bluuebunny/crossref_metadata_2025_split huggingface dataset:
Randomized study of aprotinin and DDAVP to reduce postoperative bleeding after cardiopulmonary bypass surgery.
Authors: Rocha E , Hidalgo F , Llorens R , Melero J M , Arroyo J L , Páramo J A 
Published: June 2012

BACKGROUND
Patients on cardiopulmonary bypass (CPB) have an increased susceptibility to postoperative bleeding. Previous reports using desmopressin acetate (DDAVP) for the prevention of postoperative bleeding have given contradictory results, whereas the protease inhibitor aprotinin has been shown to reduce blood loss after this type of surgery. This randomized study was performed to assess the efficacy of DDAVP versus aprotinin in the prevention of bleeding after CPB.

METHODS AND RESULTS
One hundred nine of 122 eligible patients were randomized to four different groups: Group A (n = 28) received aprotinin starting with a bolus of 2 x 10(6) KIU followed by a continuous infusion of 0.5 x 10(6) KIU/h until the end of surgery; group B (n = 25) received of DDAVP 0.3 micrograms/kg i.v. on completion of CPB; group C (n = 28) received two doses of DDAVP, the first as in group B and an additional dose 6 hours after surgery; group D (n = 28) received no treatment. There was a marked reduction of postoperative blood loss either at 12 hours (P < .01) or 72 hours (P < .02) in the aprotinin group compared with all other groups, whereas no significant effect was observed in either of the two DDAVP regimens. A significant reduction in the amount of blood used was observed only in the aprotinin group (P < .01). Of the plasma fibrinolytic components assayed, there was a significant reduction of the fibrin degradation product generation in the aprotinin group (P < .001), whereas a significant systemic hyperfibrinolysis was observed in both DDAVP-treated groups and the control group. No side effects related to the study drugs were observed in any patient.

CONCLUSIONS
Aprotinin inhibited fibrinolysis; this correlated with a significant reduction of postoperative blood loss and need for blood replacement after CPB. Neither one nor two doses of DDAVP had a beneficial effect. Aprotinin offers a better alternative than DDAVP in the prevention of bleeding after CPB.
Sex-specific determinants of increased left ventricular mass in the Tecumseh Blood Pressure Study.
Authors: Marcus R , Krause L , Weder A B , Dominguez-Meja A , Schork N J , Julius S 
Published: June 2012

BACKGROUND
Left ventricular hypertrophy (LVH) defined by either ECG or echocardiographic criteria is a risk factor for cardiovascular morbidity and mortality. A number of determinants of LVH have been described in previous studies, principally male sex, hypertension, obesity, and aortic valvular stenosis. We examined the distribution of LV mass (LVM) in a population of 18- to 42-year-old normotensive men and women who were free of valvular heart disease to establish sex-specific normal values for LVM index (LVMI) and to determine the correlates of LVMI.

METHODS AND RESULTS
LVM was derived from measurements obtained by M-mode echocardiography. Average LVMI is significantly greater in men (102.9 +/- 0.7 g/m2) than women (88.2 +/- 0.7 g/m2). By defining LVH as an LVMI greater than the 90th percentile, we developed sex-specific criteria for LVH: men, > 125.4 g/m2; women, > 110 g/m2. We found that LVH in men is associated with indices of enhanced sympathetic nervous system reactivity and with elevated fasting insulin and triglyceride levels, which may be caused by insulin resistance. In women, LVH was associated with higher body weight and obesity.

CONCLUSIONS
Before the onset of hypertension, increased LVMI appears to have different determinants in men and women. We suggest that early LVH in young men is a manifestation of hyperkinetic borderline hypertension, a state previously shown to be associated with increased sympathetic nervous system activity and insulin resistance. The hyperkinetic state is less prevalent in young women, in whom increased adiposity seems to be the predominant factor associated with LVH.
Serum antioxidants and myocardial infarction. Are low levels of carotenoids and alpha-tocopherol risk factors for myocardial infarction?
Authors: Street D A , Comstock G W , Salkeld R M , Schüep W , Klag M J 
Published: June 2012

BACKGROUND
In vitro, animal and epidemiological studies suggest that lipoprotein oxidation may play an important role in atherosclerosis. Antioxidants may protect against lipoprotein oxidation and in that way inhibit atherosclerosis and its clinical sequelae. To investigate this possibility, we examined the association between levels of several antioxidants and myocardial infarction using serum specimens collected 7 to 14 years before the onset of myocardial infarction.

METHODS AND RESULTS
A nested case-control design was used. Cases and control subjects were selected from the 25,802 persons who had donated 15 mL of blood in 1974 for a serum bank. Cases comprised 123 persons with a subsequent first diagnosis of myocardial infarction who ranged from 23 through 58 years of age in 1974 and who had had their first diagnosis of myocardial infarction during 1981 to 1988. Two groups of control subjects matched to the cases for sex and age were selected from donors to the serum bank, one from those with hospital admissions during the same period and the other from the total group of donors. Sera were assayed for four carotenoids (beta-carotene, lycopene, lutein, and zeaxanthin), alpha-tocopherol, and cholesterol. Because associations with these serum nutrients showed similar trends whether based on hospital or community controls, the two control groups were combined. There was a significantly increasing risk for subsequent myocardial infarction with decreasing levels of beta-carotene in 1974 (P value for trend, .02) and a suggestive trend with decreasing levels of lutein (P = .09). When the results were stratified by smoking status, the excess risk of myocardial infarction associated with low serum levels of carotenoids was limited to smokers. A protective association with higher levels of alpha-tocopherol was suggested only among persons with high levels of serum cholesterol.

CONCLUSIONS
Low serum levels of carotenoids were associated with an increased risk of subsequent myocardial infarction among smokers.
Platelet alpha-granule release in cocaine users.
Authors: Rinder H M , Ault K A , Jatlow P I , Kosten T R , Smith B R 
Published: June 2012

BACKGROUND
Cocaine use has been associated with arterial occlusion resulting from platelet-rich thrombi and with an accelerated, often atypical atherosclerotic lesion that could be ascribed to platelet activation and platelet alpha-granule release.

METHODS AND RESULTS
Using a flow cytometric method to quantitate the percent of circulating activated platelets in whole blood (those that express the alpha-granule membrane protein P-selectin), we found that 5 of 25 samples from 12 long-term cocaine users had a baseline level of circulating activated platelets > 3 SD (range, 19% to 60%) above the mean (4.4 +/- 3.7%, mean +/- 1 SD) for 85 nonusers (sample n = 130). This subset resulted in a significantly higher mean baseline level of circulating activated platelets (11.8 +/- 14.4%) for all cocaine users (P = .01). By contrast, cocaine and its metabolites, at concentrations documented as obtainable during in vivo cocaine use (10(-7) to 10(-5) mol/L), had no effect on in vitro platelet activation or aggregation, either directly or in concert with platelet agonists. However, in experiments in which cocaine users received blinded infusions of placebo or cocaine, the mean percent of circulating activated platelets rose significantly (P < .05) after infusion of either placebo (peak 77 +/- 31%) or cocaine (peak 65 +/- 28%), the latter at doses resulting in peak plasma cocaine levels averaging < 10(-6) mol/L.

CONCLUSIONS
Long-term cocaine use in some subjects is intermittently associated with high basal levels of circulating platelets that have undergone alpha-granule release. The inability of cocaine and its metabolites at concentrations of 10(-7) to 10(-5) mol/L to cause platelet P-selectin expression in vitro in this study, coupled with the acute increase in circulating activated platelets observed in vivo after either cocaine or placebo infusion, suggests that in vivo platelet alpha-granule release associated with cocaine use may occur through indirect rather than direct effects of the drug.
Left ventricular wall thickness and regional systolic function in patients with hypertrophic cardiomyopathy. A three-dimensional tagged magnetic resonance imaging study.
Authors: Dong S J , MacGregor J H , Crawley A P , McVeigh E , Belenkie I , Smith E R , Tyberg J V , Beyar R 
Published: June 2012

BACKGROUND
Regional performance of the hypertrophied left ventricle (LV) in hypertrophic cardiomyopathy (HCM) is still incompletely characterized with studies variably reporting that the hypertrophied myocardium is hypokinetic, akinetic, or has normal function. Different imaging modalities (M-mode or two-dimensional echocardiography) and methods of analysis (fixed or floating frame of reference for wall motion analysis) yield different results. We assessed regional function in terms of systolic wall thickening and shortening and related these parameters to end-diastolic thickness using tagged magnetic resonance imaging and the three-dimensional volume-element approach.

METHODS AND RESULTS
In 17 patients with HCM and 6 healthy volunteers, four parallel short-axis images with 12 radial tags and two mutually orthogonal long-axis images with four parallel tags were obtained at end diastole and end systole. After the LV endocardial and epicardial borders were traced, three-dimensional volume elements were constructed by connecting two matched planar segments in two adjacent short-axis image planes, accounting for translation, twist, and long-axis shortening. A total of 72 such volume elements encompassed the entire LV. From each of these elements, end-diastolic thickness and systolic function (fractional thickening and circumferential shortening) were calculated. The average end-diastolic thickness was 15.8 +/- 4.2 mm in patients with HCM, which was significantly greater than that in healthy subjects (8.6 +/- 2.1 mm, P < .001). Fractional thickening was significantly less in patients with HCM than in healthy subjects (0.31 +/- 0.22 versus 0.56 +/- 0.23, P < .001). There was a highly significant inverse correlation between fractional thickening and end-diastolic thickness that was independent of the type of hypertrophy or age group. Similar inverse relations were observed between circumferential shortening and end-diastolic wall thickness.

CONCLUSIONS
The myocardium in patients with HCM is heterogeneously thickened and the fractional thickening and circumferential shortening of the abnormally thickened myocardium are reduced compared with healthy subjects. The decrease in fractional thickening and shortening is inversely related to the local thickness.
Existence and role of substrate cycling between AMP and adenosine in isolated rabbit cardiomyocytes under control conditions and in ATP depletion.
Authors: Wagner D R , Bontemps F , van den Berghe G 
Published: June 2012

BACKGROUND
Adenosine, a physiological coronary vasodilator, has been proposed to regulate coronary circulation according to myocardial oxygen demand. In the present study, we investigated the mechanisms of adenosine formation and utilization in isolated rabbit cardiomyocytes and, in particular, the existence and the role of substrate cycling between AMP and adenosine in the regulation of its concentration.

METHODS AND RESULTS
Rabbit cardiomyocytes were isolated by collagenase perfusion and incubated in HEPES-buffered Krebs-Henseleit solution at 37 degrees C, pH 7.4, in control conditions and in ATP depletion achieved by inhibiting glycolysis with 5 mmol/L iodoacetate. Under control conditions, adenosine accumulated at a rate of 4 pmol.min-1.10(-6) cells. The 13-fold elevation of adenosine accumulation induced by iodotubercidin (ITu), an inhibitor of adenosine kinase, proves that adenosine is normally recycled into AMP. This recycling involves 95% of the adenosine formed. In ATP depletion, adenosine accumulated at the rate of 335 pmol.min-1.10(-6) cells and was no longer rephosphorylated after 20 minutes, as shown by the absence of effect of ITu after this time interval. Moreover, adenosine was deaminated, as indicated by the twofold increase of its accumulation induced by deoxycoformycin (dCF), an inhibitor of adenosine deaminase. Both in control conditions and in ATP depletion, adenosine-dialdehyde, an inhibitor of S-adenosylhomocysteine (SAH) hydrolase, had no significant effect on adenosine formation, indicating that the transmethylation pathway is not an important source of adenosine in rabbit cardiomyocytes.

CONCLUSIONS
The results indicate that recycling of adenosine into AMP is essential for the maintenance of low, nonvasodilatory concentrations of the nucleoside under control conditions and that interruption of recycling plays an important role in elevating adenosine during ATP depletion.
Effects of reperfusion on ischemic right ventricular dysfunction. Disparate mechanisms of benefit related to duration of ischemia.
Authors: Laster S B , Ohnishi Y , Saffitz J E , Goldstein J A 
Published: June 2012

BACKGROUND
Right ventricular free wall (RVFW) ischemia impairs global RV performance and may result in acute hemodynamic compromise. However, RV function and hemodynamic performance typically improve spontaneously over time. This study was designed to determine whether reperfusion facilitates recovery of function in the ischemic right ventricle.

METHODS AND RESULTS
Closed chest dogs underwent right coronary balloon occlusion for 1 hour (n = 9), 4 hours (n = 6), or 8 hours (n = 7). In all animals, occlusion depressed RVFW function and global RV performance. After 1 hour of ischemia, reperfusion led to immediate improvement in RVFW function and consequently global RV performance, with complete recovery over 4 weeks and scar in < 1% of total RVFW area. Reperfusion after 4- and 8-hour occlusions resulted in acute improvement in global RV performance but to a lesser extent and by different mechanisms, since RVFW contraction remained severely impaired. This disproportionate recovery of global RV function was attributable to diminished RVFW dyskinesis associated with reperfusion-induced increments in RVFW diastolic thickness (characterized histopathologically in 6 additional animals subjected to 4-hour occlusions but killed 1 hour after reperfusion by interstitial edema, contraction band necrosis, and hemorrhage). Although later reperfusion was associated with a slower pace and lesser extent of recovery, RVFW contraction improved markedly over time. At 4 weeks, there was trivial RVFW scar in 4-hour animals (2% of total RVFW area), and, although fibrosis was significantly greater in 8-hour animals (7% of RVFW area), infarction was minimal relative to the extent of jeopardized myocardium.

CONCLUSIONS
The responses of ischemic RV myocardium to reperfusion are complex, with disparate effects according to the duration of preceding ischemia. Early reperfusion results in prompt improvement in and subsequent complete recovery of RVFW contraction and global RV performance, with trivial or no RVFW scar. Late reperfusion leads to little acute recovery of RVFW function, but global performance improves owing to diminished RVFW dyskinesis associated with reperfusion-induced increments in RVFW diastolic thickness. Nevertheless, RVFW function improves over time, with minimal evidence of infarction. Therefore, reperfusion facilitates recovery of RV function and minimizes the extent of infarction even after prolonged ischemia.
Optical mapping of repolarization and refractoriness from intact hearts.
Authors: Efimov I R , Huang D T , Rendt J M , Salama G 
Published: June 2012

BACKGROUND
Heterogeneities of repolarization (R) across the myocardium have been invoked to explain most reentrant arrhythmias. The measurement of refractory periods (RPs) has been widely used to assess R, but conventional electrode and extrastimulus mapping techniques have not provided reliable maps of RPs.

METHODS AND RESULTS
Guinea pig hearts were stained with a voltage-sensitive dye to measure fluorescence (F) action potentials (APs) from 124 sites with a photodiode array. AP duration (APD) was defined as the time between depolarization (dF/dt)max and R time points (ie, the time when AP returns to baseline or some percent thereof). However, R time points are difficult to determine because AP downstrokes are often encumbered by drifting baselines and motion artifacts, which make this definition ambiguous. In optical and microelectrode recordings, the second derivative of AP downstrokes is shown to contain an easily detected, unique local maximum. The correlation between the position of this maximum (d2F/dt2)max and R has been tested during altered AP characteristics induced by changes in cycle length, ischemia, and hypoxia. Under these various modifications of the AP, the time points of (d2F/dt2)max fell at 97.0 +/- 2.1% of recovery to baseline. Extrastimulus techniques applied to (1) isolated myocytes, (2) intact hearts, and (3) mathematical simulations indicated that (d2V/dt2)max coincided with the effective RPs of APs. The coincidence of RPs and (d2V/dt2)max was valid within 5 milliseconds, for resting potentials of -75 to -90 mV and extrastimuli three times threshold voltage.

CONCLUSIONS
Thus, optical APs and (d2F/dt2)max can be used to map activation, R, and RPs with AP recordings from a single heartbeat.
Identification of myocardial reperfusion with echo planar magnetic resonance imaging. Discrimination between occlusive and reperfused infarctions.
Authors: Saeed M , Wendland M F , Yu K K , Lauerma K , Li H T , Derugin N , Cavagna F M , Higgins C B 
Published: June 2012

BACKGROUND
The current treatment of many cases of acute myocardial infarction involves the use of thrombolytic agents. Evaluation of this therapy requires determination of the success of reperfusion and assessment of the presence and extent of infarction in the reperfused territory. The present study was designed to simulate in rat models several possible outcomes of reperfusion therapy: (1) successful reperfusion and absence of myocardial infarction, (2) successful reperfusion and presence of myocardial infarction, and (3) unsuccessful reperfusion. The usefulness of contrast-enhanced fast magnetic resonance (MR) imaging in defining the success of reperfusion was investigated. The dynamic effects were examined of low and high doses of gadolinium-BOPTA/dimeglumine (Gd-BOPTA/dimeg) on myocardial signal using MR inversion recovery echo planar imaging (IR-EPI) and gradient recalled echo planar imaging (GR-EPI), respectively.

METHODS AND RESULTS
Rats were subjected to one of the following regimens: reperfused reversible myocardial injury (n = 9), reperfused irreversible myocardial injury (n = 9), and occlusive infarction (n = 9). MR echo planar images were acquired every 1 or 2 seconds before, during, and after administration of Gd-BOPTA/dimeg. In all groups, normal myocardial signal was sharply increased on IR-EPI and decreased on GR-EPI at the peak of the bolus, followed by a gradual decline to baseline. In animals subjected to reperfused reversible myocardial injury, normal and previously ischemic regions were indistinguishable during and after the passage of Gd-BOPTA/dimeg. On the other hand, enhancement of reperfused irreversibly injured myocardium was delayed but increased steadily to a higher level than normal myocardium on IR-EPI. The reperfused irreversibly injured myocardium was identified on IR-EPI as a zone of high signal (hot spot). On GR-EPI, signal loss in reperfused irreversibly injured myocardium was significantly less compared with normally perfused myocardium. In animals with occlusive infarctions, there was no change in signal intensity over the ischemic region on either IR-EPI or GR-EPI. Occlusive infarction was identified as zones of either low (cold spot) or high (hot spot) signal compared with normal myocardium, depending on MR pulse sequence and dose of the contrast medium.

CONCLUSIONS
The transit of Gd-BOPTA/dimeg monitored by fast MR imaging techniques can be used to distinguish between reperfused reversibly and reperfused irreversibly injured myocardium and between occlusive and reperfused infarctions.
Prevalence of hypertension in Mexico City and San Antonio, Texas.
Authors: Haffner S , González Villalpando C , Hazuda H P , Valdez R , Mykkänen L , Stern M 
Published: June 2012

BACKGROUND
Few data are available on the prevalence of hypertension in Mexico.

METHODS AND RESULTS
We compared the prevalence of mild hypertension (systolic blood pressure > or = 140 mm Hg and/or diastolic blood pressure > or = 90 mm Hg and/or use of antihypertensive medications) in 1500 low-income Mexican Americans who participated in the San Antonio Heart Study and 2280 low-income Mexicans who participated in the Mexico City Diabetes Study. The crude prevalence of mild hypertension was 17.1% in Mexican men versus 24.4% in Mexican American men (P = .001) and 17.4% in Mexican women versus 22.0% in Mexican American women (P = .005). After adjustment for age, body mass index (BMI), waist-to-hip ratio (WHR), non-insulin dependent diabetes mellitus (NIDDM), educational attainment, and percent native American genetic admixture (Caucasian and native American), the odds ratio (Mexico City/San Antonio) was 0.55 (95% CI, 0.39, 0.77; P < .001) in men and 0.81 (CI, 0.54, 1.12; P = .201) in women. In a pooled model including both men and women, the odds ratio was 0.67 (95%, CI, 0.53, 0.84; P < .001). In the pooled model, city, age, female sex, NIDDM, BMI, WHR, and low educational attainment were significantly related to the prevalence of hypertension.

CONCLUSIONS
The causes for these differences in hypertension prevalence are not known but may reflect a less modernized lifestyle in Mexico City, including greater physical activity, less obesity, and the consumption of a high-carbohydrate, low-fat diet.