bluuebunny/crossref_metadata_2025 huggingface dataset:
Indications, complications, and short-term clinical outcome of percutaneous transvenous mitral commissurotomy.
Authors: Nobuyoshi M , Hamasaki N , Kimura T , Nosaka H , Yokoi H , Yasumoto H , Horiuchi H , Nakashima H , Shindo T , Mori T
Published: June 2011

Percutaneous transvenous mitral commissurotomy was performed in 106 consecutive patients. Significant symptomatic improvement was achieved in 97 patients (92%). Mean left atrial pressure decreased (from 18 +/- 8 to 11 +/- 8 mm Hg, p less than 0.00001), mean mitral diastolic pressure gradient decreased (from 12 +/- 7 to 7 +/- 6 mm Hg, p less than 0.00001), and mitral valve area increased (from 1.40 +/- 0.40 to 2.00 +/- 0.50 cm2, p less than 0.00001). Based on echocardiographic characteristics of the mitral apparatus, patients were grouped retrospectively in three categories: pliable (group 1, n = 37), semipliable (group 2, n = 59), and rigid (group 3, n = 10). Clinical success was achieved in 36 patients of group 1 (97%) and in 55 patients of group 2 (93%). Only six patients in group 3 (60%) improved symptomatically (p less than 0.001 vs. group 1, p less than 0.001 vs. group 2). The severity of mitral regurgitation increased in five patients of group 1 (14%), in 12 of group 2 (20%), and in three of group 3 (33%). Six patients had recurrent symptoms at 9 months after commissurotomy. Recurrence of symptoms was significantly more frequent in group 3 compared with the other two groups (group 1, 3%; group 2, 4%; and group 3, 50%; p less than 0.0001 vs. groups 1 and 2). Multiple regression analysis identified the previously mentioned echocardiographic characteristics of the mitral apparatus as the significant predictor for clinical outcome. Thus, percutaneous transvenous mitral commissurotomy can be considered a safe and effective treatment for patients with pliable valves. Patients with semipliable or with rigid valves should be selected for operation very carefully.
Low-dose infusion of atrial natriuretic factor in mild essential hypertension.
Authors: Tonolo G , Richards A M , Manunta P , Troffa C , Pazzola A , Madeddu P , Towrie A , Fraser R , Glorioso N
Published: June 2011

Intra-arterial blood pressure, cardiac output, heart rate, right heart indexes, urinary electrolytes, and urinary volume were monitored in eight patients with untreated (WHO Class I) essential hypertension. The patients were given synthetic atrial natriuretic factor (ANF) (99-126 alpha-hANP) at 1 and 2 pmol/kg/min in series (phases 1 and 2, 2 hours each dose) or vehicle (hemaccel) in random order on two separate occasions while on their usual diet. Arterial plasma ANF levels increased significantly from basal and time-matched placebo values from 25 +/- 2 and 28 +/- 3 pmol/l to 50 +/- 4 and 83 +/- 9 pmol/l at the end of phases 1 and 2, respectively (p less than 0.001). After 30 minutes during phase 2, systolic blood pressure decreased significantly by 20 +/- 4 mm Hg (p less than 0.001) from basal and time-matched placebo values and remained significantly reduced (-17 +/- 4 mm Hg, p less than 0.001) by the end of the recovery period (2 hours after infusions were completed). Pulmonary systolic blood pressure decreased by 5 +/- 1 mm Hg (phase 2, p less than 0.05). Cardiac output decreased by 0.5 +/- 0.1 l/min below baseline at the end of phase 2 of ANF infusion, whereas it increased significantly (p less than 0.02) by 0.6 +/- 0.1 l/min during vehicle infusion. Systemic diastolic, pulmonary diastolic, right atrial, and wedge pressures were not significantly changed during ANF or vehicle infusions, nor were pulmonary vascular resistance or heart rate altered. Systemic vascular resistance did not change significantly during both infusions, whereas during recovery, systemic vascular resistance decreased significantly after ANF infusion was discontinued (p less than 0.05). Microhematocrit levels increased dose dependently during ANF. The maximum increase was observed at the end of phase 2 (+4.7 +/- 1.7%), whereas the microhematocrit level decreased to -2.4 +/- 0.6% with vehicle (p less than 0.001) at the end of phase 2. Urinary sodium excretion increased significantly (p less than 0.02) by the end of phase 2 under ANF infusion (+38 +/- 15%), whereas it decreased (-10 +/- 6%) under placebo infusion by the end of phase 2. Urinary magnesium excretion was significantly increased during ANF infusion from phase 1 (p less than 0.02), whereas urinary potassium levels, calcium levels, creatinine levels, volume, and glomerular filtration rate did not differ significantly between the two infusions. Plasma renin, angiotensin II, aldosterone, and catecholamine concentrations did not change significantly during ANF or vehicle infusions.(ABSTRACT TRUNCATED AT 400 WORDS)
Mitral valve dimensions and motion in Marfan patients with and without mitral valve prolapse. Comparison to primary mitral valve prolapse and normal subjects.
Authors: Pini R , Roman M J , Kramer-Fox R , Devereux R B
Published: June 2011

To determine mitral valve and extravalvular findings associated with mitral valve prolapse (MVP) in patients with the Marfan syndrome, we compared mitral leaflet and anular dimensions and motion by computerized two-dimensional echocardiography in 53 Marfan patients (28 with M-mode echocardiographic MVP) to those in 48 adults with primary MVP and in 35 normal subjects. Mitral leaflet billowing occurred in 28 of 28 Marfan patients with M-mode MVP versus 24 of 48 with primary MVP (p less than 0.00005), 0 of 25 Marfan patients without M-mode MVP, and 0 of 35 normal subjects (both, p less than 0.0001). Billowing occurred on the first systolic frame in 8 of 28 Marfan-MVP patients, in whom posterior leaflet chordae arose abnormally from the posterior ventricular wall, and in no other subjects. These patients had large mitral valves and normal anular dynamics, whereas the remaining 20 Marfan-MVP patients had increased systolic anular expansion. Marfan-MVP patients were younger than those without MVP (29 +/- 12 vs. 38 +/- 15 years, p less than 0.02) and had lower body mass index (19.8 +/- 2.7 vs. 23.9 +/- 2.9 kg/m2, p less than 0.00005) and systolic blood pressure (120 +/- 20 vs. 133 +/- 20 mm Hg, p less than 0.05), similar to differences between primary MVP and normal subjects in body mass index (21.5 +/- 3.0 vs. 23.9 +/- 4.8 kg/m2, p less than 0.01) and systolic pressure (118 +/- 14 vs. 125 +/- 18 mm Hg, p less than 0.05). Marfan patients with and without MVP had similar arm span, arm span to height ratio, upper to lower segment ratio, and prevalence of ectopia lentis and thoracic bony abnormalities, but arachnodactyly was more frequent in those with MVP (82% and 48%, respectively; p less than 0.02). We conclude that 1) leaflet billowing occurs more uniformly in Marfan patients with MVP than in primary MVP, 2) MVP in Marfan patients may be due to either valve enlargement with distinctively abnormal chordal architecture or abnormal mitral anular distensibility, 3) Marfan patients with MVP have low body weight and systolic blood pressure, similar to primary MVP, and 4) Marfan patients with MVP more commonly have arachnodactyly but otherwise have similar skeletal and anthropometric characteristics to other Marfan patients.
Treatment of acute venous thromboembolism with low molecular weight heparin (Fragmin). Results of a double-blind randomized study.
Authors: Albada J , Nieuwenhuis H K , Sixma J J
Published: June 2011

We performed a prospective, randomized, double-blind trial in 194 unselected patients to determine the safety and efficacy of low molecular weight heparin (Fragmin) compared with standard heparin as the initial treatment of acute venous thromboembolism. Ninety-eight patients received continuous intravenous heparin, and 96 patients received Fragmin for 5-10 days. Doses were adjusted to maintain anti-Xa levels between 0.3 and 0.6 unit/ml for patients with a high risk for a bleeding complication and between 0.4 and 0.9 unit/ml for patients with a low risk for bleeding. Treatment was stopped when a therapeutic level of anticoagulation (International Normalized Ratio greater than 3.5) was reached with coumarins. Thirteen patients in the heparin group and 10 patients in the Fragmin group had a major bleeding complication. The incidence of major and minor bleeding complications combined decreased from 48.9% to 38.5% (95% confidence interval for the difference, -3.5% to +24.2%), corresponding with a relative bleeding risk reduction of 21.2%. There were no significant differences in efficacy as defined by new high-probability defects on repeat ventilation-perfusion scintigraphy of the lung in 80 patients: six of 46 patients in the heparin group and 3 of 34 patients in the Fragmin group had new defects (95% confidence interval for the difference, -9.4% to +17.8%). We conclude that low molecular weight heparin (Fragmin) given in adjusted, continuous, and intravenous doses is safe and effective as initial treatment of acute venous thromboembolism compared with heparin. There is a trend in risk reduction for bleeding in favor of low molecular weight heparin, a trend, however, that is smaller than expected compared with animal studies.
End-stage dilated cardiomyopathy. Persistence of enterovirus RNA in myocardium at cardiac transplantation and lack of immune response.
Authors: Bowles N E , Rose M L , Taylor P , Banner N R , Morgan-Capner P , Cunningham L , Archard L C , Yacoub M H
Published: June 2011

Tissue from the explanted hearts of 21 patients with idiopathic dilated cardiomyopathy or 19 patients with other specific heart muscle diseases were investigated for presence of enterovirus-specific RNA with an enterovirus group-specific cDNA probe. This was complementary to coxsackievirus B2 RNA sequences between nucleotide numbers 6,550 and 7,400, which are highly conserved between enteroviruses. Hearts from six patients with dilated cardiomyopathy and one patient with ischemic heart disease were found to contain virus RNA. Serology revealed that only one patient (dilated cardiomyopathy group) was positive for coxsackievirus B-specific IgM but negative for virus RNA in the myocardium. Quantitation of leukocytes and T-lymphocytes in the myocardium and expression of major histocompatibility locus antigens revealed no significant differences associated with persistence of virus RNA. These data demonstrate that enterovirus RNA persists in myocardium of a significant proportion of patients with end-stage dilated cardiomyopathy in the absence of a continuing cell-mediated or humoral immune response.
Saphenous vein graft patency 1 year after coronary artery bypass surgery and effects of antiplatelet therapy. Results of a Veterans Administration Cooperative Study.
Authors: Goldman S , Copeland J , Moritz T , Henderson W , Zadina K , Ovitt T , Doherty J , Read R , Chesler E , Sako Y
Published: June 2011

To determine whether antiplatelet therapies improve saphenous vein graft patency after coronary artery bypass grafting, we compared 1) aspirin (325 mg once daily), 2) aspirin (325 mg three times daily), 3) aspirin and dipyridamole (325 mg and 75 mg, respectively, three times daily), 4) sulfinpyrazone (267 mg three times daily), and 5) placebo (three times daily). Therapy with dipyridamole and sulfinpyrazone was started 48 hours before bypass graft surgery, and aspirin treatment was begun 12 hours before surgery as a single 325-mg dose. Postoperative treatment was started 6 hours after surgery and continued for 1 year. Graft patency data were obtained early (median, 9 days) and late (median, 367 days) after surgery. The early graft occlusion rate was decreased with all aspirin treatment regimens compared with that of the placebo regimen. At 1 year, in 406 patients with 1,315 grafts, the graft occlusion rate in all of the aspirin groups combined was 15.8% compared with 22.6% for the placebo group (p = 0.029). The patients taking aspirin once daily had a lower occlusion rate (13.2%) compared with the patients receiving placebo (p = 0.050). At 1 year, in the vein grafts placed to vessels less than or equal to 2.0 mm in diameter (804 distal sites), the graft occlusion rate in all of the aspirin groups was 20.1% compared with 32.3% for the placebo group (p = 0.008). In the vein grafts placed to vessels greater than 2.0 mm in diameter (511 distal sites), there was no difference in the occlusion rates between aspirin and the placebo group at 1 year (8.7% vs. 9.0%, p = 0.918).(ABSTRACT TRUNCATED AT 250 WORDS)
A new method for estimating left ventricular dP/dt by continuous wave Doppler-echocardiography. Validation studies at cardiac catheterization.
Authors: Bargiggia G S , Bertucci C , Recusani F , Raisaro A , de Servi S , Valdes-Cruz L M , Sahn D J , Tronconi L
Published: June 2011

In this study, we explored the use of continuous wave Doppler-echocardiography guided by color Doppler flow-mapping as a method for noninvasively calculating the rate of pressure rise (RPR) in the left ventricle. Continuous wave Doppler determination of the velocities in mitral regurgitant jets allows calculation of instantaneous pressure gradients between the left ventricle and the left atrium. Left atrial pressure variations in early systole can be considered negligible; therefore, the rising segment of the mitral regurgitation velocity curve should reflect left ventricular pressure increase. We studied 50 patients (mean age, 51 years; range, 25-66 years) in normal sinus rhythm with color Doppler-proven mitral regurgitation and compared the Doppler-derived left ventricular RPR with peak dP/dt obtained at cardiac catheterization. Doppler studies were performed simultaneously with cardiac catheterization in 11 patients and immediately before in the remaining cases. Two points were arbitrarily selected on the steepest rising segment of the continuous wave mitral regurgitation velocity curve (point A, 1 m/sec, point B, 3 m/sec), and the time interval (t) between them was measured. Following the Bernoulli relation, the pressure rise between points A and B is 32 mm Hg (4vB2-4vA2) and the RPR is 32 mm Hg/t. Results showed a linear correlation between the Doppler RPR and peak dP/dt (r = 0.87, SEE = 316 mm Hg/sec). The RPR in the left ventricle can be derived from the continuous wave Doppler mitral regurgitation velocity curve.
Myocardial glutathione depletion impairs recovery after short periods of ischemia.
Authors: Blaustein A , Deneke S M , Stolz R I , Baxter D , Healey N , Fanburg B L
Published: June 2011

Isolated, isovolumic rat hearts, perfused by Krebs-Henseleit buffer at constant coronary flow rate, were used to explore the hypothesis that endogenous cardiac glutathione provides protection against myocardial dysfunction associated with short periods of ischemia. Experimental animals were depleted of cardiac glutathione to 35% of control levels by intraperitoneal injections of diethylmaleate (DEM). Left ventricular pressure, coronary perfusion pressure, and glutathione levels were measured in control and experimental hearts after 60 minutes of oxygenated perfusion and after 20 minutes of global, no-flow ischemia and 30 minutes of reperfusion. With each protocol, both control and glutathione-depleted hearts received either standard buffer or one supplemented with 2 mM glutathione. Recovery of systolic function after ischemia-reperfusion was impaired in DEM-treated hearts compared with controls. In addition, the rise in perfusion pressure and chamber stiffness was also greater in DEM-treated hearts compared with controls. Recovery in glutathione-depleted hearts was improved when the reperfusate was supplemented with glutathione. In addition, the supplemented reperfusate prevented the decrease in compliance and the increase in coronary perfusion pressure in the glutathione-depleted hearts. Ischemia-reperfusion alone were not associated with a significant alteration in myocardial glutathione levels. Prewashout myocardial levels of glutathione were elevated after reperfusion with glutathione-supplemented buffer but fell to baseline levels after a short washout period. These studies demonstrate that endogenous glutathione is important in protection of myocardium from injury after ischemia-reperfusion, presumably by modifying levels of active oxygen intermediates. The smaller changes in left ventricular pressure and coronary resistance after administration of GSH probably reflects an extracellular mechanism because benefit is seen soon after reperfusion.
Catheter ablation of the atrioventricular junction with radiofrequency energy.
Authors: Langberg J J , Chin M C , Rosenqvist M , Cockrell J , Dullet N , Van Hare G , Griffin J C , Scheinman M M
Published: June 2011

Catheter ablation of the atrioventricular junction using direct-current defibrillator discharges requires general anesthesia and may have serious side effects. Sixteen patients with drug-refractory supraventricular tachycardia underwent catheter ablation of the atrioventricular junction using radiofrequency energy. A standard 7F quadripolar electrode catheter was positioned to record the largest unipolar His potential (580 +/- 640 microV) from the distal electrode. An electrocoagulator (Microvasive Bicap 4005) supplied continuous, unmodulated energy at 550 kHz. One to 14 applications of radiofrequency current were delivered between the distal electrode and a large-diameter chest wall electrode. Transient, mild chest discomfort was reported by seven of 16 patients. None had significant arrhythmias or blood pressure changes during radiofrequency ablation. Complete atrioventricular block was produced in nine of 16 patients and high-grade second-degree atrioventricular block was produced in one patient with radiofrequency current. Attenuated His bundle electrograms could still be recorded in the remaining six patients, four of whom underwent successful atrioventricular junctional ablation using direct-current shock during the same session. Atrioventricular block persisted in all 10 patients successfully treated with radiofrequency ablation during a mean follow-up of 4.2 months. Compared with a group of historic control subjects treated with direct-current shock ablation, the 10 patients successfully treated with radiofrequency current had significantly less creatine kinase-MB isoenzyme release (5.7 +/- 5.1 vs. 22 +/- 13 IU, p = 0.006). A junctional escape rhythm was present in all patients after radiofrequency-induced atrioventricular block. In contrast, three of 10 control patients had an idioventricular escape after direct current shock ablation, and four patients had no escape rhythm at all.(ABSTRACT TRUNCATED AT 250 WORDS)
Conservative drug treatment in patients with moderately severe chronic occlusive peripheral arterial disease. Scandinavian Study Group.
Authors: Lindgärde F , Jelnes R , Björkman H , Adielsson G , Kjellström T , Palmquist I , Stavenow L
Published: June 2011

A double-blind, parallel group, multicenter clinical trial of pentoxifylline compared with placebo enrolled 150 patients with moderately severe chronic occlusive arterial disease (COAD) at three centers in Scandinavia. The study consisted of a 4-6 week single-blind, placebo-controlled run-in phase, during which the stabilization of the initial claudication distance of all patients was assessed before randomization to a 6-month double-blind observation period. The diagnosis of COAD was established by clinical findings, conventional angiography, and noninvasive peripheral Doppler pressure assessment at rest and after exercise. The results of the overall intention-to-treat analysis of the study population show statistically significant superiority of pentoxifylline over placebo for all absolute claudication distance summary and end point measures. By using two clinically relevant parameters, which are a resting ankle/arm pressure ratio 0.8 or less and a duration of COAD for greater than 1 year, a target population could be defined in whom trial results became highly significant. For nontarget patients with mild COAD, we conclude that basic therapeutic measures should include the treatment of risk factors and the initiation of physical training. For target patients, however, a multifactorial therapeutic approach, including the use of pentoxifylline, is justified.
Noninvasive determination of coronary artery bypass graft patency by cine magnetic resonance imaging.
Authors: Aurigemma G P , Reichek N , Axel L , Schiebler M , Harris C , Kressel H Y
Published: June 2011

Cine magnetic resonance imaging (MRI) is a gradient-recalled, retrospectively gated, fast-scan technique that depicts laminar flowing blood as bright signal and has been proposed as a useful method for determination of coronary artery bypass graft (CABG) patency. Therefore, we performed a blinded prospective study to assess the value of cine MRI determination of CABG patency in 20 patients with 45 CABG proximal anastomoses who were undergoing repeat angiography. Ten normal subjects served as controls to define normal intrathoracic vascular patterns. There were 21 left anterior descending (LAD) grafts, of which four were left internal mammary (LIMA), 12 left circumflex (Cx), and 12 right coronary (RCA) grafts. After localizing spin-echo coronal images were obtained, multiple axial multislice interleaved cine MRI acquisitions, each consisting of two to four 5-10-mm-thick slices at eight to 24 frames per cardiac cycle, were obtained from the superior main pulmonary artery to the inferior left ventricle. Each acquisition took 5-8 minutes with a subsequent 5-10 minutes of computer image reconstruction. Total study time per patient was 50-75 minutes. Known to cine MRI interpreters were the original surgical CABG insertions but not the angiographic findings. A graft was called patent if a bright graft flow signal, not corresponding to a normal vessel, was identified on multiple frames at multiple levels abutting the great vessels or epicardial surface of the heart. Angiographically, there were 33 patent grafts, of which 29 were identified as patent by cine MRI (sensitivity, 88%).(ABSTRACT TRUNCATED AT 250 WORDS)
Circadian variation of plasma fibrinopeptide A level in patients with variant angina.
Authors: Ogawa H , Yasue H , Oshima S , Okumura K , Matsuyama K , Obata K
Published: June 2011

Plasma levels of fibrinopeptide A (FPA), beta-thromboglobulin (BTG), and platelet factor 4 (PF4) were examined on venous plasma samples taken every 4 hours for 24 hours in 20 patients with variant angina and 20 patients with stable exertional angina together with 24-hour Holter recordings. The mean plasma FPA levels (ng/ml) at 2:00 PM, 6:00 PM, 10:00 PM, 2:00 AM, 6:00 AM, and 10:00 AM were 4.6 +/- 1.0, 3.1 +/- 0.5, 6.1 +/- 1.6, 9.9 +/- 2.4, 8.7 +/- 1.4, and 4.2 +/- 0.8 in patients with variant angina (p less than 0.01) and 1.8 +/- 0.2, 2.3 +/- 0.3, 1.9 +/- 0.3, and 2.3 +/- 0.2 in those with stable exertional angina. In seven patients with variant angina, we also examined the effects of heparin (3,000 units), given subcutaneously at 6:00 PM, 10:00 PM, and 2:00 AM, on the plasma FPA levels and the anginal attacks. Although heparin suppressed the elevation and circadian variation of plasma FPA levels, it did not suppress the attacks and their circadian variation in these patients. Plasma FPA levels increased significantly from 3.7 +/- 0.5 to 12.5 +/- 2.7 ng/ml during or immediately after an attack in the seven patients with no heparin. On the other hand, the plasma levels of BTG and PF4 were increased in patients with variant angina as compared with those with stable exertional angina but did not show a significant circadian variation in both groups. We conclude that 1) plasma levels of FPA, BTG, and PF4 were increased in patients with variant angina as compared with those with stable exertional angina; 2) there was a significant circadian variation in the plasma levels of FPA in parallel with that of the frequency of the attacks with the peak level occurring from midnight to early morning in patients with variant angina; and 3) elevated levels of plasma FPA are the result and not the cause of coronary spasm.
Results of the arterial switch operation for transposition of the great arteries with ventricular septal defect. Surgical considerations and midterm follow-up data.
Authors: Di Donato R M , Wernovsky G , Walsh E P , Colan S D , Lang P , Wessel D L , Jonas R A , Mayer J E , Castañeda A R
Published: June 2011

Between January 1983 and December 1987, 62 patients underwent an arterial switch operation for transposition of the great arteries with ventricular septal defect or double outlet right or left ventricle. There were three hospital deaths (4.8%), and no deaths occurred in neonates (less than 1 month of age, n = 18). There were three late deaths, one due to coronary obstruction and two due to pulmonary vascular obstructive disease. One child has been lost to follow-up. We have prospectively evaluated the remaining 55 survivors by clinical evaluation, echocardiography, cardiac catheterization, ambulatory electrocardiographic monitoring, and limited electrophysiologic studies. The mean length of follow-up has been 27 +/- 16 months since surgery. One child has required reoperation for a residual ventricular septal defect; no child has undergone reoperation for supravalvar pulmonary or aortic stenosis. Aortic regurgitation was identified in 12 children (22%), which was mild in 11 and moderate in one. One child has asymptomatic occlusion of the left main coronary artery, one child has a tiny right coronary artery-to-pulmonary artery fistula, and one child has abnormal left ventricular wall motion according to follow-up angiography. No other abnormalities of systemic (left) ventricular function have been identified at late follow-up. In addition to the two late deaths due to pulmonary vascular obstructive disease, three children, all of whom were repaired at more than 6 months of age, have elevated pulmonary vascular resistance. Notable postoperative arrhythmias include complete heart block in four patients and nonsustained supraventricular or ventricular tachycardia early after surgery in eight patients (all resolved without medication at later follow-up). Only two patients have evidence of sinus node dysfunction and have not required treatment. The low hospital mortality and encouraging early follow-up data represent a significant improvement over atrial level repairs, supporting the arterial switch operation as the procedure of choice for children who have transposition of the great arteries with ventricular septal defect or double outlet ventricle. Because of the potential for the development of early pulmonary vascular obstructive disease in these patients, repair is recommended within the first 2 months of life.
Fetal cardiac and peripheral arterial flow velocity waveforms in intrauterine growth retardation.
Authors: Groenenberg I A , Wladimiroff J W , Hop W C
Published: June 2011

Maximum flow velocity waveforms were studied at the cardiac level (ascending aorta, pulmonary artery, and ductus arteriosus) and at the peripheral level (fetal internal carotid artery, descending aorta, umbilical artery, and maternal uteroplacental artery) in 25 patients with intrauterine growth retardation and 25 normal control subjects matched for gestational age and maternal parity. Gestational age ranged from 27 to 35 weeks (median, 30 weeks). All flow velocity waveforms were obtained with a mechanical sector scanner combined with a pulsed and continuous Doppler system with a carrier frequency of 3.5 and 3.0 MHz. Normal pregnancy was characterized by low fetal and placental vascular resistances. The peak systolic velocity in the ascending aorta was significantly higher compared with the pulmonary artery. In patients with intrauterine growth retardation, reduced end-diastolic flow velocities were documented in fetal descending aorta, umbilical artery, and maternal uteroplacental artery, reflecting raised umbilical placental and uteroplacental vascular resistances. Raised end-diastolic flow velocities were observed at the cerebral level, reflecting reduced cerebral vascular resistance ("brain sparing" effect). Reduced peak systolic flow velocities documented at the cardiac level may be secondary to reduced volume flow, increased valve or vessel size, or raised afterload. The noninvasive nature of this study did not allow differentiation between these variables.
Is tau a preload-independent measure of isovolumetric relaxation?
Authors: Varma S K , Owen R M , Smucker M L , Feldman M D
Published: June 2011

Several studies have been performed in patients with a variety of myocardial diseases that have identified a prolongation of tau. However, it is not clear whether prolongation of tau represents abnormal myocardial physiology or the effect of excessive load associated with a particular disease process. Accordingly, we evaluate the effect on tau of an isolated decrease in preload induced by inferior vena cava occlusion before the appearance of reflex changes in six patients designated as normal by catheterization criteria. A computer-based digitization routine identified cardiac contractions in all patients early after inferior vena cava occlusion where left ventricular end-diastolic pressure decreased (18.3 +/- 6.3 to 9.3 +/- 5.8, p less than 0.05) while left ventricular systolic pressure (113.3 +/- 13.8 to 111.8 +/- 14.0, p = NS) and heart rate (66.0 +/- 10.0 to 65.9 +/- 10.3, p = NS) did not change. After this alteration in preload, no change in tau from baseline, as calculated by the logarithmic (TL), derivative (TD), or method of Mirsky (T1/2), was noted: TL, 47.4 +/- 6.5 to 44.6 +/- 7.6; TD, 39.3 +/- 8.1 to 39.8 +/- 8.4; T1/2, 33.0 +/- 4.0 to 31.8 +/- 4.6; all p = NS. The baseline pressure extrapolated from isovolumetric relaxation did not change in these preload beats compared with baseline (+4.26 +/- 6.20 to -0.80 +/- 4.87, p = NS). Subsequent beats were identified where left ventricular systolic pressure showed a numeric decrease compared with baseline (113.3 +/- 13.8 to 100.8 +/- 14.3, p = NS) despite no change in heart rate (66.0 +/- 10.0 to 66.8 +/- 10.5, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
Is physiologic sympathoadrenal catecholamine release exocytotic in humans?
Authors: Takiyyuddin M A , Cervenka J H , Sullivan P A , Pandian M R , Parmer R J , Barbosa J A , O'Connor D T
Published: June 2011

In cultured cells and isolated perfused organs, catecholamines are coreleased with chromogranin A (CgA) from adrenal chromaffin cells and sympathetic neurons. The corelease suggests that exocytosis is the mechanism of catecholamine secretion. To investigate whether physiologic catecholamine secretion is exocytotic in humans, we measured plasma norepinephrine, epinephrine, and CgA responses to differentiated stimuli of sympathoadrenal discharge. The CgA radioimmunoassay antibody recognized authentic CgA in normal human adrenal chromaffin vesicles. Insulin-induced hypoglycemia and caffeine ingestion, in decreasing order of potency, selectively stimulated epinephrine release from the adrenal medulla. During hypoglycemia, plasma levels of epinephrine and CgA rose, and peak plasma levels of epinephrine and CgA correlated, suggesting that gradations in epinephrine release represented gradations in exocytosis. However, significant increments in plasma CgA were not observed after caffeine ingestion. Furthermore, the rise of CgA levels during hypoglycemia lagged 60 minutes behind those of epinephrine. A less-pronounced temporal dissociation between CgA and epinephrine release was also shown in isolated chromaffin cells in vitro. Selective adrenal vein catheterization suggested a barrier to CgA transport across the adrenal capillary wall. Short-term, high-intensity dynamic exercise, assumption of the upright posture, prolonged low-intensity dynamic exercise, and smoking, in decreasing order of potency, stimulated norepinephrine release from sympathetic nerve endings. Only the first sympathetic neuronal stimulus resulted in significant increments in plasma CgA, increments considerably less than those attained during adrenal medullary activation by insulin hypoglycemia. During high-intensity exercise, peak plasma norepinephrine and CgA levels correlated, suggesting that gradations in norepinephrine release represented gradations in exocytosis. The human adrenal medulla was a far more prominent tissue source of CgA than human sympathetic nerves--adrenal medullary homogenates contained 97-fold more CgA (micrograms/g) than sympathetic nerve homogenates. In conclusion, catecholamine secretion during selective stimulation of either sympathetic nerves or the adrenal medulla is, at least in part, exocytotic. Furthermore, stimulation of the former results in comparatively modest changes in plasma CgA compared with changes attained during stimulation of the latter. CgA appears to be transported by a route different from that of catecholamines from adrenal medullary chromaffin cells to the circulation in vivo.
Prevention of platelet-rich arterial thrombosis by selective thrombin inhibition.
Authors: Jang I K , Gold H K , Ziskind A A , Leinbach R C , Fallon J T , Collen D
Published: June 2011

The effect of heparin and of the synthetic competitive thrombin inhibitor (2R,4R)-4-methyl-1-[N2-(3-methyl-1,2,3,4-tetrahydro-8-quinolinesulfon yl)-L-arginyl]-2-piperidinecarboxylic acid monohydrate (argatroban) on platelet-rich arterial thrombosis was studied in a rabbit model, consisting of a 4-6-mm everted ("inside-out") femoral arterial segment. Intravenous injection of heparin (200 units/kg) failed to prevent occlusion within 60 minutes in all 10 rabbits, whereas intravenous argatroban infusion at a rate of 100 or 200 micrograms/kg/min for 60 minutes, which prolonged the thrombin time more than fourfold, prevented thrombosis in nine of 13 rabbits (p = 0.002 vs. i.v. heparin). Intra-arterial infusion of 200 units/kg heparin over 60 minutes prevented occlusion in six of nine rabbits (p = 0.003 vs. i.v. heparin), whereas intra-arterial argatroban at a rate of 100 micrograms/kg/min for 60 minutes prevented thrombosis in all 10 rabbits (p = 0.00001 vs. i.v. heparin). Patency of femoral arterial segments was maintained after the end of the intra-arterial heparin and intravenous or intra-arterial argatroban infusion for up to 3 hours despite normalization of the thrombin time and partial thromboplastin time. Pathologic examination of the graft revealed that the inverted adventitial surface was covered by layers of platelets without platelet aggregation or fibrin deposition. These findings indicate that thrombin plays an important role in platelet-rich arterial thrombosis, and that the thrombogenic stimulus is rapidly attenuated by short-term infusion of the synthetic thrombin inhibitor. Selective thrombin inhibition can constitute an alternative approach to the prevention of arterial occlusion after angioplasty or thrombolytic therapy in patients with unstable coronary syndromes.
Circadian blood pressure changes and left ventricular hypertrophy in essential hypertension.
Authors: Verdecchia P , Schillaci G , Guerrieri M , Gatteschi C , Benemio G , Boldrini F , Porcellati C
Published: June 2011

The effects of circadian blood pressure (BP) changes on the echocardiographic parameters of left ventricular (LV) hypertrophy were investigated in 235 consecutive subjects (137 unselected untreated patients with essential hypertension and 98 healthy normotensive subjects) who underwent 24-hour noninvasive ambulatory blood pressure monitoring (ABPM) and cross-sectional and M-mode echocardiography. In the hypertensive group, LV mass index correlated with nighttime (8:00 PM to 6:00 AM) systolic (r = 0.51) and diastolic (r = 0.35) blood pressure more closely than with daytime (6:00 AM to 8:00 PM) systolic (r = 0.38) and diastolic (r = 0.20) BP, or with casual systolic (r = 0.33) and diastolic (r = 0.27) BP. Hypertensive patients were divided into two groups by presence (group 1) and absence (group 2) of a reduction of both systolic and diastolic BP during the night by an average of more than 10% of the daytime pressure. Casual BP, ambulatory daytime systolic and diastolic BP, sex, body surface area, duration of hypertension, prevalence of diabetes, quantity of sleep during monitoring, funduscopic changes, and serum creatinine did not differ between the two groups. LV mass index, after adjustment for the age, the sex, the height, and the daytime BP differences between the two groups (analysis of covariance) was 82.4 g/m2 in the normotensive patient group, 83.5 g/m2 in hypertensive patients of group 1 and 98.3 g/m2 in hypertensive patients of group 2 (normotensive patients vs. group 1, p = NS; group 1 vs. group 2, p = 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)
Lipoprotein and oxygen transport alterations in passive smoking preadolescent children. The MCV Twin Study.
Authors: Moskowitz W B , Mosteller M , Schieken R M , Bossano R , Hewitt J K , Bodurtha J N , Segrest J P
Published: June 2011

We investigated the cardiovascular effects of lifelong passive cigarette smoke exposure in preadolescent children and examined the following questions: 1) Is systemic oxygen transport altered? 2) Are coronary heart disease risk factors adversely affected? We recruited 216 families from the MCV Twin Study; 105 had at least one smoking parent. Serum thiocyanate and cotinine levels were used as measures of smoke exposure in the children and thiocyanate was proportional to the number of parental cigarettes smoked each day (p = 0.0001). Paternal smoking had no effect on these measures. Whole blood 2,3-diphosphoglycerate was higher in smoke-exposed than unexposed children (p less than 0.01) and was related to the thiocyanate level (p less than 0.02). High density lipoprotein (HDL) cholesterol was lower in passive smoking children (p less than 0.05); the HDL2 subfraction was reduced in passive smoking boys, while the HDL3 subfraction was reduced in passive smoking girls. Significant adverse alterations in systemic oxygen transport and lipoprotein profiles are already present in preadolescent children exposed to long-term passive cigarette smoke, primarily from maternal smoke. Children with long-term exposure to passive smoke may be at elevated risk for the development of premature coronary heart disease.
Transcoronary chemical ablation of atrioventricular conduction.
Authors: Brugada P , de Swart H , Smeets J , Wellens H J
Published: June 2011

In seven patients with symptomatic atrial fibrillation and uncontrollable ventricular rates, selective catheterization of the atrioventricular (AV) nodal artery was performed to chemically destroy the AV node. Ethanol at a concentration of 96% and a dose of 0.5-2 ml was used after selective catheterization of the AV nodal artery had demonstrated temporary AV block after the administration of isotonic iced saline. Complete AV block was produced in five patients and AV conduction was sufficiently modified to control symptoms in the remaining two patients. A minimal enzyme rise occurred in six patients. A severe complication in the remaining patient occurred when, after 2 ml ethanol in the AV nodal artery, occlusion developed in the midright coronary artery that led to an inferior wall myocardial infarction. It is concluded that the AV nodal artery can be selectively catheterized using presently available angioplasty techniques. Ethanol can be used to destroy the AV node and block AV conduction.
Determinants of sensitivity and specificity of electrocardiographic criteria for left ventricular hypertrophy.
Authors: Levy D , Labib S B , Anderson K M , Christiansen J C , Kannel W B , Castelli W P
Published: June 2011

Numerous electrocardiographic criteria, which are largely dependent on fixed voltage thresholds, have been proposed for the diagnosis of left ventricular hypertrophy (LVH). Electrocardiographic criteria for LVH were examined in 4,684 subjects of the Framingham Heart Study who underwent echocardiographic study for LVH. Echocardiographic LVH was detected in 290 men (14.2%) and 465 women (17.6%). Electrocardiographic features of LVH were present in 2.9% of men (60/2,042) and 1.5% of women (39/2,642). The overall sensitivity of the electrocardiographic diagnosis of LVH was 6.9%, whereas specificity was 98.8%. Sensitivity of the electrocardiogram (ECG) for LVH was marginally lower in women than in men (5.6% vs. 9.0%, p = 0.075). Obesity was inversely associated with sensitivity (p less than 0.05, both sexes combined, sex-adjusted). Smoking was also inversely related to sensitivity (p = 0.001, both sexes combined, sex-adjusted). In contrast, sensitivity of the ECG increased with age (p less than 0.001, both sexes combined, sex-adjusted). These findings suggest that electrocardiographic detection of LVH can be improved by incorporating information about noncardiac factors that impact on electrocardiographic sensitivity for LVH, presumably by attenuating QRS voltage. New strategies that take into consideration sex, age, smoking status, and obesity might improve the sensitivity of the ECG without diminishing specificity.
Effects of desmopressin acetate on platelet aggregation, von Willebrand factor, and blood loss after cardiac surgery with extracorporeal circulation.
Authors: Andersson T L , Solem J O , Tengborn L , Vinge E
Published: June 2011

The effects of desmopressin acetate (DDAVP) on platelet aggregation and the von Willebrand factor antigen (vWF:Ag) were studied in 19 patients undergoing cardiac surgery with extracorporeal circulation. The patients represented one of five blocks in a randomized double-blind placebo-controlled parallel group trial on the effects of DDAVP on postoperative bleeding after uncomplicated coronary artery bypass operations. After termination of extra-corporeal circulation, DDAVP (0.3 microgram/kg body wt) or its vehicle was infused into a peripheral vein throughout 15 minutes. The increase in factor VIII coagulant activity after infusion did not differ between the groups but there was a significantly larger increase in vWF:Ag levels in DDAVP-treated patients. The aggregatory response to adenosine-diphosphate (ADP) and ristocetin showed a normal pattern and was not significantly different between the two groups. As compared with placebo, DDAVP did not decrease the bleeding time or the postoperative blood loss. We conclude that DDAVP causes an increase in vWF:Ag levels but does not alter platelet aggregation, bleeding time, or blood loss in uncomplicated coronary artery bypass patients.
Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications.
Authors: Pfeffer M A , Braunwald E
Published: June 2011

An acute myocardial infarction, particularly one that is large and transmural, can produce alterations in the topography of both the infarcted and noninfarcted regions of the ventricle. This remodeling can importantly affect the function of the ventricle and the prognosis for survival. In the early period, infarct expansion has been recognized by echocardiography as a lengthening of the noncontractile region. The noninfarcted region also undergoes an important lengthening that is consistent with a secondary volume-overload hypertrophy and that can be progressive. The extent of ventricular enlargement after infarction is related to the magnitude of the initial damage to the myocardium and, although an increase in cavity size tends to restore stroke volume despite a persistently depressed ejection fraction, ventricular dilation has been associated with a reduction in survival. The process of ventricular enlargement can be influenced by three interdependent factors, that is, infarct size, infarct healing, and ventricular wall stresses. A most effective way to prevent or minimize the increase in ventricular size after infarction and the consequent adverse effect on prognosis is to limit the initial insult. Acute reperfusion therapy has been consistently shown to result in a reduction in ventricular volume. The reestablishment of blood flow to the infarcted region, even beyond the time frame for myocyte salvage, has beneficial effects in attenuating ventricular enlargement. The process of scarification can be interfered with during the acute infarct period by the administration of glucocorticosteroids and nonsteroidal antiinflammatory agents, which result in thinner infarcts and greater degrees of infarct expansion. Modification of distending or deforming forces can importantly influence ventricular enlargement. Even short-term augmentations in afterload have deleterious long-term effects on ventricular topography. Conversely, judicious use of nitroglycerin seems to be associated with an attenuation of infarct expansion and long-term improvement in clinical outcome. Long-term therapy with an angiotensin converting enzyme inhibitor can favorably alter the loading conditions on the left ventricle and reduce progressive ventricular enlargement as demonstrated in both experimental and clinical studies. With the former therapy, this attenuation of ventricular enlargement was associated with a prolongation in survival. The long-term clinical consequences of long-term angiotensin converting enzyme inhibitor therapy after myocardial infarction is currently being evaluated. Although studies directed at attenuating left ventricular remodeling after infarction are in the early stages, it does seem that this will be an important area in which future research might improve long-term outcome after infarction.
Efficacy and safety of perhexiline maleate in refractory angina. A double-blind placebo-controlled clinical trial of a novel antianginal agent.
Authors: Cole P L , Beamer A D , McGowan N , Cantillon C O , Benfell K , Kelly R A , Hartley L H , Smith T W , Antman E M
Published: June 2011

Despite large gains in the medical and surgical treatment of angina pectoris in the past two decades, many patients are refractory to conventional medical therapy and are unsuitable for a first or, more commonly, repeat coronary revascularization procedure. We evaluated the efficacy of perhexiline maleate, a drug with an antianginal mechanism of action in humans that is as yet unknown, by using a randomized double-blind placebo-controlled crossover design in 17 patients with refractory angina who continued to receive maximal antianginal therapy, typically including nitrates, a beta-blocker, and a calcium channel antagonist. In view of perhexiline's potential for hepatic and neurological toxicity, plasma drug levels were monitored and maintained in the 150-600 ng/ml range. Sixty-three percent of patients were judged perhexiline responders by objective exercise testing criteria, as compared with 18% of patients on placebo (p less than 0.05). By blinded review of subjective measures of anginal frequency and severity, 65% of patients noted an improvement while on perhexiline, whereas no patient identified the placebo phase with improvement. Side effects observed in 29% of patients were minor and related to transient elevations of blood levels of more than 600 ng/ml; no patient suffered hemodynamic or cardiac conduction abnormalities attributable to perhexiline. With attention to the pharmacokinetics of perhexiline's elimination in individual patients, this novel antianginal agent seems to be safe and effective and deserves further evaluation in patients already receiving maximal antianginal therapy who are not candidates for revascularization procedures.