Genomic distribution and heterogeneity of MocR-like transcriptional factors containing a domain belonging to the superfamily of the pyridoxal-5'-phosphate dependent enzymes of fold type I.

Bacterial proteins belonging to the MocR/GabR family are chimeric proteins incorporating a short N-terminal helix-turn-helix containing domain with DNA-binding properties, and a long C-terminal domain belonging to the superfamily of the pyridoxal-5'-phosphate enzymes of fold type I. The first purpose of this report is to give an overview of the distribution of these factors among the different taxonomical bacterial divisions and to determine the degree of conservation of the main structural features of the PLP binding domain. Complete proteomes of bacteria phyla were scanned with a hidden Markov model representative of the MocR family. Results indicate that presence of MocR factors is heterogeneous even within the single bacterial phylum: some species miss completely the factors, while others possess one or even more regulators. Absence of MocR factors is distinctive of some phyla such as Chlamydiae. The genomic distribution of MocR is, as expected, highly correlated to the size of the genome. At variance, phyla missing MocR regulators generally are characterized by compact genomes, of the order of 1.0-2.0 Mb, such as the case of Mollicutes or Chlamydiae. Apparently, the minimum genome size compatible with the presence of MocR genes is around 2.0-2.5 Mb. Conservation of the residues corresponding to those involved in the interaction with the cofactor pyridoxal-5'-phosphate in the homologous 2-aminoadipate aminotransferase, was analyzed in the multiple sequence alignments of MocR within each phyla considered. In the vast majority of cases, residues are conserved or conservatively replaced. This result suggests that, in most cases, MocR factors preserve at least ability to bind the cofactor and very likely some catalytic abilities.

Phenotype commitment in vascular smooth muscle cells derived from coronary atherosclerotic plaques: differential gene expression of endothelial nitric oxide synthase.

Unstable angina and myocardial infarction are the clinical manifestations of the abrupt thrombotic occlusion of an epicardial coronary artery as a result of spontaneous atherosclerotic plaque rupture or fissuring, and the exposure of highly thrombogenic material to blood. It has been demonstrated that the proliferation of vascular smooth muscle cells (VSMCs) and impaired bioavailabilty of nitric oxide (NO) are among the most important mechanisms involved in the progression of atherosclerosis. It has also been suggested that a NO imbalance in coronary arteries may be involved in myocardial ischemia as a result of vasomotor dysfunction triggering plaque rupture and the thrombotic response. We used 5' nuclease assays (TaqMan PCRs) to study gene expression in coronary plaques collected by means of therapeutic directional coronary atherectomy from 15 patients with stable angina (SA) and 15 with acute coronary syndromes (ACS) without ST elevation. Total RNA was extracted from the 30 plaques and the cDNA was amplified in order to determine endothelial nitric oxide synthase (eNOS) gene expression. Analysis of the results showed that the expression of eNOS was significantly higher (p<0.001) in the plaques from the ACS patients. Furthermore, isolated VSMCs from ACS and SA plaques confirmed the above pattern even after 25 plating passages. In situ RT-PCR was also carried out to co-localize the eNOS messengers and the VSMC phenotype. The eNOS gene was more expressed in ACS plaques and VSMCs cultured from them, thus indicating that: a) the expression of the most important differentiation markers is retained under in vitro conditions; and b) NO may play a pivotal role in coronary artery disease. Our findings suggest a new cell system model for studying the pathophysiology of unstable angina and myocardial infarction.

Multicolor fluorescence technique to detect apoptotic cells in advanced coronary atherosclerotic plaques.

Apoptosis occurring in atherosclerotic lesions has been suggested to be involved in the evolution and the structural stability of the plaques. It is still a matter of debate whether apoptosis mainly involves vascular smooth muscle cells (vSMCs) in the fibrous tissue or inflammatory (namely foam) cells, thus preferentially affecting the cell-poor lipid core of the atherosclerotic plaques. The aim of the present investigation was to detect the presence of apoptotic cells and to estimate their percentage in a series of atherosclerotic plaques obtained either by autopsy or during surgical atherectomy. Apoptotic cells were identified on paraffin-embedded sections on the basis of cell nuclear morphology after DNA staining and/or by cytochemical reactions (TUNEL assay, immunodetection of the proteolytic poly (ADP-ribose) polymerase-1 [PARP-1] fragment); biochemical procedures (identifying DNA fragmentation or PARP-1 proteolysis) were also used. Indirect immunofluorescence techniques were performed to label specific antigens for either vSMCs or macrophages (i.e., the cells which are most likely prone to apoptosis in atherosclerotic lesions): the proper selection of fluorochrome labeling allowed the simultaneous detection of the cell phenotype and the apoptotic characteristics, by multicolor fluorescence techniques. Apoptotic cells proved to be less than 5% of the whole cell population, in atherosclerotic plaque sections: this is, in fact, a too low cell fraction to be detected by widely used biochemical methods, such as agarose gel electrophoresis of low-molecular-weight DNA or Western-blot analysis of PARP-1 degradation. Most apoptotic cells were of macrophage origin, and clustered in the tunica media, near or within the lipid-rich core; only a few TUNEL-positive cells were labeled for antigens specific for vSMCs. These results confirm that, among the cell populations in atherosclerotic plaques, macrophage foam-cells are preferentially involved in apoptosis. Their death may decrease the cell number in the lipid core and generate a possibly defective apoptotic clearance: the resulting release of matrix-degrading enzymes could contribute to weakening the fibrous cap and promote the plaque rupture with the risk of acute ischemic events, while increasing the thrombogenic pultaceous pool of the plaque core.

Identification of differentially expressed genes in coronary atherosclerotic plaques from patients with stable or unstable angina by cDNA array analysis.

The composition of atherosclerotic plaques is a crucial factor in determining rupture, thrombosis and clinical events. In this study, we analyzed gene expression in coronary plaques from patients with stable or unstable angina using gene arrays. Total RNA was extracted from eight plaques collected by therapeutic directional coronary atherectomy. cDNA probes, generated by amplification, were hybridized to nylon arrays containing 482 genes. Here we report the results for the inflammation, adhesion and hemostasis subsets. Many genes not previously associated with atherosclerosis, such as the lymphocyte adhesion molecule MadCAM, were expressed in the plaques. anova analysis showed higher tissue factor (TF) expression in unstable angina samples. Five genes were expressed at lower levels in unstable angina samples: anticoagulant protein S, cyclooxygenase (COX)-1, interleukin (IL)-7 and chemokines monocyte chemotactic protein (MCP)-1 and -2. Gene arrays provide a new approach to study plaque composition and identify candidate markers of plaque instability.

Thrombogenic potential of human coronary atherosclerotic plaques.

Higher levels of tissue factor (the initiator of blood coagulation) have been found in coronary atherosclerotic plaques of patients with unstable coronary artery disease, but it is not established whether they are associated with a different thrombotic response to in vivo plaque rupture. In 40 patients undergoing directional coronary atherectomy, prothrombin fragment 1 + 2, a marker of thrombin generation, was measured in intracoronary blood samples obtained proximally and distally to the coronary atherosclerotic plaque before and after the procedure. Before the procedure, plasma prothrombin fragment 1 + 2 levels were significantly increased across the lesion in patients with unstable, but not in those with stable, coronary disease (unstable, median increase, 0.37 nM; range, -0.35-1.16 nM) (stable, median increase, -0.065 nM; range, -0.58-1.06 nM) (P =.0021). After plaque removal, an increase in prothrombin fragment 1 + 2 across the lesion was observed only in patients with unstable coronary disease (unstable, median increase, 0.25 nM; range, -1.04-4.9 nM) (stable, 0.01 nM; range, -0.48-3.59 nM) (P =.036)]. There was a correlation between the tissue factor content of the plaque and the increase in thrombin generation across the lesion (rho = 0.33; P =.038). The higher tissue factor content found in plaques obtained from patients with unstable coronary disease was associated with a local increase in thrombin generation, thus suggesting a link with the in vivo thrombogenicity of the plaque.

Tissue factor in human coronary atherosclerotic plaques.

The rupture or fissuring of a coronary atherosclerotic plaque and subsequent thrombosis is considered the key event in the pathogenesis of unstable angina and myocardial infarction. Although plaque disruption frequently occurs during the evolution of atherosclerosis, only a minority of ruptured plaques develop thrombosis. The content and procoagulant activity of tissue factor in human coronary atherosclerotic plaques varies widely, and different studies confirm that it is higher in the plaques extracted from patients with unstable angina, myocardial infarction or histologic/angiographic evidence of coronary thrombosis than in those taken from patients with stable angina or uncomplicated coronary lesions. Variations in tissue factor content and activity may be responsible for the different thrombotic responses to human coronary atherosclerotic plaque rupture.

Antithrombotic therapy of unstable angina and non-Q-wave myocardial infarction.

Unstable angina and non-Q-wave myocardial infarction still represent an unsolved problem for clinicians, owing to their unpredictable evolution and high incidence of coronary events in the follow-up. Traditional antithrombotic agents, unfractionated heparin and aspirin, have been proved to be highly effective, but show some important limitations. New potent antithrombotic therapy have been studied to improve their efficacy, with encouraging results. Among these drugs, low molecular weight heparins (for subcutaneous administration) and inhibitors of platelet glycoprotein receptor IIb/IIIa (for intravenous, and possibly oral, administration) are the most promising and are now under extensive investigation.

Adjunctive stent implantation following directional coronary atherectomy in patients with coronary artery disease.

OBJECTIVES: This prospective case-control study evaluated the acute and long-term results of stent implantation preceded by debulking of the plaque by means of directional coronary atherectomy. BACKGROUND: In comparison with balloon angioplasty, intracoronary stenting produces a larger luminal diameter, maintains artery patency and reduces the incidence of restenosis. Optimal stent deployment is a pivotal factor for achieving the best results, but the bulk of the atherosclerotic plaque opposes stent expansion and may limit the success of the procedure. Debulking of the plaque may provide a better milieu for optimal stent deployment. METHODS: Directional coronary atherectomy followed by a single Palmaz-Schatz stent implantation was attempted in 100 patients. The successes, complications and angiographic results of the combined procedure were evaluated both acutely and during follow-up. Matched patients undergoing successful Palmaz-Schatz stent implantation alone during the same period served as controls. RESULTS: Atherectomy followed by stent implantation was performed in 94 patients with 98 lesions; periprocedural complications were observed in four cases. The stenosis diameter decreased from 76+/-9% at baseline to 30+/-13% after atherectomy (p < 0.0001), and 5+/-9% after stent implantation (p < 0.0001); it increased to 27+/-15% at 6-month angiography (p < 0.0001). During the 14+/-10 months of follow-up, none of the patients died or experienced myocardial infarction, but three patients underwent target lesion revascularization. The patients undergoing stent implantation alone achieved smaller acute gains, tended to have a higher late lumen loss, had a higher restenosis rate (30.5% vs. 6.8%, p < 0.0001) and showed a greater incidence of clinical events during follow-up (p < 0.0001). CONCLUSIONS: Debulking atherosclerotic lesions by means of directional coronary atherectomy before stent implantation is a safe procedure with a high success rate and a low incidence of restenosis at follow-up.

[Coronary lesion with an aneurysm: their correction via angioplasty and the implantation of a coated stent]. / Lesione coronarica con aneurisma: correzione mediante angioplastica ed impianto di stent ricoperto.

We describe the good angiographic results obtained using a new polymeric prosthesis combining a stent with expandable polytetrafluoroethylene (PTFE) graft material in the treatment of proximal left descending coronary artery stenosis complicated by the presence of a coronary aneurysm.

[Coronary angioplasty: use and cost]. / Angioplastica coronarica: consumi e costi.

OBJECTIVES: The goal of the study was to examine the utilization of cardiac catheterization laboratory resources in surgical procedures in order to determine the cost impact of introducing new devices such as stents and atherectomy. METHODS: Detailed resource utilization and costs of each cardiac catheterization laboratory procedure performed in 1995 were determined. Costs were analyzed for single-vessel and multivessel coronary angioplasty, also taking into account the additional costs for coronary stent placement or for the use of directional atherectomy. RESULTS: The mean cost of a surgical procedure was ITL 8,280,010, while the mean cost for conventional coronary angioplasty was ITL 4,352,427 (ITL 4,293,108 for single-vessel PTCA; ITL 5,072,841 for multivessel PTCA). The mean cost for a procedure with stent implantation was ITL 10,084,563. As compared to conventional angioplasty, coronary stenting had a 131.6% higher catheterization laboratory cost and an additional cath-lab resource utilization in terms of contrast medium (257 +/- 136 ml vs 216 +/- 109 ml, p = 0.018) and balloon catheter (1.97 +/- 1.27 vs 1.54 +/- 0.78, p = 0.0009). The cost for a directional atherectomy followed by stent placement was ITL 18827545, which is 332.5% higher than the cost of a conventional angioplasty. CONCLUSIONS: Coronary stents and directional atherectomy have a significant economic impact on catheterization laboratory resource utilization and costs. This aspect should be taken into consideration in analyzing the short- and long-term results of these techniques.

Tissue-factor antigen and activity in human coronary atherosclerotic plaques.

BACKGROUND: Coronary atherosclerotic-plaque thrombosis is a key event in the pathogenesis of unstable angina and myocardial infarction. Although plaque rupture or fissuring frequently occurs in atherosclerosis, only a small proportion of ruptured plaques develop thromboses. METHODS: Tissue-factor antigen and activity were measured in atherectomy samples from 50 consecutive patients with coronary artery disease (stable angina n = 19, unstable angina n = 24, and myocardial infarction n = 7). FINDINGS: Median tissue-factor antigen and activity concentrations were significantly higher in plaques from patients with unstable angina and myocardial infarction than in those from patients with stable angina (antigen: 66.1 pg/mg [interquartile range 43.8-82.5] vs 32.4 pg/mg [9.8-43.4], p = 0.0001; activity: 0.22 mU/mg [0.17-0.41] vs 0.13 mU/mg [0.05-0.16], p = 0.0004). INTERPRETATION: Tissue-factor, an initiator of the coagulation cascade, may account for the different thrombotic responses to the rupture of human coronary atherosclerotic plaques.

[Evaluation of efficacy and mechanism of action of angioplasty and directed atherectomy assisted by intravascular ultrasonography]. / Ocena skutecznosci i mechanizmów dzialania angioplastyki oraz aterektomii kierunkowej za pomoca ultrasonografii wewnatrznaczyniowej.

Intravascular ultrasound (IVUS) is a unique method of coronary lumen visualization enabling also examination the structure of the artery wall. Aim of this study was to assess efficacy and mechanisms of action of balloon angioplasty (PTCA) and directional atherectomy by means of IVUS. IVUS examination was performed before and after mechanical revascularization procedure in 37 pts (DCA-19 pts, PTCA-18 pts). Both PTCA and DCA resulted in enlargement of the coronary artery lumen (2.29 +/- 1.19 mm2 vs 2.93 +/- 1.55 mm2) but, also external diameter of the vessel increased after the procedure (1.94 +/- 1.10 mm2 and 0.74 +/- 1.01 mm2 retrospectively). In 55.6% of cases after PTCA plaque rupture or artery wall dissection was observed, mainly in eccentric lesions (70%). IVUS allowed to recognize details of artery lumen and define efficiency of procedure. In about 15% cases decision to continue PTCA or DCA was made on the basis of IVUS images only. The mechanism in which PTCA modifies the artery lumen is diverse and depends on the structure of lesion. Factors possibly responsible for enlargement of the lumen are: stretching, squeezing and translocation of atheroma as well as cracking and dissections along the arterial wall. DCA effectiveness depends on the withdraw of the atheromatous deposit, however, in over one-half of cases also stretching has some effect.

[Histopathologic features in atherectomy samples obtained from patient with unstable angina, stable angina and restenosis. Directional Atherectomy Lombardi Group]. / Reperti histopatologici [corrected] in campioni di aterectomia ottenuti da pazienti con angina instabile, con angina stabile e con ristenosi. Gruppo Lombardo Aterectomia Direzionale, GLAD.

BACKGROUND: The present study was aimed at investigating the pathologic features of directional coronary atherectomy (DCA) samples obtained from 194 patients (14 females) with stable (n = 68) and unstable (n = 95) angina, and with restenosis (n = 27). METHODS: DCA samples were obtained from culprit lesions, using the Simpson technique. Unstable angina was classified according to E. Braunwald criteria. Stable angina was grouped according to the presence or absence of a prior myocardial infarction (MI). DCA samples were fixed, processed, serially cut and stained with hematoxilin-eosin and with Movat pentachrome stain. RESULTS: The major pathologic findings were thrombosis, inflammation of the superficial plaque layers, and neointimal hyperplasia which often coexisted within a same sample. Their frequencies, in that order, were distributed in the differing groups of patients as follows: 21% (n = 9), 29.2% (n = 12) and 51% (n = 21) of the 41 cases with stable angina without prior MI. 40.7% (n = 11), 40.7% (n = 11), and 51.8% (n = 14) of the 27 cases with stable angina with prior MI. 25% (n = 4), 56.2% (n = 9) and 68.7% (n = 11), of the 16 cases with BI unstable angina. 35.3% (n = 14), 55.8% (n = 19) and 44% (n = 15), of the 34 cases with BII unstable angina. 44.4% (n = 4), 33.3% (n = 3) and 33.3% (n = 3), of the 9 cases with BIII unstable angina. 48.2% (n = 14), 48.2% (n = 14) and 51.8% (n = 15), of the 29 cases with CII unstable angina at 35.8 days after MI. 60% (n = 3), 60% (n = 3) and 40% (n = 2), of the 5 cases with CIII unstable angina at 8.3 days after MI. 26% (n = 7), 48% (n = 13) and 85.1% (n = 23), of the 27 cases with restenosis. According to above observation, the frequency of coronary thrombosis increases with the increase of the severity of myocardial ischemia. However, thrombosis is not found in most unstable angina without prior MI (63% of BI-II-III unstable angina cases do not have thrombus). In addition, thrombus is not a specific finding of unstable angina, given its occurrence, although in a much lower percentage of cases, in stable angina and in restenosis. CONCLUSIONS: Present data show that different ischemic and plaque lesions. This observation questions on the pathogenetic role of thrombus in unstable angina and calls for further investigations on inflammation and neointimal hyperplasia, as well as on the the reciprocal relation between these findings which are often combined within a same lesion.

Correlation between clinical and morphologic findings in unstable angina.

This study was undertaken to verify the hypothesis that the discrepant findings in published reports on the prevalence of thrombus in unstable angina depend on the inclusion of different clinical subsets in the various studies. We therefore correlated the clinical characteristics of patients included under the label of unstable angina with the morphologic features assessed by coronary angiography and intravascular ultrasound, and with histopathologic findings of atherectomy specimens. Fifty-eight patients with unstable angina (class B of the Braunwald classification) undergoing coronary arteriography followed by either coronary angioplasty (n = 20) or directional coronary atherectomy (n = 38) were studied. Fifteen patients were in class IB and 43 were in class II to IIIB. Among these 43 patients with angina at rest, 28 had ST-segment elevation during pain, and 15 had ST-segment depression, and 26 developed negative T waves on the baseline electrocardiogram (ECG) as a result of prolonged or repeated episodes of resting chest pain. Intravascular ultrasound examination of the culprit lesion was performed in 43 patients before the interventional procedure, and histopathologic analysis of atherectomy specimens was performed in 38 patients. Complex lesion morphology by angiography was observed in 31 patients (53%) without any significant relation to various clinical subsets. Patients in Braunwald class IB had more calcific plaques than patients in class II to IIIB (p < 0.001). Among patients with angina at rest, those with negative T waves on the baseline ECG, as well as those with transient ST elevation during pain, had a significantly higher incidence of noncalcific lesions (p = 0.001 for both). Analysis of atherectomy specimens revealed acute coronary lesions (thrombus and/or intraplaque hemorrhage) in 18 patients (47%). The incidence of acute coronary lesions was significantly higher in patients with than without negative T waves on the baseline ECG (p = 0.005), and increased further when negative T waves were combined with ST elevation during pain (p = 0.001). Multivariate analysis revealed that the presence orf negative T waves on the baseline ECG was the only explanatory variable related to the presence of acute coronary lesions by histology (p = 0.03). Patient subsets included in the broad spectrum of unstable angina have different morphologic features and incidence of acute coronary lesions by histology. These data provide an explanation for the discrepant findings in published reports on the relevance of thrombus formation in the pathogenesis of unstable angina.

Effect of the increasing use of coronary angioplasty on outcome at one year in patients with unstable angina.

OBJECTIVE: To determine whether the increasing use of percutaneous transluminal angioplasty in patients with unstable angina has reduced the need for bypass surgery and whether this change in the choice of treatment affected the outcome at one year in patients with unstable angina who were admitted to hospital in two different periods of time. DESIGN: Retrospective analysis of consecutive patients with unstable angina (angina at rest with ST-T changes during pain) who underwent coronary arteriography in two different periods of time. PATIENTS: 158 patients were admitted to hospital between January 1988 and June 1989 (group 1) and 140 patients admitted between January 1992 and June 1993 (group 2). RESULTS: Coronary angioplasty procedures nearly doubled from 29% in group 1 to 56% in group 2 whereas bypass surgery decreased from 36% in group 1 to 23% in group 2 (P < 0.01). Coronary angioplasty increased and bypass surgery decreased in patients with one vessel disease (P < 0.01), two vessel disease (P < 0.05), and three vessel disease (P < 0.01). Coronary angioplasty also increased and bypass surgery decreased in refractory angina and in patients with ejection fraction < 0.50 (both P < 0.05). At 1-year follow up, 14 patients in group 1 (9%) and 10 in group 2 (7%) either died or had myocardial infarction (P = NS). Revascularisation procedures were needed in 16 group 1 patients (10%) and 27 group 2 patients (19%, P < 0.05). CONCLUSIONS: Coronary angioplasty became more widely used in patients with unstable angina. This reduced the need for bypass surgery in patients with multivessel disease, refractory angina, and depressed left ventricular function. This change in treatment did not affect 1-year mortality or the myocardial infarction rate. More patients in the more recent group in which angioplasty was the preferred treatment required a further revascularisation procedure than in the earlier group in which bypass grafting was more often used as the initial treatment.

Influence of plaque composition on luminal gain after balloon angioplasty, directional atherectomy, and coronary stenting.

This study was conducted to correlate the acute luminal enlargement achieved by three different nonsurgical revascularization procedures in 79 patients (32 treated by balloon angioplasty, 29 by directional atherectomy, and 18 by coronary stenting) with the morphologic characteristics of coronary plaques assessed by preprocedure intravascular ultrasound. The absolute luminal gain was 2.41 +/- 1.54 mm2 for balloon angioplasty, 3.17 +/- 1.8 mm2 for directional atherectomy, and 4.56 +/- 1.45 mm2 for coronary stenting (p = 0.00005). However, when luminal gain was corrected for the external vessel area (luminal gain index), such difference was no longer present (0.22 +/- 0.12 for balloon angioplasty, 0.24 +/- 0.15 for directional atherectomy, and 0.30 +/- 0.12 for coronary stenting, p = not significant). Concentric plaques treated by coronary stenting had a higher luminal gain index than eccentric plaques (p = 0.01). A comparison of the three devices showed that a similar luminal gain index was achieved in soft plaques, whereas coronary stenting was superior to directional atherectomy (0.41 +/- 0.10 vs 0.20 +/- 0.09, p = 0.002) and balloon angioplasty (0.41 +/- 0.10 vs 0.19 +/- 0.08, p = 0.0005) in concentric plaques. Coronary stenting also induced a greater luminal gain index than directional atherectomy in calcific plaques (0.30 +/- 0.11 vs 0.18 +/- 0.09, p = 0.04). In conclusion, these data show that plaque morphology assessed by preprocedure intracoronary ultrasound influences the acute luminal enlargement achieved by different coronary interventions. The knowledge of plaque composition may be useful in guiding the choice of the device to be used to obtain a larger acute luminal gain.

Influence of plaque morphology on the mechanism of luminal enlargement after directional coronary atherectomy and balloon angioplasty.

OBJECTIVE: To relate the mechanism of luminal gain after directional atherectomy and balloon angioplasty to the morphological characteristics of the coronary lesions, assessed by intravascular ultrasound imaging. DESIGN: Intravascular ultrasound imaging was performed before and after the revascularisation procedure to assess the contribution of wall stretching and plaque reduction in luminal gain. SUBJECTS: 32 patients undergoing balloon angioplasty and 29 undergoing directional coronary atherectomy. MAIN RESULTS: The main luminal area in vessels treated by balloon angioplasty increased from 1.51 (SD 0.30) to 3.91 (1.09) mm2 (P < 0.0001) with a concomitant increase in total vessel area from 11.44 (2.73) to 13.07 (2.83) mm2 (P < 0.0001). Therefore stretching of the vessel wall accounted for 68% of the luminal gain while plaque reduction accounted for the remaining 32%. This mechanism ranged from 45% in non-calcific plaques to 81% in echogenic plaques. The main luminal area in vessels treated by directional atherectomy increased from 1.49 (0.32) to 4.68 (1.73) mm2 (P < 0.0001), with a concomitant increase of total vessel area from 13.61 (4.67) to 15.2 (4.04) mm2 (P = 0.006). Thus stretching of the vessel wall accounted for 49% of the luminal area gain and plaque reduction for the remaining 51%. The presence of calcium influenced the relative contribution of these two mechanisms to the final luminal gain after directional atherectomy, since in calcific plaques stretching of the vessel wall accounted for only 9% of the luminal gain as compared to 56% in non-calcific plaques. After balloon angioplasty there was greater evidence of coronary dissections (32% v 3% after directional atherectomy, P < 0.01) and plaque fissure (60% v 0%, P < 0.01). Plaque fissure was more frequently seen in echolucent and concentric lesions, whereas dissections prevailed in echogenic and eccentric lesions. CONCLUSIONS: Intravascular ultrasound imaging may allow the assessment of acute changes in lumen and vessel wall after revascularisation procedures, and help in evaluating the potential effect of the structure and morphology of coronary lesions on the mechanism of luminal enlargement.

Comparison of coronary lesions obtained by directional coronary atherectomy in unstable angina, stable angina, and restenosis after either atherectomy or angioplasty.

The present study investigated the incidence of the histopathologic lesions and of growth factor expression in a consecutive series of directional coronary atherectomy (DCA) samples from 40 unstable angina pectoris patients without prior acute myocardial infarction and compared the findings with those obtained in DCA samples from 18 patients with stable angina without previous infarction and 18 patients with restenosis. We investigated coronary thrombosis, neointimal hyperplasia, and inflammation. For unstable angina, we correlated the angiographic Ambrose plaque subtypes with the histopathologic findings. The immunophenotype of plaque cells and the growth factor expression were assessed with specific antibodies for cell characterization and for the expression of basic fibroblast and platelet-derived AA and AB growth factors and receptors. The incidence of coronary thrombosis was 35% in patients with unstable angina, 17% in those with stable angina, and 11% in patients with restenosis. Neointimal hyperplasia was found in 38% of unstable angina cases, in 17% of stable angina cases, and in 83% of restenosis cases. Inflammation without thrombus or accelerated progression occurred in 20% of unstable angina and 6% of stable angina samples. In 52% of unstable angina cases, inflammation coexisted with thrombosis and/or neointimal hyperplasia. In the unstable angina group, 71% of the plaques with thrombus had a corresponding angiographic pattern of complicated lesions. The growth factor expression, reported as percentage of cells immunostaining with different growth factor antibodies, was highest in restenosis, followed by unstable angina and stable angina lesions.(ABSTRACT TRUNCATED AT 250 WORDS)