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The objective of this study was to investigate the prognostic importance of right ventricular dysfunction (RVD) and tricuspid regurgitation (TR) in patients with moderate-severe functional mitral regurgitation (FMR) receiving MitraClip procedure. RVD and TR grade are associated with cardiovascular mortality in the general population and other cardiovascular diseases. However, there are limited data from observational studies on the prognostic significance of RVD and TR in FMR receiving MitraClip procedure.

Emerging treatments for tricuspid valve (TV) regurgitation require realistic TV pathological models for preclinical testing. The aim of this work was to investigate structural features of fresh and defrosted porcine right-heart samples as models of mild and severe functional tricuspid regurgitation (FTR) condition in ex-vivo pulsatile flow platform. Ten fresh hearts were tested ex-vivo under steady and pulsatile flow in typical right-heart loading conditions. Hemodynamics and 3D echocardiographic imaging of TV and right ventricle (RV) were acquired. Hearts were then kept frozen for 14 days, defrosted, and tested again with the same protocol. Morphometric parameters of TV and RV were derived from 3D reconstructions based on echo data. Fresh samples showed a slightly dilated TV morphology, with coaptation gaps among the leaflets. Sample freezing induced worsening of TV insufficiency, with significant (p < 0.05) increases in annulus size (annulus area and perimeter 7.7-3.1% respectively) and dilation of RV (9.5%), which led to an increase in tenting volume (123.7%). These morphologic alterations reflected into a significant increment of regurgitation fraction (27%). Together, such results suggest that fresh porcine heart samples may be a reliable ex-vivo model of mild FTR condition, which can be enhanced through freezing/thawing treatment to model a severe pathological condition.

Clinical studies of a family of Saluki dogs demonstrated a spectrum of cardiac malformations, which ranged from mild thickening of a pulmonic valve leaflet to a complex condition composed of tricuspid valve insufficiency, pulmonic stenosis, patent ductus arteriosus, and mitral valve insufficiency. All affected dogs had patent ductus arteriosus or ductus diverticulum, which is an incomplete or atypical form of patent ductus arteriosus. The clinical findings varied with the type of cardiac lesion(s) found. Pedigree evaluation suggested a genetic cause, though environmental factors could not be excluded.

Nitric oxide synthase-3 (NOS3) has recently been shown to promote endothelial-to-mesenchymal transition (EndMT) in the developing atrioventricular (AV) canal. The present study was aimed to investigate the role of NOS3 in embryonic development of AV valves. We hypothesized that NOS3 promotes embryonic development of AV valves via EndMT. To test this hypothesis, morphological and functional analysis of AV valves were performed in wild-type (WT) and NOS3(-/-) mice at postnatal day 0. Our data show that the overall size and length of mitral and tricuspid valves were decreased in NOS3(-/-) compared with WT mice. Echocardiographic assessment showed significant regurgitation of mitral and tricuspid valves during systole in NOS3(-/-) mice. These phenotypes were all rescued by cardiac specific NOS3 overexpression. To assess EndMT, immunostaining of Snail1 was performed in the embryonic heart. Both total mesenchymal and Snail1(+) cells in the AV cushion were decreased in NOS3(-/-) compared with WT mice at E10.5 and E12.5, which was completely restored by cardiac specific NOS3 overexpression. In cultured embryonic hearts, NOS3 promoted transforming growth factor (TGFβ), bone morphogenetic protein (BMP2) and Snail1expression through cGMP. Furthermore, mesenchymal cell formation and migration from cultured AV cushion explants were decreased in the NOS3(-/-) compared with WT mice. We conclude that NOS3 promotes AV valve formation during embryonic heart development and deficiency in NOS3 results in AV valve insufficiency.

Musculoskeletal injuries are the most common reason for surgery in severely injured patients. In addition to direct cardiac damage after physical trauma, there is rising evidence that trauma induces secondary cardiac structural and functional damage. Previous research associates hip fractures with the appearance of coronary heart disease: As 25% of elderly patients developed a major adverse cardiac event after hip fracture. 20 male pigs underwent femur fracture with operative stabilization via nailing (unreamed, reamed, RIA I and a new RIA II; each group n = 5). Blood samples were collected 6 h after trauma and the concentration of troponin I and heart-type fatty acid binding protein (HFABP) as biomarkers for EMD were measured. At baseline and 6 h after trauma, transesophageal ECHO (TOE) was performed; and invasive arterial and left ventricular blood pressure were measured to evaluate the cardiac function after femur fracture. A systemic elevation of troponin I and HFABP indicate an early myocardial damage after femur fracture in pigs. Furthermore, various changes in systolic (ejection fraction and cardiac output) and diastolic (left ventricular end-diastolic pressure, mitral valve deceleration time and E/A ratio) parameters illustrate the functional impairment of the heart. These findings were accompanied by the development of valvular dysfunction (pulmonary and tricuspid valve). To the best of our knowledge, we described for the first time the development of functional impairment of the heart in the context of EMD after long bone fracture in pigs. Next to troponin and HFABP elevation, alterations in the systolic and diastolic function occurred and were accompanied by pulmonary and tricuspid valvular insufficiency. Regarding EMD, none of the fracture stabilization techniques (unreamed nailing, reaming, RIA I and RIA II) was superior.

Transthoracic and transesophageal echocardiography are important investigations in the intensive care unit (ICU) to diagnose acute cardiac pathologies and assess the haemodynamic status. Recommendations for critical care echocardiography (CCE) have been published recently, but these still lack an evidence-based foundation. It is not known if performing transthoracic echocardiography (TTE) on a routine basis instead of only when required in acute cases is feasible or clinically useful. In this single-centre prospective observational study, we routinely performed TTE on 111 consecutive non-cardiological, non-cardiothoracic surgical ICU patients in two surgical ICUs in a tertiary care facility. Significant cardiac pathologies were detected in 82 (76.6%) and critical cardiac pathologies in 33 (30.8%) of the 107 patients. The most common critical cardiac pathologies were sPAP > 50 mmHg (19.63%), tricuspid annular plane systolic excursion ≤ 13 mm (9.4%), grade III diastolic dysfunction (8.4%), severe tricuspid valve insufficiency (5.6%) and left ventricular ejection fraction (LV-EF) ˂ 30% (4.7%). Some of the most commonly found cardiac pathologies are not well emphasised in current recommendations and training programs. We observed a progression of the cardiac pathologies previously described in 41 of the patients (91.1%). Patients with echocardiographic abnormalities had a significant survival disadvantage in the ICU. By performing CCE routinely, we observed the range and prevalence of cardiac pathologies that can be detected by echocardiography in critically ill patients. We recommend routine transthoracic CCE in ICU patients for early detection of cardiac pathologies and to help inform early intervention regimens, since cardiac conditions carry a significant survival disadvantage for the ICU patient.

We aim to assess the theoretical impact of the atrial flow regulator (AFR) on survival in heart failure.