ISSN:0009-7322    

出版商:OVID    

年代:2003

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:2003

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:2003

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

BackgroundNatriuretic peptides play a critical role in the maintenance of salt and water homeostasis and regulation of vascular tone. Thus, interindividual variation in plasma natriuretic peptide levels may contribute to variation in susceptibility to volume overload and hypertension. It is unknown to what extent genetic factors contribute to variation in plasma natriuretic peptide levels.Methods and ResultsWe studied 1914 Framingham Study participants (mean age 57 years, 53% women) who underwent routine echocardiography and testing for plasma N‐terminal proatrial natriuretic peptide (N‐ANP) and brain natriuretic peptide (BNP). We estimated sex‐specific multivariable models and used variance‐components methods, implemented in SOLAR (Sequential Oligogenic Linkage Analysis Routines), to estimate heritability. Multipoint linkage analyses were performed using data from a 10‐cM‐density genome scan. Age, clinical, and echocardiographic variables accounted for 42% and 40% of the variation in log N‐ANP and log BNP levels, respectively, in men. Corresponding values in women were 27% and 21%. Multivariable‐adjusted heritabilities were 0.44 for log N‐ANP and 0.35 for log BNP (P<0.0001). Genome‐wide linkage analyses, based on 1142 participants from the 314 largest families, revealed 2 regions of suggestive linkage for log N‐ANP and log BNP on chromosomes 2p25 (log‐of‐odds score 2.40) and 12p13 (log‐of‐odds score 2.13), respectively.ConclusionsIn this community‐based sample, a substantial proportion of the unexplained variation in plasma natriuretic peptide levels was attributable to additive genetic effects. Additional studies using candidate gene approaches may provide insight into the genetic loci that regulate plasma natriuretic peptide levels in humans. (Circulation. 2003;108: 13‐16.)

ISSN:0009-7322    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

BackgroundAtherosclerosis preferentially develops at average low shear stress (SS) locations. SS‐related signaling maintains lumen dimensions by inducing outward arterial remodeling. Prolonged plaque accumulation at low SS predilection locations explains an inverse relation between wall thickness (WT) and SS. No data exist on WT‐SS relations when lumen narrowing and loss of compensatory remodeling commence.Methods and ResultsIn 14 patients, an angiographically normal artery (stenosis <50%) was investigated with ANGiography and ivUS (ANGUS) to provide 3D lumen and wall geometry. Selection of segments >5 mm in length, in between side branches, yielded 25 segments in 12 patients. SS at the wall was calculated by computational fluid dynamics. WT smaller than 0.2*lumen diameter was defined as normal. Largest arc of normal WT defined reference cross sections. Lumen area relative to the reference cross sections defined area stenosis (AS). Average segmental AS smaller or greater than 10% defined preserved or narrowed lumen, respectively. Total vessel area relative to the reference defined vascular remodeling (VR). For the preserved lumens (n=11, AS=1.7±5.6%,P=NS), axially averaged WT and SS were inversely related (slope, ‐0.46±0.55 mm/Pa,P<0.05) and VR was positive (7±9%,P<0.05). Narrowed segments (n=13, 1 excluded, AS=18±6%,P<0.05) showed no relation between WT and SS or vascular remodeling.ConclusionsIn patient coronary arteries, the often‐reported inverse WT‐SS relationship appears restricted to lumen preservation and positive vascular remodeling. Its disappearance with lumen narrowing suggests a growing importance of non‐SS‐related plaque progression. (Circulation. 2003;108:17‐23.)

ISSN:0009-7322    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

BackgroundThis study was designed to determine the optimal timing of vitamins E and C to prevent oxidative stress induced by a high‐fat evening meal in type 2 diabetes.Methods and ResultsEleven subjects were admitted on 4 occasions. Euglycemia was maintained for 24 hours by insulin infusion. Participants were fed a high‐fat test supper equivalent to a McDonald's Big Mac Meal. Blood was drawn for measurement of C‐reactive protein (CRP), interleukin 6 (IL‐6), plasminogen activator inhibitor‐1 (PAI‐1), malonyldialdehyde (MDA), and total radical antioxidant parameter (TRAP) before and during the 4 hours after the test meal. Studies were performed in random sequence with vitamin E 800 IU and vitamin C 1 g given either before breakfast or before supper in a double‐blind manner on the day of the test meal. Control studies were performed with no vitamins and no test meal administered. There was a significant rise in CRP and PAI‐1 after the test supper (P<0.05 compared with “no meal”). Either presupper or prebreakfast vitamins E and C prevented the meal‐induced rise in CRP (P=0.03), although presupper vitamins were more effective (P=0.03 compared with prebreakfast vitamins). Only prebreakfast vitamins prevented the meal‐induced rise in PAI‐1 (P=0.006). There were no significant meal‐related changes in the concentrations of IL‐6, MDA, or TRAP.ConclusionsThe timing of administration of antioxidant vitamins has variable effects on markers of meal‐induced inflammation and fibrinolysis. This observation may be one reason why cardiovascular disease prevention trials using these vitamins have reported conflicting results.(Circulation.2003;108:24‐31.)

ISSN:0009-7322    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

BackgroundAntidepressants, particularly selective serotonin reuptake inhibitors (SSRIs), attenuate platelet activation by depleting serotonin storage and may decrease risk of myocardial infarction (MI). These drugs differ in their affinity for the platelet serotonin transporter and therefore may vary in their effects on MI protection.Methods and ResultsA case‐control study of first MI in patients aged 40 through 75 years was conducted among 36 hospitals in a 5‐county area during a 3‐year period. Case subjects were patients hospitalized with a first MI, and control subjects were randomly selected from the same geographic area. Detailed information regarding medication use and other clinical and demographic data were obtained by telephone interview. Among the 1080 cases and 4256 controls who participated, there were 223 users of antidepressants with high serotonin transporter affinity, all of which were SSRIs (paroxetine, fluoxetine, and sertraline). After adjustment with multivariable logistic regression for age, gender, race, education, physical activity, quantity of cigarettes smoked per day, body mass index, aspirin use, family history of MI, and history of diabetes, hypertension, or hypercholesterolemia, the odds ratio for MI among current users of antidepressants with high serotonin transporter affinity compared with nonusers was 0.59 (95% CI 0.39 to 0.91;P=0.02). Increasing serotonin transporter affinity was associated with reduced odds of MI among users of all SSRIs (Pfor trend <0.01) but not tricyclic (P=0.77) or atypical (P=0.70) antidepressants. There was no association detected between non‐SSRI antidepressant use and MI.ConclusionsIncreasing serotonin transporter affinity correlates with greater MI protection with SSRI but not other antidepressant exposure.(Circulation.2003;108:32‐36.)

ISSN:0009-7322    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

BackgroundTreatment of lesions located in saphenous vein grafts (SVGs) is associated with increased procedural risk and a high rate of restenosis.Methods and ResultsWe conducted a randomized, multicenter trial to evaluate the usefulness of a polytetrafluoroethylene (PTFE)‐covered stent compared with a bare stainless steel (SS) stent for prevention of restenosis and major adverse cardiac events (MACE) in patients undergoing SVG treatment. The primary end point was angiographic restenosis at 6 months. Secondary end points were 30‐day and 6‐month MACE rates, defined as the cumulative of death, myocardial infarction (MI), and target lesion revascularization. Between September 1999 and January 2002, 301 patients with SVG lesions were randomized to either the PTFE‐covered JoStent coronary stent graft (PTFE group, n=156) or the SS JoFlex stent (control group, n=145). Angiographic and procedural success rates were similar between the 2 groups (97.4% versus 97.9% and 87.3% versus 93.8%, respectively). The incidence of 30‐day MACE was higher in the PTFE group (10.9% versus 4.1%,P=0.047) and was mainly attributed to MI (10.3% versus 3.4%,P=0.037). The primary end point, the restenosis rate at 6‐month follow‐up, was similar between the 2 groups (24.2% versus 24.8%,P=0.237). Although the 6‐month non‐Q‐wave MI rate was higher in the PTFE group (12.8% versus 4.1%,P=0.013), the cumulative MACE rate was not different (23.1% versus 15.9%,P=0.153).ConclusionsThe study did not demonstrate a difference in restenosis rate and 6‐month clinical outcome between the PTFE‐covered stent and the SS stent for treatment of SVG lesions. However, a higher incidence of nonfatal myocardial infarctions was found in patients treated with the PTFE‐covered stent. (Circulation.2003;108:37‐42.)

ISSN:0009-7322    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

BackgroundFactors leading to subacute stent thrombosis after percutaneous coronary intervention (PCI) have not been well established. We assessed the pre‐ and post‐PCI intravascular ultrasound (IVUS) characteristics of subacute stent thrombosis.Methods and ResultsWe analyzed 7484 consecutive patients without acute myocardial infarction who were treated with PCI and stenting and underwent IVUS imaging during the intervention. Twenty‐seven (0.4%) had angiographically documented subacute closure <1 week after PCI (median time to subacute closure, 24 hours). Subacute closure lesions were compared with a control group (selected to be 3 times the abrupt closer group) matched by procedure date (within 6 months), age, gender, stable or unstable angina, lesion location, and additional treatment (balloon angioplasty or atherectomy). Postintervention IVUS did not identify a cause in 22% and did identify at least 1 cause for abrupt closure in 78% of patients (versus 33% in matched lesions,P=0.0002). In 48% of the patients, there were multiple causes in 48% (versus 3% in matched lesions,P<0.0001). Causes included dissection (17%), thrombus (4%), and tissue protrusion within the stent struts leading to lumen compromise lumen (4%). A total of 83% of patients with >1 of these abnormal morphologies also had reduced lumen dimensions post‐PCI (final lumen <80% reference lumen). Preprocedural lesion characteristics were not different from matched lesions.ConclusionsSubacute stent thrombosis is infrequently related to the preintervention lesion characteristics. Inadequate postprocedure lumen dimensions, alone or in combination with other procedurally related abnormal lesion morphologies (dissection, thrombus, or tissue prolapse), contribute to this phenomenon. (Circulation.2003;108:43‐47.)

ISSN:0009-7322    

出版商:OVID    

年代:2003

数据来源: OVID