Reduction In End-diastolic Diameter Research Articles

568 Echocardiography and impedance cardiography as determinants of successful slow Levosimendan infusion in patients with acute advanced heart failure

Abstract Aims Despite new therapeutic options, patients with heart failure (HF) still progress to advanced stage. Among new therapeutic options, Levosimendan was recently approved in order to treat patients hospitalized for acute decompensated heart failure (ADHF) with severe systolic dysfunction. The pharmacological effects of Levosimendan consist of inotropy, vasodilatation, and cardioprotection through the increase of calcium sensitivity. These effects should be monitored with echocardiography and in particular with speckle tracking and tri-dimensional echocardiography which appear to be useful in LV systolic function detection and monitoring. In this study we aim to evaluate the effect of slow infusion of Levosimendan on the non-invasive measurement of cardiac output, the speckle tracking parameters and the tri-dimensional echocardiography measurements in advanced ADHF patients. Methods and results This is a prospective observational study evaluating Levosimendan efficacy through advanced echocardiography. We enrolled 11 patients with diagnosis of ADHF who respect the recent ESC criteria of ‘advanced heart failure’. Patients underwent to blood sample examination to measure electrolytes, creatinine, and NTproBNP. Patients underwent to advanced echocardiography examination (performed for each patient pre- and post-Levosimendan infusion) with tri-dimensional echocardiography and global longitudinal strain assessment. Furthermore patients underwent to non-invasive cardiac output and cardiac index collection through impedance cardiography pre- and post-Levosimendan infusion. All patients were followed for 30 days after discharge for all cause of mortality and HF re-hospitalization. A total of 11 patients affected by advanced ADHF were included in this study. Mean age was 73.8 ± 4.7 years. 72.7% (n 8) patients were men. 81.9% (n 9) of patients recognize ischaemic heart disease as HF etiology. At admission mean systolic arterial pressure was 100 ± 17 mmHg, mean NTproBNP was 24 445 ± 12 194 pg/ml and mean serum creatinine was 1.55 ± 0.84 mg/dl. At tri-dimensional echocardiography mean LV ejection fraction (LVEF) was 19.7 ± 5.7% and at bi-dimensional echocardiography mean tricuspid anular plane systolic excursion (TAPSE) and pulmonary arterial systolic pressure (PASP) were, respectively, 12.5 ± 2.7 mm and 48 ± 16 mmHg. Mean LV global longitudinal strain (GLS) was −3.0 ± 1.8. Mean furosemide in-hospital infusion was 306 ± 102 mg/die and mean urine output 1436 ± 496 ml. None developed significant ventricular or supraventricular arrhythmias. All patients were treated with betablockers during infusion. At 30 days of follow-up two patients died and 1 patient was re-hospitalized. Evaluating the differences among our variables pre- and post-Levosimendan infusion, we found that NTproBNP was significantly reduced post-Levosimendan infusion (P = 0.01). Among ICG non-invasive measurement, we found significant differences in stroke volume (SV) and cardiac output (CO) in terms of significant improvement (P = 0.001 for both). Analysing tri-dimensional echocardiography variables, we observed a significant improvement of LVEF (P = 0.003), SV (P = 0.03) and 3-D LV GLS (P = 0.002). Furthermore, we observed a significant reduction in end-systolic volume (ESV) post-Levosimendan infusion (P = 0.02). Among bi-dimensional echocardiography measurements, there was a significant reduction in end-diastolic diameter of right ventricle (EDDRV) and in B-lines count (respectively, P = 0.02 and P = 0.002). Moreover, we observed a significant improvement in TAPSE (P = 0.003) and in LV GLS (P = 0.004). Conclusions Our study showed that slow Levosimendan infusion (12.5 mg at velocity of 0.05–1 mcg/kg/min) without bolus could be considered in advanced ADHF patients to improve cardiac performance without severe adverse events. ICG and echocardiography in-hospital evaluation seemed to be necessary to understand treatment success and patients status improvement as well as cardiac function benefit.

Abstract 16795: A Trans-Ventricular Restraint to Reshape and Reduce the Left Ventricle Halts Chronic Adverse Remodeling in a Rodent Model of Ischemic Cardiomyopathy

Introduction: Elevated wall stress (WS) from chamber dilatation and wall thinning drive cause congestive heart failure(CHF) after a myocardial infarction(MI). Reducing WS by reshaping the left ventricle (LV) could decelerate or halt CHF progression, delaying need for ventricular assist devices or transplantation. In this study, we sought to investigate if a transventricular reshaping device (TRD - Fig 1A,B ) can preserve cardiac function and inhibit adverse remodeling in a rodent model of chronic ischemic cardiomyopathy. Hypothesis: Reducing left ventricular WS and sphericity index (SI) can preserve cardiac function and inhibit adverse remodeling in ischemic cardiomyopathy. Methods: Rats (n=18) were induced with an MI by left coronary artery ligation. 3 weeks post-MI, TRD was implanted on a beating heart in 9 rats (MI+TRD) ( Fig 2A-C ) and no surgery in others (MI only).TRD was tightened with echo, for 25% reduction in end-diastolic diameter and in WS. All rats were survived for another 3 weeks, with echo at 0, 2, 4, 6 weeks post-MI, and invasive hemodynamics at termination. Tissue was snap frozen for RNA-seq analysis. Results: Cardiac dysfunction were confirmed in both groups prior to TRD implantation (%EF in MI+TRD: 77.4±1.2vs. 59.6±2.1; p<0.0001; %EF in MI: 74.7±1.8 vs. 57.0±3.3; p=0.0002 ). TRD implantation and tightening, reduced LVEDD from 8.7±0.2mm to 6.7±0.2mm (23% change, p <0.0001), reduced sphericity index from 0.74±0.04 to 0.54±0.05 (27% reduction, p<0.0001), and WS from 19.9±2.0 to 14.5±1.7 (27% decrease, p=0.0662) ( Fig 3A-B ). At termination, EDV and ESV were significantly reduced in MI+TRD compared to MI alone (EDV: 647.5±39.0μl vs 500.1±14.4μl; p=0.0032; 317.5±16.9 μl vs 218.1±14.7 μl; p=0.0021), indicating halted adverse remodeling with TRD ( Fig 4A-B ). Infarct border zone wall thickness was preserved in MI+TRD, but significantly reduced/thinned in MI ( Fig 5A ), containing infarct expansion. Pre-load adjusted LV dp/dt(max), was significantly higher in MI+TRD compared to MI only ( Fig 5B ). Conclusions: Reshaping and reducing the ischemic LV with the transventricular restraint, improves cardiac contractility, preserves ventricular wall thickness and inhibits infarct expansion in this chronic rodent model of cardiomyopathy.

Hemodynamic, Echocardiographic, and Exercise‐Related Effects of the HeartWare Left Ventricular Assist Device in Advanced Heart Failure

The aim of this study was to determine the effects of the HeartWare left ventricular assist device (HVAD) (HeartWare International, Inc, Framingham, MA) on hemodynamics, ventricular function, and exercise capacity. Between July 2009 and March 2011, 46 patients with advanced heart failure had implantation of the HVAD. Of these patients, 30 had subsequent assessments for transplantation and these patients formed the study cohort. Thirty patients had assessments at a mean of 201±86 days and 13 went on to have a second assessment at 351±86 days. There were marked improvements in hemodynamics and exercise capacity at both assessments, with significant decreases in right and left heart filling pressures; increases in cardiac index, New York Heart Association class, and peak exercise oxygen consumption; and reduction in pulmonary vascular resistance (all P<.05). Left ventricular end-diastolic and end-systolic dimensions were unchanged at the first assessment, although there was a significant reduction in end-diastolic diameter at the second assessment (P<.01). There were no significant changes in a visual grade of right ventricular function. After up to 1 year of support, the HVAD system results in significant benefits in overall heart failure status, with improved hemodynamics and exercise capacity. This occurs in the absence of marked changes in left ventricular size or right ventricular function.

Clinical outcomes of mitral valve repair with the Colvin–Galloway Future Band: a single-center experience

In 2001, a semirigid band (Colvin-Galloway Future Band, Medtronic, Inc., Minneapolis, Minnesota, USA) for mitral valve repair came onto the market. We report our experience of the correction of all types of mitral regurgitation using this device. From August 2003 to December 2006, 140 patients (71% men, mean age 64 +/- 11 years) underwent valvuloplasty with this device for all types of mitral regurgitation: 94 (67%) degenerative, 34 (24%) postischemic, 11 (8%) dilative cardiomyopathy, and one (1%) postendocarditic. The patients underwent clinical and echocardiographic evaluation preoperatively, postoperatively before discharge, and after a median follow-up of 7 months (25th-75th percentile, 4-24 months). Total mortality was 6.4% (nine out of 140 patients): four patients (2.8%) died within 30 days (early death) and five died subsequently (the cause was cardiac in one case). Predischarge echocardiographic examination revealed a reduction in mitral regurgitation of at least 2 degrees in 99.2% of patients and the absence of systolic anterior movement. At the last follow-up, we recorded an improvement in New York Heart Association functional class (2.4 +/- 0.9 vs. 1.1 +/- 0.4, P < 0.0001), a significant reduction in the degree of mitral regurgitation (3.5 +/- 0.9 vs. 0.9 +/- 0.5, P < 0.0001), an increase in ejection fraction (54 +/- 11 vs. 55 +/- 9, P = 0.09), and a significant reduction in end-diastolic diameter (59 +/- 6 vs. 55 +/- 6, P < 0.0001). Two patients were reoperated on for mitral valve replacement, and no postoperative thromboembolic events occurred. Our experience shows that the Colvin-Galloway Future Band yields good results in mitral valvuloplasty for all types of mitral regurgitation. We are encouraged to continue using this device.

Structural changes in the auricles of the rat heart after local ionizing irradiation

Background and purpose: Irradiation of the heart may lead to late cardiovascular complications and depending on the dose to cardiac-related death. There is increasing evidence that left atrial appendages play an important role in left ventricular filling especially in cardiac disease. The aim of the present study was to investigate the radiation response of the atria of the rat heart (auricles in particular) at morphological, histological and transcriptional level. Material and methods: Spraque–Dawley rats were irradiated with a single dose locally on the heart (0–22.5 Gy). End-diastolic diameters of left auricles were measured during evaluation of cardiac function. Histopathological evaluations were performed at various time points up to 16 months post irradiation. Changes in mRNA expression of procollagen types I and III and pro-fibrogenic cytokines (TGF-β1 and IL-1β) were investigated using competitive PCR. Results: Irradiation leads to a dose-dependent decrease in end-diastolic diameter of the left auricles. This decrease was observed at 4 months post-irradiation, where no gross damage of the ventricle has been reported. Histologically, epicardial fibrosis was found already 1 month post irradiation, and the frequency/severity of the structural changes appeared to be dose-dependent and progressive with time post irradiation. At 9 months, fibrosis was observed in all three layers (epicardium, myocardium and endocardium) of both auricles. On the level of gene expression, increases in procollagen types I and III were observed at 12 and 3 months post irradiation, respectively. Increases in IL-1β and TGF-β1, cytokines known to influence collagen deposition at different levels, preceded the upregulation of procollagen mRNA. Conclusions: Auricles of the rat heart show a marked pathological response to ionizing radiation, characterized by generalized accumulation of collagen (fibrosis) and a reduction of end-diastolic diameter. The reduction of auricular volume and loss of elasticity will negatively contribute to the pump function of the irradiated ventricle.