scholarly journals Altered Aortic Hemodynamics and Relative Pressure in Patients with Dilated Cardiomyopathy

Author(s):  
David Marlevi ◽  
Jorge Mariscal-Harana ◽  
Nicholas S. Burris ◽  
Julio Sotelo ◽  
Bram Ruijsink ◽  
...  

AbstractVentricular-vascular interaction is central in the adaptation to cardiovascular disease. However, cardiomyopathy patients are predominantly monitored using cardiac biomarkers. The aim of this study is therefore to explore aortic function in dilated cardiomyopathy (DCM). Fourteen idiopathic DCM patients and 16 controls underwent cardiac magnetic resonance imaging, with aortic relative pressure derived using physics-based image processing and a virtual cohort utilized to assess the impact of cardiovascular properties on aortic behaviour. Subjects with reduced left ventricular systolic function had significantly reduced aortic relative pressure, increased aortic stiffness, and significantly delayed time-to-pressure peak duration. From the virtual cohort, aortic stiffness and aortic volumetric size were identified as key determinants of aortic relative pressure. As such, this study shows how advanced flow imaging and aortic hemodynamic evaluation could provide novel insights into the manifestation of DCM, with signs of both altered aortic structure and function derived in DCM using our proposed imaging protocol. Graphic Abstractr

2011 ◽  
Vol 65 (4) ◽  
pp. 207 ◽  
Author(s):  
Dardan Kocinaj ◽  
Aurora Bakalli ◽  
Masar gashi ◽  
Luljeta Begolli ◽  
Merita Berisha ◽  
...  

2016 ◽  
Vol 310 (11) ◽  
pp. H1808-H1815 ◽  
Author(s):  
Rasha M. S. M. Mohamed ◽  
Sachio Morimoto ◽  
Islam A. A. E.-H. Ibrahim ◽  
Dong-Yun Zhan ◽  
Cheng-Kun Du ◽  
...  

Glycogen synthase kinase-3β (GSK-3β) plays a central role in both cardiac physiology and pathology. Herein we want to clarify the role of GSK-3β in familial dilated cardiomyopathy. We generated a mouse model carrying a heterozygous knockout mutation of GSK-3β (GSK-3β+/− KO), together with a ΔK210 knockin mutation in cardiac troponin T (ΔK210 cTnT KI), which was proved to be one of the genetic causes of familial dilated cardiomyopathy (DCM). GSK-3β+/− KO prevented the slow and rapid deterioration in left ventricular systolic function accompanying heart failure (HF) in DCM mice with heterozygous and homozygous ΔK210 cTnT KI mutations, respectively. GSK-3β+/− KO also prevented cardiac enlargement, myocardial fibrosis, and cardiomyocyte apoptosis and markedly reduced the expression of cardiac β-myosin heavy chain isoform, indicative of HF, in DCM mice with homozygous ΔK210 cTnT KI mutation. GSK-3β+/− KO also extended the life span of these DCM mice. This study suggests that the inhibition of GSK-3β is cardioprotective in familial DCM associated with ΔK210 cTnT mutation.


2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Giv Heidari-Bateni ◽  
Lisa Goessling ◽  
Anoop Brar ◽  
Madeleine Cunningham ◽  
Pirooz Eghtesady

Introduction: Anti-cardiac myosin (CM) antibodies are induced following certain infectious diseases. We evaluated for the first time the effect of maternally-transferred anti-CM antibody on the newborn heart in a rat model. Methods: Female Lewis rats were immunized with 1 µg of emulsified CM and boosters (0.5 µg) were administered every 2 weeks, followed by mating; control rats (n=3) were injected with saline. After birth, pups were continually housed with dams. Echocardiography was performed on pups on day 20. Pups were sacrificed on day 21 and hearts were fixed, sectioned, and analyzed for morphological changes. Trichrome staining was performed to detect fibrotic changes. Results: All the pups in CM group (n=22) showed anti-CM antibody titers of more than 12800. Echocardiographic study revealed that 45.4% (10/22) of pups in the CM group had evidence of decreased left ventricular systolic function. The affected pups had both thinner anterior and inferior left ventricle walls compared with pups in control group (3.43±0.33 vs. 3.82±0.24, p=0.017 and 3.71±0.32 vs. 4.18±0.31, p=0.009 respectively). There were also evidence of underdevelopment of thoracic aorta and aortic arch (3.1±0.16 vs. 3.3±0.16 for ascending aorta diameter, p=0.002 and 2.6±0.14 vs. 2.8±0.25 for descending aorta diameter, p=0.008). Morphological changes consistent with dilated cardiomyopathy (image) and fibrosis were detected. Conclusion: Maternal anti-CM antibodies can cross the placenta and affect the development of the newborn heart; the resulting phenotype is one of dilated cardiomyopathy with associated hypoplasia of vascular structures perhaps secondary to reduced flow.


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