bluuebunny/crossref_metadata_2025_split huggingface dataset:
Responsiveness to bradykinin in veins of hypercholesterolemic humans.
Authors: Bedarida G V , Bushell E , Haefeli W E , Blaschke T F , Hoffman B B 
Published: June 2012

BACKGROUND
Hypercholesterolemia impairs endothelium-dependent dilation in arteries. We tested the hypothesis that hypercholesterolemia impairs endothelium-dependent vasodilation by an interaction between elevated plasma lipoproteins and a presumably normal endothelium using human veins in vivo; veins do not generally develop atherosclerosis and are appropriate for testing functional alterations.

METHODS AND RESULTS
Full dose-response curves were constructed in 13 hypercholesterolemic and 12 normocholesterolemic subjects by infusing bradykinin (0.25 to 508 ng/min) into hand veins preconstricted with the alpha-adrenergic agonist phenylephrine. The maximal relaxation induced by bradykinin was 80 +/- 38% in the controls and 103 +/- 40% in subjects with hypercholesterolemia (P = .08). Responsiveness to bradykinin was also determined after infusion of indomethacin (5.4 micrograms/min), a cyclooxygenase inhibitor, to block the contribution of prostaglandins; maximal responsiveness was greater in hypercholesterolemic subjects (112 +/- 41%) than in controls (81 +/- 31%) (P = .03). Hypercholesterolemic subjects were more sensitive to bradykinin, with an ED50 of 4.2 ng/min versus 10.9 ng/min in controls (P = .05); a similarly increased sensitivity was found in the presence of indomethacin. The response to a maximally effective dose of nitroglycerin was greater in hypercholesterolemic subjects (142 +/- 31%) versus 106 +/- 28% in controls (P = .007). In five hypercholesterolemic subjects, treated with lovastatin to normalize serum cholesterol concentrations, maximal responsiveness to bradykinin decreased from 103 +/- 52% to 80 +/- 28%.

CONCLUSIONS
These results demonstrate that hypercholesterolemia in humans does not impair endothelium-derived relaxing factor-mediated venodilation.
Intramural myocardial shortening in hypertensive left ventricular hypertrophy with normal pump function.
Authors: Palmon L C , Reichek N , Yeon S B , Clark N R , Brownson D , Hoffman E , Axel L 
Published: June 2012

BACKGROUND
In hypertensive left ventricular hypertrophy (LVH), intrinsic myocardial systolic function may be normal or depressed. Magnetic resonance tagging can depict intramural myocardial shortening in vivo.

METHODS AND RESULTS
Tagged left ventricular magnetic resonance images were obtained in 30 hypertensive subjects with LVH (mean LV mass index, 142 +/- 41 g/m) and normal ejection fraction (mean, 64 +/- 9%) using spatial modulation of magnetization. In 26 subjects, circumferential myocardial shortening (%S) was compared with results obtained in 10 normal subjects at endocardium, midwall, and epicardium on up to 4 short-axis slices each. Similarly, in 10 subjects, midwall long-axis shortening at basal, midventricular, and apical sites was compared with results obtained in 12 normal volunteers. Circumferential %S was reduced in hypertensive subjects. Mean shortening was 29 +/- 6% at the endocardium in hypertensive subjects versus 44 +/- 6% in normal subjects (P = .0001); 20 +/- 6% at the midwall versus 30 +/- 6% (P = .0001); and 13 +/- 5% at the epicardium versus 21 +/- 5% (P = .0002). However, the transmural gradient in percent shortening from endocardium to epicardium in hypertensive subjects paralleled that in normal subjects. The normal base-to-apex gradient in circumferential %S was absent in LVH. In contrast to normal subjects, circumferential %S showed regional heterogeneity in hypertensive subjects, being maximal in the lateral wall and least in the inferior wall. Longitudinal shortening was also uniformly depressed in hypertensive subjects: 10 +/- 9% at the base versus 21 +/- 6% in normal subjects (P = .0001); 14 +/- 8% at the midventricle versus 18 +/- 3% (P = .03); and 14 +/- 8% at the apex versus 18 +/- 4% (P = .04).

CONCLUSIONS
In hypertensive LVH with normal pump function, intramural circumferential and longitudinal myocardial shortening are depressed.
Prediction of outcome after valve replacement for rheumatic mitral regurgitation in the era of chordal preservation.
Authors: Wisenbaugh T , Skudicky D , Sareli P 
Published: June 2012

BACKGROUND
Noninvasive predictors of important outcomes after valve replacement for mitral regurgitation have not been examined in a rheumatic population (in whom the results of valve repair are suboptimal) in the era of chordal preservation. Timing of valve replacement thus remains a difficult question in rheumatic mitral regurgitation.

METHODS AND RESULTS
Of 278 patients followed after valve replacement, 66 had pure or predominant mitral regurgitation, and in 61 of these the etiology was rheumatic. The mean age was 24 years. After a mean follow-up of 24 +/- 10 months, the ability of preoperative clinical and echocardiographic data to predict outcome was assessed prospectively, and the possible impact of chordal preservation (n = 35) on survival and post-operative left ventricular function was examined retrospectively. There were no perioperative deaths. There were six postoperative deaths, all the result of heart failure and all related to left ventricular dysfunction. The mean probability of survival was .90 at 16 months. In a stepwise Cox proportional hazards regression analysis, the only independent predictor of postoperative death was preoperative end-systolic diameter. According to a logistic model, the probabilities of death (n = 6) and death or severe heart failure (n = 7) increased abruptly at a preoperative end-systolic diameter of 51 mm (probabilities, .23 and .31, respectively), and the accuracy of this cut point for predicting outcomes was 97% and 98%, respectively. Multiple linear regression analysis identified a large preoperative end-systolic diameter and the need to use tricuspid annuloplasty as significant independent predictors of postoperative fractional shortening; the use of chordal preservation (n = 35) was not a predictor of postoperative fractional shortening. A good outcome was predicted at a preoperative end-systolic diameter of 40 mm: probability of death or heart failure was .0001, and predicted mean postoperative fractional shortening was 0.27 after mitral valve replacement without tricuspid annuloplasty.

CONCLUSIONS
When preoperative end-systolic diameter is more than 50 mm, a poor postoperative outcome is predicted despite chordal preservation in relatively young patients with rheumatic mitral regurgitation, and alternative strategies should therefore be considered. When preoperative end-systolic diameter is 40 mm or less, an excellent outcome is predicted, and close observation without surgery would appear to be reasonable in the absence of symptoms.
Reconsideration of criteria for the Fontan operation. Influence of pulmonary artery size on postoperative hemodynamics of the Fontan operation.
Authors: Senzaki H , Isoda T , Ishizawa A , Hishi T 
Published: June 2012

BACKGROUND
The outcome of the Fontan operation largely depends on patient selection because this procedure is a physiological correction. Among the several selection criteria for the Fontan operation, the importance of adequate size of the pulmonary artery remains controversial. To clarify whether or not pulmonary artery size is indispensable as one of the selection criteria for the Fontan operation, we considered the physiological importance of pulmonary artery size and investigated how pulmonary artery size influenced postoperative hemodynamics of the Fontan operation.

METHODS AND RESULTS
In congenital heart disease of decreasing pulmonary blood flow, 40 patients were examined for this analysis. Pulmonary artery indexes (cross-sectional area of the right and left pulmonary arteries divided by body surface area) were measured as the expression of pulmonary artery size, and the relations of pulmonary artery index (PAI) to pulmonary vascular resistance (Rp) and compliance (Cp) were studied. There was no significant correlation between PAI and Rp, whereas a significant correlation was found between PAI and Cp (r = .71, P = .001). Furthermore, Cp influenced postoperative hemodynamics of the Fontan operation by affecting peak central venous pressure and total impedance, which was the afterload to the ventricle. Impedance increased abruptly when PAI was less than approximately 100 mm2/m2.

CONCLUSIONS
The smaller pulmonary artery size is hemodynamically disadvantageous after the Fontan operation, with resultant rise in peak control venous pressure and increased afterload to the single ventricle.
Intracoronary ultrasound assessment of morphological and functional abnormalities associated with cardiac allograft vasculopathy.
Authors: Heroux A L , Silverman P , Costanzo M R , O'Sullivan E J , Johnson M R , Liao Y , McKiernan T L , Balhan J E , Leya F S , Mullen G M 
Published: June 2012

BACKGROUND
The diffuse nature of cardiac allograft vasculopathy makes early detection of the disease by traditional noninvasive methods or coronary angiography difficult. The aim of this study was to determine if there is a relation between abnormalities in vessel wall morphology, as assessed by intracoronary ultrasound, and a decreased vasodilatory response to the endothelium-dependent vasodilator papaverine hydrochloride and if cardiac allograft vasculopathy detected by coronary angiography is associated with specific intracoronary ultrasound findings.

METHODS AND RESULTS
Twenty-three heart transplant recipients underwent 25 intracoronary ultrasound studies and 24 studies of coronary vasomotor tone 10 days to 8.3 years after surgery using a 20-mHz intracoronary ultrasound catheter. The studies were divided in two groups according to the presence (n = 7, group 1) or absence (n = 18, group 2) of angiographically evident cardiac allograft vasculopathy. Qualitative assessment of vessel wall morphology and quantitative analysis of the vasodilator response to the injection of papaverine hydrochloride into the coronary artery distal to the imaging site were performed off-line, and results for the two study groups were compared. A significantly higher percentage of patients with than without angiographic evidence of cardiac allograft vasculopathy had a three-interface vessel wall morphology by intracoronary ultrasound (100% versus 11%, P < .001). In two recipients who underwent two serial studies, the appearance of three interfaces in the vessel wall or a progressive thickening of the inner interface of the vessel wall occurred in conjunction with the appearance of angiographic cardiac allograft vasculopathy. The vasodilator response to papaverine was less in patients with than in those without angiographically evident cardiac allograft vasculopathy both in terms of absolute and relative increases in lumen diameter (+0.1 +/- 0.12 mm versus +0.3 +/- 0.17 mm, P < .05, and +5.1 +/- 5.3% versus +8.2 +/- 5.3%, P = NS) and lumen cross-sectional area (+0.5 +/- 0.6 mm2 versus +1.7 +/- 1.1 mm2, P < .02, and +7.1 +/- 8.8% versus 16.6 +/- 11.0%, P = .055), respectively.

CONCLUSIONS
Intracoronary ultrasound assessment of vessel wall morphology and evaluation of vascular response to endothelium-dependent vasodilators are useful techniques for detecting cardiac allograft vasculopathy.
Myocardial perfusion and ventricular function measurements during total coronary artery occlusion in humans. A comparison with rest and exercise radionuclide studies.
Authors: Borges-Neto S , Puma J , Jones R H , Sketch M H , Stack R , Hanson M W , Coleman R E 
Published: June 2012

BACKGROUND
The purpose of this investigation was to compare the magnitude of change in myocardial perfusion and function during exercise with that obtained during total coronary artery occlusion. Radionuclide studies are widely used for the diagnosis and determination of prognosis in patients with suspected or known coronary artery disease. These studies are based on the premise that the relative deficit of coronary blood flow, which is induced by exercise and recognized as increased demand, relates to the jeopardy experienced by the decrease or sudden absolute interruption of coronary blood flow that is recognized as decreased supply and is associated with coronary stenosis or total coronary artery occlusion. The magnitude of exercise-induced perfusion and function abnormalities compared with those induced by total coronary artery occlusion in humans has not been previously reported.

METHODS AND RESULTS
We prospectively studied 20 patients with > or = 50% diameter stenosis documented by quantitative coronary angiography in at least one vessel. A same-day rest/exercise sestamibi myocardial function and perfusion study was performed within 24 hours before percutaneous transluminal coronary angioplasty. At 1 minute after balloon inflation, while the vessel was occluded, sestamibi was injected, and a myocardial perfusion and function study was performed. Perfusion defect size was greater during occlusion (28 +/- 3%) than during exercise (13 +/- 2%) (P < .01). Ejection fraction was greater during exercise (53 +/- 3%) compared with values measured during occlusion (41 +/- 2%) (P < .01).

CONCLUSIONS
Physiological abnormalities induced by coronary occlusion are greater than those that occur during exercise, thereby indicating that stress-induced ischemia may not reflect the total potential myocardium in jeopardy from a stenotic lesion, if sudden occlusion occurs.
Does external ultrasound accelerate thrombolysis? Results from a rabbit model.
Authors: Kornowski R , Meltzer R S , Chernine A , Vered Z , Battler A 
Published: June 2012

BACKGROUND
Prior in vitro and in vivo studies have reported that external ultrasound accelerates thrombolysis at intensities too low to have a direct effect on clot dissolution in the absence of a thrombolytic agent. The present study was undertaken to examine the ultrasound effect on thrombolysis and reocclusion in a rabbit thrombosis model.

METHODS AND RESULTS
Blood clots were produced in a femoral artery segment with endothelial damage and distal stenosis. Recombinant tissue-type plasminogen activator (rTPA) was infused at 30 micrograms.kg-1.min-1 for 60 minutes. Femoral artery flow was measured every 5 minutes for 2 hours. Rabbits were randomized to four groups with continuous wave ultrasound on or off with or without intravenous injection of 17 mg/kg aspirin (+US/-US/+Asp/-Asp). Ultrasound frequency and intensity were 1 MHz and 6.3 W/cm2. In seven of eight and five of five rabbits given rTPA and -US/-Asp or -US/+Asp, respectively, reflow was observed, persisting to the end of the observation period. In five of nine and four of five rabbits given rTPA and +US/-Asp or +US/+Asp, reflow was achieved, but persistent reocclusion was subsequently observed in five of five and two of four of these rabbits, respectively. Overall, femoral artery patency was worse and reocclusion occurred more often when ultrasound was added to rTPA (P = .002 by nonparametric ANOVA). However, initial reflow occurred more rapidly with ultrasound exposure (21 +/- 10 and 33 +/- 6 minutes for the +US/+Asp and +US/-Asp groups, respectively) compared with without ultrasound (46 +/- 13 and 74 +/- 14 minutes for the -US/+Asp and -US/-Asp groups, respectively) (P = .03 by ANOVA).

CONCLUSIONS
Although time to initial reflow was shortened by ultrasound, it was associated with less reperfusion and more reocclusion in this model. A possible explanation for these results is ultrasound-induced platelet activation counterbalancing its thrombolysis-accelerating effect.
Coronary reperfusion enhances recovery of atrial natriuretic peptide secretion. Salvaging endocrine function in patients with acute right ventricular infarction.
Authors: Yasuda S , Nonogi H , Miyazaki S , Goto Y , Haze K 
Published: June 2012

BACKGROUND
The heart has been demonstrated not only to be a pumping organ but also an endocrine organ secreting atrial natriuretic peptide (ANP). We hypothesized that myocardial ischemia may affect ANP secretion and that reperfusion therapy for acute myocardial infarction can preserve endocrine function of the heart.

METHODS AND RESULTS
Twenty patients with acute right ventricular infarction were examined who underwent reperfusion therapy on admission. These patients had proximal occlusion of the dominant right coronary artery involving the right atrial branches: 9 patients with successful reperfusion (SRP group) and the remaining 11 patients with unsuccessful reperfusion (URP group). Within 24 hours after the onset of infarction, a volume loading test was performed after reperfusion therapy with measurements for plasma ANP levels and hemodynamics. Before the volume loading test, the plasma ANP level and mean right atrial pressure were similar between these two groups. However, in the URP group, percent increase in ANP in response to volume loading was strikingly smaller (URP, 45 +/- 18% versus SRP, 133 +/- 25%; P < .01) despite similar percent increase in mean right atrial pressure (URP, 100 +/- 46% versus SRP, 86 +/- 23%). The peak ANP level occurred significantly later in the URP group (69 +/- 16 hours) than in the SRP group (28 +/- 9 hours, P < .001) after the onset of infarction.

CONCLUSIONS
The response of ANP release to volume loading is attenuated in patients with right ventricular infarction without coronary reperfusion. However, successful reperfusion induces a rapid recovery of cardiac endocrine function as well as its mechanical function. A sufficiently elevated plasma ANP level may be a useful predictor of hemodynamic improvement in patients with right ventricular infarction.
Exercise technetium-99m sestamibi tomography for cardiac risk stratification of patients with stable chest pain.
Authors: Stratmann H G , Williams G A , Wittry M D , Chaitman B R , Miller D D 
Published: June 2012

BACKGROUND
This study was designed to evaluate the prognostic value of symptom-limited maximal exercise treadmill testing with tomographic technetium-99m sestamibi (MIBI) myocardial imaging in patients referred for evaluation of stable angina. Exercise stress thallium-201 myocardial imaging provides prognostic information in coronary artery disease subsets including patients with stable chest pain. The prognostic value of exercise technetium-99m MIBI myocardial tomography has not been established.

METHODS AND RESULTS
Of 548 consecutive patients with stable angina pectoris who underwent maximal exercise treadmill stress testing in combination with a same-day "rest-stress" tomographic technetium-99m MIBI myocardial imaging protocol, 521 patients were followed for 13 +/- 5 months to determine the univariate and multivariate variables associated with cardiac events and to define their cardiac event-free survival. Ten patients were lost to follow-up (98% complete), and 17 who had coronary revascularization within 6 months of testing were excluded. Major cardiac events occurred in 24 patients (9%)--nonfatal myocardial infarction in 11 and cardiac death in 13. Univariate Cox survival analysis demonstrated significant relative risk (RR) and 95% confidence intervals (CI) for exercise ST segment depression (RR = 2.3; 95% CI, 1.0 to 5.3), an abnormal MIBI scan (RR = 13.8; 95% CI, 1.9 to 102.3), and a reversible MIBI perfusion defect (RR = 3.2; 95% CI, 1.4 to 7.5). Multivariate models demonstrated that both exercise MIBI perfusion abnormalities (RR = 11.9; 95% CI, 1.6 to 89.4) and reversible MIBI perfusion defects (RR = 2.9; 95% CI, 1.2 to 7.0) had independent predictive value. During 1 year of follow-up, cardiac events occurred in only 0.5% of patients with normal MIBI scans compared with 7% of those with abnormal MIBI scans (P < .001). One-year, cardiac event-free survival was 92% in patients with reversible MIBI perfusion defects (P < .01 versus normal), 96% in patients with fixed defects (P < .01), and 93% in patients with combined reversible and fixed MIBI myocardial perfusion abnormalities (P < .02).

CONCLUSIONS
As with exercise thallium-201 myocardial imaging, exercise stress technetium-99m MIBI myocardial tomography provides significant independent information concerning the subsequent risk of serious cardiac events (death, myocardial infarction) in patients with stable angina pectoris. The identification of MIBI perfusion abnormalities, in particular, the presence of reversible MIBI defects, was associated with reduced 1-year, event-free survival. The recognized imaging and radiotracer biokinetic differences between thallium-201 and MIBI do not appear to modulate the prognostic value associated with scintigraphic evidence of ischemic myocardial jeopardy in the stable angina population.
Low-dose aspirin inhibits platelet-induced contraction of the human isolated coronary artery. A role for additional 5-hydroxytryptamine receptor antagonism against coronary vasospasm?
Authors: Bax W A , Renzenbrink G J , van der Linden E A , Zijlstra F J , van Heuven-Nolsen D , Fekkes D , Bos E , Saxena P R 
Published: June 2012

BACKGROUND
The beneficial effect of low-dose aspirin in the prevention of coronary vasospasm is well documented. In this study, we investigated the contractile effect of human washed platelets on the human isolated coronary artery. We concentrated on the effect of low-dose aspirin (40 mg/d) taken by the platelet donor and on the efficacy of thromboxane A2 (TXA2) and 5-hydroxytryptamine (5-HT) receptor antagonists.

METHODS AND RESULTS
Human coronary artery segments were suspended in an organ bath set-up for isometric tension measurement. Platelets (10(9) to 3 x 10(10)/L) elicited concentration-dependent contractile responses of the coronary artery segments, reaching 28.4 +/- 7.1% of contractions induced by 100 mmol/L K+. The contractile response tended to be decreased in vessel segments with histological signs of early atherosclerosis. Contraction was significantly attenuated after pretreatment of the vessel segments with ketanserin (5-HT2 receptor antagonist, 1 mumol/L) or SQ30741 (TXA2 receptor antagonist, 0.01 mumol/L), reaching 8.8 +/- 2.3% and 3.2 +/- 2.2% of contraction to 100 mmol/L K+, respectively. Platelets obtained from the same platelet donors after they had taken aspirin (40 mg/d for 7 to 13 days) caused significantly lower contractile responses (7.6 +/- 2.7% of 100 mmol/L K+) associated with an almost selective inhibition of the synthesis of thromboxane measured in the organ bath solution (untreated platelets, 2.19 +/- 0.43 nmol/L; aspirin-treated platelets, 0.66 +/- 0.05 nmol/L). The amount of 5-HT secreted in the organ bath remained unaltered (65.17 +/- 9.94 and 64.03 +/- 8.98 nmol/L, respectively). This explains why ketanserin significantly attenuated the residual contractile responses caused by platelets obtained from aspirin-treated subjects, whereas SQ30741 caused minor, nonsignificant additional attenuation.

CONCLUSIONS
The results of the present study therefore suggest that additional antagonism of the contractile 5-HT receptors in the coronary artery may increase the efficacy of low-dose aspirin in vivo.