Multimodal Imaging to Understand Left Ventricular Systolic Dysfunction in a Patient With Sepsis-Related Myocardial Calcification.
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ABSTRACT:
SUBMITTER: Canu M
PROVIDER: S-EPMC8311337 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundPatients with left ventricular (LV) systolic dysfunction after myocardial infarction are at a high risk of developing heart failure. The addition of neprilysin inhibition to renin angiotensin system inhibition may result in greater attenuation of adverse LV remodeling as a result of increased levels of substrates for neprilysin with vasodilatory, antihypertrophic, antifibrotic, and sympatholytic effects.MethodsWe performed a prospective, multicenter, randomized, double-blind, active-comparator trial comparing sacubitril/valsartan 97/103 mg twice daily with valsartan 160 mg twice daily in patients ≥3 months after myocardial infarction with a LV ejection fraction ≤40% who were taking a renin angiotensin system inhibitor (equivalent dose of ramipril ≥2.5 mg twice daily) and a β-blocker unless contraindicated or intolerant. Patients in New York Heart Association class ≥II or with signs and symptoms of heart failure were excluded. The primary outcome was change from baseline to 52 weeks in LV end-systolic volume index measured using cardiac magnetic resonance imaging. Secondary outcomes included other magnetic resonance imaging measurements of LV remodeling, change in NT-proBNP (N-terminal pro-B-type natriuretic peptide) and high-sensitivity cardiac troponin I, and a patient global assessment of change questionnaire.ResultsFrom July 2018 to June 2019, we randomized 93 patients with the following characteristics: mean age, 60.7±10.4 years; median time from myocardial infarction, 3.6 years (interquartile range, 1.2-7.2); mean LV ejection fraction, 36.8%±7.1%; and median NT-proBNP, 230 pg/mL (interquartile range, 124-404). Sacubitril/valsartan, compared with valsartan, did not significantly reduce LV end-systolic volume index; adjusted between-group difference, -1.9 mL/m2 (95% CI, -4.9 to 1.0); P=0.19. There were no significant between-group differences in NT-proBNP, high-sensitivity cardiac troponin I, LV end-diastolic volume index, left atrial volume index, LV ejection fraction, LV mass index, or patient global assessment of change.ConclusionsIn patients with asymptomatic LV systolic dysfunction late after myocardial infarction, treatment with sacubitril/valsartan did not have a significant reverse remodeling effect compared with valsartan. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03552575.
| S-EPMC8284373 | biostudies-literature
Project description:UnlabelledIntroductionHypothermia is a relatively rare condition, and the effects of unintentional hypothermia on the heart are not known.Case presentationThis report describes the case of an 88-year-old Japanese man found in a coma and presenting with heart failure associated with hypothermia. He experienced sinus arrest, junctional rhythm and left ventricular systolic dysfunction with prolonged ejection time. With rewarming and treatment of his heart failure, he completely recovered over a period of two weeks.ConclusionProlonged ejection time might be a characteristic finding in hypothermia.
| S-EPMC3760449 | biostudies-literature
Project description:Despite considerable advances in pharmacological, surgical and technology-based cardiovascular therapy, left ventricular dysfunction and heart failure are increasingly prevalent health problems. Recent studies suggest that angiogenic gene therapy can restore perfusion in ischaemic myocardial tissue, and that the transfer of nonangiogenic genes may correct defects in calcium handling that contribute to abnormal contractile function in patients with heart failure; however, large clinical trials of gene therapy for treatment of left ventricular dysfunction and heart failure have yet to be completed, and only a small number of genes have been evaluated in patients. Researchers continue to investigate new genes, combinations of genes and approaches that combine gene and cell therapy, and to develop novel expression vectors and delivery systems; collectively, these refinements promise to improve both patient response and safety.
| S-EPMC3123777 | biostudies-literature
Project description:To investigate the role of NBCe1-B in the heart we performed RNAseq experiments to examine genome-wide transcriptional changes in female NBCe1-B/C knockout (KO) mice compared to female wild-type (WT) mice.
2024-09-05 | GSE223324 | GEO
Project description:BackgroundThere is already extensive literature on the natural history of hypertensive heart disease (HHD) and aortic stenosis (AS). Once these patients develop severe left ventricular systolic dysfunction (LVSD) despite guideline-directed therapy for heart failure (HF), it is often thought to be end-stage from irreversible adverse remodelling. Our case series challenges this traditional paradigm. A more holistic model that factors in the interactions between the ventricle and vasculature is required. Based on a novel hypothetical concept of myocardial fatigue, we propose that occasionally LVSD is not an inherent myocardial or valvular disease but a consequence of an arterial afterload mismatch. By addressing this, the ventricle may recover and contract efficiently in unison with the arterial system.Case summaryWe present two cases of severe LVSD in a young lady with long-standing essential hypertension and a gentleman with stable severe AS. Both patients were already established on HF medications. After optimizing their blood pressure control, repeat echocardiography revealed normalization of left ventricular ejection fraction within 3 months, along with a demonstrable improvement in ventricular-arterial coupling and for AS, a reduction in valvular-arterial impedance.DiscussionJust as Frank-Starling's law was discovered by initially drawing analogies to skeletal muscle behaviour, it is biologically plausible that cardiac fatigue can occur in the setting of afterload mismatch. The chance of recovery rests upon early recognition before it transitions to irreversible myocardial damage. Only by testing new emerging theories of HF can we galvanize original research and find new avenues to understanding this complex syndrome.
| S-EPMC8186914 | biostudies-literature
Project description:Candidates for chronic warfarin therapy often have co-morbid conditions, such as heart failure, with reduced left ventricular ejection fraction. Previous reports have demonstrated an increased risk of over-anticoagulation due to reduced warfarin dose requirement in patients with decompensated heart failure. However, the influence of left ventricular systolic dysfunction (LVSD), defined as left ventricular ejection fraction <40%, on warfarin response has not been evaluated. Here, we assess the influence of LVSD on warfarin dose, anticoagulation control (percent time in target range), and risk of over-anticoagulation (international normalized ratio >4) and major hemorrhage. Of the 1,354 patients included in this prospective cohort study, 214 patients (16%) had LVSD. Patients with LVSD required 11% lower warfarin dose compared with those without LVSD (p <0.001) using multivariate linear regression analyses. Using multivariate Cox proportional hazards model, patients with LVSD experienced similar levels of anticoagulation control (percent time in target range: 51% vs 53% p = 0.15), risk of over-anticoagulation (international normalized ratio >4; hazard ratio 1.01, 95% confidence interval 0.82 to 1.25; p = 0.91), and risk of major hemorrhage (hazard ratio 1.11; 95% confidence interval 0.70 to 1.74; p = 0.66). Addition of LVSD variable in the model increased the variability explained from 35% to 36% for warfarin dose prediction. In conclusion, our results demonstrate that patients with LVSD require lower doses of warfarin. Whether warfarin dosing algorithms incorporating LVSD in determining initial doses improves outcomes needs to be evaluated.
| S-EPMC4962063 | biostudies-literature
Project description:BackgroundExperimental autoimmune myocarditis (EAM) is a common animal model for the investigation of the pathophysiology of myocarditis. Because of diverging findings from previous studies, we performed serial echocardiographic examinations throughout the course of the disease and investigated the dimensions of the murine heart and left ventricular (LV) systolic function.Materials and methodsExperimental autoimmune myocarditis was induced in male Balb/c mice by subcutaneous injection of a fragment of the ?-myosin heavy chain (MyHC-? 614-629: Ac-SLKLMATLFSTYASAD). Transthoracic echocardiography was performed on days 0, 7 and 21 in healthy animals and mice with EAM.ResultsExperimental autoimmune myocarditis was associated with a reduction in LV systolic function and an increase in LV internal diameter in diastole (LVIDd) and systole (LVIDs) 7 days postimmunization. After 21 days, EAM led to a significant increase in LV-thickness (1.3-fold increase in LV anterior wall diameter in diastole [LVAWDd]), but there was no difference in LV systolic function between immunized animals and healthy controls. LV-thickness correlated well with the severity of myocarditis in the histopathological examination (LVAWDd: rs = 0.603, P = 0.003, LV anterior wall diameter in systole (LVAWDs): rs = 0.718, P < 0.0001).ConclusionOur results indicate that EAM leads to an initial dilatation of the LV that is followed by ventricular "hypertrophy." On day 21, there was no significant difference in LV systolic function between immunized animals and controls. Furthermore, the ageing of the animals had a major impact on the echocardiographic parameters; therefore, the use of healthy age-matched controls seems warranted when echocardiography is performed in rodents.
| S-EPMC6771695 | biostudies-literature
Project description:BackgroundPOEMS syndrome (PS) is a paraneoplastic disorder from plasma cell dyscrasia, characterized by polyneuropathy, organomegaly, endocrinopathy, monoclonal protein, and skin changes. Vascular endothelial growth factors (VEGFs)-driven fluid extracellular matrix expansion plays a key role in this condition. Associated cardiac involvement has been sparsely reported thus far.Case summaryA 55-year-old woman with PS presented with a pleural effusion and respiratory failure requiring mechanical ventilation. Transthoracic echocardiogram revealed left ventricular (LV) systolic dysfunction with a moderate pericardial effusion. She developed intermittent complete heart block and ventricular standstill, requiring temporary transcutaneous pacing. Further evaluation revealed no significant coronary stenosis on coronary angiogram and cardiac magnetic resonance (CMR) showed elevated T1 and extracellular volume suggestive of myocardial oedema with possible early cardiac infiltration. She had a dual-chamber permanent pacemaker implanted in view of recurrent high-grade heart block. She was initiated on a daratumumab-based chemotherapy regimen prior to discharge. She recovered well subsequently with a promising clinical response to chemotherapy.DiscussionWe describe the first case of LV systolic dysfunction with concomitant significant bradyarrhythmia in a patient with PS. CMR revealed evidence suggestive of LV myocardial oedema and/or possible early infiltration. VEGF overexpression could explain oedema-related LV dysfunction which reversed with adequate diuresis, as well as damage to the conduction system. Early cardiac amyloidosis, which can be associated with PS, is an important differential diagnosis. Pacemaker implantation, adequate diuresis, and definitive chemotherapy are key to the management of concomitant ventricular myocardial and electrical dysfunction in such rare case.
| S-EPMC7873801 | biostudies-literature
Project description:Left ventricular systolic dysfunction (LVSD) defined by ejection fraction (EF) <40% is common, serious but treatable, and correct diagnosis is the cornerstone of effective treatment. Biomarkers may help to diagnose LVSD and give insight into the pathophysiology. The immune system is activated in LVSD, and the immunomodulatory molecule human leukocyte antigen-G (HLA-G) may be involved. The primary aim was to measure soluble HLA-G (sHLA-G) in the blood in different stages of LVSD (<30% and 30-40%), in the midrange EF 40-50%, and in preserved EF ? 50% and to validate sHLA-G as a LVSD biomarker. The secondary aim was to examine associations between HLA-G gene polymorphisms influencing expression levels and LVSD. The 260 study participants were ?75 years old, many with risk factors for heart disease or with known heart disease. Soluble HLA-G was significantly and uniformly higher in the groups with EF < 50% (<30, 30-40, and 40-50%) compared to EF > 50% (p < 0.0001). N-terminal fragment-pro-B-type natriuretic peptide (NT-proBNP) and uric acid values were inversely related to EF. According to Receiver Operating Characteristic (ROC) curves NT-proBNP outperformed both sHLA-G and uric acid as biomarkers of LVSD. Soluble HLA-G in blood plasma was elevated in LVSD regardless of EF. A novel finding was that a combined 14?bp ins-del/+3142 SNP HLA-G haplotype was associated with EF < 40%.
| S-EPMC5075317 | biostudies-literature
Project description:BackgroundRecognition of cardiomyopathy in sepsis can be challenging due to the limitations of conventional measures such as ejection fraction (EF) and fractional shortening (FS) in the context of variable preload and afterload conditions. This study correlates myocardial function using strain echocardiography (SE) with cardiomyocyte oxidative stress in a murine model of sepsis.MethodsC57BL/6J mice were randomized into control (n = 10), sham (n = 25), and a cecal ligation and puncture (CLP) (n = 33) model of sepsis. Echocardiography was performed pre-, 12, 24, and 48 h post-injury. Cardiac pro-inflammatory cytokines and mitochondrial redox scavenger expression were evaluated in a subset of each arm. To evaluate the influence of redox scavenger upregulation on oxidative injury and cardiac function, CLP was performed on mitochondrial catalase-upregulated C57BL/6J MCAT+/+ mice (n = 12) and wild-type (WT) animals for comparison.ResultsSeptic C57BL/6J mice exhibited depressed longitudinal strain (LS) when compared to sham and control at 24 h (p < 0.01) and 48 h (p = 0.04) post-CLP despite having a preserved EF. Furthermore, there was a significant association between increased odds of mortality and depressed LS (OR = 1.23, p = 0.04). Septic C57BL/6J mice concomitantly demonstrated increased expression of cardiomyocyte pro-inflammatory cytokines and decreased expression of redox scavengers at 24 and 48 h. When comparing C57Bl/6 MCAT +/+ mice and C57BL/6J WT mice, a significant decrease in LS was identified in the WT mice at 24 h (MCAT = -23 ± 5% vs. WT = -15 ± 4% p < 0.01) and 48 h (MCAT = -23 ± 7% vs. WT = -15 ± 4.3% p = 0.04) post-CLP which correlated with significant increase in the level of cardiac oxidative stress following CLP.ConclusionsIn this sepsis model, SE identified cardiomyopathy despite normal EF. SE depression temporally coincides with upregulation of inflammatory cytokines and decreases expression of key mitochondrial ROS scavengers. Upregulation of redox scavenger (CAT) abrogates oxidative stress and cardiac dysfunction in this sepsis model.
| S-EPMC5389950 | biostudies-literature