Publications by authors named "D M Gangahar"

Toward the end of the twentieth century, redo cardiac surgery accounted for approximately 15-20% of total cardiac surgical volume. Major risk factors for redo cardiac surgery include young age at time of the first operation, progression of native coronary artery disease (CAD), vein graft atherosclerosis, bioprosthetic valve failure and endocarditis, and transplantation for end stage heart failure. Historically, redo coronary artery bypass grafting (CABG) alone carried a mortality risk of around 4%.

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Background And Objective: While the risk of opioid overdose is widely accepted, the dangers of opioid withdrawal are far less clearly defined. The purpose of this publication is to provide evidence against the erroneous clinical dictum that opioid withdrawal is never life-threatening.

Methods And Results: This case report (N = 1) illustrates an unfortunate, common scenario of a man abusing prescription opioids and heroin.

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Vascular calcification predicts an increased risk for cardiovascular events in atherosclerosis, diabetes, and end-stage kidney diseases. Matrix Gla protein (MGP), an inhibitor of calcification, limits calcium phosphate deposition in the vessel wall. There are many factors contributing to the progression of atherosclerosis, including hypertension, hyperlipidemia, the renin-angiotensin system, and inflammation.

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Vascular restenosis following coronary artery bypass graft can cause major clinical complications due to intimal hyperplasia in venous conduits. However, the precise underlying mechanisms of intimal hyperplasia are still unclear. We have recently reported that increased expression of connexin43 (Cx43) is involved in the proliferation of vascular smooth muscle cells (SMCs) in human saphenous vein (SV).

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Coronary revascularization by coronary artery bypass grafting (CABG) is recommended in patients with recurrent myocardial ischemia. However, the long-term results of CABG using saphenous vein (SV) graft, compared to internal mammary artery (IMA) graft, have not been satisfactory. The SV graft failure is due to the development of intimal hyperplasia, a process characterized by abnormal migration and proliferation of smooth muscle cells (SMCs) in the intimal layer of the vein graft.

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