

Faced with a growing understanding of the causes of coronary artery disease-CAD (hardening of the arteries of the heart) and its final outcome - myocardial infarction (heart attacks), the cardiology community has worked feverishly to develop new, better and less invasive ways to counter its devastating effects. Coronary bypass surgery was introduced in the mid-sixties (see Facts about Coronary Bypass Surgery), and rapidly became the mainstay in the treatment of symptomatic CAD. While marvelously successful, bypass surgery was then, and remains, a tremendously invasive technique, with significant operative and post-operative risks. As the underlying atherosclerotic process is not altered by surgery, many patients have found it necessary to undergo repeat bypass surgery two or three times, each time carrying a higher risk.
As an outgrowth of original investigations on catheter dilatation (stretching) of peripheral arteries (arteries of the arms or legs) by Dr. Charles Dotter in 1964, Dr. Andreas Gruentzig, of Zurich, Switzerland developed and first performed catheter based dilatation of human coronary arteries in September, 1977. Using a system of coaxial catheters (one catheter inside another), he was able to direct a very thin plastic tube with a deflated plastic balloon on its end, into a coronary artery, to the site of a narrowing, and then inflate the balloon, stretching and compressing the plaque material against the wall of the artery, allowing re-establishment of normal flow down the artery. All of this was performed with the patient awake but sedated, without the necessity for incisions or suturing (stitches), and with little or no post-procedural recovery period.
Over the next decade numerous technological improvements in equipment and cardiologists experience allowed PTCA (percutaneous transluminal coronary angioplasty) to expand world-wide into one of the most frequently performed hospital based procedures. Dr. Gruentzig's original equipment would only allow for dilatation of narrowings in the beginning-most portions of any of the three major coronary arteries, and only in arteries that were relatively large in size and straight in course. Subsequent improvements allowed cardiologists to treat arteries that were smaller in size, reach narrowings that were in branch vessels or far down stream, and to dilate blockages that were of greater length. These advances also allowed interventional cardiologists to treat completely occluded arteries, especially during the first hours of a heart attack.
The technique of PTCA is quite similar to that of a heart catheterization. The patient is given an intravenous sedative to help allay fears, after which a small, hollow, long plastic tube (the catheter) is inserted into the femoral artery (an artery in the groin), the brachial artery (an artery in the elbow crease), or the radial artery (an artery at the wrist). Usually, the artery is accessed without an incision, by inserting a special needle through previously anesthetized skin, into the artery. Using a flexible, soft-tipped wire as a guide, a catheter is exchanged for the needle. The catheter is then advanced under fluoroscopic (x-ray) guidance to the origin of the coronary arteries, at the beginning of the aorta, just above the heart. Once the tip of this guiding catheter is appropriately situated, contrast media (an iodine based dye) is injected into the artery in question and the narrowing is identified. Next, an ultra-thin guide wire (0.014"-0.018" in diameter) is advanced through the guiding catheter, into the coronary artery, and across the narrowed segment. A dilating catheter (the balloon) with a central lumen is then advanced over the guide wire to the precise area of arterial narrowing, and the balloon is inflated by a hand-held inflation device until it has reached its predetermined size. The balloon may be left inflated for seconds to minutes, but once deflated, it is withdrawn into the guiding catheter and more dye is injected into the artery to define the effect of the dilatation. (PTCA Video) After the artery in question is fully dilated, and no significant residual narrowing is seen, the balloon catheter, guide wire, and guiding catheter are removed from the body.
As experience has broadened and PTCA success rates have routinely exceeded 90%, several additional facts have became apparent:
1. Balloon angioplasty, as with bypass surgery, does not cure the underlying disease, but only alleviates a mismatch in the heart's supply and demand for blood. Once this mismatch is corrected, the atherosclerotic process continues and additional blockages may develop at other sites in the coronary arteries at a later date.
2. The initial successful result attained during balloon dilatation of an artery is a combination of stretching of the entire artery ("remodeling"), compression of plaque material against the arterial wall, and tearing of the plaque material ("dissection").
3. The injury created in the inner arterial wall triggers a very complex coagulation process that frequently leads to blood clot formation within the treated artery at the site of the PTCA. If not prevented by special medicines, this may cause a sudden and catastrophic arterial occlusion, resulting in a heart attack.
4. Angiography, always considered to be the "gold standard" of arterial visualization, is a fairly tarnished standard that misses much of the information obtained by other imaging techniques, such as intravascular ultrasound and angioscopy.
5. The arterial wall injury that is always a component of PTCA also triggers a "healing-type" process in which new material is laid down in the inner arterial wall, at the site of this injury. Excessive amounts of this material may accumulate, especially within the first six months post-PTCA, resulting in repeat narrowing (restenosis) in a large percentage of patients - 25-50%. When excessive, restenosis may require repeating the angioplasty.
6. Soft plaque is usually readily treated with PTCA, whereas densely calcified plaques, elongated plaques, and lesions containing large amounts of thrombus (clot), do not fair as well by plain balloon angioplasty.
The last decade of investigation in coronary angioplasty has seen many of these problems answered. Interventional cardiologists now regularly visualize the treated coronary artery with a combination of angiography and intravascular ultrasound. While angiography gives an excellent measure of blood flow rates, ultrasound allows for precise accuracy in measuring the size of the artery as well as the integrity of the dilated plaque. When the angiogram suggests that the artery is fully dilated, but the ultrasound shows that there is a significant tear in the arteries inner lining, additional work is done to assure that the artery will stay open. In fact, it was this knowledge that led to the development of intracoronary stents.
Coronary stents are metallic, tubular devices, compressed on a deflated angioplasty balloon, that expand into the wall of the artery when the balloon is inflated. Once the balloon is deflated, the stent remains expanded, and stays in the artery permanently. The stent acts as a scaphold, keeping any torn arterial inner lining from falling into the arterial lumen and blocking blood flow, as well as by reducing vessel wall remodeling. Many stents are either now available or are being tested and the majority are made of stainless steel. Some are shaped like a coiled spring, others like a slotted tube, and still others like the diamond pattern of a chain link fence. In general, stented vessels tend to have lower restenosis rates, and clearly have a lower incidence of sudden, acute closure.
Intense study of the coagulation system has resulted in the development of a variety of medications that can inhibit clotting inside the treated artery. Most of the medications now used before, during and after angioplasty reduce the adhesive properties (stickiness) of platelets (the microscopic blood particles that are primarily responsible in forming arterial clots). The use of some of these agents has also resulted in better short and long-term angioplasty results.
Atherectomy devices, tools that physically remove some of the plaque, have made the treatment of long calcified narrowings, or lesions containing considerable thrombus, more successful. A directional atherectomy catheter (DCA) has a miniature tubular blade that slices off layers of plaque and removes them from the body. The Rotablator atherectomy catheter is a diamond incrusted burr that spins at remarkably high speeds while drilling through hardened plaque, pulverizing the plaque into a fine dust. The TEC transluminal extraction catheter is a spinning cutter combined with a vacuum system to suck out the drilled particulate matter, especially thrombus, and the Possis Angiojet uses a very powerful suction apparatus to suck out thrombotic material from a diseased artery. Laser assisted angioplasty utilizes a high intensity laser to vaporize small quantities of plaque material. Each one of these new devices has its own unique indication, and each one is usually used in concert with balloon angioplasty.
Techniques to reduce or prevent restenosis are being heavily investigated. Some of these techniques involve impregnating stents with various drugs, delivering radiation directly to the injured inner arterial wall, and introducing genetic material directly into the injured tissue that will locally "turn off" the healing process.
It is most important to note that all of these exciting developments only allow us to buy time for an individual. Patients requiring any of these treatments, or bypass surgery, must aggressively work to change their life style; losing weight, ceasing all tobacco use, altering their diets to keep total and LDL cholesterol levels at their lowest possible levels, reducing elevated blood pressure, and, if necessary, deftly managing diabetes.
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