摘要:

ABSTRACTTo investigate whether ergonovine acts directly on coronary arteries or via remote neurohumoral reflexes, we administered small titrated increments of intracoronary ergonovine up to a maximum cumulative dose of 50 gg to 15 patients. In six patients with variant angina (group 1), ischemic electrocardiographic ST changes, angina, and localized coronary spasm (local coronary diameter reduction of 87.8 18.9% [mean ± SD]) followed after 6 to 50 gℒg (mean 20.7) cumulative intracoronary ergonovine. In nine patients with atypical chest pain, normal baseline coronary arteriograms, and no evidence of variant angina (group 2), there was no ischemic ST segment change or localized coronary spasm after 6 to 50 ug (mean 31.6) intracoronary ergonovine. Coronary diameter of proximal vessels of patients in group 2 was reduced by 16.2 ± 6.5% and did not differ from the response of nonspastic vessels of comparable size of group 1 (20.5 13.8%; p = .7). There was no significant difference in the median effective dose values in the dose-response curves of the spastic and nonspastic segments between groups 1 and 2. Ergonovine causes coronary spasm by a direct local effect, which seems to be caused by localized arterial hyperreactivity rather than supersensitivity. Intracoronary delivery may be safer than intravenous administration because negligible drug recirculation may prevent perpetuation of spasm and selective coronary administration can avoid branches with critical stenoses.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

ABSTRACTThe first successful application of a transcatheter closure technique for patent ductus arteriosus (PDA) suitable for use in infants and children was performed by us in 1977. Since that time, there has been continued improvement and simplification of the equipment as well as in the implantation technique. Following a Food and Drug Administration protocol, a multicenter study was conducted to test the safety and effectiveness of this interventional method. The clinical results from three major regional test centers (Philadelphia, Houston, and New Haven) are presented. One hundred fortysix patients from a test population of 156 were treated for PDA with use of the Rashkind PDA Occluder Systems. Successful closure was accomplished in 94 (66%) of the total cases. Ten patients (7%) retained residual ductal murmurs despite correct placement of the occlusion devices; five additional patients (3%) were considered failures due to the presence of abnormal Doppler flow patterns after the procedure. Postrelease embolizations occurred in 19 (15%) instances. One patient required emergency surgical intervention after attempted retrieval of an embolized occluder. With the improvements in the manufacturing of the double-disk occluder systems as well as the perfection of the transvenous delivery technique, the incidences of closure failure and postrelease complications have decreased. Since January 1984, 78% of all transcatheter closure attempts were successful, with 10% embolization.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

ABSTRACTBetween October 1984 and September 1986, we attempted transcatheter umbrella closure, using the Rashkind PDA occluder, of 12 congenital or postoperative cardiovascular defects (other than patent ductus arteriosus [PDA]) in 11 patients. In each, we used the umbrella for closure because the defect was too short and/or too large to close with conventional transcatheter methods. The defects included three post-Glenn venous communications (superior vena cava-right atrium, n = 2; azygos vein to inferior vena cava), four congenital “interatrial defects” producing cyanosis (“coronary sinus” septal defect, left superior vena cava to left atrium, patent foramen ovale, left inferior vena cava to left atrium), and five non-PDA systemic-to-pulmonary arterial communications (two congenital and three postoperative). Ten of 12 defects were embolized successfully; nine had complete or subtotal closure, and one was partially closed. The first attempted closure resulted in embolization of a 12 mm device to a lower-lobe pulmonary artery, without clinical sequelae. No other complications occurred. Clinical improvement was most dramatic in those patients whose cyanosis was relieved and less obvious when pulmonary blood flow was reduced. The Rashkind umbrella device, originally designed for closure of PDA, considerably expands the list of congenital or operative defects that can be closed nonsurgically.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

ABSTRACTBalloon coarctation angioplasty (BCA) was performed in seven consecutive patients (five boys and two girls) 18 months to 18 years old (mean 9.5) with isolated discrete unoperated coarctation of the aorta. A No. 8F or 9F catheter was chosen with balloon lengths of 30 or 40 mm and maximum inflation diameters 1 mm less than the smallest measured aortic diameter determined 1 cm proximal to the coarctation site. A 10 sec inflation-deflation cycle of 6 to 8 atmospheres (90 to 120 psi) was perforined. The peak systolic pressure gradient (PSG) before BCA ranged from 35 to 70 mm Hg (mean 58), and immediately after BCA it decreased to 0 to 20 mm Hg (mean 7). One to two year follow-up (mean 14 months) of the seven patients revealed a PSG range of 10 to 30 mm Hg (mean 19). Repeat angiography was performed immediately proximal to the coarctation site. Three patients (43%) had evidence of aneurysm formation at or immediately distal to the balloon dilatation site. One patient had coarctation restenosis. While initial results with BCA for unoperated coarctation were encouraging, current data raise serious concerns about its long-term safety and efficacy.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

ABSTRACTBetween 1968 and 1977, 32 patients who underwent the Fontan operation for tricuspid atresia at Bordeaux, France, or Leiden, The Netherlands, survived at least 1 year after surgery. These patients were evaluated clinically 7 to 16 years (mean 8.9 years) after surgery by review of clinical records, questionnaire, or direct examination. There were five deaths: one during arrhythmia, the second sudden and unexplained, and three others after reoperation. Four of the five patients had evidence of obstruction of the atriopulmonary or atrioventricular conduit. There were eight reoperations. Two were for residual atrial septal defects, one for an atrial septal defect and an intrapulmonary arteriovenous fistula, and one for a residual ventricular septal defect. The other four were reoperated for severe conduit or homograft obstruction. One of these four also had a residual shunt, severe mitral regurgitation, and reduced left ventricular function. One patient was found to have left ventricular dysfunction 3 months after surgery, which persisted. Another patient had left ventricular dysfunction unmasked after successful mitral annuloplasty for severe mitral regurgitation. No other patients had clinical evidence of left ventricular dysfunction. Recurrent supraventricular tachycardia occurred in four patients and was eventually fatal in one patient with associated conduit obstruction. Of the 27 survivors, 13 are in NYHA class I, 13 are in class II, and one is in class III. We conclude that clinical results of the Fontan operation remain good in most patients 7 to 16 years after surgery. Conduit or homograft obstruction has been associated with mortality, reoperation, and poor hemodynamic tolerance of arrhythmia.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

ABSTRACTPreviously, technetium-99m-stannous pyrophosphate (99mTc-PPi) has been used to localize and estimate the size of myocardial infarcts in animals after permanent coronary artery occlusion. This study tested the hypothesis that 99mTc-PPi accurately sizes myocardial infarctions produced by temporary coronary artery occlusion and reflow in dogs. Three groups of dogs were studied: group A underwent 3 hr of occlusion followed by 2 hr of reperfusion, with 99mTc-PPi injected 10 min after reflow (n = 10); group B underwent 3 hr of occlusion followed by 2 hr of reperfusion, with 99mTc-PPi injected 90 min after reflow (n = 11); and group C underwent 3 hr of occlusion followed by reflow with 99mTc-PPi injected at 10 min and again at 48 hr after reflow (n = 5). Myocardial slices from group A and B dogs were imaged in vitro. Group C dogs were imaged with single photon-emission computed tomography (SPECT) in vivo, and myocardial slices were imaged in vitro at the conclusion of the study. The extent of myocardial infarction was defined with triphenyltetrazolium chloride (TTC) staining, and coronary blood flow was estimated with radioactive microspheres. In addition, transmural myocardial tissue samples were taken from the center of the myocardial infarction, the lateral portion of the myocardial infarction, the normal myocardium adjacent to the lateral aspect of the infarcts, and from the normal myocardium and counted for 99mTc-PPi activity. A significant correlation was found between infarct size determined by areas of increased 99mTc-PPi uptake and that estimated from TTC staining for both group A (r = .89) and group B animals (r = .98). However, the intercepts and slopes relating estimates of infarct size from 99mTc-PPi uptake and TTC staining indicated that 99mTc-PPi overestimated size of infarction when injected early after reflow (group A), especially that of small infarcts (.5 g). Results in group C dogs confirmed that, in the same dogs, estimates of infarct size were smaller when 99mTc-PPi was injected relatively late as compared with early after reperfusion. Thus, 99mTc-PPi injected 90 min or later after reperfusion provides an excellent means to identify and size myocardial infarcts produced by temporary coronary artery occlusion and reflow in this canine preparation. 99mTc-PPi uptake early, but not late, after reperfusion probably occurs in some myocardial cells that are severely injured but viable after reperfusion, and possibly in cells with excess cytosolic calcium that recover with longer periods of reperfusion.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

ABSTRACTRegression of left ventricular hypertrophy after control of blood pressure has been documented with some antihypertensive agents but not with others. To determine whether similar differences in regression of wall thickening also occur in resistance vessels during treatment, matched groups of spontaneously hypertensive rats (SHR) were treated for 12 weeks with either hydralazine (H) or captopril and hydrochlorothiazide (C-D) and they were compared with untreated SHR and Wistar- Kyoto rats (WKY). Perfusion pressure was then determined in the hindlimbs of pithed rats under conditions of constant blood flow (4.0 ml/min) and maximal vasodilation (hemodilution to 22% hematocrit combined with continuous nitroprusside and papaverine infusion). This perfusion pressure, which has been validated as an index of thickening (hypertrophy) of resistance vessels walls, averaged 26.8 ± 0.4(SE) mm Hg in untreated WKY (n = 12) and 37.6 ± 0.4 mm Hg in untreated SHR (n = 11) (p > .01). Treatment with H or C-D controlled blood pressure equally in SHR, but the two drugs had significantly different effects on both left ventricular hypertrophy and resistance vessels. Perfusion pressure was reduced from 37.6 ± 0.4 mm Hg to 34.0 + 0.5 mm Hg (p > .01) with C-D but only to 36.5 ± 0.5 mm Hg with H (NS). Left ventricular weight was significantly reduced by C-D (2.02 + 0.02 vs 2.63 + 0.05 mg/g, p > .01) but only to 2.44 ± 0.05 mg/g by H. Close correlations were found both before and after treatment, between perfusion pressure and left ventricular weight (y = 0.68, p > .01), but not between either of these two variables and arterial pressure. Thus, despite equal blood pressure control, wall thickness of resistance vessels regressed more with C-D than with H, suggesting that vascular hypertrophy, like left ventricular hypertrophy, is not determined by blood pressure levels alone. Moreover, thickening of resistance vessels and increased left ventricular mass, although changing in the same direction, were related to each other to a limited degree (y2 = 0.46) both during the development of hypertension and in its response to treatment.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

ABSTRACTThe inhibitory effect of Separan AP-30, an anionic polyacrylamide, on atherosclerotic plaque formation in aortas of rabbits on a high (2%) cholesterol diet was tested over a period extending from 37 to 170 days. Atherogenesis was quantified morphometrically by application of a computerassisted image analysis of histologic cross sections of the aorta. The area of vessel wall-atheroma interface, fraction of lumen occluded, and other indexes of atherogenesis were measured in each of 26 segments of aorta excised from the animals, half of which were administered injections (intravenous) of Separan three times a week. Regression analysis of the morphometric data indicates that the polyelectrolyte exerts a powerful antiatherogenic effect in all regions of the aorta, inhibiting the formation of plaque mass to less than half in the aortic arch and about one-fifth in the descending aorta as compared with the aortic plaque masses in untreated rabbits. Results are compatible with the suggestion that a novel hemodynamic principle in vivo, polymer drag reduction, might be effectively applied against atherosclerosis.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

ABSTRACTSince platelet accumulation may be an important determinant of restenosis after angioplasty, the time course of 11Cr-labeled platelet accumulation after experimental angioplasty was evaluated in a deendothelialized, hypercholesterolemic rabbit preparation of atherosclerosis. Marked platelet accumulation (39.5 ± 8.7 × 106 platelets/1 cm vessel length) was observed at 30 min and remained active until 4 hr after angioplasty. Total accumulation over 24 hr was 56.4 ± 4.7 × 106 platelets/1 cm length. Histologic dissection was directly related to the degree of platelet accumulation, with 64 ± 15 x 106 platelets/1 cm in the group with marked dissection and 8.7 3.7 × 106 platelets/1 cm in the group with minimal dissection (p > .05). Increasing angiographic dissection also resulted in a trend toward increased platelet accumulation, and angiographic change in luminal diameter showed a significant correlation with platelet accumulation. It is concluded that marked platelet accumulation occurs early after transluminal angioplasty and is related to the extent of dissection. Restenosis may result from a complex interaction of platelet accumulation, vascular damage, and blood flow.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

ABSTRACTInjection of serotonin (5-HT) into the left atrium or ventricle activates a hypertensive chemoreflex. The primary purpose of our study was to determine the afferent pathway(s) that mediates this response. A secondary goal was to localize the receptive sites of this reflex. We measured (1) changes in arterial pressure, (2) reflex vascular responses in skeletal muscle and paw, and (3) changes in renal nerve traffic that occurred after the left atrial or left ventricular injection of 5-HT. Injection of 5- HT (100 to 600 gg) into left atrium or ventricle produced large reflex increases in vascular resistance and sympathetic outflow. These responses were not reduced after bilateral cervical vagotomy. In separate experiments, increases in renal nerve traffic with left ventricular injection of 5-HT were assessed before and after cardiac sympathetic deafferentation. Interruption of cardiac sympathetic afferent pathways did not significantly attenuate increases in renal nerve activity with 5-HT. Injection of 5-HT (300 ulg) into the aortic root produced large increases in arterial pressure but this was not observed after injections into the vertebral or common carotid arteries or descending aorta. Injection of 5-HT (100 jig) into the left main coronary artery (perfused via a Gregg cannula from an external reservoir) resulted in a depressor reflex (Bezold-Jarisch). In contrast, injection of 5-HT (200 μg) into the left ventricle when the drug was prevented from reaching the left coronary artery produced a large pressor response. We conclude that the left atrial, left ventricular, or aortic root injection of 5-HT elicits a hypertensive chemoreflex response from receptors that receive their blood supply from arteries other than the major branches of the left coronary artery. The afferent limb of this reflex does not travel in cardiopulmonary vagal or sympathetic afferent fibers.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID