The Facts Karla M. Ku - The Methodist Hospital

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PPARa agonists diminishes myocardial TG accumulation, inhibits production of inflammatory factors such as tumor necrosis factor, attenuates cardiac fibrosis and improves cardiac function. 11 Theoretically, PPARa activation could also induce the expression of FA importing proteins and thus increase FA uptake from the circulation. Therefore, the question of whether PPARa agonists induce or normalize an imbalance between the uptake and utilization of FAs requires further investigation. There are no reports to date of deteriorating cardiac function in humans treated with fibrates — synthetic PPARa agonists — despite widespread use to treat hyperlipidemia in patients with known cardiac disease, suggesting that PPARa agonists may provide a net benefit to the cardiovascular system. C o n C l u s I o n PPARs transcriptionally regulate every aspect of fatty acid metabolism. Therefore, development of efficient and targeted PPAR agonists may serve as a novel strategy to combat heart disease complicated by myocyte lipid imbalance. R e f e R e n C e s 1. Unger RH. Lipotoxic diseases. Annu Rev Med. 2002;53:319-36. 2. Barger PM, Kelly DP. PPAR signaling in the control of cardiac energy metabolism. Trends Cardiovasc Med. 2000 Aug;10(6):238-45. 3. Tian Q, Barger PM. Do PPARs play a role in cardiac hypertrophy and heart failure? Drug Discovery Today: Disease Mechanism. 2005;2(1):109-14. 4. Cheng L, Ding G, Qin Q, Huang Y, Lewis W, He N, et al. Cardiomyocyte-restricted peroxisome proliferator-activated receptordelta deletion perturbs myocardial fatty acid oxidation and leads to cardiomyopathy. Nat Med. 2004 Nov;10(11):1245-50. 5. Watanabe K, Fujii H, Takahashi T, Kodama M, Aizawa Y, Ohta Y, et al. Constitutive regulation of cardiac fatty acid metabolism through peroxisome proliferator-activated receptor alpha associated with age-dependent cardiac toxicity. J Biol Chem. 2000 Jul;275(29):22293-9. 6. Leone TC, Weinheimer CJ, Kelly DP. A critical role for the peroxisome proliferatoractivated receptor alpha (PPARalpha) in the cellular fasting response: the PPARalpha-null mouse as a model of fatty acid oxidation disorders. Proc Natl Acad Sci U S A. 1999 Jun;96(13):7473-8. 7. Petersen KF, Dufour S, Befroy D, Garcia R, Shulman GI. Impaired mitochondrial activity in the insulin-resistant offspring of patients with type 2 diabetes. N Engl J Med. 2004 Feb;350(7):664-71. 8. Young ME, Guthrie PH, Razeghi P, Leighton B, Abbasi S, Patil S, et al. Impaired long-chain fatty acid oxidation and contractile dysfunction in the obese Zucker rat heart. Diabetes. 2002 Aug;51(8):2587-95. 9. Zhou YT, Grayburn P, Karim A, Shimabukuro M, Higa M, Baetens D, et al. Lipotoxic heart disease in obese rats: implications for human obesity. Proc Natl Acad Sci U S A. 2000 Feb;97(4):1784-9. 10. Sack MN, Disch DL, Rockman HA, Kelly DP. A role for Sp and nuclear receptor transcription factors in a cardiac hypertrophic growth program. Proc Natl Acad Sci USA. 1997 Jun;94(12):6438-43. 11. Aasum E, Belke DD, Severson DL, Riemersma RA, Cooper M, Andreassen M, et al. Cardiac function and metabolism in type 2 diabetic mice after treatment with BM 17.0744, a novel PPAR-alpha activator. Am J Physiol Heart Circ Physiol. 2002 Sept;283(3):H949-57. 2 II (1) 2006 | JMDHC
C O M B I N E d O P E N A N d S T E N T G R A F T R E PA I R O F A N A R C H A N d d E S C E N d I N G T H O R AC I C AO R T I C A N E U RYS M : T H E H Y B R I d P R O C E d U R E M i c h a e l J . R e a r d o n , W e i Z h o u , J o n - C e c i l W a l k e s , A l a n B . L u m s d e n F r o m M e t h o d i s t D e B a k e y H e a r t C e n t e r, H o u s t o n , Te x a s IntRoduCtIon surgeons at the methodist Hospital and the methodist deBakey Heart Center have a long history of contributions to the treatment of thoracic aortic aneurysms. In the 1950s, dr. michael e. deBakey pioneered the use of artificial grafts for aortic replacement and drs. deBakey and denton Cooley introduced the use of cardiopulmonary bypass to repair aneurysms of the ascending aorta and aortic arch. dr. stanley Crawford then introduced surgical repair of the descending and thoracoabdominal aneurysm. Half a century later, the methodist deBakey Heart Center has now performed more descending and thoracoabdominal aortic aneurysm repairs than any other institution in the world. despite these advances, treatment of aneurysms involving both the ascending aorta/aortic arch segment and the descending thoracic aorta have continued to pose a formidable surgical challenge: aortic arch repair traditionally requires circulatory arrest and profound hypothermia via median sternotomy followed by a later descending thoracic aorta repair through a left thoracotomy. Recently, a patient who had undergone previous ascending thoracic aortic aneurysm repair for dissection presented with a large arch and descending thoracic aortic aneurysm and a high risk of standard surgical repair. a unique, minimally-invasive hybrid approach of open and stent graft repair with aortic arch debranching was successfully employed, again advancing the field of thoracic aortic surgery at the methodist deBakey Heart Center. C a s e H I s t o R Y Mr. TF is an 81-year-old male with a history of previous graft replacement of his ascending thoracic aorta for dissection in 1996. His current medical history included hypertension, COPD with a 120-pack-year history of smoking, history of a CVA and parkinsonism. He presented with chest and back pain and a chest X-ray showing a wide mediastinum (Figure 1). Arteriography evaluation revealed a large aneurysm beginning at his distal ascending aortic graft and extending through his aortic arch into the distal descending thoracic aorta (Figure 2). Evaluation by the consulting medical services placed his risk of standard surgical repair at 30-50%. Further, the patient refused consideration of a standard open, twostage repair because of prior difficulty in recovering from his initial dissection surgery. A hybrid procedure of minimallyinvasive debranching of the aortic arch and stent graft repair of the arch and C L I N C I A L B R I E F figure 1. Chest X-ray showing wide mediastinum JMDHC | II (1) 2006 2
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