cardiac remodelling
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2022 ◽  
pp. 101728
Author(s):  
Patoomporn Prasartthong ◽  
Poungrat Pakdeechote ◽  
Putcharawipa Maneesai ◽  
Sariya Meephat ◽  
Siwayu Rattanakanokchai ◽  
...  

2022 ◽  
Vol 145 ◽  
pp. 112411
Author(s):  
Marija Kosić ◽  
Zorica Nešić ◽  
Sofija Glumac ◽  
Marko Vasić ◽  
Vladislav Pajović ◽  
...  
Keyword(s):  

2021 ◽  
Author(s):  
Dean R Perkins ◽  
Jack S Talbot ◽  
Rachel N Lord ◽  
Tony G Dawkins ◽  
Aaron L Baggish ◽  
...  

2021 ◽  
Author(s):  
Giedrė Balčiūnaitė ◽  
Justinas Besusparis ◽  
Darius Palionis ◽  
Edvardas Žurauskas ◽  
Viktor Skorniakov ◽  
...  

Abstract PurposeMyocardial fibrosis in aortic stenosis (AS) is associated with worse survival following aortic valve replacement (AVR). We assessed myocardial fibrosis in severe AS patients, integrating echocardiographic, cardiovascular magnetic resonance (CMR) and histological data. MethodsA total of 83 severe AS patients (age 66.4 ± 8.3, 42% male) who were scheduled for surgical AVR underwent CMR with late gadolinium enhancement (LGE) and T1 mapping and global longitudinal strain (GLS) analysis. Collagen volume fraction (CVF) was measured in myocardial biopsies (71) that were sampled at the time of AVR. ResultsCVF correlated with imaging and serum biomarkers of LV systolic dysfunction and left side chamber enlargement and was higher in the sub-endocardium compared with midmyocardium (p<0.001). CVF median values were higher in LGE-positive versus LGE-negative patients [28.7% (19-33) vs 20.7% (15-30), respectively, p=0.040]. GLS was associated with invasively (CVF; r=-0.303, p=0.013) and non-invasively (native T1; r=-0.321, p<0.05) measured myocardial fibrosis. GLS and native T1 correlated with parameters of adverse LV remodelling, systolic and diastolic dysfunction and serum biomarkers of heart failure and myocardial injury. ConclusionOur data highlight the role of myocardial fibrosis in adverse cardiac remodelling in AS. GLS has potential as a surrogate marker of myocardial fibrosis, and high native T1 and low GLS values differentiated patients with more advanced cardiac remodelling.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Emanuele F. Osimo ◽  
Mark Sweeney ◽  
Antonio de Marvao ◽  
Alaine Berry ◽  
Ben Statton ◽  
...  

AbstractCardiovascular diseases are the leading cause of death in schizophrenia. Patients with schizophrenia show evidence of concentric cardiac remodelling (CCR), defined as an increase in left-ventricular mass over end-diastolic volumes. CCR is a predictor of cardiac disease, but the molecular pathways leading to this in schizophrenia are unknown. We aimed to explore the relevance of hypertensive and non-hypertensive pathways to CCR and their potential molecular underpinnings in schizophrenia. In this multimodal case–control study, we collected cardiac and whole-body fat magnetic resonance imaging (MRI), clinical measures, and blood levels of several cardiometabolic biomarkers known to potentially cause CCR from individuals with schizophrenia, alongside healthy controls (HCs) matched for age, sex, ethnicity, and body surface area. Of the 50 participants, 34 (68%) were male. Participants with schizophrenia showed increases in cardiac concentricity (d = 0.71, 95% CI: 0.12, 1.30; p = 0.01), indicative of CCR, but showed no differences in overall content or regional distribution of adipose tissue compared to HCs. Despite the cardiac changes, participants with schizophrenia did not demonstrate activation of the hypertensive CCR pathway; however, they showed evidence of adipose dysfunction: adiponectin was reduced (d = −0.69, 95% CI: −1.28, −0.10; p = 0.02), with evidence of activation of downstream pathways, including hypertriglyceridemia, elevated C-reactive protein, fasting glucose, and alkaline phosphatase. In conclusion, people with schizophrenia showed adipose tissue dysfunction compared to body mass-matched HCs. The presence of non-hypertensive CCR and a dysmetabolic phenotype may contribute to excess cardiovascular risk in schizophrenia. If our results are confirmed, acting on this pathway could reduce cardiovascular risk and resultant life-years lost in people with schizophrenia.


2021 ◽  
Vol 23 (Supplement_G) ◽  
Author(s):  
Denise Zaffalon ◽  
Efstathios Papatheodorou ◽  
Ahmed Merghani ◽  
Harshil Dhutia ◽  
Eleonora Moccia ◽  
...  

Abstract Aims Physiological cardiac remodelling in highly trained athletes may overlap with dilated cardiomyopathy (DCM). The aim of this study was to investigate the role of the ECG in differentiating between physiological and pathological remodelling. Methods and results The study population consisted of 30 patients with DCM who revealed a pathogenic variant at genetic testing and 30 elite athletes with significant cardiac remodelling defined by a left ventricular (LV) end-diastolic diameter &gt; 62 mm and/or LV ejection fraction between 45% and 50%. The ECG was abnormal in 22 (73%) patients with DCM. The most common abnormalities were low voltages (n = 14, 47%), lateral TWI (n = 6, 20%), ventricular ectopic beats (n = 5, 17%) and anterior TWI (n = 4, 13). Two athletes revealed an abnormal ECG: complete left bundle branch block (LBBB) in one case and atrial flutter in the other. The sensitivity, specificity and accuracy of the ECG in differentiating DCM from physiological adaptation to exercise in athletes was 73% [confidence interval (CI: 54–88%), 93% (CI: 78–99%), and 0.83 (CI: 0.71–0.92), respectively. Conclusions While the ECG is usually normal in athletes exhibiting significant LV dilatation and/or systolic dysfunction, this test is often abnormal in patients with DCM harbouring a pathogenic variant. Low voltages in the limb leads and lateral TWI are the most common abnormalities.


2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Jan E. Engvall ◽  
Meriam Åström Aneq ◽  
Eva Nylander ◽  
Lars Brudin ◽  
Eva Maret

Abstract Background Elite athletes have been the subject of great interest, but athletes at an intermediate level of physical activity have received less attention in respect to the presence of cardiac enlargement and/or hypertrophy. We hypothesized that playing football, often defined as demanding less endurance components than running or cycling, would still induce remodelling similar to sports with a dominating endurance component. Methods 23 male football players, age 25+/− 3.9 yrs. underwent exercise testing, 2D- and 3D- echocardiography and cardiac magnetic resonance (CMR). The results were compared with a control group of engineering students of similar age. The athletes exercised 12 h/week and the control subjects 1 h/week, p < 0.001. Results The football players achieved a significantly higher maximal load at the exercise test (380 W vs 300 W, p < 0.001) as well as higher calculated maximal oxygen consumption, (49.7 vs 37.4 mL x kg− 1 x min− 1, p < 0.001) compared to the sedentary group. All left ventricular (LV) volumes assessed by 3DEcho and CMR, as well as CMR left atrial (LA) volume were significantly higher in the athletes (3D-LVEDV 200 vs 154 mL, CMR-LVEDV 229 vs 185 mL, CMR-LA volume 100 vs 89 mL, p < 0.001, p = 0.002 and p = 0.009 respectively). LVEF and RVEF, LV strain by CMR or by echo did not differentiate athletes from sedentary participants. Right ventricular (RV) longitudinal strain, LA and right atrial (RA) strain by CMR all showed similar results in the two groups. Conclusion Moderately trained intermediate level football players showed anatomical but not functional cardiac remodelling compared to sedentary males.


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