bluuebunny/crossref_metadata_2025_split huggingface dataset:
Quantification of left-to-right atrial shunting and defect size after balloon mitral commissurotomy using biplane transesophageal echocardiography, color flow Doppler mapping, and the principle of proximal flow convergence.
Authors: Rittoo D , Sutherland G R , Shaw T R 
Published: June 2012

BACKGROUND
The flow convergence region (FCR), a zone of progressive laminar velocity acceleration, can be imaged by color Doppler proximal to stenotic and regurgitant orifices. Theoretically, FCR proximal to a discrete circular and planar orifice consists of concentric hemispheric shells of equal and accelerating velocities centered at the orifice. According to the continuity principle, flow rate across any of these isovelocity surfaces equals flow rate through the orifice. The aim of this study was to investigate whether these principles could be applied to quantify left-to-right shunting and the size of atrial septal defects after balloon mitral commissurotomy.

METHODS AND RESULTS
Biplane transesophageal echocardiography (TEE) with color flow imaging was performed on 36 consecutive patients (mean age, 57 +/- 16 years; range, 14-78 years) immediately before and within 24 hours of balloon (Inoue, n = 33; Mansfield, n = 3) mitral commissurotomy. Left-to-right atrial shunting was detected by TEE in 33 patients (92%) and by oximetry in 11 patients (31%). The radius r of FCR was measured from the first aliasing limit, at a Nyquist velocity reduced to 11 cm/sec by zero-shifting, to the orifice in the atrial septum. FCR was assumed to be hemispherical. Hence, flow rate (Q) was calculated as 2 pi r2 Vr, where Vr is the velocity at a radial distance r. The velocity profile of transatrial flow was assessed by means of high pulse repetition frequency, from which the maximum flow velocity (Vp) and the velocity-time integral (VTI) were obtained. The flow area of the atrial septal defect was calculated as Qm, the maximal flow rate, divided by Vp. Hence, shunt flow was calculated as flow area x VTI x heart rate. FCR was analyzed in two orthogonal planes. Mean Qm (38.1 +/- 26.5 versus 5.3 +/- 2.7 mL/sec), flow area (22.1 +/- 11.2 versus 4.4 +/- 2.0 mm2), and shunt flow (1,590 +/- 1,070 versus 200 +/- 130 mL/min) on transverse plane imaging were all significantly higher in patients with shunts detected by oximetry than in those without. Similar results were obtained from longitudinal plane imaging. Qm correlated well with oximetric shunt flow (r = 0.89-0.94, p < 0.001) and shunt ratio (r = 0.91-0.94, p < 0.001). Flow area correlated closely (r = 0.93-0.94, p < 0.001) with area determined by direct measurement from two-dimensional echocardiography. Shunt flow determined by FCR also correlated closely (r = 0.94-0.98, p < 0.001) with that determined by oximetry and that derived from two-dimensional echocardiography and pulsed Doppler (r = 0.96, p < 0.001).

CONCLUSIONS
The flow convergence region imaged by TEE color flow mapping provides new and accurate quantitative information on atrial shunt flow and defect size after balloon mitral valvotomy. It is a quick, reliable, and fairly simple method that can be readily incorporated into routine clinical practice.
Scintigraphic pattern of regional cardiac sympathetic innervation in patients with familial long QT syndrome using positron emission tomography.
Authors: Calkins H , Lehmann M H , Allman K , Wieland D , Schwaiger M 
Published: June 2012

BACKGROUND
The purpose of this study was to determine whether scintigraphic evidence of cardiac sympathetic neuronal dysinnervation is present in patients with the familial long QT syndrome. The "sympathetic imbalance" hypothesis for the familial long QT syndrome proposes that the long QT syndrome results from a congenital imbalance of sympathetic innervation of the heart caused by lower-than-normal right cardiac sympathetic activity. Although the majority of clinical features of the long QT syndrome can be understood according to this hypothesis, its validity has never been shown. Noninvasive scintigraphic evaluation of the pattern of sympathetic innervation of the heart has recently become possible with catecholamine analogues that can be taken up by sympathetic nerve terminals: radioiodinated metaiodobenzyl guanidine or C-11 hydroxyephedrine (HED).

METHODS AND RESULTS
Nine affected patients, each from a separate family with familial long QT syndrome, were enrolled in this study (three men, six women; mean age, 39 +/- 16 years). Scintigraphic evaluation of the pattern of cardiac sympathetic innervation in each patient was performed with HED in conjunction with positron emission tomography. The results of scintigraphic imaging in these patients were compared with those obtained in 14 asymptomatic volunteers. Scintigraphic evaluation demonstrated that HED retention index and HED uptake normalized to blood flow were no different in patients with the familial long QT syndrome than in normal control patients.

CONCLUSIONS
Patients with the long QT syndrome have normal cardiac sympathetic innervation as assessed by HED. This finding, although not incompatible with the sympathetic imbalance hypothesis of the long QT syndrome, suggests that if a decrease in right sympathetic activity is present in patients with familial long QT syndrome, it is unlikely to be attributed to an abnormal distribution of cardiac sympathetic nerves.
Acute intravenous cocaine causes transient depression followed by enhanced left ventricular function in conscious dogs.
Authors: Stambler B S , Komamura K , Ihara T , Shannon R P 
Published: June 2012

BACKGROUND
Prior studies in experimental canine models have demonstrated that intravenous cocaine administration causes myocardial depression. The purpose of the present study was to establish the mechanisms of cocaine's actions on myocardial and left ventricular performance after single intravenous bolus doses in conscious, chronically instrumented dogs, in which the full autonomic influences of cocaine would be manifest.

METHODS AND RESULTS
In the intact state, cocaine (1 mg/kg) caused a transient decrease in left ventricular dP/dt (baseline; 3,086 +/- 107 mm Hg/sec; 2.5 minutes, 2,649 +/- 114 mm Hg; p < 0.05) followed by a 25 +/- 4% increase in left ventricular dP/dt that peaked at 15 minutes (left ventricular dP/dt, 3,751 +/- 127 mm Hg/sec, p < 0.01) and remained elevated during the 30-minute period of observation. Both the initial depression and the sustained increase in left ventricular contractile response were dose related. The increase in left ventricular dP/dt persisted under circumstances in which the responses were normalized for changes in heart rate and preload that accompanied cocaine administration. The positive inotropic effects were abolished by full autonomic or selective beta-adrenergic blockades. Finally, both cardiac output (baseline, 2,461 +/- 142 min/mL; peak [5 minutes], 3,434 +/- 218 mL/min; p < 0.05) and left ventricular stroke work (baseline, 39 +/- 5 g.m; peak, 49 +/- 6 g.m; p < 0.05) were increased at all times after cocaine administration, suggesting that pump performance was enhanced, despite early reductions in myocardial contractility. Similarly, indexes of early diastolic filling were enhanced despite transient early prolongation in isovolumic relaxation.

CONCLUSIONS
Acute intravenous cocaine administration (0.1-2 mg/kg) has a biphasic effect on myocardial and left ventricular function with a transient depression followed by significant sustained increases in left ventricular contractility. The results are in keeping with an early local effect followed by significant adrenergic stimulation, which may be obscured by anesthesia or masked by changes in loading conditions.
Role of oscillatory potential and pacemaker shifts in digitalis intoxication of the sinoatrial node.
Authors: Gonzalez M D , Vassalle M 
Published: June 2012

BACKGROUND
Digitalis intoxication causes tachycardia, pacemaker shifts, and conduction disturbances in the sinoatrial (SA) node, but the mechanisms underlying these changes have not been clarified. We studied the role played by oscillatory potentials, electrical inhomogeneity, and calcium overload in cardiac steroid intoxication of the SA node.

METHODS AND RESULTS
Guinea pig SA nodes (isolated from atrial tissue) were perfused in vitro. Transmembrane potentials and force were recorded. Strophanthidin (1 mumol/L) induced minor changes, although it was perfused for more than 30 minutes. In contrast, ouabain (0.5 mumol/L) and digoxin (1 mumol/L) intoxicated the SA node in 10-20 minutes. Ouabain and digoxin increased spontaneous rate and slope of diastolic depolarization, shifted the plateau to more negative values, and decreased the maximum diastolic potential. These cardiac steroids increased and then decreased contractile force and eventually caused the action potential and twitch to become irregular in amplitude and rhythm. In the presence of acetylcholine (ACh, 0.01-1 mumol/L), cardiac steroids decreased the resting potential, caused spontaneous activity, and increased force and, eventually, oscillatory potentials (Vos) and aftercontractions as well as overdrive excitation. To make the SA node electrically homogeneous (only slow responses), the SA node was perfused with high extracellular potassium concentration (with and without norepinephrine), tetrodotoxin (2.61 mumol/L), or lidocaine (50 mumol/L). Adding ouabain or digoxin to these solutions increased the rate but far less than in Tyrode's solution. Recovery in Tyrode's solution initially caused fast and irregular rhythms, which then subsided. Low extracellular calcium concentration ([Ca]o) (0.54 mmol/L) decreased force; adding ouabain markedly increased force and induced Vos. High [Ca]o (8.1 mmol/L) increased force; adding ouabain decreased force and made action potentials as well as contractions quite irregular.

CONCLUSIONS
Ouabain and digoxin quickly intoxicate the SA node by inducing calcium overload and its manifestations (Vos, decrease in contractile force and aftercontractions), whereas strophanthidin does not, possibly because of the lack of a sugar moiety. The intoxication is less pronounced when sodium influx is decreased (slow responses), and this accounts for the shifts from dominant to subsidiary pacemakers. Marked conduction disturbances result from calcium overload, leading to the fractionation of SA node activity.
X-linked dilated cardiomyopathy. Molecular genetic evidence of linkage to the Duchenne muscular dystrophy (dystrophin) gene at the Xp21 locus.
Authors: Towbin J A , Hejtmancik J F , Brink P , Gelb B , Zhu X M , Chamberlain J S , McCabe E R , Swift M 
Published: June 2012

BACKGROUND
X-linked cardiomyopathy (XLCM) is a rapidly progressive primary myocardial disorder presenting in teenage males as congestive heart failure. Manifesting female carriers have later onset (fifth decade) and slower progression. The purpose of this study was to localize the XLCM gene locus in two families using molecular genetic techniques.

METHODS AND RESULTS
Linkage analysis using 60 X-chromosome-specific DNA markers was performed in a previously reported large XLCM pedigree and a smaller new pedigree. Two-point and multipoint linkage was calculated using the LINKAGE computer program package. Deletion analysis included multiplex polymerase chain reaction (PCR). Dystrophin protein was evaluated by Western blotting with N-terminal and C-terminal dystrophin antibody. Linkage of XLCM to the centromeric portion of the dystrophin or Duchenne muscular dystrophy (DMD) locus at Xp21 was demonstrated with combined maximum logarithm of the scores of +4.33, theta = 0 with probe XJ1.1 (DXS206) using two-point linkage and +4.81 at XJ1.1 with multipoint linkage analysis. LOD scores calculated using other proximal DMD genomic and cDNA probes and polymerase chain reaction polymorphisms supported linkage. No deletions were observed. Abnormalities of cardiac dystrophin were shown by Western blotting with N-terminal dystrophin antibody, whereas skeletal muscle dystrophin was normal, suggesting primary involvement of the DMD gene with preferential involvement of cardiac muscle.

CONCLUSIONS
XLCM is due to an abnormality within the centromeric half of the dystrophin genomic region in heart. This abnormality could be due to 1) a point mutation in the 5' region of the DMD coding sequence preferentially affecting cardiac function, 2) a cardiac-specific promoter mutation that alters expression in this tissue, 3) splicing abnormalities, resulting in an abnormal cardiac protein, or 4) deletion mutations undetectable by Southern and multiplex polymerase chain reaction analysis.
Increased left ventricular mass after thoracotomy and pericardiotomy. A role for relief of pericardial constraint?
Authors: Tischler M D , Rowan M , LeWinter M M 
Published: June 2012

BACKGROUND
Myocardial stretch and increased ventricular filling can lead to increased rates of myocardial protein synthesis. In animal studies, left ventricular mass increases after pericardiectomy, suggesting relief of a biologically meaningful restraining role and a resultant stimulus for growth. The present study was designed to test the hypothesis that combined thoracotomy and pericardiotomy leads to left ventricular hypertrophy in patients with normal left ventricular ejection fraction undergoing elective bypass surgery.

METHODS AND RESULTS
Twenty-five patients with normal left ventricular ejection fraction without active myocardial ischemia underwent Doppler and quantitative two-dimensional echocardiography 1 day before and 6 weeks and 7 months after elective coronary artery bypass surgery. The pericardium was left widely incised in all patients. Left ventricular end-systolic volume, end-diastolic volume, stroke volume, ejection fraction, end-systolic circumferential wall stress, and mass were measured. Left ventricular end-diastolic volume index increased from 51 +/- 11 mL/m2 to 62 +/- 14 mL/m2 (p < 0.05) at 6 weeks and to 66 +/- 14 mL/m2 (p < 0.05 versus baseline, p = NS versus 6 weeks) at 7 months. Left ventricular mass index increased from 109 +/- 23 g/m2 to 127 +/- 24 g/m2 (p < 0.05) at 6 weeks and to 131 +/- 23 g/m2 (p < 0.05 versus baseline, p = NS versus 6 weeks) at 7 months. There were no changes in systolic or diastolic blood pressures, end-systolic circumferential wall stress, or end-systolic volume.

CONCLUSIONS
Patients with normal left ventricular ejection fraction develop increases in left ventricular end-diastolic volume and mass after coronary artery bypass surgery. These findings support the hypothesis that the increase in left ventricular end-diastolic volume associated with thoracotomy and pericardiotomy leads to myocardial growth and an increase in left ventricular mass.
Intimal thickening of the coronary arteries in infants in relation to family history of coronary artery disease.
Authors: Kaprio J , Norio R , Pesonen E , Sarna S 
Published: June 2012

BACKGROUND
Intimal thickenings of the coronary arteries of newborn children are composed mainly of smooth muscle cell proliferations. To investigate whether thickening of the intima in infants is associated with a family history of coronary artery disease (CAD), we studied the relation of coronary death of grandparents to intimal thickening of 136 infants.

METHODS AND RESULTS
The length of internal elastic lamina of the artery and the areas of arterial layers in cross section were measured, and the arteries were transformed to idealized round circles. Intimal thickening was assessed as the degree of luminal narrowing (ratio of intimal area to the area on the luminal side of the arterial media). Among 136 infants, luminal narrowing varied between 0% and 58%. CAD deaths accounted for 108 of the total 281 deaths among the grandparents of the infants. Family history of CAD (defined as at least one CAD death among the four grandparents) was positive for 77 infants. Family history of CAD was significantly more common in the infants with luminal narrowing of both the left and right coronary arteries compared with the infants with no narrowing in at least one artery (odds ratio adjusted for sex, infection status, and age of infant, 5.69; 95% confidence interval, 1.46-22.2). After adjustment for sex and age, infants with both a positive family history and presence of infection had an increased degree of luminal narrowing compared with infants with a negative family history and no infection.

CONCLUSIONS
The association of coronary artery intimal thickening in infancy with family history of CAD suggests that intimal thickening is a morphological manifestation of predisposition to CAD.
Age thresholds for prophylactic replacement of Björk-Shiley convexo-concave heart valves. A clinical and economic evaluation.
Authors: van der Meulen J H , Steyerberg E W , van der Graaf Y , van Herwerden L A , Verbaan C J , Defauw J J , Habbema J D 
Published: June 2012

BACKGROUND
Björk-Shiley convexo-concave heart valves have an increased risk of mechanical failure. One might consider prophylactic rereplacement as a preventive measure to avert the disastrous consequences of these failures. We investigated the effect that prophylactic rereplacement has on survival of individual patients and on the medical costs.

METHODS AND RESULTS
Quantitative estimates for the surgical risks of prophylactic replacement of Björk-Shiley valves, long-term survival, and the risk of outlet strut fracture were derived insofar as possible from a detailed analysis of a follow-up study conducted in The Netherlands, including 2303 patients with a mean follow-up of 6.6 years. On the basis of these estimates, we calculated life expectancy with and without prophylactic replacement. For the various valve types, age thresholds were determined below which rereplacement prolongs (discounted quality-adjusted) life expectancy. We also calculated the cost per year of life gained as a function of age. The age thresholds below which prophylactic rereplacement increases life expectancy (expressed in simple future years of life) for male patients without comorbidity, if the surgical mortality after rereplacement is equivalent to that of primary replacement, are 27, 48, 51, and 65 years for small and large 60 degrees and for small and large 70 degrees mitral valves, respectively. For aortic valves, these age thresholds lie somewhat higher: 39, 52, 56, and 76 years, respectively. Repeat analyses indicated that for women, all age thresholds lie about 1 or 2 years higher. These age thresholds decrease considerably if the surgical mortality after rereplacement is considered to be higher after prophylactic rereplacement than after primary replacement or if comorbidity is present. The costs per discounted and quality-adjusted year of life gained depend on type and position of the Björk-Shiley convexo-concave heart valve and rise steeply as the patient's age approaches the threshold for rereplacement.

CONCLUSIONS
The results of the Dutch follow-up study allow guidance for prophylactic replacement of the Björk-Shiley convexo-concave valve on an individual basis. Rereplacement compares favorably with expectant management in some patient subgroups with both 60 degrees and 70 degrees valves. Age thresholds may serve as a first step in identifying patients in whom rereplacement might be beneficial.
Heparin accelerates coronary collateral development in a porcine model of coronary artery occlusion.
Authors: Carroll S M , White F C , Roth D M , Bloor C M 
Published: June 2012

BACKGROUND
Coronary collaterals develop in response to an ischemic stimulus. However, collateral growth is not sufficient to result in the complete recovery of coronary reserves. Using a porcine model of gradual coronary artery occlusion, we investigated the effect of continuous heparin infusion on coronary collateral development.

METHODS AND RESULTS
We placed ameroid constrictors on the left circumflex coronary artery of 16 minipigs; the ameroid constrictors completely occluded the left circumflex coronary artery at 10 +/- 1 days. Half of the animals also were instrumented with subcutaneously placed osmotic pumps and catheters that delivered heparin (300 units/h) into the external jugular vein. At 2, 3, and 4 weeks, we assessed blood flow at rest and during vasodilation using radioactive microspheres. Our results indicate that the animals receiving heparin restored resting myocardial blood flow to normal levels at or before 2 weeks; in contrast, we did not see normal resting myocardial blood flow levels in the untreated-ameroid animals until 3 weeks. Under vasodilated conditions, untreated-ameroid animals experienced a severe loss of coronary reserves at 2 weeks. Although this improved with time, these animals still were significantly underperfused at 4 weeks. In contrast, in the heparin-treated animals, coronary reserves returned to near-normal levels between 3 and 4 weeks. In addition, infarct size was significantly smaller in the heparin-treated animals.

CONCLUSIONS
These experiments suggest that the administration of heparin in the early phases of gradual coronary occlusion accelerates the rate of return of normal blood flow under resting conditions, substantially increases the recovery of coronary reserve, and reduces the risk of infarction.
Enhanced revascularization of the ischemic limb by angiogenic therapy.
Authors: Pu L Q , Sniderman A D , Brassard R , Lachapelle K J , Graham A M , Lisbona R , Symes J F 
Published: June 2012

BACKGROUND
This study tests the efficacy of an angiogenic growth factor, endothelial cell growth factor, in a rabbit model of persistent hindlimb ischemia.

METHODS AND RESULTS
Ischemia was induced in the left hindlimb of 22 New Zealand White rabbits by ligation of the distal external iliac artery and complete excision of the common and superficial femoral arteries. Two groups of animals were studied: Group 1 consisted of 11 animals who for 10 days received daily intramuscular injections of 4 mg of endothelial cell growth factor beginning on postoperative day 11, and group 2 consisted of 11 animals who underwent the same surgical ischemic procedure but received only injections of saline daily for the same postoperative period. Perfusion of the ischemic left limb was compared with the normal right limb in each animal on postoperative days 10, 20, 30, and 40 using the calf blood pressure ratio, 99mTc macroaggregate radioisotopic perfusion scans, and serial angiography. Neovascularization in the left thigh at day 40 was quantified from the angiograms. Each technique documented that animals in group 1 had significantly better perfusion than animals in group 2; that is, the calf pressure ratio was higher in group 1 than in group 2 (0.56 versus 0.32 at day 20, 0.64 versus 0.44 at day 30, and 0.70 versus 0.50, P < .0001), and the calf radioisotopic perfusion ratio was also higher in group 1 than in group 2 (0.88 versus 0.74 at day 20, P < .02; 0.93 versus 0.76 at day 30, and 0.96 versus 0.79 at day 40, P < .008). Angiographic studies correlated well with these results demonstrating much earlier distal arterial reconstitution and enhanced neovascularization (23.8 versus 9.0 vessels, P < .007).

CONCLUSIONS
The data clearly indicate that an angiogenic growth factor, endothelial cell growth factor, promotes revascularization in this experimental ischemic hindlimb model, raising the possibility that in the future such agents might be of value in humans.