Atrial Dyssynchrony Measured by Strain Echocardiography as a Marker of Proarrhythmic Remodeling and Oxidative Stress in Cardiac Surgery Patients

Abstract

Aging leads to structural and electrophysiological changes that increase the risk of postoperative atrial arrhythmias; however, noninvasive preoperative markers of atrial proarrhythmic conditions are still needed. This study is aimed at assessing whether interatrial dyssynchrony determined using two-dimensional speckle tracking echocardiography relates to proarrhythmic structural and functional remodeling. A cohort of 45 patients in sinus rhythm referred for cardiac surgery was evaluated by echocardiography and surface electrocardiogram the day before the intervention. Transmembrane potential, connexin, and potassium channel distribution, inflammatory, and nitrooxidative markers were measured from right atrial tissue obtained from patients. A difference greater than 40 milliseconds between right and left atrial free wall contraction confirmed the presence of interatrial dyssynchrony in 21 patients. No difference in relation with age, previous diseases, and 2-dimensional echocardiographic findings as well as average values of global longitudinal right and left atrial strain were found between synchronic and dyssynchronic patients. Postoperative atrial fibrillation incidence increased from 8.3% in the synchronic group to 33.3% in the dyssynchronic ones. P wave duration showed no difference between groups. Action potentials from dyssynchronous patients decreased in amplitude, maximal rate of depolarization, and hyperpolarized. Duration at 30% of repolarization increased, being markedly shorter at 90% of repolarization. Only the dyssynchronous group showed early and delayed afterdepolarizations. Atrial tissue of dyssynchronous patients displayed lateralization of connexin 40 and increased connexin 43 expression and accumulation of tumor necrosis factor-α in the intercalated disc. Tumor necrosis factor-α did not colocalize, however, with lateralized connexin 40. Nitroxidative marks and KATP channels increased perivascularly and in myocytes. Our results demonstrate that, as compared to a traditional surface electrocardiogram, the novel noninvasive echocardiographic evaluation of interatrial dyssynchrony provides a better identification of nonaged-related proarrhythmic atrial remodeling with increased susceptibility to postoperative atrial fibrillation.

Strain Echocardiography to Predict Postoperative Atrial Fibrillation

“…Patients with POAF have increased RA basal superoxide release, associated with higher tissue protein level of monoamine oxidase, NADPH oxidase 2, and p22phox subunits of NADPH oxidase. Although causality is yet to be demonstrated, atrial NADPH oxidase may be a key mediator of atrial oxidative stress that leads to the development of POAF [14]. Additionally, a study demonstrated the role of exogenous nitric oxide in reducing the incidence of POAF by using nitroprusside as a nitric oxide donor [15].…”

“…The substrates and mechanisms mentioned above are summarized in Table 2. [14,[22][23][24][25] calcium handling…”

“…Atrial synchrony, size (total atrial volume), and function (pump, compliance) are all significant landmarks in the evaluation of the atria that can reveal pathological states (Figure 3). More recently, atrial synchrony has proved to be another useful tool for atrial functional assessment [14,59,60]. Doppler evaluation has been used to determine atrial function and pressure [61].…”

“…It also disrupts Cx43 forward trafficking to the intercalated disk resulting in abnormal gap junction coupling [88]. Cx lateralization is associated with interatrial dyssynchrony measured by strain echocardiography [14].…”

(E)-5-Benzyl-7-(3,4-dimethoxybenzylidene)-3-(3,4-dimethoxyphenyl)-2-phenyl-3,3a,4,5,6,7-hexahydro-2H-pyrazolo[4,3c] Pyridine

“…A good balance between ROS and RNS with antioxidants is necessary for proper physiological function. Both ROS and RNS participate in the emergence of oxidative stress [1,2]. Oxidative stress plays an important role in the development of age-related diseases including arthritis, diabetes, dementia, cancer, atherosclerosis, vascular disease, osteoporosis, and metabolic syndrome [3,4].…”