the GHRH antagonist group had decreased IM ratio (1.33 ± 0.58 SD, p < 0.05) and percent area of stenosis (78.84% ± 24.97, p < 0.05) compared to control (2.38 ± 1.09). Conclusions The significant decrease in both IM ratio and percent area of stenosis in the GHRH antagonist group supports the hypothesis that this peptide may reduce neointimal hyperplasia and restenosis. [ABSTRACT FROM AUTHOR]
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- 2017
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3. Drug-eluting stents versus bare-metal stents in saphenous vein grafts: a double-blind, randomised trial
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Brilakis, Emmanouil S, Edson, Robert, Bhatt, Deepak L, Goldman, Steven, Holmes, David R, Rao, Sunil V, Shunk, Kendrick, Rangan, Bavana V, Mavromatis, Kreton, Ramanathan, Kodangudi, Bavry, Anthony A, Garcia, Santiago, Latif, Faisal, Armstrong, Ehrin, Jneid, Hani, Conner, Todd A, Wagner, Todd, Karacsonyi, Judit, Uyeda, Lauren, Ventura, Beverly, Alsleben, Aaron, Lu, Ying, Shih, Mei-Chiung, Banerjee, Subhash, Ahmed, Bina, Ratliff, D Michelle, Ricciardi, Mark, Sheldon, Mark, Icenogle, Milton, Snider, Richard, Ardati, Amer, Nallamothu, Brahmajee, Duvernoy, Claire, Menees, Daniel S, Gurm, Hitinder, Thomas, Michael P, Grossman, Paul, Owen, Kristine, Topaz, On, Kumar, Gautam, Mavromatis, Kreton, Block, Peter, Zidar, David A, Bezerra, Hiram, Goldberg, Jonathan, Ortiz, Jose, Jozic, Joseph, Osman, Mohammed, Rosenthal, Noah, Parikh, Sahil A, Lassar, Tom A, Chan, Albert, Kumar, Arun, Aggarwal, Kul, Cyrus, Tillmann, Brilakis, Emmanouil S, Grodin, Jerrold, Banerjee, Subhash, Hattler, Brack, Armstrong, Ehrin, Casserly, Ivan, Messenger, John, Kim, Michael, Rogers, R Kevin, Waldo, Stephen, Tsai, Thomas, Morris, Kenneth, Krucoff, Mitchell, Rao, Sunil, Povsic, Thomas J, Jones, William S, Bavry, Anthony, Choi, Calvin, Park, Ki, Liu, Jayson, Kar, Biswajit, Paniagua, David, Jneid, Hani, Breall, Jeffrey, Bolad, Islam, Mukerji, Rita, Subbarao, Roopa, Abdel-Latif, Ahmed, Booth, David C, Ziada, Khaled M, Rajan, Lawrence, Hakeem, Abdul, Uretsky, Barry F, Agrawal, Mayank, Sachdeva, Rajesh, Ahmed, Zubair, McGee, Jesse, Ramanathan, Kodangudi, Shah, Rahman, Sharma, Alok, McFalls, Edward, Siddiqui, Rizwan, Garcia, Santiago, Adabag, Selcuk, Bertog, Stefan, Irimpen, Anand, Baldwin, Drew, Abi Rafeh, Nidal, Mogabgab, Owen, Delafontaine, Patrice, Lorin, Jeffrey, Sedlis, Steven, Schechter, Eliot, Latif, Faisal, Abu-Fadel, Mazen, Rousan, Talla, Thadani, Udho, Malik, Fady, Zimmet, Jeffrey, Shunk, Kendrick, Chou, Tony, Beatty, Alexis, Lehmann, Kenneth, Stadius, Michael, Klein, Andrew, Rowe, Caroline, Taniuchi, Megumi, Klein, Andrew J, Forsberg, Michael, Kapoor, Divya, Juneman, Elizabeth, Truong, Huu Tam, Lotun, Kapildeo, Tsuda, Ryan, Thai, Sergio, Goldman, Steven, Thai, Hoang, Lu, David, Papademetriou, Vasilios, Faxon, David, Bhatt, Deepak L, Croce, Kevin, Elmariah, Sammy, and Kinlay, Scott
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Few studies have examined the efficacy of drug-eluting stents (DES) for reducing aortocoronary saphenous vein bypass graft (SVG) failure compared with bare-metal stents (BMS) in patients undergoing stenting of de-novo SVG lesions. We assessed the risks and benefits of the use of DES versus BMS in de-novo SVG lesions.
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- 2018
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4. Abstract 11537: IGF-1 Reduces Atherosclerosis in Rapacz Pigs
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sukhanov, sergiy, Higashi, Yusuke, Danchuk, Svitlana, Alfortish, Mitzi, Goodchild, Traci, Scarborough, Amy, Sharp, Thomas E, GARCIA, DANIEL C, Jenkins, James S, Schumacher, Jeffrey, Ivey, Jan, Tharp, Darla, Bowles, Douglas K, Lefer, David J, and Delafontaine, Patrice
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Introduction:Cardiovascular disease, including atherosclerosis is the leading cause of mortality in the Western world. We have reported that insulin-like growth factor I (IGF-1) reduced atherosclerosis in the murine model, however it is unknown whether IGF-1 exerts protective effect on human-like atherosclerosis.Hypothesis:Rapacz pigs with familial hypercholesterolemia (FH pigs) fed with high-cholesterol diet develop human-like advanced plaques in coronary arteries. We hypothesize that IGF-1 suppresses atherosclerosis in FH pigs.Methods:Human recombinant IGF-1 (50 ug/kg) or saline (control) was injected daily into high-fat diet fed FH swine (n=9/group) for 6 months. Atherosclerotic burden was quantified by intravascular ultrasound (IVUS) at basal level (T0), after 3 months on diet (T3) and at sacrificing (T6).Results:IGF-1-injected pigs had 2.6-fold increase in total plasma IGF-1 (ELISA, p<0.001 vs. control pigs). Pigs in IGF-1 and control groups had a gradual increase in vessel volume in the right coronary artery (RCA), and left anterior descending artery (LAD) with time as quantified by IVUS. However, IGF-1-injected pigs had a larger increase in vessel volume after 3 and 6 months compared to controls suggesting vascular hypertrophy. The atherosclerotic burden was increased in RCA, and LAD in both groups after 3 and 6 months of injections compared to the pre-injection time point. We found a significant reduction in atherosclerotic burden in RCA and LAD in IGF-1 group compared to control at 6 months’ time-point (RCA: IGF-1, 203±13%, vs. control, 244±8; LAD: IGF-1, 200±6%, vs. control, 228±11%). The lumen volume of coronaries was decreased in both groups, however, coronaries in IGF-1-injected pigs had on average 24±3% larger lumen volume compared to control pigs at 6 months’ time-point.Conclusions:We found that IGF-1 increased total volume of pig coronaries suggesting hypertrophy and these data are consistent with growth-stimulating effects of IGF-1. We found reduction in atherosclerotic burden and increase in lumen volume in coronaries in the IGF-1 group after 6 months of injections consistent with an anti-atherosclerotic effect of IGF-1. Our data support the feasibility of using IGF-1 for as an anti-atherogenic therapy.
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- 2022
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5. Abstract 13040: Insulin-Like Growth Factor-1 Upregulates Larp6 via Translational and Post-Translational Mechanisms in Vascular Smooth Muscle Cells, Leading to Elevated Collagen Production
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Danchuk, Svitlana W, Delafontaine, Patrice, and Higashi, Yusuke
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Introduction:Collagen content in atherosclerotic plaque is a hallmark of plaque stability. We have shown that insulin-like growth factor-1 (IGF1) increased collagen content in atherosclerotic plaques of Apoe-/-mice. We have identified LARP6 (La Ribonucleoprotein Domain Family, Member 6), a type I collagen mRNA-binding protein, as a mediator of IGF1-dependent type I collagen upregulation and increased mature fibril formation by smooth muscle cells (SMC), however specific mechanism has not been elucidated yet.Methods and Results:Micro-RNAs, including miR-1976 have been shown to bind to LARP6 mRNA. We found that SMC treatment with IGF1 significantly downregulated miR-1976 by 41±5% after 3h (P<0.05), consistent with the IGF1-induced LARP6 upregulation. In fact, miR-1976 mimic (20 nM) decreased LARP6 by 67% (P<0.05) and reduced type I procollagen protein levels by 85% (P<0.05). MiR-1976 mimic inhibits IGF1-induced LARP6 upregulation showing miR-1976 involvement in IGF1 effect on LARP6. It has been reported that LARP6-mediated promotion of procollagen synthesis may be regulated by phosphorylation of LARP6, therefore we investigated whether IGF1 induces LARP6 phosphorylation in cultured human aortic SMCs. For this experiment, SMCs were serum-starved and treated for 0-48h with 10 ng/mL IGF1. LARP6 protein was detected by immunoblots as a single 67kDa band in untreated SMC. However, after 6h of IGF1 treatment there was additional phosphorylated LARP6 band detected at 70 kDa. The levels of 70kDa LARP6 time-dependently increased up to 18h of treatment, with a concomitant increase of type I procollagen and collagen expression levels.Conclusions:In summary, our data suggests that (i) IGF1 downregulates miR-1976, thereby increasing LARP6 expression levels and (ii) IGF1 induces phosphorylation of LARP6, thereby promoting LARP6 activity. Our study revealed novel mechanisms underlying IGF1-induced type I collagen upregulation in vascular SMC and potentially in atherosclerotic plaques.
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- 2022
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6. Insulin-Like Growth Factor-1 Receptor Deficiency in Macrophages Accelerates Atherosclerosis and Induces an Unstable Plaque Phenotype in Apolipoprotein E–Deficient Mice
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Higashi, Yusuke, Sukhanov, Sergiy, Shai, Shaw-Yung, Danchuk, Svitlana, Tang, Richard, Snarski, Patricia, Li, Zhaohui, Lobelle-Rich, Patricia, Wang, Meifang, Wang, Derek, Yu, Hong, Korthuis, Ronald, and Delafontaine, Patrice
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Supplemental Digital Content is available in the text.
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- 2016
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7. Angiotensin II upregulates protein phosphatase 2Cα and inhibits AMP-activated protein kinase signaling and energy balance leading to skeletal muscle wasting.
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Tabony, A. Michael, Yoshida, Tadashi, Galvez, Sarah, Higashi, Yusuke, Sukhanov, Sergiy, Chandrasekar, Bysani, Mitch, William E., and Delafontaine, Patrice
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Congestive heart failure and chronic kidney disease are characterized by chronically elevated angiotensin II (Ang II) and muscle wasting. Ang II causes skeletal muscle wasting by reducing appetite and by enhancing catabolism. The serine/threonine kinase AMP-activated protein kinase (AMPK) functions mainly as a sensor of cellular energy status. It is energy sparing and favors ATP generation. We hypothesized that Ang II induces muscle wasting in part by inhibiting AMPK signaling and altering cellular energy balance. Our results show that Ang II infusion in mice reduced gastrocnemius muscle weight by 26% and depleted ATP by 74%. In addition, Ang II upregulated protein phosphatase 2Cα by 2.6-fold and reduced AMPK phosphorylation and signaling in muscle. Importantly, the pharmacological AMPK activator 5-aminoimidazole-4-carboxamide ribonucleoside restored AMPK activity to levels of pair-fed controls and reversed Ang II-mediated ATP depletion and muscle wasting. Moreover, 5-aminoimidazole-4-carboxamide ribonucleoside activated Akt and inhibited Ang II-induced increases in E3 ubiquitin ligase expression. These novel results demonstrate critical roles for energy depletion and AMPK inhibition in Ang II-induced skeletal muscle wasting and suggest a therapeutic potential for AMPK activators in diseases characterized by muscle wasting. [ABSTRACT FROM AUTHOR]
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- 2011
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8. The effect of nebivolol versus metoprolol succinate extended release on asymmetric dimethylarginine in hypertension.
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Kandavar, Ramprasad, Higashi, Yusuke, Chen, Wei, Blackstock, Christopher, Vaughn, Charlotte, Sukhanov, Sergiy, Sander, Gary E., Roffidal, Louise E., Delafontaine, Patrice, and Giles, Thomas D.
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HYPERTENSION ,METOPROLOL ,ADRENERGIC beta blockers ,BIOAVAILABILITY ,NITRIC oxide ,ARGININE ,SOMATOMEDIN ,ENZYME-linked immunosorbent assay ,MONOCLONAL antibodies - Abstract
Abstract: This study sought to determine if metoprolol succinate ER (MET), and nebivolol (NEB), a β1-AR with increased bioavailability of nitric oxide (NO), would have differing effects on plasma asymmetric dimethylarginine concentration in hypertensives. It was hypothesized that NEB, a β1-AR antagonist and β3-AR agonist with NO-releasing properties, and MET, only a β1-AR antagonist, would have different effects on plasma asymmetric dimethylarginine (ADMA) concentration. Forty-one hypertensive subjects randomly received either 50 mg of MET (n = 19) or 5 mg of NEB (n = 22) for 4 weeks followed by 100 mg MET and 10 mg NEB for 4 weeks. ADMA and insulin-like growth factor-1 (IGF-1) were measured by enzyme-linked immunosorbent assay kit; endothelial progenitor cells were estimated using fluorescein-labeled monoclonal antibody to KDR and CD133 receptors; arterial augmentation index was measured by radial tonometry. Baseline systolic/diastolic blood pressure was 155.1 ± 18.7/85.3 ± 12.5 mm Hg for MET subjects and 157.6 ± 20.7/87.1 ± 14.0 mm Hg for NEB subjects. Baseline ADMA was 0.32 ± 0.123 μmol/L in the MET group and 0.4035 ± 0.1378 in the NEB group. ADMA increased 44.78% and 72% in the MET group at weeks 4 and 8 (P < .05 for both), respectively, without increase in the NEB group. At week 8, augmentation index was increased in the MET group (P < .05). IGF-1 and endothelial progenitor cells were unchanged by treatment. Plasma ADMA and augmentation index are increased in a dose-dependent fashion by MET but not with NEB. [Copyright &y& Elsevier]
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- 2011
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9. Symptoms Characteristic of Heart Failure Among CKD Patients Without Diagnosed Heart Failure.
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Shlipak, Michael G., Lash, James P., Yang, Wei, Teal, Valerie, Keane, Martin, Cappola, Tom, Keller, Chris, Jamerson, Kenneth, Kusek, John, Delafontaine, Patrice, He, Jiang, Miller, Edgar R., Schreiber, Martin, and Go, Alan S.
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Abstract: Background: Epidemiological studies typically diagnose heart failure (HF) at the time of hospitalization, and have not evaluated the prevalence of HF symptoms in CKD patients without a prior HF diagnosis. Methods and Results: We modified the Kansas City Cardiomyopathy Questionnaire (KCCQ) to detect and quantify symptoms characteristic of HF (dyspnea, edema, and fatigue) among 2883 chronic kidney disease (CKD) patients without diagnosed heart failure in the Chronic Renal Insufficiency Cohort (CRIC). The KCCQ is a 23-item instrument that quantifies the impact of dyspnea, fatigue, and edema on physical, social, and emotional functions (scored 0 to 100). The median KCCQ score was 92, and 25% had KCCQ scores <75. Compared with cystatin C‑based estimated glomerular filtration rate >50 mL·min·1.73m
2 (reference), estimated glomerular filtration rate 40 to 50, 30 to 40, and <30 were independently associated with lower KCCQ scores (<75); adjusted odds ratios and (95% CI): 1.38 (1.06–1.78), 1.39 (1.09–1.82), and 2.15 (1.54–3.00), respectively. Lower hemoglobin (Hb) levels also had independent associations with KCCQ <75: Hb >14 g/dL (reference), Hb 13 to 14 g/dL (1.03; 0.76–1.40), Hb 12 to 13 g/dL (1.41; 1.04–1.91), Hb 11 to 12 g/dL (1.56; 1.12–2.16); and Hb <1 g/dL (1.65; 1.15–2.37). Conclusion: CKD patients without diagnosed HF have a substantial burden of symptoms characteristic of HF, particularly among those with lower estimated glomerular filtration rate and hemoglobin levels. [ABSTRACT FROM AUTHOR]- Published
- 2011
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10. Intravenous hMSCs Improve Myocardial Infarction in Mice because Cells Embolized in Lung Are Activated to Secrete the Anti-inflammatory Protein TSG-6.
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Ryang Hwa Lee, Pulin, Andrey A., Min Jeong Seo, Kota, Daniel J., Ylostalo, Joni, Larson, Benjamin L., Semprun-Prieto, Laura, Delafontaine, Patrice, and Prockop, Darwin J.
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DNA ,MESSENGER RNA ,MYOCARDIAL infarction ,STEM cells ,PROTEINS ,GENES - Abstract
Quantitative assays for human DNA and mRNA were used to examine the paradox that intravenously (i.v.) infused human multipotent stromal cells (hMSCs) can enhance tissue repair without significant engraftment. After 2 × 10
6 hMSCs were i.v. infused into mice, most of the cells were trapped as emboli in lung. The cells in lung disappeared with a half-life of about 24 hr, but <1000 cells appeared in six other tissues. The hMSCs in lung upregulated expression of multiple genes, with a large increase in the anti-inflammatory protein TSG-6. After myocardial infarction, i.v. hMSCs, but not hMSCs transduced with TSG-6 siRNA, decreased inflammatory responses, reduced infarct size, and improved cardiac function. l.v. administration of recombinant TSG-6 also reduced inflammatory responses and reduced infarct size. The results suggest that improvements in animal models and patients after i.v. infusions of MSCs are at least in part explained by activation of MSCs to secrete TSG-6. [ABSTRACT FROM AUTHOR]- Published
- 2009
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11. Angiotensin II as candidate of cardiac cachexia.
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Delafontaine P, Akao M, Delafontaine, Patrice, and Akao, Makoto
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Purpose Of Review: Congestive heart failure is increasing in prevalence and represents a major public health problem. The syndrome of advanced heart failure often includes muscle wasting, commonly termed cardiac cachexia, which is a predictor of poor outcome. Mechanisms of cardiac cachexia are poorly understood, but there is recent evidence that increased angiotensin II, interacting with the insulin-like growth factor-1 system, plays an important role.Recent Findings: In animals, angiotensin II produces weight loss through a pressor-independent mechanism, accompanied by decreased levels of circulating and skeletal muscle insulin-like growth factor-1 and increased mRNA levels of the ubiquitin ligases atrogin-1 and Muscle RING finger-1 in skeletal muscle. Reduced insulin-like growth factor-1 action in muscle leads to increased proteolysis, through the ubiquitin-proteasome pathway, and increased apoptosis. These changes are blocked by muscle-specific expression of insulin-like growth factor-1, likely to be via the Akt/mTOR/p70S6K signaling pathway.Summary: The link between insulin-like growth factor-1, the ubiquitin-proteasome pathway, and angiotensin II effects has widespread clinical implications for the understanding of mechanisms of catabolic conditions. Therapeutic interventions targeting cross-talk mechanisms between angiotensin II and insulin-like growth factor-1 effects could provide new approaches for the treatment of muscle wasting. [ABSTRACT FROM AUTHOR]- Published
- 2006
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12. Natural Disasters and Myocardial Infarction: The Six Years After Hurricane Katrina
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Peters, Matthew N., Moscona, John C., Katz, Morgan J., Deandrade, Kevin B., Quevedo, Henry C., Tiwari, Sumit, Burchett, Andrew R., Turnage, Thomas A., Singh, Kanwar Y., Fomunung, Edmond N., Srivastav, Sudesh, Delafontaine, Patrice, and Irimpen, Anand M.
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To determine the prolonged effect of Hurricane Katrina on the incidence and timing of acute myocardial infarction (AMI) in the city of New Orleans.
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- 2014
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13. Mammographically Detectable Breast Arterial Calcification and Atherosclerosis
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Shah, Neeraj, Chainani, Vinod, Delafontaine, Patrice, Abdo, Abir, Lafferty, James, and Rafeh, Nidal Abi
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Breast arterial calcification (BAC), observed as an incidental finding on screening mammograms, represents degenerative calcific changes occurring in the mammary arteries, with increasing age. The aim of this review is to discuss relevant literature examining relation between BAC and atherosclerosis. After a thorough literature search, in OVID and PubMed, 199 studies were identified, of which 25 were relevant to our review. Data were abstracted from each study and statistical analysis was done, including calculation of odds ratios and construction of forest plots. A total of 35,542 patients were enrolled across 25 studies looking at an association between BAC and coronary artery disease, cardiovascular disease, stroke, cerebral artery disease, carotid and peripheral artery diseases, and coronary artery calcification. A majority of the studies showed a statistically significant relation between BAC and presence of coronary artery disease cardiovascular disease and associated mortality. Sensitivity of BAC in predicting cardiovascular events was low, but specificity was high. BAC was predictive of incident and prevalent stroke but not mortality of stroke. Similarly, BAC was predictive of cerebral, carotid, and peripheral artery diseases. The role of BAC as a surrogate marker of coronary and systemic atherosclerosis is currently uncertain. Its role may be further elucidated by more large-scale prospective studies and clinical experience.
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- 2014
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14. Authors' Reply
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Tian, Di, Lin, Zhen, Kriner, Ellie M., Esneault, Dalton J., Tran, Jonathan, DeVoto, Julia C., Okami, Naima, Greenberg, Rachel, Yanofsky, Sarah, Ratnayaka, Swarnamala, Tran, Nicholas, Livaccari, Maeghan, Lampp, Marla, Wang, Noel, Tim, Scott, Norton, Patrick, Scott, John, Hu, Tony Y., Garry, Robert, Hamm, Lee, Delafontaine, Patrice, and Yin, Xiao-Ming
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- 2022
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15. Effect of Hurricane Katrina on the Incidence of Acute Coronary Syndrome at a Primary Angioplasty Center in New Orleans
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Gautam, Sandeep, Menachem, Jonathan, Srivastav, Sudesh K., Delafontaine, Patrice, and Irimpen, Anand
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ABSTRACTBackground:In August 2005, New Orleans was hit by Hurricane Katrina, the costliest natural disaster in US history. Previous studies have shown an increase in acute myocardial infarction (AMI) in the immediate hours to weeks after natural disasters. The goals of our study were to detect any long-term increase in the incidence of AMI after Katrina and to investigate any pertinent contributing factors.Methods:This was a single-center retrospective cohort observational study. Patients admitted with AMI to Tulane Health Sciences Center hospital in the 2 years before Katrina and in the 2 years after the hospital reopened (5 months after Katrina) were identified from hospital records. The 2 groups (pre- and post-Katrina) were compared for prespecified demographic and clinical data.Results:In the post-Katrina group, there were 246 admissions for AMI, out of a total census of 11,282 patients (2.18%), as compared with 150 AMI admissions out of a total of 21,229 patients (0.71%) in the pre-Katrina group (P< 0.0001). The post-Katrina group had a significantly higher prevalence of unemployment (P= 0.0003), lack of medical insurance (P< 0.0001), medication noncompliance (P= 0.0001), smoking (P= 0.001), substance abuse (P= 0.03), first-time hospitalization (P< 0.001), local residents rather than visitors affected (P< 0.0001), and people living in temporary housing (P= 0.003).Discussion:The role of chronic stress in the pathogenesis of AMI is poorly understood, especially in the aftermath of natural disasters. Our data suggest that Katrina was associated with prolonged loss of employment and insurance, decreased access to preventive health services, and an increased incidence of AMI. In addition, it appears that chronic stress after a natural disaster can be associated with tobacco abuse and medication and therapeutic noncompliance.Conclusions:We found a 3-fold increased incidence of AMI more than 2 years after Hurricane Katrina. Even allowing for the loss of some local hospitals after the disaster, this represents a significant change in overall health of the study population and supports the need for further study into the health effects of chronic stress. (Disaster Med Public Health Preparedness. 2009;3:144–150)
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- 2009
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16. Abstract 9073: Profiling of Metabolic Remodeling in Rat Model of Pressure Overload Induced Early Systolic Dysfunction and in Progression to Overt Systolic Heart Failure
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Chaanine, Antoine H, Delafontaine, Patrice, and Busija, David W
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Introduction:We have previously shown left ventricular (LV) structural and hemodynamic differences in two models of rat pressure overload induced moderate remodeling and early systolic dysfunction (MOD) and overt systolic heart failure (SHF). The MOD and SHF phenotypes develop 8 weeks post ascending aortic banding via a vascular clip, area of 2 mm2and 1.5 mm2, respectively.Hypothesis:Metabolic remodeling play significant role in the development of MOD and SHF phenotypes, but is more evident in SHF than MOD.Methods:Shotgun proteomics and phospho-(p)-proteomics and non-targeted metabolomics analysis was performed in LV myocardium tissue from Sham, MOD and SHF using liquid chromatography mass spectrometry (LC-MS); n=3 biological samples per group. Raw proteomics, p-proteomics and metabolomics MS data were uploaded into Qlucore bioinformatics software for statistical analysis and data visualization. Statistically analyzed data were then uploaded into Ingenuity Pathway Analysis bioinformatics software for data validation and assessment of highly enriched canonical pathways related to metabolism that were up or down-regulated in MOD and SHF relative to Sham. Some of the proteomics and p-proteomics data were validated by immunoblotting.Results:Canonical pathways of oxidative phosphorylation, fatty acid β-oxidation, Kreb’s cycle, branched-chain amino acid and amino acid (Glutamine and Tryptophan) degradation were downregulated in MOD vs Sham and were further downregulated in SHF vs MOD. Whilst glycogen degradation and glucose degradation were upregulated in MOD and SHF vs Sham, but more so in MOD than SHF. Metabolomics data revealed that long chain and very long chain acyl-carnitines were decreased in abundance in MOD and SHF relative to Sham, while short and medium chain acyl-carnitines were decreased in abundance in SHF only. Moreover, Isoleucine degradation and glycolysis decreased and Taurine biosynthesis increased in SHF vs MOD. p-Proteomics data showed mild decrease in protein kinase A (PKA) and AMPK signaling in MOD vs Sham, which were more profoundly decreased in SHF than MOD.Conclusion:The interplay between PKA and AMPK signaling play an important role in metabolic remodeling and transitioning from MOD to SHF phenotype.
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- 2021
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17. Abstract 13092: Macrophage Specific IGF1 Overexpression on ApoE Deficient Mice Decreases Atherosclerosis, Reduces CXCL12 Chemokine Expression, and Increases Cholesterol Efflux
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Snarski, Patricia, Sukhanov, Sergiy, Yoshida, Tadashi, Danchuk, Svitlana, Shai, Shaw-Yung, Bysani, Chandrasekar, and Delafontaine, Patrice
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Increased bioavailability of Insulin Like Growth Factor I (IGF1) has been shown to reduce cardiovascular events. Systemic IGF1 administration in ApoE deficient (Apoe-/-) mice fed a high fat diet reduced atherosclerosis and reduced plaque macrophages. Results of our previous in vitroexperiments suggest that macrophages play a predominant role in mediating IGF1 effects in atherosclerotic plaque. We hypothesized that increasing IGF1 levels strictly in macrophages will prevent atherosclerosis. After breeding a novel macrophage-specific IGF1 overexpressing transgenic mouse to an Apoe-/-background (MF-IGF1 mice), we assessed atherosclerotic plaque burden, stability, and monocyte recruitment. Macrophage IGF1 overexpression downregulated plaque burden by 30% (P<0.01), reduced plaque macrophages by 47% (P<0.001) and promoted a stable plaque phenotype. Monocyte recruitment was reduced by 70% (P<0.05) in MF-IGF1 mice and was associated with a decrease in circulating levels of CXC Chemokine Ligand 12 (CXCL12) (27% reduction, P<0.05). CXCL12 protein levels were reduced in plaque and peritoneal macrophages in MF-IGF1 mice. IGF1 completely blocked oxidized low-density lipoprotein (oxLDL)-dependent increase of CXCL12 mRNA transcription (98% reduction, P<0.01) and IGF1 treatment reduced CXCL12 protein (56% decrease, P<0.001) in vitro.ATP-binding cassette transporter A1 (ABCA1) is the key cholesterol transporter mediating macrophage cholesterol efflux and CXCL12 reduces its expression. We found that peritoneal macrophages isolated from MF-IGF1 mice have a 2 fold increase in ABCA1 protein levels. We loaded peritoneal macrophages with oxLDL to measure changes in cholesterol efflux and found that MF-IGF1 mice have a 42% increase in efflux (P<0.01). We also found a 27% increase in cholesterol efflux in IGF1 (100 ng/mL) treated THP-1 cells (P<0.01) with Apolipoprotein AI as a cholesterol acceptor. Overall, our results indicate that macrophage IGF1 reduces atherosclerosis and decreases CXCL12, a chemokine newly implicated in atheroprogression. IGF1 potentially exerts its atheroprotective effect via this reduction in CXCL12 by reducing monocyte recruitment and by increasing ABCA1, thereby increasing cholesterol efflux capacity.
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- 2021
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18. Angiotensin II as candidate of cardiac cachexia
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Delafontaine, Patrice and Akao, Makoto
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Congestive heart failure is increasing in prevalence and represents a major public health problem. The syndrome of advanced heart failure often includes muscle wasting, commonly termed cardiac cachexia, which is a predictor of poor outcome. Mechanisms of cardiac cachexia are poorly understood, but there is recent evidence that increased angiotensin II, interacting with the insulin-like growth factor-1 system, plays an important role.
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- 2006
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19. Endothelial dysfunction its role in hypertensive coronary disease
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Bolad, Islam and Delafontaine, Patrice
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Coronary artery disease is the major cause of death worldwide. Hypertension is a major risk factor for developing coronary disease. It is now recognized that endothelial dysfunction is an early marker of coronary artery disease before structural changes to the vessel wall are apparent on angiography or intravascular ultrasound and that it has a prognostic value in predicting cardiovascular events in hypertensive patients. This review addresses recent developments in hypertension-induced endothelial dysfunction.
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- 2005
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20. Endovascular Stent-Graft Repair of Ascending Aortic Dissection With a Commercially Available Thoracic Endograft.
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Atianzar, Kimberly, Mohamad, Almois, Galazka, Patrycja, Keller, V. Antoine, Delafontaine, Patrice, and Sam II, Albert D.
- Abstract
We describe the endovascular treatment of a type A thoracic aortic dissection (TAAD) in a patient deemed unfit for surgical repair with a commercially available thoracic endograft. A patient with a symptomatic acute TAAD, multiple medical comorbidities, and ascending thoracic aortic and arch dilation underwent successful endovascular repair with the use of a commercially available stent graft, resulting in complete resolution of his symptoms despite slight but persistent perigraft false lumen perfusion. Although surgical repair remains the gold standard, endografting has promise and may have a positive impact on the current treatment algorithm for TAAD. Advances must occur in graft manufacturing, and further data will be required before wider application is appropriate. [ABSTRACT FROM AUTHOR]
- Published
- 2014
- Full Text
- View/download PDF
21. Estrogen regulates insulin-like growth factor 1, platelet-derived growth factor A and B, and their receptors in the vascular wall
- Author
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Savolainen-Peltonen, Hanna, Loubtchenkov, Michael, Petrov, Loubomir, Delafontaine, Patrice, and Häyry, Pekka
- Abstract
Peptide growth factors induce vascular smooth muscle cell (SMC) proliferation and migration after vascular injury, leading to arterial stenosis. Estrogen provides vasculoprotective effects by regulating endothelial and vascular SMC function.
- Published
- 2004
- Full Text
- View/download PDF
22. Decreased Expression of Insulin-like Growth Factor-1 and Apoptosis of Vascular Smooth Muscle Cells in Human Atherosclerotic Plaque
- Author
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Okura, Yoshifumi, Brink, Marijke, Zahid, Aliya Aftab, Anwar, Asif, and Delafontaine, Patrice
- Abstract
Insulin-like growth factor-1 (IGF-1) plays an important role in migration, cell cycle progression and survival of vascular smooth muscle cells (VSMC). We investigated the specific localization of IGF-1 and its receptor (IGF-1R) and their association with apoptosis and the expression of apoptosis-related proteins in early and advanced atherosclerotic lesions. Human atherosclerotic plaques (n=23) from patients undergoing aortic, carotid or femoral arterial surgery were studied. Immunohistochemistry and in situhybridization revealed significantly higher expression of IGF-1 and IGF-1R in the media than in the intima of early atherosclerotic lesions (P<0.01). Medial VSMC positive for BAX, a proapoptotic protein of the B-cell CLL/lymphoma 2 (BCL2) family, showed colocalization of IGF-1. Apoptosis, as detected by DNA in situterminal deoxynucleotidyl transferase end labeling (TUNEL), was not present in these early lesions. In advanced atherosclerotic plaques, the expression of IGF-1 and IGF-1R was significantly lower in the intimal regions with macrophage infiltration than in those without macrophage infiltration or than in the media (P<0.01). Furthermore, IGF-1 and IGF-1R immunoreactivity was markedly lower in intimal TUNEL-positive VSMC compared with intimal BAX-positive and medial VSMC (P<0.01). We conclude that IGF-1 and IGF-1R expression are reduced in the deep intima of early atherosclerotic lesions and in areas of advanced plaques with macrophage infiltration. Since IGF-1 is a potent survival factor for VSMC, poor expression of IGF-1 and IGF-1R in intimal regions with macrophage infiltration would likely contribute to triggering VSMC apoptosis potentially leading to plaque weakening, plaque rupture and acute coronary events.
- Published
- 2001
- Full Text
- View/download PDF
23. Coronary angiographic significance of hyperacute ST-T changes associated with regadenoson stress.
- Author
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Peters, Matthew N., Bhattasli, Onita, Burchett, Andrew R., Howell, Lucius A., Turnage, Thomas A., Katz, Morgan J., Delafontaine, Patrice, and Irimpen, Anand M.
- Abstract
An abnormal electrocardiographic stress test is typically characterized by ST segment depression. In rare cases, ST segment elevation is observed, which, in the absence of diagnostic Q waves, has anatomic specificity for localized myocardial ischemia. Most instances of ST elevation occurring during cardiac stress testing have been observed with exercise, with only six cases reported with pharmacologic stress. Despite different physiologic mechanisms for inducing myocardial ischemia, development of ST segment elevation during pharmacologic stress, as illustrated by the present case, may also be indicative of critical coronary stenoses, warranting urgent coronary arteriography. [ABSTRACT FROM AUTHOR]
- Published
- 2013
24. Coronary angiographic significance of hyperacute ST-T changes associated with regadenoson stress.
- Author
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Peters, Matthew N., Bhattasli, Onita, Burchett, Andrew R., Howell, Lucius A., Turnage, Thomas A., Katz, Morgan J., Delafontaine, Patrice, and Irimpen, Anand M.
- Abstract
An abnormal electrocardiographic stress test is typically characterized by ST segment depression. In rare cases, ST segment elevation is observed, which, in the absence of diagnostic Q waves, has anatomic specificity for localized myocardial ischemia. Most instances of ST elevation occurring during cardiac stress testing have been observed with exercise, with only six cases reported with pharmacologic stress. Despite different physiologic mechanisms for inducing myocardial ischemia, development of ST segment elevation during pharmacologic stress, as illustrated by the present case, may also be indicative of critical coronary stenoses, warranting urgent coronary arteriography. [ABSTRACT FROM AUTHOR]
- Published
- 2013
- Full Text
- View/download PDF
25. Vitamin C and Percutaneous Coronary Intervention ⁎ [⁎] Editorials published in JACC: Cardiovascular Interventions reflect the views of the authors and do not necessarily represent the views of JACC: Cardiovascular ...
- Author
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Delafontaine, Patrice and Anwar, Asif
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- 2010
- Full Text
- View/download PDF
26. Ct Values Do not Predict SARS-CoV-2 Transmissibility in College Students
- Author
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Tian, Di, Lin, Zhen, Kriner, Ellie M., Esneault, Dalton J., Tran, Jonathan, DeVoto, Julia C., Okami, Naima, Greenberg, Rachel, Yanofsky, Sarah, Ratnayaka, Swarnamala, Tran, Nicholas, Livaccari, Maeghan, Lampp, Marla, Wang, Noel, Tim, Scott, Norton, Patrick, Scott, John, Hu, Tony Y., Garry, Robert, Hamm, Lee, Delafontaine, Patrice, and Yin, Xiao-Ming
- Abstract
Severe acute respiratory syndrome coronavirus 2 is highly contagious, and the global spread has caused significant medical/socioeconomic impacts. Other than vaccination, effective public health measures (including contact tracing, isolation, and quarantine) are critical for deterring viral transmission, preventing infection progression, and resuming normal activities. Viral transmission is affected by many factors, but the viral load and vitality could be among the most important ones. Although in vitrostudies have indicated that the amount of virus isolated from infected people affects the successful rate of virus isolation, whether the viral load carried at the individual level would determine the transmissibility was unknown. We aimed to examine, from a diagnostic point of view, whether the cycle threshold (Ct) value, a measurement of viral load by RT-PCR assay, could differentiate the spreaders from the nonspreaders in a population of college students. Our results indicate that although at the population level the Ct value is lower (suggesting a higher viral load) in the symptomatic spreaders than in the asymptomatic nonspreaders, there is significant overlap in the Ct values between the two groups. Thus, the Ct value, or the viral load, at the individual level could not predict transmissibility. Our studies also suggest that a sensitive method to detect the presence of virus is needed to identify asymptomatic persons who may carry a low viral load but can still be infectious.
- Published
- 2021
- Full Text
- View/download PDF
27. Coronary Angiographic Significance of Hyperacute St-T Changes Associated with Regadenoson Stress
- Author
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Peters, Matthew N., Bhattasli, Onita, Burchett, Andrew R., Howell, Lucius A., Turnage, Thomas A., Katz, Morgan J., Delafontaine, Patrice, and Irimpen, Anand M.
- Abstract
An abnormal electrocardiographic stress test is typically characterized by ST segment depression. In rare cases, ST segment elevation is observed, which, in the absence of diagnostic Q waves, has anatomic specificity for localized myocardial ischemia. Most instances of ST elevation occurring during cardiac stress testing have been observed with exercise, with only six cases reported with pharmacologic stress. Despite different physiologic mechanisms for inducing myocardial ischemia, development of ST segment elevation during pharmacologic stress, as illustrated by the present case, may also be indicative of critical coronary stenoses, warranting urgent coronary arteriography.
- Published
- 2013
- Full Text
- View/download PDF
28. Persistent giant U wave inversion with anoxic brain injury.
- Author
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Peters, Matthew N., Katz, Morgan J., Howell, Lucius A., Moscona, John C., Turnage, Thomas A., and Delafontaine, Patrice
- Abstract
Various electrocardiographic changes have been reported in the setting of acute neurological events, among them large, upright U waves. In contrast, the occurrence of inverted U waves is strongly suggestive of cardiovascular disease, most commonly hypertension, coronary artery disease, or valvular abnormalities. Presented herein is the case of a 29-year-old man with previous anoxic brain injury (but without apparent cardiovascular disease) whose electrocardiogram demonstrated persistent giant inverted U waves. [ABSTRACT FROM AUTHOR]
- Published
- 2013
29. Persistent giant U wave inversion with anoxic brain injury.
- Author
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Peters, Matthew N., Katz, Morgan J., Howell, Lucius A., Moscona, John C., Turnage, Thomas A., and Delafontaine, Patrice
- Abstract
Various electrocardiographic changes have been reported in the setting of acute neurological events, among them large, upright U waves. In contrast, the occurrence of inverted U waves is strongly suggestive of cardiovascular disease, most commonly hypertension, coronary artery disease, or valvular abnormalities. Presented herein is the case of a 29-year-old man with previous anoxic brain injury (but without apparent cardiovascular disease) whose electrocardiogram demonstrated persistent giant inverted U waves. [ABSTRACT FROM AUTHOR]
- Published
- 2013
- Full Text
- View/download PDF
30. Preoperative Electrocardiogram in an 89-Year-Old Man.
- Author
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Peters, Matthew N., Katz, Morgan J., Irimpen, Anand M., and Delafontaine, Patrice
- Published
- 2013
31. Persistent Giant U Wave Inversion with Anoxic Brain Injury
- Author
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Peters, Matthew N., Katz, Morgan J., Howell, Lucius A., Moscona, John C., Turnage, Thomas A., and Delafontaine, Patrice
- Abstract
Various electrocardiographic changes have been reported in the setting of acute neurological events, among them large, upright U waves. In contrast, the occurrence of inverted U waves is strongly suggestive of cardiovascular disease, most commonly hypertension, coronary artery disease, or valvular abnormalities. Presented herein is the case of a 29-year-old man with previous anoxic brain injury (but without apparent cardiovascular disease) whose electrocardiogram demonstrated persistent giant inverted U waves.
- Published
- 2013
- Full Text
- View/download PDF
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