Arman Arghami

Transcriptional and phenotypic changes in aorta and aortic valve with aging and MnSOD deficiency in mice

The purpose of this study was to characterize changes in antioxidant and age-related gene expression in aorta and aortic valve with aging, and test the hypothesis that increased mitochondrial oxidative stress accelerates age-related endothelial and aortic valve dysfunction. Wild-type (MnSOD(+/+)) and manganese SOD heterozygous haploinsufficient (MnSOD(+/-)) mice were studied at 3 and 18 mo of age. In aorta from wild-type mice, antioxidant expression was preserved, although there were age-associated increases in Nox2 expression. Haploinsufficiency of MnSOD did not alter antioxidant expression in aorta, but increased expression of Nox2. When compared with that of aorta, age-associated reductions in antioxidant expression were larger in aortic valves from wild-type and MnSOD haploinsufficient mice, although Nox2 expression was unchanged. Similarly, sirtuin expression was relatively well-preserved in aorta from both genotypes, whereas expression of SIRT1, SIRT2, SIRT3, SIRT4, and SIRT6 were significantly reduced in the aortic valve. Expression of p16(ink4a), a marker of cellular senescence, was profoundly increased in both aorta and aortic valve from MnSOD(+/+) and MnSOD(+/-) mice. Functionally, we observed comparable age-associated reductions in endothelial function in aorta from both MnSOD(+/+) and MnSOD(+/-) mice. Interestingly, inhibition of NAD(P)H oxidase with apocynin or gp91ds-tat improved endothelial function in MnSOD(+/+) mice but significantly impaired endothelial function in MnSOD(+/-) mice at both ages. Aortic valve function was not impaired by aging or MnSOD haploinsufficiency. Changes in antioxidant and sirtuin gene expression with aging differ dramatically between aorta and aortic valve. Furthermore, although MnSOD does not result in overt cardiovascular dysfunction with aging, compensatory transcriptional responses to MnSOD deficiency appear to be tissue specific.

Quadruple valve replacement in patients with carcinoid heart disease

with interarterial course and no intramural component, we favor pulmonary artery translocation to create space between the aortic and pulmonic roots, thereby decreasing the risk of pulmonary compression of the coronary artery. Intraoperative inspection determines which procedure will be performed. If the orientation of the aortic and pulmonic roots is such that anterior movement of the MPAwill create space, a LeCompte maneuver is done. Alternatively, if moving the MPA laterally will create space, the MPA is translocated distally toward the left pulmonary artery. At the current time there is not sufficient data to form firm management guidelines for asymptomatic children with ACAs from the contralateral sinus. Because of the documented risk of sudden death without antecedent symptoms, our policy is to surgically correct all lesions at risk, regardless of symptoms. Although we believe pulmonary artery translocation is protective of subsequent ischemic episodes, long-term follow-up has not been achieved. Whether it will

Origins of Cardiovascular Surgery at the Mayo Clinic

Sixty years ago, at the Mayo Clinic in Rochester, Minnesota, an ambitious group of pioneers, led by Dr John W. Kirklin and supported by a multidisciplinary team of physicians and technicians embarked on a planned series of surgical cases using a heart-lung machine to allow direct visualization of the inside of the opened human heart to repair otherwise fatal congenital intracardiac defects. Their success sparked the beginning of a new era of open-heart surgery. In this historical article, we discuss the contributions of a few key figures of this revolution and also share the story of the first successful cardiac surgery operation using cardiopulmonary bypass performed at Mayo Clinic.

Reoperations for Mitral Valve Disease: Surgical Approaches and Techniques

Approximately 10% of all adult cardiac operations involve redo thoracotomy, and clinically significant hemorrhage occurs in up to 8% of patients with a resultant increase in operative morbidity and mortality (Ann Thorac Surg 68: 2215–9, 1999). Indeed, in some reports, prior cardiac surgery increases the operative risk of mitral valve (MV) surgery almost twofold (J Am Coll Cardiol 37: 885–92, 2001; J Thorac Cardiovasc Surg 131: 547–57, 2006). Reoperation for MV disease is necessary for a wide variety of problems, such as failure of a previously placed prosthesis, development of a paravalvular leak, endocarditis, or newly diagnosed valve disease in a patient with prior aortic valve replacement or coronary artery bypass. Careful attention to the planning and execution of the operation can minimize surgical risks, and this chapter details those methods that have proved helpful at Mayo Clinic (Rochester, MN)