scholarly journals 280 Role of the electrocardiogram in differentiating genotype positive dilated cardiomyopathy from cardiac remodelling in athletes

2021 ◽  
Vol 23 (Supplement_G) ◽  
Author(s):  
Denise Zaffalon ◽  
Efstathios Papatheodorou ◽  
Ahmed Merghani ◽  
Harshil Dhutia ◽  
Eleonora Moccia ◽  
...  
Keyword(s):  
Dilated Cardiomyopathy ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Pathogenic Variant ◽  
Cardiac Remodelling ◽  
Physiological Adaptation ◽  
Study Population ◽  
Ectopic Beats ◽  
Sensitivity Specificity

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 > 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.

The role of inflammation in recent-onset dilated cardiomyopathy

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Chaloupka ◽  
J Krejci ◽  
H Poloczkova ◽  
P Hude ◽  
E Ozabalova ◽  
...  
Keyword(s):  
Dilated Cardiomyopathy ◽  
Left Ventricular ◽  
Pcr Analysis ◽  
Myocardial Inflammation ◽  
Gene Variants ◽  
Absolute Increase ◽  
Recent Onset ◽  
Cardiotropic Viruses

Abstract Background The aetiology of recent-onset dilated cardiomyopathy (RODCM) includes inflammatory, genetic, toxic and metabolic causes. Delineating the role of inflammation on the genetic background could improve risk stratification. Purpose We aimed to ascertain the role of inflammation evaluated by serum CRP immunohistochemical and PCR analysis of endomyocardial biopsy (EMB) in conjunction with genetic testing in left ventricular reverse remodelling (LVRR) in 12-month follow-up. Methods 83 RODCM patients enrolled in this prospective observational study underwent 12-month echocardiographic follow up whole-exome sequencing, and EMB. Presence of cardiotropic viruses was determined by PCR analysis of the EMB samples. Inflammation was defined according to TIMIC immunohistochemical criteria as the presence of >7 CD3+ lymphocytes/mm2 and/or >14 infiltrating leukocytes (LCA+ cells/mm2). LVRR was defined as an absolute increase in LV ejection fraction > +10% and a relative decrease of LV end-diastolic diameter >−10% at 12 months. Results LVRR occurred in 28 (34%) of all cases. PCR analysis uncovered cardiotropic viruses in 55 (66%) patients, with highest prevalence of parvovirus B19 (47%). (Figure 1) EMB analysis detected inflammation in 28 (34%) cases and inflammation significantly positively predicted LVRR (P=0.019). Sequencing identified disease-related gene variants (ACMG class 3–5) in 45 (54%) patients. Carriers of non-titin gene variants showed a lowest probability of 12-month LVRR (19%) P=0.041. Combination of genetic findings and inflammation did not improve the prediction of LVRR in 12 months. (Table 1) Conclusion Both myocardial inflammation and disease-causing variants can be identified in a large proportion of RODCM cases. Prognostic value of CRP and virus detection is low. Non-titin disease-related variants carriers of are less likely to reach LVRR. In contrast, myocardial inflammation detected by EMB predicts favourable remodelling in 12 months. Figure 1 Funding Acknowledgement Type of funding source: None

scholarly journals Torsion Mechanics as an Indicator of More Advanced Left Ventricular Systolic Dysfunction in Secondary Mitral Regurgitation in Patients with Dilated Cardiomyopathy: A 2D Speckle-Tracking Analysis

Cardiology ◽  
2018 ◽  
Vol 139 (3) ◽  
pp. 187-196 ◽  
Author(s):  
Elena Kinova ◽  
Natalia Spasova ◽  
Angelina Borizanova ◽  
Assen Goudev
Keyword(s):  
Mitral Regurgitation ◽  
Dilated Cardiomyopathy ◽  
Speckle Tracking ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Functional Mitral Regurgitation ◽  
Compensatory Mechanism ◽  
Structural Wall ◽  
Group 2 ◽  
Group 1

Left ventricular (LV) twist serves as a compensatory mechanism in systolic dysfunction and its degree of reduction may reflect a more advanced stage of disease. Aim: The aim was to investigate twist alterations depending on the degree of functional mitral regurgitation (MR) by speckle-tracking echocardiography. Methods: Sixty-three patients with symptomatic dilated cardiomyopathy (DCM) were included. Patients were divided according to MR vena contracta width (VCW): group 1 with VCW <7 mm (mild/moderate MR) and group 2 with VCW ≥7 mm (severe MR). Results: There were no differences in LV geometry and function between groups. Group 2 showed lower endocardial basal rotation (BR) (–2.04° ± 1.83° vs. –3.23° ± 1.83°, p = 0.012); epicardial BR (–1.54° ± 1.18° vs. –2.31° ± 1.22°, p = 0.015); endocardial torsion (0.41°/cm ± 0.36°/cm vs. 0.63°/cm ± 0.44°/cm, p = 0.033) and mid-level circumferential strain (CSmid) (–6.12% ± 2.64% vs. –7.75% ± 2.90%, p = 0.028), when compared with group 1. Multivariable linear regression analysis identified endocardial BR, torsion and CSmid, as the best predictors of larger VCW. In the ROC curve analysis, endocardial BR and CSmid values greater than or equal to –3.63° and –9.35%, respectively, can differentiate patients with severe MR. Conclusions: In DCM patients, torsional profile was more altered in severe MR. Endocardial BR, endocardial torsion, and CSmid, can be used as indicators of advanced structural wall architecture damage.

scholarly journals The Role of Cardiac T-Cadherin in the Indicating Heart Failure Severity of Patients with Non-Ischemic Dilated Cardiomyopathy

Medicina ◽  
2020 ◽  
Vol 56 (1) ◽  
pp. 27
Author(s):  
Vaida Baltrūnienė ◽  
Ieva Rinkūnaitė ◽  
Julius Bogomolovas ◽  
Daiva Bironaitė ◽  
Ieva Kažukauskienė ◽  
...  
Keyword(s):  
Heart Failure ◽  
Dilated Cardiomyopathy ◽  
Experimental Studies ◽  
Left Ventricular ◽  
Human Myocardium ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cox Regression Analysis ◽  
Non Ischemic Dilated Cardiomyopathy ◽  
The Mean

Background and objectives: T-cadherin (T-cad) is one of the adiponectin receptors abundantly expressed in the heart and blood vessels. Experimental studies show that T-cad sequesters adiponectin in cardiovascular tissues and is critical for adiponectin-mediated cardio-protection. However, there are no data connecting cardiac T-cad levels with human chronic heart failure (HF). The aim of this study was to assess whether myocardial T-cad concentration is associated with chronic HF severity and whether the T-cad levels in human heart tissue might predict outcomes in patients with non-ischemic dilated cardiomyopathy (NI-DCM). Materials and Methods: 29 patients with chronic NI-DCM and advanced HF were enrolled. Patients underwent regular laboratory investigations, echocardiography, coronary angiography, and right heart catheterization. TNF-α and IL6 in serum were detected by enzyme-linked immunosorbent assay (ELISA). Additionally, endomyocardial biopsies were obtained, and the levels of T-cad were assessed by ELISA and CD3, CD45Ro, CD68, and CD4- immunohistochemically. Mean pulmonary capillary wedge pressure (PCWP) was used as a marker of HF severity, subdividing patients into two groups: mean PCWP > 19 mmHg vs. mean PCWP < 19 mmHg. Patients were followed-up for 5 years. The study outcome was composite: left ventricular assist device implantation, heart transplantation, or death from cardiovascular causes. Results: T-cad shows an inverse correlation with the mean PCWP (rho = −0.397, p = 0.037). There is a tendency towards a lower T-cad concentration in patients with more severe HF, as indicated by the mean PCWP > 19 mmHg compared to those with mean PCWP ≤ 19 mmHg (p = 0.058). Cardiac T-cad levels correlate negatively with myocardial CD3 cell count (rho = −0.423, p = 0.028). Conclusions: Univariate Cox regression analysis did not prove T-cad to be an outcome predictor (HR = 1, p = 0.349). However, decreased T-cad levels in human myocardium can be an additional indicator of HF severity. T-cad in human myocardium has an anti-inflammatory role. More studies are needed to extend the role of T-cad in the outcome prediction of patients with NI-DCM.

P595Characteristics of the right ventricle in patients with nonischemic dilated cardiomyopathy

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Becker ◽  
C P Allaart ◽  
M Wubben ◽  
J H Cornel ◽  
A C Van Rossum ◽  
...  
Keyword(s):  
Ejection Fraction ◽  
Right Ventricular ◽  
Dilated Cardiomyopathy ◽  
Ventricular Function ◽  
Left Atrial ◽  
Systolic Dysfunction ◽  
Underlying Mechanism ◽  
Left Ventricular ◽  
End Diastolic Volume ◽  
Nonischemic Dilated Cardiomyopathy

Abstract Background In nonischemic dilated cardiomyopathy (DCM), diagnosis and prognosis is based on left ventricular function. Although concomitant right ventricular (RV) dysfunction is frequently observed, the underlying mechanism is currently not fully understood. Purpose We aimed to describe the characteristics of right ventricular function in DCM patients with cardiac magnetic resonance (CMR) imaging using cine and late-gadolinium enhancement (LGE) imaging. Methods Patients with DCM and left ventricular (LV) dysfunction (ejection fraction (EF) <50%) on LGE-CMR were included prospectively. LV and RV volumes and function were quantified and RV systolic dysfunction was defined as RV ejection fraction (RVEF)<45%. The presence and pattern of LGE were assessed visually and the extent was quantified using the full-width half maximum method. Septal midmyocardial LGE pattern was defined as midwall striae or hinge-point myocardial hyperenhancement. Moreover, left atrial (LA) volumes were calculated using the bi-plane area-length method. Results The study included 214 DCM patients (42% female, age 58±14 years) with a mean LVEF of 34±12% and RVEF of 46±12%. RV systolic dysfunction was present in 39% and was associated with the presence of septal midwall LGE (OR 1.96 (95% CI 1.09–3.54) p=0.026). In patients with RV dysfunction, LV dilation was more severe (LV end diastolic volume (EDV) 242±97mL vs. 212±58mL, p=0.011) and LVEF was lowere (26±12% vs. 39±8%, p<0.001) (figure A). There was a weak correlation between septal LGE amount and LVEDV and RVEDV (respectively r=0.36, p=0.003 and r=0.35, p=0.005) In patients with RV dysfunction, left atrial volumes were enlarged (56±23mL/m2 vs. 46±14mL/m2, p<0.001) and LA emptying fraction was moderately correlated to RVEF (figure B), also after exclusion of patients with a history of atrial fibrillation. RVEF in DCM patients Conclusion In DCM, reduced RVEF predominantly occurred in patients with a) LVEF lower than 30%, b) septal midwall enhancement, indicating progressive LV remodeling, c) LA dilation and d) LA dysfunction. This suggests that RV dysfunction in advanced DCM is drive by LV diastolic dysfunction resulting in increased afterload of the RV.

scholarly journals P784 Cardiac remodelling in elite rowers - insights from novel echocardiographic techniques

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
G Kleinnibbelink ◽  
N M Panhuyzen-Goedkoop ◽  
H G Hulshof ◽  
A P J Van Dijk ◽  
K P George ◽  
...  
Keyword(s):  
Exercise Training ◽  
Elite Athlete ◽  
Left Ventricular ◽  
Cardiac Remodelling ◽  
Physiological Adaptation ◽  
Training Volume ◽  
Short Term ◽  
Apical Rotation ◽  
Elite Rowers ◽  
The Impact

Abstract Funding Acknowledgements No financial support Background Chronic exercise training leads to cardiac remodelling; the so-called Athlete’s Heart. Previous studies are often limited by a cross-sectional design whilst longitudinal training studies are often constrained to the assessment of non-athletes. Echocardiography provides comprehensive assessment of mechanics and may give additional insight into short-term changes in training volume in the elite athlete. Purpose To examine the impact of a short-term (9 months) increase in training volume on cardiac structure and mechanics in elite international competing rowers. Methods As part of the work-up to the 2012 Olympic Games, twenty-seven elite rowers (26.4 ± 3.7 years, 19 male) underwent baseline echocardiography prior to and post (9-months) a planned increase in training volume. Conventional echocardiographic indices including mechanics of all cardiac chambers were assessed. Results In response to increased training volume, there was a significant increase in left ventricular (LV) size (IVSd 9.2 ± 1.2 to 9.7 ± 1.1 mm, p = 0.001; PWd 8.3 ± 1.3 to 8.7 ± 1.4 mm, p = 0.013), LVIDd (56.5 ± 4.6 to 57.9 ± 4.2 mm, p = 0.001), and LVMi (90.2 ± 17.8 to 100.8 ± 17.1 g/m2, p = 0.000), see table. There was a significant increase in LV twist (9.2 ± 4.5 to 11.2 ± 4.7 °, p = 0.04; basal rotation -4.4 ± 3.1 to -4.5 ± 3.4 °, p = 0.84; apical rotation 5.8 ± 3.4 to 7.1 ± 3.7 °, p = 0.011), see figure, however, there were no changes in any other conventional indices of function or any other cardiac mechanics. There was a significant increase in left atrial (LA) volume (58.8 ± 15.2 to 65.3 ± 17.6 mm, p = 0.01) whilst no changes were observed in right heart structure. Conclusion An increase in exercise training volume in elite rowers across 9-months induced mild balanced structural remodelling of the LV and LA with a concomitant increase in LV twist. Contradictory to findings in non-athletes, there was no increase in right ventricular or atrial structure or function which may be representative of the elite athlete status and possibly already at threshold for physiological adaptation. Abstract P784 Figure.

scholarly journals Orai1 Channel Inhibition Preserves Left Ventricular Systolic Function and Normal Ca 2+ Handling After Pressure Overload

Circulation ◽  
2020 ◽  
Vol 141 (3) ◽  
pp. 199-216 ◽  
Author(s):  
Fiona Bartoli ◽  
Marc A. Bailey ◽  
Baptiste Rode ◽  
Philippe Mateo ◽  
Fabrice Antigny ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Systolic Function ◽  
Systolic Dysfunction ◽  
Pressure Overload ◽  
Left Ventricular Systolic Function ◽  
Left Ventricular ◽  
Specific Expression ◽  
Channel Inhibition

Background: Orai1 is a critical ion channel subunit, best recognized as a mediator of store-operated Ca 2+ entry (SOCE) in nonexcitable cells. SOCE has recently emerged as a key contributor of cardiac hypertrophy and heart failure but the relevance of Orai1 is still unclear. Methods: To test the role of these Orai1 channels in the cardiac pathophysiology, a transgenic mouse was generated with cardiomyocyte-specific expression of an ion pore-disruptive Orai1 R91W mutant (C-dnO1). Synthetic chemistry and channel screening strategies were used to develop 4-(2,5-dimethoxyphenyl)-N-[(pyridin-4-yl)methyl]aniline (hereafter referred to as JPIII), a small-molecule Orai1 channel inhibitor suitable for in vivo delivery. Results: Adult mice subjected to transverse aortic constriction (TAC) developed cardiac hypertrophy and reduced ventricular function associated with increased Orai1 expression and Orai1-dependent SOCE (assessed by Mn 2+ influx). C-dnO1 mice displayed normal cardiac electromechanical function and cellular excitation-contraction coupling despite reduced Orai1-dependent SOCE. Five weeks after TAC, C-dnO1 mice were protected from systolic dysfunction (assessed by preserved left ventricular fractional shortening and ejection fraction) even if increased cardiac mass and prohypertrophic markers induction were observed. This is correlated with a protection from TAC-induced cellular Ca 2+ signaling alterations (increased SOCE, decreased [Ca 2+ ] i transients amplitude and decay rate, lower SR Ca 2+ load and depressed cellular contractility) and SERCA2a downregulation in ventricular cardiomyocytes from C-dnO1 mice, associated with blunted Pyk2 signaling. There was also less fibrosis in heart sections from C-dnO1 mice after TAC. Moreover, 3 weeks treatment with JPIII following 5 weeks of TAC confirmed the translational relevance of an Orai1 inhibition strategy during hypertrophic insult. Conclusions: The findings suggest a key role of cardiac Orai1 channels and the potential for Orai1 channel inhibitors as inotropic therapies for maintaining contractility reserve after hypertrophic stress.

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