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Catheter balloon valvuloplasty of stenotic aortic valves has met with generally poor short- and long-term clinical results. Part of this problem resides with the lack of recognition of various etiologies of aortic stenosis. Part I of this review discusses the various etiologies of aortic stenosis and provides an anatomic basis for successful valve dilation. Results of an in vitro study indicate stenotic aortic valves are dilated by various mechanisms (cracking, stretching) based in part upon the etiology of the aortic valve stenosis.

This report describes clinical, morphologic and histologic findings at necropsy late (range 1.6 to 24.1 months [average 8.2 months]) after clinically successful coronary balloon angioplasty in 20 patients with coronary angioplasty restenosis. Clinical evidence of restenosis occurred in 14 patients (70%), including 6 patients with sudden coronary death. Of the 20 patients, 14 (70%) had a cardiac cause of death and 6 (30%) had a noncardiac cause of death. Two major subgroups of histologic findings were observed: 1) intimal proliferation (60%), and 2) atherosclerotic plaque only (40%). Of the eight sites with atherosclerotic plaque only, six were eccentric lesions and two were concentric lesions. No morphologic evidence of previous angioplasty injury (cracks, breaks, tears) was observed in the eight patients with atherosclerotic plaque only. Proposed mechanisms for the development of intimal proliferation involve the reaction of smooth muscle cells and platelets, whereas elastic recoil of overstretched eccentric or concentric atherosclerotic lesions represents the most likely explanation for the findings in the latter subgroup. On the basis of these morphologic findings at angioplasty restenosis sites, specific treatment strategies for restenosis after coronary artery balloon angioplasty are proposed.

This report describes clinical, morphological, and histological findings late (1.6-24.1 months [average, 8.2 months]) after clinically successful coronary balloon angioplasty in 20 necropsied patients with coronary angioplasty restenosis. Clinical evidence of restenosis occurred in 14 (70%) of patients, including six patients with sudden coronary death. Of the 20 patients, 14 (70%) had cardiac causes of death and six (30%) had noncardiac causes of death. Two major subgroups of histological findings were observed: 1) intimal proliferation (60%) and 2) atherosclerotic plaques only. Of the eight sites with atherosclerotic plaques only, six were eccentric lesions and two were concentric lesions. No morphological evidence of previous angioplasty injury (cracks, breaks, or tears) was observed in the eight patients with atherosclerotic plaques only. Proposed mechanisms for the development of intimal proliferation involve the reaction of smooth muscle cells and platelets, whereas elastic recoil of overstretched eccentric or concentric atherosclerotic lesions represents the most likely explanation for the findings in the latter subgroup. On the basis of these morphological findings at angioplasty restenosis sites, specific treatment strategies for coronary artery balloon angioplasty restenosis are proposed.

This report provides the anatomic basis for catheter balloon valvuloplasty procedures. The morphologic hallmark of mitral stenosis is commissural fusion and the major mechanism of successful balloon valvuloplasty is commissural splitting. Single and double dilating balloons are used to increase the cross-sectional orifice area of stenotic mitral valves. Double balloons appear to improve the luminal diameter and cross-sectional area compared with single balloons. This report also illustrates the anatomic basis for single and double balloon catheter placement and position using the transseptal approach.

Despite widespread use of coronary balloon angioplasty, advances in angioplasty technology, and improvements in operator technique, restenosis at the angioplasty site is the major problem limiting the long-term efficacy of this procedure. The article reviews morphologic-histologic observations at angioplasty restenosis sites, speculates about the connection between the acute injury patterns of balloon angioplasty and the development of restenosis, and briefly reviews the currently understood pathways to restenosis and possible approaches to its reduction or elimination.

Percutaneous transluminal coronary angioplasty (PTCA) was performed unsuccessfully, resulting in disruption and near-total closure of the proximal right coronary artery at the site of stenosis following balloon inflation. The artery could not be reopened in the catheterization laboratory despite intracoronary nitroglycerin, sublingual nifedipine, and multiple balloon inflations. Myocardial revascularization surgery was immediately performed with excellent graft flow. No apparent myocardial infarction resulted. Catheterization performed at one year showed normal left ventriculography, total occlusion of the bypass graft, and reopening and normalization of the right coronary artery at the site of PTCA-induced occlusion. Possible mechanisms for this phenomenon and its clinical implications are discussed.

This report updates the current indications, techniques and investigational devices used in a busy interventional cardiology practice. Specific attention is devoted toward the problem areas of thrombolytic treatment of acute myocardial infarction, restenosis after angioplasty and the use of angioplasty in the treatment of multivessel coronary artery disease.

Direct myocardial revascularization surgery using either the saphenous vein or internal mammary artery has become the definitive surgical treatment for coronary artery occlusive disease. Certain patients who have undergone these procedures, however, have recurrent myocardial ischemia due to progression of disease in unbypassed vessels, to obstruction in the arteries distal to the insertion of the bypass conduit, or to disease of the conduit itself. Balloon angioplasty may be used to relieve myocardial ischemia in these situations; however, initial studies suggested a low primary success rate coupled with excessive mortality and morbidity. Improvements in patient selection, equipment and technical expertise now allow angioplasty to be performed in this patient population with results comparable to that in the general coronary angioplasty population. Of the 3,016 angioplasty procedures performed between September 1980 and June 1987, 236 patients had previously undergone revascularization surgery. The primary success rate was 93% (390 of 419 stenoses successfully dilated). Overall, clinical restenosis was observed in 39%, including a 43% restenosis rate in patients undergoing only saphenous vein graft angioplasty. This did not differ appreciably from the restenosis rate in postbypass patients undergoing angioplasty of only native vessels (37%) or internal mammary arteries (42%). Emergency revascularization surgery was required in 7 of 236 patients (3%), each of whom had myocardial infarction. One of 236 patients (0.4%) died. Thus, angioplasty may be used to relieve recurrent myocardial ischemia in patients with prior direct myocardial revascularization procedures with a high initial success rate and acceptable risk. Early (less than 6 months) restenosis is not infrequent and remains the largest obstacle to a satisfactory clinical outcome.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute dissection of the left main coronary artery during diagnostic cardiac catheterization with selective coronary arteriography is an uncommon but recognized complication of the procedure. That similar dissection may occur during percutaneous transluminal coronary angioplasty is less well recognized. This report describes two cases of left main coronary dissection resulting in acute occlusion that occurred during percutaneous transluminal coronary angioplasty and demonstrates that survival with essentially complete functional recovery may result if immediate surgical intervention is undertaken. Recognition and treatment of this potentially catastrophic complication of angioplasty is described.

Percutaneous transluminal coronary angioplasty is an effective technique for the treatment of selected patients with ischemic heart disease due to coronary artery stenosis. Successful angioplasty in saphenous vein bypass grafts has been documented, but little experience has been reported using angioplasty in internal mammary artery to coronary artery bypass grafts. Nine of ten patients with stenosis in the internal mammary artery to coronary artery anastomosis or in the coronary vessel distal to the anastomosis site were successfully treated with angioplasty. One patient developed restenosis 1 month after the procedure, and a repeat angioplasty was successful. In one patient, the balloon catheter could not be advanced through the left internal mammary artery to the stenosis site. Technical features of internal mammary artery angioplasty are discussed, including the use of specially designed guiding wires, guiding catheters, and balloon catheters that facilitate angioplasty involving internal mammary arteries from the femoral approach.