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Mitral regurgitation(MR) imposes left ventricular (LV)volume overload, triggering rapid ventricular dilatation, increased myocardial compliance and ultimately cardiac dysfunction. Breakdown of extracellular matrix(ECM) is hypothesized to drive these rapid changes, partially from an imbalance in the matrix metalloproteinases(MMPs) and their tissue inhibitors(TIMPs). In this study, we developed a rat model of severe MR that mimics the human condition, and investigated the temporal changes in ECM related genes, collagen biosynthesis proteins, and proteolytic enzymes, over 20 weeks. Male Sprague-Dawley rats were anesthetized to a surgical plane with mechanical ventilation, and a thoracotomy was performed to expose the apex. Using transesophageal ultrasound guidance, a needle was inserted into the beating heart to perforate the anterior mitral leaflet and create severe MR. Animals were survived for 20 weeks, with some animals terminated at 2,10 and 20 weeks for analysis of LV tissue. A sham group that underwent the same surgery without mitral leaflet perforation and MR were used as controls. At 2 weeks post-MR, increased collagen gene expression was measured, but protein levels of collagen did not corroborate this finding. In parallel, MMP1-TIMP4, MMP2-TIMP1, MMP2-TIMP3 ratios were significantly elevated indicating a proteolytic milieu in the myocardium, possibly causing collagen degradation. By 20 weeks, may of the initial differences seen in the proteolytic ratios were not observed, with an increase in collagen compared to the 2-week timepoint. Altogether this data indicates that imbalance in MMP-TIMP ratio may occur early and potentially contribute to the early dilatation and compliance observed structurally.

Background: Undersizing mitral annuloplasty (UMA) to repair functional mitral regurgitation (FMR) lacks durability, as it forces leaflet coaptation without relieving the subleaflet tethering forces. In this biomechanical study, we demonstrate that papillary muscle approximation (PMA) before UMA can drastically relieve tethering forces and improve valve function, without the need for significant annular downsizing.Methods: An ex vivo model of FMR was used, in which pig mitral valves were geometrically perturbed to induce FMR, and the repairs were performed. Nine pig mitral valves were studied in the following sequence: normal (baseline), FMR, true-sized annuloplasty to 30 mm (true-sized ring [TSR]), and undersized annuloplasty to 26 mm (down-sized ring [DSR]), along with concomitant PMA at both ring sizes. Mitral regurgitation, valve kinematics, and chordal forces were measured and compared among the groups.Results: FMR geometry induced a mean regurgitant fraction of 16.31 AE 7.33% compared with 0% at baseline. TSR reduced the regurgitant fraction to 6.05 AE 5.63%, whereas DSR reduced it to 5.06 AE 6.76%. The addition of PMA before the use of these rings reduced the mean regurgitant fraction to 3.87 AE 6.79% with the TSR (TSR þ PMA) and 3.71 AE 6.25% with the DSR (DSR þ PMA). Mean peak anterior and posterior marginal chordal forces were elevated to 0.09 AE 0.1 N and 0.12 AE 0.1 N, respectively, with FMR and were not reduced by annuloplasty of either sizes. The addition of PMA significantly reduced these forces to 0.23 AE 0.02 N and 0.51 AE 0.04 N.

Right heart thrombus represents a mobilized deep venous thrombosis that is lodged temporarily in the right atrium and ventricle, and is often referred to as "emboli in transit." Floating right heart thrombus is an uncommon but life-threatening condition, and usually coexists with an already massive pulmonary embolism. The presence of floating right heart thrombus appears to substantially increase the risk of mortality compared to the presence of pulmonary embolism alone. Floating right heart thrombus needs emergency treatment, but there is no clear consensus regarding optimal management, e.g., thrombolytic therapy, anticoagulation therapy, or surgical removal. We present the case of an 80-year-old female with a floating right heart thrombus in conjunction with an acute massive pulmonary embolism, who presented in cardiogenic shock. We successfully carried out surgical embolectomy. The patient's postoperative course was uneventful, and she remained in good health without recurrence of pulmonary embolism. This success was based on rapid diagnosis by transthoracic echocardiography and computed tomography, prompt decision-making to proceed with surgical intervention and efficient postoperative care. In this case, surgical embolectomy was effective for a floating right heart thrombus with acute massive pulmonary embolism.Keywords: thrombus, right heart, pulmonary embolism, surgical embolectomy IntroductionFloating right heart thrombus (FRHTh) is uncommon, and is generally diagnosed when echocardiography is performed in patients with suspected or proven pulmonary embolism (PE). FRHTh is regarded as being in transit from the legs to the pulmonary arteries and thus is a form of venous thromboembolic disease. 1�2�Mortality rates with FRHTh are high, at over 40% of cases.3� Moreover, the presence of FRHTh appears to substantially increase the risk of mortality compared to the presence of PE alone. 4� The thrombus is very unstable, and migration towards the pulmonary trunk is often fatal. 5�6� Thus FRHTh needs emergency treatment; however, there is no clear consensus regarding optimal management, e.g., thrombolytic therapy, anticoagulation therapy, or surgical removal. 3�4� We herein present the case of a patient who presented with a floating thrombus in the right atrium accompanied by acute massive PE. Case ReportAn 80-year-old female was admitted with sudden dyspnea and chest pain. On admission she presented in cardiogenic shock with a systolic blood systolic pressure of 60 mm Hg, a heart rate of 96 beats/min, and oxygen saturation of 92% while breathing 100% oxygen. The electrocardiogram showed sinus tachycardia and ST-T wave depression in leads V1 to V3. The chest radiogram documented no abnormalities. Right heart thrombus represents a mobilized deep venous thrombosis that is lodged temporarily in the right atrium and ventricle, and is often referred to as "emboli in transit." Floating right heart thrombus is an uncommon but life-threatening condition, and usually coexists with an already massive pulmonary embolism. ...

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