30 research outputs found

    Reverse ventricular remodeling reduces ischemic mitral regurgitation: echo-guided device application in the beating heart. Circulation

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    Background-In ischemic mitral regurgitation (MR), mitral leaflet closure is restricted by ventricular remodeling with displacement of the papillary muscles (PMs). Therapy is uncertain because ring annuloplasty does not alleviate PM displacement. We tested the hypothesis that echo-guided PM repositioning using an external device can reduce MR without compromising left ventricular (LV) function. Methods and Results-We studied 10 sheep with ischemic MR produced by circumflex ligation with inferior infarction, 6 acutely and 4 eight weeks after myocardial infarction (MI). A Dacron patch containing an inflatable balloon was placed over the PMs and adjusted under echo guidance to reverse LV remodeling and reposition the infarcted PM. 3D echo assessed mitral valve geometric changes. In 7 sheep, sonomicrometry and Millar catheters assessed changes in end-systolic and end-diastolic pressure-volume relationships, and microspheres were injected to assess coronary flow. Moderate MR after MI resolved with patch application alone (nϭ3) or echo-guided balloon inflation, which repositioned the infarcted PM, decreasing the PM tethering distance from 31.1Ϯ2.5 mm after MI to 26.8Ϯ1.8 with patch (PϽ0.01; baselineϭ25.5Ϯ1.5). LV contractility was unchanged (end-systolic slopeϭ3.4Ϯ1.6 mm Hg/mL with patch versus 2.8Ϯ1.6 after MI). Although there was a nonsignificant trend for a mild increase in stiffness constant (0.07Ϯ0.05 m

    Mechanical effects of MitraClip on leaflet stress and myocardial strain in functional mitral regurgitation - A finite element modeling study.

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    PurposeMitraClip is the sole percutaneous device approved for functional mitral regurgitation (MR; FMR) but MR recurs in over one third of patients. As device-induced mechanical effects are a potential cause for MR recurrence, we tested the hypothesis that MitraClip increases leaflet stress and procedure-related strain in sub-valvular left ventricular (LV) myocardium in FMR associated with coronary disease (FMR-CAD).MethodsSimulations were performed using finite element models of the LV + mitral valve based on MRI of 5 sheep with FMR-CAD. Models were modified to have a 20% increase in LV volume (↑LV_VOLUME) and MitraClip was simulated with contracting beam elements (virtual sutures) placed between nodes in the center edge of the anterior (AL) and posterior (PL) mitral leaflets. Effects of MitraClip on leaflet stress in the peri-MitraClip region of AL and PL, septo-lateral annular diameter (SLAD), and procedure-related radial strain (Err) in the sub-valvular myocardium were calculated.ResultsMitraClip increased peri-MitraClip leaflet stress at end-diastole (ED) by 22.3±7.1 kPa (pConclusionsMitraClip for FMR-CAD increases mitral leaflet stress and radial strain in LV sub-valvular myocardium. Mechanical effects of MitraClip are augmented by LV enlargement

    Acute leukemia is associated with cardiac alterations before chemotherapy

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    Background: Patients with acute leukemia (AL) have a higher rate of congestive heart failure than patients with other cancers. AL may predispose to cardiac dysfunction before chemotherapy because of high cytokine release or direct leukemic myocardial infiltration. The aims of this study were to evaluate whether AL is associated with abnormalities of myocardial structure and function before chemotherapy and to identify possible risk factors associated with these myocardial changes. Methods: Using an echocardiographic database, 76 patients with AL and 76 patients without cancer matched for age, gender, hypertension, and the presence of diabetes were retrospectively selected. Subsequently, to assess the effect of a nonhematologic malignancy, 28 women in each group were matched with women with breast cancer. Left ventricular (LV) mass, volumes, ejection fraction, and global longitudinal strain (GLS) were measured before chemotherapy. Results: The patients were predominantly male (63%), with a median age of 51 years, and had low prevalence of cardiovascular risk factors. Despite similar LV ejection fractions, patients with AL had higher LV mass and volumes and lower GLS (-19.3 ± 2.7% vs -20.9 ± 1.9%, P < .001) than patients without cancer. Similarly, GLS was lower in women with AL compared with women with breast cancer or without cancer. Among patients with AL, high body mass index, low LV ejection fraction, and a small number of circulating lymphocytes were all independently associated with low GLS. Conclusions: Patients with AL had higher LV volumes and lower GLS than patients without cancer and lower GLS than patients with breast cancer, suggesting that AL by itself may be associated with these cardiac alterations

    Effects of cyproheptadine on mitral valve remodeling and regurgitation after myocardial infarction

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    BACKGROUND Ischemic mitral regurgitation (MR) is primarily caused by left ventricle deformation, but leaflet thickening with fibrotic changes are also observed in the valve. Increased levels of 5-hydroxytryptamine (5-HT; ie, serotonin) are described after myocardial infarction (MI); 5-HT can induce valve fibrosis through the 5-HT type 2B receptor (5-HT2BR). OBJECTIVES This study aims to test the hypothesis that post-MI treatment with cyproheptadine (5-HT2BR antagonist) can prevent ischemic MR by reducing the effect of serotonin on mitral biology. METHODS Thirty-six sheep were divided into 2 groups: inferior MI and inferior MI treated with cyproheptadine (0.5 mg/kg/d). Animals were followed for 90 days. Blood 5-HT, infarct size, left ventricular volume and function, MR fraction and mitral leaflet size were assessed. In a complementary in vitro study, valvular interstitial cells were exposed to pre-MI and post-MI serum collected from the experimental animals. RESULTS Increased 5-HT levels were observed after MI in nontreated animals, but not in the group treated with cyproheptadine. Infarct size was similar in both groups (11 ± 3 g vs 9 ± 5 g; P = 0.414). At 90 days, MR fraction was 16% ± 7% in the MI group vs 2% ± 6% in the cyproheptadine group (P = 0.0001). The increase in leaflet size following MI was larger in the cyproheptadine group (+40% ± 9% vs +22% ± 12%; P = 0.001). Mitral interstitial cells overexpressed extracellular matrix genes when treated with post-MI serum, but not when exposed to post-MI serum collected from treated animals. CONCLUSIONS Cyproheptadine given after inferior MI reduces post-MI 5-HT levels, prevents valvular fibrotic remodeling, is associated with larger increase in mitral valve size and less MR

    Left atrial cross-sectional area is a novel measure of atrial shape associated with cardioembolic strokes

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    Objective Cardioembolic (CE) stroke carries significant morbidity and mortality. Left atrial (LA) size has been associated with CE risk. We hypothesised that differential LA remodelling impacts on pathophysiological mechanism of major CE strokes. Methods A cohort of consecutive patients hospitalised with ischaemic stroke, classified into CE versus non-CE strokes using the Causative Classification System for Ischaemic Stroke were enrolled. LA shape and remodelling was characterised by assessing differences in maximal LA cross-sectional area (LA-CSA) in a cohort of 40 prospectively recruited patients with ischaemic stroke using three-dimensional (3D) echocardiography. Flow velocity profiles were measured in spherical versus ellipsoidal in vitro models to determine if LA shape influences flow dynamics. Two-dimensional (2D) LA-CSA was subsequently derived from standard echocardiographic views and compared with 3D LA-CSA. Results A total of 1023 patients with ischaemic stroke were included, 230 (22.5%) of them were classified as major CE. The mean age was 68±16 years, and 464 (45%) were women. The 2D calculated LA-CSA correlated strongly with the LA-CSA measured by 3D in both end-systole and end-diastole. In vitro flow models showed shape-related differences in mid-level flow velocity profiles. Increased LA-CSA was associated with major CE stroke (adjusted relative risk 1.10, 95% CI 1.04 to 1.16; p<0.001), independent of age, gender, atrial fibrillation, left ventricular ejection fraction and CHA 2 DS 2 -VASc score. Specifically, the inclusion of LA-CSA in a model with traditional risk factors for CE stroke resulted in signifi cant improvement in model performance with the net reclassification improvement of 0.346 (95% CI 0.189 to 0.501; p=0.00001) and the integrated discrimination improvement of 0.013 (95% CI 0.003 to 0.024; p=0.0119). Conclusions LA-CSA is a marker of adverse LA shape associated with CE stroke, reflecting importance of differential LA remodelling, not simply LA size, in the mechanism of CE risk
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