Ventricular electrical instability

Author(s):  
Günter Breithardt ◽  
Martin Borggrefe ◽  
Antoni Martínez-Rubio
Author(s):  
R. E. Worsham ◽  
J. E. Mann ◽  
E. G. Richardson

This superconducting microscope, Figure 1, was first operated in May, 1970. The column, which started life as a Siemens Elmiskop I, was modified by removing the objective and intermediate lenses, the specimen chamber, and the complete vacuum system. The large cryostat contains the objective lens and stage. They are attached to the bottom of the 7-liter helium vessel and are surrounded by two vapor-cooled radiation shields.In the initial operational period 5-mm and 2-mm focal length objective lens pole pieces were used giving magnification up to 45000X. Without a stigmator and precision ground pole pieces, a resolution of about 50-100Å was achieved. The boil-off rate of the liquid helium was reduced to 0.2-0.3ℓ/hour after elimination of thermal oscillations in the cryostat. The calculated boil-off was 0.2ℓ/hour. No effect caused by mechanical or electrical instability was found. Both 4.2°K and 1.7-1.9°K operation were routine. Flux pump excitation and control of the lens were quite smooth, simple, and, apparently highly stable. Alignment of the objective lens proved quite awkward, however, with the long-thin epoxy glass posts used for supporting the lens.


Author(s):  
Dongming Wang ◽  
Guangwei Wang ◽  
Yanbo Cai ◽  
Lingling Wu ◽  
Peng Zhu ◽  
...  

2021 ◽  
Vol 10 (11) ◽  
pp. 2385
Author(s):  
Paweł Muszyński ◽  
Tomasz A. Bonda

Despite the enormous progress in the treatment of atrial fibrillation, mainly with the use of invasive techniques, many questions remain unanswered regarding the pathomechanism of the arrhythmia and its prevention methods. The development of atrial fibrillation requires functional changes in the myocardium that result from disturbed ionic fluxes and altered electrophysiology of the cardiomyocyte. Electrical instability and electrical remodeling underlying the arrhythmia may result from a cellular energy deficit and oxidative stress, which are caused by mitochondrial dysfunction. The significance of mitochondrial dysfunction in the pathogenesis of atrial fibrillation remains not fully elucidated; however, it is emphasized by the reduction of atrial fibrillation burden after therapeutic interventions improving the mitochondrial welfare. This review summarizes the mechanisms of mitochondrial dysfunction related to atrial fibrillation and current pharmacological treatment options targeting mitochondria to prevent or improve the outcome of atrial fibrillation.


2009 ◽  
Vol 297 (4) ◽  
pp. H1235-H1242 ◽  
Author(s):  
Gregory S. Hoeker ◽  
Rodolphe P. Katra ◽  
Lance D. Wilson ◽  
Bradley N. Plummer ◽  
Kenneth R. Laurita

Abnormalities in calcium handling have been implicated as a significant source of electrical instability in heart failure (HF). While these abnormalities have been investigated extensively in isolated myocytes, how they manifest at the tissue level and trigger arrhythmias is not clear. We hypothesize that in HF, triggered activity (TA) is due to spontaneous calcium release from the sarcoplasmic reticulum that occurs in an aggregate of myocardial cells (an SRC) and that peak SCR amplitude is what determines whether TA will occur. Calcium and voltage optical mapping was performed in ventricular wedge preparations from canines with and without tachycardia-induced HF. In HF, steady-state calcium transients have reduced amplitude [135 vs. 170 ratiometric units (RU), P < 0.05] and increased duration (252 vs. 229 s, P < 0.05) compared with those of normal. Under control conditions and during β-adrenergic stimulation, TA was more frequent in HF (53% and 93%, respectively) compared with normal (0% and 55%, respectively, P < 0.025). The mechanism of arrhythmias was SCRs, leading to delayed afterdepolarization-mediated triggered beats. Interestingly, the rate of SCR rise was greater for events that triggered a beat (0.41 RU/ms) compared with those that did not (0.18 RU/ms, P < 0.001). In contrast, there was no difference in SCR amplitude between the two groups. In conclusion, TA in HF tissue is associated with abnormal calcium regulation and mediated by the spontaneous release of calcium from the sarcoplasmic reticulum in aggregates of myocardial cells (i.e., an SCR), but importantly, it is the rate of SCR rise rather than amplitude that was associated with TA.


2018 ◽  
Vol 83 (1) ◽  
pp. 91-100 ◽  
Author(s):  
Yoshinori Kobayashi ◽  
Kaoru Tanno ◽  
Akira Ueno ◽  
Seiji Fukamizu ◽  
Hiroshige Murata ◽  
...  

2021 ◽  
Vol 1 (1) ◽  
pp. 150-154
Author(s):  
I. Yu. Melnikova ◽  
Yu. A. Tokarevа

The purpose of the research. The optimization of the method electrocardiogram’s interpretation (ECG) for diagnosis and prognosis of fatal cardiogenic situations among children and teenagers depending on the severity of myocardial electrical instability.Materials and methods. The authors propose to use a modified method for assessing the “electrical quality of the heart”, proposed by A. N. Volobuev and co-authors in order to assess the electrical instability of the myocardium among children and teenagers. There is a formula which helps to estimate the index of “electrical quality factor of the heart” among children and teenagers: D=(aR/aT):(QT/QRS), where D is the index of “electrical quality factor of the heart”, aT and aR is the amplitude of R wave and T, QT — QT interval, QRS — interval, QRS. ECG was recorded in 12 leads, ECG assessment was carried out according to generally accepted rules.Results. Based on the analysis of 234 ECG of children and teenagers from the neonatal period to 18 years, the criteria of the average value of the index of “electrical quality factor of the heart” (D) were defined, D =1,09 +/- 0,03. It is proved that the value of the index “electrical quality factor of the heart” does not depend on the sex and age of the child. There was a decrease in the index of “electrical quality factor of the heart” was revealed among children with the lengthening of the QT interval.Conclusion. The index of “electrical quality factor of the heart” in pediatric practice allows to predict the risk of fatal cardiogenic conditions, to develop tactics of dynamic monitoring of patients, to evaluate the efficiency of treatment. When D<0.55 it is possible to predict high risk, at a value of 0.55≤D<0.80 — average risk, and at D≥0.80 — low risk of fatal cardiogenic conditions among children and teenagers.


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