首页> 外文期刊>The Annals of Thoracic Surgery: Official Journal of the Society of Thoracic Surgeons and the Southern Thoracic Surgical Association >Unusual Gastrointestinal Bleeding After Sutureless Aortic Valve Replacement: A Word of Caution
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Unusual Gastrointestinal Bleeding After Sutureless Aortic Valve Replacement: A Word of Caution

机译:无主动脉瓣置换术后不常见的胃肠道出血:注意事项

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We report the clinical case of a male patient who presented, after an aortic valve replacement with a rapid deployment bioprosthesis, a Heyde-like syndrome, secondary to a moderate aortic paravalvular leakage. All the digestive and hematologic investigations confirmed the diagnosis. A redo surgery to fill the paravalvular gap was accomplished and the postoperative course was uneventful, with a normalization of the biological parameters. To our knowledge, this is the first described case of such a complication with the new generation of sutureless bioprosthesis.;The Heyde syndrome, initially described in 1958, combines a calcific aortic stenosis (AS) with an occult digestive bleeding. In fact, it is an association between an intestinal angiodysplasia, frequently seen in older people, and hemostasis troubles because of the denaturation of the von Willebrand factor (vWF), in which high-weighted molecules are cut because of the hemodynamic stress in an AS flow [1, 2, 3].We report a case of an unusual gastrointestinal bleeding occurring in a patient with an aortic sutureless paravalvular leakage (PVL), cured by surgical repair of PVL. This led us to suspect a Heyde-like syndrome as observed after transcatheter aortic valve replacement (TAVR) complicated with PVL.A 77-year-old male patient with a history of metabolic syndrome, chronic kidney injury, and hypertension, but without any history of gastrointestinal bleeding, was admitted in our department for a surgical treatment of a severe AS (New York Heart Association class 2; AS murmur; aortic valve area, 0.8 cm2; maximal velocity, 4.4?m/s; and transvalvular mean gradient, 48 mm Hg).We opted for an aortic valve replacement through a J-shaped upper hemisternotomy with a rapid-deployment Edwards Intuity Elite 23-mm bioprosthesis (Edwards LifeScience, Irvine, CA). The postoperative course was uneventful. Before discharge, echocardiographic control showed mild PVL, without any hemodynamic effects.The 3-month follow-up was marked by the unexpected occurrence of iterative episodes of hematemesis and melena, leading to a severe anemia with a hemoglobin level at 5 g/dL, requiring multiple blood transfusions, up to 32 units in a month.Digestive endoscopy revealed an uncomplicated colic diverticulitis. Capsule endoscopy showed sparse areas of angiodysplasia in the small bowel without any hemorrhagic ulceration.Hematologic investigations concluded that the cause of anemia was principally iron deficiency, with discrete hemolysis and a direct bilirubin plasma level that was not increased and only scarce schizocytes found on direct examination. Coagulation vitamin K–dependent factors were normal, with a normal platelet count, but platelet occlusion time (measured by PFA-100 test) was elongated (187 s for a normal range between 68 and 121 s). A primary coagulation acquired anomaly, such as a Willebrand-like syndrome, was suspected. The Heyde-like syndrome was then evoked. Transesophageal echocardiography showed the persistence of the initial aortic PVL.After a heart team discussion, we decided to treat this PVL by a redo aortic surgery. Next, under cardiopulmonary bypass and through full sternotomy, we found a well-seated bioprosthesis with two small dehiscences (Fig?1Fig?1) associated with a large defect of endothelialization. Leaving the prosthesis in place, we easily occluded the dehiscences with mattress sutures (Fig 2Fig 2). Postoperative course was uneventful, with a discharge on the 13th postoperative day and no subsequent need for blood transfusion. The 1-year follow-up showed a complete regression of PVL. There was no recurrent gastric bleeding notified. Biological hemostasis investigations showed a normalization of the PFA-100 test.Fig 1Surgical view of the prosthesis with the endothelial defect responsible of the paravalvular leakage.;To our knowledge, this is the first reported case of a putative acquired von Willebrand syndrome caused by a paravalvular leak after sutureless aortic val
机译:我们报告了一名男性患者的临床病例,该患者在用快速部署的生物假体置换主动脉瓣后,继发于中度主动脉瓣周漏继发的Heyde样综合征。所有消化和血液学检查均证实了诊断。完成了一项重做手术以填补瓣周间隙,术后过程顺利进行,生物学参数正常化。据我们所知,这是第一次出现这种并发症,并伴随着新一代的无缝合生物假体。Heyde综合征最初于1958年进行了描述,将钙化主动脉瓣狭窄(AS)与隐匿性消化道出血结合在一起。实际上,这是老年人中常见的肠道血管增生与由于von Willebrand因子(vWF)变性而引起的止血麻烦之间的联系,其中由于AS中的血流动力学压力,高分子量分子被切断了流程[1、2、3]。我们报告了一例发生主动脉无缝合线瓣周漏(PVL)的患者发生胃肠道异常出血的情况,该患者通过手术修复。这使我们怀疑在经导管主动脉瓣置换术(TAVR)并发PVL后观察到的Heyde样综合征.77岁的男性患者有代谢综合征,慢性肾脏损伤和高血压病史,但没有任何病史因消化道出血而入院,用于外科手术治疗严重的AS(纽约心脏协会2级; AS杂音;主动脉瓣面积0.8 cm2;最大速度4.4?m / s;经瓣膜平均梯度48)毫米汞柱)。我们选择通过J形上半切开术和快速部署的Edwards Intuity Elite 23毫米生物假体(Edwards LifeScience,Irvine,CA)选择主动脉瓣置换术。术后过程很顺利。出院前,超声心动图检查显示轻度PVL,无任何血流动力学影响。随访3个月的结果是意外出现呕血和黑便反复发作,导致严重贫血,血红蛋白水平为5 g / dL,需要多次输血,一个月内最多输注32个单位。消化内镜检查发现未发生绞痛性憩室炎。胶囊内窥镜检查显示小肠血管发育不良的区域稀疏,没有出血性溃疡。血液学研究表明,贫血的原因主要是铁缺乏,离散溶血和直接胆红素血浆水平没有增加,直接检查仅发现了稀少的分裂细胞。 。凝血维生素K依赖性因子正常,血小板计数正常,但血小板闭塞时间(通过PFA-100测试测量)延长(187 s,正常范围为68到121 s)。怀疑有原发性凝血异常,例如Willebrand样综合征。然后诱发了类似海德的综合症。经食道超声心动图检查显示了初始主动脉PVL的持续性。经过心脏小组讨论后,我们决定通过重做主动脉手术治疗该PVL。接下来,在体外循环下并通过完全胸骨切开术,我们发现了一个根基固定的生物假体,其中有两个小裂口(图1图1),并伴有较大的内皮化缺损。假体就位后,我们很容易用褥式缝线缝合开裂(图2图2)。术后过程平稳,术后第13天出院,以后无需输血。 1年的随访显示PVL完全消退。没有复发胃出血的通知。生物止血研究显示PFA-100测试正常化。图1假体的外科视图,其内皮缺损导致瓣周漏。据我们所知,这是首例报道的由假性血管性痴呆引起的后天性von Willebrand综合征病例。无缝合主动脉瓣后瓣周漏

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