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2. Cough as a cause and consequence of heart dysfunction - current state of art

Creator:
Grabczak, Elzbieta M., Stec, Sebastian , Dąbrowska, Marta , Plevkova, Jana , and Krenke, Rafal
Format:
počítač and online zdroj
Type:
model:article and TEXT
Subject:
cough, cardiopulmonary reflexes, and arrhythmia
Language:
English
Description:
The cough reflex is an airway defensive process that can be modulated by afferent inputs from organs located also out of the respiratory system. A bidirectional relationship between cough and heart dysfunctions are presented in the article, with the special insights into an arrhythmia-triggered cough. Albeit rare, cough induced by cardiac pathologies (mainly arrhythmias) seems to be an interesting and underestimated phenomenon. This condition is usually associated with the presence of abnormal heart rhythms and ceases with successful treatment of arrhythmia either by pharmacotherapy or by radiofrequency ablation of arrhythmogenic substrate. The two main hypotheses on cough-heart relationships – reflex and hemodynamic - are discussed in the review, including the authors’ perspective based on the experiences with an arrhythmia-triggered cough.
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public

3. Effects of bepridil on stretch-activated BKca channels and stretch-induced extrasystoles in isolated chick hearts

Creator:
Jin, H., Iribe, G., and Naruse, K.
Format:
print, bez média, and svazek
Type:
article, články, journal articles, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, fyziologie, physiology, stretch-activated channels, arrhythmia, SAKca channels, bepridi, 14, and 612
Language:
English
Description:
Various types of mechanosensitive ion channels, including cationic stretch-activated channels (SAC NS ) and stretch-activated BKca (SAKca) channels, modulate heart rhythm. Bepridil has been used as an antiarrhythmic drug with multiple pharmacological effects; however, whether it is effective for mechanically induced arrhythmia has not been well investigated. To test the effects of Bepridil on SAKca channels activity, cultured chick embryo nic ventricular myocytes were used for single - channel recordings. Bepridil significantly reduced the open probability of the SAKca channel (PO). Next, to test the effects of bepridil on stretch-induced extrasystoles (SIE), we used an isolated 2-week-old Langendorff-perfused chick heart. The left ventricle (LV) volume was rapidly changed, and the probability of SIE was calculated in the presence and absence of bepridil, and the effect of the drug was compared with that of Gadolinium (Gd3+). Bepridil decreased the probability of SIE despite its suppressive effects on SAKca channel activity. The effects of Gd3+, which blocks both SAKca and SACNS , on the probability of SIE were the same as those of bepridil. Our results suggest that bepridil blocks not only SAKc a channels but possibly also blocks SACNS , and thus decreases the stretch -induced cation influx (stabilizing membrane potential) to compensate and override the effects of the decrease in outward SAKca current (destabilizing membrane potential)., H. Jin, G. Iribe, K. Naruse., and Obsahuje bibliografii
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public

4. JAK2/STAT3 pathway mediates beneficial effects of pterostilbene on cardiac contractile and electrical function in the setting of myocardial reperfusion injury

Creator:
Li, Sanjun, Wang, Hong, and Zhou, Yuxuan
Format:
počítač and online zdroj
Type:
model:article and TEXT
Subject:
arrhythmia, ischemia, reperfusion, signaling pathway, pterostilbene, and JAK2/STAT3
Language:
English
Description:
Contractile dysfunction and fatal arrhythmias are the hallmarks of myocardial ischemia/reperfusion (I/R) injury. Pterostilbene has notable cardioprotective effects, but its main mechanisms are not fully understood. Here, we investigated the effect of PTE on myocardial hemodynamics, arrhythmias, inflammatory/oxidative responses, and the causal role of the JAK2/STAT3 pathway in rats with acute myocardial I/R injury. Sixty male 7-8 months Sprague-Dawley rats (n=10/each group) experienced in vivo model of myocardial I/R injury through 40-min LAD coronary artery occlusion and subsequent 24-h reperfusion. PTE at concentrations of 5 and 25 mg/kg was intraperitoneally administered to rats five min before reperfusion. Cardiac hemodynamics, reperfusion-induced ventricular arrhythmias, infarct size, inflammatory cytokines, oxidative stress markers, the activity of the JAK2/STAT3 pathway were measured as the endpoints. Administration of PTE to I/R-injured rats recovered myocardial contractile function and reduced infarct size and ventricular arrhythmias counts and incidence in a dosedependent manner. PTE at 25 mg/kg significantly and more potently reduced the levels of inflammatory mediators NF-κB, TNF-α, and IL-1β, suppressed intracellular ROS production, augmented the activity of glutathione, and manganesesuperoxide dismutase, and upregulated the JAK2 and STAT3 phosphorylation. Importantly, pretreatment of rats with Ag490 as a JAK2 inhibitor significantly abolished the cardioprotective and signaling effects of PTE in I/R rats. PTE exerts significant protective effects on reducing arrhythmias and myocardial infarction and enhancing cardiac function by stimulating JAK2/STAT3-related suppression of inflammatory and oxidative reactions in the I/R injury setting.
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

5. The impact of atrial fibrillation and atrial tachycardias on the hemodynamic status of patients with pulmonary hypertension

Creator:
Dusik, Milan, Fingrova, Zdenka, Marek, Josef, Dytrych, Vladimir, Jansa, Pavel, and Havranek, Stepan
Format:
počítač and online zdroj
Type:
model:article and TEXT
Subject:
pulmonary hypertension, hemodynamics, arrhythmia, atrial fibrillation, and pulmonary artery catheterization
Language:
English
Description:
The impact of atrial fibrillation and atrial tachycardias (AF/AT), and their optimal treatment strategy in PH patients is still being discussed. The goal of this study was to evaluate the effect of AF/AT termination on the hemodynamic parameters in PH patients. We compared patients with pre-capillary pulmonary hypertension (PH group), left ventricular heart failure (LV-HF group), and a Control group. A repeated right heart catheterization was performed during the catheter ablation (CA) procedure. The first measurement was done in arrhythmia, the second after the sinus rhythm (SR) was restored. High frequency atrial stimulation was used to simulate AT in patients without arrhythmia presence at the time of the CA. The variation of pressure parameters in PH patients did not differ significantly from the Controls. There was a significant increase in the right ventricle pressure after the SR restoration in the LV-HF group compared to the Controls and PH group (+4 vs. -2 vs. -3 mmHg, p<0.05). The cardiac index (CI) variation was not significant when compared between the study groups. An increase of the CI after the SR restoration was found in those patients with AF (+0.31 l/min/m² [IQR 0.18; 0.58]) in contrast to those patients with organized AT/high frequency atrial stimulation (-0.09 l/min/m², [IQR - 0.45; 0.19]). This difference was statistically significant (p<0.05). The acute hemodynamic response to arrhythmia termination was not significantly different in the PH patients when compared to the Controls. In contrast to AT/high frequency stimulation, the restoration of SR in AF patients leads to an increased CI, irrespective of the presence or absence of PH.
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public