CoenzymeQ in Cellular Redox Regulation and Clinical Heart Failure

: Pacemaker induced cardiomyopathy (PICM) is commonly defined as a reduction in left ventricular (LV) function in the setting of right ventricular (RV) pacing. This condition may be associated with the onset of clinical heart failure in those affected. Recent studies have focused on potential methods of identifying patients at risk of this condition, in addition to hypothesizing the most efficacious ways to manage these patients. Newer pacing options, such as His bundle pacing, may avoid the onset of PICM entirely.

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Overview of Pathophysiology of Clinical Heart Failure

Congestive Heart Failure ◽

10.1007/978-1-4613-8315-4_2 ◽

1994 ◽

pp. 11-16 ◽

Cited By ~ 3

Author(s):

Jay N. Cohn

Keyword(s):

Heart Failure ◽

Clinical Heart Failure

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Cell type-specific differences in redox regulation and proliferation after low UVA doses

10.1101/425793 ◽

2018 ◽

Author(s):

Sylwia Ciesielska ◽

Patryk Bil ◽

Karolina Gajda ◽

Aleksandra Poterala-Hejmo ◽

Dorota Hudy ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Redox Regulation ◽

Cellular Proliferation ◽

Reactive Oxygen ◽

Oxygen Species ◽

Cell Type ◽

Redox Systems ◽

Human Colon Cancer ◽

Cellular Redox ◽

Hct116 Cells

AbstractUltraviolet A (UVA) radiation is harmful for living organisms but in low doses may stimulate cell proliferation. Our aim was to examine the relationships between exposure to different low UVA doses, cellular proliferation, and changes in cellular reactive oxygen species levels. In human colon cancer (HCT116) and melanoma (Me45) cells exposed to UVA doses comparable to environmental, the highest doses (30-50 kJ/m2) reduced clonogenic potential but some lower doses (1 and 10 kJ/m2) induced proliferation. This effect was cell type and dose specific. In both cell lines the levels of reactive oxygen species and nitric oxide fluctuated with dynamics which were influenced differently by UVA; in Me45 cells decreased proliferation accompanied the changes in the dynamics of H2O2 while in HCT116 cells those of superoxide. Genes coding for proteins engaged in redox systems were expressed differently in each cell line; transcripts for thioredoxin, peroxiredoxin and glutathione peroxidase showed higher expression in HCT116 cells whereas those for glutathione transferases and copper chaperone were more abundant in Me45 cells. We conclude that these two cell types utilize different pathways for regulating their redox status. Many mechanisms engaged in maintaining cellular redox balance have been described. Here we show that the different cellular responses to a stimulus such as a specific dose of UVA may be consequences of the use of different redox control pathways. Assays of superoxide and hydrogen peroxide level changes after exposure to UVA may clarify mechanisms of cellular redox regulation and help in understanding responses to stressing factors.

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Abstract 13073: ECG, Clinical, and Imaging Characteristics of Arrhythmogenic Right Ventricular Cardiomyopathy With Fat and Fibrotic Invasion Into the Left Ventricular Myocardium Revealed by Four-dimensional (4D) Cardiac CT

Circulation ◽

10.1161/circ.142.suppl_3.13073 ◽

2020 ◽

Vol 142 (Suppl_3) ◽

Author(s):

Nobusada FUNABASHI ◽

Yoshio Kobayashi

Keyword(s):

Heart Failure ◽

Right Ventricular ◽

Cardiac Ct ◽

4D Ct ◽

Imaging Characteristics ◽

Group 3 ◽

Clinical Heart Failure ◽

Group 2 ◽

Group 1 ◽

T Waves

Introduction: 4D cardiac CT can reveal characteristics of arrhythmogenic right ventricular (RV) cardiomyopathy (ARVC) such as fat and fibrotic invasion into the RV and LV myocardium (RVM, LVM), an enlarged RV, reduced RV motion and bulging. Hypothesis: We could differentiate ARVC patients with fat and fibrotic invasion into the LVM from those without, using ECG, clinical, and other imaging characteristics. Methods: Retrospective analysis of 17 patients (11 males, 57±17 years) with suspected ARVC who underwent 4D cardiac CT. Results: 9 patients met the 2010 ARVC task force criteria. 4 had fat and fibrotic invasion into the LVM (group 1) but 5 did not (group 2). The remaining 8 did not fulfill the ARVC criteria (group 3). The proportion of males and age did not differ between groups. In groups 1, 2 and 3, respectively, 3 (75%), 4 (80%), and 1 (13%) patients had epsilon waves in V1-3 (group 1>3, P=0.033, group 2>3, P=0.005). 2 (50%), one (20%) and 4 (50%) had complete right bundle branch block (CRBBB) (all P=NS). Three (75%), 3 (60%), and 1 (13%) had inverted T waves in V1-3 or beyond (group 1>3, P=0.033). One (50%), 3 (75%), and 2 (50%) had terminal activation duration of QRS ≥55 ms measured from the nadir of the S wave to the end of the QRS, including R’, in V1, V2, or V3, in the absence of CRBBB (all P=NS). One (25%), 4 (80%) and 1 (13%) had sustained ventricular tachycardia (SVT; group 2>3, P=0.005). Two (50%), 1 (20%), and 3 (38%) had non-SVT (all P=NS). 4 (100%), 2 (40%), and 2 (25%) had clinical heart failure (group 1>2, P=0.019, group 1>3, P<0.001). Finally, 4 (100% and 80%) and 6 (75%) had RV enlargement on TTE (all P=NS). On 4D CT, 4 (100%), 5 (100%), and 5 (63%) of patients in groups 1, 2 and 3, showed RV enlargement (all P=NS); 4 (100%), 2 (40%), and 1 (13%) showed reduced RV motion (group 1>2, P=0.019, group 1>3, P<0.001); 75, 100, and 0%, had RV fat invasion (group 1>3, P=0.002, group 2>3, P<0.001); and 25, 0, and 0% showed bulging (all P=NS). Conclusions: Most patients had RV enlargement on TTE and/or 4D CT. Presence of epsilon waves, reduced RV motion, and RV fat invasion on 4D CT may differentiate groups 1 and 2 from group 3, inverted T waves in V1-3 leads or beyond may differentiate group 1 from group 3, SVT may differentiate group 2 from group 3 but only clinical heart failure may differentiate groups 1 and 2.

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