Sundin Jonathan, Bustamante Mariana, Ebbers Tino, Dyverfeldt Petter, Carlhäll Carl-Johan
Unit of Cardiovascular Sciences, Department of Health, Medicine and Caring Sciences, Linköping University, Linköping, Sweden.
Center for Medical Image Science and Visualization, Linköping, Sweden.
Front Physiol. 2022 May 25;13:869701. doi: 10.3389/fphys.2022.869701. eCollection 2022.
The blood flow in the normal cardiovascular system is predominately laminar but operates close to the threshold to turbulence. Morphological distortions such as vascular and valvular stenosis can cause transition into turbulent blood flow, which in turn may cause damage to tissues in the cardiovascular system. A growing number of studies have used magnetic resonance imaging (MRI) to estimate the extent and degree of turbulent flow in different cardiovascular diseases. However, the way in which heart rate and inotropy affect turbulent flow has not been investigated. In this study we hypothesized that dobutamine stress would result in higher turbulence intensity in the healthy thoracic aorta. 4D flow MRI data were acquired in twelve healthy subjects at rest and with dobutamine, which was infused until the heart rate increased by 60% when compared to rest. A semi-automatic segmentation method was used to segment the thoracic aorta in the 4D flow MR images. Subsequently, flow velocity and several turbulent kinetic energy (TKE) parameters were calculated in the ascending aorta, aortic arch, descending aorta and whole thoracic aorta. With dobutamine infusion there was an increase in heart rate (66 ± 9 vs. 108 ± 13 bpm, < 0.001) and stroke volume (88 ± 13 vs. 102 ± 25 ml, < 0.01). Additionally, there was an increase in Peak Average velocity (0.7 ± 0.1 vs. 1.2 ± 0.2 m/s, < 0.001, Peak Max velocity (1.3 ± 0.1 vs. 2.0 ± 0.2 m/s, < 0.001), Peak Total TKE (2.9 ± 0.7 vs. 8.0 ± 2.2 mJ, < 0.001), Peak Median TKE (36 ± 7 vs. 93 ± 24 J/m3, = 0.002) and Peak Max TKE (176 ± 33 vs. 334 ± 69 J/m3, < 0.001). The relation between cardiac output and Peak Total TKE in the whole thoracic aorta was very strong (R = 0.90, < 0.001). TKE of blood flow in the healthy thoracic aorta increases with dobutamine stress and is strongly related to cardiac output. Quantification of such turbulence intensity parameters with cardiac stress may serve as a risk assessment of aortic disease development.
在正常心血管系统中,血流主要呈层流状态,但接近湍流阈值。血管和瓣膜狭窄等形态学畸变可导致血流转变为湍流,进而可能损害心血管系统中的组织。越来越多的研究使用磁共振成像(MRI)来估计不同心血管疾病中湍流的范围和程度。然而,心率和心肌收缩力对湍流的影响方式尚未得到研究。在本研究中,我们假设多巴酚丁胺负荷试验会导致健康胸主动脉中的湍流强度更高。对12名健康受试者在静息状态下以及使用多巴酚丁胺时进行了四维血流MRI数据采集,多巴酚丁胺持续输注直至心率相较于静息时增加60%。采用半自动分割方法在四维血流MR图像中分割胸主动脉。随后,计算升主动脉、主动脉弓、降主动脉和整个胸主动脉中的流速和几个湍流动能(TKE)参数。输注多巴酚丁胺后,心率增加(66±9对108±13次/分钟,<0.001),每搏输出量增加(88±13对102±25毫升,<0.01)。此外,峰值平均速度增加(0.7±0.1对1.2±0.2米/秒,<0.001),峰值最大速度增加(1.3±0.1对2.0±0.2米/秒,<0.001),峰值总TKE增加(2.9±0.7对8.0±2.2毫焦,<0.001),峰值中位数TKE增加(36±7对93±24焦/立方米,=0.002),峰值最大TKE增加(176±33对334±69焦/立方米,<0.001)。整个胸主动脉的心输出量与峰值总TKE之间的关系非常密切(R=0.90,<0.001)。健康胸主动脉中血流的TKE随多巴酚丁胺负荷试验增加,且与心输出量密切相关。通过心脏负荷试验对这种湍流强度参数进行量化,可作为主动脉疾病发展的风险评估。