bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of baffle fenestration on outcome of the modified Fontan operation.
Authors: Bridges N D , Mayer J E , Lock J E , Jonas R A , Hanley F L , Keane J F , Perry S B , Castaneda A R 
Published: June 2012

BACKGROUND
The "fenestrated Fontan" (surgical baffle fenestration followed by transcatheter test occlusion and permanent closure after postoperative recovery) was adopted in an effort to reduce perioperative mortality and morbidity. This study assesses the effect of baffle fenestration on outcome.

METHODS AND RESULTS
Patients having a modified Fontan operation with a cavocaval baffle and cavopulmonary anastomosis were retrospectively selected for study. Those with baffle fenestration (n = 91) were compared with those without baffle fenestration (n = 56) with respect to preoperative risk factors, age, anatomy, surgical date, and presence or absence of a previous bidirectional cavopulmonary anastomosis. Outcome variables were failure (death or take-down) and duration of postoperative pleural effusions and hospitalization. Survival and clinical status after hospital discharge were ascertained. The two groups did not appear to differ with respect to age or anatomic diagnosis. Patients having baffle fenestration were at significantly greater preoperative risk by univariate and multivariate analysis (p < 0.01). Operative failure was low in both groups (11% without and 7% with baffle fenestration, p = NS). Durations of pleural effusions and hospitalization were significantly shorter with baffle fenestration (p < 0.01). Neither date of surgery nor a previous bidirectional cavopulmonary anastomosis appeared to contribute to improved outcome. Patients with baffle fenestration had lower postoperative systemic venous pressure (p < 0.01). There were no late deaths. Functional status in both groups is good (82% in New York Heart Association class I).

CONCLUSIONS
Baffle fenestration is associated with low mortality, significantly less pleural effusion, and significantly shorter hospitalization among high-risk patients having a modified Fontan operation.
Angiotensin converting enzyme inhibition restores cardiac and hormonal responses to volume overload in patients with dilated cardiomyopathy and mild heart failure.
Authors: Volpe M , Tritto C , DeLuca N , Rubattu S , Mele A F , Lembo G , Enea I , deCampora P , Rendina V , Romano M 
Published: June 2012

BACKGROUND
Angiotensin converting enzyme (ACE) inhibition exerts a favorable effect on the response to exercise in heart failure. This study was planned to define the influence of ACE inhibition on the adaptation to volume overload.

METHODS AND RESULTS
We studied the hemodynamic, hormonal, and renal responses to acute volume expansion (sodium chloride, 0.9%, 0.25 ml.kg-1.min-1 for 2 hours) in patients with idiopathic or ischemic dilated cardiomyopathy and mild heart failure (New York Heart Association class I or II, ejection fraction < or = 50%). The patients were studied without any pretreatment (n = 14) or after 1 week of treatment with the oral ACE inhibitor quinapril at a dosage of 10 mg/day (n = 11). Seven patients were studied during constant intravenous infusion with nitroglycerin (0.1 micrograms.kg-1.min-1). The study groups had similar hemodynamic and clinical characteristics and hormonal profile at baseline evaluation. In the untreated patients, volume expansion did not increase left ventricular end-diastolic volume measured by echocardiography and was associated with a reduction in ejection fraction (p < 0.05) and with a paradoxical increase in forearm vascular resistance (p < 0.05) estimated by plethysmography. In addition, plasma atrial natriuretic factor did not change, and plasma norepinephrine was increased by saline loading. In contrast, in the patients treated with quinapril, volume expansion induced an increase of both left ventricular volumes (p < 0.001) without changing ejection fraction and reduced forearm vascular resistance (p < 0.05). In addition, in this group, plasma atrial natriuretic factor levels increased (p < 0.05) and plasma norepinephrine did not change during volume overload. During nitroglycerin infusion, volume expansion was associated with peripheral vasodilatation, increases of left ventricular volumes, and no change in ejection fraction. In this group, however, plasma atrial natriuretic factor levels did not change in response to volume overload.

CONCLUSIONS
We conclude that pretreatment with the ACE inhibitor quinapril significantly improves compromised responses to acute isotonic volume overload in patients with dilated cardiomyopathy and mild heart failure. The favorable influence of ACE inhibition on cardiovascular and hormonal responses to volume expansion seems to be related to the cardiac unloading produced by this treatment.
Angiotensin II directly stimulates release of atrial natriuretic factor in isolated rabbit hearts.
Authors: Focaccio A , Volpe M , Ambrosio G , Lembo G , Pannain S , Rubattu S , Enea I , Pignalosa S , Chiariello M 
Published: June 2012

BACKGROUND
Previous studies have shown that infusion of angiotensin II (Ang II) increases plasma concentrations of atrial natriuretic factor (ANF) in vivo. This phenomenon has been considered secondary to the effects of Ang II on cardiac and systemic hemodynamics. The present study was designed to assess whether Ang II may exert a direct stimulatory effect on ANF release from the heart independent of changes in hemodynamics.

METHODS AND RESULTS
Isolated rabbit hearts were perfused in the Langendorff mode. Heart rate, coronary flow, and atrial and left ventricular (LV) volumes were kept constant. After stabilization, Ang II was infused intracoronary at increasing doses (10(-11) to 10(-8) M) in nine hearts and at a single dose of 10(-10) M in 10 hearts. Each infusion lasted for 5 minutes and was followed by a 10-minute washout period. Four hearts received vehicle alone for 80 minutes. Ang II induced a dose-dependent increase in coronary perfusion pressure and in LV developed pressure. ANF release, measured by radioimmunoassay on the extracts of the cardiac effluent, also increased during Ang II infusion and returned to the basal values during the 10-minute washout period. In the control group, coronary perfusion pressure, LV developed pressure, and LV end-diastolic pressure did not change appreciably over the observation period, whereas ANF release progressively decreased during perfusion.

CONCLUSIONS
Ang II can directly stimulate cardiac release of ANF in isolated rabbit hearts independently of changes in hemodynamics.
Ischemic preconditioning increases adenosine release and 5'-nucleotidase activity during myocardial ischemia and reperfusion in dogs. Implications for myocardial salvage.
Authors: Kitakaze M , Hori M , Takashima S , Sato H , Inoue M , Kamada T 
Published: June 2012

BACKGROUND
Adenosine has been reported to mediate the necrosis-limiting effects of ischemic preconditioning; however, it is unclear how this mediation occurs. The present study was undertaken to test the hypothesis that ischemic preconditioning increases 5'-nucleotidase activity and adenosine release during sustained ischemia and subsequent reperfusion.

METHODS AND RESULTS
After thoracotomy, the left anterior descending coronary artery was cannulated and perfused with blood redirected from the left carotid artery in 32 dogs. Ischemic preconditioning was produced by four cycles in which the coronary artery was occluded and then reperfused for 5 minutes each. After the last cycle of ischemia and reperfusion, the coronary artery was occluded for 40 minutes. This was followed by 120 minutes of reperfusion. In the control group, the coronary artery was occluded for 40 minutes and reperfused for 120 minutes without ischemic preconditioning. The plasma adenosine concentration was measured and blood gases were analyzed in coronary arterial and venous blood samples taken during 120 minutes of reperfusion. Myocardial 5'-nucleotidase activity was measured before and at 40 minutes of sustained ischemia with and without ischemic preconditioning. The adenosine concentration in coronary venous blood during reperfusion was significantly higher in preconditioned hearts than in the control hearts: 1 minute after the onset of reperfusion, 546 +/- 57 versus 244 +/- 41 pmol/ml; 10 minutes after, 308 +/- 30 versus 114 +/- 14 pmol/ml; 30 minutes after, 175 +/- 24 versus 82 +/- 16 pmol/ml, respectively (p < 0.01). Ectosolic and cytosolic 5'-nucleotidase activities increased in both endocardial and epicardial myocardium in the ischemia-preconditioned hearts. Furthermore, 40 minutes of ischemia increased 5'-nucleotidase activity in ischemia-preconditioned hearts more than in control hearts.

CONCLUSIONS
Ischemic preconditioning increases adenosine release and 5'-nucleotidase activity during sustained ischemia and subsequent reperfusion.
Effects of subendocardial ablation on anodal supernormal excitation and ventricular vulnerability in open-chest dogs.
Authors: Chen P S , Wolf P L , Cha Y M , Peters B B , Topham S L 
Published: June 2012

BACKGROUND
In Langendorff-perfused hearts and in hearts on cardiopulmonary bypass, chemical ablation of the subendocardium of both ventricles decreases ventricular vulnerability to fibrillation. It was hypothesized that the effects of ablation are a result of the elimination of the subendocardial Purkinje fiber network. This hypothesis has been supported by recent observations that the supernormal excitability that is demonstrable in the Purkinje fibers is associated with arrhythmogenesis.

METHODS AND RESULTS
We tested this hypothesis on 10 open-chest dogs by evaluating the strength-interval curves of anodal and cathodal stimulation with the assistance of computerized mapping techniques. The ventricular fibrillation threshold was also determined. The same test was then performed after chemical ablation of the subendocardium of either the right ventricle (six dogs) or both ventricles (four dogs). Anodal supernormality was consistently demonstrated in all the dogs studied both before and after subendocardial ablation. The ventricular fibrillation thresholds were 23 +/- 5 mA both before and after right ventricular subendocardial ablation (p = NS). The ventricular fibrillation thresholds before and after biventricular subendocardial ablation were 25 +/- 3 and 22 +/- 10 mA, respectively (p = NS).

CONCLUSIONS
We conclude that 1) subendocardial ablation does not decrease ventricular vulnerability when the heart is in situ and is not on cardiopulmonary bypass and 2) anodal supernormal excitability can be demonstrated in ventricles without a subendocardial Purkinje fiber network.
Variable effects of explosive or gradual increase of intracranial pressure on myocardial structure and function.
Authors: Shivalkar B , Van Loon J , Wieland W , Tjandra-Maga T B , Borgers M , Plets C , Flameng W 
Published: June 2012

BACKGROUND
Studies done in potential donors for heart transplantation and in experimental animals have suggested that brain death can have major histopathological and functional effects on the myocardium.

METHODS AND RESULTS
We developed experimental models of brain death using dogs to study the hemodynamic and catecholamine changes, the extent of myocardial structural damage, and the recovery potential of donor hearts obtained from brain-dead donors. Brain death was caused by increasing the intracranial pressure (ICP) suddenly or gradually by injecting saline in an epidural Foley catheter. In a first series of experiments, dogs given a sudden rise in ICP (n = 5) showed a hyperdynamic response and a 1,000-fold increase in the level of epinephrine after brain death. Histology revealed 93 +/- 2% of the myocardium to be severely ischemic. Dogs given a gradual rise in ICP (n = 6) showed a lesser hyperdynamic response, almost 200-fold increase in the level of epinephrine after brain death, and mild ischemic damage to the myocardium (23 +/- 1%). In a second series, hearts obtained from brain-dead and non-brain-dead donors were transplanted in recipients, and the weaning and recovery potential were studied. All four recipients with hearts from non-brain-dead donors were weaned with good functional recovery. Also, all four recipients with hearts from brain-dead dogs given a gradual rise in ICP were weaned with only moderate functional recovery. However, only two of four recipients with hearts from donors given a sudden rise in ICP were weaned and showed poor functional recovery.

CONCLUSIONS
Our results indicate that a sudden rise in ICP can cause irreversible myocardial damage.
Vascular injury induces angiotensinogen gene expression in the media and neointima.
Authors: Rakugi H , Jacob H J , Krieger J E , Ingelfinger J R , Pratt R E 
Published: June 2012

BACKGROUND
Angiotensin II promotes growth of vascular smooth muscle cells in vitro via the autocrine production of growth factors such as platelet-derived growth factor, basic fibroblast growth factor, and transforming growth factor-beta. Furthermore, experimental studies have demonstrated that angiotensin infusion can enhance smooth muscle proliferation after balloon injury in vivo. Consistent with this, angiotensin converting enzyme inhibitors have been shown to prevent myointimal proliferation. The origin of vascular angiotensin that participate in this process is of interest. We have demonstrated the presence of angiotensinogen messenger RNA (mRNA) in the adventitial and medial layers of the rat aorta and have speculated that local angiotensinogen production may play an important role during myointimal proliferation. To provide further evidence toward this hypothesis, we compared the localization and expression of angiotensinogen mRNA in control and balloon injured vessels using in situ hybridization.

METHODS AND RESULTS
Abdominal aorta of Sprague-Dawley rats were studied before or after injury with a balloon catheter. Neointimal hyperplasia developed as documented morphologically by a progressive increase in the ratio of neointimal to medial thickness from 0.17 at 1 week to 1.17 at 6 weeks after injury. Angiotensinogen mRNA was detected clearly in the adventitia and media of control and injured aorta. However, at 1 week after injury, the medial-to-adventitial angiotensinogen mRNA ratio was higher in the injured aorta, suggesting increased gene expression in the media compared with control. Of potential importance, angiotensinogen mRNA was also detected in the neointima of the injured aorta, and this was also highest at 1 week after injury.

CONCLUSIONS
These data are consistent with the hypothesis that balloon injury leads to activation of the vascular renin-angiotensin system, which may participate in the myointimal proliferation.
Fat-suppressed breath-hold magnetic resonance coronary angiography.
Authors: Manning W J , Li W , Boyle N G , Edelman R R 
Published: June 2012

BACKGROUND
The ability to image the coronary arteries noninvasively would represent an advance in patient care. We have developed a magnetic resonance (MR) angiographic technique that allows the acquisition of complete images of coronary flow within a single breath-hold. By this method, the feasibility of noninvasive MR coronary angiography was evaluated in 25 subjects, including 19 healthy adult volunteers and six patients after diagnostic coronary angiography.

METHODS AND RESULTS
Noninvasive MR coronary angiography was performed with a fat-suppressed ECG-gated gradient-echo sequence with k-space segmentation. Overlapping transverse sections were initially used to image coronary flow, with oblique images obtained after identification of proximal anatomy. The left main coronary artery was seen in 24 subjects (96%), with a mean diameter of 4.8 mm (range, 3.4-6.2 mm) and average length of 10 mm (range, 8-14 mm). The left anterior descending coronary artery was seen in 100% of subjects, with a mean proximal diameter of 3.6 mm (range, 2.6-4.3 mm) and for an average length of 44 mm (range, 28-93 mm). The left circumflex coronary artery was seen in 76% of subjects, with a mean proximal diameter of 3.5 mm (range, 2.6-4.3 mm) and for an average length of 25 mm (range, 9-42 mm). The right coronary artery was also identified in 100% of subjects, with a mean proximal diameter of 3.7 mm (range, 2.7-5.1 mm) and for an average length of 58 mm (range, 24-122 mm). Quantitative angiography of normal proximal segments demonstrated a good correlation with MR-determined lumen diameters (r = 0.86, p < 0.002). Occluded vessels in patients with coronary artery disease displayed an absence of flow signal distal to the occlusion, whereas vessels with significant angiographic stenoses demonstrated signal loss corresponding to the area of the stenosis, with visualization of the more distal vessel.

CONCLUSIONS
Breath-hold MR coronary angiography provides visualization of the major epicardial vessels. In the future, MR coronary angiography may provide a noninvasive means for the evaluation of patients with known or suspected coronary artery disease.
Time course of functional improvement in stunned myocardium in risk area in patients with reperfused anterior infarction.
Authors: Ito H , Tomooka T , Sakai N , Higashino Y , Fujii K , Katoh O , Masuyama T , Kitabatake A , Minamino T 
Published: June 2012

BACKGROUND
The beneficial effect of coronary reflow on myocardial salvage may be assessed more accurately than in previous studies if the size of risk area is taken into account, particularly because the size of risk area varies significantly among patients. In this study, the risk area was determined with myocardial contrast echocardiography to investigate the time course of functional recovery of postischemic myocardium within the risk area in patients with reperfused anterior myocardial infarction.

METHODS AND RESULTS
The study population consisted of 21 patients with anterior myocardial infarction who achieved coronary reflow within 6 hours of onset by means of thrombolysis or coronary angioplasty. Myocardial contrast echocardiography was performed with the injection of hand-agitated Haemaccel (5 ml) into the right and left coronary arteries before coronary reflow, and the risk area was defined as the area of contrast perfusion defect in the apical long-axis view. The ratio of the endocardial length of abnormal contraction (dyskinesis/akinesis) segment to that of contrast defect segment (AS/CD) was determined at days 1, 2, 3, 7, 14, and 28 of reflow. Before reflow, the length of contrast defect correlated well with the segment length of dyskinesis/akinesis. The values for AS/CD in patients with successful reperfusion significantly and progressively decreased until day 14; 1.00 +/- 0.02 at day 1, 0.93 +/- 0.11 at day 2 (p < 0.05 versus day 1), 0.84 +/- 0.16 at day 3 (p < 0.05 versus day 2), 0.80 +/- 0.13 at day 7 (p < 0.01 versus day 2), 0.73 +/- 0.10 at day 14, and 0.72 +/- 0.10 at day 28. Greater improvement in function was obtained in patients reperfused within 4 hours than in those reperfused at > or = 4 hours (AS/CD at day 28, 0.64 +/- 0.12 versus 0.75 +/- 0.09, p < 0.05).

CONCLUSIONS
Thus, a significant amount of myocardium, an average of 28% in segment length of the risk area, is salvaged in patients with reperfused anterior myocardial infarction. Major functional improvement seems to be achieved within 14 days of reflow.
Chronic changes in skeletal muscle histology and function in peripheral arterial disease.
Authors: Regensteiner J G , Wolfel E E , Brass E P , Carry M R , Ringel S P , Hargarten M E , Stamm E R , Hiatt W R 
Published: June 2012

BACKGROUND
Peripheral arterial disease (PAD) is associated with an impairment in exercise performance and muscle function that is not fully explained by the reduced leg blood flow during exercise. This study characterized the effects of PAD on muscle function, histology, and metabolism.

METHODS AND RESULTS
Twenty-six patients with PAD and six age-matched control subjects were studied. Ten of the PAD patients had unilateral disease, which permitted paired comparisons between their diseased and nonsymptomatic legs. All PAD patients had a lower peak treadmill walking time and peak oxygen consumption than controls. Vascular disease (diseased leg in unilateral patients and the most severely diseased leg in bilateral patients) was associated with decreased calf muscle strength compared with control values. In patients with unilateral disease, the diseased legs had a greater percentage of angular fibers (indicating chronic denervation) and a decreased type II fiber cross-sectional area (expressed as percent of total fiber area) compared with the nonsymptomatic, or control, legs. In diseased legs, gastrocnemius muscle strength was correlated with the total calf cross-sectional area (r = 0.78, p < 0.05) and type II fiber cross-sectional area (r = 0.63, p < 0.05). Activities of citrate synthase, phosphofructokinase, and lactate dehydrogenase in all 26 PAD patients (most diseased leg) did not differ from control values. Despite a wide range in citrate synthase activity in PAD patients, activity of this enzyme was not correlated with muscle strength or treadmill exercise performance.

CONCLUSIONS
In patients with PAD, gastrocnemius muscle weakness is associated with muscle fiber denervation and a decreased type II fiber cross-sectional area. In contrast, the PAD patients displayed substantial heterogeneity in muscle enzyme activities that was not associated with exercise performance. Denervation and type II fiber atrophy may contribute to the muscle dysfunction in patients with PAD and further confirm that the pathophysiology of chronic PAD extends beyond arterial obstruction.
Impairment of endothelium-dependent pulmonary artery relaxation in children with congenital heart disease and abnormal pulmonary hemodynamics.
Authors: Celermajer D S , Cullen S , Deanfield J E 
Published: June 2012

BACKGROUND
Endothelial injury may be an important event in the pathophysiology of pulmonary hypertension. We therefore investigated whether endothelial dysfunction occurs early in children with congenital heart defects who are at risk of developing pulmonary vascular disease.

METHODS AND RESULTS
In 25 children aged 3-16 years, we studied the response of the pulmonary circulation to graded infusions of acetylcholine (an endothelium-dependent vasodilator) and nitroprusside (a dilator not dependent on endothelial function). Diameter of a bronchopulmonary segment artery and pulmonary blood flow velocity were measured using quantitative angiography and intra-arterial Doppler catheters in 10 children aged 4-16 years with normal pulmonary hemodynamics (controls), seven children aged 3-12 years with left-to-right shunt lesions resulting in increased pulmonary flow, and eight children aged 3-14 years with established pulmonary vascular disease. In the controls, there was a dose-dependent increase in flow velocity in response to acetylcholine (maximal increase, 93 +/- 7%) and in response to nitroprusside (51 +/- 8%). In contrast, in patients with pulmonary vascular disease, the response of flow velocity to similar doses of acetylcholine (33 +/- 7%, p < 0.01) and nitroprusside (7 +/- 13%, p < 0.01) were impaired. In the patients with high pulmonary flow, there was an impaired response to acetylcholine (46 +/- 9%, p < 0.01), but response to nitroprusside was preserved (42 +/- 8%, p > 0.10), consistent with endothelial dysfunction. Arterial diameter was unchanged during acetylcholine infusion in all subjects and increased only modestly in response to nitroprusside (< or = 10%), indicating that the major site of action of each agent is distal to the segmental pulmonary arteries.

CONCLUSIONS
Endothelium-dependent pulmonary artery relaxation can be demonstrated in vivo and is impaired in young patients with increased pulmonary flow secondary to congenital heart disease. This impairment may be an important early event in the pathogenesis of pulmonary vascular disease.