bluuebunny/crossref_metadata_2025_split huggingface dataset:
Left ventricular diastolic Doppler characteristics in beta-thalassemia major.
Authors: Kremastinos D T , Tsiapras D P , Tsetsos G A , Rentoukas E I , Vretou H P , Toutouzas P K 
Published: June 2012

BACKGROUND
Diastolic left ventricular function expressed by diastolic Doppler characteristics of the left ventricle has never been properly investigated.

METHODS AND RESULTS
Left ventricular inflow and pulmonary vein flow patterns were assessed by Doppler echocardiography in 88 beta-thalassemia major patients with normal left ventricular systolic function; 34 were young (age, 15.1 +/- 3.2 years) and 54 were adults (age, 25.1 +/- 3.6 years). The findings were compared with those obtained from 22 young (age, 13.8 +/- 2.4 years) and 24 adult (age, 25.3 +/- 4.1 years) normal individuals. In both groups of patients, peak flow velocities in early (E) and late (A) diastole were higher than in the control subjects (young E: P < .01; adult E: P < .001; young A: P < .05; adult A: P < .05), whereas no difference was found in the E/A ratio, deceleration time, or isovolumic relaxation time. Pulmonary vein systolic (S) and diastolic (D) velocities were also higher in beta-thalassemia major patients compared with the control subjects (young S: P < .05; adult S: P < .05; young D: P < .05; adult D: P < .05). Restrictive left ventricular abnormalities were only found in 7 patients who were among the oldest beta-thalassemia major population of the adult group (P < .01) with highly elevated mean serum ferritin. In comparison to the remaining adult patients, interventricular septum and left ventricular posterior wall thickness were increased (P < .01 and P < .01, respectively). The left atrium and right ventricle were dilated (P < .05 and P < .01, respectively).

CONCLUSIONS
Doppler diastolic indexes in beta-thalassemia major patients with normal left ventricular systolic function are similar to those seen in conditions with an increased preload, probably because of chronic anemia. Only severe iron loading and deposition in the myocardium leads to the restrictive abnormalities of left ventricular filling.
On-line assessment of left atrial area and function by echocardiographic automatic boundary detection.
Authors: Waggoner A D , Barzilai B , Miller J G , Pérez J E 
Published: June 2012

BACKGROUND
Direct assessment of left atrial (LA) function has not been previously performed by noninvasive techniques; rather, LA function has been evaluated only indirectly via the analysis of transmitral flow velocity by Doppler. The recent development of real-time two-dimensional echocardiographic automatic boundary detection suggests that LA dimensions can be measured instantaneously to provide on-line assessment of its systolic and diastolic functions.

METHODS AND RESULTS
We performed echocardiographic assessment of LA dimensions and function with automatic boundary detection in 45 patients by using the apical four-chamber view. Thirty-seven patients had structural or functional cardiac abnormalities, 35 patients were in sinus rhythm, and 10 patients had atrial fibrillation. Moderate to severe mitral regurgitation (MR) was noted in 16 patients. We also studied 10 control subjects to assess normal values of LA cavity area and indexes of function. From the instantaneously derived LA area, we derived indexes of systolic atrial expansion and diastolic atrial emptying. There were excellent correlations between the on-line-derived LA areas and those measured off line from videotaped images of conventional echocardiography (r = .91 for end-diastolic and .93 for end-systolic areas; SEE, 4.0 and 3.8 cm2, respectively). Patients in atrial fibrillation had depressed diastolic emptying index (0.17 +/- 0.05) compared with those in sinus rhythm (0.28 +/- 0.12; P < .02). Furthermore, patients with chronic MR exhibited larger LA cavity areas and depressed systolic and diastolic LA function as compared with those without MR. In addition, the Doppler-determined mitral E/A ratio was related to the ratio of early diastolic-to-late diastolic change in LA cavity area (r = .79; SEE 0.6; n = 35).

CONCLUSIONS
Instantaneous LA cavity area measurement by echocardiographic automatic boundary detection is accurate and feasible in patients with diverse cardiac disorders. Patients with atrial fibrillation had a depressed diastolic emptying index and those with significant mitral regurgitation had depressed systolic expansion index as well. LA functional indexes in both systole and diastole can be derived providing an approach for quantitative evaluations of left atrial-left ventricular interactions based on geometric assessment noninvasively.
Effect of endothelin-1 on neutrophil adhesion to endothelial cells and perfused heart.
Authors: López Farré A , Riesco A , Espinosa G , Digiuni E , Cernadas M R , Alvarez V , Montón M , Rivas F , Gallego M J , Egido J 
Published: June 2012

BACKGROUND
Based on recent evidence showing that endothelin-1 stimulates several activation mechanisms on neutrophils, the aim of the present study was to analyze the effects of endothelin-1 on neutrophil adhesion to endothelial cells and neutrophil accumulation in the heart.

METHODS AND RESULTS
The experiments included (1) adhesion of 51Cr-labeled human neutrophils to bovine endothelial cells in culture both in the presence and absence of monoclonal antibodies against the alpha- and beta-subunits of integrins; (2) surface expression of the alpha- and beta-integrin antigens; (3) accumulation of 51Cr-labeled neutrophils on the isolated perfused rabbit heart; (4) in vivo accumulation of autologous neutrophils in the heart, as assessed by myeloperoxidase activity. Endothelin-1 stimulated neutrophil adhesion to endothelial cells (increase of 1 x 10(5) +/- 1 x 10(4) neutrophils per well). The endothelin-1-induced adhesion was blocked (83 +/- 6%) by the anti-CD18 antibody TS1/18 and by several anti-alpha-subunit antibodies. The expression of CD18 and CD11b on the neutrophil surface was also increased by endothelin-1. Endothelin-1 enhanced neutrophil accumulation in the isolated rabbit heart by 4.2 times throughout a TS1/18-inhibitable mechanism. Myeloperoxidase activity increased by 4.2 times in hearts infused in vivo with endothelin-1.

CONCLUSIONS
Endothelin-1 stimulates neutrophil adhesion to endothelial cells by an effect on the expression of adhesive molecules on the neutrophil surface. Endothelin-1 stimulates neutrophil accumulation in vivo and in vitro in the heart. Antibodies against the integrin complex block the endothelin-1-dependent neutrophil adhesion. These findings have potential importance in the pathophysiology of endothelin-1-increased states.
Pinacidil-induced electrical heterogeneity and extrasystolic activity in canine ventricular tissues. Does activation of ATP-regulated potassium current promote phase 2 reentry?
Authors: Di Diego J M , Antzelevitch C 
Published: June 2012

BACKGROUND
Pinacidil is known to augment a time-independent outward current in cardiac tissues by activating the ATP-regulated potassium channels. Activation of this current, IK-ATP, is thought to be responsible for increased potassium permeability in ischemia. The contribution of IK-ATP activation to arrhythmogenesis and the role of activation of this current in suppression of arrhythmias are areas of great interest and debate. Because electrical depression attending myocardial ischemia is more accentuated in ventricular epicardium than in endocardium, we endeavored to contrast the effects of pinacidil-induced IK-ATP activation on the electrophysiology of canine ventricular epicardium and endocardium.

METHODS AND RESULTS
Standard microelectrode techniques were used. Pinacidil (1 to 5 mumol/L) produced a marked dispersion of repolarization and refractoriness in isolated canine ventricular epicardium as well as between epicardium and endocardium. In endocardium, pinacidil abbreviated action potential duration (APD90) and refractoriness by 8.0 +/- 2.3%. In epicardium, the effects of pinacidil were nonhomogeneous. At some sites, pinacidil induced an all-or-none repolarization at the end of phase 1 of the action potential, resulting in 55.5 +/- 8.7% abbreviation of APD90 and refractoriness. Adjacent to these were sites at which the dome was maintained with only minor changes in APD and refractoriness. Extrasystolic activity displaying features of reentry was observed in isolated sheets of epicardium (63.2%) after exposure to pinacidil (1 to 5 mumol/L) but never in its absence. Dispersion of repolarization and ectopic activity was most readily induced in epicardium by a slowing of the stimulation rate in the presence of pinacidil. Electrical homogeneity was restored and arrhythmias abolished after washout of pinacidil or addition of either a transient outward current blocker, 4-aminopyridine, or a blocker of the ATP-regulated potassium channels, glybenclamide.

CONCLUSIONS
Our data suggest that the activation of IK-ATP can produce a marked dispersion of repolarization and refractoriness in epicardium as well as between epicardium and endocardium, leading to the development of extrasystolic activity via a mechanism that we have called phase 2 reentry. The available data also suggest that blockade of the transient outward current and/or the ATP-regulated potassium channels may be useful antiarrhythmic interventions under ischemic or "ATP depleted" conditions.
Angiotensin I and II exert inotropic effects in atrial but not in ventricular human myocardium. An in vitro study under physiological experimental conditions.
Authors: Holubarsch C , Hasenfuss G , Schmidt-Schweda S , Knorr A , Pieske B , Ruf T , Fasol R , Just H 
Published: June 2012

BACKGROUND
The renin-angiotensin system with its renal-humoral and local myocardial components plays an important role in the development and progression of chronic heart failure. Whereas angiotensin receptors have been found in atrial and ventricular myocardium of different species including humans, its influence on myocardial contractility is not yet defined in human failing myocardium and especially in human nonfailing myocardium.

METHODS AND RESULTS
We measured force development of right atrial and right and left ventricular myocardial preparations of patients with a variety of cardiac diseases. To evaluate the physiological effects of angiotensin, experimental temperature and stimulation rates were 37 degrees C and 60 beats per minute, respectively. Angiotensin I and II increased peak developed force in atrial myocardial preparations obtained from patients without heart failure in a concentration-dependent manner. At optimal concentrations, peak developed force is increased from 10.2 +/- 1.8 to 12.3 +/- 1.9 mN/mm2 by angiotensin I (P < .05) and from 15.4 +/- 2.1 to 20.5 +/- 3.3 mN/mm2 by angiotensin II (P < .05). This effect was not influenced by pretreatment with propranolol (10(-6) mol/L) and prazosin (10(-5) mol/L) but was completely blocked by saralasin (10(-6) mol/L). The positive inotropic effect of angiotensin I could be blocked by enalaprilate (10(-5) mol/L). Neither angiotensin I nor angiotensin II had any effect in preparations of the left ventricle from patients with idiopathic dilated cardiomyopathy, mitral valve stenosis, and incompetence or in patients with no significant heart disease. Additionally, no effect could be seen when angiotensin II was applied to right ventricular preparations from infants undergoing reconstructive heart surgery for tetralogy of Fallot.

CONCLUSIONS
Angiotensin I and II exert positive inotropic effects via angiotensin receptors in atrial preparations but not in right or left ventricular preparations. Furthermore, the existence of a local myocardial angiotensin converting enzyme with functional importance is shown.
Effects of active compression-decompression resuscitation on myocardial and cerebral blood flow in pigs.
Authors: Lindner K H , Pfenninger E G , Lurie K G , Schürmann W , Lindner I M , Ahnefeld F W 
Published: June 2012

BACKGROUND
This study was designed to assess the effects of a modified cardiopulmonary resuscitation (CPR) technique that consists of both active compression and active decompression of the chest (ACD CPR) versus standard CPR (STD CPR) on myocardial and cerebral blood flow during ventricular fibrillation both before and after epinephrine administration.

METHODS AND RESULTS
During a 30-second period of ventricular fibrillation cardiac arrest, 14 pigs were randomized to receive either STD CPR (n = 7) or ACD CPR (n = 7). Both STD and ACD CPR were performed using an automated pneumatic piston device applied midsternum, designed to provide either active chest compression (1.5 to 2.0 in.) and decompression or only active compression of the chest at 80 compressions per minute and 50% duty cycle. Using radiolabeled microspheres, median total myocardial blood flow after 5 minutes of ventricular fibrillation was 14 (7 to 30, minimum to maximum) STD CPR versus 30 (9 to 46) mL.min-1 x 100 g-1 with ACD CPR (P < .05). Median cerebral blood flow was 15 (10 to 26) mL.min-1 x 100 g-1 with STD CPR and 30 (21 to 39) with ACD CPR (P < .01). When comparing STD with ACD CPR, aortic systolic (62 mm Hg [48 to 70] vs 80 [59 to 86]) and diastolic (22 [18 to 28] vs 28 [21 to 36]) pressures, calculated coronary systolic (30 [22 to 36] vs 49 [37 to 56]) and diastolic (18 [16 to 23] vs 26 [21 to 31]) perfusion pressures, end-tidal CO2 (1.4% [0.8 to 1.8] vs 2.1 (1.8 to 2.4]), cerebral O2 delivery (3.1 mL.min-1 x 100 g-1 [1.5 to 4.5] vs 5.3 [3.8 to 7.5]), and cerebral perfusion pressure (14 mm Hg [4 to 22] vs 26 [6 to 34]) were all significantly higher with ACD CPR: To compare these parameters before and after vasopressor therapy, a bolus of high-dose epinephrine (0.2 mg/kg) was given to all animals after 5 minutes of ventricular fibrillation. Organ blood flow and calculated perfusion pressures increased significantly in both the STD and ACD groups after epinephrine. The differences observed between STD and ACD CPR before epinephrine were diminished 90 seconds after epinephrine but were again statistically significant when assessed 5 minutes later, once the acute effects of epinephrine had decreased. No difference in short-term resuscitation success was found between the two groups.

CONCLUSIONS
We conclude that ACD CPR significantly increases myocardial and cerebral blood flow during cardiac arrest in the absence of vasopressor therapy compared with STD CPR:
Luminal narrowing after percutaneous transluminal coronary angioplasty. A study of clinical, procedural, and lesional factors related to long-term angiographic outcome. Coronary Artery Restenosis Prevention on Repeated Thromboxane Antagonism (CARPORT) Study Group.
Authors: Rensing B J , Hermans W R , Vos J , Tijssen J G , Rutch W , Danchin N , Heyndrickx G R , Mast E G , Wijns W , Serruys P W 
Published: June 2012

BACKGROUND
The renarrowing process after successful percutaneous transluminal coronary angioplasty (PTCA) is now believed to be caused by a response-to-injury vessel wall reaction. The magnitude of this process can be assessed by the change in minimal lumen diameter (MLD) at follow-up angiography. The aim of the present study was to find independent patient-related, lesion-related, and procedure-related risk factors for this luminal narrowing process. A model that accurately predicts the amount of luminal narrowing could be an aid in patient or lesion selection for the procedure, and it could improve assessment of medium-term (6 months) prognosis. Modification or control of the identified risk factors could reduce overall restenosis rates, and it could assist in the selection of patients at risk for a large loss in lumen diameter. This population could then constitute the target population for pharmacological intervention studies.

METHODS AND RESULTS
Quantitative angiography was performed on 666 successfully dilated lesions at angioplasty and at 6-month follow-up. Multivariate linear regression analysis was performed to obtain variables with an independent contribution to the prediction of the absolute change in minimal lumen diameter. Diabetes mellitus, duration of angina < 2.3 months, gain in MLD at angioplasty, pre-PTCA MLD, lesion length > or = 6.8 mm, and thrombus after PTCA were independently predictive of change in MLD. Overall prediction of the model was poor, however, percentage-correct classification for a predicted change between -0.1 to -0.4 mm was approximately 10%. Lesions showing no change or regression (change > -0.1 mm) and lesions showing large progression (< or = -0.4 mm) were more predictable (correct classification, 59.5% and 49.7%, respectively).

CONCLUSIONS
Renarrowing after successful PTCA as determined with contrast angiography is a process that cannot be accurately predicted by simple clinical, morphological, and lesion characteristics.
Transcatheter occlusion of patent ductus arteriosus with Gianturco coils.
Authors: Lloyd T R , Fedderly R , Mendelsohn A M , Sandhu S K , Beekman R H 
Published: June 2012

BACKGROUND
Transcatheter occlusion with Gianturco coils has been attempted in a small number of patients with tiny (< or = 1.5-mm diameter) patent ductus arteriosus, and preliminary results have been encouraging. The present study extends this method to larger ductus sizes and makes recommendations for proper coil size selection.

METHODS AND RESULTS
Coil occlusion was attempted in 24 consecutive patients with patent ductus arteriosus who did not require other cardiac surgery. Median patient age was 4.2 years (8 months to 30 years), and mean ductus diameter was 1.7 +/- 0.8 mm. Two instances of coil embolization occurred in the first 4 patients, with successful coil retrieval. Based on this experience, we proposed that the coil helical diameter should be twice or more the minimum ductus diameter, with coil length sufficient for three or more loops. With these recommendations, coils were successfully implanted in the subsequent 20 consecutive patients. Of the 22 patients with successful coil implantation, 15 (68%) had no residual shunting, and 7 had trace residual shunting by angiography. The continuous murmur was abolished in all 22 patients. No significant complications occurred, and all patients were discharged within 24 hours of successful coil implantation. No change in the systolic pressure gradient between main and left pulmonary artery or ascending and descending aorta was observed.

CONCLUSIONS
Transcatheter occlusion of patent ductus arteriosus can be safely and effectively achieved in patients with ductus diameters up to 3.3 mm. Coil occlusion does not cause obstruction to flow in the left pulmonary artery or descending aorta. Coils should be selected to provide a helical diameter twice or more the minimum ductus diameter and a length sufficient for three or more loops.
Lipids and lipoproteins predicting coronary heart disease mortality and morbidity in patients with non-insulin-dependent diabetes.
Authors: Laakso M , Lehto S , Penttilä I , Pyörälä K 
Published: June 2012

BACKGROUND
The aim of this study was to investigate the association of lipoprotein fractions with the future risk of coronary heart disease (CHD) in patients with non-insulin-dependent diabetes (NIDDM).

METHODS AND RESULTS
At baseline, lipoprotein fractions were determined in 313 diabetic patients with NIDDM (153 men and 160 women), and these patients were followed up for 7 years with respect to CHD events (CHD death or all CHD events including CHD death or nonfatal myocardial infarction). Altogether, 56 NIDDM patients (28 men and 28 women) died from CHD and 25 had a nonfatal myocardial infarction (17 men and 8 women) during the follow-up. NIDDM patients having these CHD events during the follow-up had higher levels of total and very-low-density lipoprotein (VLDL) triglycerides and VLDL cholesterol and lower levels of high-density lipoprotein (HDL) and HDL2 cholesterol than those without CHD events. The risk for CHD death was fourfold and for all CHD events, twofold higher among diabetics with low HDL cholesterol (< 0.9 mmol/L) than among diabetics with HDL cholesterol > or = 0.9 mmol/L. High triglyceride level (> 2.3 mmol/L) was associated with a twofold increase in the risk of CHD events. In multiple logistic regression analyses, HDL was inversely associated with CHD events and VLDL triglycerides with CHD events in NIDDM patients with low HDL cholesterol level (< or = 1.12 mmol/L).

CONCLUSIONS
Our 7-year follow-up study gives evidence that low HDL and HDL2 cholesterol, high VLDL cholesterol, and high total and VLDL triglycerides are powerful risk indicators for CHD events in patients with NIDDM:
Insulin resistance is an important determinant of left ventricular mass in the obese.
Authors: Sasson Z , Rasooly Y , Bhesania T , Rasooly I 
Published: June 2012

BACKGROUND
Obesity in adults is associated with increased left ventricular (LV) mass. The mechanism for this is unclear, however. We tested the hypothesis that insulin resistance is an important independent contributing factor to LV mass in the healthy obese population.

METHODS AND RESULTS
The study population consisted of 40 normotensive, nondiabetic, otherwise healthy obese subjects with body mass index (BMI) > 25 kg/m2. LV mass was echocardiographically determined according to the Penn convention, using the formula of Devereux and Reichek. Insulin resistance was assessed using indices derived from Intravenous Glucose Tolerance Test (IVGTT): insulin level at baseline, insulin level at 90 minutes of IVGTT (insulin-90), insulin integration over 90 minutes of IVGTT, and rate of glucose disposal (k value). Insulin-90 (r = .61, P = .0001), k value (r = .55, P = .003), insulin integration over 90 minutes (r = .46, P = .003), basal insulin (r = .44, P = .005), and BMI (r = .59, P = .0001) were all strongly correlated with LV mass by univariate analysis. No significant correlation was found with blood pressure or age. In multivariate regression analysis, only insulin-90 and k value correlated significantly with LV mass (P = .03, P = .02, respectively), accounting for 50% of the variance of LV mass, whereas the association with BMI became insignificant (P = .2).

CONCLUSIONS
LV mass in the normotensive nondiabetic obese population is strongly associated with, and may be mediated by, the degree of insulin resistance and its associated hyperinsulinemia, independent of BMI and blood pressure.