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(1/1777) Disease pattern in cranial and large-vessel giant cell arteritis.

OBJECTIVE: To identify variables that distinguish large-vessel giant cell arteritis (GCA) with subclavian/axillary/brachial artery involvement from cranial GCA. METHODS: Seventy-four case patients with subclavian/axillary GCA diagnosed by angiography and 74 control patients with temporal artery biopsy-proven GCA without large vessel involvement matched for the date of first diagnosis were identified. Pertinent initial symptoms, time delay until diagnosis, and clinical symptoms, as well as clinical and laboratory findings at the time of diagnosis, were recorded by retrospective chart review. Expression of cytokine messenger RNA in temporal artery tissue from patients with large-vessel and cranial GCA was determined by semiquantitative polymerase chain reaction analysis. Distribution of disease-associated HLA-DRB1 alleles in patients with aortic arch syndrome and cranial GCA was assessed. RESULTS: The clinical presentation distinguished patients with large-vessel GCA from those with classic cranial GCA. Upper extremity vascular insufficiency dominated the clinical presentation of patients with large-vessel GCA, whereas symptoms related to impaired cranial blood flow were infrequent. Temporal artery biopsy findings were negative in 42% of patients with large-vessel GCA. Polymyalgia rheumatica occurred with similar frequency in both patient groups. Large-vessel GCA was associated with higher concentrations of interleukin-2 gene transcripts in arterial tissue and overrepresentation of the HLA-DRB1*0404 allele, indicating differences in pathogenetic mechanisms. CONCLUSION: GCA is not a single entity but includes several variants of disease. Large-vessel GCA produces a distinct spectrum of clinical manifestations and often occurs without involvement of the cranial arteries. Large-vessel GCA requires a different approach to the diagnosis and probably also to treatment.  (+info)

(2/1777) Endothelial function in Marfan syndrome: selective impairment of flow-mediated vasodilation.

BACKGROUND: The cardiovascular complications of Marfan syndrome arise due to alterations in the structural and functional properties of fibrillin, a constituent of vascular connective tissues. Fibrillin-containing microfibrils are closely associated with arterial endothelial cells, indicating a possible functional role for fibrillin in the endothelium. Plasma concentrations of endothelial cell products are elevated in Marfan subjects, which indirectly indicates endothelial dysfunction. This study directly assessed flow- and agonist-mediated endothelium-dependent brachial artery reactivity in Marfan subjects. METHODS AND RESULTS: In 20 Marfan and 20 control subjects, brachial artery diameter, blood flow, and blood pressure were measured by ultrasonic wall tracking, Doppler ultrasound, and photoplethysmography, respectively. Measurements were taken during hand hyperemia (a stimulus for endothelium-derived nitric oxide [NO] release in the upstream brachial artery) and after sublingual administration of the endothelium-independent vasodilator nitroglycerin. In 9 Marfan and 6 control subjects, the above parameters were also assessed during intra-arterial infusions of acetylcholine and bradykinin (agonists that stimulate NO production) and NG-monomethyl-L-arginine (L-NMMA, an inhibitor of NO production). Flow-mediated responses differed markedly between Marfan and control subjects (-1.6+/-3.5% versus 6. 50+/-4.1%, respectively; P<0.0001), whereas nitroglycerin produced similar vasodilation (14.2+/-5.7% versus 15.2+/-7.8%; P=NS). Agonist-induced vasodilation to incremental intra-arterial infusions of acetylcholine and bradykinin were not significantly different between Marfan and control subjects, and intra-arterial L-NMMA produced similar reductions in brachial artery diameter in both groups. CONCLUSIONS: These data demonstrate impaired flow-mediated but preserved agonist-mediated endothelium-dependent vasodilation in Marfan subjects and suggest preservation of basal NO release. Selective loss of flow-mediated dilation suggests a role for fibrillin in endothelial cell mechanotransduction.  (+info)

(3/1777) Flow-mediated vasodilation and distensibility of the brachial artery in renal allograft recipients.

BACKGROUND: Alterations of large artery function and structure are frequently observed in renal allograft recipients. However, endothelial function has not yet been assessed in this population. METHODS: Flow-mediated vasodilation is a useful index of endothelial function. We measured the diameter and distensibility of the brachial artery at rest using high-resolution ultrasound and Doppler frequency analysis of vessel wall movements in the M mode. Thereafter, changes in brachial artery diameter were measured during reactive hyperemia (after 4 min of forearm occlusion) in 16 cyclosporine-treated renal allograft recipients and 16 normal controls of similar age and sex ratio. Nitroglycerin-mediated vasodilation was measured to assess endothelium-independent vasodilation. Brachial artery blood pressure was measured using an automatic sphygmomanometer, and brachial artery flow was estimated using pulsed Doppler. RESULTS: Distensibility was reduced in renal allograft recipients (5.31 +/- 0. 74 vs. 9.10 +/- 0.94 x 10-3/kPa, P = 0.003, mean +/- sem), while the brachial artery diameter at rest was higher (4.13 +/- 0.14 vs. 3.25 +/- 0.14 mm, P < 0.001). Flow-mediated vasodilation was significantly reduced in renal allograft recipients (0.13 +/- 0.08 vs. 0.60 +/- 0.08 mm or 3 +/- 2 vs. 19 +/- 3%, both P < 0.001). However, nitroglycerin-mediated vasodilation was similar in renal allograft recipients and controls (0.76 +/- 0.10 vs. 0.77 +/- 0.09 mm, NS, or 19 +/- 3 vs. 22 +/- 2%, NS). There were no significant differences in brachial artery flow at rest and during reactive hyperemia between both groups. The impairments of flow-mediated vasodilation and distensibility in renal allograft recipients remained significant after correction for serum cholesterol, creatinine, parathyroid hormone concentrations, end-diastolic diameter, as well as blood pressure levels, and were also present in eight renal allograft recipients not treated with cyclosporine. Flow-mediated vasodilation was not related to distensibility in either group. CONCLUSIONS: The results show impaired endothelial function and reduced brachial artery distensibility in renal allograft recipients. The impairments of flow-mediated vasodilation and distensibility are not attributable to a diminished brachial artery vasodilator capacity, because endothelium-independent vasodilation was preserved in renal allograft recipients.  (+info)

(4/1777) Endothelial dysfunction by acute hyperhomocyst(e)inaemia: restoration by folic acid.

Recent evidence demonstrates that hyperhomocyst(e)inaemia is a novel risk factor for cardiovascular diseases. In patients with chronic hyperhomocyst(e)inaemia, endothelial function is impaired. However, whether hyperhomocyst(e)inaemia per se is a cause or an epiphenomenon of endothelial dysfunction remains unknown. In this study, we examined the effects of methionine-induced acute hyperhomocyst(e)inaemia on human endothelial function. In healthy volunteers we administered methionine (0.1 g/kg body weight, per os), a substrate of homocyst(e)ine, with or without folic acid (20 mg, per os) and examined flow-mediated vasodilatation of the brachial artery by high-resolution ultrasonography as a non-invasive measure of endothelial function. We also measured plasma levels of homocyst(e)ine before and 3, 8 and 24 h after methionine loading. Methionine administration increased plasma levels of homocyst(e)ine by four times the basal level at 8 h (P<0.0001, ANOVA). The plasma levels returned to baseline at 24 h. Flow-mediated vasodilatation was significantly decreased to half of the baseline value at 8 h and returned to baseline at 24 h (P<0.0001, ANOVA), whereas endothelium-independent vasodilatation by glyceryl trinitrate was not affected by the methionine loading. Co-administration of folic acid did not attenuate methionine-induced hyperhomocyst(e)inaemia but completely prevented endothelial dysfunction. Our results suggest that in humans a methionine-rich diet may acutely impair endothelial function, which can be prevented by folic acid supplementation.  (+info)

(5/1777) Demonstration of rapid onset vascular endothelial dysfunction after hyperhomocysteinemia: an effect reversible with vitamin C therapy.

BACKGROUND: Hyperhomocysteinemia is a major and independent risk factor for vascular disease. The mechanisms by which homocysteine promotes atherosclerosis are not well understood. We hypothesized that elevated homocysteine concentrations are associated with rapid onset endothelial dysfunction, which is mediated through oxidant stress mechanisms and can be inhibited by the antioxidant vitamin C. METHODS AND RESULTS: We studied 17 healthy volunteers (10 male and 7 female) aged 33 (range 21 to 59) years. Brachial artery diameter responses to hyperemic flow (endothelium dependent), and glyceryltrinitrate (GTN, endothelium independent) were measured with high resolution ultrasound at 0 hours (fasting), 2 hours, and 4 hours after (1) oral methionine (L-methionine 100 mg/kg), (2) oral methionine preceded by vitamin C (1g/day, for 1 week), and (3) placebo, on separate days and in random order. Plasma homocysteine increased (0 hours, 12.8+/-1.4; 2 hours, 25.4+/-2.5; and 4 hours, 31. 2+/-3.1 micromol/l, P<0.001), and flow-mediated dilatation fell (0 hours, 4.3+/-0.7; 2 hours, 1.1+/-0.9; and 4 hours, -0.7+/-0.8%) after oral L-methionine. There was an inverse linear relationship between homocysteine concentration and flow-mediated dilatation (P<0. 001). Pretreatment with vitamin C did not affect the rise in homocysteine concentrations after methionine (0 hours, 13.6+/-1.6; 2 hours, 28.3+/-2.9; and 4 hours, 33.8+/-3.7 micromol/l, P=0.27), but did ameliorate the reduction in flow-mediated dilatation (0 hours, 4. 0+/-1.0; 2 hours, 3.5+/-1.2 and 4 hours, 2.8+/-0.7%, P=0.02). GTN-induced endothelium independent brachial artery dilatation was not affected after methionine or methionine preceded by vitamin C. CONCLUSIONS: We conclude that an elevation in homocysteine concentration is associated with an acute impairment of vascular endothelial function that can be prevented by pretreatment with vitamin C in healthy subjects. Our results support the hypothesis that the adverse effects of homocysteine on vascular endothelial cells are mediated through oxidative stress mechanisms.  (+info)

(6/1777) Isolated femoropopliteal bypass graft for limb salvage after failed tibial reconstruction: a viable alternative to amputation.

PURPOSE: Femoropopliteal bypass grafting procedures performed to isolated popliteal arteries after failure of a previous tibial reconstruction were studied. The results were compared with those of a study of primary isolated femoropopliteal bypass grafts (IFPBs). METHODS: IFPBs were only constructed if the uninvolved or patent popliteal segment measured at least 7 cm in length and had at least one major collateral supplying the calf. When IFPB was performed for ischemic lesions, these lesions were usually limited to the digits or small portions of the foot. Forty-seven polytetrafluoroethylene grafts and three autogenous reversed saphenous vein grafts were used. RESULTS: Ankle brachial pressure index (ABI) increased after bypass grafting by a mean of 0.46. Three-year primary life table patency and limb-salvage rates for primary IFPBs were 73% and 86%, respectively. All eight IFPBs performed after failed tibial bypass grafts remained patent for 2 to 44 months, with patients having viable, healed feet. CONCLUSION: In the presence of a suitable popliteal artery and limited tissue necrosis, IFPB can have acceptable patency and limb-salvage rates, even when a polytetrafluoroethylene graft is used. Secondary IFPB can be used to achieve limb salvage after failed tibial bypass grafting.  (+info)

(7/1777) Surgical transluminal iliac angioplasty with selective stenting: long-term results assessed by means of duplex scanning.

PURPOSE: The safety of iliac angioplasty and selective stenting performed in the operating room by vascular surgeons was evaluated, and the short- and long-term results were assessed by means of serial duplex scanning. METHODS: Between 1989 and 1996, 281 iliac stenotic or occlusive lesions in 235 consecutive patients with chronic limb ischemia were treated by means of percutaneous transluminal angioplasty (PTA) alone (n = 214) or PTA with stent (n = 67, 23.8%). There were 260 primary lesions and 21 restenosis after a first PTA, which were analyzed separately. Stents were implanted in selected cases, either primarily in totally occluded arteries or after suboptimum results of PTA (ie, residual stenosis or a dissection). Data were collected prospectively and analyzed retrospectively. Results were reported in an intention-to-treat basis. Clinical results and patency were evaluated by means of symptom assessment, ankle brachial pressure index, and duplex scanning at discharge and 1, 3, 6, and every 12 months after angioplasty. To identify factors that may affect outcome, 12 clinical and radiological variables, including the four categories of lesions defined by the Standards of Practice Committee of the Society of Cardiovascular and Interventional Radiology, were analyzed separately. The statistical significances of life-table analysis of patency were determined by means of the log-rank test. RESULTS: There were no postoperative deaths or amputations. Local, general, and vascular complications occurred in 2.1%, 1.3% and 4.7% of cases, respectively (total, 8.1%). The mean follow-up period was 29.6 months. The cumulative patency rates +/- SE of the 260 PTAs (including 55 PTAs plus stents) were 92.9% +/- 1.5% at 1 month, 86. 5% +/- 1.7% at 1 year, 81.2% +/- 2.3% at 2 years, 78.8% +/- 2.9% at 3 years, and 75.4% +/- 3.5% at 5 and 6 years. The two-year patency rate of 21 redo PTAs (including 11 PTAs plus stents) was 79.1% +/- 18.2%. Of 12 predictable variables studied in the first PTA group, only the category of the lesion was predictive of long-term patency. The two-year patency rate was 84% +/- 3% for 199 category 1 lesions and 69.7% +/- 6.5% for 61 category 2, 3, and 4 lesions together (P =. 02). There was no difference of patency in the stented and nonstented group. CONCLUSION: Iliac PTA alone or with the use of a stent (in cases of occlusion and/or suboptimal results of PTA) offers an excellent long-term patency rate. Categorization of lesions remains useful in predicting long-term outcome. PTA can be performed safely by vascular surgeons in the operating room and should be considered to be the primary treatment for localized iliac occlusive disease.  (+info)

(8/1777) Normal pregnancy is associated with enhanced endothelium-dependent flow-mediated vasodilation.

Normal pregnancy is characterized by reduced systemic vascular resistance, which may be mediated by nitric oxide (NO). We compared endothelial vasomotor function in 71 normal pregnant women (13 in first, 29 in middle, and 29 in last trimester) to 37 healthy age-matched controls. With external ultrasound, brachial artery diameter was measured at rest, during reactive hyperemia [with increased flow causing endothelium-dependent dilation (FMD)], and after sublingual nitroglycerin (causing endothelium-independent dilation). Compared with controls, resting flow and brachial artery diameter were significantly higher during the middle and last trimesters. Reactive hyperemia was reduced in all pregnant groups. FMD increased from the first trimester (by 26%), reaching the highest value in the last trimester (to 47% above nonpregnant values). FMD was significantly correlated to pregnancy status (nonpregnant or pregnant) and to vessel size. Nitroglycerin-induced dilation was similar in pregnant and nonpregnant women. A longitudinal study of eight women evaluated in the first, middle, and last trimesters confirmed an increase in FMD throughout pregnancy. The study supports the idea that basal and stimulated NO activity is enhanced in normal pregnancy and may contribute to the decrease in peripheral resistance.  (+info)