bluuebunny/crossref_metadata_2025_split huggingface dataset:
Electrophysiological properties in chronic lone atrial fibrillation.
Authors: Kumagai K , Akimitsu S , Kawahira K , Kawanami F , Yamanouchi Y , Hiroki T , Arakawa K 
Published: June 2012

BACKGROUND
Although the electrophysiological mechanisms underlying self-sustaining atrial fibrillation (AF) are unclear, recent studies suggest that one requirement for reentry, slow conduction, is frequently present in patients with AF. However, these observations limited to paroxysmal AF may not necessarily apply to chronic AF. Therefore, electrophysiological properties of the atrium and sinus nodal function in chronic lone AF were evaluated.

METHODS AND RESULTS
Electrophysiological studies were performed after electrocardioversion in 12 patients with chronic lone AF. Atrial enlargement was absent in the patients with AF. Twelve patients without atrial arrhythmias served as the control group. The patients with AF had a higher incidence of sinus nodal dysfunction, a shorter atrial effective refractory period (215 +/- 19 msec versus 238 +/- 23 msec, p less than 0.02), and a longer P wave duration than control patients (115 +/- 16 msec versus 86 +/- 16 msec, p less than 0.01). The conduction delay zone was significantly greater in patients with AF (60 +/- 12 msec) than that in the control patients (8 +/- 13 msec, p less than 0.01), and the maximal conduction delay was also greater in the study patients than those in the control group, both to the His bundle region (31 +/- 12 msec versus 10 +/- 15 msec, p less than 0.01) and to the coronary sinus (41 +/- 15 msec versus 15 +/- 11 msec, p less than 0.01). The fragmented atrial activity zone was wider in the study group (23 +/- 25 msec) than in control subjects (1.7 +/- 4 msec, p less than 0.02). Repetitive atrial firing was observed in four patients with AF but it was not seen in the control group.

CONCLUSIONS
These electrophysiological features, which are manifestations of the abnormal atrial electrophysiology, would favor production of atrial reentry in chronic lone AF.
Effect of alpha-adrenergic stimulation on regional contractile function and myocardial blood flow with and without ischemia.
Authors: Miyamoto M I , Rockman H A , Guth B D , Heusch G , Ross J 
Published: June 2012

BACKGROUND
The effect of alpha-adrenergic receptor activation on regional contractile function and transmural myocardial blood flow is controversial. Accordingly, the effects of selective alpha 1-(methoxamine) and alpha 2-(BHT 933) receptor stimulation on regional contractile function and transmural myocardial blood flow distribution were studied in 15 anesthetized open-chest dogs.

METHODS AND RESULTS
The alpha-adrenergic agonists were separately infused into the cannulated left circumflex coronary artery during control and ischemic conditions in the same animal. Mean coronary perfusion pressure was held constant by a servocontrolled pump in an extracorporeal circuit. Ischemia was created by reducing coronary perfusion pressure to the level at which percent systolic wall thickening (%WT) decreased by 54%. Contractile function during control conditions was unchanged, whereas under ischemic conditions a further significant decrease in %WT of 27% occurred with either alpha 1- or alpha 2-receptor stimulation without any change in the anterior (control) wall function. Both alpha 1- and alpha 2-receptor stimulations during control conditions resulted in a relatively uniform transmural decrease in blood flow with no change in the subendocardial-to-subepicardial blood flow ratio. With alpha 1-stimulation during ischemia (n = 13), there was a tendency toward decreased subepicardial blood flow with no change in subendocardial flow, resulting in an increased subendocardial-to-subepicardial blood flow ratio (0.61 +/- 0.23 to 0.82 +/- 0.40, p less than 0.05). alpha 2-Receptor stimulation during ischemia (n = 12) produced a significant decrease in subepicardial blood flow (0.45 +/- 0.20 to 0.35 +/- 0.12 ml/min/g, p less than 0.01) with no change in subendocardial blood flow, also resulting in an increased subendocardial-to-subepicardial blood flow ratio.

CONCLUSIONS
These results indicate the selective vasoconstriction in outer wall layers during ischemia mediated by either alpha 1- or alpha 2-receptors can cause a decrease in regional contractile function despite unchanged subendocardial blood flow and improved subendocardial-to-subepicardial flow ratio. This suggests an adverse effect of alpha-adrenergic vasoconstriction during ischemia in this coronary perfusion pressure-controlled canine model.
Dietary fish oil reduces leukocyte/endothelium interaction following systemic administration of oxidatively modified low density lipoprotein.
Authors: Lehr H A , Hübner C , Finckh B , Nolte D , Beisiegel U , Kohlschütter A , Messmer K 
Published: June 2012

BACKGROUND
In vitro and in vivo experiments have demonstrated the role of oxidatively modified low density lipoprotein (oxLDL) in eliciting leukocyte/endothelium interaction during early atherogenesis.

METHODS AND RESULTS
In the present study we investigated the effect of dietary fish oil on oxLDL-induced leukocyte/endothelium interaction using intravital fluorescence microscopy in the dorsal skinfold chamber model in awake Syrian golden hamsters. Hamsters were fed for 4 weeks prior to the experiments with either standard laboratory chow or a diet supplemented with 5% of a fish oil concentrate (18% eicosapentaenoate, 12% docosahexaenoate). The efficacy of the fish oil diet was demonstrated by the incorporation of fish oil-derived omega-3 fatty acids into plasma, leukocyte, and erythrocyte lipids. In control hamsters (n = 7) and fish oil-fed hamsters (n = 7), leukocyte/endothelium interaction was assessed in the time course after intravenous injection of human LDL (4 mg/kg), oxidized by 7.5 microM Cu2+ (6 hours, 37 degrees C). In control hamsters, injection of oxLDL elicited the rolling and sticking of leukocytes to the endothelium of arterioles and postcapillary venules with a maximum 15 minutes after injection (arterioles: from 3 +/- 1 to 91 +/- 25 cells/mm2 at 15 minutes; venules: from 13 +/- 6 to 150 +/- 46 cells/mm2 at 15 minutes; mean +/- SD). This phenomenon was significantly reduced in fish oil-fed hamsters, where 15 minutes after injection of oxLDL leukocyte sticking reached a maximum of only 15 +/- 7 and 20 +/- 5 cells/mm2 in arterioles and postcapillary venules, respectively (p less than 0.01 versus control animals).

CONCLUSIONS
The results of the present study suggest that inhibition of leukocyte/endothelium interaction may be one of the mechanisms by which dietary fish oil exerts its protective effects on experimental and clinical atherogenesis.
Cellular electrophysiological basis for oxygen radical-induced arrhythmias. A patch-clamp study in guinea pig ventricular myocytes.
Authors: Cerbai E , Ambrosio G , Porciatti F , Chiariello M , Giotti A , Mugelli A 
Published: June 2012

BACKGROUND
Oxygen radicals have been implicated in the pathogenesis of reperfusion arrhythmias. However, the basic electrophysiological alterations accompanying the effects of oxygen radicals on action potential (AP) are poorly understood.

METHODS AND RESULTS
We investigated the effects of oxygen radicals generated by dihydroxyfumarate (DHF, 5 mM) on AP parameters and on ionic currents in patch-clamped guinea pig ventricular myocytes. DHF consistently caused a marked prolongation of AP duration, which was already significant after 60 seconds of exposure and continued to increase over time. Within 5 minutes, the majority of cells developed early afterdepolarizations (EADs) or became unexcitable. Both AP prolongation and occurrence of EADs were completely prevented in the presence of the oxygen radical scavengers superoxide dismutase (SOD) and catalase (CAT). Prolongation of AP duration was accompanied by a marked decreased in time-dependent potassium current (IK) and calcium current (ICa). The inward rectifier K current (IK1) was unaffected, suggesting no widespread changes in membrane properties. IK and ICa alterations were also significantly reduced by SOD and CAT. In additional experiments, intracellular calcium levels were kept constantly low by addition of 200 microM ethyleneglycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetra-acetic acid (EGTA) to the pipette solution. Under these conditions, the effects of DHF on AP duration and the occurrence of EADs were largely prevented. However, EGTA did not prevent cells from becoming unexcitable, nor did it affect the decrease in both IK and ICa upon exposure to DHF.

CONCLUSIONS
Exposure to an exogenous source of oxygen radicals may induce major electrophysiological alterations in isolated myocytes, which might be related to changes in specific ionic currents and in level of intracellular calcium. These alterations occur with a time course consistent with the rapid onset of ventricular arrhythmias in reperfused hearts.
Functional distribution of alpha 1- and alpha 2-adrenergic receptors in the coronary microcirculation.
Authors: Chilian W M 
Published: June 2012

BACKGROUND
The goal of this study was to determine the functional distribution of alpha 1- and alpha 2-adrenergic receptors in the epicardial coronary microcirculation. This goal was accomplished by intracoronary administration of the selective alpha 1-adrenergic agonist phenylephrine and the selective alpha 2-adrenergic agonist BHT-933 during measurements of coronary microvascular diameters in the beating heart.

METHODS AND RESULTS
Experimental measurements were made under conditions with intact vasomotor tone and during coronary hypoperfusion (i.e., under conditions with autoregulatory mechanisms intact and blunted, respectively). Administration of selective alpha 1- and alpha 2-adrenergic antagonists, prazosin and SKF 104078, respectively, confirmed that the agonists were preferentially activating the desired adrenergic receptor subtype because the vasoconstrictor effects of the agonists were completely blocked by the appropriate antagonist. With baseline coronary vasomotor tone intact, phenylephrine caused constriction (8 +/- 3% decrease in diameter, p less than 0.05) of small coronary arteries (vessels greater than 100 microns in diameter) but did not produce constriction of coronary arterioles (vessels less than 100 microns in diameter). During coronary hypoperfusion, phenylephrine caused constriction (p less than 0.05) of both small coronary arteries and arterioles, 6 +/- 2% and 11 +/- 3% decreases in diameter, respectively. BHT-933 did not cause significant changes in microvascular diameters under control conditions but substantially and selectively decreased arteriolar diameters during hypoperfusion (24 +/- 6% decrease in diameter, p less than 0.05).

CONCLUSIONS
In the intact, autoregulating coronary circulation, coronary arterioles escape from the effects of adrenergic activation but coronary arteries do not; rather, they can exhibit alpha 1-adrenergic coronary vasoconstriction. During coronary hypoperfusion, when autoregulatory adjustments are blunted, coronary arterioles are sensitive to both alpha 1- and alpha 2-adrenergic agonists, demonstrating significant constrictor responses. Also, the magnitude of coronary alpha 2-adrenergic arteriolar constriction (24% decrease in diameter) is significantly greater than that of alpha 2-adrenergic constriction (11% decrease in diameter) (p less than 0.05). Thus, alpha 1- and alpha 2-adrenergic activation produce different constrictor effects in the coronary microcirculation under baseline conditions when autoregulatory adjustments are intact and during coronary hypoperfusion when autoregulation is blunted. The data suggest that alpha 2-adrenergic receptors are preferentially distributed in arterioles, whereas alpha 1-adrenergic receptors are located throughout the coronary microcirculation. Importantly, the data also suggest that intrinsic autoregulatory adjustments in tone (i.e., autoregulatory escape) can override either alpha 1- or alpha 2-adrenergic constriction in coronary arterioles.
Single-lung transplantation for pulmonary hypertension. Three-month hemodynamic follow-up.
Authors: Pasque M K , Trulock E P , Kaiser L R , Cooper J D 
Published: June 2012

BACKGROUND
Shorter waiting times, relative technical simplicity, and satisfactory application to a broad spectrum of patients has made single-lung transplantation an attractive option in the treatment of patients with end-stage pulmonary hypertension.

METHODS AND RESULTS
Seven patients with pulmonary hypertension underwent single-lung transplantation. Simultaneous closure of associated atrial septal defects was accomplished in two patients. Despite severely compromised pretransplant right ventricular function in all patients, there was no early or late mortality. Right ventricular functional recovery as characterized by hemodynamic assessment before and at a mean of 13 weeks posttransplant was nearly uniform and characterized by a drop in 1) pulmonary arterial systolic pressure from 92 +/- 7 mm Hg to 29 +/- 6 mm Hg (p = 0.001), 2) central venous pressure from 10 +/- 6 mm Hg to 1 +/- 2 mm Hg (p = 0.02), and 3) pulmonary vascular resistance index from 1,924 +/- 663 to 232 +/- 73 dyne.sec.cm-9 (p = 0.001). Radionuclide ventriculography before and at a mean of 17 weeks posttransplant documented a significant (p = 0.006) increase in right ventricular ejection fraction from 22 +/- 15% to 51 +/- 11%. Quantitative pulmonary perfusion scintigraphy at a mean of 17 weeks posttransplant demonstrated a significant (p = 0.001) increase in perfusion to the transplanted lung from 56 +/- 6% to 89 +/- 7%. There was a concomitant, slight but significant (p = 0.004) decrease in ventilation to the transplanted side from 56 +/- 6% to 49 +/- 8%. After transplantation, all patients returned to New York Heart Association functional class I or II from their preoperative levels of class III or IV.

CONCLUSIONS
These early follow-up data cautiously support the option of single-lung transplantation in patients with pulmonary hypertension, although long-term durability of these hemodynamic changes deserves documentation before widespread application.
Inappropriate constriction of small coronary vessels as a possible cause of a positive exercise test early after successful coronary angioplasty.
Authors: el-Tamimi H , Davies G J , Sritara P , Hackett D , Crea F , Maseri A 
Published: June 2012

BACKGROUND
The mechanism responsible for exercise-induced myocardial ischemia early after successful coronary angioplasty (PTCA) is poorly understood.

METHODS AND RESULTS
Twelve patients who underwent one-vessel PTCA were studied. Exercise testing was performed before and on day 7 after PTCA, which was repeated after 10 mg sublingual isosorbide dinitrate if the test was positive. Quantitative coronary arteriography was also performed on day 8 after PTCA in the basal state, after intracoronary infusion of 0.9% saline, 1, 5, 10, and 20 micrograms ergonovine, and after 300 micrograms nitroglycerin. All patients had a positive exercise test before PTCA but on day 7, six patients had a positive exercise test (group 1) and six patients (group 2) had a negative exercise test. In group 1, all positive exercise tests on day 7 became negative when repeated after isosorbide dinitrate. Intracoronary ergonovine was associated with a dose-dependent constriction of the PTCA segment, a segment distal to it, and a control segment, with no significant difference in the magnitude of the response between the two groups; maximum constriction for group 1 was 19 +/- 3%, 23 +/- 2%, and 16 +/- 3% (p less than 0.001 versus basal), and in group 2 was 20 +/- 4%, 18 +/- 4%, and 9 +/- 2% (p less than 0.01 versus basal). No angina, ischemic ST segment changes, occlusive, or subocclusive spasm occurred in any patient of either group.

CONCLUSIONS
We could find no evidence that exercise-induced myocardial ischemia early after PTCA is related to the presence of fixed angiographic restenosis or to dynamic constriction of any epicardial coronary segment. Therefore, inappropriate small coronary vessel constriction responsive to nitrates should be considered as a possible alternative explanation.
Single-catheter approach to radiofrequency current ablation of left-sided accessory pathways in patients with Wolff-Parkinson-White syndrome.
Authors: Kuck K H , Schlüter M 
Published: June 2012

BACKGROUND
Catheter ablation with the use of radiofrequency current has been introduced as a therapeutic option for patients with tachyarrhythmias mediated by an accessory atrioventricular pathway. The technique conventionally implies the introduction of several catheters into the heart for assessment of electrophysiological parameters as well as for localization of the accessory pathway and may last for several hours.

METHODS AND RESULTS
Thirty-four patients with Wolff-Parkinson-White syndrome and a delta wave pattern indicative of an overt (i.e., capable of consistent antegrade conduction) left-sided free-wall accessory pathway underwent attempts at radiofrequency current ablation of the pathway with the use of just one catheter. No patient had a previous electrophysiological study. The catheter was introduced into the left ventricle close to the mitral annulus and was used for pathway localization as well as for ablation. The approach was completely successful in 30 patients (88%). In the remaining four patients, ablation of the pathway was achieved by using the multiple-catheter approach. Overall procedure duration was 2.0 +/- 1.1 hours; radiation exposure time was 22.8 +/- 20.4 minutes (median, 17.3 minutes). There were no acute complications.

CONCLUSIONS
The single-catheter approach to radiofrequency current ablation of overt left-sided free-wall accessory pathways is feasible, safe, and effective in the majority of patients. The approach requires considerable investigator experience but significantly reduces procedure duration and radiation exposure time.
Ischemic preconditioning preserves creatine phosphate and intracellular pH.
Authors: Kida M , Fujiwara H , Ishida M , Kawai C , Ohura M , Miura I , Yabuuchi Y 
Published: June 2012

BACKGROUND
Ischemic preconditioning slows ATP depletion and ultrastructural damage during the final episode of ischemia. To define the influence of creatine phosphate (CP) and intracellular pH (pHi) on this effect, CP and pHi were serially measured in porcine hearts without collateral circulation by using 31P-NMR spectroscopy and ultrastructural examination.

METHODS AND RESULTS
Farm pigs weighing 12-15 kg were anesthetized with Fluothane. The control group underwent a single occlusion (20 minutes or 60 minutes); the preconditioned group underwent four episodes of 5-minute occlusion and 5-minute reperfusion followed by a sustained occlusion (20 minutes or 60 minutes). After ischemic preconditioning, CP increased to 115 +/- 11% (p less than 0.05) of preischemic value and ATP decreased to 84 +/- 8% (p less than 0.05) of preischemic value, but pHi returned to preischemic value. At 5 and 10 minutes of sustained ischemia, CP was significantly preserved in the preconditioned group (control group, 19 +/- 3% versus preconditioned group, 29 +/- 4% at 5 minutes; control group, 5 +/- 3% versus preconditioned group, 11 +/- 3% at 10 minutes; p less than 0.05). At 15 and 20 minutes of sustained ischemia, ATP was significantly preserved in the preconditioned group (control group, 64 +/- 3% versus preconditioned group, 73 +/- 3% at 15 minutes; control group, 51 +/- 7% versus preconditioned group, 62 +/- 2% at 20 minutes; p less than 0.05). At 10, 15, 20, and 25 minutes of sustained ischemia, pHi was significantly higher in the preconditioned group (control group, 6.5 +/- 0.05 versus preconditioned group, 6.7 +/- 0.1 at 10 minutes; control group, 6.3 +/- 0.05 versus preconditioned group, 6.6 +/- 0.06 at 15 minutes; control group, 6.1 +/- 0.1 versus preconditioned group, 6.4 +/- 0.1 at 20 minutes; control group, 6.0 +/- 0.2 versus preconditioned group, 6.3 +/- 0.1 at 25 minutes; p less than 0.05). Ultrastructural changes were milder in the preconditioned group at 20 minutes of sustained ischemia.

CONCLUSIONS
In addition to ATP and ultrastructure, preconditioning preserved CP and pHi during sustained ischemia. These protective effects might be due to overshoot phenomenon of CP and/or reduced ATP consumption. The relatively longer period of preservation of pHi, which probably is the result of reduced ATP consumption, indicates its greater contribution to reducing infarct size than that of CP and ATP.
Noninvasive arterial thrombus imaging with 99mTc monoclonal antifibrin antibody.
Authors: Cerqueira M D , Stratton J R , Vracko R , Schaible T F , Ritchie J L 
Published: June 2012

BACKGROUND
The T2G1s monoclonal antifibrin antibody binds specifically to fibrin but not to fibrinogen.

METHODS AND RESULTS
In a canine model of acute arterial thrombosis, we determined the feasibility of imaging thrombi using a 99mTc-labeled Fab' fragment. In 14 dogs, 10 carotid and 13 femoral artery thrombi were produced using 2-hour temporary occlusion, crush injury, and local thrombin injection methods. A sham-operated carotid artery served as control. Antifibrin antibody was injected intravenously at the end of temporary occlusion. Serial planar radionuclide images were obtained immediately and at 1 and 2 hours. Following killing the dogs at 2 hours, we measured antibody uptake ex vivo in 5-mm-long segments of thrombus, the adjacent injured artery, and a control artery. Antibody was cleared from the blood with a mean +/- SD t1/2 of 121 +/- 23 minutes. The thrombi weighed 218 +/- 140 mg. Antibody uptake in the thrombi was patchy, and the thrombi were closely adherent to the injured arterial wall. In the segment with maximal ex vivo antibody uptake, the ratio of control artery to blood counts/g/sec was 0.65 +/- 0.46, the injured artery-to-blood ratio was 2.35 +/- 1.01 (p less than 0.0001 versus control), and the thrombus-to-blood ratio was 4.24 +/- 2.58 (p less than 0.0001 versus control). In three dogs, an isotype-matched ovarian tumor antibody labeled with 111In was injected with T2G1s but was not taken up in the thrombus or the adjacent arterial wall. Visual analysis of the in vivo carotid radionuclide images showed uptake by 2 hours in all 10 carotid thrombi. Quantitative image analysis, measured as the thrombus-to-opposite carotid artery ratio, showed increasing uptake over time with ratios of 1.1 +/- 0.3, 1.6 +/- 2.0, and 2.2 +/- 1.3 on the immediate, 1-hour, and 2-hour images, respectively. All quantitative ratios of 1.3 or greater were visually identified.

CONCLUSIONS
99mTc-labeled Fab' fragments of the T2G1s antibody are taken up specifically by acute arterial thrombi after intravenous injection. Uptake is progressive over a 2-hour period, and all thrombi are detected by radionuclide imaging at 2 hours. These results show that it is feasible to noninvasively detect arterial thrombi within 2 hours of formation.