Myocardial disease

1991 ◽  
pp. 133-144
Author(s):  
Martin Kaltenbach ◽  
Ronald E. Vlietstra
Keyword(s):  
2019 ◽  
Vol 14 (4) ◽  
pp. 343-353 ◽  
Author(s):  
Yanbin Zhao ◽  
Kun Zhang ◽  
Patrick Sips ◽  
Calum A. MacRae
Keyword(s):  

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J Boidol ◽  
M Koziel ◽  
K Miszalski-Jamka ◽  
J Klys ◽  
Z Kalarus ◽  
...  

Abstract Background The clinical course and ventricular remodeling in inflammatory myocardial disease could be unpredictable. No single functional parameter has been confirmed as a powerful predictor of clinical course and functional recovery assessment in patients with acute inflammatory myocardial disease. Purpose The aim of the study was to assess the mechanical properties of the myocardium in patients with active myocarditis at baseline and follow-up. Methods Database from a high volume, tertiary cardiology center was analysed to identify patients with active myocarditis, based on clinical presentation and ≥1 diagnostic criteria from different categories (including electrocardiography/holter, elevated troponin T/I levels, functional or structural abnormalities on cardiac imaging or tissue characterization by cardiac magnetic resonance) between 2016 and 2019. Conventional and speckle tracking echocardiography including global longitudinal strain (GLS) mechanical dispersion (MD) was completed at baseline and at 17±13 months follow-up. MD was calculated as a standard deviation of time to peak longitudinal strain derived from all left ventricle segments in 3 apical views. Results 61 consecutive patients [50 M, 11F, end-diastolic volume 212±84 ml, end-systolic volume 130±90ml, ejection fraction (EF) 42±16%] were enrolled. During the entire follow-up 1 patient died at early observation. Implantable cardioverter-defibrillator was implanted in 5 patients (primary prevention 4, secondary 1), cardiac resynchronization therapy pacemaker in 1 patient. Despite of significant global improvement (EF 42±16% vs 52±10%, p<0.001) the limited regional improvement was noticed (GLS 14±6% vs 15±4%, p = NS; MD 47±18 ms vs 45±20 ms, p=NS) in all patients at 17±13 months follow-up. There was a strong negative association between GLS and MD at baseline (Figure 1), and slightly weaker at follow-up (R=0.47, Pearson's correlation). Moreover, the GLS correlated well the change of MD in each individual patient. Conclusions Mechanical dispersion and global longitudinal strain may serve as an additional markers of myocardial damage and potential predictive markers in non ischemic cardiomyopathy patients with proven inflammatory origin. Funding Acknowledgement Type of funding source: None


Author(s):  
Jeong Hoon Yang ◽  
William R Miranda ◽  
Rick A Nishimura ◽  
Kevin L Greason ◽  
Hartzell V Schaff ◽  
...  

Abstract Aims  Increased medial mitral annulus early diastolic velocity (e′) plays an important role in the echocardiographic diagnosis of constrictive pericarditis (CP) and mitral e′ velocity is also a marker of underlying myocardial disease. We assessed the prognostic implication of mitral e′ for long-term mortality after pericardiectomy in patients with CP. Methods and results  We studied 104 surgically confirmed CP patients who underwent echocardiography and cardiac catheterization within 7 days between 2005 and 2013. Patients were classified as primary CP (n = 45) or mixed CP (n = 59) based on the clinical history of concomitant myocardial disease. On multivariable analysis, medial e′ velocity and mean pulmonary artery pressure were independently associated with long-term mortality post-pericardiectomy. There were significant differences in survival rates among the groups divided by cut-off values of 9.0 cm/s and 29 mmHg for medial e′ and mean pulmonary artery pressure, respectively (both P < 0.001). Ninety-two patients (88.5%) had elevated pulmonary artery wedge pressure (PAWP) (≥15 mmHg); there was no significant correlation between medial E/e′ and PAWP (r = 0.002, P = 0.998). However, despite the similar PAWP between primary CP and mixed CP groups (21.6 ± 5.4 vs. 21.2 ± 5.8, P = 0.774), all primary CP individuals with elevated PAWP had medial E/e′ <15 as opposed to 34 patients (57.6%) in the mixed CP group (P < 0.001). Conclusion  Increased mitral e′ velocity is associated with better outcomes in patients with CP. A paradoxical distribution of the relationship between E/e′ and PAWP is present in these patients but there is no direct inverse correlation between them.


IRBM ◽  
2021 ◽  
Author(s):  
K. Brahim ◽  
A. Qayyum ◽  
A. Lalande ◽  
A. Boucher ◽  
A. Sakly ◽  
...  

2013 ◽  
Vol 10 (9) ◽  
pp. 489-489
Author(s):  
Gregory B. Lim
Keyword(s):  

2007 ◽  
Vol 28 (3) ◽  
pp. 284-293 ◽  
Author(s):  
Sarah Glyn-Jones ◽  
Sarah Song ◽  
Michael A. Black ◽  
Anthony R. J. Phillips ◽  
Soon Y. Choong ◽  
...  

Heart disease is the major cause of death in diabetes, a disorder characterized by chronic hyperglycemia and cardiovascular complications. Diabetic cardiomyopathy (DCM) is increasingly recognized as a major contributor to diastolic dysfunction and heart failure in diabetes, but its molecular basis has remained obscure, in part because of its multifactorial origins. Here we employed comparative transcriptomic methods with quantitative verification of selected transcripts by reverse transcriptase quantitative PCR to characterize the molecular basis of DCM in rats with streptozotocin-induced diabetes of 16-wk duration. Diabetes caused left ventricular disease that was accompanied by significant changes in the expression of 1,614 genes, 749 of which had functions assignable by Gene Ontology classification. Genes corresponding to proteins expressed in mitochondria accounted for a disproportionate number of those whose expression was significantly modified in DCM, consistent with the idea that the mitochondrion is a key target of the pathogenic processes that cause myocardial disease in diabetes. Diabetes also induced global perturbations in the expression of genes regulating cardiac fatty acid metabolism, whose dysfunction is likely to play a key role in the promotion of oxidative stress, thereby contributing to the pathogenesis of diabetic myocardial disease. In particular, these data point to impaired regulation of mitochondrial β-oxidation as central in the mechanisms that generate DCM pathogenesis. This study provides a comprehensive molecular snapshot of the processes leading to myocardial disease in diabetes.


Circulation ◽  
1967 ◽  
Vol 35 (4) ◽  
pp. 638-652 ◽  
Author(s):  
W. K. NASSER ◽  
J. F. WILLIAMS ◽  
M. E. MISHKIN ◽  
R. H. CHILDRESS ◽  
C. HELMEN ◽  
...  

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