Atrial Giant Cell Myocarditis as a Cause of Heart Failure: Diagnostic Pathway and Successful Treatment.
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ABSTRACT:
SUBMITTER: Paitazoglou C
PROVIDER: S-EPMC8743871 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BACKGROUND AND PURPOSE:The pleiotropic properties of HDL may exert beneficial effects on the myocardium. The effect of recombinant HDLMilano on established heart failure was evaluated in C57BL/6 mice. EXPERIMENTAL APPROACH:Mice were subjected to transverse aortic constriction (TAC) or sham operation at the age of 14 weeks. Eight weeks later, TAC and sham mice were each randomized into three different groups. Reference groups were killed at day 56 after the operation for baseline analysis. Five i.p. injections of recombinant HDLMilano (MDCO-216), 100 mg·kg-1 , or an equivalent volume of control buffer were administered with a 48 h interval starting at day 56. Endpoint analyses in the control buffer groups and in the MDCO-216 groups were executed at day 65. KEY RESULTS:Lung weight in MDCO-216 TAC mice was 25.3% lower than in reference TAC mice and 27.9% lower than in control buffer TAC mice and was similar in MDCO-216 sham mice. MDCO-216 significantly decreased interstitial fibrosis and increased relative vascularity compared to reference TAC mice and control buffer TAC mice. The peak rate of isovolumetric relaxation in MDCO-216 TAC mice was 30.4 and 36.3% higher than in reference TAC mice and control buffer TAC mice respectively. Nitro-oxidative stress and myocardial apoptosis were significantly reduced in MDCO-216 TAC mice compared to control buffer TAC mice. CONCLUSIONS AND IMPLICATIONS:MDCO-216 improves diastolic function, induces regression of interstitial fibrosis and normalizes lung weight in mice with established heart failure. Recombinant HDL may emerge as a treatment modality in heart failure.
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Project description:Heart failure is becoming a global epidemic. It exerts a staggering toll on quality of life, and substantial medical and economic impact. In a pre-clinical model of cardiac hypertrophy and heart failure, we were able to overcome loss of heart function by administering the TRPV1 antagonist BCTC (4-(3-Chloro-2-pyridinyl)-N-[4-(1,1-dimethylethyl)phenyl]-1-piperazinecarboxamide). The results presented here identify TRPV1 antagonists as new treatment options for cardiac hypertrophy and heart failure.
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Project description:Various clinical presentations of the 2019 coronavirus disease (COVID-19) have been described, including post-infectious acute and fulminant myocarditis. Here, we describe the case of a young patient admitted for COVID-19-associated post-infectious fulminant myocarditis. Despite optimal pharmacologic management, haemodynamic status worsened requiring support by veno-arterial extracorporeal membrane oxygenation. Emergent heart transplantation was required at Day 11 given the absence of cardiac function improvement. The diagnosis of post-infectious COVID-19-associated myocarditis was made from both pathologic examination of the explanted heart and positive SARS-CoV-2 serology.
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Project description:Background?Dyspnoea is very common in elderly patients and can be caused by a variety of different diseases. However, the initial diagnosis of patent ductus arteriosus (PDA) as a cause of left heart failure is very rare in this patient population.Case summary?A 69-year-old physically active woman with known hypertension presented with worsening exertional dyspnoea. Echocardiography showed a dilated left ventricle with moderately reduced left ventricular ejection fraction, and evidence for PDA. The PDA was confirmed by computed tomography angiography and successfully closed by implantation of an Amplatzer PDA occluder II 06-06?mm. As a result, the heart failure symptoms receded completely.Discussion?Congenital heart diseases should be considered as heart failure causes even in older adults. In addition to the standard medical therapy, there may be effective interventional treatment options to reverse the symptoms of heart failure in such patients.
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Project description:AimsLeft atrial (LA) remodelling is an important predictor of cardiovascular events of heart failure (HF) and atrial fibrillation. Data regarding diagnostic value of LA remodelling on diastolic dysfunction (DD) and preclinical HF remain largely unexplored.Methods and resultsWe assessed LA dimension (LAD) in 8368 consecutive asymptomatic Asians (mean age: 49.7, 38.9% women) and related such measure to updated American Society of Echocardiography (ASE) DD criteria and newly revised N-terminal pro-brain natriuretic peptide (NT-proBNP) cut-off (?125 pg/mL) and HF with preserved ejection fraction criteria incorporating NT-proBNP and echocardiography parameters by the European Society of Cardiology (ESC). LAD and indexed LAD (LADi) were both inversely correlated with myocardial relaxation e' and positively associated with indexed LA volume, left ventricular E/e', and tricuspid regurgitation velocity (all P < 0.001) and showed significantly graded increase across ASE-defined 'normal', 'inconclusive', and 'DD' categories (30.9, 34.4, and 36.5 mm; 16.7, 19.1, and 20.6 mm/m2 , for LAD/LADi, both P for trend: <0.001, respectively). Substantial differences of LAD/LADi (31.3 vs. 33.6 mm/16.7 vs. 19.2 mm/m2 , both P < 0.001) between ESC low and high HF probability using NT-proBNP cut-off were also observed. Multivariate linear and logistic models demonstrated that LAD set at 34 mm was independently associated with ASE-defined diastolic indices, DD existence, and elevated NT-proBNP (all P < 0.05). The use of LAD further yielded high diagnostic accuracy in DD (area under receiving operative characteristic curve: 0.77, 95% confidence interval [0.73, 0.80]; negative predictive value: 97.9%) and in ESC-recommended HF with preserved ejection fraction criteria (area under receiving operative characteristic curve: 0.70, 95% confidence interval [0.65, 0.75]; negative predictive value: 98.7%) with high predictive value in LA remodelling (>34 mL/m2 ; positive predictive value: 96%) and well-discriminated ESC-recommended NT-proBNP (?125 pg/mL, LAD: 37 mm) for HF.ConclusionsSingle utilization of atrial remodelling is highly useful for ruling out presence of DD and provides practical threshold for identifying preclinical HF based on most updated guidelines.
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Project description:BackgroundGiant cell myocarditis (GCM) is a rare cause of fulminant heart failure (HF). The most common presentation is progressive hemodynamic deterioration, and a few cases present with idiopathic complete atrioventricular block (cAVB). The prognosis of GCM is poor, and GCM patients usually die of HF and ventricular arrhythmia unless cardiac transplantation is performed. Few reports have described the effects of treatments such as immunosuppression and detailed reverse remodelling in GCM patients.Case summaryA 69-year-old female presented with cAVB. Transvenous pacemaker was implanted via the left subclavian vein. One and a half months later, she exhibited left ventricular dyssynchrony and lower left ventricular ejection fraction (LVEF), resulting in hospitalization for HF. She received cardiac resynchronization therapy; however, this had no apparently positive effects on her cardiac function. To investigate the cause of the lower LVEF, an endomyocardial biopsy was taken from the right ventricular septum. She was diagnosed with GCM and immediately received immunosuppression therapy with prednisolone and ciclosporin. This resulted in the functional recovery of the right ventricle; on the other hand, the left ventricle had still not recovered based on transthoracic echocardiography. Fortunately, she successfully recovered from severe HF without recurrence.DiscussionThis is a case of fulminant HF due to GCM which initially presented as cAVB. Moreover, this case demonstrates the quite difference of the functional recovery between the left ventricle and the right ventricle with immunosuppression therapy.
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Project description:Coronary artery fistula is a rare congenital cardiac anomaly that is often found incidentally during computed tomography angiography. Coronary fistula between the left circumflex coronary artery and the coronary sinus is among the less common forms of coronary artery fistula. A 60-yea\r-old female patient presented to our outpatient cardiology department with symptoms of severe, de novo heart failure. Echocardiogram revealed severe mitral regurgitation and a dilated duct that turbulently accelerated colour Doppler flow behind the left ventricle with significant left-to-right shunt. Cardiac magnetic resonance imaging and computed tomography angiography revealed a massively dilated fistula between the left circumflex coronary artery and the coronary sinus with a diameter of 3-4 cm. The patient underwent combined heart surgery involving mitral ring annuloplasty and fistula ligation and was discharged in stable condition on guideline-based medical therapy. At 18 months of follow-up, minimal residual shunt flow and mild-to-moderate mitral regurgitation were found. We report a rare case of congenital coronary disorder resulting in heart failure and highlight the importance of complex non-invasive cardiac diagnostic procedures before planning and performing heart surgery.
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Project description:In human myocarditis and its sequela dilated cardiomyopathy (DCM), the mechanisms and immune phenotype governing disease and subsequent heart failure are not known. Here, we identified a Th17 cell immunophenotype of human myocarditis/DCM with elevated CD4+IL17+ T cells and Th17-promoting cytokines IL-6, TGF-β, and IL-23 as well as GM-CSF-secreting CD4+ T cells. The Th17 phenotype was linked with the effects of cardiac myosin on CD14+ monocytes, TLR2, and heart failure. Persistent heart failure was associated with high percentages of IL-17-producing T cells and IL-17-promoting cytokines, and the myocarditis/DCM phenotype included significantly low percentages of FOXP3+ Tregs, which may contribute to disease severity. We demonstrate a potentially novel mechanism in human myocarditis/DCM in which TLR2 peptide ligands from human cardiac myosin stimulated exaggerated Th17-related cytokines including TGF-β, IL-6, and IL-23 from myocarditic CD14+ monocytes in vitro, and an anti-TLR2 antibody abrogated the cytokine response. Our translational study explains how an immune phenotype may be initiated by cardiac myosin TLR ligand stimulation of monocytes to generate Th17-promoting cytokines and development of pathogenic Th17 cells in human myocarditis and heart failure, and provides a rationale for targeting IL-17A as a therapeutic option.
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