The use of percutaneous transluminal coronary angioplasty (PTCA) has increased exponentially during each of the last 5 years. Because PTCA is a procedure that can normally be under taken safely in the cardiac catheterization laboratory and which requires only a short hospital stay, its appeal is obvious. Until prospective randomized trails comparing PTCA with coronary bypass graft surgery or medical therapy are completed, however, subjective decisions concerning selection of patients for a particular form of treatment for coronary artery disease will continue.

The use of PTCA was initially confined to patients with proximal, discrete, and single-vessel coronary artery disease and objective evidence of coronary ischaemia in whom the success rate exceeds 90 per cent and complication rates are low.

PTCA is frequently used in patients with multivessel or complex single vessel disease. The latter is defined as anatomical lesions that have a high risk of occlusion or of dissection of the media during dilatation. These lesions may have evidence of calcification in the vessel wall, severe eccentricity of the lumen, thrombus formation near or at the site of stenosis, diffuse areas of occlusion, location of disease near the coronary ostia, ostial location, or may involve major vessel bifurcations, and areas of occlusion next to each other.

Disease of several coronary arteries increases the difficulty of PTCA. Some authorities define multivessel disease as at least one stenosis of 70 per cent in one artery and a stenosis of 50 per cent or more in another. Others define multivessel disease as 70 per cent stenosis in two vessels or more. The definition used substantially changes the assessment of outcome and long-term results of PTCA. Reported rates of complete revascularization may reach 40 to 50 per cent, but depend on the selection of patients (Table 1) 485.

The most common reason for failure to achieve complete revascularization is the presence of a chronic total occlusion or a lesion in a small vessel, which is not amenable to PTCA. In the National Heart Lung and Blood Institutes PTCA registry, at least one occluded vessel was present in 52 per cent of patients who had incomplete revascularization, whereas only 6 per cent of patients in whom complete revascularization was achieved had an occluded vessel. Whether complete revascularization is necessary or even important is controversial. Although some studies have shown lower incidences of death, myocardial infarction, and recurrent angina pectoris, other show that when differences in left ventricular function and degree of coronary disease are considered, the outcome in patients with complete and incomplete revascularization does not differ. The outcome of PTCA for patients with multivessel disease is shown in Table 2 486. Selection of patients might bias the long-term result of PTCA in patients with multivessel disease. Clinical results are difficult to assess without angiography because of differences in end-points and between subsets of patients used for analysis. However, the incidence of death is less than 5 per cent, and that of non-fatal myocardial infarction is less than 3 per cent. Sixty per cent of patients are asymptomatic at follow-up. Restenosis occurs in approximately 25 to 35 percent of patients, and repeat PTCA may be necessary in up to 30 per cent of patients. An initial PTCA may therefore only be the first step in the treatment of a patient with multivessel disease. Long-term analysis of patients who have undergone multiple PTCA procedures in different vessels is also confounded by progression of coronary disease in the same vessels or in other sites of the coronary vasculature.

Restenosis may only play a small part in the recurrence of symptoms: the concept of the ‘culprit lesion’ has been advanced. The culprit lesion can be identified reliably by electrocardiographic evidence of ischaemia, radionuclide imaging, or by angiographic assessment. Following treatment of only this lesion, 17 per cent of patients had recurrent angina during a mean follow-up in 16 months. However, new occlusions causing myocardial infarction only rarely occur at the site of the most severe pre-existing stenosis. Thus, the ability to predict which may be the culprit lesion for future ischaemic events is low.

PTCA is highly successful in the treatment of unstable angina pectoris (progressive angina or new onset angina, chronic angina of increasing severity, angina at rest, early post-infarction angina). However, major complications appear to be more common in such patients, due to thrombosis at the site of coronary stenosis or instability of the atherosclerotic plaque. Urgent surgery is required in 3 to 12.5 per cent of patients treated with PTCA for unstable angina, and the incidence of infarction is more than 5 per cent. Recurrent angina pectoris occurs in approximately one-third of the patients within 6 to 12 months. Because of the high incidence of complications, restenosis, and recurrence of angina, unstable angina should be treated with pharmacological agents, followed by rapid revascularization by either PTCA or surgery.

PTCA for total coronary occlusions is appropriate if the occlusion is recent (within 6 months), if the vessel stump is visible at angiography, and if the patient has symptoms and limitation of activity because of ischaemia related to the occluded vessel. In many patients retrograde or antegrade collaterals to the distal vessel maintain viability of the myocardium at risk. The decision to use PTCA should weigh the duration and length of the occlusion (the risk of the procedure) against the risks of the current symptoms and the limitations produced by coronary insufficiency. The amount of viable myocardium at risk must also be considered.

To achieve successful recanalization a guidewire must be advanced antegrade through the site of total occlusion until the distal vessel lumen is encountered and entered. Once the guidewire has traversed the lesion, progressively larger dilating balloon catheters are advanced over it until an adequate lumen is achieved. Injection of contrast material is necessary to establish that the wire is in the distal lumen. About 50 per cent of totally occluded arteries can be successfully recanalized. Duration of an occlusion is an important predictor of success. Complications following attempts at recanalization are low, presumably because most myocardium at jeopardy is protected by collateral circulation. Nevertheless, side-branch occlusion, embolism, or perforation of coronary arteries are hazards associated with this technique. The major problem with recanalization of completed occluded coronary vessels using PTCA is recurrence, which occurs in 55 per cent of patients (range 20–75 per cent). This restenosis rate is approximately twice as high as that following PTCA of open vessels.

Recurrence of coronary insufficiency after coronary bypass graft surgery is common. It is due to both new sites of disease and to progression of native coronary atherosclerotic disease in both grafted and ungrafted vessels. Many patients who have undergone coronary bypass graft surgery become candidates for PTCA.

Progression of disease in native coronary arteries occurs in 5 per cent of patients annually. Saphenous vein bypass grafts have a 10 to 20 per cent incidence of occlusion during the first year after surgery and a 2 per cent per year occlusion rate thereafter. At about 10 years, only 40 per cent of vein grafts are free of significant stenoses. The results of angioplasty in bypass conduits is not as certain as the results of PTCA of native coronary vessels. Outcome is dependent on the underlying variety of occlusive disease, which in turn is dependent on the ‘age’ of the bypass conduit.

Although intimal thickening is common in vein grafts, even early after coronary artery bypass graft surgery, early stenosis is most often caused by technical problems with surgery, thrombus formation, or both. Fibroproliferative lesions, which are relatively focal, occur 3 to 5 years after implantation. Degenerative atherosclerotic plaques appear in vein grafts thereafter. The plaques are frequently composed of foam cells and cholesterol crystals as well as friable necrotic debris. Plaques in vein grafts more than 5 years old may be more diffuse, and prone to distal embolization if angioplasty is performed. Thus, older grafts are not candidates for treatment with angioplasty unless lesions are focal and of recent onset. Other therapies, such as laser angioplasty, are likely to be more applicable for treatment of old and diffuse bypass lesions. The restenosis rate is higher than that in native coronary arteries, ranging from 25 to 50 per cent.

Ostial lesions at the aortic anastomosis site are difficult to treat with angioplasty because of elastic recoil of the aorta and focal fibroproliferative disease. Lesions in mid- or distal saphenous vein grafts, particularly at the insertion site with the native coronary artery, are best treated with angioplasty. PTCA of internal mammary artery stenoses after implantation into the left anterior descending or left anterior descending diagonal coronary artery has become possible with recent technical advances, requiring stiffer guidewires. Although lesions may occur along the length of the internal mammary artery graft, most are found at the anastomosis of the mammary with the native coronary artery. The lesions often occur early after surgery and are responsive to PTCA.

The major risk of internal mammary artery angioplasty is dissection of the artery, particularly where it leaves the left subclavian system. Spasm may occur, though this is treatable with intra-arterial nitrates. The short-term results of angioplasty of lesions in the internal mammary artery are promising.

Atherectomy (transcatheter selective excision and removal of atheromatous material or tissue causing restenosis) was developed to overcome some of the drawbacks of PTCA. Following PTCA, coronary occlusion due to focal dissection, restenosis, eccentric lesions, ulcerated lesions and lesions exhibiting calcification, lesions longer than 1 cm in length, and lesions in left main locations or old bypass grafts, as well as ostial lesions cannot easily be treated with further PTCA. Atherectomy devices have been designed that are coaxial over a guidewire system: these remove tissue by directional shaving, using a high-speed (150000 r.p.m.) rotating catheter with an abrasive tip, which pulverizes atherosclerotic plaque, or by extractive atherectomy using a conical cutter. The latter may be used with simultaneously applied suction, and extract plaque fragments. All of these devices can be used successfully to open segments of coronary arteries not suitable for PTCA, but technological advances will be necessary before catheters can be made small enough and flexible enough to treat more than proximal lesions in the coronary circulation.

Coronary bypass graft stenosis may be better treated with atherectomy than angioplasty because of the embolization risk mentioned previously. Long-term results in patients who have undergone atherectomy are still sparse: however, restenosis is still a problem. At present the use of extraction atherectomy is limited to eccentric lesions or proximal lesions in the coronary vasculature which are not ideally treated with angioplasty.

The placement of stents in the coronary vasculature or in the peripheral vasculature was envisioned in the late 1960s when Dotter experimentally implanted metal spirals into arteries. Palmaz and coworkers have developed a balloon expandable stent of deformable metal which has been successful in human trials. Rubin and Gianturco have designed a balloon expandable stent which has been most frequently used to maintain patency of vessels that are dissected at the time of PTCA to prevent acute coronary occlusion. A self-expanding mesh stent has been proposed by Sigwart.

Stenting of coronary vessels might be feasible for the short-term prevention of acute occlusion after unsuccessful PTCA. However, thrombosis is common in stents with large surface areas, and high doses of anticoagulants are needed to maintain patency of the stented region. Restenosis appears to be as much of a problem after stenting as after PTCA itself. Stents may enlarge the coronary lumen enough to prevent ingrowth that would normally narrow the native coronary artery from impacting sufficiently on the coronary lumen. If the proliferative response can be minimized, possibly by antiproliferative agents or other chemicals incorporated in stent material, stenting may become used more widely. The coating of stents with biologically active agents to prevent thrombosis and cellular ingrowth is a subject of intense investigation. Until the ease of deployment and longer follow-up of stented arteries is available, however, only selected patients should be considered for this treatment.

Treatment of atheroslerotic lesions using catheter-guided laser energy has taken many forms. Laser thermal angioplasty in which laser light is used to heat a metal tip on the catheter can be used to ablate atherosclerotic material. Laser thermal angioplasty initially seemed to hold great promise, but the incidence of perforation and difficulty in passing the laser probe through tortuous lesions have reduced the feasibility of the procedure in most patients with coronary artery disease. Treatment of peripheral atherosclerotic lesions has a high success rate, however. Doppler scanning and clinical evaluation show good improvement in more than 75 per cent of patients at 1 year.

The excimer laser (using 308 nm energy) is undergoing clinical trials for use in coronary angioplasty and bypass graft angioplasty. The advantage of excimer laser angioplasty is that the pulsed energy ablates tissue with a minimal thermal effect. There is a direct correlation between the number of pulses and the depth of ablation, making precise calculation of the depth of plaque ablation possible. Even distal lesions in the coronary vasculature can be treated with small laser probes (1.3, 1.6, 2.0 mm in diameter).

According to the excimer laser coronary angioplasty registry in the United States, 75 to 97 per cent of attempts are successful. A 20 per cent reduction of diameter in stenosis was achieved in 75 per cent of patients in whom the 1.3 mm probe was used, 92 per cent of patients in whom the 1.6 mm probe was used, and 95 per cent of patients in whom the 2.0 mm probe was used. A channel diameter of more than 1 mm was achieved with the 1.6 mm probe and of more than 1.5 mm with the 2.0 mm probe. There was no difference in success rates according to site of the lesion within the coronary arteries. Coronary stenoses were more easily treated (92 per cent success rate) than coronary occlusions (85 per cent). Laser angioplasty is particularly suitable for lesions longer than 1.5 cm and for eccentric lesions. Clinical complications are few. Myocardial infarctions have occurred in less than 1 per cent of the patients. Emergency coronary artery bypass graft surgery was necessary in 1 per cent, and 0.3 per cent died. In many patients, laser angioplasty using a 1.6 or 2.0 mm probe alone was sufficient to produce adequate patency of the vessel and a residual of less than 50 per cent. In many situations, however, the laser probe does not produce a lumen size adequate to maintain patency of the coronary artery. A combination of laser angioplasty followed by balloon PTCA has been particularly useful.

Follow-up studies of laser angioplasty are incomplete. Issues of restenosis, and recurrent angina pectoris due to inadequate ablation remain to be clarified. The use of laser energy to treat coronary lesions is therefore still under development, but with refinement of technology it should serve as an adjunct to PTCA in many instances, and serve as an alternative for treating atherosclerotic lesions in others.

Percutaneous mitral balloon valvotomy is an alternative to surgical commissurotomy for patients with symptomatic mitral stenosis. There are many variations of the procedure. The use of single expandable balloons, the double balloon technique, retrograde placement of two balloons, trefoil balloons, and two trans-septal punctures all allow adequate commissurotomy of a stenotic mitral valve. The antegrade approach, using trans-septal puncture to gain access to the stenotic mitral valve is most commonly used. The sequence of double balloon mitral valvotomy is shown in Fig. 1 1666. Two balloons are placed across the stenotic mitral valve and inflated simultaneously. Placement is facilitated by positioning two guidewires across the valve before the catheters are advanced.

All patients with symptomatic mitral stenosis are potential candidates for percutaneous mitral balloon valvotomy. Careful transthoracic two-dimensional and Doppler echocardiographic examination is important when selecting patients for the procedure. Valve rigidity, thickening, calcification, and subvalvular agglutination are graded 0 (least) to 4 (most): the sum of the gradings of these four components gives a ‘score’. Patients with a cumulative score of 8 or less are good candidates for percutaneous mitral balloon valvotomy. The procedure has variable success in patients with a score between 9 and 11: many have valves that are too thickened or have too much subvalvular fibrosis to allow opening by balloon techniques. Percutaneous mitral balloon valvotomy should only be undertaken in a patient with an echocardiographic score greater than 12 if he or she is not fit for surgery. Contraindications to percutaneous mitral balloon valvotomy include evidence of left atrial thrombus, severe mitral valve calcification, severe subvalvular agglutination, or the presence of left ventricular thrombus in or near an area of old myocardial infarction. Patients with atrial fibrillation should receive anticoagulation therapy with warfarin for 2 to 3 months before balloon valvotomy. The presence of left atrial thrombus should be excluded by echocardiography. A transoesophageal echocardiogram may allow better visualization of the left atrium. If left atrial thrombus is suspected, percutaneous mitral balloon valvotomy should not be performed.

Immediate haemodynamic and clinical improvement occur in the majority of patients, accompanied by a mean increase in mitral valve area from 0.9 to approximately 2.0 cm². Pulmonary vascular resistance falls gradually over the first 24 h following the procedure. A final mitral valve area of 1.5 cm² or more can be expected in more than 90 per cent of patients with echocardiographic scores of 8 or less. Only 52 per cent of patients with a higher score will have a satisfactory result. Valve thickening and calcification appear to be the major predictors of outcome (Fig. 2) 1667.

Percutaneous mitral balloon valvotomy produces marked functional improvement in most patients. The best long-term functional, echocardiographic, and haemodynamic results are seen in patients with echocardiographic scores of less than 8. Figure 3 1668 shows the post-treatment New York Heart Association classification of 119 patients whose initial echocardiographic scores were less than 8: 83 per cent of patients were class I and 13 per cent were class II (follow-up 17 &plusmin; 0.6 months).

Complications related to trans-septal catheterization include pericardial tamponade, which occurs in less than 1 per cent of patients and is usually treated successfully by pericardiocentesis in the catheterization laboratory without the need for emergency surgery. Cardiac pulsations should be observed fluoroscopically before the beginning of the procedure. If hypotension occurs in association with diminished cardiac pulsations, tamponade is present. The balloon valvotomy procedure itself carries a mortality rate of less than 1 per cent; the incidence of systemic embolism, including stroke, is also less than 1 per cent. Fewer than 1 per cent of patients develop severe mitral regurgitation. However, more than 15 per cent of patients develop a left to right shunt through the created atrial communication. Two-thirds of these close spontaneously within 6 months. If left atrial pressure remains high (usually because of an inadequate mitral valvotomy) a persistent shunt may be present. If surgical repair is contemplated, the surgeon should be aware of the possibility of finding an atrial septal defect, and closure should be undertaken at the time of mitral valve surgery.

Mitral regurgitation is increased in approximately half of all patients undergoing percutaneous mitral valvotomy: this is usually slight. Severe mitral regurgitation is usually caused by tearing of a mitral leaflet, ruptured chordae, or rupture of a papillary muscle. The increase in regurgitation seems to be related to the balloon size used. A ration of effective balloon dilating area to body surface area between 3.2 and 3.8 cm².m² maximizes the degree of mitral valve opening and minimizes the development of mitral valve regurgitation.

Although early studies showed that percutaneous balloon aortic valvuloplasty improved both aortic valve area and symptoms of aortic stenosis, there is a high rate of restenosis within 1 year of the procedure.

Most commonly, 15 to 23 mm dilating balloon catheters are passed retrogradely over guidewires in the left ventricular apex. The balloon sizes should be increased until transient hypotension occurs with inflation, indicating that the aortic outflow tract has been completely occluded by the expanded balloon. If the aortic gradient is not sufficiently decreased, a larger balloon may produce a better result, but too large a balloon may produce aortic outflow tract rupture or aortic regurgitation. In patients with severe iliac occlusive disease, a trans-septal antegrade approach to aortic valvuloplasty produces similar results to those obtained with the retrograde approach.

Final aortic valve areas are usually around 1 cm². In one series, 27 per cent of the patients had final aortic valve areas above 1cm², 32 per cent had valve areas of 0.8 to 0.9 cm², and 41 per cent had valve areas of 0.7 cm² or less.

Although approximately half of the patients show improvement in symptoms (New York Association classification) immediately after the procedure, symptoms usually recur within 6 months to 1 year.

It has proved difficult to identify the subset of patients with symptomatic aortic stenosis who benefit most from the procedure. The initial systolic function of the left ventricle and the haemodynamic results following percutaneous balloon aortic valvuloplasty are the best predictors of long-term improvement. The aetiology of the aortic stenosis may also be important: in patients with an element of rheumatic disease and commissural fusion of the aortic valve, commissural opening produced by the expanding balloon will produce better long-term results. Lysis of commissural fusion is also the mechanism underlying clinical improvement in children with congenital aortic stenosis following treatment with percutaneous balloon aortic valvuloplasty. In patients with degenerative calcific aortic stenosis, cracking of calcific deposits within the valve produces only transient increases in valvular mobility. Percutaneous balloon aortic valvuloplasty has little effect on the mortality of patients with aortic stenosis, but the quality of life is improved in approximately 50 per cent (Table 3) 487.

The procedure is suitable for use in patients who are not candidates for aortic valve replacement, but who have an urgent need for surgical treatment of disease affecting other organs in the face of severe aortic stenosis, and those with severe heart failure, who need intervention before valve replacement.

Balloon valvotomy has now replaced surgery as the treatment of choice for treating pulmonary stenosis. The patient is treated under local anaesthesia in the cardiac catheterization laboratory: the approach is percutaneous, transfemoral through the femoral vein, and antegrade across the stenotic pulmonic valve. A guidewire is placed in the distal pulmonary artery and a balloon valvotomy catheter is advanced over an exchanged wire. The use of a balloon with an inflated diameter 30 to 50 per cent larger than the diameter of pulmonary valve annulus size maximizes the effectiveness of the valvotomy and minimizes the chance of injury to the pulmonary valve annulus or outflow tract.

In patients with pulmonic stenosis, balloon pulmonary valvotomy provides excellent relief of outflow tract obstruction with a reduction of the peak systolic gradient in most patients to 30 mmHg or less.

Complications of the procedure are rare. Perforation of the right ventricular outflow tract can occur. Right bundle branch block and premature ventricular contractions are common, but there are no reports of long-term rhythm disturbances or conduction defects after the procedure. Arterial blood pressure transiently decreases, but returns to normal promptly when the balloon is deflated. Use of a double balloon technique may minimize hypotension during the procedure by allowing blood flow past the adjoining segments of the two balloons.

Balloon pulmonary valvotomy is indicated in any patient with isolated pulmonic stenosis whose resting peak gradient is more than 50 mmHg in the presence of a normal cardiac output. Patients with dysplastic pulmonary valves and those in whom the valve annulus is hypoplastic may require cardiac surgery for relief of right ventricular obstruction.

Ambrose JA, Tannenbaum MA, Alenopoulos A. Angiographic progression of coronary artery disease and the development of myocardial infarction. J Am Coll Cardiol 1988; 12: 56–62.

Babic UU, Pejcic P, Djurisic Z, Vucinic M, Grujici SM. Percutaneous transarterial balloon valvuloplasty for mitral valve stenosis. Am J Cardiol 1986; 57: 1101–4.

Block PC, Palacios IF. Comparison of hemodynamic results of antegrade versus retrograde percutaneous balloon aortic valvuloplasty. Am J Cardiol 1987; 60: 659–62.

Block PC, Palacios IF. Clinical and hemodynamic follow-up after percutaneous aortic valvuloplasty in the elderly. Am J Coll Cardiol 1988; 62: 760–3.

Block PC, Cowley MJ, Kaltenbach M, Kent KN, Simpson J. Percutaneous angioplasty of stenoses of bypass grafts or of bypass graft anastomotic sites. Am J Cardiol 1984; 53: 666–8.

Block PC, Palacios IF, Jacobs M. The mechanism of successful percutaneous mitral valvotomy in humans. Am J Cardiol 1987; 178: 179.

Bourassa MG, Enjalbert M, Campeau L, Lesperance J. Progression of coronary artery disease between 10 and 12 years after coronary artery bypass graft surgery. In: Roskamann H, ed. Prognosis of Coronary Heart Disease. Progression of Atherosclerosis. Berlin: Springer Verlag, 1983: 150.

Cowley MJ, Vetrovec GW, DiSciascio G, Lewis SA, Hirsch PD, Wolfgang TC. Coronary angioplasty of multiple vessels: short term outcome and long term results. Circulation 1985; 72: 1314.

deFeyter PJ, et al. Emergency coronary angioplasty in refractory unstable angina. N Engl J Med 1985; 313: 342–7.

Deligonul U, Vandormael MG, Kern MJ, Zelman R, Gelan K, Chartman BR. Coronary angioplasty: a therapeutic option for symptomatic patients with two and three vessel coronary disease. J Am Coll Cardiol 1988; 11: 1173.

DiSciascio G, Cowley MJ, Vetrovec GW, Kelly KM, Lewis SA. Triple vessel coronary angioplasty: acute outcome and long term results. J Am Coll Cardiol 1988; 12: 42.

Dorros G, Lewin RF, Jenkl L. Multiple lesion transluminal coronary angioplasty in single or multivessel coronary artery disease: acute outcome and long-term effect. J Am Coll Cardiol 1987; 10: 1007.

Fawzi ME, Mercer EN, Dunn B. Late results of pulmonary balloon valvuloplasty in adults using double balloon technique. J Intervent Cardiol 1988; 1: 35–42.

Fitzgibbon GM, Burton JR, Leach AJ. Coronary artery bypass graft fate. Angiographic grading of 1400 consecutive grafts early after operation and after one year. Circulation 1978; 57: 1070.

Gruentzig AR, Senning A, Siegenthaler WE. Non-operative dilatation of coronary artery stenosis: percutaneous transluminal angioplasty. N Engl J Med 1979; 301: 61.

Hartzler GO, Rutherford BD, McConahy DR, Johnson WL, Giorgi LV. ‘High-risk’ percutaneous transluminal angioplasty. Am J Cardiol 1988; 61: 33G.

Kan JS, White RI, Mitchell SE, Gardner T. Percutaneous balloon valvuloplasty: a new method for treatment of congenital pulmonary valve stenosis. N Engl J Med 1882; XX: 540–2.

Letac B, Cribler A, Konig R, Bellefleur J-P. Results of percutaneous transluminal vavuloplasty in 218 adults with valvular aortic stenosis. J Am Coll Cardiol 1988; 598: 605.

Little WC, Constantinescu M, Applegate RJ. Can coronary angiography predict the site of a subsequent myocardial infarction in patients with mild to moderate coronary artery disease? Circulation 1988; 78: 1157–66.

Litvack F, et al. Percutaneous excimer laser coronary angioplasty. Lancet 1989; ii: 102–3.

Litvack F, et al. Percutaneous excimer laser coronary angioplasty: results of the first 110 procedures. J Am Coll Cardiol 1990; 15: 25A.

Locke JE, Kajlilullah M, Shrivasta S, Bahl V, Keane JF. Percutaneous catheter commissurotomy in rheumatic mitral stenosis. N Engl J Med 1985; 313: 1515–8.

Mobin TA, et al. Follow-up clinical results in patients undergoing percutaneous transluminal angioplasty. Circulation 1985; 71: 754.

Meier B. Chronic total occlusion. In: Meier B, ed. Coronary Angioplasty. Orlando: Grune and Stratton, 1987: 190–9.

Melchior JP, et al. Percutaneous transluminal coronary angioplasty for chronic total coronary arterial occlusions. Am J Cardiol 1987; 59: 535–8.

Myler RK, et al. Multiple vessel coronary angioplasty: classification, results and patterns of re-stenosis in 494 consecutive patients. Catheterization Cardiovasc Diagnosis 1987; 13:1.

Nobuyoshi M, et al. Re-stenosis of successful percutaneous transluminal coronary angioplasty. Serial angiographic follow-up of 229 patients. J Am Coll Cardiol 1988; 12: 616.

Palac RT, et al. Progression of coronary artery disease in medically and surgically treated patients 5 years after randomization. Circulation 1981; Suppl. II: II–17.

Palacios IF, Block PC, Wilkins GT, Weyman AE. Follow-up of patients undergoing mitral balloon valvotomy. Analysis of factors determining re-stenosis. Circulation 1989; 573: 579.

Reeder GS, Holmes DR Jr, Detre K, Castigan T, Kelsey SF. Degree of revascularization in patients with multivessel coronary disease: a report from the National Heart, Lung and Blood Institute Percutaneous Transluminal Coronary Angioplasty Registry. Circulation 1988; 77: 638.

Roth RB, Block PC, Palacios IF. Percutaneous aortic balloon valvuloplasty: its role in the management of patients with aortic stenosis requiring major non-cardiac surgery. J Am Coll Cardiol 1989; 13: 1039–41.

Roth RB, Block PC, Palacios IF. Mitral regurgitation after percutaneous mitral valvuloplasty: predictors and follow-up. Circulation 1988; 78: 1947A.

Roubin GS, et al. Early and late results of intracoronary arterial stenting after coronary angioplasty in dogs. Circulation 1987; 76: 891–7.

Safian RD, et al. Balloon aortic valvuloplasty in 170 consecutive patients. N Engl J Med 1988; 319: 125–30.

Sanborn TA, et al. Peripheral laser assisted balloon angioplasty: initial experience in 219 peripheral arteries. Arch Surg 1989; 124: 1099–1103

Serruys PW, et al. Elective PTCA of totally occluded coronary arteries not associated with acute myocardial infarction. Short term and long term results. Eur Heart J 1985; 6: 212.

Sjharma B, Wyeth RP, Koltah GS, Giminez HJ, Franciosa JA. Percutaneous transluminal coronary angioplasty of one vessel for refractory unstable angina pectoris. Br Heart J 1988; 59: 280–372.

Shimshack TM, et al. Application of percutaneous transluminal angioplasty to the internal mammary artery graft. J Am Coll Cardiol 1988; 12: 1205–14.

Sigwart U, Puel J, Mirkovitch V, Joffre F, Kappenberger L. Intravascular stents to prevent occlusion and restenosis after transluminal angioplasty. N Engl J Med 1987; 316: 701–6.

Stigwart U, et al. Emergency stenting for acute occlusion after balloon angioplasty. Circulation 1988; 78: 1121–7.

Simpson JB, Johnson DE, Braden LJ, Gifford HS, Thapliyal HV, Selmon MR. Transluminal coronary atherectomy (TCA): results in 21 human cadaver vascular segments. Circulation 1986; 74: 202.

Simpson JB, et al. Transluminal atherectomy for occlusive peripheral vascular disease. Am J Cardiol 1988; 61: 96G–101G.

Thomas ES, Most AS, Williams EO. Coronary angioplasty for patients with multi-vessel coronary artery disease: follow-up of clinical status. Am Heart J 1988; 115: 8.

Timmis AD, Griffin B, Crick JCP, Sowton E. Early percutaneous transluminal coronary angioplasty in the management of unstable angina. Int J Cardiol 1987; 14: 255–31.

Wohlgelernter D, Cleman M, Highman HA, Zaret BL. Percutaneous transluminal coronary angioplaty of the ‘culprit lesion’ in management of unstable angina pectoris in patients with multivessel coronary artery disease. Am J Cardiol 1986; 58: 460.