diastolic heart failure
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Author(s):  
Chihiro Miyagi ◽  
Kiyotaka Fukamachi ◽  
Barry D. Kuban ◽  
Shengquiang Gao ◽  
Takuma Miyamoto ◽  
...  

2021 ◽  
pp. 60-72
Author(s):  
Irina V. Opalinskaya ◽  
Galina V. Danilova ◽  
Natalya Yu. Isaeva ◽  
Ekaterina S. Petrova ◽  
Elena I. Busalaeva ◽  
...  

Primary amyloidosis is a disease with a complex and not fully understood pathogenesis, which is characterized by a wide range of clinical manifestations. Light chain amyloidosis is the most common form of systemic amyloidosis. At this, the heart is the dominant target organ in systemic amyloidosis. Cardiac amyloidosis (amyloid cardiomyopathy) is most often manifested by diastolic heart failure resulting from restrictive cardiomyopathy. Therapy of amyloid cardiopathy includes optimal treatment of heart failure and chemotherapy. To reduce the symptoms of heart failure, diuretics are the main means, since other pathogenetic agents cannot be used due to hypotension and a possible decrease in cardiac output. With the introduction of new medicinal products into clinical practice, such as the proteosome inhibitor Bortezomib, the prognosis for patients has improved. However, amyloidosis remains a difficult disease to diagnose and treat.


Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Alexander J Lu ◽  
Li Lai ◽  
Hyeon-Ju R Ali ◽  
Guha Ashrith ◽  
John P Cooke

Description of the Case: Patient 1 is a 61-year-old woman with a history of rheumatoid arthritis-related interstitial lung disease (ILD). Six months after initiation of nintedanib, she was diagnosed with new-onset heart failure. Cardiac magnetic resonance imaging (CMR) was consistent with nonischemic cardiomyopathy (NICM) with ejection fraction (EF) of 15-25%. EKG showed new bifascicular block (right bundle branch block and left anterior fascicular block). Nintedanib was discontinued, and four months later, echocardiogram showed recovered EF (50-54%). EKG abnormalities resolved with biventricular pacing. Patient 2 is a 57-year-old-man with a history of scleroderma-related ILD and stable diastolic heart failure (EF = 55-60%). Six months after initiation of nintedanib, he was admitted for heart failure exacerbation. CMR showed NICM with EF = 35%, and EKG showed prolonged QRS (130 ms). Given the rapid progression of cardiomyopathy, nintedanib was discontinued. Discussion: We report two patients with underlying connective tissue disease who developed significant nonischemic cardiomyopathy in temporal association with initiation of nintedanib. Nintedanib is a tyrosine kinase inhibitor, antagonizing three angiogenic signaling pathways mediated by vascular endothelial growth factor receptor (VEGFR), fibroblast growth factor receptor (FGFR), and platelet derived growth factor receptor (PDGFR). The nintedanib-treated cohorts of the TOMORROW and INPULSIS trials for idiopathic pulmonary fibrosis showed a high incidence of myocardial infarction (MI). With the recent SCENSIS trial, nintedanib was approved in 2019 for ILD associated with systemic sclerosis. There are likely multifactorial effects of this triple angiokinase inhibitor, seeing that it inhibits multiple growth factors essential for vascular homeostasis, the balance between mesenchymal and endothelial cell fates. Thus, there may be multiple pathways for cardiomyopathy due to “vascular failure,” including MI and importantly, cardiac fibrosis. Based on our observations, we urge other clinicians to report their experience with nintedanib use in patients with underlying connective tissue disease and to carefully monitor these patients for adverse cardiovascular effects.


Author(s):  
Daniel Soetkamp ◽  
Romain Gallet ◽  
Sarah J Parker ◽  
Ronald Holewinski ◽  
Vidya Venkatraman ◽  
...  

Rationale: Phosphorylation of sarcomeric proteins has been implicated in heart failure with preserved ejection fraction (HFpEF); such changes may contribute to diastolic dysfunction by altering contractility, cardiac stiffness, Ca 2+ -sensitivity and mechanosensing. Treatment with cardiosphere-derived cells (CDCs) restores normal diastolic function, attenuates fibrosis and inflammation, and improves survival in a rat HFpEF model. Objective: Phosphorylation changes that underlie HFpEF and those reversed by CDC therapy, with a focus on the sarcomeric subproteome were analyzed. Methods and Results: Dahl salt-sensitive rats fed a high-salt diet, with echocardiographically-verified diastolic dysfunction, were randomly assigned to either intracoronary CDCs or placebo. Dahl salt-sensitive rats receiving low salt diet served as controls. Protein, and phosphorylated Ser, Thr and Tyr residues from left ventricular tissue, were quantified by mass spectrometry. HFpEF hearts exhibited extensive hyperphosphorylation with 98% of the 529 significantly changed phospho-sites increased compared to control. Of those 39% were located within the sarcomeric subproteome, with a large group of proteins located or associated with the Z-disk. CDC treatment partially reverted the hyperphosphorylation, with 85% of the significantly altered 76 residues hypophosphorylated. Bioinformatic upstream analysis of the differentially phosphorylated protein residues revealed PKC as the dominant putative regulatory kinase. PKC isoform analysis indicated increases in PKC α, β and δ concentration, whereas CDC treatment led to a reversion of PKCβ. Use of PKC isoform specific inhibition and overexpression of various PKC isoforms strongly suggests PKCβ is the dominant kinase involved in hyperphosphorylation in HFpEF and is altered with CDC treatment. Conclusions: Increased protein phosphorylation at the Z-disk is associated with diastolic dysfunction, with PKC isoforms driving most quantified phosphorylation changes. Because CDCs reverse the key abnormalities in HFpEF and selectively reverse PKCβ upregulation, PKCβ merits being classified as a potential therapeutic target in HFpEF, a disease notoriously refractory to medical intervention,


2021 ◽  
Author(s):  
Naghmeh Ziaie ◽  
Khadijeh Ezoji ◽  
Seyedeh Golnaz Ziaei ◽  
Mohammad Chehrazi ◽  
Parviz Amri Maleh ◽  
...  

Abstract Background: Diastolic dysfunction has been reported in patients with COVID-19. Due to the role of N-terminal pro-brain natriuretic peptide (NT-proBNP) in the diagnosis of heart failure, this study investigated the relationship between serum NT-proBNP levels and diastolic heart failure in COVID-19 patients.Methods: This descriptive-analytical study was performed at Ayatollah Rouhani Hospital in Babol. Fifty-four patients with confirmed COVID-19 diagnosis who were admitted to the ICU were included in the study. The primary outcome was the relationship and predictive role of NT-proBNP and diastolic heart failure in patients with severe SARS-COV-2 infection. Patients with pro BNP >125 pg/mL underwent echocardiography and the relationship between echocardiographic indices and NT-proBNP was assessed as a secondary outcome.Results: Our study showed that plasma NT-proBNP levels in patients with increased diastolic dysfunction were associated with disease severity. It was also found that the cut-off point of NT-proBNP = 799 pg/mL could be a predictor of diastolic dysfunction grades two and three. In this study, patients with a serum NT-proBNP level equal or above 799 had 37 times higher chance of having diastolic dysfunction than those with a serum NT-proBNP level below 799. Patients with NT-proBNP above 556 had RV_EA> 2 in echocardiography, indicating increased right-sided filling pressures.Conclusion: Despite the confounding factors in the interpretation of the pro BNP level in COVID-19, its level can be used to estimate the presence of high-grade diastolic heart failure on the left and right sides of the heart and the presence of high filling pressures. Lower levels of NT-proBNP are associated with right-sided diastolic failure.


2021 ◽  
Vol 07 (09) ◽  
Author(s):  
S. Faid ◽  

Objective: Chronic constrictive pericarditis (CCP) is a rare entity responsible of diastolic heart failure. The true prevalence is yet to be defined. The purpose of this study was to describe the clinical and para-clinical characteristics of patients with CCP, the therapeutic management, the outcomes and impacting factors. Materials and Methods: We conducted a retrospective descriptive study from 2017 to 2020 including 9 patients hospitalized for CCP in our cardiovascular surgery department. Results: The mean age was of 32.6 years. Majority were men (n=7). Dyspnea was the most common sign. Peripheral signs were dominated by signs of right heart failure. Cardiac ultrasonography showed pericardial thickening and calcifications with Doppler adiastolic signs in 90% of cases. Thoracic CT was performed in 7 patients, cardiac MRI in one patient, showing calcifications and measuring the pericardial thickening. Cardiac catheterization performed in 6 patients showed the aspect of Dip plateau. Tuberculosis etiology was retained in 55.6%; post-radiation origin in one patient and 33.4 % of cases were idiopathic. All of patients benefited from subtotal pericardiectomy with good results in the medium and long term. Two deaths occurred, the first patient died following multi-visceral failure, the second died 3 years later from neoplasia. Conclusion: The CCP is a rare condition with poor prognosis. The diagnosis should be raised when there are signs of right heart failure associated with signs of hemodynamic adiastolia. The echocardiography, with computed tomography or cardiac MRI and especially cardiac catheterization confirm the diagnosis and also etiological orientation. Tuberculosis and idiopathic etiologies were the most common at our country. Medical treatment options are limited. Pericardiectomy remains the only radical treatment with good results in immediate, medium and long term.


2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Katie Anne Fopiano ◽  
Yanna Tian ◽  
Vadym Buncha ◽  
Liwei Lang ◽  
Zsolt Bagi

Coronary microvascular dysfunction (CMD) develops in patients with heart failure with preserved ejection fraction (HFpEF, also known as diastolic heart failure), but the nature of the underlying pathomechanisms behind this prevalent disease remain poorly understood. The hypothesis tested was that coronary microvascular rarefaction contributes to left ventricle (LV) diastolic function in HFpEF. The obese ZSF1 rat model of human HFpEF was employed and using transthoracic echocardiography it was found that 18-week-old male obese ZSF1 rats exhibited a significantly reduced E/A ratio (E=early, A=late mitral inflow peak velocities) and increased DT (E wave deceleration time) with no change in ejection fraction, indicating diastolic dysfunction. Coronary arteriolar and capillary trees were labeled using Tomato Lectin (Lycopersicon esculentum) DyLight®594 and were imaged by fluorescent confocal microscopy to generate image stacks for 3D reconstruction. Unbiased automated tracing of the microvasculature was done using VesselLucida360 software (MBF) followed by a morphometric analysis (VesselLucida Explorer). It was found that total vessel length and the number of vessel’s branching nodes were reduced in the obese ZSF1 rats, whereas the total vessel’s volumes remained consistent, when compared to the lean ZSF1 controls. These changes in the microvasculature were accompanied by decreased angiogenesis in the coronary arteries in the obese ZSF1 rats when compared to the lean ZSF1 rats using an ex vivo endothelial sprouting assay. From these results, it was concluded that vascular rarefaction and decreased angiogenesis both play a role in the development of LV diastolic dysfunction in the obese ZSF1 rat model of human HFpEF.


2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Man Liu ◽  
Hong Liu ◽  
Richard T Clements ◽  
Feng Feng ◽  
Jin O-Uchi ◽  
...  

Introduction: The prevalence of heart failure with preserved ejection fraction (HFpEF) is increasing, although there is no specific treatment for HFpEF yet because of poor understanding of the underlying pathophysiology. Our previous studies show that hypomagnesemia contributes to diastolic dysfunction and HFpEF by regulation of mitochondrial function and that Mg supplementation improves diastolic function. In this study, we investigated how mitochondria were affected by Mg deficiency. Methods: C57BL/6J mice were fed with a low-Mg diet (HypoMg mice, 15-30 mg/kg Mg) or a normal Mg diet (control mice, 600 mg/kg Mg) for 6 weeks. Mg repletion was achieved by feeding HypoMg mice with normal diet for another 6 weeks. Results: HypoMg mice showed significantly decreased serum Mg (0.38±0.03 mM vs. 1.14±0.03 mM of control, P<0.0001), diastolic dysfunction (E/e’=21.1±1.1 vs. 15.4±0.4 of control, P=0.011), increased mitochondrial ROS (1.9±0.2-fold of control, P<0.0001), decreased total mitochondrial Mg content (3.6±1.8 vs. 18.3±4.7 μM total Mg/mg mitochondrial protein of control, P=0.019), decreased ATP production in hearts (1.2±0.2 vs. 2.7±0.2 μmol/g heart tissue of control, P=0.0002), decreased complex I activity (ΔOCR NADH-rotenone =0.27±0.10 vs. 1.02±0.04 of control, P=0.0004 measured with Seahorse), and decreased complex I protein levels (50.2% reduction compared with control mice, P=0.009). Mg repletion reversed all these changes. Conclusion: HypoMg-induced diastolic dysfunction likely results from HypoMg-induced electron transport chain dysfunction resulting from a decrease in mitochondrial Mg content. Mg repletion reverses these changes, reinforcing the known correlation of increased Mg intake and reduced heart failure symptoms. In deficiency states, Mg supplementation may represent a novel treatment for diastolic heart failure by improving mitochondrial function.


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