Biomedical subjects
Publications and source records attributed to W Wijns.
Antiphospholipid antibodies are associated with arterial and venous thromboembolism, thrombocytopenia and fetal loss. According to several studies the obstetrical problems associated with antiphospholipid antibodies can be successfully treated with immunosuppressive or anticoagulant drugs. The detection of these antibodies is difficult owing to the lack of standardization and of specificity of the laboratory tests.
Asynchronous segmental early relaxation, defined as a localized early segmental outward motion of the left ventricular endocardium during isovolumetric relaxation, has been associated with an altered left ventricular relaxation rate. To determine whether asynchronous segmental early relaxation also results in impaired left ventricular filling, early diastolic ventricular wall motion and Doppler-derived left ventricular filling indexes were examined in 25 patients with documented coronary artery disease and normal systolic function. Patients were further classified into two groups according to the presence (n = 15, group 1) or absence (n = 10, group 2) of asynchronous early relaxation at left ventriculography. A third group of 10 age-matched normal subjects served as a control group. No differences were observed between the two patient groups with coronary artery disease with respect to age, gender distribution, heart rate, left ventricular systolic and diastolic pressures or extent and severity of coronary artery disease. No differences in transmitral filling dynamics were observed between group 2 patients and age-matched control subjects. Conversely, group 1 patients had significantly lower peak early filling velocities (44 +/- 11 vs. 58 +/- 11 cm/s, p less than 0.01), larger atrial filling fraction (45 +/- 4% vs. 38 +/- 4%, p less than 0.001), lower ratio of early to late transmitral filling velocities (0.6 +/- 0.08 vs. 0.99 +/- 0.18, p less than 0.001) and a longer isovolumetric relaxation period (114 +/- 12 vs. 90 +/- 6 ms, p less than 0.001) compared with group 2 patients and control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
Percutaneous transluminal angioplasty (PTCA) of coronary stenoses involving major bifurcations carries a small but significant risk of side branch occlusion which can be avoided by simultaneously using multiple dilatation systems. Among 1,275 PTCA procedures performed between 1984 and 1988 in 1,035 consecutive patients, 42 double wire procedures were applied (4%) to protect and/or dilate major coronary side branches. A total of 80 coronary stenoses were attempted of which 76 were located on a bifurcation and 4 on other segments. In the first 11 patients (group A), 2 guiding catheters were used and PTCA of each vessel was successfully performed by means of separate double lumen over-the-wire balloon catheters. In the next 31 patients (group B), 2 guidewires were advanced through a single guiding catheter and PTCA was attempted using "Monorail" balloon catheters sequentially advanced over the wires. In group B, a successful PTCA was obtained in 29 patients (93%) but twisting of the wires hampered balloon progression in 5 cases, such that dilatation could only be performed by stepping back to a single wire technique. The procedure time in group B was significantly shorter than in group A: 144 +/- 30 versus 230 +/- 52 minutes (p = .01). Repeat angiography was performed in 35 out of 40 patients (87%) after a mean of 180 +/- 46 days following successful PTCA. Angiographic restenosis was present in 37% (24/65) of bifurcation segments which, in our experience, is not significantly different from the angiographic restenosis rate in less complex lesions (248/740; 34%; NS).(ABSTRACT TRUNCATED AT 250 WORDS)
Case report of a woman with the characteristics of dominant exudative vitreoretinopathy. These anomalies are however unilateral and the family study is not very contributive. A platelet aggregation study carried out on the patient and 3 family members is normal.
The safety and therapeutic benefits of percutaneous transluminal coronary angioplasty of the left anterior descending coronary artery, the left circumflex coronary artery or both were assessed in 61 patients with chronic (greater than 3 months) occlusion of the right coronary artery. Recanalization of the right coronary artery was not performed before dilatation of left coronary artery lesions. All lesions could be dilated without an acute ischemic event in the catheterization laboratory. However, three patients underwent coronary artery bypass surgery within the first 8 days after coronary angioplasty. There were no in-hospital deaths. Of the remaining 58 patients, 51 (88%) had repeat angiography at a mean of 5.2 +/- 2.5 months. Patients were divided into two groups according to the presence (n = 17) or absence (n = 34) of restenosis defined as greater than or equal to 50% diameter stenosis at the dilated site. Baseline characteristics were comparable. The mean value for angina functional class at follow-up was significantly better in the group without than in the group with restenosis (0.4 +/- 0.6 vs 2.1 +/- 1.1, respectively; p less than 0.001). Sixty-five percent of the patients without restenosis were asymptomatic at follow-up. Seventy-five percent of the predicted maximal physical capacity was reached by 76% of the patients without restenosis compared with 33% in the group with restenosis (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
After successful coronary angioplasty, the minimal luminal diameter of the dilated coronary artery segment is generally smaller than the diameter of the largest balloon catheter at the maximal inflation pressure. The determinants of this phenomenon were studied in 28 patients. Biplane angiograms were obtained after intracoronary administration of isosorbide dinitrate (1 mg) before, immediately and 24 h after coronary angioplasty. Balloon and coronary luminal diameters were measured by automated contour detection. Immediately after the procedure, the difference between inflated balloon diameter and minimal luminal diameter averaged 0.93 +/- 0.43 mm for the entire group and was greater both in eccentric stenoses (1.13 +/- 0.39 vs. 0.70 +/- 0.36 mm; p less than 0.01) and after angioplasty with an oversized balloon (1.20 +/- 0.37 vs. 0.71 +/- 0.33 mm; p less than 0.005). At 24 h, the balloon - minimal luminal diameter difference was unchanged at the group level (0.86 +/- 0.38 mm, but the minimal luminal diameter increased significantly in the subgroup of coronary segments dilated with an oversized balloon (1.97 +/- 0.37 vs. 1.81 +/- 0.28 mm; p less than 0.05). Thus, the difference between the minimal diameter of a dilated coronary segment immediately after a successful coronary balloon angioplasty procedure and the maximal diameter of the inflated balloon catheter is dependent both on eccentricity of the stenosis and on the balloon/artery diameter ratio. Moreover, the increase in minimal luminal diameter 24 h after angioplasty performed with an oversized balloon suggest that in addition to elastic recoil partly reversible factors related to vessel barotrauma are involved.
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BACKGROUND: GR32191B is a novel thromboxane A2-receptor antagonist with potent antiagregational and antivasoconstrictive properties. We have conducted a randomized, double-blind placebo-controlled trial to study its usefulness in restenosis prevention. METHODS AND RESULTS: Patients received either GR32191B (80 mg orally before angioplasty and 80 mg/day orally for 6 months) or 250 mg i.v. aspirin before angioplasty and placebo for 6 months. Coronary angiograms before angioplasty, after angioplasty, and at 6-month follow-up were quantitatively analyzed. Angioplasty was attempted in 697 patients. For efficacy analysis, quantitative angiography at follow-up was available in 522 compliant patients (261 in each group). Baseline clinical and angiographic parameters did not differ between the two treatment groups. The mean difference in coronary diameter between postangioplasty and follow-up angiogram (primary end point) was -0.31 +/- 0.54 mm in the control group and -0.31 +/- 0.55 mm in the GR32191B group. Clinical events during 6-month follow-up, analyzed on intention-to-treat basis, were ranked according to the highest category on a scale ranging from death (control, six; GR32191B, four) to nonfatal infarction (control, 22; GR32191B, 18), bypass grafting (control, 19; GR32191B, 22) and repeat angioplasty (control, 52; GR32191B, 48). No significant difference in ranking was detected. Six months after angioplasty, 75% of patients in the GR32191B group and 72% of patients in the control group were symptom free. CONCLUSIONS: Long-term thromboxane A2-receptor blockade with GR32191B does not prevent restenosis and does not favorably influence the clinical course after angioplasty.
Increasing blood flow results in endothelium-dependent vasodilation of angiographically normal epicardial coronary arteries in humans. To compare the ability of internal mammary artery (IMA) and saphenous vein (SV) used as coronary artery bypass grafts to adapt their vasomotor tone to an increase in myocardial blood flow demand induced by tachycardia, 10 IMA and seven SV grafts were studied by quantitative angiography more than 6 months (range, 6-82 months) after surgery in 17 patients. All grafts were angiographically smooth and implanted to large nonakinetic perfusion zones. Angiograms were obtained in basal sinus rhythm (71 +/- 10 beats/min), during atrial pacing (129 +/- 9 beats/min), and after intragraft infusion of 1 mg isosorbide dinitrate (ISDN). In basal sinus rhythm, the cross-sectional area of SV was superior to that of IMA (10.7 +/- 3.6 versus 5.4 +/- 1.7 mm2; p less than 0.01). All IMA dilated during pacing (+14.8 +/- 11.5%; p less than 0.005) and a further increase in IMA cross-sectional area occurred after ISDN (+27.4 +/- 20.1% versus basal; p less than 0.005). In contrast, SV failed to dilate during pacing (+0.3 +/- 5.4%; p = NS) and after ISDN (+0.7 +/- 6.0% versus basal; p = NS). Thus, an increase in myocardial blood flow demand induced by tachycardia results in dilation of IMA but not of SV grafted on coronary vessels. The ability of the endothelium to modulate the vasomotor tone of IMA grafts in response to changes in blood flow could contribute to their excellent long-term functional results after coronary artery bypass surgery.
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A prospective study of 111 patients who underwent repeat coronary angiography and exercise thallium-201 scintigraphy 6 +/- 2 months after complete revascularization by percutaneous transluminal coronary angioplasty was performed to assess whether clinical, procedure-related and postangioplasty exercise variables yield independent information for the prediction of angiographic restenosis after angioplasty. Complete revascularization was defined as successful angioplasty of one or more vessels that resulted in no residual coronary lesion with greater than 50% diameter stenosis. Restenosis was defined as a residual stenosis at the time of repeat angiography of greater than 50% of luminal diameter. Restenosis occurred in 40% of the patients. The 111 patients were randomly subdivided into a learning group (n = 84) and a testing group (n = 27). A logistic discriminant analysis was performed in the learning group and the logistic model was used to estimate a logistic probability of restenosis. This probability of restenosis was validated in the testing group. In the learning group of 84 patients univariate analysis of 39 factors revealed 8 factors related to restenosis: recurrence of angina (p less than 0.0001), postangioplasty abnormal finding on exercise thallium-201 scintigram (p less than 0.0001), exercise thallium-201 scintigram score (p less than 0.0001), difference between exercise and rest ST segment depression (p less than 0.001), postangioplasty exercise ST segment depression (p less than 0.001), absolute postangioplasty stenosis diameter (p less than 0.003), postangioplasty exercise work load (p less than 0.03) and postangioplasty exercise heart rate (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
To evaluate the significance of persistent negative T waves during severe ischemia, we prospectively studied 62 patients admitted for unstable angina without evidence of recent or ongoing myocardial infarction. A critical stenosis on the left anterior descending coronary artery (LAD), considered as the culprit lesion, was successfully treated by percutaneous transluminal coronary angioplasty (PTCA). The patients were divided into two groups according to the admission electrocardiogram: T NEG group (n = 32) had persistent negative T waves, and the T POS group (n = 30) had normal positive T waves on precordial leads. The two groups had similar baseline clinical, hemodynamic, and angiographic characteristics. All patients underwent a complete clinical and angiographic evaluation (coronary arteriography and left ventriculography) before undergoing PTCA and 8 +/- 3 months later. Left ventricular anterior wall motion was evaluated by the percent shortening of three areas (S1, S2, and S3) considered as LAD-related segments on left ventriculograms. Before PTCA, there was no significant difference in global ejection fraction between the two groups despite a significant depression in anterior mean percent area shortening in the T NEG compared with the T POS group (S1, 44 versus 54, p less than 0.01; S2, 39 versus 48, p less than 0.01; S3, 44 versus 50, NS). At repeated angiography, the anterior mean percent area shortening improved significantly in the T NEG group (S1, from 44 to 61, p less than 0.001; S2, from 39 to 58, p less than 0.001; S3, from 44 to 61, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
In a canine model of reperfused myocardial infarction, we tested the hypothesis that after reperfusion, technetium-99m-hexakis-2-methoxyisobutyl isonitrile (Tc-MIBI) tomographic imaging still reflects occlusion blood flow when the tracer is injected before reperfusion. Nine anesthetized dogs underwent 2 hours of coronary occlusion followed by 3 hours of reperfusion ending by being killed. Reference coronary blood flow was determined by radioactive microspheres injected during occlusion and after reperfusion. Biopsies in normal and ischemic myocardium and single photon emission computed tomography were obtained during occlusion and after reperfusion. Circumferential profiles were applied to axial slices divided into 5-degree sectors. The sectors were divided into 3 groups selected on the occlusion acquisition (normal, mildly reduced, and severely reduced) and compared with the postreperfusion acquisition. Tissular Tc-MIBI kinetics was assessed both by Tc-MIBI time-activity curves of normal and ischemic tissue obtained by biopsy and by the relative gradient between normal, ischemic, and necrotic postmortem tissue samples. In biopsy samples, Tc-MIBI content remained unchanged during occlusion and after reperfusion in normal as well as in ischemic tissue (4,662 +/- 2,237 counts/min/mg vs. 4,599 +/- 1,577 counts/min/mg in normal tissue, NS; 941 +/- 903 counts/min/mg vs. 1,087 +/- 721 counts/min/mg in ischemic tissue, NS). In postmortem tissue samples, there was a good correlation between occlusion microsphere blood flow and Tc-MIBI activity (r = 0.91). In the necrotic samples, mean normalized Tc-MIBI activity (10 +/- 17%) was slightly higher than the normalized microsphere blood flow (3 +/- 3%, p less than 0.001) but markedly lower than the normalized microsphere reperfusion blood flow (63 +/- 31%, p less than 0.001). Comparing the single photon emission computed tomographic acquisitions before and after reperfusion, Tc-MIBI activity remained unchanged in normal as well as in mildly reduced or severely reduced segments. Thus, our data are consistent with the hypothesis that Tc-MIBI traces blood flow, does not redistribute significantly despite reperfusion, and can be used for imaging the area at risk.
Both 201Tl redistribution and persistent glucose uptake have been proposed as markers of viability after reperfusion. In the present study, they have been compared in the same open-chest canine preparation of occlusion and reperfusion. Ten fasting dogs were subjected to 2 hr of left anterior descending coronary artery occlusion and 4 hr of reperfusion. Myocardial blood flow was determined by a microsphere technique 100 min after occlusion and 3 hr after reperfusion. 201Tl was injected intravenously 20 min before reperfusion. Serial biopsy samples were obtained from ischemic and normal areas. 18F-2-deoxyglucose, a tracer of exogenous glucose uptake, was injected 3 hr after reperfusion. Thirty minutes before the animals were killed, simultaneous blood samples were taken from the femoral artery and the regional coronary veins draining the reperfused and the remote areas. Dogs were killed 4 hr after reperfusion was established. Area at risk was assessed by dye injection in vivo and area of necrosis by triphenyl tetrazolium chloride (TTC) staining, with confirmation by electron microscopy. Immediately after death, endocardial and epicardial samples were taken from regions characterized as risk regions, areas of necrosis, areas of patchy necrosis, and normal areas. These samples were counted in a scintillation well counter. Four hours after reperfusion, in ischemic myocardium (TTC positive) the relative 201Tl gradient between ischemic and normal regions was 26 +/- 13%, whereas in necrotic samples, this gradient was 71 +/- 26%.(ABSTRACT TRUNCATED AT 250 WORDS)
Polymorphonuclear leukocytes may participate in reperfusion injury. Whether leukocytes affect viable or only irreversibly injured tissue is not known. Therefore, we assessed the accumulation of 111In-labeled leukocytes in tissue samples characterized as either ischemic but viable or necrotic by metabolic, histochemical, and ultrastructural criteria. Six open-chest dogs received left anterior descending coronary occlusion for 2 hr followed by 4 hr reperfusion. Myocardial blood flow was determined by microspheres and autologous 111In-labeled leukocytes were injected intravenously. Fluorine-18-2-deoxyglucose, a tracer of exogenous glucose utilization, was injected 3 hr after reperfusion. The dogs were killed 4 hr after reperfusion. The risk and the necrotic regions were assessed following in vivo dye injection and postmortem tetrazolium staining. Myocardial samples were obtained in the ischemic but viable, necrotic and normal zones, and counted for 111In and 18F activity. Compared to normal, leukocytes were entrapped in necrotic regions (111In activity: 207 +/- 73%) where glucose uptake was decreased (26 +/- 15%). A persistent glucose uptake, marker of viability, was mainly seen in risk region (135 +/- 85%) where leukocytes accumulation was moderate in comparison to normal zone (146 +/- 44%). Thus, the glucose uptake observed in viable tissue is mainly related to myocytes metabolism and not to leukocytes metabolism.
The respective roles of peripheral and myocardial determinants of exercise ventricular performance were studied in 10 normal volunteers and in 9 mildly hypertensive patients without evidence of coronary disease. Hemodynamic measurements and equilibrium blood pool scintigraphy were simultaneously performed at rest and during maximal upright exercise. In hypertensive patients, mean systolic and diastolic blood pressure were, respectively, 199 +/- 23 and 102 +/- 12 mm Hg at rest, and 271 +/- 28 and 113 +/- 8 mm Hg at peak exercise. Ejection fraction response to exercise was normal (increase by more than 5%) in 4 hypertensive patients (normal hypertensive group: 63 +/- 4 to 77 +/- 6%) and in volunteers (65 +/- 3 to 78 +/- 4%) and abnormal in 5 hypertensive patients (abnormal hypertensive group: 66 +/- 6 to 58 +/- 10% at peak exercise). The abnormal response in the abnormal hypertensive group was not due to an inadequate decrease in systemic vascular resistance during exercise. By contrast, the ratio systolic blood pressure/end-systolic volume, an index of contractility, decreased by 2.3 +/- 4.9 in the abnormal hypertensive group, whereas it increased by 9.8 +/- 9.1 in the normal hypertensive group and by 7.3 +/- 2 in volunteers. Thus, abnormal exercise ejection fraction response in mild hypertension was not related to increased afterload but rather to intrinsic myocardial factors.
Positron emission tomography allows the noninvasive assessment of regional myocardial blood flow and metabolism. The purpose of this study was to correlate N-13 ammonia uptake as a measure of regional blood flow and C-11 palmitate kinetics as a marker for fatty acid metabolism in ischemic canine myocardium using positron emission tomography. Furthermore, the metabolic results were compared with ultrastructural findings obtained in the same animal model. Regional ischemia was induced by balloon occlusion of the left anterior descending artery in a closed chest dog model. The three myocardial sites studied were the center and "border" of the ischemic segment as well as the control myocardium. C-11 palmitate uptake closely correlated with blood flow (r = 0.88). In the center of ischemia uptake of C-11 palmitate was decreased and clearance of C-11 activity significantly prolonged. In the "border" of the ischemic segment with only mild reduction of flow and C-11 palmitate uptake (approximately 20%) clearance halftime and residual activity were significantly different from control. The residual activity normalized for initial uptake of C-11 palmitate was highest in the "border" regions consistent with increased deposition of C-11 palmitate in lipid pools. The electron microscopic studies showed in 8 of 11 dogs lipid droplets as the only abnormality in corresponding segments with only mild reduction in microsphere blood flow. Thus, these data indicate the potential of metabolic imaging to characterize ischemia on a cellular level. Positron emission tomography provides a sensitive means to detect mild ischemia and to define extent and severity. Metabolic imaging may prove clinically useful to identify not only necrosis, but also myocardium at risk.
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