class='kwd-title'>Keywords: Heyde Syndrome, Aort'/> A Vicious Circle: Heyde Syndrome in Mild Aortic Stenosis
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A Vicious Circle: Heyde Syndrome in Mild Aortic Stenosis

机译:恶性循环:轻度主动脉瓣狭窄的海德综合症

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摘要

class="kwd-title">Keywords: Heyde Syndrome, Aortic stenosis, von Willebrand factor, High-output cardiac failure class="head no_bottom_margin" id="sec1title">IntroductionPatients with severe aortic stenosis have an increased risk of gastrointestinal (GI) bleeding that can be due to angiodysplasias in the GI tract; this association has been termed Heyde syndrome. High gradients across a severely stenotic aortic valve cause disruption of the von Willebrand factor and deficiency of large von Willebrand multimers. In one study, nine out of 42 (21%) patients with severe aortic stenosis had a history of bleeding, most often from skin or mucosal sites. In the same study, two out of eight patients with moderate aortic stenosis also had a history of hemorrhagic syndrome that required treatment. True mild aortic stenosis has, at least to our knowledge, not been described in the literature as a cause for Heyde syndrome. We here present a case of a 42-year-old man with a body weight of 160 kg who was diagnosed with Heyde syndrome in mild aortic stenosis. Loss of large von Willebrand multimers were proven by multimeric analysis. Gradients across a mildly stenotic aortic valve were significantly increased secondary to high-output cardiac state, which was itself caused by the combination of anemia and high body weight. Once the anemia was corrected and the patient lost 20% of his body weight (30 kg) with diuresis, the high-output state and flow across the aortic valve improved, gradients decreased, and the patient had no further episode of GI bleeding. We conclude that the patient was in a vicious circle where anemia eventually triggered further GI blood loss caused by Heyde syndrome in high-output cardiac state.
机译:<!-fig ft0-> <!-fig @ position =“ anchor” mode =文章f4-> <!-fig mode =“ anchred” f5-> <!-fig / graphic | fig / alternatives / graphic mode =“ anchored” m1-> class =“ kwd-title”>关键字: Heyde综合征,主动脉瓣狭窄,von Willebrand因子,高输出心脏衰竭 class =“ head no_bottom_margin“ id =” sec1title“>简介患有严重主动脉瓣狭窄的患者胃肠道(GI)出血的风险增加,这可能是由于胃肠道血管增生所致;这种联系被称为海德综合症。严重狭窄的主动脉瓣上的高梯度会导致von Willebrand因子的破坏和大型von Willebrand多聚体的缺乏。在一项研究中,在42位严重主动脉瓣狭窄患者中,有9位(21%)有出血史,通常是皮肤或粘膜部位出血。在同一项研究中,八分之二的中度主动脉瓣狭窄患者也有出血综合征的病史,需要治疗。至少据我们所知,真正的轻度主动脉瓣狭窄在文献中没有被描述为海德综合征的病因。我们在这里介绍了一个体重160公斤的42岁男性患者,该患者被诊断患有轻度主动脉瓣狭窄的海德综合症。大型von Willebrand多聚体的损失已通过多聚体分析证明。继发于高输出心率的继发于轻度狭窄主动脉瓣的梯度明显增加,这本身是由贫血和高体重共同引起的。贫血得到纠正后,利尿使患者体重减轻20%(30 kg),高输出状态和主动脉瓣血流改善,梯度降低,患者不再有GI出血发作。我们得出的结论是,该患者处于恶性循环中,贫血最终引发了由高输出心脏状态下的海德综合症引起的胃肠道失血。

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