Isolated pulmonary regurgitation causes decreased right ventricular longitudinal function and compensatory increased septal pumping in a porcine model.

Isolated pulmonary regurgitation causes decreased right ventricular longitudinal function and compensatory increased septal pumping in a porcine model.
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DOI:
10.1111/apha.12904
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发表时间:
2017-11
期刊:
Acta physiologica (Oxford, England)
影响因子:
--
通讯作者:
Carlsson M
Carlsson M
中科院分区:
其他
文献类型:
--
作者:
Kopic S;Stephensen SS;Heiberg E;Arheden H;Bonhoeffer P;Ersbøll M;Vejlstrup N;Søndergaard L;Carlsson M

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室壁纵向收缩是心功能的一个参数,具有较强的预测能力。法洛四联症(TOF)矫治术后自由肺返流(PR)患者右室(RV)纵向功能受损。目前尚不清楚这是手术修复的结果,还是PR固有的结果。本研究的目的是在猪孤立PR模型中评估纵向泵、侧泵和间隔泵之间的关系。将仔猪分为对照组(n=8)和治疗组(n=12),在肺动脉瓣口置入支架,诱发PR。2-3个月后,对动物进行心脏磁共振成像。一组动物(n=6)随后接受经皮肺瓣膜置换术(PPVR),并在1个月后进行随访。通过测量心脏短轴和长轴从舒张末到收缩末期的体积位移来量化每搏输出量(SV)的纵向、横向和间隔贡献。PR对RV每搏量的纵向贡献低于对照组(60.0±2.6%vs.73.6±3.8%;P=0.012)。此外,室间隔对室间隔的代偿性增加(11.0±1.6%对−3.1±1.5%;P<0.0001)。左心室(LV)呈逆调节,纵向LVSV增大。PPVR可逆转右室纵向功能的改变。这些发现表明,在心脏手术中没有瘢痕形成的情况下,PR有助于降低RV纵向功能。测量纵向rVSV有助于TOF患者PR介入治疗的风险分层和时机选择。
Longitudinal ventricular contraction is a parameter of cardiac performance with predictive power. Right ventricular (RV) longitudinal function is impaired in patients with free pulmonary regurgitation (PR) following corrective surgery for Tetralogy of Fallot (TOF). It remains unclear whether this is a consequence of the surgical repair, or whether it is inherent to PR. The aim of this study was to assess the relationship between longitudinal, lateral and septal pumping in a porcine model of isolated PR. Piglets were divided into a control (n = 8) group and a treatment (n = 12) group, which received a stent in the pulmonary valve orifice, inducing PR. After 2–3 months, animals were subjected to cardiac magnetic resonance imaging. A subset of animals (n = 6) then underwent percutaneous pulmonary valve replacement (PPVR) with follow‐up 1 month later. Longitudinal, lateral and septal contributions to stroke volume (SV) were quantified by measuring volumetric displacements from end‐diastole to end‐systole in the cardiac short axis and long axis. PR resulted in a lower longitudinal contribution to RV stroke volume, compared to controls (60.0 ± 2.6% vs. 73.6 ± 3.8%; P = 0.012). Furthermore, a compensatory increase in septal contribution to RVSV was observed (11.0 ± 1.6% vs. −3.1 ± 1.5%; P < 0.0001). The left ventricle (LV) showed counter‐regulation with an increased longitudinal LVSV. Changes in RV longitudinal function were reversed by PPVR. These findings suggest that PR contributes to decreased RV longitudinal function in the absence of scarring from cardiac surgery. Measurement of longitudinal RVSV may aid risk stratification and timing for interventional correction of PR in TOF patients.
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