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RV Failure (rv + failure)
Selected AbstractsExtracorporeal Life Support: A Simple and Effective Weapon for Postcardiotomy Right Ventricular FailureARTIFICIAL ORGANS, Issue 7 2009Kuo-Sheng Liu Abstract Postcardiotomy right ventricular (RV) failure develops during the perioperative period following pulmonary hypertensive crisis or acute myocardial infarction. This study reports our institutional experience in treating these patients with extracorporeal life support (ECLS). Between June 2002 and July 2005, 46 adults were treated with ECLS for postcardiotomy shock. Acute RV failure was the cause of support in 14 (30%). Patient mean age was 55.7 ± 15.4 years. Cardiac pathologies were valvular (n = 7), coronary (n = 1), combined coronary and valvular disease (n = 2), complex congenital heart (n = 2), aortic aneurysm (n = 1), and cardiomyopathy post heart transplant (n = 1). The triggers of RV failure were pulmonary hypertension (n = 6), RV infarction (n = 4), and not defined (n = 4). Patients were supported on ECLS for a mean duration of 71 ± 52 h (range, 10,183 h). Major complications included acute renal failure requiring hemodialysis (n = 4), reexploration for bleeding (n = 2), and acute subdural hematoma (n = 1). Nine (64%) patients were successfully weaned from ECLS, and seven (50%) survived to discharge. Preexisting pulmonary hypertension had a favorable tendency for weaning, and acute renal failure requiring hemodialysis correlated with in-hospital mortality. ECLS is beneficial for treating postcardiotomy RV failure when conventional therapy is exhausted. As it can be deployed rapidly and does not require resternotomy for weaning, ECLS could be regarded as the first choice of mechanical support for postcardiotomy RV failure. [source] Assessment of a New Experimental Model of Isolated Right Ventricular FailureARTIFICIAL ORGANS, Issue 3 2009Petronio G. Thomaz Abstract We assessed a new experimental model of isolated right ventricular (RV) failure, achieved by means of intramyocardial injection of ethanol. RV dysfunction was induced in 13 mongrel dogs via multiple injections of 96% ethanol (total dose 1 mL/kg), all over the inlet and trabecular RV free walls. Hemodynamic and metabolic parameters were evaluated at baseline, after ethanol injection, and on the 14th postoperative day (POD). Echocardiographic parameters were evaluated at baseline, on the sixth POD, and on the 13th POD. The animals were then euthanized for histopathological analysis of the hearts. There was a 15.4% mortality rate. We noticed a decrease in pulmonary blood flow right after RV failure (P = 0.0018), as well as during reoperation on the 14th POD (P = 0.002). The induced RV dysfunction caused an increase in venous lactate levels immediately after ethanol injection and on the 14th POD (P < 0.0003). The echocardiogram revealed a decrease in the RV ejection fraction on the sixth and 13th PODs (P = 0.0001). There was an increased RV end-diastolic volume on the sixth (P = 0.0001) and 13th PODs (P = 0.0084). The right ventricle showed a 74% ± 0.06% transmural infarction area, with necrotic lesions aged 14 days. Intramyocardial ethanol injection has allowed the creation of a reproducible and inexpensive model of RV failure. The hemodynamic, metabolic, and echocardiographic parameters assessed at different protocol times are compatible with severe RV failure. This model may be useful in understanding the pathophysiology of isolated right-sided heart failure, as well as in the assessment of ventricular assist devices. [source] Phenotyping the Right Ventricle in Patients with Pulmonary HypertensionCLINICAL AND TRANSLATIONAL SCIENCE, Issue 4 2009M.S., Marc A. Simon M.D. Abstract Right ventricular (RV) failure is associated with poor outcomes in pulmonary hypertension (PH). We sought to phenotype the RV in PH patients with compensated and decompensated RV function by quantifying regional and global RV structural and functional changes. Twenty-two patients (age 51 ± 11, 14 females, mean pulmonary artery (PA) pressure range 13,79 mmHg) underwent right heart catheterization, echocardiography, and ECG-gated multislice computed tomography of the chest. Patients were divided into three groups: Normal, PH with hemodynamically compensated, and decompensated RV function (PH-C and PH-D, respectively). RV wall thickness (WT) was measured at end-diastole (ED) and end-systole (ES) in three regions: infundibulum, lateral free wall, and inferior free wall. Globally, RV volumes progressively increased from Normal to PH-C to PH-D and RV ejection fraction decreased. Regionally, WT increased and fractional wall thickening (FWT) decreased in a spatially heterogeneous manner. Infundibular wall stress was elevated and FWT was lower regardless of the status of global RV function. In PH, there are significant phenotypic abnormalities in the RV even in the absence of overt hemodynamic RV decompensation. Regional changes in RV structure and function may be early markers of patients at risk for developing RV failure. [source] |