Response by Kass et al to Letter Regarding Article, "Chronic Atrial and Ventricular Pacing in the Mouse: Application to Model Cardiac Dyssynchrony and Resynchronization in Heart Failure".
Response by Kass et al to Letter Regarding Article, "Chronic Atrial and Ventricular Pacing in the Mouse: Application to Model Cardiac Dyssynchrony and Resynchronization in Heart Failure".
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Kass 等人对有关文章“小鼠慢性心房和心室起搏：在心力衰竭中心脏不同步和再同步模型的应用”的信件的回应。
DOI：
10.1161/circheartfailure.119.006094
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发表时间：
2019
期刊：
影响因子：
--
通讯作者：
Ståhlberg,Marcus
中科院分区：
文献类型：
--
作者：
Kass,DavidA;Nakagawa,Ryo;Ståhlberg,Marcus
Etzion和Mulla博士指出，我们使用房室（AV）分离的右心室（RV）起搏而不是AV延迟缩短的AV起搏存在局限性。1我们同意这些是限制。理想的方法是感知心房，以缩短的AV延迟起搏RV，然后使用双心室刺激和相同的短AV延迟（最佳）或恢复到正常窦性（次佳）。相比之下，我们的方法结合了不同步/失步和AV定时的丢失/恢复。然而，每个因素的影响是不同的，前者是内在的左心室（LV）收缩性能，后者的前负荷。在之前的大鼠研究中，Mulla等人2比较了急性AV顺序起搏与仅RV起搏。由于失去了适当的心房计时，相对于AV顺序起搏，仅RV起搏可预见地减少了前负荷，因此与较低的收缩压、每搏输出量、每搏功和dP/dt max相关。然而，收缩期的较低前负荷敏感性测量，例如射血分数或收缩末期压力/容积比（后者可从表1中估计），如果仅RV起搏的话，则更高。考虑到体内平衡机制会提高前负荷以帮助恢复动脉压和心输出量，RV起搏的低前负荷也不太可能持续数周（正如我们所研究的那样）。小鼠心脏比大鼠小10倍，这使得多腔刺激成为一项极端的技术挑战。不能使用Hulsman等人3的市售起搏装置，因为其仅提供一根电极导线，虽然我们的方法可以处理双腔刺激，但电极导线植入仍然很困难。重要的是，我们的小鼠数据与使用RV快速起搏并忽略AV协调的犬模型（大多数已发表的分子/细胞数据的来源）的报告结果匹配良好。器官和有限的可用分子人类数据也与该动物模型的发现很好地匹配。4犬的研究还发现，从RV快速起搏过渡到双心室或心房快速起搏，也会产生类似的改善。总之，这表明单部位心室起搏及其逆转为心房起搏的主导效应源于不同步，而房室协调是次要因素。在微引线技术的进步之前，我们认为我们的模型提供了不同步/非同步化生理学的关键要素，但在小鼠中这样做提供了适合基因工程的额外优势。
Drs Etzion and Mulla note limitations from our use of right ventricular (RV) pacing with atrial ventricular (AV) dissociation rather than AV pacing with a shortened AV delay. 1 We agree these are limitations. The ideal approach would be to sense the atria, pace the RV with a shortened AV delay, and then resynchronize either with biventricular stimulation and the same short AV delay (best) or revert to normal sinus (next best). By contrast, our approach combined both dyssynchrony/resynchronization and loss/recovery of AV timing. However, the impact of each factor differs, the former being on intrinsic left ventricular (LV) systolic performance, the latter on preload. In their prior rat study, Mulla et al 2 compared acute AV sequential to RV-only pacing. RV-only pacing predictably reduced preload relative to AV sequential pacing because of loss of proper atrial timing and was thus associated with lower systolic pressure, stroke volume, stroke work, and dP/dt max. However, less preload-sensitive measures of systole, such as ejection fraction or end-systolic pressure/volume ratio (the latter can be estimated from their Table 1) were if anything higher with RV-only pacing. It is also unlikely lower preload from RV-pacing would be sustained over weeks (as we studied) given that homeostatic mechanisms would raise preload to help restore arterial pressure and cardiac output.The mouse heart is 10× smaller than the rat, making multi-chamber stimulation an extreme technical challenge. The commercial pacing unit in Hulsman et al 3 cannot be used as it provides only one lead, and while our method can handle dual chamber stimulation, lead implantation remains difficult. Importantly, our mouse data matches well with reported findings from canine models (the source of most published molecular/cellular data) using RV tachypacing and ignoring AV coordination. Organ and limited available molecular human data also matches well with findings from this animal model. 4 The canine work also found transitioning from RV tachypacing to either biventricular or atrial tachypacing, yields similar improvements. Together, this suggests the dominant effect from single-site ventricular pacing and its reversal to atrial pacing stems from dyssynchrony, whereas atrial ventricular coordination is a secondary contributor. Pending advances in microlead technology, we feel our model provides the key elements of dyssynchrony/resynchronization physiology but does so in mice providing the added advantage being amenable to genetic engineering.
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