ESC Heart Failure ( IF 3.8 ) Pub Date : 2024-04-05 , DOI: 10.1002/ehf2.14791 Kristína Burýšková Salajová 1 , Jan Malík 1 , Anna Valeriánová 1
We have read with interest the recent paper in this journal by Lee et al.1 The authors examined 109 haemodialysis patients by detailed echocardiography and measured haemodialysis arteriovenous fistula (AVF) flow in a retrospective study. Then they followed them for a mean of 25 months, and during this time, 19 (17.4%) patients were hospitalized for high-output cardiac failure (HOCF). Lower estimated systemic vascular resistance (eSVR) was the best predictor of the hospitalization. Systemic vascular resistance (SVR) was estimated by the ratio of systemic blood pressure and velocity time integral of the left ventricular outflow tract.
HOCF (or sometimes HOHF) is a relatively rare HF phenotype characterized by the combination of HF signs and symptoms together with cardiac index (CI) above 3.9 L/min/m2.2 High AVF flow represents one of the common aetiologies and is thus more frequent in patients on chronic haemodialysis where AVF is used as the vascular access,3, 4 and the study by Lee et al. was unique by the hospitalization records.
- The authors recorded hospitalizations for HOCF. However, there is no information whether they were for heart failure decompensation/oedema or just elective hospitalizations for some flow-reducing procedure on the AVF. How were the patients treated during the hospitalizations?
- The authors included only patients having AVF flow >1500 mL/min (n = 109) at the first/index visit when 50 patients of this group had high-output status (defined in the paper by CI > 4 L/min/m2). However, the presence of HF symptoms at the first visit is not described. Several studies, including ours, have documented that a surgical AVF flow reduction leads to the alleviation of the heart failure signs and symptoms.2, 5 Were the patients with HOCF diagnosed at the index visit sent to reducing surgery just after this visit? Moreover, the authors cite studies by Basile et al. that generally define high-flow AVF with risk of HOCF development as AVF with blood flow over 2000 mL/min.6 It would be interesting to know why the authors decreased the blood flow threshold to 1500 mL/min.
- The authors used a less common method for the estimation of the systemic vascular resistance (eSVR)7—see above. Generally, the presence of a high-flow AVF affects the vascular resistance significantly. The latter could be calculated non-invasively by using mean arterial pressure (MAP = 1/3 of the systolic blood pressure + 2/3 of the diastolic blood pressure) and the central venous pressure (CVP) that could be estimated by echocardiography.8 Therefore, two terms are sometimes used: ‘total vascular resistance’ (TVR) calculated as (MAP-CVP)/CO—with the use of the total cardiac output (CO), and SVR calculated as (MAP-CVP)/COeff—with the use of the effective CO (difference of the total CO and AVF flow).5, 9 Therefore, in these terms, Lee et al. estimated TVR. We calculated both SVR and TVR in a study of non-invasively assessed haemodynamic changes caused by high-flow AVF reduction.5 While SVR decreased significantly after the flow reduction, the opposite occurred with TVR (although with P = 0.08), which documented the reaction of the resistant arteries on the lower AVF flow. We have applied the method of eSVR (or rather eTVR) calculation that was used by Lee et al. and observed no significant change after the surgical AVF flow reduction (from 5.4 ± 1.1, to 5.3 ± 1.1, P-value 0.8). When we re-analysed our data, we observed only a significant decrease of the velocity time interval of the left ventricular outflow tract (from 0.27 ± 0.07 to 0.24 ± 0.06 m/s, P-value 0.02), while the systemic blood pressure and heart rate did not change significantly. End-stage kidney disease (ESKD) patients are known to have stiff aortas and arteries due to calcification and subsequently high pulse pressure.10 Therefore, the estimation of the SVR that was used by Lee et al. could also have been dampened by this phenomenon. Did the Authors also calculate the cardiac output (derived from the LVOT), effective cardiac output and estimated the CVP? If yes, it would be interesting to recalculate SVR and TVR as we summarized above and that, according to our opinion, corresponds better to the invasive haemodynamic examinations.
中文翻译：
无创评估高流量动静脉瘘和高输出量心力衰竭患者的血流动力学
我们饶有兴趣地阅读了 Lee 等人最近在该杂志上发表的论文。1作者通过详细的超声心动图检查了 109 名血液透析患者，并在一项回顾性研究中测量了血液透析动静脉瘘 (AVF) 流量。然后他们平均跟踪了 25 个月，在此期间，19 名 (17.4%) 患者因高输出量心力衰竭 (HOCF) 住院。较低的估计全身血管阻力（eSVR）是住院的最佳预测指标。全身血管阻力（SVR）通过全身血压与左心室流出道速度时间积分的比值来估计。
HOCF（或有时 HOHF）是一种相对罕见的 HF 表型，其特征是 HF 体征和症状以及心脏指数 (CI) 高于 3.9 L/min/m 2。2高 AVF 流量是常见病因之一，因此在使用 AVF 作为血管通路的慢性血液透析患者中更为常见，3、4以及 Lee 等人的研究。住院记录是独一无二的。
- 作者记录了 HOCF 的住院情况。然而，没有信息表明他们是因为心力衰竭代偿失调/水肿，还是只是为了进行 AVF 的某些减流手术而选择性住院。患者住院期间的治疗情况如何？
- 作者仅纳入了 首次/初次就诊时AVF 流量 >1500 mL/min 的患者 ( n = 109)，而该组中有 50 名患者处于高输出状态（本文中定义为 CI > 4 L/min/m 2）。然而，没有描述第一次就诊时是否存在心力衰竭症状。包括我们在内的几项研究已经证明，手术 AVF 流量减少可以缓解心力衰竭的体征和症状。2, 5在首次就诊时诊断出 HOCF 的患者是否在本次就诊后立即进行减容手术？此外，作者引用了 Basile 等人的研究。通常将具有发生 HOCF 风险的高流量 AVF 定义为血流超过 2000 mL/min 的 AVF。6了解作者为何将血流量阈值降低至 1500 mL/min 将会很有趣。
- 作者使用了一种不太常见的方法来估计全身血管阻力 (eSVR) 7 — 见上文。一般来说，高流量 AVF 的存在会显着影响血管阻力。后者可以通过使用平均动脉压（MAP = 1/3 收缩压 + 2/3 舒张压）和可通过超声心动图估计的中心静脉压（CVP）进行无创计算。8因此，有时会使用两个术语：“总血管阻力”(TVR)，计算公式为 (MAP-CVP)/CO——使用总心输出量 (CO)，而 SVR 计算公式为 (MAP-CVP)/COeff —使用有效 CO（总 CO 和 AVF 流量之差）。5, 9因此，在这些方面，Lee 等人。估计的TVR。我们在一项对高流量 AVF 减少引起的无创评估血流动力学变化的研究中计算了 SVR 和 TVR。5虽然 SVR 在流量减少后显着下降，但 TVR 却出现相反的情况（尽管P = 0.08），它记录了阻力动脉对较低 AVF 流量的反应。我们应用了 Lee 等人使用的 eSVR（或更确切地说 eTVR）计算方法。手术 AVF 流量减少后没有观察到显着变化（从 5.4 ± 1.1 到 5.3 ± 1.1，P值 0.8）。当我们重新分析数据时，我们仅观察到左心室流出道的速度时间间隔显着降低（从 0.27 ± 0.07 到 0.24 ± 0.06 m/s，P值 0.02），而全身血压和心率没有明显变化。众所周知，终末期肾病（ESKD）患者由于钙化和随后的高脉压而出现主动脉僵硬。10因此，Lee 等人使用的 SVR 估计。也可能受到这种现象的抑制。作者是否还计算了心输出量（源自 LVOT）、有效心输出量并估计了 CVP？如果是，那么重新计算 SVR 和 TVR 将会很有趣，正如我们上面总结的那样，根据我们的观点，这更符合侵入性血流动力学检查。
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