WHAT HAPPENS DURING STENTING?

The stenting procedure takes place in a catheterization laboratory. To the patient, the “cath. Lab.” may resemble an operating room with its many monitoring devices, video displays and x-ray cameras. The patient will lie down on a table under an x-ray camera. He or she will be given a mild sedative and remain awake but relaxed for the duration of the procedure. Once the patient is comfortable, heart monitoring begins, an intravenous line (IV) is established and the area where the sheath is to be inserted is made sterile and locally anesthetized. The majority of stent procedures are performed via the femoral artery in the groin. However, the brachial artery in the arm or the radial artery in the wrist can be utilized as well. The injection of the local anesthesia may result in discomfort. An anticoagulant is then administered through the IV to prevent blood clot formation within the artery during the procedure. The guiding catheter is then advanced through the sheath to the heart and is positioned near the origin of the coronary artery. The physician will inject dye (contrast medium) through the catheter. The dye can be seen on a special x-ray (fluoroscope) and serves as a road map for the procedure. The physician and other attending medical staff may ask the patient to perform tasks such as coughing, turning the head, taking a deep breath or not speaking for a while. Guide wire is then passed through the catheter into the coronary artery and to the narrowing of the coronary artery. In most cases, the physician then performs a balloon angioplasty. Stenting is then performed. Equipped with a premounted stent, a balloon-tipped catheter is advanced to the target area. The balloon is inflated for several seconds to several minutes, expanding the stent, which adheres to the wall of the artery. The balloon catheter is removed while the stent remains permanently fixed to the artery.

REBLOCKAGE WHY DOES IT OCCUR?       

Over 1 million balloon angioplasty and stenting procedures are performed worldwide each year. While these procedures have a high rate of initial success, the chronic problem of restenosis develops in a large percentage of patients. Let’s examine the mechanisms that underlie the process of restenosis.

In standard angioplasty, a balloon is inserted into a coronary artery and inflated until the plaque is compressed and the lumen is enlarged.

The first mechanism of restenosis during angioplasty is “elastic recoil”, where the walls of the artery tend to spring back immediately after the procedure.

A second mechanism of restenosis is “chronic remodeling”. In remodeling, the vessel wall slowly contracts as it heals, producing a smaller lumen.

The third mechanism of restenosis involves excessive growth of smooth muscle tissue known as neointimal hyperplasia. Neointima consists of smooth muscle cells and surrounding matrix that proliferate in the vessel wall and migrate into the arterial lumen.

Now let’s see what happens when a stent is used during balloon angioplasty. The balloon delivers and expands the stent at the lesion, where it remains in place as a permanent scaffold. The stent is strong enough to prevent elastic recoil and chronic remodeling, but neointimal hyperplasia continues to be a problem because stents do not stop smooth muscle cell proliferation.

MECHANISMS

While true in-stent restenosis (ISR) represents a neointimal proliferative response to the implanted stent,’pseudo ISR’ may be due to a variety of mechanical factors, including acute recoil of neointimal tissue bck into the lumen, missing the lesion, stent crush, having the stent stripped off the balloon, and stent under expansion. Unlike restenosis after PTCA which is caused by a combination of acute elastic recoil, intimal hyperplasia, and negative vascular remodeling, ISR is almost exclusively the result of neointimal hyperplasia (growth of new cells). The placement of a stent leads to chronic, prolonged damage resulting in more exaggerated intimal growth and greater late lumen loss, compared with PTCA. In some individuals, contact allergy to certain ions released from stainless steel stents (eg nickel, chromat, and molybdenum) may potentially trigger ISR.

After the initial damage by the angioplasty balloon, ISR progresses through four distinct phases: thrombosis, inflammation, proliferation, and vessel remodeling. Focal thrombosis is universally observed after stent implantation, usually within the first 1 to 3 days, and is proportional to the depth of injury of the artery wall by the stent struts. Platelets and macropahges (body’s defence cells in blood) are believed to secrete a variety of growth factors, notably platelet-derived growth factor, which induce a brisk inflammatory reaction at the site of injury and encourage smooth muscle cell migration and proliferation, leading to the formation of the neointimal hyperplastic (excessive new cell growth) lesion. There is evidence from animal and human studies that the degree of inflammation and subsequent neointima formation is proportional to the degree of penetration of the vessel wall by the stent struts.

                                                                         

DRAWBACKS OF SURGERY                                                                                                                                                         

The cardiologist entered the examination room with a grim look on his face. After exchanging a few formalities, he came to the main reason for the consultation. “Mr. Rahul Sharma, I’ve reviewed your angiograms again, and there is no option. You will need to have a bypass surgery.” Rahul was clearly shaken. “But doctor, are you sure? I nearly died on the operating table the last time I had surgery. Are there no other operations? What about the balloon procedure, or new medications?”

“Rahul, I am really sorry. I know how much you dread the thought of surgery but there is simply no other option.”

Dialogues like this take place thousands of time each year. In spite of reblockages surgeons still perform bypass surgeries. The darling of heart specialists today, however, appears to be coronary angioplasty. Often referred to as the “balloon procedure” in lay circles, this technique opens up blocked heart arteries by forcibly opening a sturdy balloon inside the clogged vessels. The balloon inside the clogged vessels. The balloon flattens out the obstructing fatty deposits, and thus allows more blood to pass through the previously narrowed area. If the cardiologist believes there is a high likelihood of repeat closure of the artery, a stainless steel wire mesh circular tube, called a “stent”, will be placed where the angioplasty was performed to decrease the possibility of short-term repeated clogging.          

Many lay persons today have become so familier with both bypass surgery and angioplasty that they might think that Rahul is a bit childish to fear such well known therapies. Yet, experts who recognize the results of these common procedures would likely share Rahul’s sentiments. One of the greatest concern with these methods is that they do not address the underlying disease process. The disease causes a slow but steadily increasing blockage of major arteries. Bypass surgery and angioplasty do nothing to change this gradual accumulation of fatty deposits throughout the body. These high-tech procedures only “buy time” by addressing what are often the most life threatening areas of blockage- the blood vessels nourishing the heart. If the process of atherosclerosis is not addressed, the arteries that have been bypassed will again clog up; the vessels that have been angioplastied or stented will again be obstructed with fatty material.

                                                                                                                                                 

Hope you liked this article!

This article is written by Dr. Bimal Chhajer (India’s best heart doctor)