bluuebunny/crossref_metadata_2025_split huggingface dataset:
Adenosine deaminase and carcinoembryonic antigen in pericardial effusion diagnosis, especially in suspected tuberculous pericarditis.
Authors: Koh K K , Kim E J , Cho C H , Choi M J , Cho S K , Kim S S , Kim M H , Lee C J , Jin S H , Kim J M 
Published: June 2012

BACKGROUND
Adenosine deaminase (ADA) and carcinoembryonic antigen (CEA) have been measured in pleural fluid to help distinguish malignant from benign effusions, especially in tuberculous pleurisy. We investigated ADA and CEA levels in patients with moderate to large pericardial effusions of different etiologies.

METHODS AND RESULTS
We performed diagnostic and therapeutic pericardiostomy with drainage and biopsy. We measured ADA and CEA levels in the pericardial fluid in 26 patients with moderate to large pericardial effusion and 19 control patients. Patients were included in a prospective protocol from August 1991 to August 1993. Patients were grouped as follows: group 1, 9 patients with tuberculous pericarditis (TP) confirmed by bacteriologic culture or histology of pericardial biopsy; group 2, 5 patients with clinically strongly suspected TP; group 3, 12 patients with malignancy (8) and acute pericarditis (4); group 4, 19 control patients without pericardial disease. We treated patients with TP with isoniazid, rifampin, and either streptomycin or ethambutol for 12 months and pyrazinamide for 2 months. We observed for symptoms and signs of recurrent pericarditis or constrictive pericarditis on follow-up. In group 1 the ADA activity was significantly higher (101 +/- 14 U/L) than that in group 3 (22 +/- 5 U/L) or that in group 4 (17 +/- 2 U/L) (P < .05). There was no significant difference between ADA activity in group 1 (101 +/- 14 U/L) and that in group 2 (100 +/- 26 U/L). With a cutoff value for ADA activity of 40 U/L, sensitivity was 93% and specificity 97% in the diagnosis of TP. In benign diseases, the CEA level was significantly lower (1.0 +/- 0.3 ng/mL) than that in malignant diseases (135.1 +/- 79.7 ng/mL) (P < .05). With a cutoff value for CEA level of 5 ng/mL, sensitivity was 75% and specificity 100% in the diagnosis of malignant pericarditis. Follow-up study (mean, 12.9, 19.8, and 11.8 months in groups 1, 2, and 3, respectively, showed no symptoms or signs of constrictive pericarditis, except for 1 patient.

CONCLUSIONS
Pericardial fluid ADA and CEA are useful for the differential diagnosis of pericardial effusion of various causes. They also have great value in early diagnosis of TP, particularly when the results of other clinical and laboratory tests are negative.
Reduced calcium currents in subendocardial Purkinje myocytes that survive in the 24- and 48-hour infarcted heart.
Authors: Boyden P A , Pinto J M 
Published: June 2012

BACKGROUND
The abnormal transmembrane action potentials of subendocardial Purkinje fibers that survive 24 to 48 hours after coronary artery occlusion can be a source of the multiform ventricular tachycardias that occur during this time. A change in the density or function of either or both the T-type and L-type cardiac Ca2+ channels may contribute to the altered electrical activity of these Purkinje myocytes.

METHODS AND RESULTS
The purpose of this study was to determine the function of the T- and L-type Ca2+ currents (iCat and iCaL, respectively) in Purkinje myocytes dispersed from the subendocardium of the left ventricle 24 and 48 hours after coronary artery occlusion (IZPC24 and IZPC48, respectively). To do this we compared whole-cell Ca2+ currents from Purkinje myocytes enzymatically dispersed from free-running fiber bundles (SPCs), from the subendocardium of the noninfarcted canine heart (NZPCs), and from IZPC24 and IZPC48. ICaL and iCat were recorded with Cs(+)- and EGTA-rich pipettes and in Na(+)-K(+)-free external solutions to eliminate overlapping currents. ICaL density was significantly reduced in IZPC48 compared with NZPC or IZPC24. This was not accompanied by a shift in the current-voltage relation or by a change in the time course of decay of iCaL. Replacement of Ca2+ with equimolar Ba2+ increased iCaL density in all cell types, but peak iBaL of IZPC48 remained reduced compared with control iBaL values. T-type Ca2+ currents were recorded in all SPCs and NZPCs. In IZPC24 and IZPC48 there was a reduction in peak iCat amplitudes and densities. This was not accompanied by a shift in the current-voltage relation or by a change in the time course of decay of peak iCat. However, there was a hyperpolarizing shift in the steady-state availability relations in both IZPC24 and IZPC48. In addition, the maximally available iCat in IZPC24 was not different from control, whereas it was significantly reduced in IZPC48.

CONCLUSIONS
The L-type ICa density in subendocardial Purkinje myocytes that survive in the infarcted heart is significantly decreased by 48 hours after the time of coronary artery occlusion. The peak T-type ICa density is decreased in subendocardial Purkinje myocytes that survive in the infarcted heart at 24 hours, but further reduction occurs in these myocytes by 48 hours. This loss in Ca2+ channel function could contribute to the abnormal transmembrane potentials of these myocytes surviving in the infarcted heart.
Differences in compensatory vessel enlargement, not intimal formation, account for restenosis after angioplasty in the hypercholesterolemic rabbit model.
Authors: Kakuta T , Currier J W , Haudenschild C C , Ryan T J , Faxon D P 
Published: June 2012

BACKGROUND
In de novo human atherosclerosis, compensatory vessel enlargement limits the effect of intimal plaque formation on lumen narrowing. We hypothesized that arterial remodeling may also play an important role in determining the chronic lumen size after angioplasty and tested this hypothesis using the hypercholesterolemic rabbit iliac artery angioplasty model.

METHODS AND RESULTS
Morphometric analysis of histological cross-sectional areas of vessels from animals killed immediately after angioplasty (acute group, n = 11) were compared with the same areas from animals killed 4 weeks after the procedure (chronic group, n = 37), when restenosis occurs in this model. The area circumscribed by the internal elastic lamina (IEL) increased by 20% from acute to 4 week follow-up after angioplasty (acute group, 2.36 +/- 0.45 mm2, chronic group, 2.84 +/- 0.89 mm2). Over the same time period, intimal area increased by 0.82 mm2. Despite this increase in intimal area, lumen area decreased by only 0.34 mm2 because of the compensatory enlargement of the IEL area. In the chronic group, polynomial regression analysis revealed a quadratic relation between intimal area and lumen area (R2 = .35, P < .001). A lumen area of 0.45 mm2 (the nadir of the quadratic relation) was used to divide the chronic group into two subgroups: restenotic (n = 21; lumen area, < 0.45 mm2) and nonrestenotic (n = 16; lumen area, > 0.45 mm2). By definition, there was a significant difference in lumen area between the two subgroups (0.15 +/- 0.15 mm2 for restenotic; 0.73 +/- 0.18 mm2 for nonrestenotic). Surprisingly, the intimal areas in the two subgroups were virtually identical (2.41 +/- 0.92 mm2 for restenotic, 2.49 +/- 0.69 mm2 for nonrestenotic, P = NS). The difference in the lumen area between restenotic and nonrestenotic vessels was a result of the significantly greater IEL area in the nonrestenotic subgroup (3.22 +/- 0.83 mm2 for nonrestenotic, 2.56 +/- 0.84 mm2 for restenotic, P < .05). In both restenotic and nonrestenotic vessels, the IEL area increased with increases in intimal area. In the restenotic arteries, the slope of this correlation was < 1, showing inadequate compensatory enlargement for the intimal plaque. In the nonrestenotic vessels, the slope was > 1, limiting the effect of intimal plaque on luminal narrowing.

CONCLUSIONS
These data indicate that the iliac artery in an atherosclerotic rabbit model compensates for intimal formation after angioplasty by vessel enlargement. Furthermore, the degree of vessel enlargement is more important than intimal area in determining the chronic lumen size.
Exercise-induced ST-segment depression in patients without restenosis after coronary angioplasty. Relation to preprocedural impaired left ventricular function.
Authors: Beregi J P , Bauters C , McFadden E P , Quandalle P , Bertrand M E , Lablanche J M 
Published: June 2012

BACKGROUND
ST-segment depression during exercise testing is frequently observed in the absence of restenosis after coronary angioplasty.

METHODS AND RESULTS
We studied the determinants of this phenomenon in 70 consecutive patients with unstable angina related to a single left anterior descending coronary artery lesion who had successful angioplasty without restenosis (< 50% stenosis by quantitative angiography). We compared preangioplasty clinical, angiographic, and hemodynamic variables in the group with positive (ExT Pos, n = 35; ST depression, 2.3 +/- 0.9 mm) and negative (ExT Neg, n = 35; ST depression, 0.3 +/- 0.5 mm) results on exercise testing at follow-up angiography. At this time, minimal lumen diameter (1.7 +/- 0.4 mm) and mean residual stenosis (34 +/- 11%) in the ExT Pos group were not significantly different from the values (1.9 +/- 0.5 mm, 38 +/- 10%) in the ExT Neg group. Before angioplasty, the ExT Pos group had a lower ejection fraction (63 +/- 8% versus 68 +/- 9%, P < .05), more marked anterior hypokinesis estimated by the extent of anterior wall contraction on quantitative ventriculography (P < .05), and a greater end-systolic volume (30 +/- 11 versus 25 +/- 9 mL/m2, P < .05) than the ExT Neg group. At follow-up angiography, regional anterior wall motion was normal in 68 patients (97%). Anterior hypokinesis before angioplasty was strongly associated (P < .01) with a positive exercise test at control (71% compared with 31% in patients with normal wall motion before angioplasty).

CONCLUSIONS
In the absence of significant epicardial stenosis after angioplasty, ST-segment depression is strongly associated with the presence of preprocedural regional ventricular dysfunction that has recovered at follow-up angiography.
Forearm vascular responsiveness to alpha 1- and alpha 2-adrenoceptor stimulation in patients with congestive heart failure.
Authors: Indolfi C , Maione A , Volpe M , Rapacciuolo A , Esposito G , Ceravolo R , Rendina V , Condorelli M , Chiariello M 
Published: June 2012

BACKGROUND
The alpha-adrenergic component of the sympathetic nervous system plays a major role in the pathophysiology, clinical manifestations, and natural history of human congestive heart failure (CHF). However, the functional integrity of vascular alpha 1- and alpha 2-adrenoceptors in CHF remains to be elucidated. The present study was designed to assess the vascular responsiveness of alpha 1- and alpha 2-adrenoceptors in patients with CHF.

METHODS AND RESULTS
To evaluate alpha 1- and alpha 2-adrenoceptor responsiveness, we studied the effects of the regional infusion into the brachial artery of increasing doses of phenylephrine (a selective alpha 1-adrenoceptor agonist) and BHT 933 (a selective alpha 2-adrenoceptor agonist) on vascular responses in 12 healthy subjects and in 24 patients with CHF secondary to primary dilated cardiomyopathy or ischemic heart disease. Left ventricular ejection fraction was measured by radionuclide angiography, and forearm blood flow was determined by venous occlusion plethysmography. Phenylephrine reduced forearm blood flow in normal subjects from 5.2 +/- 0.9 to 2.5 +/- 0.6 mL per 100 mL of tissue/min (P < .05) at the highest dose (-50.8 +/- 4.8% versus baseline). A similar vasoconstriction was obtained in patients with CHF (from 3.5 +/- 0.5 to 1.5 +/- 0.2 mL per 100 mL of tissue/min (P < .05) (-58.7 +/- 5.0% versus baseline). The dose-response curves produced by phenylephrine in the two groups were comparable. The highest dose of BHT 933 reduced forearm blood flow in normal subjects from 5.3 +/- 0.9 to 2.3 +/- 0.6 mL per 100 mL of tissue/min (P < .05) (-59.0 +/- 4.9% versus baseline). In patients with CHF, a similar vasoconstriction was obtained (from 4.2 +/- 0.8 to 1.5 +/- 0.3 mL per 100 mL of tissue/min, P < .05, -62.1 +/- 6.5% versus baseline). The dose-response curves produced by BHT 933 also were comparable in the two groups. In patients with CHF, plasma concentrations of norepinephrine were significantly higher than in normal subjects.

CONCLUSIONS
The results of the present study demonstrate that alpha 1- and alpha 2-adrenoceptor stimulations produced an equivalent vasoconstriction in patients with CHF and in normal subjects. This indicates that the vascular responsiveness to alpha-adrenoceptor agonists may be preserved in the limb vessels of patients with CHF.
Catheter-induced mechanical conduction block of right-sided accessory fibers with Mahaim-type preexcitation to guide radiofrequency ablation.
Authors: Cappato R , Schlüter M , Weiss C , Siebels J , Hebe J , Duckeck W , Mletzko R U , Kuck K H 
Published: June 2012

BACKGROUND
Accessory pathways originating at the tricuspid annulus that exhibit decremental antegrade conduction properties (Mahaim-type preexcitation) are amenable to radiofrequency (RF) current catheter ablation. However, a reliable and reproducible strategy for mapping and ablation of these fibers is lacking.

METHODS AND RESULTS
Eleven patients with preexcited atrioventricular tachycardia involving a decrementally conducting antegrade accessory pathway underwent complete electrophysiological evaluation and subsequent attempts at RF catheter ablation. Mechanical conduction block at the subannular level of the atrial input to the accessory fiber was induced by catheter manipulation in 8 patients, in 2 of them during atrial fibrillation. RF current was delivered, after resumption of preexcitation, to the site of mechanical block during atrial pacing (n = 6) or atrial fibrillation (n = 2) and eliminated the accessory pathway in all 8 patients. In another patient, mechanical block was not observed, but ablation of the atrial accessory fiber insertion was achieved at the subannular level during atrioventricular tachycardia. The anatomic site of ablation along the tricuspid annulus was anterolateral (n = 1), lateral (n = 3), or posterolateral (n = 5). Failures were encountered in the first patient of the series in whom ablation attempts were directed at the ventricular insertion of the accessory fiber and in a patient in whom ablation of the atrial insertion was attempted at the supraannular level. Recurrence of preexcitation within 12 hours was observed in 5 of 6 patients in whom ablation had been achieved during atrial pacing. Eventually successful repeat sessions were performed the following day using a simplified ablation approach. Thus, a median of 5 RF pulses (range, 1 to 26) per accessory fiber eliminated conduction in 9 (82%) of the 11 patients in 1.9 +/- 0.9 sessions. During a follow-up of 9.5 +/- 2.3 months, preexcitation recurred in 1 patient.

CONCLUSIONS
The atrial origin of accessory connections with Mahaim-type preexcitation is apparently confined to the anterolateral-to-posterolateral region of the tricuspid annulus. Mechanical conduction block in the atrial input to the accessory fiber induced at the subannular level by catheter manipulation provides an optimal marker to locate the ablation site, even during atrial fibrillation. To expose early recurrence of antegrade accessory pathway conduction, intermittent atrial pacing in the 12 hours after ablation is advisable; in cases of recurrence, a repeat procedure can readily be performed using just the ablation catheter advanced to the target site at the tricuspid annulus.
Role of spin echo and cine magnetic resonance imaging in presurgical planning of heterotaxy syndrome. Comparison with echocardiography and catheterization.
Authors: Geva T , Vick G W , Wendt R E , Rokey R 
Published: June 2012

BACKGROUND
Patients with heterotaxy syndrome frequently have complex congenital cardiac and noncardiac malformations requiring detailed diagnostic evaluation by noninvasive as well as invasive imaging modalities for management planning. Recent advances in magnetic resonance imaging (MRI) techniques allow detailed delineation of cardiovascular anatomy and blood flow in young infants with rapid heart rates. The present study was undertaken to prospectively evaluate the role of MRI in the presurgical evaluation of patients with heterotaxy syndrome.

METHODS AND RESULTS
Between January 1 and December 31, 1992, 14 consecutive patients with heterotaxy syndrome and complex congenital heart disease were enrolled in a prospective protocol. After evaluation by echocardiography and cardiac catheterization, a tentative management plan was recorded. Subsequently, a MRI study was performed and surgical planning was reevaluated. MRI was found to be comparable to echocardiography in terms of length of examination and sedation requirements. Surgical planning was altered in four patients because MRI provided additional data not evident on echocardiography and catheterization. Comparison of diagnostic yield between echocardiography, catheterization, and MRI showed that MRI is superior to echocardiography and often to catheterization in delineation of systemic and pulmonary venous anatomy and their relation to mediastinal structures. When the anatomic and hemodynamic data obtained by echocardiography and MRI were considered together, cardiac catheterization data were necessary only to determination of pulmonary vascular resistance before Fontan operation.

CONCLUSIONS
MRI provides excellent anatomic and functional information that in some patients was not available by echocardiography or catheterization. Combined with echocardiography, MRI provides the high-quality diagnostic information necessary for management planning in most patients with heterotaxy syndrome. Cardiac catheterization is indicated when determination of pulmonary vascular resistance is necessary for decision making or when an interventional procedures is indicated.
Myocardial and cerebral hemodynamics during tachyarrhythmia-induced hypotension in the rat.
Authors: Hagendorff A , Dettmers C , Danos P , Pizzulli L , Omran H , Manz M , Hartmann A , Lüderitz B 
Published: June 2012

BACKGROUND
The different vulnerabilities of heart and brain to hypotension and hypoxia have been discussed. Hemorrhagic or cardiogenic hypotension appears to cause greater cerebral lesions than drug-induced hypotension. The present model was established to evaluate myocardial blood flow (MBF) and function of the heart and cerebral blood flow (CBF) during tachyarrhythmias and to characterize the capacity of blood flow regulation in the heart and brain during tachycardia-induced borderline hypotension.

METHODS AND RESULTS
MBF and CBF were determined with radiolabeled microspheres. Coronary and central venous oxygen tensions were measured to estimate myocardial and cerebral oxygen consumption (MVO2 and CVO2). Measurements were performed in 62 Sprague-Dawley rats during sinus rhythm and high-rate left ventricular pacing and after hemorrhage. In control rats, MBF and CBF were 5.08 +/- 1.07 and 1.09 +/- 0.29 mL.g-1.min-1. MBF increased (7.21 +/- 1.98 mL.g-1.min-1, P < .05), whereas CBF decreased (0.99 +/- 0.29 mL.g-1.min-1, P = NS) during normotensive high-rate pacing. MBF and CBF dropped to 4.27 +/- 2.24 mL.g-1.min-1 (P = NS) and 0.68 +/- 0.29 mL.g-1.min-1 (P < .05) during pacing-induced borderline hypotension and decreased further during severe hypotension (1.77 +/- 0.81 mL.g-1.min-1, P < .01; 0.45 +/- 0.18 mL.g-1.min-1, P < .01). During borderline hypotension due to hemorrhage, MBF and CBF were 4.05 +/- 0.95 mL.g-1.min-1 (P = NS) and 0.71 +/- 0.23 mL.g-1.min-1 (P < .05). MVO2 and CVO2 were 72.7 +/- 15.4 and 12.7 +/- 3.3 mL.100 g-1.min-1 in control rats. MVO2 increased during normotensive pacing (100.3 +/- 27.4 mL.100 g-1.min-1, P = NS). Mean MVO2 was reduced during pacing-induced borderline hypotension (64.1 +/- 35.6 mL.100 g-1.min-1, P = NS) and severe hypotension (29.8 +/- 15.4 mL.100 g-1.min-1, P < .05). CVO2 decreased in correlation to CBF. Coronary and cerebrovascular resistance and autoregulation indexes indicated a maintenance of MBF regulation and a failure of CBF regulation during borderline hypotensive tachycardias. These results show a dissociation of MBF and CBF after onset of hypotensive tachycardias. Thus, brain tissue appears to be jeopardized at an earlier stage than myocardial muscle during tachyarrhythmias.

CONCLUSIONS
The proposed hypotension model is suitable to analyze tachyarrhythmia-induced hemodynamic changes and end-organ perfusion in the presence of myocardial dysfunction. It has the potential to test therapeutic strategies in the treatment of tachycardias.
Decreased platelet deposition and smooth muscle cell proliferation after intramural heparin delivery with hydrogel-coated balloons.
Authors: Azrin M A , Mitchel J F , Fram D B , Pedersen C A , Cartun R W , Barry J J , Bow L M , Waters D D , McKay R G 
Published: June 2012

BACKGROUND
In vitro and in vivo studies have demonstrated both anticoagulant and antiproliferative effects of heparin. The purpose of this study was to assess the effect of local intramural delivery of heparin, using heparin-coated hydrogel balloons, on platelet deposition and early smooth muscle cell proliferation after in vivo balloon angioplasty.

METHODS AND RESULTS
The effects of local heparin delivery were assessed during balloon angioplasty of porcine peripheral arteries. All balloon dilatations were performed with oversized hydrogel balloons coated with a known quantity of heparin. Balloon dilatations in contralateral vessels with uncoated hydrogel balloons served as study controls. The pharmacokinetics of heparin delivery were assessed using 3H-heparin to quantitate heparin wash-off from the balloon surface, heparin delivery to the arterial wall, and intramural persistence of drug. Platelet deposition at 1 hour after balloon injury was quantified using 111In-labeled platelets. Smooth muscle cell proliferation was assessed 6 to 7 days after angioplasty with immunohistochemical staining for proliferating cell nuclear antigen. 3H-heparin wash-off from the hydrogel balloon surface occurred rapidly, with approximately 95% of the heparin coating disappearing within 10 seconds in the intact circulation. Approximately 2% of heparin on the balloon surface was delivered intramurally at the time of angioplasty. Intramural heparin dissipated rapidly, although small amounts of intramural heparin could still be detected for at least 48 hours. In comparison to control vessels, there was less 111In-platelet deposition (P = .002) and less medial smooth muscle cell proliferation (P = .03) in heparin-treated vessels.

CONCLUSIONS
Local intraluminal delivery of heparin at the time of balloon angioplasty with heparin-coated hydrogel balloons results in intramural deposition of drug that persists for at least 48 hours. This in vivo technique significantly decreases platelet deposition and early smooth muscle cell proliferation after angioplasty injury.