bluuebunny/crossref_metadata_2025_split huggingface dataset:
Functional significance of intimal thickening as detected by intravascular ultrasound early and late after cardiac transplantation.
Authors: Anderson T J , Meredith I T , Uehata A , Mudge G H , Selwyn A P , Ganz P , Yeung A C 
Published: June 2012

BACKGROUND
Detection of transplant coronary disease remains difficult. Both intravascular ultrasound (IVUS) imaging and functional coronary vasomotion studies have been used to evaluate this process. However, the time course of intimal thickening as assessed by IVUS and the relation between structure and function have not been explored.

METHODS AND RESULTS
In 40 patients 1 to 8 years after transplantation, 108 coronary artery segments were analyzed by IVUS. Intimal index [% intimal area (lumen+intimal area)] and maximal thickness were used to quantify intimal thickening. Abnormal IVUS was present in 53 of 108 segments (49%) (mean intimal index of diseased segments, 23 +/- 2%; maximal thickness, 530 +/- 47 microns). For those patients with intimal thickening in all segments of the analyzed artery, more time had elapsed since transplantation (4.3 +/- 0.6 years) than for those whose arteries contained some normal (2.6 +/- 0.3 years) or all normal segments (2.2 +/- 0.6 years, P < .05). Both the proportion of segments with intimal thickening and the degree of thickening increased as a function of time after transplantation (P < .5). By multivariate analysis, the independent predictors of intimal thickening were increasing time after transplantation and pretransplantation hypercholesterolemia (P = .02). Within the cohort of 40 patients, endothelium-dependent vasomotor function was evaluated in 26 matched segments from 11 patients studied 1 year after transplantation and in 15 matched segments from 8 patients studied > or = 5 years after transplantation by serial infusions of acetylcholine (10(-8) to 10(-6) mol/L). Of the 26 segments assessed for structure/function correlation at 1 year after transplantation, 22 had no intimal thickening by IVUS. However, endothelial dysfunction was present in 13 of these normal segments (mean diameter constriction, 18.8 +/- 2.3%). Of the 15 segments studied > or = 5 years after transplantation, 11 had intimal thickening. Nine of these 11 segments had preserved endothelial function (mean diameter dilation, 8.6 +/- 2.9%). There was no relation between the degree of intimal thickening and the magnitude of the endothelium-dependent response to acetylcholine.

CONCLUSIONS
This study has shown that intimal thickening after transplantation begins as a heterogeneous process and increases in extent and magnitude over time. Also, endothelial dysfunction occurs early before the intimal thickening; yet in those patients surviving > or = 5 years, endothelial function may recover even in the presence of moderate intimal pathology. The variable relation between intimal pathology and endothelial function is probably a result of the episodic nature of immune injury.
Endothelin antiserum decreases volume-stimulated and basal plasma concentration of atrial natriuretic peptide.
Authors: Fyhrquist F , Sirviö M L , Helin K , Saijonmaa O , Metsärinne K , Paakkari I , Järvinen A , Tikkanen I 
Published: June 2012

BACKGROUND
Endothelin-1 (ET-1) is the most powerful factor known to release atrial natriuretic peptide (ANP) in vivo and in cultured cardiac myocytes or preparations of atrium. We tested the role of endogenous ET-1 in the regulation of ANP release by passive immunization in anesthetized rats.

METHODS AND RESULTS
Intravenous injection of antiserum against ET-1 was shown to decrease basal and volume-stimulated plasma concentrations of ANP, whereas control serum was without effect. Antiserum generated in rabbits cross-reacted 100% with endothelin-2 and -3. In pentobarbital-anesthetized Wistar rats treated with ET-1 antiserum, plasma ANP concentration measured by radioimmunoassay was reduced by 37% from starting level after 10 minutes and by 30% after 60 minutes. Control rat serum had no effect on plasma ANP. Rapid intravenous infusion of 8 mL of 0.9% NaCl caused a sixfold increase of plasma ANP concentration in control rats but only twofold in rats pretreated with ET-1 antiserum (P < .01). This effect of ET-1 antiserum was dose dependent. ET-1 antiserum changed neither blood pressure nor heart rate significantly in anesthetized rats. Pretreatment with ET-1 antiserum did not affect the initial hypotensive response to intravenous ET-1 0.5 nmol/kg but significantly attenuated the subsequent hypertensive response to endothelin.

CONCLUSIONS
Endothelin may be a physiological modulator of both basal and stimulated ANP release.
Both increased and decreased platelet adhesion to thermally injured subendothelium is caused by denaturation of von Willebrand factor.
Authors: Bos A N , Post M J , de Groot P G , Sixma J J , Borst C 
Published: June 2012

BACKGROUND
Thermal angioplasty methods heat the arterial wall. We related platelet adhesion to the temperature to which subendothelium and purified adhesive proteins had been exposed.

METHODS AND RESULTS
Cultured subendothelium, purified von Willebrand factor, collagen types I and III, or fibronectin was applied to glass coverslips. Coverslips were mounted on a heating device that applied a temperature gradient from 30 to 100 degrees C. De-endothelialized umbilical arteries were heated by immersion in phosphate-buffered saline. After cooling to room temperature, the surfaces were perfused with blood at 37 degrees C (shear rate, 1600 sec-1). Compared with 37 degrees C, platelet adhesion to endothelial cell matrix was significantly reduced by 25%, 50% or 75% after heating to 69 +/- 1 degree C (mean +/- SEM, P < .05), 72 +/- 1 degree C, or 75 +/- 1 degree C, respectively. Platelet coverage to umbilical artery subendothelium was in the same way significantly reduced after heating to 71 +/- 1 degree C, or 77 +/- 1 degree C, respectively. In contrast to endothelial cell matrix, however, heating to about 55 degrees C increased platelet coverage from 30 +/- 5% to 54 +/- 6% (P < .05). Both platelet adhesion to von Willebrand factor and monoclonal antibody binding against the GpIb binding site of von Willebrand factor showed a comparable temperature dependence as platelet adhesion to subendothelium, provided the proper von Willebrand factor concentration was used. Platelet adhesion to heated collagen types I and III was increased and maximal at 57 +/- 2 degrees C and 62 +/- 2 degrees C, respectively. Preincubation of collagen III with proteins resulted in decreased platelet adhesion with increasing temperatures. Heating did not affect the reactivity of fibronectin.

CONCLUSIONS
In vitro platelet adhesion to human subendothelium is reduced by more than 50% after heating it briefly to more than 74 degrees C. Temperatures in excess of 80 degrees C reduce platelet adhesion by at least 85%. Thermal denaturation of von Willebrand factor is responsible not only for the decreased thrombogenicity above 71 degrees C but also for the increased thrombogenicity near 55 degrees C, provided that the von Willebrand factor concentration is low.
Ankle-arm index as a marker of atherosclerosis in the Cardiovascular Health Study. Cardiovascular Heart Study (CHS) Collaborative Research Group.
Authors: Newman A B , Siscovick D S , Manolio T A , Polak J , Fried L P , Borhani N O , Wolfson S K 
Published: June 2012

BACKGROUND
Peripheral arterial disease measured noninvasively by the ankle-arm index (AAI) is common in older adults, largely asymptomatic, and associated with clinically manifest cardiovascular disease (CVD). The criteria for an abnormal AAI have varied in previous studies. To determine whether there is an inverse dose-response relation between the AAI and clinical CVD, subclinical disease, and risk factors, we examined the relation of the AAI to cardiovascular risk factors, other noninvasive measures of subclinical atherosclerosis using carotid ultrasound, echocardiography and electrocardiography, and clinical CVD.

METHODS AND RESULTS
The AAI was measured in 5084 participants > or = 65 years old at the baseline examination of the Cardiovascular Health Study. All subjects had detailed assessment of prevalent CVD, measures of cardiovascular risk factors, and noninvasive measures of disease. Participants were stratified by baseline clinical CVD status and AAI (< 0.8, > or = 0.8 to < 0.9, > or = 0.9 to < 1.0, > or = 1.0 to < 1.5). Analyses tested for a dose-response relation of the AAI with clinical CVD, risk factors, and subclinical disease. The cumulative frequency of a low AAI was 7.4% of participants < 0.8, 12.4% < 0.9, and 23.6% < 1.0. participants with an AAI < 0.8 were more than twice as likely as those with an AAI of 1.0 to 1.5 to have a history of myocardial infarction, angina, congestive heart failure, stroke, or transient ischemic attack (all P < .01). In participants free of clinical CVD at baseline, the AAI was inversely related to history of hypertension, history of diabetes, and smoking, as well as systolic blood pressure, serum creatinine, fasting glucose, fasting insulin, measures of pulmonary function, and fibrinogen level (all P < .01). Risk factor associations with the AAI were similar in men and women free of CVD except for serum total and low-density lipoprotein cholesterol, which were inversely associated with AAI level only in women. Risk factors associated with an AAI of < 1.0 in multivariate analysis included smoking (odds ratio [OR], 2.55), history of diabetes (OR, 3.84), increasing age (OR, 1.54), and nonwhite race (OR, 2.36). In the 3372 participants free of clinical CVD, other noninvasive measures of subclinical CVD, including carotid stenosis by duplex scanning, segmental wall motion abnormalities by echocardiogram, and major ECG abnormalities were inversely related to the AAI (all P < .01).

CONCLUSIONS
There was an inverse dose-response relation of the AAI with CVD risk factors and subclinical and clinical CVD among older adults. The lower the AAI, the greater the increase in CVD risk; however, even those with modest, asymptomatic reductions in the AAI (0.8 to 1.0) appear to be at increased risk of CVD.
Late potentials and ventricular enlargement after myocardial infarction. A new role for high-resolution electrocardiography?
Authors: Zaman A G , Morris J L , Smyllie J H , Cowan J C 
Published: June 2012

BACKGROUND
Arrhythmias are common in patients who have developed ventricular enlargement after myocardial infarction.

METHODS AND RESULTS
A prospective study was undertaken to assess the relation between ventricular dilatation and the development of late potentials after myocardial infarction. Echocardiograms and signal-averaged ECGs were recorded on days 1,3,7, and 42 in 52 patients with a first anterior myocardial infarction. Twenty-nine percent of patients were late potential-positive on their initial signal-averaged ECG recorded on the day of admission. The incidence of late potentials rose during the next week to a peak of 42% at day 7, declining to 13% by day 42. The presence of late potentials on the day of admission was associated with an increase in end-diastolic volume index of 16.1 +/- 6.0 mL/m2 (mean +/- SEM), compared with a decreased of 4.7 +/- 2.7 mL/m2 among late potential-negative patients (P < .006). Qualitatively similar results were evident for late potentials on day 3 and day 7. By contrast, there was no association between late potentials on day 42 and ventricular dilatation. Marked dynamic changes in late potentials were evident during the first week. Patients with persistent late potentials (n = 9) on all three recordings in the first week showed a marked increase in end-diastolic volume index of 21.3 +/- 8.1 mL/m2 (P < .005 in comparison with patients who were persistently negative [n = 20]). Patients demonstrating dynamic positivity (n = 15) not present on all three recordings in the first week showed no significant increase in end-diastolic volume index.

CONCLUSION
It is concluded that late potentials during the first week after infarction are associated with subsequent ventricular dilatation. These early-phase late potentials may be a manifestation of cell slippage. They arise before gross topographical enlargement and may serve as a predictor of ventricular dilatation.
Determination of the most appropriate velocity threshold for applying hemispheric flow convergence equations to calculate flow rate: selected according to the transorifice pressure gradient. Digital computer analysis of the Doppler color flow convergence region.
Authors: Deng Y B , Shiota T , Shandas R , Zhang J , Sahn D J 
Published: June 2012

BACKGROUND
While flow convergence methods have been promising for calculating volume flows from color Doppler images, it appears that the velocity threshold used and the transorifice pressure gradient dramatically influence the accuracy of application of the simple hemispheric flow convergence equation for calculation of flow rate. The present in vitro study was performed to determine whether the value of velocity threshold at which the shape of proximal isovelocity surface best fits given shape assumptions with different orifice sizes and flow rates is predictable as a function independent of orifice size from clinically measurable peak velocity or transorifice pressure gradient information.

METHODS AND RESULTS
In an in vitro model built to facilitate ultrasound imaging, steady flow was driven through circular discrete orifices with diameters of 3.8, 5.5, and 10 mm. Flow rates ranged from 2.88 to 8.28 L/min with corresponding driving pressure gradients from 14 to 263 mm Hg. At each flow rate, Doppler color-encoded M-mode images through the center of the flow convergence region were obtained and transferred into the microcomputer (Macintosh IIci) in their original digital format. Then, the continuous wave Doppler traces of maximal velocity through the orifice were derived for the calculation of driving pressure gradient. Direct numerical spatial velocity measurements were obtained from the digital color encoded M-mode velocities with computer software. For each flow rate, we could calculate flow volume from any number of velocity distance combinations with a number of assumptions and use the results to assess expected flow convergence shape based on a priori knowledge of the progression from oblate hemispheroid to hemisphere to prolate hemispheroid changes observed previously. Our results showed that for a given ratio of calculated flow rate to actual flow rate (0.7 and 1), the velocity threshold that could be used for the calculation of flow rate with a hemispheric flow convergence equation correlated well with the pressure gradient for a given orifice size, and the differences in velocity threshold that could be used this way among different orifice sizes once they were adjusted for the covariate pressure gradients were not statistically significant (P = .79 for ratio = 0.7, and P = .81 for ratio = 1).

CONCLUSIONS
Our present study provides an orifice size-independent quantitative method that can be used to select the most suitable velocity threshold for applying a simple hemispheric flow convergence equation based on clinically predictable pressure gradients ranging from 40 to 200 mm Hg, and it offers a correction factor that can be applied to the hemispheric flow convergence equation when the pressure gradient is less than 40 mm Hg.
Sustained activation of vascular cells and leukocytes in the rabbit aorta after balloon injury.
Authors: Tanaka H , Sukhova G K , Swanson S J , Clinton S K , Ganz P , Cybulsky M I , Libby P 
Published: June 2012

BACKGROUND
To improve understanding of the cellular basis of the arterial response to injury, we tested whether balloon withdrawal can induce certain inflammatory functions of vascular cells and leukocytes and whether such "activation" persists even after the acute phase of injury.

METHODS AND RESULTS
We examined the expression of several inducible cell surface molecules in the rabbit aorta at 2, 5, 10, and 30 days after balloon injury. Longitudinal sections encompassing parts of the uninjured, border, and injured zones were examined for expression of vascular adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), class II major histocompatibility (MHC) antigens, and markers for smooth muscle cells (SMCs), macrophages, endothelial cells, and T-lymphocytes. Endothelial cell healing involved true endothelial regeneration as well as migration, as shown by nuclear incorporation of bromodeoxyuridine. Luminal endothelial cells at the leading edge of repopulation at each time point expressed VCAM-1. As healing progressed, VCAM-1 expression decreased in the regenerated endothelial cells. The neointimal endothelium also expressed high levels of ICAM-1 that persisted longer than the elevation of VCAM-1. SMCs in the neointima also showed increased levels of ICAM-1. Some neointimal endothelial cells, SMCs, and macrophages also expressed high levels of class II MHC antigens during 30 days after injury.

CONCLUSIONS
Local inflammatory activation of endothelial cells, SMCs, and leukocytes occurs in a predictable sequence and persists up to 30 days after balloon injury to the rabbit aorta. Our findings suggest that ongoing local signals persisting after the original balloon injury may contribute to later phases of intimal thickening.
Response of human coronary arteries to serotonin after injury by coronary angioplasty.
Authors: Mc Fadden E P , Bauters C , Lablanche J M , Quandalle P , Leroy F , Bertrand M E 
Published: June 2012

BACKGROUND
Atherosclerotic stenoses that have exaggerated vasomotor responses are especially prone to restenosis after coronary angioplasty. Experimental studies show that vasomotor responses in normal vessels are altered by acute mechanical injury, an alteration that in part reflects changes in the functional characteristics of endothelium that has regenerated after injury.

METHODS AND RESULTS
We examined, by quantitative coronary arteriography, the response of dilated and control coronary segments to intracoronary infusions of graded doses of serotonin, an endothelium-dependent vasoactive agent, and to intracoronary injection of isosorbide dinitrate, an endothelium-independent smooth muscle dilator in 15 patients who had undergone a single percutaneous transluminal coronary angioplasty procedure and who had no clinical features of variant angina. Dose-dependent constriction to serotonin occurred at all measured sites. The mean +/- SEM diameter reductions, expressed as percent reduction in baseline diameter that was observed at proximal (18.1 +/- 2.9, 18.8 +/- 2.2) and distal (30.9 +/- 4.4, 35.4 +/- 5.3) control sites in the dilated and nondilated vessels, respectively, at the highest dose, were similar. The degree of constriction in distal segments was significantly (P < .01) greater than that in proximal segments. Total or subtotal occlusion occurred at the angioplasty site in 4 patients at the highest infused dose (10(-4) mol/L). The mean percent reduction in baseline diameter at previously dilated sites (53.8 +/- 5.9) at this dose was significantly (P < .05) greater than that observed at the adjacent proximal control sites and similar to that observed at distal control sites. All segments dilated significantly after intracoronary injection of isosorbide dinitrate.

CONCLUSIONS
In dilated and nondilated vessels, serotonin caused significantly more marked constriction in distal than in proximal vessel segments. In dilated vessels, the vessel segments that had been subjected to angioplasty had a constrictor response to serotonin that was more marked than at adjacent proximal control sites and equivalent to that in the distal vessel segments. This enhanced constrictor response could be related to changes in endothelial cell function after regeneration or to hyperreactivity of smooth muscle cells at the angioplasty site.
Differences between men and women in hospital mortality associated with coronary artery bypass graft surgery. The Northern New England Cardiovascular Disease Study Group.
Authors: O'Connor G T , Morton J R , Diehl M J , Olmstead E M , Coffin L H , Levy D G , Maloney C T , Plume S K , Nugent W , Malenka D J 
Published: June 2012

BACKGROUND
A prospective study of patients undergoing coronary artery bypass graft surgery (CABG) was conducted to examine differences in hospital mortality by sex. Outcome data on 3055 CABG patients undergoing operation between 1987 and 1989 were examined for differences in patient, disease, and treatment factors.

METHODS AND RESULTS
Odds ratios (OR), risk differences, and 95% confidence intervals (CI95%) were calculated. Mortality rates for women (7.1%) and men (3.3%) differed, the OR (women versus men) being 2.23 (CI95%, 1.58 to 3.15). Women were older, more often diabetic, and had more urgent or emergent surgery; adjustment yielded an OR (women versus men) of 1.75 (CI95%, 1.17 to 2.63). Body surface area (BSA) was associated with risk of death in both sexes (P = .007) and positively associated with coronary artery luminal diameters. After adjustment for BSA, sex was no longer significantly associated with mortality (OR [women versus men] of 1.18; CI95%, 0.72 to 1.95). Internal mammary artery (IMA) grafting was performed less frequently among women than men (64.8% versus 78.4%, P < .001). Smaller BSA and absence of IMA grafting were each associated with increased risk of death (RD) from heart failure. Risk of death from heart failure (RD [women minus men] = 2.05; CI95%, 0.89 to 3.22) and hemorrhage (RD [women minus men] = 0.63; CI95%, 0.13 to 1.13) was greater among women; these accounted for 71.1% of the sex-specific difference in mortality rates.

CONCLUSIONS
Excess risk of hospital mortality among women having CABG was largely the consequence of death from heart failure and, to a lesser extent, from hemorrhage. Smaller BSA (probably because of its association with coronary artery luminal diameter) and the absence of IMA grafting were each associated with increased risk of death from heart failure.