Cardiomyopathy Dilated Publications (20372)

Search

Cardiomyopathy Dilated Publications

2017Jan
Arch. Biochem. Biophys.
Arch Biochem Biophys 2017 Jan 11. Epub 2017 Jan 11.
Department of Pediatric Cardiac Surgery, UH Hospitals Cleveland, Cleveland, OH 44106, United States. Electronic address:

Mutations in the human cardiac motor protein beta-myosin heavy chain (βMHC) have been long recognized as a cause of familial hypertrophic cardiomyopathy. Recently, mutations (P830L and A1004S) in the less abundant but faster isoform alpha-myosin heavy chain (αMHC) have been linked to dilated cardiomyopathy (DCM). In this study, we sought to determine the cellular contractile phenotype associated with these point mutations. Read More

Ventricular myocytes were isolated from 2 month male Sprague Dawley rats. Cells were cultured in M199 media and infected with recombinant adenovirus containing the P830L or the A1004S mutant human αMHC at a MOI of 500 for 18 h. Uninfected cells (UI), human βMHC (MOI 500, 18 h), and human αMHC (MOI 500, 18 h) were used as controls. Cells were loaded with fura-2 (1 μM, 15 min) after 48 h. Sarcomere shortening and calcium transients were recorded in CO2 buffered M199 media (36°±1 C) with and without 10 nM isoproterenol (Iso). The A1004S mutation resulted in decreased peak sarcomere shortening while P830L demonstrated near normal shortening kinetics at baseline. In the presence of Iso, the A1004S sarcomere shortening was identical to the βMHC shortening while the P830L was identical to the αMHC control. All experimental groups had identical calcium transients. Despite a shared association with DCM, the P830L and A1004S αMHC mutations alter myocyte contractility in completely different ways while at the same preserving peak intracellular calcium.

2017Jan
Circ Arrhythm Electrophysiol
Circ Arrhythm Electrophysiol 2017 Jan;10(1)
From the Stephenson Cardiac Imaging Centre (Y.M., B.H., C.P.L., A.G.H., J.W.) and Department of Cardiac Sciences (Y.M., B.H., M.P., C.P.L., A.G.H., J.W.), Libin Cardiovascular Institute of Alberta, University of Calgary, Canada; Department of Diagnostic Imaging, University of Calgary, Alberta, Canada (B.H., C.P.L., A.G.H., J.W.); and Department of Medicine, London Health Sciences Centre, Ontario, Canada (U.J., F.A., M.Z., M.B., J.S., R.Y.).

Left ventricular ejection fraction remains the primary risk stratification tool used in the selection of patients for implantable cardioverter defibrillator therapy. However, this solitary marker fails to identify a substantial portion of patients experiencing sudden cardiac arrest. In this study, we examined the incremental value of considering right ventricular ejection fraction for the prediction of future arrhythmic events in patients with systolic dysfunction using the gold standard of cardiovascular magnetic resonance. Read More


Three hundred fourteen consecutive patients with ischemic cardiomyopathy or nonischemic dilated cardiomyopathy undergoing cardiovascular magnetic resonance were followed for the primary outcome of sudden cardiac arrest or appropriate implantable cardioverter defibrillator therapy. Blinded quantification of left ventricular and right ventricular (RV) volumes was performed from standard cine imaging. Quantification of fibrosis from late gadolinium enhancement imaging was incrementally performed. RV dysfunction was defined as right ventricular ejection fraction ≤45%. Among all patients (164 ischemic cardiomyopathy, 150 nonischemic dilated cardiomyopathy), the mean left ventricular ejection fraction was 32±12% (range, 6-54%) with mean right ventricular ejection fraction of 48±15% (range, 7-78%). At a median of 773 days, 49 patients (15.6%) experienced the primary outcome (9 sudden cardiac arrest, 40 appropriate implantable cardioverter defibrillator therapies). RV dysfunction was independently predictive of the primary outcome (hazard ratio=2.98; P=0.002). Among those with a left ventricular ejection fraction >35% (N=121; mean left ventricular ejection fraction, 45±6%), RV dysfunction provided an adjusted hazard ratio of 4.2 (P=0.02).
RV dysfunction is a strong, independent predictor of arrhythmic events. Among patients with mild to moderate LV dysfunction, a cohort greatly contributing to global sudden cardiac arrest burden, this marker provides robust discrimination of high- versus low-risk subjects.

2017Jan
Biochim. Biophys. Acta
Biochim Biophys Acta 2017 Jan 10. Epub 2017 Jan 10.
Department of Internal Medicine III (Cardiology, Angiology, Intensive Care), University Medical Center Kiel, 24105 Kiel, Germany; DZHK (German Centre for Cardiovascular Research), partner site Hamburg/Kiel/Lübeck, 24105 Kiel, Germany. Electronic address:
2017Jan
PLoS ONE
PLoS One 2017 13;12(1):e0170066. Epub 2017 Jan 13.
University of Ottawa, Dept. CMM, Ottawa, Ontario, Canada.

The E2F pathway plays a critical role in cardiac growth and development, yet its role in cardiac metabolism remains to be defined. Metabolic changes play important roles in human heart failure and studies imply the ketogenic enzyme β-hydroxybutyrate dehydrogenase I (BDH1) is a potential biomarker.
To define the role of the E2F pathway in cardiac metabolism and dilated cardiomyopathy (DCM) with a focus on BDH1. Read More


We previously developed transgenic (Tg) mice expressing the transcriptional repressor, E2F6, to interfere with the E2F/Rb pathway in post-natal myocardium. These Tg mice present with an E2F6 dose dependent DCM and deregulated connexin-43 (CX-43) levels in myocardium. Using the Seahorse platform, a 22% decrease in glycolysis was noted in neonatal cardiomyocytes isolated from E2F6-Tg hearts. This was associated with a 39% reduction in the glucose transporter GLUT4 and 50% less activation of the regulator of glucose metabolism AKT2. The specific reduction of cyclin B1 (70%) in Tg myocardium implicates its importance in supporting glycolysis in the postnatal heart. No changes in cyclin D expression (known to regulate mitochondrial activity) were noted and lipid metabolism remained unchanged in neonatal cardiomyocytes from Tg hearts. However, E2F6 induced a 40-fold increase of the Bdh1 transcript and 890% increase in its protein levels in hearts from Tg pups implying a potential impact on ketolysis. By contrast, BDH1 expression is not activated until adulthood in normal myocardium. Neonatal cardiomyocytes from Wt hearts incubated with the ketone β-hydroxybutyrate (β-OHB) showed a 100% increase in CX-43 protein levels, implying a role for ketone signaling in gap junction biology. Neonatal cardiomyocyte cultures from Tg hearts exhibited enhanced levels of BDH1 and CX-43 and were not responsive to β-OHB.
The data reveal a novel role for the E2F pathway in regulating glycolysis in the developing myocardium through a mechanism involving cyclin B1. We reveal BDH1 expression as an early biomarker of heart failure and its potential impact, through ketone signaling, on CX-43 levels in E2F6-induced DCM.

2017Jan
Cardiol Young
Cardiol Young 2017 Jan;27(S1):S80-S88
Departments of Pediatrics and Internal Medicine,Division of Pediatric Cardiology,Children's Specialty Physicians,Children's Hospital & Medical Center,University of Nebraska Medical Center,Creighton University Medical Center,Omaha,Nebraska,United States of America.

Chronic physical training has been shown to produce multiple changes in the heart, resulting in the athlete's heart phenotype. Some of the changes can make it difficult to discern athlete's heart from true cardiac disease, most notably hypertrophic cardiomyopathy. Other diseases such as dilated cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy may be difficult to rule in or out. Read More

In this article, the physiological cardiac changes of chronic athletic training are reviewed. A methodological approach using electrocardiography and echocardiography to differentiate between athlete's heart and cardiac disease is proposed.

2017Jan
Asian Cardiovasc Thorac Ann
Asian Cardiovasc Thorac Ann 2017 Jan 1:218492316689177. Epub 2017 Jan 1.
1 Department of Cardiovascular Diseases, Clínica Dávila, Santiago, Chile.

Background Durable mechanical support devices are prohibitively expensive in our health system and may be unsuitable for critically ill patients. CentriMag is an alternative bridge to transplantation or recovery. Methods We retrospectively reviewed 28 patients (23 males) aged 13-60 years who received CentriMag support. Read More

The etiology was ischemic in 13 (46%), dilated cardiomyopathy in 8 (29%), and others in 7 (25%). All patients were in Interagency Registry for Mechanically Assisted Circulatory Support class I, and 27 (96%) had multiorgan failure; 2 (7%) were post-cardiotomy and 12 (43%) had a previous cardiac arrest (mean arrest time 21 ± 17 min). Results Thirty-day post-implant survival was 79% (22 patients). Twenty (71%) patients were successfully bridged to transplantation or recovery. The mean support time was 40 days; 12 (43%) patients had >4-weeks' support (longest was 292 days). Eight (29%) patients died on support. Complications included bleeding in 10 (36%) cases, immediate stroke in 4 (14%), and dialysis in 8 (29%). There was no stroke during subsequent support. Eighteen (64%) patients underwent transplantation, and 17 of them were discharged. Two (7%) patients recovered and were discharged. Two-year survival was 62% ± 10%. Mean follow-up was 21 months (total follow-up 579 months). Two (7%) patients died during follow-up. All survivors were in New York Heart Association class I. Conclusions CentriMag is useful for medium-term support for cardiogenic shock in a developing country. Support for >4 weeks is feasible. The stroke rate is low during support. The major drawback is prolonged intensive care unit stay.

2017Jan
Pak J Med Sci
Pak J Med Sci 2016 Nov-Dec;32(6):1430-1433
Ghulam Mustafa, MBBS, MSPH. Assistant Professor of Community Medicine, Sheikh Zayed Medical College/Hospital, Rahim Yar Khan, Punjab, Pakistan.

To see the role of Vitamin D supplementation on physical status of patients suffering from Congestive Heart Failure (dilated cardiomyopathy).
In this nonrandomized clinical trial, Forty three Patients with dilated cardiomyopathy who were not showing any significant improvements in physical performance on optimal treatment of heart failure were included. Vitamin D (200,000 IU) supplementation on weekly basis for a period of 12 weeks was added to heart failure treatment. Read More

And its effect was seen on 6 minutes' walk distance and Pro-BNP levels. SPSS version 19 was used for data analysis. Dependent sample t-test was used to see the significant effect of vitamin D supplementation on pre- intervention vitamin D levels, 6MWD and Pro-BNP. Taking p-value <0.05 as significant.
On clinical assessment most of the patients were in NYHA class II (65%), the percentages of NYHA Class I, III and IV was 19%, 9% and 7% respectively. The baseline mean vitamin D level of the study group was 16.59±3.54ng/ml and it raised to 31.97±3.64ng/ml after 12 weeks of supplementation with vitamin D, p value<0.0005. The mean distance travelled by the study group before the intervention was 806±380ft while it increased to 945±393ft after the intervention, p value of 0.008. The mean of pro-BNP level of the study group before the intervention was 1024±635 while it improved to 159±80 after the intervention with a significant p value<0.0005.
Vitamin D supplementation decreases the severity of HF as reflected by reduction in serum pro-BNP levels and significant increase in six minutes' walk distance.

2017Jan
Eur J Cardiothorac Surg
Eur J Cardiothorac Surg 2017 Jan 12. Epub 2017 Jan 12.
Department of Cardiovascular Surgery, Chukyo Children's Heart Center, Nagoya, Japan.
2016Dec
Int. J. Cardiol.
Int J Cardiol 2016 Dec 27. Epub 2016 Dec 27.
Center of Microbiology and Parasitology, Public Health Institute Niš, Serbia, Blvd Zorana Djindjica 81, 18000 Niš, Serbia; Department of Microbiology and Immunology, Faculty of Medicine, University of Niš, Serbia, Blvd Zorana Djindjica 81, 18000 Niš, Serbia.

Although a subtype of hypertrophic cardiomyopathy (HCM), dilated phase of HCM (D-HCM) characterized by left ventricular (LV) systolic dysfunction, has been reported to have a poor prognosis, some patients with D-HCM survive for a relatively long period. The degree of LV dilatation and functional mitral regurgitation (MR) are generally thought to be important predictors of poor prognosis in patients with LV systolic dysfunction. However, there is little information available on the relations among LV size, presence of significant MR, and prognosis in D-HCM patients. Read More

We retrospectively studied 31 patients with D-HCM to determine whether echocardiographic assessment of LV size and MR provides incremental prognostic information.During a follow-up period of 5.6 ± 4.2 years, there were 13 cardiovascular deaths. When the patients were divided into two groups by LV size at diagnosis of D-HCM, a non-dilated LV group (LV end-diastolic diameter (LVEDD) < 50 mm, n = 9) and a dilated LV group (LVEDD ≥ 50 mm, n = 22), the clinical course in the non-dilated LV group was significantly worse. As for the clinical impact of MR, no patient in the non-dilated LV group showed significant MR and 7 of the patients with dilated LV size showed significant MR during follow-up. Once significant MR was reached, cardiovascular deaths were significantly more frequent in patients with MR.Patients with D-HCM, particularly those with less LV dilatation at diagnosis of dilated phase and with significant MR during follow-up, have a poor prognosis.