Thomas F. Peters

Restenosis 1 to 24 months after clinically successful coronary balloon angioplasty: A necropsy study of 20 patients

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.

Comparison of six-month outcome of coronary artery stenting in patients 75 years of age

We studied 1,238 patients receiving 1,880 coronary stents. In-hospital outcomes were divided by age into <65 years (n = 747, group 1), 65 to 75 years (n = 326, group 2), and >75 years (n = 165, group 3). Procedural success was 97.2%, 95.1%, and 98.8% in groups 1, 2, and 3, respectively (p = NS). There was 1 death (group 1). Myocardial infarction occurred in 1.2%, 2.8%, and 1.8%, bypass surgery occurred in 0.9%, 1.8%, and 1.2%, and repeat balloon angioplasty in 0.3%, 0.6%, and 0% of patients in groups 1, 2, and 3, respectively (p = NS for all comparisons). Vascular complications occurred in 2.8%, 4.9%, and 6.1% in groups 1, 2, and 3, respectively (p <0.05). Six-month follow-up of patients was divided by age: <65 years (n = 564, group 1); 65 to 75 years (n = 221, group 2); and >75 years (n = 122, group 3). Event-free survival was 94.5%, 90.5%, and 89.3% for groups 1, 2, and 3, respectively (p = NS). Death occurred in 0.4%, 0.5%, and 1.6%; myocardial infarction occurred in 1.2%, 2.3%, and 1.6%, and target vessel revascularization in 4.3%, 8.6%, and 7.4% for groups 1, 2, and 3, respectively (p = NS for all comparisons). Thus, coronary stenting produced favorable in-hospital and 6-month outcomes in all 3 age groups. Age itself should not preclude patients from undergoing coronary stenting.

Late coronary artery stenosis regression within the gianturco-roubin intracoronary stent

The late angiographic outcome of the Gianturco-Roubin intracoronary stent has not been well defined. To investigate serial changes within the stent, we studied 23 patients (15 men and 8 women, median age 63) who had late angiographic follow-up ( > 1 year) after undergoing Gianturco-Roubin stenting for angioplasty-associated acute or threatened native coronary artery closure. Coronary angiography before and after stenting, at 6-month follow-up, and at late return was analyzed with quantitative coronary angiography. The median time from stent deployment to late angiographic follow-up was 27 months. As expected, stenting significantly increased the median minimal lumen diameter (MLD) acutely from 1.0 to 2.46 mm. Median percent diameter stenosis decreased from 66% to 18%. Although at 6 months there was a significant loss of the acute gain (median MLD decreased from 2.46 to 1.9 mm), with a corresponding increase in percent stenosis from 18% to 31%, late angiography demonstrated lesion regression, median MLD increasing from 1.9 to 2.15 mm (p = 0.004), and percent stenosis decreasing from 31% to 21% (p = 0.0026). No patient had a significant decline in minimal lesion diameter, and 5 patients had a > 50% increase in MLD at late follow-up. Linear regression analysis of 6-month MLD and late lumen gain suggested that lesions with the greatest regression were those with the lowest lumen diameters at 6-month angiography. Late angiographic analysis demonstrated significant lesion regression within the Gianturco-Roubin stent, which was sometimes dramatic. In suggesting that coronary arteriography at 6 months may underestimate the late angiographic benefit of intracoronary stenting, these data have important clinical implications, and imply that patients with a stable clinical course and angiographic stent restenosis may often be followed rather than routinely redilated.

Coronary balloon angioplasty dissections: “The good, the bad and the ugly”☆

Since the tntraduction of percutanewi coronary b&on lion simply means mvolvement or penetratton of the vessei angioplasty nearly IS years ago (I). there has been cow& media 117,. C’inically. however. it often conveys a sense of erable interest in the recognition of angiographic pa;.erns of failure. complication (“bad”) car impending doom P~ply”). successful dilation. angiogmphic predictors oi angopla<ty Angiographir evidence of dissection. Angiographically. complications and identification of angiographic factors usthe term dissection has been freelv used (and oerhaos sociated with restenosis. Similarly, there has been considerable morphologic interest in distinguishing mechanisms of wrongly so) for vartous luminographif appearker iIS-36.

Rotational ablation and stent placement for severe calcific coronary artery stenosis after Kawasaki disease

We report on a 5‐year‐old child who had an episode of Kawasaki disease with giant coronary artery aneurysms at the age of 4 months. Surveillance coronary angiography showed severe calcific stenosis in the proximal left anterior descending artery. Balloon angioplasty failed to resolve the obstruction. Rotational ablation was therefore performed. Surveillance angiogram performed 6 months after rotational ablation showed critical restenosis. Rotational ablation was therefore repeated, followed by stent placement. To the best of our knowledge, this is the youngest child who has undergone coronary stenting after Kawasaki disease. Cathet Cardiovasc Intervent 2002;56:549–552.

Coronary artery and saphenous vein graft remodeling: A review of histologic findings after various interventional procedures—part V

Catheter balloon angioplasty is a well accepted form of nonsurgical treatment of acutely and chronically obstructed coronary artery vessels. It is also the centerpiece for various new intervention techniques. Their morphologic effects on the site of obstruction has been termed “remodeling.” Part IV of this six‐part series focuses on morphologic correlates of coronary angiographic patterns of remodeling after balloon angioplasty and discusses effects of angioplasty on adjacent, nondilated vessels.

Histologic Basis of Vessel Remodeling after Various Interventional Procedures: A Comparison of Acute (Cracks, Breaks, Tears, Stretching) and Chronic (Tissue Proliferation, Recoil) Changes

During the past two decades, there has been an explosive increase in the number of techniques and devices used to treat obstructed coronary arteries. Since its introduction in 1977 (1), catheter balloon angioplasty has gained wide acceptance as a nonsurgical form of therapy for acutely and chronically obstructed coronary arteries, and this technique forms the centerpiece around which newer tools and techniques have been developed. Of the many interventional devices currently used or under study, their morphologic effects (“remodeling”) on vessel luminal shape or obstruction can be separated into two underlying processes (2): (a) remodeling (“displacing,” “expanding,” “attaching”) and (b) removing (“heating,” “drilling,” “excising”) (Tables 1, 2). This chapter will review acute and chronic changes of remodeling after balloon angioplasty and other interventional techniques.

Quantitative and Qualitative Coronary Angiography

Although the technical quality of coronary angiographic images has dramatically improved, the method by which the great majority of clinical cardiac catheterization laboratories estimate coronary lesion severity has remained essentially unchanged. Most laboratories continue to rely on visual assessments of percent diameter stenosis, so called “eyeball” estimates, to define lesion severity. Unfortunately, these visual estimates are neither accurate nor precise [1–3]. Created to circumvent the weaknesses of “eyeball” measurements, quantitative coronary angiography (QCA) was developed to more reproducibly and accurately guage the magnitude of coronary obstructions [4–6]. Hand-held calipers were the first form of QCA. Subsequently, computer-assisted, quantitative angiographic systems were introduced.