Excitation-contraction coupling and cardiac contractile force: by Donald M. Bers, Kluwer Academic Publishers, 1991, $96.50 (xviii + 258 pages) ISBN 0 7923 1186 8

Pulsed-field ablation (PFA) is a promising new ablation modality for the treatment of atrial fibrillation. This energy form employs a train of microsecond duration high amplitude electrical pulses that ablate myocardium by electroporation of the sarcolemmal membrane without measurable tissue heating. The ablation pulse waveform has multiple variable components that can affect ablation efficacy, thus each proprietary system has unique properties that cannot be generalized to other systems. Success with PFA depends upon the proximity of the electrode to the target tissue, but not necessarily upon contact. A unique feature of PFA is tissue specificity. Myocardium is very susceptible to irreversible injury whereas the esophagus, phrenic nerves, pulmonary veins, and coronary arteries are relatively resistant to injury. The tissue specificity of PFA may result in a wide therapeutic range and improved safety profile during atrial fibrillation ablation. Vein isolation can be achieved very rapidly (seconds) promising that PFA may reduce procedure time to 1 hour or less. This attractive new technology promises to be a major advance in the field of atrial fibrillation ablation.

Pulsed field ablation for pulmonary vein isolation in the treatment of atrial fibrillation.

Evidence has shown that the sarcoplasmic reticulum (SR) of cardiac cells releases Ca not only during excitation-contraction coupling but also during diastole, albeit at a much lower rate. This diastolic SR Ca release (leak) has also been implicated in the generation of spontaneous depolarization in latent atrial pacemaker cells of the cat right atrium. In the present work, we sought to measure Ca transients in pacemaker and nonpacemaker cells of the cat using the fluorescent Ca indicator indo 1. Atrial latent pacemaker cells develop a slow Ca transient when rested in the presence of both Na- and Ca-free solution and thapsigargin [used to inhibit Na/Ca exchange and SR Ca adenosinetriphosphatase (Ca-ATPase), respectively]. This increase in cytosolic Ca concentration ([Ca]i) is probably caused by the rate of SR Ca leak exceeding the capacity of the remaining Ca transport systems (e.g., sarcolemmal Ca-ATPase and mitochondrial Ca uptake). However, neither cat sinoatrial (SA) node cells nor myocytes from cat atrium or ventricle exhibited a similar increase in [Ca]i during the same protocol. This indicates that SR Ca leak in these cells occurred at a rate low enough to be within the capacity of the slow Ca transporters, as observed previously in rabbit ventricular myocytes. When atrial and ventricular myocytes were stimulated at higher frequencies, sufficient to markedly increase diastolic and systolic [Ca]i and approach Ca overload (and spontaneous activity), they responded to inhibition of SR Ca-ATPase and Na/Ca exchange with a slow Ca transient similar to that normally observed in atrial latent pacemaker cells. Furthermore, the SR Ca depletion by thapsigargin did not affect spontaneous activity of SA node cells, but it prevented or slowed pacemaker activity in the atrial latent pacemaker cells. These findings suggest that enhanced diastolic SR Ca efflux contributes significantly to the generation of spontaneous activity in atrial subsidiary pacemakers under normal conditions and in Ca-overloaded myocytes but not in SA node cells.

Diastolic Sr Ca Efflux In Atrial Pacemaker Cells And Ca-overloaded Myocytes.

INTRODUCTION Opening of voltage-gated sodium channels takes tens to hundreds of microseconds, and mechanisms of their opening by nanosecond pulsed electric field (nsPEF) stimuli remain elusive. This study was aimed at uncovering the mechanisms of how nsPEF elicits action potentials (APs) in cardiomyocytes. METHODS AND RESULTS Fluorescent imaging of optical APs (FluoVolt) and Ca2+ -transients (Fluo-4) was performed in enzymatically isolated murine ventricular cardiomyocytes stimulated by 200-nanosecond trapezoidal pulses. nsPEF stimulation evoked tetrodotoxin-sensitive APs accompanied or preceded by slow sustained depolarization (SSD) and, in most cells, by transient afterdepolarization waves. SSD threshold was lower than the AP threshold (1.26 ± 0.03 vs 1.34 ± 0.03 kV/cm, respectively, P < 0.001). Inhibition of l-type calcium and sodium-calcium exchanger currents reduced the SSD amplitude and increased the AP threshold ( P < 0.05). The threshold for Ca 2+ -transients (1.40 ± 0.04 kV/cm) was not significantly affected by a tetrodotoxin-verapamil cocktail, suggesting the activation of a Ca 2+ entry pathway independent from the opening of Na + or Ca 2+ voltage-gated channels. Removal of external Ca 2+ decreased the SSD amplitude ( P = 0.004) and blocked Ca 2+ -transients but not APs. The incidence of transient afterdepolarization waves was decreased by verapamil and by removal of external Ca 2+ ( P = 0.002). CONCLUSIONS The study established that nsPEF stimulation caused calcium entry into cardiac myocytes (including routes other than voltage-gated calcium channels) and SSD. Tetrodotoxin-sensitive APs were mediated by SSD, whose amplitude depended on the calcium entry. Plasma membrane electroporation was the most likely primary mechanism of SSD with additional contribution from l-type calcium and sodium-calcium exchanger currents.

Excitation of murine cardiac myocytes by nanosecond pulsed electric field.

Pulsed Field Ablation: a New Paradigm for Catheter Ablation of Arrhythmias

Much of the academic and professional discourse within the design disciplines over the last century has been bereft of a critical reflection on the politics of design practice, and on the politics of the artifacts, systems and practices that designerly activity produces. Our premise is that— notwithstanding important and valued exceptions—design theory, practice, and pedagogy as a whole are not geared towards delivering the kinds of knowledge and understanding that are adequate to addressing longstanding systemic issues of power.

These issues are products of modernity and its ideologies, regimes, and institutions reiterating, producing and exerting continued colonial power upon the lives of oppressed, marginalised, and subaltern peoples in both the ‘developed’ and ‘developing’ world. This planet, shared and co- inhabited by a plurality of peoples, each inhabiting different worlds, each orienting themselves within and towards their environments in different ways, and with different civilisational histories, is being undermined by a globalised system of power that threatens to flatten and eradicate ontological and epistemological difference, rewriting histories and advance visions of a future for a privileged few at the expense of their human and nonhuman others.

/pdf/a-manifesto-for-decolonising-design-2tvyqn2lz3.pdf

A Manifesto for Decolonising Design

Although high-intensity electric fields (HEF) application is currently the only effective therapy available to terminate ventricular fibrillation, it may cause injury to cardiac cells. In this study we determined the relation between HEF pulse length and cardiomyocyte lethal injury. We obtained lethality curves by survival analysis, which were used to determine the value of HEF necessary to kill 50% of cells (E50) and plotted a strength-duration (SxD) curve for lethality with 10 different durations: 0.1, 0.2, 0.5, 1, 3, 5, 10, 20, 35 and 70 ms. For the same durations we also obtained an SxD curve for excitation and established an indicator for stimulatory safeness (stimulation safety factor - SSF) as the ratio between the SxD curve for lethality and one for excitation. We found that the lower the pulse duration, the higher the HEF intensity required to cell death. Contrary to expectations, the highest SSF value does not correspond to the lowest pulse duration but to the one of 0.5 ms. As defibrillation threshold has been described as duration-dependent, our results imply that the use of shorter stimulus duration - instead of the one typically used in the clinic (10 ms) - might increase defibrillation safeness.

/pdf/ventricular-myocyte-injury-by-high-intensity-electric-field-2ovptbcope.pdf

Ventricular myocyte injury by high-intensity electric field: Effect of pulse duration.

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A Manifesto for Decolonising Design

Ventricular myocyte injury by high-intensity electric field: Effect of pulse duration.