Balloon angioplasty of the coronary artery, or percutaneous transluminal coronary angioplasty (PTCA), was introduced in the late 1970's. PTCA is a non-surgical procedure that relieves narrowing and obstruction of the arteries to the muscle of the heart (coronary arteries). This allows more blood and oxygen to be delivered to the heart muscle. PTCA, is now referred to as percutaneous coronary intervention, or PCI, as this term includes the use of balloons, stents, and atherectomy devices. PCI is accomplished with a small balloon catheter inserted into an artery in the groin or arm, and advanced to the narrowing in the coronary artery. The balloon is then inflated to enlarge the narrowing in the artery. When successful, PCI can relieve chest pain of angina, improve the prognosis of patients with unstable angina, and minimize or stop a heart attack without having the patient undergo open heart coronary artery bypass graft (CABG) surgery.
Clinical indications and contraindications to PTCA
- Stable angina
- Unstable angina
- Anginal equivalent (eg, dyspnea, arrhythmia, dizziness/syncope)
- Acute myocardial infarction
- Objective evidence of reversible ischemia on the following:
- Resting electrocardiogram
- Positive result on exercise stress test
- Positive result on exercise or pharmacologic scintigraphy
- Stress echocardiography
- Holter monitoring
- Significant comorbidities (relative contraindication)
Angiographic indications and contraindications to PTCA
- Hemodynamically significant lesion in a vessel serving viable myocardium (vessel diameter >1.5 mm)
- Left main stenosis or left main equivalent stenosis (Coronary artery bypass graft [CABG] surgery is still the preferred treatment for left main stenosis. However, this area is rapidly evolving toward safe and feasible PCI options.)
- Chronic total occlusion (CTO) with the following:
- No proximal stump visible
- Extensive bridging collaterals present
- Diffusely diseased small-caliber artery or vein graft
- Other coronary anatomy not amenable to percutaneous intervention
Recent advances in guidewires, stents, and devices to cross chronically occluded arteries are evolving so that more patients with CTOs are now being successfully treated percutaneously.
POSSIBLE COMPLICATIONS AND RISK
With advancements in technique, devices, and adjuvant medical therapy, percutaneous transluminal coronary intervention is now associated with mortality and emergency bypass rates of less than 1%. Restenosis after balloon angioplasty requiring a second revascularization procedure is a major limitation occurring in about 30-50% of patients, depending on the definition of restenosis applied. Today, success rates are as high as 95% following conventional balloon angioplasty and are even higher with the use of DESs and adjunctive pharmacotherapy.
Acute complications. The mechanism by which balloon angioplasty or stenting improves luminal diameter is associated with significant local trauma to the vessel wall, which can in turn lead to occlusive complications in a minority of patients. Coronary artery dissection typically results from the vessel injury secondary to balloon expansion. Angiographic follow-up typically shows no residual evidence of a dissection as early as 6 weeks after angioplasty in most of the cases studied. However, larger dissections can lead to complications.
Abrupt vessel closure may occur in as many as 5% of balloon angioplasty cases and typically develops when compression of the true lumen by a large dissection flap occurs, thrombus formation, superimposed coronary vasospasm, or a combination of these processes. The presence of large coronary dissections immediately after balloon angioplasty is associated with a 5-fold increase in the risk of abrupt closure. This underscores the importance of a good postprocedure angiographic result on clinical outcomes.
Today, the use of intracoronary stents and new antiplatelet drugs has decreased the incidence of abrupt closure significantly (to <1%).>
Restenosis. Following balloon angioplasty or stent implantation, the vessel wall undergoes a number of changes. Platelets and fibrin adhere to the site within minutes of vessel injury. Within hours to days, inflammatory cells infiltrate the site and vascular smooth muscle cells begin to migrate toward the lumen. The vascular smooth muscle cells then hypertrophy and excrete an extensive extracellular matrix. During this period of vascular smooth muscle cell proliferation, endothelial cells colonize the surface of the lumen and regain their normal function. Over the course of several weeks to months, multiple forces interact to cause remodeling of the vessel wall with either a decrease in lumen diameter (negative remodeling) or an increase in lumen diameter (positive remodeling). The amount of late loss in lumen diameter is dependent on the amount of neointimal proliferation and the degree of remodeling following intervention. After 6 months, the repair process stabilizes and the risk of restenosis decreases significantly.
Today, DESs have reduced restenosis rates to less than 10%. Poststent lumen diameter and lesion complexity are still the major predictors of restenosis with these newer stents.
While DESs have significantly reduced restenosis events, concerns of stent thrombosis with these newer stents still exist. In fact, the rate of thrombosis with DES is virtually identical to that for bare metal stent (BMS) (0.4-1.5%). The biggest factor contributing to stent thrombosis is interruption of antiplatelet therapy. Another important factor is final stent diameter and area. Underdeployment or incomplete apposition of the DES may also increase the risk for stent thrombosis. This is extremely important because acute and subacute stent thrombosis often have a fatal outcome. Late stent thrombosis is another consideration. DES may take up to 4 years to endothelialize on the coronary vessel wall and discontinuing antiplatelet therapy may expose these patients to an increased risk for sent thrombosis over time.
Someother complications that might be happened are: severe bruising/bleeding into the groin area of the procedure leg, changes in your heart rhythm, allergic reaction to the contrast or dye or to other medications used, a tear in the lining of the artery which is being dilated, possibility of a heart attack during or following inflation of the balloon or stent implantation, and possibility of a blood clot in the artery in which the catheter is inserted.