bluuebunny/crossref_metadata_2025_split huggingface dataset:
A new noninvasive method for the estimation of peak dP/dt.
Authors: Rhodes J , Udelson J E , Marx G R , Schmid C H , Konstam M A , Hijazi Z M , Bova S A , Fulton D R 
Published: June 2012

BACKGROUND
Peak dP/dt is a good index of ventricular performance that is not influenced by afterload, wall motion abnormalities, or the variations in ventricular anatomy and morphology commonly encountered among patients with congenital heart disease. Unfortunately, the clinical utility of peak dP/dt has been limited by the fact that its measurement generally requires an intraventricular catheter. However, peak dP/dt occurs during isovolumetric contraction, and the pressure rise during isovolumetric contraction is almost linear. Therefore, the mean dP/dt during isovolumetric contraction (mean dP/dtic), ie, the ratio of the rise in pressure during isovolumetric contraction (aortic diastolic pressure minus the systemic ventricular end-diastolic pressure [VEDP]) over the isovolumetric contraction time, should provide a good estimate of peak dP/dt that could be generated noninvasively.

METHODS AND RESULTS
Echo/phonocardiography was used to measure the isovolumetric contraction time and a blood pressure cuff to estimate aortic diastolic pressure of 27 patients (age, 1 day to 77 years) with congenital or acquired heart disease. VEDP was determined by three methods: (1) intraventricular catheter, (2) assumed VEDP of 10 mm Hg, and (3) assignment of a normal or elevated value on the basis of clinical history. The three estimates of mean dP/dtic thus generated were compared with simultaneous measurements of peak dP/dt obtained during cardiac catheterization. Invasively measured peak dP/dt correlated well with the indirect determinations (r = .95, .89, and .92 for methods 1, 2, and 3, respectively; P < .0001).

CONCLUSIONS
Echo/phonocardiography can be used in conjunction with a blood pressure cuff and indirect estimates of VEDP to generate mean dP/dtic, an index of ventricular function that approximates and closely correlates with peak dP/dt. This noninvasive measurement can be obtained in almost any patient and may be useful in the assessment of ventricular performance in a variety of cardiovascular disorders.
Plasma lipoproteins and progression of coronary artery disease evaluated by angiography and clinical events.
Authors: Phillips N R , Waters D , Havel R J 
Published: June 2012

BACKGROUND
There is considerable evidence that remnants of triglyceride-rich lipoproteins may be particularly atherogenic.

METHODS AND RESULTS
Levels of lipoprotein lipids and of apolipoprotein B in low-density lipoproteins were measured in 335 men and women enrolled in a study in which quantitative coronary angiography was carried out at 2-year intervals. Clinical events related to coronary disease occurred in 129 patients during the trial and in the subsequent follow-up period of 4 to 6 years. In multivariate analysis controlled for a number of nonlipid risk factors, high-density lipoprotein cholesterol was inversely related to the mean percentage increase in coronary artery stenosis in both men and women. Neither plasma triglycerides nor low-density lipoprotein cholesterol, triglycerides, or apolipoprotein B was related to change in stenosis, but a measure of remnants of triglyceride-rich lipoproteins, which included cholesterol in intermediate-density lipoproteins, was directly related to lesion progression. The same relations for these measures of plasma lipoprotein concentrations were found to hold for clinical events related to coronary artery atherosclerosis.

CONCLUSIONS
In patients with established coronary heart disease, increased levels of remnants of triglyceride-rich lipoproteins and decreased levels of high-density lipoproteins appear to promote progression of coronary artery atherosclerosis, which in turn may lead to an untoward clinical event. No such relation could be shown for the level of components of low-density lipoproteins. These and other observations call for reevaluation of relations between particular species of lipoproteins containing apolipoprotein B and the pathogenesis of coronary artery atherosclerosis and coronary heart disease.
Mitral valve replacement versus mitral valve repair. A Doppler and quantitative stress echocardiographic study.
Authors: Tischler M D , Cooper K A , Rowen M , LeWinter M M 
Published: June 2012

BACKGROUND
Standard mitral valve replacement (MVR) in patients with chronic mitral regurgitation results in consistent reductions in resting postoperative ejection fraction. This has been attributed to removal of the low-impedance ejection pathway into the left atrium or to disruption of the chordal apparatus. Mitral valve repair (MVP) does not reduce ejection fraction at rest. However, whether MVP confers any advantages with regard to dynamic left ventricular performance has not been investigated. The aim of this study was to directly compare standard MVR with MVP and to determine their respective influences on ventricular ejection performance during bicycle exercise.

METHODS AND RESULTS
Ten consecutive patients with pure chronic mitral regurgitation who underwent MVP and 10 patients matched for age, sex, and preoperative ejection fraction who underwent standard MVR for pure chronic mitral regurgitation performed symptom-limited, graded upright bicycle exercise with simultaneous Doppler and quantitative two-dimensional echocardiography. Patients with MVP had significantly greater rest (55 +/- 12%) and exercise (63 +/- 11%) ejection fractions than matched patients with MVR (40 +/- 13% [P < .0001] and 42 +/- 17% [P < .005], respectively). End-systolic circumferential wall stress was significantly lower at rest (190 +/- 36 versus 244 +/- 46; P < .03) and at peak exercise (231 +/- 46 versus 300 +/- 52; P < .02) in patients with MVP. At peak exercise, left ventricular shape was significantly more spherical in patients with MVR than those with MVP (1.84 +/- 0.31 versus 2.45 +/- 0.59; P < .02).

CONCLUSIONS
MVR with chordal transection resulted in significant reductions in rest and exercise ejection fraction. This was caused in part by a significant increase in end-systolic circumferential wall stress. MVP resulted in improved rest and exercise ejection indexes, primarily due to a marked reduction in end-systolic stress and maintenance of a more ellipsoidal chamber geometry.
Gamma-globulin treatment of acute myocarditis in the pediatric population.
Authors: Drucker N A , Colan S D , Lewis A B , Beiser A S , Wessel D L , Takahashi M , Baker A L , Perez-Atayde A R , Newburger J W 
Published: June 2012

BACKGROUND
Myocardial damage in myocarditis is mediated, in part, by immunological mechanisms. High-dose intravenous gamma-globulin (IVIG) is an immunomodulatory agent that is beneficial in myocarditis secondary to Kawasaki disease, as well as in murine myocarditis. Since 1990, the routine management of presumed acute myocarditis at Children's Hospital, Boston, and Children's Hospital, Los Angeles, has included administration of high-dose IVIG.

METHODS AND RESULTS
We treated 21 consecutive children presenting with presumed acute myocarditis with IVIG, 2 g/kg, over 24 hours, in addition to anticongestive therapies. A comparison group comprised 25 recent historical control patients meeting identical eligibility criteria but not receiving IVIG therapy. Left ventricular function was assessed during five time intervals: 0 to 7 days, 1 to 3 weeks, 3 weeks to 3 months, 3 to 6 months, and 6 to 12 months. At presentation, the IVIG and non-IVIG groups had comparable left ventricular enlargement and poor fractional shortening. Compared with the non-IVIG group, those treated with IVIG had a smaller mean adjusted left ventricular end-diastolic dimension and higher fractional shortening in the periods from 3 to 6 months (P = .008 and P = .033, respectively) and 6 to 12 months (P = .072 and P = .029, respectively). When adjusting for age, biopsy status, intravenous inotropic agents, and angiotensin-converting enzyme inhibitors, patients treated with IVIG were more likely to achieve normal left ventricular function during the first year after presentation (P = .03). By 1 year after presentation, the probability of survival tended to be higher among IVIG-treated patients (.84 versus .60, P = .069). We observed no adverse effects of IVIG administration.

CONCLUSIONS
These data suggest that use of high-dose IVIG for treatment of acute myocarditis is associated with improved recovery of left ventricular function and with a tendency to better survival during the first year after presentation.
Ventricular proarrhythmic effects of ventricular cycle length and shock strength in a sheep model of transvenous atrial defibrillation.
Authors: Ayers G M , Alferness C A , Ilina M , Wagner D O , Sirokman W A , Adams J M , Griffin J C 
Published: June 2012

BACKGROUND
Synchronized cardioversion is generally accepted as safe for the treatment of ventricular tachycardia and atrial fibrillation when shocks are synchronized to the R wave and delivered transthoracically. However, others have shown that during attempted transvenous cardioversion of rapid ventricular tachycardia, ventricular fibrillation (VF) may be induced. It was our objective to evaluate conditions (short and irregular cycle lengths [CL]) under which VF might be induced during synchronized electrical conversion of atrial fibrillation with transvenous electrodes.

METHODS AND RESULTS
In 16 sheep (weight, 62 +/- 7.8 kg), atrial defibrillation thresholds (ADFT) were determined for a 3-ms/3-ms biphasic shock delivered between two catheters each having 6-cm coil electrodes, one in the great cardiac vein under the left atrial appendage and one in the right atrial appendage along the anterolateral atrioventricular groove. A hexapolar mapping catheter was positioned in the right ventricular apex for shock synchronization. In 8 sheep (group A), a shock intensity 20 V less than the ADFT was used for testing, and in the remaining 8 sheep (group B), a shock intensity of twice ADFT was used. With a modified extrastimulus technique, a basic train of eight stimuli alone (part 1) and with single (part 2) and double (part 3) extrastimuli were applied to right ventricular plunge electrodes. Atrial defibrillation shocks were delivered synchronized to the last depolarization. In part 4, shocks were delivered during atrial fibrillation. The preceding CL was evaluated over a range of 150 to 1000 milliseconds. Shocks were also delayed 2, 20, 50, and 100 milliseconds after the last depolarization from the stimulus (parts 1 through 3) or intrinsic depolarization (part 4). The mean ADFT for group A was 127 +/- 48 V, 0.71 +/- 0.60 J and for group B, 136 +/- 37 V, 0.79 +/- 0.42 J (NS, P > .15). Of 1870 shocks delivered, 11 episodes of VF were induced. Group A had no episodes of VF in part 1, two episodes of VF in part 2 (CL, 240 and 230 milliseconds with 2-millisecond delay), and one episode each in parts 3 (CL, 280 milliseconds with 2-millisecond delay) and 4 (CL, 240 milliseconds with 100-millisecond delay). Group B had two episodes in part 1 (CL, 250 and 300 milliseconds with 20-millisecond delay), three episodes in part 2 (CL, 230, 230, and 250 milliseconds with 2-millisecond delay), and one episode each in parts 3 (CL, 260 milliseconds with 2-millisecond delay) and 4 (198 milliseconds with 100-millisecond delay). No episodes of VF were induced for shocks delivered after a CL > 300 milliseconds.

CONCLUSIONS
Synchronized transvenous atrial defibrillation shocks delivered on beats with a short preceding ventricular cycle length (< 300 milliseconds) are associated with a significantly increased risk of initiation of VF. To decrease the risk of ventricular proarrhythmia, short CLs should be avoided.
Abrupt complement activation and transient neutropenia in patients with acute myocardial infarction treated with streptokinase.
Authors: Frangi D , Gardinali M , Conciato L , Cafaro C , Pozzoni L , Agostoni A 
Published: June 2012

BACKGROUND
Whether and to what extent complement is activated in acute myocardial infarction (AMI) and how it contributes to inflammation of the ischemic area are not yet clear. Fibrinolytic agents used for thrombolysis are known to activate complement in vitro and may contribute to its activation in vivo. The aim of this study was to measure the extent of complement activation in AMI patients, some treated and some not treated with streptokinase. In addition, because abrupt complement activation in vivo is usually associated with leukocyte margination, plugging of cells in the microcirculation, and hypotension, we correlated complement activation with leukocyte numbers and mean arterial pressure.

METHODS AND RESULTS
Forty AMI patients were studied: 20 were treated with streptokinase (1.5 million IU IV over 60 minutes), and 20 were not given any fibrinolytic agent. The extent and severity of AMI were not significantly different in both groups. Blood samples were drawn on arrival at the hospital, during streptokinase infusion, and then daily for 1 week. Time-matched samples were also drawn from patients not treated with streptokinase. We measured plasma levels of anaphylatoxin C4a, C3a, and C5a by radioimmunoassay and membrane attack complexes SC5b-9 by enzyme immunoassay. Leukocytes and arterial pressure also were measured when samples were obtained. C4a, C3a, and SC5b-9 levels increased about 10-fold (P < .0001) during infusion of streptokinase. There were no significant increases in complement catabolic products in AMI patients not treated with streptokinase. There was a significant transient leukopenia (mean +/- SEM, -29.5 +/- 7.0%; P = .001) and decreases in systolic and diastolic pressures (systolic, -29.3 +/- 3.2%, P < .0001; diastolic, -27.5 +/- 3.4%, P < .0001) after 15 minutes of streptokinase infusion in coincidence with the peak of anaphylatoxins in plasma.

CONCLUSIONS
Streptokinase treatment of AMI causes abrupt activation of the complement system, whereas no significant complement activation can be detected in plasma of AMI patients not treated with fibrinolytic agents. Complement activation causes a transient leukopenia, as reported for such other clinical conditions as dialysis and cardiopulmonary bypass, and possibly contributes to the hypotension observed during streptokinase treatment.
Two-dimensional left ventricular deformation during systole using magnetic resonance imaging with spatial modulation of magnetization.
Authors: Young A A , Imai H , Chang C N , Axel L 
Published: June 2012

BACKGROUND
Myocardial tissue tagging with the use of magnetic resonance imaging allows noninvasive regional analysis of heart wall motion and deformation. However, any evaluation of the effect of disease or treatment requires a baseline reference of normal values and variation. We studied the two-dimensional motion of material points imaged within the left ventricular wall using spatial modulation of magnetization (SPAMM) in 12 normal human volunteers.

METHODS AND RESULTS
Five parallel short-axis and five parallel long-axis slices were acquired at five times during systole. SPAMM tags were generated at end diastole using a 7-mm grid. Intersection point data were analyzed for displacement, rotation, and torsion, and triangles of points were analyzed for local rotation and principal strains. Short-axis displacement was the least in the septum for all longitudinal levels (P < .001). Torsion about the long axis was uniform circumferentially because of the motion of the centroids used to reference the rotation. In the long-axis images, the base displaced longitudinally toward the apex, with the posterior wall moving farther than the anterior wall (13.4 +/- 2.2 versus 9.7 +/- 1.8 mm, P < .001) in this direction. The largest principal strain (maximum lengthening) was approximately radially oriented in both views. In the short-axis images, the minimum principal strain (maximum shortening) increased in magnitude toward the apex (P < .001) with little circumferential variation, except at midventricle, where the anterior wall showed greater contraction than the posterior wall (-0.21 +/- 0.03 versus -0.19 +/- 0.02, P < .02).

CONCLUSIONS
Consistent regional variations in deformation are seen in the normal human heart. Displacement and maximum shortening strains are well characterized with two-dimensional magnetic resonance tagging; however, higher-resolution images will be required to study transmural variations.
Visualization of penetrating transmural arteries in situ by monochromatic synchrotron radiation.
Authors: Mori H , Hyodo K , Tobita K , Chujo M , Shinozaki Y , Sugishita Y , Ando M 
Published: June 2012

BACKGROUND
Penetrating transmural arteries with a diameter of < 500 microns are considered to be a critical vascular component that causes a transmural variation of myocardial blood flow under various pathophysiological conditions. However, the conventional coronary angiographic system is not oriented to the visualization of such small arteries as these.

METHODS AND RESULTS
We magnified and monochromatized the inherently narrow beam (3 mm along the vertical direction) of synchrotron radiation by using an asymmetrically cut silicon crystal with 311 reflecting planes to obtain a monochromatic x-ray with relatively large beam size (60 x 25 mm) and with an energy of just above (+130 eV) the K-absorption edge of the contrast materials (33.17 and 37.41 ke V for iodine and barium, respectively). We irradiated dogs or excised hearts with the monochromatic x-ray and obtained coronary angiograms using an image intensifier and video system with a spatial resolution of 170 microns. In the anesthetized dog experiments, we visualized the transmural penetrating arteries (5 to 15 mm in length) arising every 4 to 7 mm from the epicardial branch. Visualization of these arteries filled with heavy element-loaded microspheres (15 microns in diameter) in the excised-heart experiments, in which the monochromatic x-ray was irradiated to the hearts through a 10- to 20-cm acrylic plate, indicated that this system could be used for human patients, in whom body absorption of x-ray is substantial.

CONCLUSIONS
Coronary angiogram by means of monochromatic x-ray is useful for a precise evaluation of coronary circulation, both in clinical setting and in physiological animal experiments.
Effects on left ventricular hypertrophy of long-term nonpharmacological treatment with sodium restriction in mild-to-moderate essential hypertension.
Authors: Jula A M , Karanko H M 
Published: June 2012

BACKGROUND
Cross-sectional studies on human hypertension have suggested an association between sodium intake and left ventricular hypertrophy (LVH).

METHODS AND RESULTS
The effects on LVH of a nonpharmacological treatment program based mainly on sodium restriction were examined by serial echocardiography in a 12-month controlled, randomized study that included 76 previously untreated subjects with uncomplicated mild-to-moderate hypertension. The mean daily sodium excretion of 38 subjects randomized into the treatment group decreased from 195 +/- 95 to 94 +/- 73 mmol (P < .001) at 6 months and to 109 +/- 74 mmol (P < .001) at 12 months. This was accompanied by a weight decrease from 81.4 +/- 18.0 to 79.2 +/- 17.4 kg (P < .001) at 6 months and to 80.6 +/- 17.5 kg (NS) at 12 months. The net blood pressure decrease (difference in change from baseline between the treatment and control groups) was 8.9 mm Hg (P < .001) in systolic blood pressure and 6.5 mm Hg (P < .001) in diastolic blood pressure during the first 6 months and 6.7 mm Hg (P < .01) in systolic blood pressure and 3.8 mm Hg (P < .01) in diastolic blood pressure during the last 6 months. After 12 months of sodium restriction, left ventricular mass (LVM) had decreased by 5.4% (from 238 +/- 63 to 225 +/- 51 g, P < .01), and LVM index (LVMI) had decreased by 4.7% (from 123 +/- 26 to 117 +/- 22 g/m2, P < .05), whereas no changes occurred in these parameters in the control group. In treated subjects with baseline LVMI of more than the median value of 133 g/m2 in men and 107 g/m2 in women, LVM decreased by 8.6% (from 272 +/- 62 to 249 +/- 51 g, P < .01), and LVMI decreased by 7.1% (from 140 +/- 23 to 130 +/- 22 g/m2, P < .01). LVM and LVMI remained unchanged in treated subjects with LVMI values equal to or less than the median.

CONCLUSIONS
Our data suggest that long-term nonpharmacological treatment with moderate sodium restriction decreases LVH.
Shortening of fast pathway refractoriness after slow pathway ablation. Effects of autonomic blockade.
Authors: Natale A , Klein G , Yee R , Thakur R 
Published: June 2012

BACKGROUND
Shortening of the anterograde effective refractory period (ERP) of the fast pathway has been reported after radiofrequency ablation of the slow pathway. We hypothesized that ERP shortening may be related to autonomic changes, possibly catecholamine release, as a result of ablation.

METHODS AND RESULTS
To test this, 10 consecutive patients with atrioventricular node reentry undergoing slow pathway ablation were given autonomic blockade before the ablation procedure. This was achieved by atropine 0.03 mg/kg and propranolol 0.15 mg/kg IV supplemented by half the initial dose after ablation and before the final study. A control group of 10 patients underwent the protocol without autonomic blockade. Before ablation, autonomic blockade did not alter the ERP of either the fast pathway (295 +/- 22 versus 298 +/- 26 milliseconds) or the slow pathway (264 +/- 36 versus 269 +/- 38 milliseconds). Autonomic blockade obscured dual pathway physiology in 2 patients and brought it out in another 2 without dual pathway physiology initially. Slow pathway ablation shortened the ERP of the fast pathway for the group as a whole (331.5 +/- 54 versus 305.5 +/- 60 milliseconds, mean +/- SD, n = 20, P < .04). There was no difference in degree of ERP shortening in control patients (23.5 +/- 58 milliseconds) or autonomic blockade patients (25.5 +/- 52 milliseconds).

CONCLUSIONS
These data suggest that shortening of the ERP of the fast pathway after slow pathway ablation is not mediated by autonomic changes.
The Australian Schools Health and Fitness Survey. Physical fitness related to blood pressure but not lipoproteins.
Authors: Dwyer T , Gibbons L E 
Published: June 2012

BACKGROUND
Recent research indicates that levels of conventional coronary heart disease risk factors in children are related to the premature development of atheroma. It is therefore important to determine how risk factors might be modified on a population scale in children.

METHODS AND RESULTS
In 1985, the Australian Schools Health and Fitness Survey was conducted on a representative sample of Australian schoolchildren aged 7 to 15 years. In children aged 9, 12, and 15, data on plasma cholesterol, triglycerides, and high-density lipoprotein cholesterol were obtained along with measurements of blood pressure, fitness, and body fatness. From an original sample of 2400 in these three age categories 1919 underwent the full set of measurements. Univariate analysis of these data revealed a strong association between body fatness and plasma lipids. There was no significant association between fitness (measured as physical work capacity at a heart rate of 170 beats per minute per kilogram of lean body mass) and plasma lipids, but a significant negative association was found for fitness and systolic blood pressure (r = -.12, P < .001). Multiple regression analysis revealed that the association of fitness with systolic blood pressure was only partly accounted for by the confounding effect of lower body fatness in fitter children.

CONCLUSIONS
These data collected on a representative sample of children under standardized conditions confirm a previous finding of a link between fitness and blood pressure in schoolchildren and also support a growing consensus that fitness is only weakly linked to plasma lipids and lipoproteins in children and adolescents.