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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.

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To study the immediate and long-term results of balloon aortic valvuloplasty (BAV) in a large cohort of patients with rheumatic valvular aortic stenosis. Single tertiary care center retrospective data analysis of immediate and long-term outcomes in patients following BAV from 2000 to 2008. Ninety-two patients with rheumatic aortic stenosis (AS) were studied who underwent BAV. Mean age of patients was 21.7 years (95 % CI 14.3-28.9) with mean follow-up period of 5.7 years (±SD 1.3). Intervention resulted in successful BAV (more than 50 % reduction in baseline gradient) in 79 (85.9 %) subjects (Group A) and partially successful BPV (<50 % reduction in baseline gradient) in 8 (8.7 %) subjects (Group B). BAV failed in 5 (5.4 %) subjects (Group C). Concomitant balloon mitral valvuloplasty was done in 23/92 cases. Mean left ventricular systolic pressure decreased from 165.6 (95 % CI 142.7-196.3) to 110.9 mmHg (95 % CI 92.1-129.6), ( P < 0.001) and mean aortic valve (AV) gradient from 50.7 (95 % CI 35.12-66.22) to 27.2 mmHg (95 % CI 25.83-31.23), ( P < 0.001). The mean change in ejection fraction and mean AV gradient were significantly different between success (Groups A and B) and failure groups ( P < 0.001). Different grades of aortic regurgitation were noted in 32 (34.78 %) patients post BAV (severe regurgitation in 2.18 %). Anova post hoc analysis showed sustained gradient reductions at 1- and 5-year follow-up ( P > 0.05). The need for surgery was much lower in Group A (2.5 %) compared to Group B (50 %) and C (100 %). BAV is an effective treatment strategy in dominant AS in multi valvular rheumatic disease situations. Combined aortic and mitral valvuloplasty was performed in one-fourth of study patients. [ABSTRACT FROM AUTHOR]

Background: Percutaneous balloon mitral valvotomy (BMV) is the gold standard treatment for rheumatic mitral stenosis (MS) in that it causes significant changes in mitral valve area (MVA) and improves leaflet mobility. Development of or increase in mitral regurgitation (MR) is common after BMV. This study evaluated MR severity and its changes after BMV in Iranian patients. Methods: We prospectively evaluated consecutive patients with severe rheumatic MS undergoing BMV using the Inoue balloon technique between February 2010 and January 2013 in Madani Heart Center, Tabriz, Iran. New York Heart Association (NYHA) functional class and echocardiographic and catheterization data, including MVA, mitral valve mean and peak gradient (MVPG and MVMG), left atrial (LA) pressure, pulmonary artery systolic pressure (PAPs), and MR severity before and after BMV, were evaluated. Results: Totally, 105 patients (80% female) at a mean age of 45.81 ± 13.37 years were enrolled. NYHA class was significantly improved after BMV: 55.2% of the patients were in NYHA functional class III before BMV compared to 36.2% after the procedure (p value < 0.001). MVA significantly increased (mean area = 0.64 ± 0.29 cm² before BMV vs. 1.90 ± 0.22 cm² after BMV; p value < 0.001) and PAPs, LA pressure, MVPG, and MVMG significantly decreased. MR severity did not change in 82 (78.1%) patients, but it increased in 18 (17.1%) and decreased in 5 (4.8%) patients. Patients with increased MR had a significantly higher calcification score (2.03 ± 0.53 vs. 1.50 ± 0.51; p value < 0.001) and lower MVA before BMV (0.81 ± 0.23 vs. 0.94 ± 0.18; p value = 0.010). There were no major complications. Conclusion: In our study, BMV had excellent immediate hemodynamic and clinical results inasmuch as MR severity increased only in some patients and, interestingly, decreased in a few. Our results, underscore BMV ejficacy in severe MS. The echocardiographic calcification score was useful for identifying patients likely to have MR development or MR increase after BMV. [ABSTRACT FROM AUTHOR]

There are few histologic studies of intracoronary stents found at autopsy. We studied histologic findings of 87 intracoronary stents from 45 autopsy hearts. There were 40 patients with chronically implanted stents and five shorter than 30 days. Of five patients with recent stent placement, the cause of death was related to the stent (in-stent thrombosis) in one case. Of the 40 patients with chronic stents, there were 16 sudden coronary deaths and 24 noncoronary deaths (controls). There were no late stent thromboses in the coronary deaths. In the coronary deaths, 26% of stents showed restenosis versus 11% in controls ( p = 0.1). The rate of healed infarcts and cardiomegaly was similar in the coronary and noncoronary groups, and acute thrombi in native arteries were seen only in three hearts in the coronary group. We conclude that the cause of death is rarely impacted by in-stent findings at autopsy, especially in chronically implanted stents. [ABSTRACT FROM AUTHOR]

Copyright of Advances in Interventional Cardiology / Postępy w Kardiologii Interwencyjnej is the property of Termedia Publishing House and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Aortic stenosis is a congenital or acquired reduction in the area of the aortic valve, resulting in obstruction of the blood flow from the left ventricle to the aorta. Aortic stenosis accounts for 2-5% of all congenital heart defects and is a potentially life-threatening disorder. In adults aortic stenosis represents 34% of all valvular heart diseases. Degenerative etiology is present in 80% of cases. Patients with mild aortic stenosis are usually asymptomatic. Symptoms of the disease occur along with the disappearance of effective compensatory mechanisms. These are symptoms of low cardiac output syndrome manifested as fainting, dizziness, ischemic pains, exercise intolerance, arrhythmias with the risk of sudden cardiac death, and heart failure. As soon as the symptoms occur the prognosis significantly worsens, which is associated with a high risk of death. Percutaneous aortic valvuloplasty is a palliative method of treatment of aortic stenosis. The aim of the procedure is to relieve left ventricular outflow tract obstruction, thereby improving cardiac output. The etiology, course of the aortic stenosis and treatment methods, including invasive procedures, vary depending on the patients' age. The purpose of this paper is to present the characteristics of the aortic valve disease and the strategy of aortic balloon valvuloplasty in different age groups. [ABSTRACT FROM AUTHOR]

To develop a strategy for gene therapy of restenosis following coronary angioplasty, we examined the effects of a recombinant adenovirus vector encoding a hammerhead ribozyme specific for rat platelet-derived growth factor (PDGF) A-chain mRNA (Ad.Ribozyme) and a control recombinant adenovirus vector encoding the Escherichia coli LacZ gene (Ad.LacZ) on neointima formation in rat carotid artery after balloon injury. Ad.Ribozyme (108 PFU/ml) markedly reduced the increased expression of PDGF A-chain mRNA and protein. Ad.Ribozyme significantly decreased the intima/media ratio (68%) of the injured artery, whereas Ad.LacZ had no effect on the intima/media ratio. Most carotid arteries developed thrombi by 14 days after balloon injury, whereas Ad.Ribozyme completely inhibited thrombus formation. Expression of thromboxane A2 (TXA2) receptor mRNA was significantly increased after balloon injury. Ad.Ribozyme significantly decreased the levels of TXA2 receptor. Expression of prostaglandin I2 (PGI2) synthase mRNA was significantly decreased after balloon injury. Ad.Ribozyme significantly increased levels of PGI2 synthase mRNA after balloon injury. The observation that adenovirus-encoded ribozyme to PDGF A-chain inhibits neointima formation may serve as a novel strategy to prevent restenosis after coronary angioplasty. Inhibition of growth factors by genetic approaches may yield new insights into the mechanisms underlying responses to vascular injury and lead to new therapeutic applications. Copyright © 2004 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Based on recent advances, this article aims to review the biological basis for the use of either radiation or drug-eluting stents for the prevention of restenosis, and to elucidate the complementary role that they may play in the future. Vascular restenosis is a multifactorial process primarily driven by the remodeling of the arterial wall, as well as by the hyperproliferation of smooth muscle cells (SMC). These pathophysiological features are the target of therapeutic strategies aimed at inhibiting constrictive remodeling as well as inhibiting SMC proliferation. The success of radiation as well as anti-proliferative drugs such as paclitaxel and sirolimus lies in the primary and/or multifactorial inhibition of cell proliferation. Radiation has the additional feature of preventing constrictive remodeling while sirolimus has the potential property of being anti-inflammatory, which may be a desirable feature. The effects of radiation are not reliant on any uptake and “metabolism” by the target cells, as in the case with drugs, and thus radiation potentially may be more effective as a result of its more-direct action. However, radiation does have some significant drawbacks compared to drug-eluting stents, including a much delayed re-endothelialization resulting in the need for prolonged anti-platelet therapy. Based on recent clinical data, drug-eluting stents have been shown to markedly reduce the likelihood of restenosis, which actually favors this approach for the prevention of restenosis. From a biological perspective, drug-eluting stents and radiation have certain differences, which are reviewed in this article. [Copyright &y& Elsevier]

Successful percutaneous intervention of unprotected left main coronary artery (LMCA) in lieu of surgical revascularization represents the next wave of challenges that the field of interventional cardiology will try to overcome. Significant LMCA stenosis, commonly secondary to atherosclerosis, is seen in about 4–10% of cases presenting to the cardiac catheterization laboratory. Currently, the vast majority of these patients undergo surgical revascularization unless there are prohibitive reasons for surgical revascularization. Several challenges of percutaneous revascularization have been overcome with stents, intravascular brachytherapy, and other technical improvements. Yet, several remaining limitations of percutaneous intervention, such as in-stent restenosis, have to be improved further before randomized clinical trials of surgical and percutaneous revascularization of unprotected LMCA disease can be contemplated to establish a new standard of care. (J Interven Cardiol 2003;16:281–288). [ABSTRACT FROM AUTHOR]

Presents a study which examined whether the selective inhibition of Rho kinase by adenovirus-mediated gene transfer of its dominant negative form suppresses the vascular lesion formation after balloon injury in porcine femoral arteries in vivo. Methodology; Results; Discussion.

Standard guiding catheters for coronary interventions may not selectively engage the coronary ostium despite a successful cannulation with a diagnostic catheter of the same curve. This discrepancy is explained by a slight difference in shape between the two catheters (shorter tip of the guiding, absence of tip tapering, etc.). The authors report on the use of 6 F. coronary diagnostic catheters as guiding catheters for coronary angioplasty and stent implantation in two patients with critical stenoses: in the right coronary artery distal to a right internal mammary artery anastomosis in one and in the ostial right coronary artery in the other. In both cases, the use of diagnostic catheters was the key to success despite the vessel orifice being unfavourable for the use of different types of guiding catheters. [ABSTRACT FROM AUTHOR]

We developed a rat double-balloon injury model and studied the thickened neointima using immunohistochemical and RT-PCR methods. Fourteen days after the first balloon injury of the rat left common carotid artery, a second balloon injury was inflicted in the same place. Histochemical sections taken 14 days after the single- and double-balloon injuries were used for calculating intimal/medial (I/M) area ratios, as an indicator of neointimal formation, and were subjected to immunohistochemical staining. Total RNA was also purified from some arteries and mRNA expression of some extracellular matrices (ECM) and cytokine receptors related to ECM metabolism was estimated using the RT-PCR method. The I/M ratio in the rat double-balloon injury model (II) (1.84±0.62 (mean±SE, n=5)) was significantly (p<0.05) higher than that in the single-balloon injury model (I) (1.30±0.19, n=10). The cell number per neointimal area was less in II than in I. As for the phenotype of smooth muscle cells, α-actin staining showed that the neointima of II consisted of more contractile form than synthetic, whereas that of I consisted of more synthetic form than contractile. The neointima of II was strongly stained with laminin and fibronectin, but that of I was stained only weakly. Consistent with these data, laminin and fibronectin mRNAs were markedly expressed in the neointima of II. Neointimas of both I and II were also stained positively with PDGF (α and β) and TGF-β (types I and II) receptors to the same extent. These results show: that ECM accumulation, particularly of laminin and fibronectin, characterizes the double-balloon injury model; that the marked accumulation of ECM in this model is due to a mechanism other than the PDGF or TGF-β signalling pathway; and that this model resembles the lesion of post-PTCA re-stenosis, and therefore provides the key for its investigation. [ABSTRACT FROM AUTHOR]

Examines the radiation inhibition of arterial restenosis. Effectiveness of different radiation modalities; Use of catheter-based system; Application of dose fractionation.

The role of remodeling in restenosis of coronary arteries on which percutaneous transluminal coronary angioplasty (PTCA) had been performed was investigated. At autopsy, presence (n = 6) or absence of restenosis (n = 5) based on the cross-sectional area of stenosis was determined in 11 coronary lesions. Remodeling was defined as a ratio of the artery area at the PTCA site to that at the reference site of <1.0. According to this definition, remodeling had occurred in all of the lesions in the restenosis group, and in only 1 lesion in the group with no restenosis which had the least residual plaque (p < 0.05). Dense caps of collagen fibers in the adventitia in the vicinity of the disrupted internal elastic laminae were present in all of the remodeling lesions. We suggest that remodeling, which results in adventitial scarring, is one of the major causative factors of restenosis. [ABSTRACT FROM AUTHOR]

AimsThere is increased late loss in luminal diameter following long-term coronary stenting, compared with balloon angioplasty. We evaluated short- and long-term vessel wall injury after experimental implantation of two stent designs as well as balloon angioplasty and their relationship to neointimal hyperplasia.Methods and ResultsWiktor stents and Palmaz-Schatz stents were implanted in normal coronary arteries of pigs (balloon/artery ratio: 0·9–1·1). In control coronary arteries, balloon angioplasty was performed. At 1, 4 and 12 weeks, the vessel injury score, neointimal thickness and inflammatory response were assessed by histology.The vessel injury score increased over time in both Wiktor and Palmaz-Schatz stents: 0·9±0·1, 1·5±0·5 and 1·7±0·6 (mean±SD) for Wiktor stents and 0·7±0·2, 1·0±0·1 and 1·2±0·3 for Palmaz-Schatz stents at 1, 4 and 12 weeks follow-up, respectively. No increase in injury was seen in balloon angioplasty controls. Inflammation was seen in both stented groups but was absent 12 weeks after balloon angioplasty. No strong correlation between injury and neointimal thickness was apparent.ConclusionStents induce chronic injury in contrast to balloon angioplasty. Stent design (coil vs slotted tube) as well as inflammation may influence vessel response. [ABSTRACT FROM PUBLISHER]

The authors describe a new approach to percutaneous transluminal coronary angioplasty (PICA) of bifureational lesions with a single-guide. "kissing balloon" technique, utilizing two probe dilatation systems, inserted simultaneously into the guiding catheter and across both diseased branches. The versatility of the probe dilatation system in complex angioplasty is portrayed, both for simultaneous or alternate balloon inflations, and the low-profile characteristics of the system are highlighted, which allow a double-probe introduction into a single guiding catheter, good visualization still being retained by guide injections. [ABSTRACT FROM AUTHOR]

Percutaneous transluminal coronary angioplasty (PTCA) is a proven nonoperative method of direct myocardial revascularization. Acute complications occurring during PTCA center primarily around acute disruption at the site of dilatation, arrhythmias, or vascular problems at the site of guide catheter access. Late complications include restenosis or aneurysm formation at the site of dilatation. Subacute stenosis of the left main coronary artery occurred in three of 440 patients who had PTCA performed between September 1980 and December 1983 and may be an infrequent but potentially critical complication of PTCA. The serious clinical course of patients with left main coronary stenosis requires prompt recognition and intervention. [ABSTRACT FROM AUTHOR]

Objective: Restenosis after percutaneous transluminal coronary angioplasty (PTCA) still remains a serious late complication. Many growth factors induced in restenotic lesions may be responsible for restenosis after PTCA. Most of the receptors for such growth factors possess tyrosine kinase activity. This study was designed to determine whether or not a specific tyrosine kinase inhibitor, ST 638, can prevent (re)stenotic changes of the coronary artery after balloon injury. Methods: A segment of the porcine coronary artery was aseptically wrapped with cotton mesh absorbing either ST 638 or vehicle, followed by balloon injury. Two weeks after the procedure, coronary stenosis and vasoconstricting responses were examined by coronary arteriography and (re)stenotic changes of the coronary artery were histologically examined. Antiphosphotyrosine immunoblotting was also performed to examine the inhibitory effects of ST 638. Results: Coronary arteriography showed the development of mild stenotic lesions at the balloon-injured sites, where hyperconstrictive responses were repeatedly induced by intracoronary serotonin and histamine. Histologically, neointimal formation was noted at the balloon-injured site, where the total vessel area also tended to decrease (geometric remodeling). The treatment with ST 638 suppressed all the hyperconstrictive responses, the neointimal formation, and the geometric remodeling induced by balloon injury. Immunoblotting for phosphotyrosine proteins demonstrated the elevation of proteins at the balloon-injured site, which was suppressed by ST 638. Conclusions: These results indicate that tyrosine kinases are activated at the balloon-injured site and the inhibition of such kinase activities is effective in reducing both the (re)stenotic changes (neointimal formation and geometric remodeling) and the hyperconstrictive responses of the coronary artery after balloon injury. [ABSTRACT FROM PUBLISHER]

The expression and localization of hepatocyte growth factor/scatter factor (HGF/SF) were examined immunohistochemically in 59 human coronary artery lesions retrieved by directional coronary atherectomy and compared with the localization of transforming growth factor beta isoforms (TGF-β1, -β2, and -β3). In 21 of the 59 specimens (35.6%) HGF-like immunoreactivity (HGF-IR) was revealed. The HGF immunopositivity rate of 45% (14/31) in thrombotic tissue was significantly ( P < 0.05) higher than the rates of 7.3% (4/55), 7.1% (3/42), and 0% (0/14) in fibrous tissue, neointimal hyperplasia and atheromatous gruel, respectively. Immunoreactivity for HGF was much weaker than that for TGF-β isoforms in these components except in thrombotic tissue. These cells exhibiting strong HGF-IR were inflammatory cells such as monocytes/macrophages in thrombotic tissue, in tissue lesions adjacent to a thrombus, and outside the capillary walls in a portion of the neovascularized lesions. Smooth muscle cells (SMCs) hardly demonstrated HGF-IR. In contrast, in control coronary arteries obtained at autopsy, the HGF-IR was strongly expressed in SMCs. These findings suggest that HGF produced by macrophages play a part in the process of coronary plaque formation attributable to thrombus in man. [ABSTRACT FROM AUTHOR]