bluuebunny/crossref_metadata_2025_split huggingface dataset:
Color Doppler regurgitant characteristics of normal mechanical mitral valve prostheses in vitro.
Authors: Baumgartner H , Khan S , DeRobertis M , Czer L , Maurer G 
Published: June 2012

BACKGROUND
To evaluate normal regurgitant characteristics of St. Jude (SJ) and Medtronic-Hall (MH) mitral valves, four sizes (25-31 mm) of each were studied in a pulsatile flow model.

METHODS AND RESULTS
Regurgitant flow was measured by flowmeter at left ventricular pressures of 80, 130, and 180 mm Hg. Peak regurgitant flow rates ranged from 6.2 to 12.7 cm3/sec in SJ valves and from 7.9 to 17.5 cm3/sec in MH valves. Regurgitant orifice areas calculated from the Doppler continuity equation ranged from 1.6 to 2.0 mm2 in SJ valves and from 2.2 to 2.9 mm2 in MH valves. Regurgitant volumes across the closed valve at a left ventricular pressure of 130 mm Hg were normalized to an ejection time of 280 msec and ranged from 1.5 to 1.9 cm3 in SJ valves and from 2.1 to 2.8 cm3 in MH valves. Jets were imaged by color Doppler in six rotational planes, and jet size and morphology were compared with those of regurgitant jets from circular orifices with sizes comparable to the calculated prosthetic valve regurgitant orifices (1.1-3.1 mm2). SJ valves showed two converging jets from the pivot points, one central jet, and a variable number of peripheral jets. The mean color jet area derived from the six image planes ranged from 1.6 to 5.3 cm2. Aliasing occurred only close to the valve (maximal distance 0.5-2.0 cm). MH valves showed a large central jet with a maximal length of aliased flow between 2.0 and 5.5 cm. Depending on valve size, driving pressure, and image plane, one or two small peripheral jets were found. These jets did not show aliasing in any case. The mean color jet area ranged from 5.1 to 11.0 cm2. Jets originating from circular orifices of comparable size showed jet areas from 5.5 to 13.9 cm2 and aliasing distances from 3.3 to 7.3 cm. At similar regurgitant orifice areas, driving pressures, and regurgitant flows, the measured color areas and aliasing distances were smallest in SJ valves, larger in MH valves, and largest in simple circular orifices.

CONCLUSIONS
Large, complex regurgitant jets can be found in normal closed SJ and MH valves by color Doppler, although regurgitant flow volume is minimal. Jet size and velocity distribution differs markedly between SJ valves, MH valves, and circular orifices, even with comparable driving pressure, regurgitant orifice area, and regurgitant volume. The characteristic patterns of normal regurgitation must be recognized to avoid incorrect diagnoses of pathological regurgitation in SJ and MH prosthetic valves. MH valves should not be removed solely on the basis of a central regurgitant jet with a long aliasing distance. Peripheral jets in MH valves and all jets in SJ valves should be considered normal as long as no or only minimal aliasing is present. In contrast, peripheral jets with significant aliasing may represent strong evidence of pathological regurgitation.
Complications and validity of pulmonary angiography in acute pulmonary embolism.
Authors: Stein P D , Athanasoulis C , Alavi A , Greenspan R H , Hales C A , Saltzman H A , Vreim C E , Terrin M L , Weg J G 
Published: June 2012

BACKGROUND
The Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) addressed the value of ventilation/perfusion scans in acute pulmonary embolism (PE). The present study evaluates the risks and diagnostic validity of pulmonary angiography in 1,111 patients who underwent angiography in PIOPED:

METHODS AND RESULTS
Complications were death in five (0.5%), major nonfatal complications in nine (1%), and less significant or minor in 60 (5%). More fatal or major nonfatal complications occurred in patients from the medical intensive care unit than elsewhere: five of 122 (4%) versus nine of 989 (1%) (p less than 0.02). Pulmonary artery pressure, volume of contrast material, and presence of PE did not significantly affect the frequency of complications. Renal dysfunction, either major (requiring dialysis) or less severe, occurred in 13 of 1,111 (1%). Patients who developed renal dysfunction after angiography were older than those who did not have renal dysfunction: 74 +/- 13 years versus 57 +/- 17 years (p less than 0.001). Angiograms were nondiagnostic in 35 of 1,111 (3%), and studies were incomplete in 12 of 1,111 (1%), usually because of a complication. Surveillance after negative angiograms showed PE in four of 675 (0.6%). Angiograms, interpreted on the basis of consensus readings, resulted in an unchallenged diagnosis in 96%.

CONCLUSIONS
The risks of pulmonary angiography were sufficiently low to justify it as a diagnostic tool in the appropriate clinical setting. Clinical judgment is probably the most important consideration in the assessment of risk.
Elevated endothelin-1 in heart failure and loss of normal response to postural change.
Authors: Stewart D J , Cernacek P , Costello K B , Rouleau J L 
Published: June 2012

BACKGROUND
The possible contribution of endothelin-1, a potent endothelium-derived vasoconstrictor peptide, to neurohumoral compensation for hemodynamic stress was examined in nine normal volunteers and six patients with severe congestive heart failure.

METHODS AND RESULTS
Plasma levels of endothelin-1 were measured with a sensitive and specific radioimmunoassay. Venous blood samples were obtained after 90 minutes of supine rest and serially during 30 minutes of 60 degrees upright tilt. Endothelin-1 levels were compared with those of known neurohumoral mediators of compensation. In normal subjects, the resting levels of endothelin-1 were low (0.74 +/- 0.11 pg/ml), and there was a rapid increase to 1.37 +/- 0.07 pg/ml at 5 minutes of upright tilting (p less than 0.05). This increase was not sustained at 10 and 15 minutes of tilt, but there was a trend toward a second rise at 30 minutes (1.14 +/- 0.17 pg/ml; p = 0.06). This biphasic pattern of response was shared by dopamine and reflected the response of systemic blood pressure to postural change. In contrast, slower and more sustained increases in circulating levels were observed for norepinephrine, epinephrine, aldosterone, plasma renin activity, and vasopressin, whereas atrial natriuretic peptide tended to decrease progressively. Patients with congestive heart failure had markedly higher basal levels of circulating endothelin-1 than normal subjects (3.7 +/- 0.5 pg/ml; p less than 0.01), and there was no further increase on postural change. Similar patterns were observed for the other neurohumoral mediators measured, with the degree of blunting of the response to upright tilting in heart failure being inversely related to the magnitude of increase in basal levels.

CONCLUSIONS
Alterations in plasma levels of endothelin in congestive heart failure and in response to postural change were qualitatively and quantitatively similar to the alterations of known mediators of neurohumoral compensation. In addition, the increase in plasma endothelin-1 during upright tilting in normal subjects preceded the increases in circulating levels of the other vasoconstrictor mediators, consistent with a role of endothelin-1 in neurohumoral compensation for hemodynamic stress.
Evidence implicating nonmuscle myosin in restenosis. Use of in situ hybridization to analyze human vascular lesions obtained by directional atherectomy.
Authors: Leclerc G , Isner J M , Kearney M , Simons M , Safian R D , Baim D S , Weir L 
Published: June 2012

BACKGROUND
Identification of genes that are specifically activated in restenosis lesions after percutaneous transluminal angioplasty represents a necessary step toward molecular manipulation designed to inhibit cellular proliferation responsible for such lesions. Whereas quiescent smooth muscle cells (contractile phenotype) preferentially express smooth muscle myosin, proliferating smooth muscle cells (synthetic phenotype) have been shown to preferentially express nonmuscle myosin in vitro. Accordingly, we analyzed the expression of a recently cloned isoform of human nonmuscle myosin heavy chain (MHC-B) in fresh human restenotic lesions.

METHODS AND RESULTS
A total of 10 lesions, including four restenosis (three superficial femoral arterial lesions and one saphenous vein bypass lesion) and six primary (four superficial femoral arterial lesions and two coronary arterial lesions) obtained percutaneously by directional atherectomy, were processed for examination by in situ hybridization. In total, 150 tissue sections of restenotic lesions (66 sections), primary lesions (78 sections), and normal internal mammary artery (six sections) were hybridized with the nonmuscle MHC-B probe. Restenotic lesions showed intense hybridization to the nonmuscle MHC-B cRNA probe, as demonstrated by a clustering of more than 20 grains per cell nucleus in 80% of the cells examined within a high-power field (x250); in contrast, an equivalent degree of hybridization was observed in only 7% of cells within primary lesions (p less than 0.001). Results of immunocytochemistry using monoclonal antibody to smooth muscle actin indicated that cells demonstrating strong hybridization were smooth muscle in origin.

CONCLUSIONS
These findings demonstrate that 1) human vascular tissue obtained by percutaneous directional atherectomy constitutes appropriate biopsy material for gene expression studies at the mRNA level, and 2) nonmuscle MHC-B mRNA is present in greater abundance among restenotic versus primary vascular stenoses. These observations thus provide a rational basis to explore restenotic lesions on a larger scale to identify genes that are activated in these lesions and establish potential targets for future gene therapy.
Prevalence, circumstances, mechanisms, and risk stratification of sudden cardiac death in unipolar single-chamber ventricular pacing.
Authors: Zehender M , Büchner C , Meinertz T , Just H 
Published: June 2012

BACKGROUND
Permanent cardiac pacing is well established for the improvement of prognosis and quality of life in patients with severe bradycardia. However, sudden cardiac death still remains an unresolved problem, as it occurs in approximately 20-30% of paced patients. This 2-year follow-up study was directed at prospectively assessing prevalence, circumstances, and mechanisms of sudden death in 2,021 permanently paced patients.

METHODS AND RESULTS
During the observation period, 220 patients (11%) died (mean pacing interval, 50.5 +/- 7 months). Lethal cerebrovascular events in 66 of 220 patients (30%) and sudden death in 49 of 220 patients (23%) were the two most frequently reported modes of death. Nonsudden (first year, 20%; subsequent years, 6.9%; p less than 0.01) and sudden death mortality rate (4% versus 1.8%, p less than 0.05) were highest during the first year. Mortality was unrelated to the patient's activity status at the time of death. Sudden cardiac death occurred more often in male patients (increased risk, 1.7 versus female patients; p less than 0.001) and patients younger than 60 years of age (5.2 versus patients older than 60 years, p less than 0.001). Patients with severe bradycardia (sudden death rate, 28%), severe atrioventricular block (25%), or atrial fibrillation with low ventricular rate (25%) before pacemaker implantation were more likely to suffer from sudden cardiac death than patients with previous syncopal attacks (sudden death rate, 15%) or sick sinus syndrome (17%). The highest incidence of sudden death was observed in patients with bifascicular and trifascicular bundle branch block. In this group, 35% of patients died suddenly during the follow-up period compared with 18% of patients without bundle branch block. In a subsequent study in 90 consecutive patients with various types of bundle branch block, undersensing of up to 13% of ectopic ventricular beats occurred in patients with bifascicular block. Pacing-induced tachyarrhythmias and ventricular fibrillation were documented in 10% of undersensed ectopic ventricular beats as well as in the setting of atrial fibrillation associated with ventricular arrhythmias.

CONCLUSIONS
Young age, male sex, and a severely diseased heart indicated by the presence of bifascicular and trifascicular bundle branch block are the strongest predictive clinical parameters for sudden cardiac death, especially in the first year after pacemaker implantation.
Myocardial adrenergic denervation supersensitivity depends on a postreceptor mechanism not linked with increased cAMP production.
Authors: Hammond H K , Roth D A , Ford C E , Stamnas G W , Ziegler M G , Ennis C 
Published: June 2012

BACKGROUND
Two major hypotheses have been proposed to explain catecholamine supersensitivity after myocardial denervation, but neither sufficiently explains certain features of the phenomenon. In addition, a nonsurgical method for long-term myocardial adrenergic denervation is desirable but has not been accomplished or described with respect to catecholamine supersensitivity.

METHODS AND RESULTS
We have accomplished chronic myocardial adrenergic denervation by using 6-hydroxydopamine (6-OHDA). Sixteen weeks after 6-OHDA administration to newborn pigs, we found substantial myocardial adrenergic denervation associated with beta-adrenergic receptor (beta AR) downregulation. Despite decreased beta AR number, the dose of isoproterenol yielding 50% maximal heart rate change (ED50) was decreased, and heart rates during exercise showed increased responsiveness despite decreased circulating catecholamines. Thus, stimulation of fewer receptors yielded an increased response, implying improved signal transduction efficiency. Competitive binding studies with isoproterenol showed an increased proportion of beta AR with high-affinity binding in myocardial membranes from 6-OHDA pigs, suggesting that interaction between beta AR and cardiac G, may contribute to improved signal transduction efficiency. However, measures of adenylyl cyclase activity indicated marked reduction in beta AR-dependent and G2-dependent cAMP production in myocardial membranes from denervated animals despite a normal amount of cardiac Gs and decreased Gi.

CONCLUSIONS
We have demonstrated that substantial, long-term myocardial adrenergic denervation is possible using 6-OHDA. Denervation supersensitivity in this model does not depend on enhanced cAMP stimulation but rather depends on postreceptor elements in the beta AR-responsive pathway that may be independent of Gs-activated adenylyl cyclase activity. In this model of adrenergic denervation supersensitivity, beta-receptors, through Gs, may be linked to an alternative effector that drives heart rate responsiveness.
High-current stimuli to the spared epicardium of a large infarct induce ventricular tachycardia.
Authors: Kavanagh K M , Kabas J S , Rollins D L , Melnick S B , Smith W M , Ideker R E 
Published: June 2012

BACKGROUND
Previous studies have demonstrated that both ventricular tachycardia (VT) and ventricular fibrillation (VF) may begin as figure-eight reentry: VT with a longer cycle length from spared tissue adjacent to an infarct by programmed stimulation and VF with a shorter cycle length from noninfarcted tissue by a large premature S2 stimulus. These results suggest that the type of tissue or cycle length of the arrhythmia rather than the mode of induction determines whether the figure eight becomes sustained VT or degenerates into VF. Thus, a protocol similar to that by which a VF threshold is determined may induce VT rather than VF when performed in the spared tissue over an infarct.

METHODS AND RESULTS
In 10 dogs, 4 days after occlusion-reperfusion of the left anterior descending coronary artery, 10 S1 stimuli were delivered from a total of 34 right and left ventricular sites outside the infarct. An epicardial S2 stimulus over the infarct was increased in 10-mA steps and introduced in diastole at decreasing cycle lengths of 5 msec until VT or VF was induced. Sustained monomorphic figure-eight VT was induced from 24 S1 sites and VF from nine (p = 0.03). The mean cycle lengths for the initial six arrhythmic cycles was 152 +/- 33 msec for VT and 115 +/- 13 msec for VF (p less than 0.001). Mean transmural infarct extent was 80% in five dogs with only VT, 63% in three dogs with both VT and VF, and 15% in two dogs with only VF. Different morphologies of VT were induced by changing the S1 site, the S2 strength, or the S1S2 coupling interval. In 25 of the 34 arrhythmias, the central part of the initial figure-eight pathway was oriented opposite the S1 activation sequence in that region.

CONCLUSIONS
A large S2 stimulus over a nontransmural infarct induces VT if the spared myocardium is thin. This study introduces a useful technique for inducing sustained monomorphic VT in which the location and direction of the figure-eight pathway are known a priori and in which different morphologies of sustained VT can be produced by changing the S1 site.
Low level in vivo gene transfer into the arterial wall through a perforated balloon catheter.
Authors: Flugelman M Y , Jaklitsch M T , Newman K D , Casscells W , Bratthauer G L , Dichek D A 
Published: June 2012

BACKGROUND
Gene transfer into the arterial wall may provide a novel therapeutic strategy for the treatment of coronary artery restenosis. Previously described methods for gene transfer into the arterial wall require total vessel occlusion for 30 minutes. We sought to develop a protocol for gene transfer within a more clinically relevant time frame.

METHODS AND RESULTS
We used a perforated balloon (Wolinsky) catheter to inject retroviral vector-containing virions into rabbit aortas in vivo. The virions were injected within 1 minute. Aortas were removed 5-14 days after injection and analyzed for evidence of gene transfer. In initial studies, nine rabbits were injected with a vector expressing the beta-galactosidase gene, and nine rabbits were injected with either non-beta-galactosidase-containing vectors or with a vehicle control. Histochemical staining of aortic tissues revealed blue (positive) cells in eight of nine experimental rabbits and six of nine controls. Because of the lack of specificity of the beta-galactosidase detection system, we adopted a polymerase chain reaction-based protocol in which oligonucleotide primers were used to amplify specific vector-related sequences from aortic tissue extracts. The polymerase chain reaction protocol, calibrated with standards containing known numbers of transduced cells, revealed low amounts of vector-related sequences in six of 12 vector-injected rabbits and in one of 13 controls (p less than 0.03). Comparison with standards indicated that fewer than 100 transduced cells were present in a 2-cm length of the injected aortic tissue.

CONCLUSIONS
Although in vivo gene transfer through an infusion balloon catheter can be accomplished within 1 minute, the therapeutic use of this protocol is limited by the small number of cells that are transduced.
Success, safety, and late electrophysiological outcome of low-energy direct-current ablation in patients with the Wolff-Parkinson-White syndrome.
Authors: Lemery R , Talajic M , Roy D , Coutu B , Lavoie L , Lavallée E , Cartier R 
Published: June 2012

BACKGROUND
Percutaneous ablation of accessory pathways with the use of a defibrillator can be accomplished with high-energy direct-current (DC) shocks of 150-400 J, but complications include cardiac tamponade and sudden cardiac death, mostly resulting from significant electrical arcing and barotrauma. A new low-energy DC power source with a brief time-constant capacitive discharge delivers shocks of 2-40 J and eliminates or greatly reduces arcing. This report describes our initial experience with this device in 60 consecutive patients (mean age, 34 years; range, 9-67 years) with Wolff-Parkinson-White syndrome. Accessory pathways were located in the left free wall in 36 patients, in the right free wall in two, were posteroseptal in 18, and anteroseptal in four. Most patients (77%) had their initial diagnostic electrophysiological study and catheter ablation during the same session.

METHODS AND RESULTS
Selective ablation of accessory pathways was successful in 55 patients (92%). The mean cumulative energy was 312 +/- 284 J and the mean creatine kinase MB peak (normal, 0-30 units) was 42 +/- 27 units. Patients with left free wall accessory pathways required less procedure time for ablation (2.7 +/- 0.8 versus 3.6 +/- 1.5 hours, p less than 0.0007) and less fluoroscopy time (46 +/- 24 versus 66 +/- 33 minutes, p less than 0.002). Complications were limited to transient pericarditis (three patients), one iliac artery dissection, and cardiac tamponade probably caused by catheter repositioning in the coronary sinus (one patient). An electrophysiological study was repeated in 50 of the 55 successful cases at a mean of 9 +/- 5 months. This study was normal in 48 of 50 (96%) patients.

CONCLUSIONS
Low-energy DC ablation is safe and effective treatment for accessory pathways in children and adults. The long-term outcome is excellent as documented by electrophysiological restudy.
Regression of coronary artery dimensions after successful aortic valve replacement.
Authors: Villari B , Hess O M , Meier C , Pucillo A , Gaglione A , Turina M , Krayenbuehl H P 
Published: June 2012

BACKGROUND
The effect of regression of myocardial hypertrophy on coronary artery dimensions was evaluated in patients with aortic valve disease who underwent valve replacement.

METHODS AND RESULTS
Cross-sectional area (CSA) of the three major coronary arteries (left anterior descending [LAD], left circumflex [LCx], and right coronary artery) was determined by quantitative coronary arteriography in 15 patients with aortic valve disease before and 38 months (range, 14-113 months) after successful aortic valve replacement. Twelve normal subjects served as controls. Left ventricular (LV) angiographic mass was calculated according to the method of Rackley. CSA of the left coronary artery was larger in aortic valve disease than in controls (LAD, 15 versus 8 mm2, p less than 0.001; LCx, 14 versus 6 mm2, p less than 0.001). After valve replacement, CSA of the left coronary artery decreased (LAD, 12 mm2, p less than 0.05 versus before surgery; LCx, 11 mm2, p less than 0.05 versus before surgery) but remained significantly larger than in controls. CSA of the right coronary artery in patients with aortic valve disease was not different from controls. LV muscle mass was significantly increased in aortic valve disease patients before (364 g) and after (250 g) valve replacement compared with controls (135 g). The appropriateness of coronary artery size with respect to muscle mass was evaluated by normalizing CSA of the left coronary artery (LAD + LCx) per 100 g of LV muscle mass (mm2/100 g). This index amounted to 11 mm2/100 g in controls, to 8 mm2/100 g in preoperative patients (p less than 0.05 versus controls), and to 10 mm2/100 g in postoperative patients with aortic valve disease (p = NS versus controls).

CONCLUSIONS
In patients with aortic valve disease, CSA of the proximal LAD and LCx is increased, but this increase is not sufficient to keep CSA per 100 g of LV mass within normal limits. The postoperative decrease in muscle mass is associated with a decrease in the size of LAD and LCx, whereas the size of the right coronary artery remains unchanged. In contrast to the preoperative state, the residually hypertrophied LV myocardium after aortic valve replacement is supplied by an enlarged but adequately sized LAD and LCx.