A finite element analysis of diaphragmatic hernia repair on an animal model.

The diaphragm is a mammalian skeletal muscle that plays a fundamental role in the process of respiration. Alteration of its mechanical properties due to a diaphragmatic hernia contributes towards compromising its respiratory functions, leading to the need for surgical intervention to restore the physiological conditions by means of implants. This study aims to assess via numerical modeling biomechanical differences between a diaphragm in healthy conditions and a herniated diaphragm surgically repaired with a polymeric implant, in a mouse model. Finite Element models of healthy and repaired diaphragms are developed from diagnostic images and anatomical samples. The mechanical response of the diaphragmatic tendon is described by assuming an isotropic hyperelastic model. A similar constitutive model is used to define the mechanical behavior of the polymeric implant, while the muscular tissue is modeled by means of a three-element Hill's model, specifically adapted to mouse muscle fibers. The Finite Element Analysis is addressed to simulate diaphragmatic contraction in the eupnea condition, allowing the evaluation of diaphragm deformation in healthy and herniated-repaired conditions. The polymeric implant reduces diaphragm excursion compared to healthy conditions. This explains the possible alteration in the mechanical functionality of the repaired diaphragm. Looking to the surgical treatment of diaphragmatic hernia in human neonatal subjects, this study suggests the implementation of alternative approaches based on the use of biological implants.

Uranium beam characterization at CIRCE for background and contamination determinations.

The Accelerator Mass Spectrometry (AMS) is the most sensitive technique, compared either to the Inductively Coupled Plasma (ICP-MS) or Thermal Ionization (TI-MS) mass spectrometer, for the actinide (e.g. (236)U, (x)Pu isotopes) measurements. They are present in environmental samples at the ultra trace level since atmospheric tests of Nuclear Weapons (NWs) performed in the past, deliberate dumping of nuclear waste, nuclear fuel reprocessing, on a large scale, and operation of Nuclear Power Plants (NPPs), on a small scale, have led to the release of a wide range of radioactive nuclides in the environment. At the Center for Isotopic Research on Cultural and Environmental heritage (CIRCE) in Caserta, Italy, an upgraded actinide AMS system, based on a 3-MV pelletron tandem accelerator, has been developed and routinely operated. At CIRCE a charge state distribution as a function of terminal voltage, the beam emittance, measured in the 20° actinides dedicated beam line, as well as the energy and position validation of the U ions were performed in order to determine the best measurement conditions. A (236)U/(238)U isotopic ratio background level of about 5×10(-12) or 3×10(-13), depending on the Time of Flight-Energy (TOF-E) configurations, as well as the spatial distribution of the (235)U, (238)U interferences ions and a (236)U contamination mass of about 0.5 fg have been determined.

Stellar and primordial nucleosynthesis of 7Be: measurement of 3He(alpha,gamma)7Be.

The 3He(alpha,gamma)7Be reaction presently represents the largest nuclear uncertainty in the predicted solar neutrino flux and has important implications on the big bang nucleosynthesis, i.e., the production of primordial 7Li. We present here the results of an experiment using the recoil separator ERNA (European Recoil separator for Nuclear Astrophysics) to detect directly the 7Be ejectiles. In addition, off-beam activation and coincidence gamma-ray measurements were performed at selected energies. At energies above 1 MeV a large discrepancy compared to previous results is observed both in the absolute value and in the energy dependence of the cross section. Based on the available data and models, a robust estimate of the cross section at the astrophysical relevant energies is proposed.

[Implantation of the Palmaz-Schatz stent in coronary vessels irrigating and non-irrigating necrotic myocardial areas: comparison of acute results and at mid-term]. / Impianto di stent di Palmaz-Schatz in vasi coronarici tributari e non tributari di aree miocardiche necrotiche: confronto dei risultati acuti e a medio termine.

Recent evidence suggests that higher restenosis rate is observed after coronary angioplasty of an infarct-related artery. Furthermore, angiographic restenosis seems associated with a deterioration of left ventricular function at follow-up. The aim of this study was to assess the acute results and angiographic restenosis following coronary artery stenting of infarct-related (Group 1) and non infarct-related coronary arteries (Group 2). We retrospectively analyzed the results of 381 consecutive patients treated with Palmaz-Schatz coronary stent implantation between May 1992 and January 1996. Stenting of the infarct-related artery was performed in 154 patients (Group 1), while 227 patients (Group 2) received stenting of the non infarct-related artery. Both groups had similar age, gender, clinical conditions and coronary angiographic pattern. There were no significant differences between groups, concerning type of stented coronary vessel (left anterior descending-LAD 52.4% vs non-LAD 47.6%, Group 1, LAD 59.5% vs non-LAD 40.5%, Group 2) and number of stents per patient (1.31 +/- 0.48 in Group 1, 1.18 +/- 0.56 in Group 2) and per coronary vessel (1.17 +/- 0.54 in Group 1, 1.09 +/- 0.46 in Group 2). The procedure was performed using similar maximal inflation pressures in both groups (13.3 +/- 2.9 atm in Group 1, 13.40 +/- 3.17 atm in Group 2). Technical success was achieved in 96.8% of Group 1 and in 96% of Group 2 patients. Acute coronary stenting success and major adverse events (acute myocardial infarction, emergency bypass, death) were similar in both groups of patients. No difference was found in restenosis rate at 6-month angiographic follow-up (Group 1 = 29.8%, Group 2 = 27%). In conclusion, this study indicates that stenting of infarct and non infarct-related coronary arteries has similar success and 6-month restenosis rates.

Local heparin delivery prior to coronary stent implantation: acute and six-month clinical and angiographic results.

Stents increase smooth muscle cell proliferation, which may also lead to in-stent restenosis. A local delivery strategy provides higher drug concentration at the angioplasty site and may limit the proliferative response following stenting. Local heparin delivery was attempted in 35 patients following balloon angioplasty using an "over-the-balloon" style catheter (infusion sleeve). The infusion sleeve was successfully tracked and heparin was delivered in 33 (94%) patients. Heparin (1,000 IU/ml) was delivered under low (45 psi, 2 ml, n = 4), intermediate (75 psi, 4 ml, n = 11), and high (100 psi, 4 ml, n = 18) proximal infusion pressures. Stent placement was successful in all cases. Acute and in-hospital complications were a severe arterial spasm after heparin delivery, a non Q-wave myocardial infarction, and two vascular complications. Ten dissections were observed after PTCA and prior to heparin delivery. Of these dissections, 7 remained unchanged, 2 worsened, and 1 improved with local delivery. When heparin was delivered in the absence of dissection, no new dissections were observed. Of the 33 patients who received heparin, 30 (91%) had no symptoms and a negative exercise test at clinical follow-up. QCA analysis of 6-month follow-up angiograms, performed in 32 of 33 (97%) patients, demonstrated an acute gain of 1.98 +/- 0.67 mm, a late loss of 0.94 +/- 0.78 mm, a net gain of 1.04 +/- 0.78 mm, and a loss index of 0.48 +/- 0.32. Restenosis (> or = 50% stenosis) was observed in 4 of 32 (12%) patients. Local delivery of heparin via the infusion sleeve following PTCA and prior to stent deployment is feasible with an acceptable safety profile and a low clinical and angiographic restenosis rate at 6 months.

Evidence of multifocal activity of coronary disease in patients with acute myocardial infarction.

BACKGROUND: Destabilization of the fibrous cap facilitates plaque rupture, thrombus formation, and myocardial infarction. Because systemic stimuli, such as lipoproteins, infectious agents, and autoantigens, may incite this reaction, one may wonder whether disruption mechanisms are only local or systemic and infarction is caused by an arbitrary plaque event or by a systemic, acute activity of the coronary disease. METHODS AND RESULTS: Early (3 to 5 days) and late (1 month) peri-infarction coronary angiographic data in 23 patients with first infarction were compared with that in 23 similar patients, with angiography performed because of stable angina and repeated after 1 month before angioplasty. Nonculprit lesion changes at the narrowest point defined progression or regression when exceeding 0.27 mm. In patients with recent infarction we found that 16 had progression, 4 had regression, 1 had both, 2 were steady (values in patients with stable angina being 2 [P<.0011, 1 [NS], 0 [NS], and 20 [P<.001]); 27 lesions were infarct related; 17 of the 45 nonculprit lesions progressed and 5 regressed (values in stable angina being 2 [P<.001] and 1 [P<.05] out of 78); minimal diameter reduction of progressing stenoses averaged 0.39 mm; lumen increase of regressing lesions averaged 0.30 mm; 3 patients developed interim rest angina associated with progression of a nonculprit lesion. CONCLUSIONS: A greater proportion of subjects and lesions with progression or regression (in infarction versus stable angina) supports the hypothesis that infarction is a hallmark of systemic coronary disease activity. Changes might vary according to the "maturation" stage of an atheroma, and maximal expression would be at the level of the offending plaque. Shrinkage, thrombolysis, or vascular remodeling would determine the residual plaque morphology.

Changes in right ventricular filling dynamics during left anterior descending, left circumflex and right coronary artery balloon occlusion.

AIM: Transient coronary artery occlusion during percutaneous transluminal coronary angioplasty may cause left ventricular diastolic dysfunction. The aim of this study was to evaluate the effect of left anterior descending, left circumflex and right coronary artery balloon occlusion on right ventricular diastolic function. METHODS: Thirty-five patients with single-vessel coronary artery disease and no previous myocardial infarction were selected. Left and right ventricular filling pressures were monitored by Doppler echocardiography and haemodynamic monitoring. This was performed during and immediately after 60 s of coronary balloon occlusion of the left anterior descending artery in 21 cases (Group 1), the left circumflex artery in eight cases (Group 2) and the right coronary artery in six cases (Group 3). Doppler analysis of left and right ventricular filling included peak velocity of early (PFVE) and late ventricular filling (PFVA) and PFVE to PFVA ratio (PFVE/PFVA). RESULTS: In all three groups, balloon inflation induced a significant increase in left and right filling pressures (P < 0.05). No qualitative difference in haemodynamic changes was found between groups during inflation. Significant impairment in the Doppler pattern of left and right ventricular filling occurred after 20 s of coronary occlusion: PFVE values in mitral and tricuspid valves decreased by 14% and 25% in Group 1, 13% and 25% in Group 2, and 10% and 21% in Group 3, respectively, as PFVA remained unchanged in all groups, the PFVE/PFVA ratio of mitral and tricuspid valve flows significantly decreased (Group 1: -12% and -20%, Group 2: -10% and -21%, Group 3: -14% and -21%, respectively). All parameters returned to baseline within 30 s after each balloon deflation. CONCLUSION: Our data suggest that brief episodes of acute myocardial ischaemia, such as those induced by 60 s of coronary artery occlusion during percutaneous transluminal coronary angioplasty, elicit simultaneous diastolic dysfunction of both ventricles, independent of the coronary artery involved.

[Peri-infarct angiographic behavior of "non-culprit" coronary infarct lesions]. / Comportamento angiografico perinfartuale delle lesioni coronariche "non colpevoli" di infarto.

Because systemic factors, such as lipoproteins, autoantigens, infectious agents, may facilitate plaque rupture, thrombus formation and coronary occlusion, the question may arise of whether thrombosis be only a local plaque event or the consequence of an acute activity of the entire coronary tree. Taking changes at the narrowest point of non culprit lesions as reflecting progression or regression of the disease when > 0.27 mm, early (within a few days) and late (within 1 month) coronarographic findings in 23 patients with first infarction were compared with those of patients with stable angina, in whom coronary angiography was performed for diagnostic purposes and was repeated 1 month later, before angioplasty. Sixteen infarction patients had progression, 4 had regression, 1 had both, and 2 had steadiness; corresponding values in stable angina group were 2 (p < 0.001), 1 (NS), 0 (NS) and 20 (p < 0.001). In the infarction group, 17 out of the 45 non culprit lesions progressed and 5 regressed; corresponding figures in stable angina group were 2 (p < 0.001) and 1 (p < 0.05). Three of the infarction patients developed interim angina at rest that was associated with progression of a culprit lesion in each of them. These results support the hypothesis that in a number of cases infarction may not reflect an arbitrary plaque event but rather a systemic coronary disease activity with maximal expression at the level of the offending plaque.

Treatment of ostial lesions of the left anterior descending coronary artery with Palmaz-Schatz coronary stent.

We evaluated acute and long-term clinical and angiographic results of elective Palmaz-Schatz coronary stent implantation for left anterior descending coronary artery (LAD) ostial stenosis in 23 consecutive patients. Eight patients had stable angina, 14 had unstable angina, and 1 had recent myocardial infarction. Sixteen patients had single-vessel, 5 had double-vessel, and 2 had triple-vessel disease. Clinical success without major complications (death, acute myocardial infarction, emergency coronary artery bypass grafting) was obtained in all cases and technical success in 20 cases (86.9%). After stenting, minimal lumen diameter increased from 1.05 +/- 0.45 mm to 2.89 +/- 0.52 mm (p < 0.001), and percent diameter stenosis decreased from 65.49% +/- 13.36% to 2.94% +/- 19.93% (p < 0.001). One case of subacute thrombosis and no major bleeding occurred. Twenty patients were followed-up for 6 months, during which no acute cardiac event (death, acute myocardial infarction) was observed. Eighteen patients were eligible for follow-up coronary angiography; restenosis (> or = 50% diameter stenosis) was observed in 4 (22.2%). Minimal lumen diameter was 1.77 +/- 0.55 mm, percent diameter stenosis was 39.66% +/- 17.62%, late loss was 1.01 +/- 0.69 mm, net gain was 0.79 +/- 0.55 mm, and loss index (late loss/acute gain) was 0.53 +/- 0.37. This study suggests that elective Palmaz-Schatz stent implantation may be a safe and successful treatment of LAD ostial lesions and provides a large increase in lumen diameter.

Prompt and safe femoral hemostasis with a collagen device after intracoronary implantation of Palmaz-Schatz stents.

We report the safety and efficacy of sealing the femoral puncture site with percutaneously applied collagen after Palmaz-Schatz stent implantation in 100 consecutive patients. Patients were anticoagulated with continuous heparin infusion, overlapping oral anticoagulants, and antiplatelet therapy by dextran, aspirin, and dipyridamole. At the time of sheath removal and collagen application, the mean activated partial thromboplastin time and prothrombin time values expressed as international normalized ratio were 3.2 +/- 2.1 and 1.6 +/- 0.7, respectively. The hemostasis time ranged from 1 to 8 minutes (mean 2.18 +/- 2.08 minutes). Only two (2%) patients had major puncture-site bleeding (not seal related in one case) that required surgery and blood transfusions. Small (< 6 cm) and medium (6 to 10 cm) hematomas observed in 12 (12%) and 2 (2%) patients, respectively, resolved spontaneously without sequelae. Local infection developed in 2 (2%) patients, who were successfully treated with antibiotics without clinical consequences. Subacute stent thrombosis was observed in only 1 (1%) patient. Repeat catheterization through the same femoral artery was performed at 6-month follow-up in 55 patients without difficulty or vascular complications. These findings suggest that percutaneous collagen application after coronary stenting is a secure method of achieving prompt and effective femoral hemostasis with a low incidence of major vascular bleeding complications despite intense anticoagulation. Stable hemostasis may allow continued full-dose anticoagulation, reducing the risk of stent subacute thrombosis.

Obstruction of the right pulmonary artery by an aortic aneurysm complicating previous coronary bypass grafting.

We report a case of right main pulmonary artery compression due to a type II dissecting aortic aneurysm simulating massive pulmonary artery embolism. Aortic tear and intimal splitting developed around an aortocoronary bypass graft performed 11 months earlier. Ultrasound detected the aortic aneurysm and pulmonary hypertension, and excluded emboli in the pulmonary artery. Pulmonary angiography explained the lung involvement, showing compression of the right main pulmonary artery. Coronary and aortic angiograms demonstrated that the aortic aneurysm developed around the right venous bypass graft. Surgery confirmed the angiographic findings and the pathogenesis of the syndrome.

Facilitation of coronary spasm by propranolol in Prinzmetal's angina: fact or unproven extrapolation?

BACKGROUND: Alpha-adrenergic activation enhances coronary vascular tone; beta-blockade leaves alpha-adrenergic vasoconstriction unopposed. Whether beta-adrenergic blockade facilitates coronary spasm in patients with Prinzmetal's angina is unknown. METHODS: Using quantitative angiography, we evaluated the response of normal and narrowed coronary arteries to intravenous propranolol, a cold pressor test (an alpha-stimulus), and the combination of the two in 15 patients with Prinzmetal's (group 1) and in 19 with classic (group 2) angina. From measurements of heart rate, systemic and pulmonary arterial pressures, and left and right ventricular ejection times, we derived the tension-time index per minute as a measure of the oxygen need (O2 demand) of the whole heart. RESULTS: In group 1, cold invariably constricted normal and diseased vessels, and in two patients elicited spasm at sites of significant lesions; these changes did not correlate with those in O2 demand. In group 2, the vasomotor reaction of normal and narrowed vessels in response to cold correlated with the modifications in O2 demand. After propranolol administration, (1) in normal vessels in both groups, the baseline luminal diameter varied in parallel with the changes in myocardial O2 demand; (2) narrowings in group 1 patients invariably dilated and in group 2 the caliber varied according to changes in O2 demand; (3) during cold stimulation, luminal narrowing in group 1 varied in parallel with O2 demand, and, in group 2, vessels were uniformly constricted. CONCLUSION: These results do not support the facilitation of coronary spasm by propranolol in Prinzmetal's angina and support the hypothesis that the contractility of coronary vessels in patients with this form of angina is different from that in the classic form.

Quantitative analysis of factors influencing late lumen loss and restenosis after directional coronary atherectomy.

Although encouraging initial results have been demonstrated after directional atherectomy, the mechanisms and predictors of late lumen loss and restenosis after this procedure have not been evaluated. To examine these issues, clinical and angiographic follow-up were obtained in 262 (96%) and 212 (77%) of 274 patients undergoing successful directional coronary atherectomy. Symptom recurrence developed in 87 (33%) patients and angiographic restenosis was found in 93 (44%). Restenosis was highest in re-stenotic lesions in saphenous vein grafts (78% [95% confidence interval (CI): 56 to 100%]) and lowest in new-onset lesions in the left anterior descending (27% [95% CI: 15 to 39%]) and circumflex (14% [95% CI: 0 to 43%]) coronary arteries. Residual lumen diameter immediately after atherectomy was smaller in re-stenotic lesions (p = 0.002) and in lesions > or = 10 mm in length (p = 0.02). Late lumen loss was associated with the minimal lumen diameter immediately after atherectomy (p < 0.001), saphenous vein graft lesion location (p = 0.008), and male gender (p = 0.02). Re-stenotic lesions (p < 0.001), lesions > or = 10 mm in length (p = 0.018), saphenous vein graft lesion location (p = 0.025) and male gender (p = 0.045) were independent predictors for restenosis. It is concluded that restenosis after directional atherectomy is related both to factors resulting in a suboptimal initial result and to factors contributing to excessive late lumen loss. These results may have implications for lesion selection in patients undergoing directional coronary atherectomy.

Early reocclusion after successful thrombolysis is related to lesion length and roughness.

BACKGROUND: Reocclusion is a significant problem after thrombolysis. Results of previous studies conflict regarding the association of various features of postlytic lesions that might predict reocclusion. METHODS: A computer-assisted algorithm was therefore used to quantitatively measure edge roughness in the 90-minute postlysis angiogram of 84 patients receiving recombinant tissue plasminogen activator within 6 hours of chest pain. RESULTS: Twenty-five patients had reocclusion, and 59 did not. The baseline angiogram showed no differences between these two groups with respect to minimal dimensions or relative percentage of stenosis. Length was greater in the reocclusion group (12.2 +/- 5.0 vs 10.0 +/- 4.2 mm, P < 0.05). Three of four roughness indices based on curvature analysis indicated greater roughness in those patients with reocclusion. These differences were largely due to the increased length of these lesions. The scaled edge-length ratio, an index of roughness that is independent of length, was, however, significantly greater in the reocclusion group (1.15 +/- 0.10 vs 1.09 +/- 0.08, P < 0.006). Multiple regression analysis showed that lesion length, the scaled edge-length ratio, and the number of features (invaginations and evaginations) per cm correlated independently with the risk for reocclusion. CONCLUSIONS: The length and roughness of postlytic residual lesions are determinants of reocclusion.

Clinical angiographic and histologic correlates of ectasia after directional coronary atherectomy.

Directional coronary atherectomy can cause ectasia (final area stenosis less than 0%), presumably due to an excision deeper than the angiographically "normal" arterial lumen. In a multicenter series in which quantitative coronary arteriography was performed after directional atherectomy in 382 lesions (372 patients), ectasia after atherectomy occurred in 50 (13%) lesions. By univariate analysis, ectasia was seen more often within the circumflex coronary artery (p = 0.008), in complex, probably thrombus-containing lesions (p = 0.015), and with higher device:artery ratios (p less than 0.001). Ectasia occurred less often in lesions within the right coronary artery (p = 0.008). Histologic analysis demonstrated adventitia or media, or both, in all patients with angiographic ectasia. Repeat angiography was performed in 188 of 271 eligible patients (69%) 6.1 +/- 2.4 months after atherectomy. Restenosis, defined as a follow-up area stenosis greater than or equal to 75%, was present in 50% of patients without procedural ectasia and in 70% of patients with marked ectasia (residual area stenosis less than -20%; p = 0.12). It is concluded that excision beyond the normal arterial lumen may occur after directional coronary atherectomy, related, in part, to angiographic and procedural features noted at the time of atherectomy. Restenosis tends to occur more often in patients with marked ectasia after coronary atherectomy.

Establishing comprehensive, quantitative criteria for detection of restenosis and remodeling after percutaneous transluminal coronary angioplasty.

To establish comprehensive criteria for detecting restenosis and remodeling, inter- and intraobserver reproducibility of quantitative arteriography in the analysis of 20 lesions immediately after and 6 months after percutaneous transluminal coronary angioplasty (PTCA) were assessed. Geometric single-plane (minimum, maximum, mean diameter and percent diameter stenosis), biplane (absolute and relative cross-sectional area stenosis), relative densitometric area stenosis and the average of densitometric area stenosis in orthogonal views were compared. A high intra- and interobserver reproducibility of all absolute measurements was found, with the highest correlations for minimum diameter and cross-sectional area (interobserver, r = 0.85 and 0.85; intraobserver, r = 0.93, and 0.95 for minimum diameter and cross-sectional area, respectively). Of the relative measurements, biplane geometric percent cross-sectional area stenosis was the most reliable and percent densitometric area stenosis was the most variable (interobserver, r = 0.67; intraobserver, r = 0.71). Only small differences were demonstrated for the absolute measurements between the analysis of lesions immediately after PTCA and after follow-up, whereas a greater variability was found for relative measurements, especially videodensitometry. In both circumstances, a poor correlation between relative densitometric cross-sectional area from orthogonal views was found, whereas geometric elliptical cross-sectional area correlated quite well with the average of densitometric percent cross-sectional area in orthogonal views (interobserver, r = 0.86; intraobserver, r = 0.84). Thus, data in this study support the suitability of geometric quantitative analysis for the assessment of PTCA results. Densitometry was the least reliable quantitative parameter.

Coronary adrenergic hyperreactivity in patients with syndrome X and abnormal electrocardiogram at rest.

Syndrome X is characterized by an abnormal vasomotility of coronary microvessels. It is unknown whether the presence of an ischemic-like pattern in the electrocardiogram at rest (T-wave inversion) reflects a more severe vasomotion disturbance. Changes in coronary sinus flow (thermodilution) and epicardial vessel diameter (quantitative angiography) during adrenergic activation were measured with a standard cold pressor test in patients with syndrome X whose electrocardiogram at rest was normal (group 1: 17 patients) or showed stable, symmetrically inverted T waves (group 2: 22 patients). Cold pressor test increased mean blood pressure and rate-pressure product to a similar extent in both groups, increased coronary sinus flow in group 1 (88 +/- 29 to 119 +/- 36 ml/min; p less than 0.05) and not in group 2 (109 +/- 37 vs 104 +/- 36 ml/min; p = not significant), and decreased coronary resistance in group 1 (1.38 +/- 0.42 to 1.19 +/- 0.38 mm Hg/ml/min; p less than 0.05) and augmented it in group 2 (1.06 +/- 0.32 to 1.28 +/- 0.43 mm Hg/ml/min; p less than 0.02). During cold stimulus, the proximal and middle segments of epicardial arteries showed negligible changes in their lumen, whereas the distal segment dilated in group 1 (1.81 +/- 0.27 to 2.01 +/- 0.32 mm; p less than 0.05) and constricted in group 2 (1.82 +/- 0.12 to 1.62 +/- 0.20 mm; p less than 0.05). Differences in coronary hemodynamic and angiographic responses between the groups were statistically significant (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical, angiographic and procedural correlates of quantitative coronary dimensions after directional coronary atherectomy.

To define the clinical, angiographic and procedural correlates of quantitative coronary dimensions after directional coronary atherectomy, 400 lesions in 378 patients were analyzed with use of qualitative morphologic and quantitative angiographic methods. Successful atherectomy, defined by a less than 75% residual area stenosis, tissue retrieval and the absence of in-hospital ischemic complications, was performed in 351 lesions (87.7%). After atherectomy, minimal cross-sectional area increased from 1.2 +/- 1.1 to 6.6 +/- 4.4 mm2 (p less than 0.001) and percent area stenosis was reduced from 87 +/- 10% to 31 +/- 42% (p less than 0.001). By univariate analysis, device size (p less than 0.001) and left circumflex artery lesion location (p = 0.004) were associated with a larger final minimal cross-sectional area. Conversely, restenotic lesion (p = 0.002), lesion length greater than or equal to 10 mm (p = 0.018) and lesion calcification (p = 0.035) were quantitatively associated with a smaller final minimum cross-sectional area. With use of stepwise multivariate analysis to control for the reference area, atherectomy device size (p = 0.003) and left circumflex lesion location (p = 0.007) were independently associated with a larger final minimal cross-sectional area, whereas restenotic lesion (p = 0.010), diffuse proximal disease (p = 0.033), lesion length greater than or equal to 10 mm (p = 0.026) and lesion calcification (p = 0.081) were significantly correlated with a smaller final minimal cross-sectional area. The number of specimens excised, the number of atherectomy passes and atherectomy balloon inflation pressure did not correlate with the final minimal cross-sectional area. Thus, directional atherectomy results in marked improvement of coronary lumen dimensions, at least in part correlated with the presence of certain clinical, angiographic and procedural factors at the time of atherectomy.