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.

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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.

Summary:Catheter balloon valvuloplasty of stenotic aortic valves has met with generally poor short-and longtemi 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.Key words: aortic stenosis, aortic balloon valvuloplasty, bicuspid aortic valve, rheumatic disease, degenerative aortic stenosis percutaneous balloon aortic valvuloplasty may improve some symptoms, the high incidence of recurrence of clinical symptoms within several weeks and the high mortality within 8 months of the dilation limits the procedure to selected patients.The results of aortic balloon valvuloplasty described above represent no clinical or morphologic attempt to separate patients (aortic valves) into subgroups of specific aortic valve etiology. Specific morphologic selection of stenotic aortic valves for balloon dilation may greatly improve these initial dismal clinical results of dilation. Part 1 of this review provides an anatomic basis for aortic balloon valvuloplasty and indicates mechanisms of successful balloon dilation for various causes of aortic valve stenosis.

Summary:During the last several years dilating balloons have been applied in the treatment of stenotic cardiac valves. This interest has been extended to stenotic porcine bioprosthetic valves. Part I of this review discusses the pathologic changes producing stenotic porcine prosthetic valves. Part I1 of this review describes an in vitro study of porcine prosthetic valve valvuloplasty defining the mechanisms, complications, and clinical applications. Results of this study indicate a limited and cautious role in balloon dilation of stenotic bioprosthetic valves.