摘要:

Background Catheter-induced mechanical trauma is unfavorable during electrophysiological study. However, its incidence, significance, and pharmacological responses in patients receiving radiofrequency ablation for supraventricular tachycardia have not been investigated.Methods and Results A prospective study was performed in 666 consecutive patients with documented, symptomatic supraventricular tachycardia. All had been referred for electrophysiological study and radiofrequency ablation. Catheter-induced mechanical trauma was defined by either disappearance of or change in preexcitation pattern induced by the electrode catheters or noninducibility of tachycardia after the electrode catheter-induced termination of tachycardia, confirmed by electrophysiological study. Adenosine, isoproterenol, and atropine were serially administered 1 hour after the mechanical trauma to study pharmacological response. "Rescue" radiofrequency ablation was defined as delivery of radiofrequency energy just at the presumed ablation site immediately after the mechanical trauma. Of the 666 patients, 254 had atrioventricular (AV) nodal reentrant tachycardia, 367 patients had accessory pathways, 30 patients had atrial tachycardia, and 15 had atrial flutter. Catheter-induced mechanical trauma occurred in 17 patients (2.6%): 4 patients had AV nodal reentrant tachycardia, 9 had accessory pathways, and 4 had atrial tachycardia. Five patients had such episodes during the placement of electrode catheters and 12, during mapping and ablation procedures. Of the 4 patients with AV nodal reentrant tachycardia, 3 had mechanical trauma on the retrograde fast pathway and 1, on the antegrade slow pathway. In the 9 patients with accessory pathways, those pathways were located in the left free wall in 4 patients, right free wall in 1, right posteroseptum in 1, and right anteroseptum in 3. Atrial tachycardia was more easily traumatized than AV nodal reentrant tachycardia (P<.01) and than accessory pathways (P<.01). The clinical courses of mechanical trauma were variable: 1 patient had spontaneous recovery within 1 week, 5 patients had recurrence of tachycardia within 3 months, and the rest have been free of tachycardia from 3 to 35 months. The recurrence rate was higher in patients with mechanical trauma than in those without (33.3% versus 3.5%, P<.0001) despite rescue radiofrequency ablation given in 7 patients. Pharmacological agents were generally unable to revive the traumatized tissues, and recurrence was unpredictable.Conclusions Catheter-induced mechanical trauma was not common in patients receiving radiofrequency ablation for supraventricular tachycardia. Their clinical courses were variable, and pharmacological manipulation offered little assistance. More than half of the patients had long-term cures. However, the recurrence rate was, on the whole, significantly high despite rescue radiofrequency ablation. There is a need for great caution in the placement of electrode catheters in every patient during electrophysiological study and radiofrequency ablation. (Circulation. 1994;90:1847-1854.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Patients with Takayasu's disease, a chronic inflammatory arteriopathy of unknown cause, have variable clinical courses, and predictors of the long-term outcome are not well understood. We studied prognostic factors of this disease, based on follow-up results, and a new prognostic classification was proposed.35 years and <=35 years, and 79.9% versus 96.5% for patients diagnosed in 1957 through 1975 and in 1976 through 1990, respectively. The delay in diagnosis and the erythrocyte sedimentation rate (ESR) were of marginal significance. The multivariate Cox analysis showed that only two of the above variables were statistically independent predictors, ie, the major complication and the progressive course. In addition to these two factors, ESR was the third predictor, if the Cox stepwise elimination procedure was performed. These three predictors used in various combinations made a total of 1822 classifications theoretically feasible. Of these, a three-stage classification was selected as the best one, based on the Akaike information criterion. The presence of both major complication and progressive course (stage 3) was the worst prognostic indicator (43% survival at 15 years). In contrast, no patient died who had neither of these manifestations or who had a progressive course but an elevated ESR as well (stage 1).Conclusions The long-term outcome for patients with Takayasu's disease seems best predicted by two major prognostic factors, ie, complications and the pattern of the past clinical course, as well as by ESR. Aggressive medical and surgical treatment may be considered for patients with a major complication and a progressive course (stage 3). (Circulation. 1994;90:1855-1860.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background This study was undertaken to expand the understanding of ultrasound-guided compression repair (UGCR) of postcatheterization femoral artery injuries.Methods and Results In a series of 62 patients with pseudoaneurysms (n=53) or arteriovenous (AV) fistulas (n=9), UGCR was performed as a nonsurgical method in the treatment of postcatheterization femoral artery injuries. When the communicating channel could be visualized (43 cases), pressure was focused on it; otherwise (10 cases) the extraluminal cavity itself was compressed. In 45 cases, the elimination of flow in the pseudoaneurysm and/or the communicating channel could be achieved only with simultaneous temporary complete occlusion of the femoral artery. UGCR was successfully performed in 25 of 27 cases of false aneurysms (93%) in patients without anticoagulation and in 14 of 26 patients (54%) on anticoagulants. Three of 9 AV fistulas could be repaired by this method. No apparent correlation could be found between the therapeutic success and the size of the pseudoaneurysm or the age of the lesion.Conclusions In patients on anticoagulants and in patients with AV fistulas, the detection of a communicating channel that could be obliterated by direct mechanical compression was discerned as a discriminant factor of success. (Circulation. 1994;90:1861-1865.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background In patients with intermittent claudication, a supervised walking exercise program increases peak exercise performance and community-based functional status. Patients with peripheral arterial disease also have muscle weakness in the affected extremity that may contribute to the walking impairment. However, the potential benefits of training modalities other than walking exercise, such as strength training, have not been critically evaluated in this patient population. The present study tested the hypothesis that a strength training program would be as effective as treadmill walking exercise and that combinations of strengthening and walking exercise would be more effective than either alone in improving exercise performance.Methods and Results Twenty-nine patients with disabling claudication were randomized to 12 weeks of supervised walking exercise on a treadmill (3 h/wk at a work intensity sufficient to produce claudication), strength training (3 h/wk of resistive training of five muscle groups of each leg), or a nonexercising control group. Graded treadmill testing was performed to maximally tolerated claudication pain to define changes in peak exercise performance. After 12 weeks, patients in the treadmill training program had a 74+-58% increase in peak walking time as well as improvements in peak oxygen consumption (Vo2) and the onset of claudication pain. Patients in the strength-trained group had a 36+-48% increase in peak walking time but no change in peak Vo2or claudication onset time. Control subjects had no changes in any of these measures over the 12-week period. After the first 12 weeks, patients in the initial walking exercise group continued for 12 more weeks of supervised treadmill training. This resulted in an additional 49+-53% increase in peak walking time (total of 128+-99% increase over the 24 weeks). After the initial 12 weeks, patients in the strength-trained group began 12 weeks of supervised treadmill training, and patients in the control group participated in a 12-week combined program of strengthening and treadmill walking exercise. The combined strength and treadmill training program and treadmill training after 12 weeks of strength training resulted in increases in peak exercise performance similar to those observed with 12 weeks of treadmill training alone.Conclusions A supervised treadmill walking exercise program is an effective means to improve exercise performance in patients with intermittent claudication, with continued improvement over 24 weeks of training. In contrast, 12 weeks of strength training was less effective than 12 weeks of supervised treadmill walking exercise. Finally, strength training, whether sequential or concomitant, did not augment the response to a walking exercise program. (Circulation. 1994;90:1866-1874.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Evaluation of regional aortic elastic properties in humans has been hampered by the need for invasive techniques to access instantaneous aortic pressure, wall thickness, and cross-sectional area or diameter. In this study, a new noninvasive method is presented for quantification of regional aortic elastic properties.Methods and Results Twenty-five patients were studied during transesophageal echocardiographic procedures. Measurements of instantaneous aortic cross-sectional area were obtained with an automated border detection algorithm applied to short-axis transesophageal two-dimensional echocardiographic images of the proximal descending thoracic aorta. Instantaneous aortic wall thickness was derived from combined two-dimensional targeted M-mode end-diastolic wall thickness and instantaneous aortic area measurements. Instantaneous aortic pressures were estimated from calibrated subclavian pulse tracings recorded simultaneously. Data were digitized to generate aortic area-pressure loops. Regional aortic mechanical properties were quantified in terms of compliance per unit length (C is the slope of the area-pressure regression), aortic midwall radius (R sub m), and incremental elastic modulus of the aortic wall (Einc). To assess the independent effect of age, Rmand Eincvalues were compared at a common level of aortic midwall stress (0.666 x 106dynes/cm2). Mean values (+-SD) for C, Rm, and Eincwere 0.01+-0.004 cm2/mm Hg, 1.14+-0.17 cm, and 7.059+-4.091 x 106dynes/cm2, respectively. An inverse linear correlation was found between aortic compliance per unit length and age (r=-.68, P<.0007). Incremental elastic modulus was related to age (r=+.80, P<.00003) in a nonlinear fashion such that it increased sharply after the age of 60 years. Finally, midwall radius was less tightly correlated with age (r=+.45, P<.05). Values for C, Rm, and Eincas well as the age dependency of these properties are similar to those reported previously when invasive techniques were used.Conclusions This methodology constitutes a new tool to improve the clinical evaluation of regional aortic elastic properties in multiple disease states. (Circulation. 1994;90:1875-1882.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Control of renal hemodynamics by the arterial baroreflex has never been proved in humans. Apart from the physiological viewpoint, this issue is relevant because altered baroreflex function has been implicated in the pathogenesis of human hypertension.Methods and Results Renal function studies were performed in seated healthy volunteers (n=12; age range, 20 to 34 years) during sustained neck suction at -60 mm Hg, aiming to selectively activate the carotid sinus arterial baroreceptors. Two protocols were followed. One group of 6 volunteers taking a 20 mmol/d sodium diet underwent 90 minutes of neck suction. Compared with a time-control study, neck suction decreased arterial pressure and heart rate; increased glomerular filtration rate (inulin clearance) from 104+-6 to 114+-8 mL/min (P<.01), renal plasma flow (para-aminohippurate clearance) from 616+-52 to 665+-42 mL/min (P<.01), and renal blood flow (from 1120+-95 to 1209+-77 mL/min, P<.01); and decreased renal vascular resistance (from 86+-8 to 76+-6 mm Hg x min x L sup -1, P<.01). Neck suction had no effect on plasma renin activity, aldosterone, atrial natriuretic peptide, catecholamines, and renal sodium excretion. The other 6 volunteers took a normal sodium diet and underwent sustained neck suction for 60 minutes. In this group, no effects on renal hemodynamics could be discerned, despite a modest decrease in blood pressure and heart rate.Conclusions These data show, for the first time, that the arterial baroreflex is involved in the control of renal hemodynamics in humans. However, basal arterial baroreflex control of renal hemodynamics is probably low, and arterial baroreflex activation with subsequent renal vasorelaxation may be found only in conditions in which basal arterial baroreflex control of kidney function is significant, as is presumably the case in seated sodium-restricted subjects. (Circulation. 1994;90: 1883-1890.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Animal data indicate that ATP derived from aggregating thrombocytes or endothelium induces an endothelium-dependent vasodilator response that is mediated by P2y-purinergic receptors and is reduced when high dosages are administered. This reduced vasodilator response to high ATP doses has been associated with the concomitant release of endothelium-derived contracting factors. In contrast to the endothelium-dependent vasodilator response, ATP as released from sympathetic nerve endings induces a P2x-purinergic receptor-mediated vasoconstrictor response that may contribute to the attenuated vasodilator response to high dosages of luminally applied ATP. The dual action of ATP might be important in the pathophysiology of disease states characterized by an impaired endothelial function and increased thrombocyte aggregation. This study was performed to characterize the vascular response to ATP in humans.Methods and Results The brachial artery was cannulated in 50 healthy male volunteers (age, 18 to 44 years) for drug infusion and measurement of mean arterial pressure. Forearm blood flow was recorded by venous occlusion strain-gauge plethysmography. ATP induced a dose-dependent vasodilator response that was significantly higher than the effect of equimolar adenosine infusion and that was not reduced by concomitant infusion of the P sub 1 -purinergic receptor antagonist theophylline. The infusion of the NO synthase antagonist NG.1 for ATP versus SNP). In contrast to animal data, high dosages of intra-arterially infused ATP (up to 1000 micrograms x 100 mL forearm sup -1 x min sup -1) did not reveal a reduction in the forearm vasodilator response but appeared to be similar to the maximal forearm vasodilation as observed during postocclusive reactive hyperemia.Conclusions These observations indicate that ATP induces a potent dose-dependent vasodilator response that is not mediated by P1-purinergic receptor stimulation or by the release of nitric oxide. Moreover, in healthy volunteers, the vasodilator response to high intra-arterial dosages of ATP is not reduced by the release of endothelium-derived contracting factors or by the stimulation of P2x-purinergic receptors on the smooth muscle cells. (Circulation. 1994;90:1891-1898.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Increases in both leukocyte and endothelial cytosolic free (Ca sup 2+) may be involved in intercellular adhesion by regulating the affinity of surface adhesion molecules or by facilitating transendothelial leukocyte migration. The purpose of this study was to examine the effect of initial contact and subsequent adhesion of human neutrophils or monocytes on human aortic endothelial (Ca2+).Methods and Results Endothelial monolayers were loaded with the fluorescent Ca sup 2+ indicator indo 1 and exposed to isolated human peripheral blood neutrophils or to a cultured human monocyte cell line. A rapid, fourfold to fivefold increase in endothelial cytosolic (Ca2+) occurred within seconds of leukocyte contact. No increase in endothelial (Ca sup 2+) occurred on contact of 18.25- microns inert microspheres, isolated red blood cells, or suspensions of cultured human aortic endothelial cells. In experiments performed on monolayers grown in 1-mm2capillary flow tubes, the increase in endothelial cytosolic (Ca2+) on initial leukocyte contact was found to be related to the subsequent resistance to leukocyte detachment during exposure to arterial levels of shear stress (13.4 dyne x cm sup -2). The increase in endothelial cytosolic (Ca2+) during leukocyte contact was not inhibited in Ca2+ -free buffer but was abolished by prior depletion of an endoplasmic reticulum Ca2+ store by thapsigargin. Pretreatment of neutrophils with R15.7, a specific monoclonal antibody to the adhesion protein CD-18, inhibited the increase in endothelial cytosolic (Ca2+) on neutrophil contact.Conclusions Initial contact leading to subsequent adhesion of human leukocytes to human aortic endothelial cells releases an endothelial intracellular Ca sup 2+ store. This may, in part, be mediated by specific adhesion proteins and may in turn regulate the affinity of surface adhesion molecules or facilitate transendothelial migration of leukocytes. (Circulation. 1994;90:1899-1907.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Platelet-mediated mechanisms have been implicated in intimal lesion formation following vascular injury. Although the participation of peptide growth factors has been suspected in this process, little has been known about the possible mitogenic role of other platelet factors that are released at sites of vascular injury.Methods and Results We tested the hypothesis that platelet products, which are not peptide growth factors, are important modulators of the platelet-induced smooth muscle cell (SMC) proliferative response by acting as growth amplification factors. In these studies, cell proliferation was assessed by (Hydrogen-3)thymidine incorporation, flow cytometry, and direct cell counting. We examined the potential mitogenicity of several platelet products, including serotonin, ADP, norepinephrine, histamine, platelet-activating factor, the thromboxane A2mimetic U46619, and bradykinin. Of the platelet products tested, serotonin and ADP induced a synergistic response with peptide growth factors. This synergy was greatest at low growth-factor concentrations. Addition of nonaggregated platelets to quiescent SMC cultures strongly stimulated cell proliferation. Since the addition of suramin to platelet-treated cultures markedly inhibited SMC proliferation, peptide growth factors are most likely the primary mitogens mediating this response. However, platelet-induced proliferation was also markedly reduced by the serotonin antagonists ketanserin and LY53857 (44%), and by the ADP antagonist apyrase (35%).Conclusions Therefore, serotonin and ADP contribute significantly, in synergy with peptide growth factors, to the platelet-induced SMC proliferative response. We propose that in vivo serotonin and ADP act as amplification factors for SMC proliferation at sites of vascular injury. (Circulation. 1994;90: 1908-1918.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Background Recent studies indicate that serotonin (5-HT) has a growth-promoting effect on several different cell types, including smooth muscle cells. After percutaneous transluminal coronary angioplasty, there is damage and denudation of vascular endothelial cells, which promotes platelet aggregation at the site of injury. Aggregating platelets release 5-HT; thus, a high concentration of the amine may be present at sites of endothelial damage, which may act as a mitogen to endothelial cells.Methods and Results The mitogenic effect of 5-HT was examined on canine and bovine aortic endothelial cells by (1) assessing the increase in (Hydrogen-3)thymidine incorporation into DNA and (2) assessing the increase in the absolute number of cells after stimulation with 5-HT. 5-HT at an added concentration of 200 to 1000 micromole/L in the media induced a significant increase in (Hydrogen-3)thymidine incorporation into endothelial cells and an increase in cell number. This effect was not observed with fibroblasts. As the concentrations of added 5-HT were decreased, the endothelial cells had to be stimulated with 5-HT for longer periods to induce the same degree of cellular proliferation. The precursors and metabolic breakdown products of 5-HT were inactive. The 5-HT-induced endothelial proliferation was reversed by 5-HT2receptor antagonists and pertussis toxin. These data suggest that the mitogenic effect of 5-HT on endothelial cells is mediated by the 5-HT2receptor, which is coupled to a G protein.Conclusions 5-HT is a mitogen for endothelial cells at concentrations likely to be present at sites of vascular injury. This effect is probably mediated via the 5-HT2receptor. The growth-promoting effects of 5-HT on endothelial cells may facilitate the healing of intima after vascular damage. (Circulation. 1994;90:1919-1926.)

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID