Left ventricular dysfunction in the newborn.
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ABSTRACT:
SUBMITTER: Menahem S
PROVIDER: S-EPMC10248935 | biostudies-literature | 2023 May
REPOSITORIES: biostudies-literature
Publications
Left ventricular dysfunction in the newborn.
Menahem Samuel S Sehgal Arvind A
Translational pediatrics 20230418 5
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Project description:We describe a rare case of spontaneous coronary artery thrombosis in a newborn leading to rapid severe ventricular dysfunction. Early diagnosis is critical and management strategies are varied including hemodynamic support with extracorporeal membrane oxygenation, systemic/local thrombolytic therapy with tissue plasminogen activator, or surgical thrombectomy. (Level of Difficulty: Advanced.).
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Project description:A 73-year-old male patient presented with shortness of breath at rest resulting from new-onset severe primary mitral regurgitation with a flail posterior leaflet, left ventricular dysfunction, and cardiogenic shock. After initial stabilization in the intensive care unit, multiple treatment options were considered for this patient, all associated with significant mortality. Ultimately, operative mitral valve repair with Impella 5.5 placement was performed for postoperative hemodynamic support. Surgical repair provided elimination of mitral regurgitation. Impella support was maintained for 7 days to provide unloading of the left ventricle. After device removal, the patient had sustained left ventricular recovery with significantly improved ejection fraction. Full left ventricular support and unloading may decrease operative risk and promote left ventricular recovery in patients with severe mitral regurgitation and left ventricular dysfunction. This case emphasizes the value of ventricular unloading to facilitate the recovery of left ventricular function as a treatment option for patients with challenging cases of severe mitral regurgitation and left ventricular dysfunction.
| S-EPMC10178643 | biostudies-literature
Project description:BackgroundCoronavirus Disease-2019 (COVID-19) is associated with cardiovascular injury, but left ventricular (LV) function is largely preserved. We aimed to evaluate for subclinical LV dysfunction in patients with COVID-19 through myocardial strain analysis.MethodsWe performed a single-center retrospective cohort study of all patients hospitalized with COVID-19 who underwent echocardiography. Traditional echocardiographic and global longitudinal strain (GLS) values were compared with prior and subsequent echocardiograms.ResultsAmong 96 patients hospitalized with COVID-19 with complete echocardiograms, 67 (70%) had adequate image quality for strain analysis. The cohort was predominantly male (63%) and 18% had prevalent cardiovascular disease (CVD). Echocardiograms were largely normal with median [IQR] LV ejection fraction (EF) 62% [56%, 68%]. However, median GLS was abnormal in 91% (-13.5% [-15.0%, -10.8%]). When stratified by CVD, both groups had abnormal GLS, but presence of CVD was associated with worse median GLS (-11.6% [-13.4%, -7.2%] vs -13.9% [-15.0%, -11.3%], p = 0.03). There was no difference in EF or GLS when stratified by symptoms or need for intensive care. Compared to pre-COVID-19 echocardiograms, EF was unchanged, but median GLS was significantly worse (-15% [-16%, -14%] vs -12% [-14%, -10%], p = 0.003). Serial echocardiograms showed no significant changes in GLS or EF overall, however patients who died had stable or worsening GLS, while those who survived to discharge home showed improved GLS.ConclusionsPatients with COVID-19 had evidence of subclinical cardiac dysfunction manifested by reduced GLS despite preserved EF. These findings were observed regardless of history of CVD, presence of COVID-19 symptoms, or severity of illness.
| S-EPMC7988446 | biostudies-literature
Project description:BackgroundThe aim of this study was to evaluate the possible presence of diastolic dysfunction and its possible effects in terms of respiratory mechanics, gas exchange and lung recruitability in mechanically ventilated ARDS.MethodsConsecutive patients admitted in intensive care unit (ICU) with ARDS were enrolled. Echocardiographic evaluation was acquired at clinical PEEP level. Lung CT-scan was performed at 5 and 45 cmH2O. In the study, 2 levels of PEEP (5 and 15 cmH2O) were randomly applied.ResultsA total of 30 patients were enrolled with a mean PaO2/FiO2 and a median PEEP of 137 ± 52 and 10 [9-10] cmH2O, respectively. Of those, 9 patients (30%) had a diastolic dysfunction of grade 1, 2 and 3 in 33%, 45% and 22%, respectively, without any difference in gas exchange and respiratory mechanics. The total lung weight was significantly higher in patients with diastolic dysfunction (1669 [1354-1909] versus 1554 [1146-1942] g) but the lung recruitability was similar between groups (33.3 [27.3-41.4] versus 30.6 [20.0-38.8] %). Left ventricular ejection fraction (57 [39-62] versus 60 [57-60]%) and TAPSE (20.0 [17.0-24.0] versus 24.0 [20.0-27.0] mL) were similar between the two groups. The response to changes of PEEP from 5 to 15 cmH2O in terms of oxygenation and respiratory mechanics was not affected by the presence of diastolic dysfunction.ConclusionsARDS patients with left ventricular diastolic dysfunction presented a higher amount of lung edema and worse outcome.
| S-EPMC9604741 | biostudies-literature
Project description: Not available
| S-EPMC5516273 | biostudies-literature
Project description:Studies of Left Ventricular Dysfunction (SOLVD-BioLINCC)
| PRJNA1120512 | ENA
Project description:Studies of Left Ventricular Dysfunction (SOLVD-BioLINCC)
| PRJNA1120513 | ENA
Project description:BackgroundCardiac magnetic resonance (CMR) has been used to diagnose and risk-stratify patients with left ventricular noncompaction (LVNC). The prognostic value of CMR parameters for LVNC, especially feature tracking (CMR-FT), is not well known in LVNC patients with left ventricular dysfunction. The present study aimed to investigate whether the combination of CMR-FT with traditional CMR parameters can increase the prognostic value of CMR for LVNC patients with reduced left ventricular ejection fraction (LVEF).MethodsA total of 123 candidates were retrospectively included in this multicenter study and 55 LVNC patients (mean age, 45.7 ± 16.2 years; 61.8% men) remained after applying the exclusion criteria. Clinical features, left ventricular (LV) function parameters, global and segment myocardial strain, and late gadolinium enhancement (LGE) were evaluated. The outcomes include the composite events of cardiovascular death, heart transplantation, hospitalization for heart failure, thromboembolic events, and ventricular arrhythmias.ResultsAfter a median follow-up of 5.17 years (interquartile range: 0.17 to 10.58 years), 24 (36.8%) patients experienced at least one major adverse cardiovascular event (MACE). The myocardial strain parameters of patients with events were lower than those of patients without events. In the univariable Cox analysis, LVEF, the presence of LGE, global longitudinal strain (GLS) and segmental strains, including longitudinal strain at the apical level and radial and circumferential strain at the basal level, were significantly associated with MACEs. In the multivariate analysis, LGE (hazard ratio (HR) 3.452, 95% CI 1.133 to 10.518, p = 0.029) was a strong predictor of MACEs and significantly improved the predictive value (chi-square of the model after adding LGE: 7.51 vs. 13.47, p = 0.009). However, myocardial strain parameters were not statistically significant for the prediction of MACEs after adjusting for age, body mass index, LVEF and the presence of LGE and did not increase the prognostic value (chi-square of the model after adding GLS: 13.47 vs. 14.14, p = 0.411) in the multivariate model.ConclusionsThe combination of CMR-FT with traditional CMR parameters may not increase the prognostic value of CMR in LVNC patients with reduced LVEF, while the presence of LGE was a strong independent predictor of MACEs and significantly improved the predictive value.
| S-EPMC9724297 | biostudies-literature
Project description:ObjectivesWe aimed to assess prevalence of left ventricular (LV) systolic and diastolic function in stable cohort of COPD patients, where LV disease had been thoroughly excluded in advance.Methods100 COPD outpatients in GOLD II-IV and 34 controls were included. Patients were divided by invasive mean pulmonary artery pressure (mPAP) in COPD-PH (≥25 mmHg) and COPD-non-PH (<25 mmHg), which was subdivided in mPAP ≤20 mmHg and 21-24 mmHg. LV myocardial performance index (LV MPI) and strain by tissue Doppler imaging (TDI) were used for evaluation of LV global and systolic function, respectively. LV MPI ≥0.51 and strain ≤-15.8% were considered abnormal. LV diastolic function was assessed by the ratio between peak early (E) and late (A) velocity, early TDI E´, E/E´, isovolumic relaxation time, and left atrium volume.ResultsLV MPI ≥0.51 was found in 64.9% and 88.5% and LV strain ≤-15.8% in 62.2.% and 76.9% in the COPD-non-PH and COPD-PH patients, respectively. Similarly, LV MPI and LV strain were impaired even in patients with mPAP <20 mmHg. In multiple regression analyses, residual volume and stroke volume were best associated to LV MPI and LV strain, respectively. Except for isovolumic relaxation time, standard diastolic echo indices as E/A, E´, E/E´ and left atrium volume did not change from normal individuals to COPD-non-PH.ConclusionsSubclinical LV systolic dysfunction was a frequent finding in this cohort of COPD patients, even in those with normal pulmonary artery pressure. Evidence of LV diastolic dysfunction was hardly present as measured by conventional echo indices.
| S-EPMC7365599 | biostudies-literature
Project description:AimsInterleukin 11 (IL11) was initially thought important for platelet production, which led to recombinant IL11 being developed as a drug to treat thrombocytopenia. IL11 was later found to be redundant for haematopoiesis, and its use in patients is associated with unexplained and severe cardiac side effects. Here, we aim to identify, for the first time, direct cardiomyocyte toxicities associated with IL11, which was previously believed cardioprotective.Methods and resultsWe injected recombinant mouse lL11 (rmIL11) into mice and studied its molecular effects in the heart using immunoblotting, qRT-PCR, bulk RNA-seq, single nuclei RNA-seq (snRNA-seq), and assay for transposase-accessible chromatin with sequencing (ATAC-seq). The physiological impact of IL11 was assessed by echocardiography in vivo and using cardiomyocyte contractility assays in vitro. To determine the activity of IL11 specifically in cardiomyocytes, we made two cardiomyocyte-specific Il11ra1 knockout (CMKO) mouse models using either AAV9-mediated and Tnnt2-restricted (vCMKO) or Myh6 (m6CMKO) Cre expression and an Il11ra1 floxed mouse strain. In pharmacologic studies, we studied the effects of JAK/STAT inhibition on rmIL11-induced cardiac toxicities. Injection of rmIL11 caused acute and dose-dependent impairment of left ventricular ejection fraction (saline: 62.4% ± 1.9; rmIL11: 32.6% ± 2.9, P < 0.001, n = 5). Following rmIL11 injection, myocardial STAT3 and JNK phosphorylation were increased and bulk RNA-seq revealed up-regulation of pro-inflammatory pathways (TNFα, NFκB, and JAK/STAT) and perturbed calcium handling. snRNA-seq showed rmIL11-induced expression of stress factors (Ankrd1, Ankrd23, Xirp2), activator protein-1 (AP-1) transcription factor genes, and Nppb in the cardiomyocyte compartment. Following rmIL11 injection, ATAC-seq identified the Ankrd1 and Nppb genes and loci enriched for stress-responsive, AP-1 transcription factor binding sites. Cardiomyocyte-specific effects were examined in vCMKO and m6CMKO mice, which were both protected from rmIL11-induced left ventricular impairment and molecular pathobiologies. In mechanistic studies, inhibition of JAK/STAT signalling with either ruxolitinib or tofacitinib prevented rmIL11-induced cardiac dysfunction.ConclusionsInjection of IL11 directly activates IL11RA/JAK/STAT3 in cardiomyocytes to cause acute heart failure. Our data overturn the earlier assumption that IL11 is cardioprotective and explain the serious cardiac side effects associated with IL11 therapy.
| S-EPMC11687394 | biostudies-literature