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Biomedical subjects

C Bauters

Publications and source records attributed to C Bauters.

At least 73 records · Page 4Linked to original sources
PubMed1997

Effects of stenting of recent or chronic coronary occlusions on late vessel patency and left ventricular function.

Due to high rates of late vessel reocclusion, balloon angioplasty of recent or chronic coronary occlusions is not associated with a sustained improvement in left ventricular function. Recent studies have suggested that stent implantation at coronary occlusions significantly reduces late vessel occlusion. We thus designed a study to analyze the effect of stent implantation at coronary occlusions on late vessel potency and left ventricular function. Twenty-four consecutive patients with recent or chronic coronary occlusions had successful stent implantation and were enrolled in a 6-month angiographic follow-up program. Contrast left ventricular cineangiography, at baseline and 6-month follow-up, as well as preprocedural, postprocedural, and follow-up angiograms analyzed with quantitative angiography were available in 22 of the patients (92%). At follow-up, no vessel reocclusion was observed and 32% of the patients, as analyzed by the >50% diameter stenosis criterion, had restenosis. There was a significant improvement in global left ventricular function with a decrease in both left ventricular end-diastolic volume index (LVEDVI, p <0.01) and left ventricular end-systolic volume index (LVESVI, p <0.0001) and an increase in left ventricular ejection fraction (LVEF, p <0.0001). Similarly, regional wall motion in the territory of the recanalized artery was also significantly improved (p <0.05). These effects were associated with a reduction in left ventricular filling pressure (p <0.0001). Stent implantation following balloon angioplasty of recent or chronic coronary occlusion is associated with a low rate of late vessel reocclusion, a reduction in cardiac volume, and an increase in ejection fraction. Such effects on left ventricular volumes could have a significant impact on patient survival.

Angioplasty, Balloon, Coronary↗
PubMed1997

Hypercholesterolemia attenuates angiogenesis but does not preclude augmentation by angiogenic cytokines.

BACKGROUND: The impact of hyperlipidemia on collateral vessel development in vivo remains enigmatic. We sought to determine the anatomic extent and functional capacity of the collateral bed that develops in response to limb ischemia in a well characterized animal model of spontaneous hypercholesterolemia, the Watanabe heritable hyperlipidemic (WHHL) rabbit. We further characterized the impact of exogenous angiogenic cytokine administration on collateral vessel development and function in the same animal model. METHODS AND RESULTS: Weight-matched 6-month-old male homozygous WHHL (n=9) and normal New Zealand White (NZW) (n=9) rabbits underwent surgical resection of one femoral artery. Ten days later, the ischemic hindlimb was evaluated for collateral vessel formation, blood flow, and tissue damage. Collateral vasculature was less extensive among WHHL than NZW, as indicated by a significant reduction in angiographic score (0.19+/-0.02 versus 0.35+/-0.03, P<.001) and capillary density (46.4+/-4.1 versus 78.9+/-4.6/mm2, P<.0002). This was associated with a reduction in calf blood pressure index (9.5+/-3.5% versus 32.8+/-2.8%, P<.0001), arterial blood flow (7.5+/-0.6 versus 13.6+/-0.7 mL/min, P<.0001), and muscle perfusion index (40.1+/-3.2% versus 65.9+/-2.0%, P<.0001) and an increase in muscle necrosis (48.16+/-5.41% versus 25.90+/-3.83% negative 2,3,5-triphenyltetrazolium chloride staining, P<.004). Treatment of WHHL rabbits (n=9) with recombinant human vascular endothelial growth factor produced a statistically significant improvement in all functional as well as anatomic indices of collateral development. CONCLUSIONS: Collateral vessel development associated with hindlimb ischemia in vivo is severely attenuated in an animal model of spontaneous hypercholesterolemia but nevertheless may be augmented by administration of angiogenic cytokines.

Animals↗
PubMed1997

Restenosis rates in diabetic patients: a comparison of coronary stenting and balloon angioplasty in native coronary vessels.

BACKGROUND: Diabetes is a major risk factor for restenosis after coronary balloon angioplasty. Recent studies have shown that coronary stenting significantly reduces restenosis compared with balloon angioplasty alone. However, limited information is available on the effect of coronary stenting in diabetic patients. METHODS AND RESULTS: We designed this study to analyze the effect of diabetes on restenosis in patients treated with either balloon angioplasty or coronary stenting who were enrolled in a 6-month angiographic follow-up program. Three hundred consecutive patients, 19% of whom were diabetics, who underwent coronary stent implantation during a single-vessel procedure on native coronary vessels and who had 6-month angiographic follow-up constituted the study group (stent group). Three hundred consecutive patients who underwent 6-month angiographic follow-up after single-vessel conventional balloon angioplasty served as control patients (balloon group). Preprocedural, postprocedural, and follow-up angiograms were analyzed with quantitative angiography. In the balloon group, the restenosis rate was almost twofold higher in diabetic than in nondiabetic patients (63% versus 36%; P=.0002) owing to both a greater late loss (0.79+/-0.70 versus 0.41+/-0.61 mm, respectively; P<.0001) and a higher rate of late vessel occlusion (14% versus 3%, respectively; P<.001). In the stent group, restenosis rates were similar in diabetics and nondiabetics (25% versus 27%, respectively). Furthermore, in the stent group, late loss (0.77+/-0.65 versus 0.79+/-0.57 mm, respectively) and the rate of late vessel occlusion (2% versus 1%, respectively) did not differ significantly between diabetic and nondiabetic patients. CONCLUSIONS: Although diabetics have increased rates of restenosis and late vessel occlusion after simple balloon angioplasty, they have the same improved outcome with coronary stenting that has been documented in nondiabetic patients.

Aged↗
PubMed1997

D allele of the angiotensin I-converting enzyme is a major risk factor for restenosis after coronary stenting.

BACKGROUND: Although intracoronary stent implantation significantly reduces restenosis compared with balloon angioplasty, a minority of patients still develop restenosis predominantly due to neointimal hyperplasia. Experimental studies suggest that the renin-angiotensin system is involved in neointimal hyperplasia after arterial injury. In humans, the plasma and cellular levels of ACE are associated with an I/D genetic polymorphism in the ACE gene, DD patients having higher levels. METHODS AND RESULTS: We investigated a possible relation between the ACE I/D polymorphism and restenosis in 146 patients who underwent successful implantation of a Palmaz-Schatz stent and had 6-month follow-up angiography. The minimal lumen diameter (MLD) before and after the procedure did not differ significantly among the three groups of genotypes (DD, ID, and II). At follow-up, MLD had a significant inverse relationship to the number of D alleles present (DD, 1.65 +/- 0.71 mm; ID, 1.84 +/- 0.60 mm; II, 2.05 +/- 0.61 mm; P < .007). Late luminal loss during the follow-up period was significantly related to the number of D alleles (DD, 0.89 +/- 0.61 mm; ID, 0.60 +/- 0.52 mm; II, 0.40 +/- 0.53 mm; P < .0001). The relative risk of restenosis (defined as a > 50% diameter stenosis at follow-up) approximated by the adjusted odds ratio was 2.00 per number of D alleles (95% confidence interval, 1.03 to 3.88, P < .04). CONCLUSIONS: The ACE I/D polymorphism influences the level of late luminal loss after coronary stent implantation. These results suggest that the renin-angiotensin system may be implicated in the pathogenesis of restenosis after coronary stenting.

Aged↗
PubMed1997

The angiotensin II type 1 receptor gene polymorphism is associated with coronary artery vasoconstriction.

OBJECTIVES: This study sought to assess the potential association of the angiotensin-converting enzyme (ACE) and angiotensin II type 1 (AT1) receptor gene polymorphisms on coronary vasomotion in humans. BACKGROUND: Abnormal coronary vasomotion plays a role in the clinical expression of coronary atherosclerosis. The components of the renin-angiotensin system are important determinants of vasomotor tone. Furthermore, epidemiologic evidence suggests that these components are involved in the pathogenesis of coronary artery disease. Indeed, two genetic polymorphisms of the ACE and AT1 receptor genes were synergistically associated with the occurrence of myocardial infarction. The influence of these genetic polymorphisms on the risk of myocardial infarction may be related, at least in part, to a deleterious effect on coronary vasomotion. METHODS: We studied the response of angiographically normal human coronary arteries after intravenous injection of methylergonovine maleate, a potent vasoconstrictor whose effects have been previously explored in various aspects of coronary artery disease. We characterized the ACE and AT1 receptor genotypes in a consecutive series of 140 patients with normal coronary arteries. Coronary vasomotion was assessed with quantitative coronary angiography. RESULTS: No effect of the ACE gene polymorphism was detected. Conversely, the patients carrying the AT1 receptor CC genotype (n = 13) had significantly greater vasoconstriction in distal coronary vessels (p < 0.009). CONCLUSIONS: The AT1 receptor gene polymorphism is associated with coronary vasomotion in humans.

Adult↗
PubMed1997

ACE inhibition accelerates endothelial regrowth in vivo: a possible explanation for the benefit observed with ACE inhibitors following arterial injury.

Recent in vitro studies suggest that angiotensin converting enzyme (ACE) inhibitors stimulate endothelial cell proliferation and migration. The present study was designed to test the hypothesis that an ACE inhibitor may accelerate endothelial regrowth in vivo. Twenty eight New Zealand White rabbits were randomized to receive placebo or the ACE inhibitor perindopril and underwent iliac balloon denudation. Endothelial regrowth, quantified 28 days after injury using Evans blue, was significantly greater in perindopril-treated animals than in controls (131 +/- 9 mm2 vs 69 +/- 8 mm2; P < .001). These results were confirmed by scanning electron microscopy and by specific immunostaining for endothelial cells. These data provide the first in vivo demonstration that ACE inhibitors accelerate endothelial regrowth after arterial injury. This effect may contribute to the benefit observed with ACE inhibition following arterial injury.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

[Primary pulmonary hypertension: a rare but often fatal complication of Crest syndrome].

In a retrospective study of 194 systemic sclerosis, we selected 37 Crest syndrome patients. Among these 37 patients, five presented a primary pulmonary hypertension. For three of these patients, the evolution of this primary pulmonary hypertension was rapidly fatal, one died of another cause. One died without certitude that death is imputable to HTAP. Diagnosis and management of the evolution of primary pulmonary hypertension may be easily assessed by doppler-echocardiography.

Aged↗
PubMed1997

Influence of late reopening of the infarct-related artery on left ventricular remodelling after myocardial infarction. IRIS Study Group.

AIMS: This trial was undertaken to assess the impact of late reopening of the infarct-related artery on left ventricular remodelling in post-myocardial infarction patients. METHODS: One hundred and fifty seven patients with recent myocardial infarction were routinely submitted to delayed (second week) catheterization. They also underwent systematic angioplasty of a significantly narrowed infarct-related artery with a suitable anatomy, or reopening of a totally occluded infarct-related artery, and repeat follow-up catheterization after 4 months. Changes in left ventricular ejection fraction, left ventricular volumes, and percent of regional hypokinesia were assessed over the study period. RESULTS: One hundred and thirty-two patients had two interpretable left ventriculograms and two interpretable coronary angiograms. At initial angiography, 56 out of 96 patients with a patent infarct-related artery were successfully submitted to percutaneous coronary angioplasty, of whom 25 had restenosis and eight had total reocclusion at follow-up angiography. Percutaneous transluminal coronary angioplasty was not attempted in the remaining 40 patients due to unsuitable anatomy in 18 or a nonsignificant lesion in 22. The infarct-related artery was totally occluded in 36 patients at initial angiography, and successfully reopened by means of angioplasty in 19, of whom seven showed a reocclusion at follow-up angiography. The independent predictors of left ventricular enlargement, identified by means of multivariate regression analysis, were initial stroke volume index < 40 ml.m-2 (odds ratio = 6.3, 95% confidence interval = [2.5; 16.6]), initial end-systolic volume index > 50 ml.m-2 (odds ratio = 7.1, 95% confidence interval = [1.5; 25.8]), anterior infarct location (odds ratio = 4.1, 95% confidence interval = [1.4; 11.5]) and reocclusion of the infarct-related artery (odds ratio = 7.3, 95% confidence interval = [1.3; 27.3]). Angioplasty of a patent but significantly narrowed infarct-related artery was not found predictive. CONCLUSIONS: This study demonstrates that reocclusion of a previously open infarct-related artery, as well as the initial low stroke volume index, enlarged end-systolic volume index and anterior infarct location are independent predictors of long-term left ventricular enlargement. These results emphasize the impact of long-term sustained patency of the infarct-related artery on the prevention of left ventricular dysfunction. The need for a larger randomized trial is recognised.

Adrenergic beta-Antagonists↗
PubMed1997

Association of angiotensin converting enzyme and angiotensin II type 1 receptor genotypes with left ventricular function and mass in patients with angiographically normal coronary arteries.

OBJECTIVE: To analyse the potential association of the angiotensin converting enzyme (ACE) and angiotensin II type 1 receptor (AT1R) gene polymorphisms on left ventricular function and mass in patients with normal coronary arteries. DESIGN: Consecutive sample. SETTING: University hospital. SUBJECTS: 141 consecutive white patients referred for coronary angiography and with angiographically normal coronary arteries. Patients with valvar diseases, cardiomyopathies, or a history of myocardial infarction were excluded. MAIN OUTCOME MEASURES: Left ventricular variables were measured for all patients. The ACE and AT1R genotypes were determined with a polymerase chain reaction based protocol using DNA prepared from white blood cells. A general linear model was used to compare data according to the ACE and to the AT1R genotypes. RESULTS: A strong association was observed between left ventricular mass and systemic hypertension (mean (SD) hypertension: 114 (31) g/m2; no hypertension 98 (23) g/m2; P < 0.003). However, no influence of ACE and AT1R polymorphisms on left ventricular mass was found, regardless of systemic hypertension. The subjects homozygous for the AT1R CC mutation had a significantly lower ejection fraction than those with allele A (AC+AA) (mean (SD) 62(12)% and 68(10)%, respectively, P < 0.05). No synergistic interaction of ACE and AT1R gene polymorphisms on left ventricular function and mass was found. CONCLUSIONS: These data do not support an association of the ACE and AT1R genotypes on left ventricular hypertrophy in white patients with normal coronary arteries.

Angiotensin II↗
PubMed1997

bFGF restores endothelium-dependent responses of hypercholesterolemic rabbit thoracic aorta.

In animal models, a hypercholesterolemic diet induces areas of deendothelialization and impairs endothelium-dependent vasorelaxation. Angiogenic growth factors increase endothelial cell growth in vivo. This study was thus designed to test the hypothesis that chronic administration of basic fibroblast growth factor (bFGF) in hypercholesterolemic rabbits might restore normal physiological responses to endothelium-dependent agonists. After feeding on a 2% cholesterol diet for 6 wk, 14 New Zealand White rabbits received twice-weekly intravenous boluses of either 2.5 microg bFGF (hypercholesterolemic bFGF group, n = 6) or placebo (hypercholesterolemic control group, n = 8) for 3 wk and were killed for assessment of in vitro vasoreactivity and for histological analysis. Six animals fed with standard rabbit diet were used to assess normal responses. Endothelium-dependent responses to acetylcholine and to the calcium ionophore A-23187 were reduced in the hypercholesterolemic control group compared with normal rabbits. Hypercholesterolemic animals treated with bFGF had significantly better endothelium-dependent responses than hypercholesterolemic rabbits not treated with bFGF. Endothelium-independent responses did not differ significantly among the three groups. A similar degree of plaque formation was observed in control- and bFGF-treated hypercholesterolemic rabbits. These results show that, in this model of atherosclerosis, bFGF has a highly beneficial effect on the functional responses of atherosclerotic vessels and does not have a deleterious effect on the degree of plaque formation.

Acetylcholine↗
PubMed1997

[Coronary angioscopy].

Coronary angioscopy evaluates the composition of the atherosclerotic plaque by direct examination of the arterial wall. The angioscope is fitted with a balloon which prevents assessment of the proximal segment of the vessels. The fibre optic system provides and excellent view of the mid and distal segments of the coronary arteries. The coronary arteries appear smooth and white on angioscopy. The atherosclerotic plaque is a white or yellowish incursion. Unstable plaques are characterised by the presence of thrombus. In unstable angina, thrombus is observed in 64% of cases and in 75% of cases during the first month after myocardial infarction. The colour of the plaque seems to be related to its fragility: the yellow plaque is much more common during myocardial infarction than in unstable angina (75% versus 47% of cases). Finally, after coronary angioplasty restenosis is more commonly white, covered by neo-intimal proliferation. Angioscopy has been shown to be feasible and safe and it is a better method of identifying thrombus. At present, it is a tool for clinical research in coronary thrombosis and interventional cardiology.

Angioplasty, Balloon, Coronary↗
PubMed1997

Growth factors as a potential new treatment for ischemic heart disease.

Growth factors such as fibroblast growth factor (FGF) and vascular endothelial growth factor (VEGF) exert important effects on endothelial cells in vitro and in vivo. This article reviews the effect of these two growth factors on endothelial dysfunction in various animal models of vascular disease: (1) collateral circulation supplying an ischemic territory, (2) balloon injury, and (3) diet-induced experimental atherosclerosis. Endothelial dysfunction may limit the beneficial effects of collateral vessels on tissue perfusion. Administration of VEGF or basic FGF (bFGF) augments collateral development in different models of hindlimb ischemia by enhancing neovascularity and by facilitating the recovery of endothelial function in the collateral circulation. Similarly, studies performed after balloon angioplasty have demonstrated abnormal responses of previously dilated sites to endothelium-dependent agonists. Administration of VEGF or bFGF increases endothelial regrowth and normalizes endothelium-dependent responses after experimental angioplasty. Finally, endothelium-dependent relaxation is impaired in diet-induced experimental atherosclerosis. It was recently demonstrated that hypercholesterolemic rabbits treated with bFGF had significantly better endothelium-dependent responses than those not treated with bFGF. These results show that in vivo administration of the endothelial cell growth factors VEGF and bFGF leads to significant improvement in endothelium-dependent responses and supports the concept of using these growth factors as a new therapeutic strategy for patients with vascular diseases.

Animals↗
PubMed1997

[Endothelial dysfunction in cardiovascular diseases: therapeutic implications after coronary angioplasty].

Restenosis remains the principal limitation of coronary angioplasty; its main mechanisms are neointimal hyperplasia and vascular remodeling. The endothelium destroyed at angioplasty will progressively recover the denuded zone. However, dysfunction of this neo-endothelium persists for quite a period and may participate in restenosis by influencing these two components (hyperplasia and remodeling). Several therapeutic strategies are under evaluation to try and accelerate the regeneration of the endothelium and make it functional more rapidly. Increasing available nitric oxide (NO) decreases the hyperplasia and improves endothelial function. Growth factors accelerate the endothelial regeneration and improves its function: the effect on hyperplasia depends on the growth factor used. The angiotensin converting enzyme inhibitors decrease hyperplasia by improving endothelial function. These therapeutic strategies merit evaluation in the clinical setting.

Angioplasty, Balloon, Coronary↗
PubMed1997

[Recanalization of complete coronary occlusions followed by STENT implantation. An angiographic study after 6 months].

The restenosis and reocclusion rate after coronary recanalization by conventional angioplasty are high. The role of stent implantation in this context is unknown. The authors assessed a group of 49 patients who underwent implantation of one or more stent after a recanalization procedure by angiography at 6 months. The restenosis rate assessed by quantitative angiography was 24%; no cases of reocclusion were observed. These angiographic results were accompanied with a significant improvement of the anginal symptoms (p < 0.01). These results suggest that stent implantation following recanalization of a coronary occlusion may be beneficial on the restenosis and reocclusion rates and anginal symptoms. However, they should be confirmed by randomised study. It would also be important to analyse the impact of this procedure on the outcome of left ventricular function.

Aged↗
PubMed1996

Therapeutic angiogenesis following arterial gene transfer of vascular endothelial growth factor in a rabbit model of hindlimb ischemia.

The plasmid phVEGF165, expressing the 165-amino-acid isoform of vascular endothelial growth factor (VEGF), an endothelial cell specific mitogen, was applied to the polymer coating of an angioplasty balloon and delivered percutaneously to the iliac artery of rabbits in which the femoral artery had been excised to cause hindlimb ischemia. Site-specific transfection of phVEGF165 resulted in augmented development of collateral vessels documented by serial angiograms, and increased capillary density as well as increased capillary/myocyte ratio documented histochemically at necropsy. Consequent amelioration of the hemodynamic deficit in the ischemic limb was documented by improvement in the calf blood pressure ratio (ischemic/normal limb) to 0.70 +/- 0.08 in the VEGF-transfected group vs 0.50 +/- 0.18 in controls (p < 0.05). These findings suggest that site-specific arterial gene transfer of VEGF165 may achieve physiologically meaningful therapeutic modulation of vascular insufficiency.

Animals↗
PubMed1996

ACE polymorphism, a genetic predictor of occlusion after coronary angioplasty.

In this study, restenosis after coronary angioplasty is evaluated in a series of 291 consecutive patients according to ACE genotypes. The authors conclude that the ACE 2ID polymorphism has no effect on progressive restenosis after balloon angioplasty, but it is implicated in a distinct mechanism of restenosis (thrombosis and occlusion) that could explain discrepancies among previously published studies.

Angioplasty, Balloon, Coronary↗
PubMed1996

Basic fibroblast growth factor restores endothelium-dependent responses after balloon injury of rabbit arteries.

BACKGROUND: After experimental angioplasty, partial or complete reendothelialization of the denuded surface occurs; the function of the regenerated endothelium has, however, been shown to be abnormal. Basic fibroblast growth factor (bFGF) is mitogenic for endothelial cells in vitro and in vivo. We investigated whether chronic administration of bFGF in a rabbit model of balloon denudation might not only improve endothelial regrowth but also restore normal physiological responses to endothelium-dependent agonists. METHODS AND RESULTS: Thirty-nine New Zealand White rabbits underwent balloon denudation of the right iliac artery. Twenty rabbits received intravenous administration of bFGF (2.5 micrograms twice a week for 2 weeks). Nineteen rabbits receiving saline injections served as controls. Animals were killed on day 28 for assessment of reendothelialization and neointimal thickening and for analysis of in vitro vasoreactivity. Animals in the bFGF group had a significantly (P<.005) greater degree of reendothelialization than controls (115 +/- 13 versus 55 +/- 6 mm2). Neointimal thickening was similar in the two groups. Four weeks after denudation, endothelium-independent responses did not differ significantly between the two groups. In contrast, the maximal endothelium-dependent acetylcholine-induced relaxation of the bFGF-treated animals (Emax, 40 +/- 7%) was significantly greater than that of the control group (Emax, 11 +/- 9%; P<.05). CONCLUSIONS: Systemic administration of bFGF restores, in large part, the responses of previously denuded arterial segments to endothelium-dependent vasodilators. Angiogenic growth factors may help to reestablish normal endothelial cell function in patients who have undergone angioplasty.

Acetylcholine↗