scholarly journals Stabilisation of a Segment of Autologous Vascularised Stomach as a Patch for Myocardial Reconstruction with Degradable Magnesium Alloy Scaffolds in a Swine Model

Crystals ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 438 ◽  
Author(s):  
Tobias Schilling ◽  
Michael Bauer ◽  
Dagmar Hartung ◽  
Gudrun Brandes ◽  
Igor Tudorache ◽  
...  
Keyword(s):  
Heart Failure ◽  
Magnesium Alloy ◽  
Degradation Kinetics ◽  
Therapeutic Option ◽  
Severe Heart Failure ◽  
Left Ventricular ◽  
Surgical Reconstruction ◽  
Left Ventricular Myocardium ◽  
Swine Model ◽  
Coronary Vasculature

In patients with severe heart failure, the surgical reconstruction of the damaged myocardium with regenerative biological grafts is an innovative therapeutic option. However, natural patch materials are often too delicate for a full wall repair of the left ventricle. A degradable magnesium scaffold could provide temporary mechanical stability until the sufficient physiological remodeling of such grafts. An autologous vascularised gastric patch was employed for the reconstruction of the left ventricular myocardium in a porcine model. Magnesium alloy (LA63) scaffolds were fixed over the biological patch. The function of the implant was assessed via magnetic resonance imaging. Angiography was carried out to detect a connection between the gastric and coronary vasculature. The explants were examined via µ-computer tomography and light microscopy. All the test animals survived. The prostheses integrated biologically and functionally into the myocardium. No rupture of the prostheses occurred. An anastomosis of the gastric and coronary vasculature had developed. The magnesium scaffolds degraded, on average, to 30.9% of their original volume. This novel technique responds to the increasing demand for regenerative myocardial grafts. The magnesium scaffolds’ biocompatibility and degradation kinetics, as well as their stabilizing effects, indicate their applicability in the surgical treatment of terminal heart failure.

Cardiac mitofusin-1 is declined in non-responding patients with idiopathic dilated cardiomyopathy

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
Y Hsiao ◽  
I Shimizu ◽  
T Wakasugi ◽  
S Jiao ◽  
T Watanabe ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Heart Failure ◽  
Ventricular Myocytes ◽  
Severe Heart Failure ◽  
Left Ventricular ◽  
Neonatal Rat ◽  
Heart Failure Patients ◽  
Underlying Mechanisms ◽  
Neonatal Rat Ventricular Myocytes ◽  
Mitofusin 1

Abstract Background/Introduction Mitochondria are dynamic regulators of cellular metabolism and homeostasis. The dysfunction of mitochondria has long been considered a major contributor to aging and age-related diseases. The prognosis of severe heart failure is still unacceptably poor and it is urgent to establish new therapies for this critical condition. Some patients with heart failure do not respond to established multidisciplinary treatment and they are classified as “non-responders”. The outcome is especially poor for non-responders, and underlying mechanisms are largely unknown. Purpose Studies indicate mitochondrial dysfunction has causal roles for metabolic remodeling in the failing heart, but underlying mechanisms remain to be explored. This study tried to elucidate the role of Mitofusin-1 in a failing heart. Methods We examined twenty-two heart failure patients who underwent endomyocardial biopsy of intraventricular septum. Patients were classified as non-responders when their left-ventricular (LV) ejection fraction did not show more than 10% improvement at remote phase after biopsy. Fourteen patients were classified as responders, and eight as non-responders. Electron microscopy, quantitative PCR, and immunofluorescence studies were performed to explore the biological processes or molecules involved in failure to respond. In addition to studies with cardiac tissue specific knockout mice, we also conducted functional in-vitro studies with neonatal rat ventricular myocytes. Results Twenty-two patients with IDCM who underwent endomyocardial biopsy were enrolled in this study, including 14 responders and 8 non-responders. Transmission electron microscopy (EM) showed a significant reduction in mitochondrial size in cardiomyocytes of non-responders compared to responders. Quantitative PCR revealed that transcript of mitochondrial fusion protein, Mitofusin-1, was significantly reduced in non-responders. Studies with neonatal rat ventricular myocytes (NRVMs) indicated that the beta-1 adrenergic receptor-mediated signaling pathway negatively regulates Mitofusin-1 expression. Suppression of Mitofusin-1 resulted in a significant reduction in mitochondrial respiration of NRVMs. We generated left ventricular pressure overload model with thoracic aortic constriction (TAC) in cardiac specific Mitofusin-1 knockout model (c-Mfn1 KO). Systolic function was reduced in c-Mfn1 KO mice, and EM study showed an increase in dysfunctional mitochondria in the KO group subjected to TAC. Conclusions Mitofusin-1 becomes a biomarker for non-responders with heart failure. In addition, our results suggest that therapies targeting mitochondrial dynamics and homeostasis would become next generation therapy for severe heart failure patients. Funding Acknowledgement Type of funding source: None

Anaemia and heart failure

Open Medicine ◽  
2011 ◽  
Vol 6 (1) ◽  
pp. 11-25
Author(s):  
Enrico Vizzardi ◽  
Tania Bordonali ◽  
Elena Tanghetti ◽  
Marco Metra ◽  
Livio Cas
Keyword(s):  
Heart Failure ◽  
Ventricular Dysfunction ◽  
Severe Heart Failure ◽  
Left Ventricular ◽  
Favourable Effect ◽  
Heart Failure Trial ◽  
Patients With Heart Failure ◽  
Darbepoetin Alpha ◽  
Main Determinants ◽  
Independent Determinant

AbstractAnaemia is one of the most frequent co-morbidities in patients with heart failure. Its prevalence increases from 4% to7% in subjects with asymptomatic left ventricular dysfunction to >30% in patients with severe heart failure. Renal insufficiency, activation of inflammatory mediators and treatment with renin-angiotensin antagonists seem to be its main determinants. The results of many studies agree in providing evidence that anaemia is a powerful independent determinant of survival in patients with heart failure. However, the mechanisms of this relation are still not fully understood. Moreover a favourable effect of the correction of anaemia on prognosis has not yet been shown. Also In addition to this, controlled studies assessing its effects on exercise tolerance have yielded controversial results. Further research is needed to assess the effect of correcting anaemia in chronic heart failure (CHF) patients; ongoing reduction of events with RED-HF (Darbepoetin alpha in heart failure) trial will help define the role.

scholarly journals Linearity of the left ventricular end-systolic pressure-volume relation in patients with severe heart failure

1989 ◽  
Vol 14 (1) ◽  
pp. 127-134 ◽  
Author(s):  
Constantine N. Aroney ◽  
Howard C. Herrmann ◽  
Marc J. Semigran ◽  
G. William ◽  
Charles A. Boucher ◽  
...  
Keyword(s):  
Heart Failure ◽  
Severe Heart Failure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Volume Relation

scholarly journals Levosimendan treatment of severe acute congestive heart failure refractory to dobutamine/milrinone in children

2011 ◽  
Vol 68 (11) ◽  
pp. 979-984
Author(s):  
Sergej Prijic ◽  
Sanja Rakic ◽  
Ljubica Nikolic ◽  
Bosiljka Jovicic ◽  
Mila Stajevic ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Myocardial Contractility ◽  
Severe Heart Failure ◽  
Oxygen Demand ◽  
Left Ventricular ◽  
Myocardial Oxygen Demand ◽  
Univentricular Heart ◽  
Dilatative Cardiomyopathy ◽  
Hemodynamic Improvement

Introduction. Levosimendan is a novel positive inotropic agent which, improves myocardial contractility through its calcium-sensitizing action, without causing an increase in myocardial oxygen demand. Also, by opening ATP-sensitive potassium channels, it causes vasodilatation with the reduction in both afterload and preload. Because of the long halflife, its effects last for up 7 to 9 days after 24-hour infusion. Case report. We presented three patients 2, 15 and 17 years old. All the patients had severe acute deterioration of the previously diagnosed chronic heart failure (dilatative cardiomyopathy; univentricular heart with bidirectional Glenn anastomosis and restrictive bulboventricular foramen; bacterial endocarditis on artificial aortic valve with severe stenosis and regurgitation). Signs and symptoms of severe heart failure, cardiomegaly (cardio-thoracic index 0.65) and left ventricular dilatation (end-diastolic diameter z-score 2.6; 4.1 and 4.0) were confirmed on admission. Also, myocardial contractility was poor with ejection fraction (EF - 27%, 25%, 35%), fractional shortening (FS - 13%, 11%, 15%) and stroke volume (SV - 40, 60, 72 mL/m2). The treatment with standard intravenous inotropic agents resulted in no improvement but in clinical deterioration. Thus, standard intravenous inotropic support was stopped and levosimendan treatment was introduced. All the patients received a continuous 24-h infusion 0.1 ?g/kg/min of levosimendan. In a single patient an initial loading dose of 11 ?g/kg over 10 min was administrated, too. Levosimendan treatment resulted in both clinical and echocardiography improvement with the improved EF (42%, 34%, 44%), FS (21%, 16%, 22%) and SV (59, 82, 93 mL/m2). Hemodynamic improvement was registered too, with the reduction in heart rate in all the treated patients from 134-138 bpm before, to less than 120 bpm after the treatment. These parameters were followed by the normalization of lactate levels. Nevertheless, left ventricular end-diastolic diameter did not change after the levosimendan treatment. Conclusion. Our initial experience demonstrates that administration of levosimendan in patients with severe chronic heart failure not responsive to standard intravenous inotropic treatment might result in a significant clinical and hemodynamic improvement and that, in selected patients, it might be life saving. According to our best knowledge patients presented are the first pediatric patients treated with levosimendan in our country.

scholarly journals Exertional dyspnea after myocardial infarction: thinking beyond the diagnosis of heart failure

2018 ◽  
Vol 46 (11) ◽  
pp. 4769-4774
Author(s):  
Konstantinos Koutsampasopoulos ◽  
Savvas Grigoriadis ◽  
Ioannis Vogiatzis
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Aneurysm ◽  
Left Ventricular Myocardium ◽  
Inferior Wall ◽  
Delayed Presentation ◽  
Exertional Dyspnea ◽  
St Elevation

Introduction We herein present an unusual case of a pseudoaneurysm of the left ventricular myocardium, which is a rare and fatal complication of myocardial infarction. Case report A 64-year-old man with a history of bipolar disorder and arterial hypertension was hospitalized for delayed presentation ST-elevation myocardial infarction. He was admitted to our hospital 24 hours after symptom onset. Diagnostic coronary angiography revealed 95% stenosis at the distal third of the right coronary artery, and he underwent a primary percutaneous coronary intervention to the culprit lesion. Despite administration of a diuretic and optimization of other pharmaceutical treatment, his heart failure deteriorated. Electrocardiography showed a sinus rhythm with Q-wave formation in the inferior wall leads (II, III, aVF), T-wave inversion in the same leads, and borderline QT prolongation (QTc of 490 ms). No ST elevation suggestive of left ventricular aneurysm formation was noticed. Forty days later, cardiac ultrasound revealed a dyskinetic cavity (pseudoaneurysm) in continuity with the posterior–inferior wall of the myocardium, resulting in severe mitral valve regurgitation. Unfortunately, the patient died while awaiting surgical treatment. Conclusion Although most patients with left ventricular pseudoaneurysm have a relatively benign outcome, those with symptoms of heart failure must be urgently diagnosed and treated.

scholarly journals Increasing veno-arterial extracorporeal membrane oxygenation flow reduces electrical impedance of the lung regions in porcine acute heart failure

2020 ◽  
pp. 609-620 ◽  
Author(s):  
M Popková ◽  
E Kuriščák ◽  
P Hála ◽  
D Janák ◽  
L Tejkl ◽  
...  
Keyword(s):  
Heart Failure ◽  
Extracorporeal Membrane Oxygenation ◽  
Acute Heart Failure ◽  
Electrical Impedance ◽  
Severe Heart Failure ◽  
Left Ventricular ◽  
Fluid Accumulation ◽  
Impedance Tomography ◽  
Membrane Oxygenation ◽  
Ventricular Afterload

Veno-arterial extracorporeal membrane oxygenation (VA ECMO) is a technique used in patients with severe heart failure. The aim of this study was to evaluate its effects on left ventricular afterload and fluid accumulation in lungs with electrical impedance tomography (EIT). In eight swine, incremental increases of extracorporeal blood flow (EBF) were applied before and after the induction of ischemic heart failure. Hemodynamic parameters were continuously recorded and computational analysis of EIT was used to determine lung fluid accumulation. With an increase in EBF from 1 to 4 l/min in acute heart failure the associated increase of arterial pressure (raised by 44 %) was accompanied with significant decrease of electrical impedance of lung regions. Increasing EBF in healthy circulation did not cause lung impedance changes. Our findings indicate that in severe heart failure EIT may reflect fluid accumulation in lungs due to increasing EBF.

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