Percutaneous Transluminal Coronary Angioplasty
Percutaneous Transluminal Coronary Angioplasty (PTCA) is the procedure used to widen the coronary stenosis without the need for an open-surgical procedure. PTCA is also applied for treating stenosis of carotid arteries, which supply blood to the brain. To carry out the procedure, a catheter, which has small inflatable balloon on the end, is positioned within the artery's narrowed portion. The balloon is then inflates causing dilation of the artery's stenosed segment through compression of the atherosclerotic plaque thereby stretching the artery wall. PTCA is usually followed by inserting a stent at the stenosis's site.

Every year in the United States, around 1.5 million patients experience percutaneous coronary intervention. Depending on the diagnostic criteria used and the local practices followed, nearly 6 to 30 percent of these patients have shown evidence of periprocedural myocardial infarction (MI). If the cardiac biomarker level (cardiac troponin) is three times higher than the upper-reference limit, it indicates periprocedural MI.

Coronary Stents
A coronary stent is a small mesh-tube, expandable in size and made from medical-grade stainless steel. A stent is implanted in the coronary artery after being delivered on a balloon catheter; it keeps the artery open after balloon angioplasty procedure. The stent fully expands into position after the plaque compresses against the artery wall thereby acting as small "scaffolding" for the artery. After the balloon deflates, it is removed and the stent is left behind in the blood vessel of the patient. Depending on the blockage length, one more stent may be placed. The artery's inside lining heals around the stent.

The narrowing or re-closure of an artery is called as Restenosis. This is concerned with balloon angioplasty procedures and coronary stents. Restenosis usually occurs when a blockage returns for few weeks or months following the stent procedure. Abnormal growth seen in the smooth muscle that lines the arterial walls plays a vital role in vascular occlusion during coronary heart diseases (CAD) contributing to coronary arteries blockage, which have been either replaced by bypass operations or opened by billon angioplasty. Despite the PTCA achieving a 95 percent success in opening blocked coronary arteries, restenosis occurs at angioplasty site.
Out of the 1 million coronary stents that are implanted annually, nearly 20 to 25 percent of the patients who are treated with bare, conventional metal stents require a second procedure less than 6 months for the vessel can develop a possible re-blockage.

The restenosis mechanism following angioplasty procedure has been researched extensively. The mechanism of pathophysiology involves the healing response of smooth muscle to vascular injury. Proliferation and migration of the smooth muscle cells to the sub-intimal layer occurs after being induced by the injury. Neo-intimal mass expands because of these processes and subsequently impinges on the coronary lumen. Some of the explanations include:

• Sometimes, atherosclerosis is considered as a form of benign neoplasia.

• There is higher intrinsic movement in restenotic-derived smooth-muscle cells than those derived from primary lesions. Lesions with high proportions of aggressive biological cells develop more stenosis than lesions without the same biological characteristics.

• Removing inhibitory influences. Generally, endothelial cells secrete heparan sulphate and nitric acid. Both inhibit smooth-muscle cell proliferation. They are removed by angioplasty (mechanical trauma) contributing to a proliferative setting.

• Inducting stimulatory influences. Platelets cause thrombosis at the injured site by adhering to the injured vessel. Various cytokines and free radicals that are released during vascular injury increase cell adhesion molecule expression.

• By activating the cell signal pathways, the cell moves from quiescent to proliferative state.

The Role of Nitric Acid in Coronary Restenosis Management
Renarrowing of the vessel, also called restenosis, is the main problem related to PTCA procedure. Non-steroidal anti-inflammatory drugs (NSAIDs) and Nitric acid (NO) play a role in this pathology. Several mechanisms that are involved in the restenotic process following coronary angioplasty are counteracted by nitric acid. Injury to the NO-dependent pathways occurs during restenosis. Nitric acid inhibits interactions between leukocyte-vessel wall, platelet adhesion and aggression, and mediates an anti-proliferative influence on smooth-muscle cells.

Since these effects are primarily dependent of dose, NO-releasing drugs are applied at high dosage in order to influence restenotic mechanisms. Convectional NO donors affect blood flow and pressure and because of these reasons they are not used in clinical practices. Methods for NO delivery are currently researched using modified NO-releasing stents, NO donors, and eNOS gene therapy.

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