<p>In the case report described in this issue, Bell et al. (<span>2024</span>) describe a previously unreported occurrence of aortic, mitral and tricuspid valve dysplasia (TVD) in a 7-month-old, Warmblood-cross colt. The prevalence of congenital heart disease (CHD) in the horse is limited to historical studies that suggest a prevalence of 0.03%–0.2% (Buergelt, <span>2003</span>; Michaëlsson & Ho, <span>2000</span>). Valvular dysplasia appears to make up an even smaller group of CHD in horses, and was identified in only 8/18 foals in one report (Hall et al., <span>2010</span>). The reported numbers likely underestimate total occurrence, as the true numbers include foals with severe cardiac malformations who die during or shortly after birth, as well as clinically silent defects that go undetected. Despite the suspectedly low occurrence of congenital valvular disease, the equine practitioner must still be aware of these conditions and be familiar with the clinical presentation and available diagnostics for detection and management of congenital valvular dysplasia.</p><p>The horse in this report had changes consistent with congenital dysplasia of the aortic, mitral and tricuspid valves. Individual case reports of dysplasia of the mitral valve (Marr & Bowen, <span>2010</span>; McGurrin et al., <span>2003</span>; Schober et al., <span>2000</span>) and mitral and tricuspid valves (Duz et al., <span>2013</span>) in horses have been published. Anecdotal observation of TVD as an isolated congenital defect has also been previously reported by the authors. Most congenital abnormalities of the tricuspid valve in horses are forms of atresia (Hall et al., <span>2010</span>; Krüger et al., <span>2016</span>; Meurs et al., <span>1997</span>), with some investigators suggesting it is among the most common form of equine CHD (Hall et al., <span>2010</span>). Atrioventricular valvular dysplasia can also be a component of complex CHD (Bayly et al., <span>1982</span>; Kohnken et al., <span>2018</span>; van der Luer & van der Linde-Sipman, <span>1978</span>). Dysplasia of the aortic valve has been described as an isolated abnormality (Clark et al., <span>1987</span>; Taylor et al., <span>2007</span>), as well as in combination with other CHD (Michlik et al., <span>2014</span>).</p><p>The clinical signs of valvular dysplasia tend to manifest early in life, particularly when disease is severe. The clinical presentation of horses with CHD varies greatly based on disease severity. Most foals diagnosed with one or more forms of valvular dysplasia present with lethargy, exercise intolerance, failure to thrive, dyspnoea, cyanosis or syncope within the first days to weeks of life (Scansen, <span>2019</span>). Clinical signs are often nonspecific, which can complicate diagnosis and delay management. Recognition of disease requires that the practitioner consider CHD as a differential. Abnormal cardiac auscultation is often the first diagnostic that triggers suspicio
在本期的病例报告中,Bell 等人(2024 年)描述了一匹 7 个月大的温血杂交马驹的主动脉瓣、二尖瓣和三尖瓣发育不良 (TVD) 病例,该病例此前从未报道过。马匹先天性心脏病(CHD)的发病率仅限于历史研究,其发病率为 0.03%-0.2%(Buergelt,2003 年;Michaëlsson & Ho,2000 年)。瓣膜发育不良在马的先天性心脏病中似乎占的比例更小,在一份报告中,仅在8/18的马驹中发现了瓣膜发育不良(Hall等人,2010年)。报告中的数字很可能低估了总发生率,因为真实数字包括在出生时或出生后不久死亡的严重心脏畸形马驹,以及未被发现的临床无声缺陷马驹。尽管先天性瓣膜病的疑似发生率很低,但马术从业人员仍必须了解这些疾病,熟悉先天性瓣膜发育不良的临床表现和可用的诊断方法。有关马匹二尖瓣发育不良(Marr & Bowen, 2010; McGurrin 等人, 2003; Schober 等人, 2000)以及二尖瓣和三尖瓣发育不良(Duz 等人, 2013)的个案报告已经发表。作者以前也曾报道过 TVD 作为一种孤立的先天性缺陷的轶事。马的三尖瓣先天性畸形大多为闭锁(Hall 等人,2010 年;Krüger 等人,2016 年;Meurs 等人,1997 年),一些研究者认为这是马类先天性心脏病中最常见的一种(Hall 等人,2010 年)。房室瓣发育不良也可能是复杂性先天性心脏病的一个组成部分(Bayly 等人,1982 年;Kohnken 等人,2018 年;van der Luer & van der Linde-Sipman, 1978 年)。主动脉瓣发育不良已被描述为一种孤立的异常(Clark 等人,1987 年;Taylor 等人,2007 年),也可与其他先天性心脏病合并出现(Michlik 等人,2014 年)。患有心脏瓣膜发育不良的马匹的临床表现因疾病的严重程度而有很大不同。大多数被诊断出患有一种或多种瓣膜发育不良的马驹在出生后几天到几周内会出现嗜睡、运动不耐受、无法茁壮成长、呼吸困难、发绀或晕厥等症状(Scansen,2019)。临床症状通常没有特异性,这会使诊断复杂化并延误治疗。要识别疾病,医生必须将心脏疾病作为鉴别诊断的一个因素。心脏听诊异常通常是引发对心脏瓣膜发育不良怀疑的第一诊断依据,因为大多数形式的瓣膜发育不良都伴有响亮的心脏杂音。由于马驹的胸壁较薄,心脏紧贴胸壁,因此通常很容易听诊到马驹的心音。在 4 天龄以内的新生儿中,由于动脉导管未闭导致血流不畅,通常可听到生理性杂音。这些杂音可能是收缩期杂音,但也可能是连续性杂音。连续性杂音通常会在出生后 24 小时内消失,如果在 4 日龄后发现,则被视为异常杂音(Reef,1985 年)。正常纯血马驹在出生后最初 5 分钟内的心率为 30 至 90 次/分,到 10 h 大时心率逐渐变为 72 至 133 次/分(Rossdale,1967 年)。二尖瓣发育不良(MVD)可能导致二尖瓣反流(MR)和/或狭窄;但二尖瓣狭窄(MS)并不常见。二尖瓣反流的杂音通常很大(IV/VI 级或更大),在左侧胸腔向心尖方向听得最清楚,应出现在心动周期的收缩期。在多发性硬化症病例中,也可能在同一位置听到柔和的舒张期杂音。严重 MVD 患者通常会出现左侧充血性心力衰竭(CHF)的体征。这些体征包括呼吸急促、虚弱和肺水肿。三尖瓣发育不良也会导致继发于三尖瓣反流的收缩期杂音,但这种杂音通常比 MR 的杂音更小,而且在右侧胸腔听到的杂音最大。这种杂音不能与室间隔缺损(VSD)引起的右侧收缩期心脏杂音混淆,室间隔缺损是最常报道的马驹先天性心脏缺损(Hall et al. , 2010).主动脉瓣发育不良可能伴有收缩期或舒张期杂音,这取决于是否存在左心室流出道梗阻或主动脉瓣关闭不全(AI)。并非所有主动脉瓣发育不良患者都会出现可闻杂音(Taylor 等人,2007 年)。Bell 等人(2024 年)的病例报告描述了 IV/VI 级、双侧、持续性杂音。结合超声心动图和死后检查的结果,可以推断杂音的舒张期成分很可能是由人工心动过速引起的。收缩期和舒张期杂音也可能被描述为 "来来回回 "的杂音,而不是真正的连续性杂音。人工心动过速的杂音可能具有音乐性的渐弱音质,有时被描述为 "嘎吱嘎吱 "的声音。虽然杂音分级与 AI 严重程度有很强的正相关性,但动脉脉搏质量是最好的临床指南。AI 引起的舒张期径流会导致舒张压过低,严重患病马匹的舒张期动脉压会低于 50 mmHg。严重 AI 的最终结果是左心室容量超负荷和随后的左侧心房颤动。患有严重 AI 的马可能会表现出与患有 MR 的马相同的左侧心脏病症状。患有先天性心脏病的动物的临床症状可能很难与其他后天性非心脏病相鉴别,如肺炎、发育不良、败血症、寄生虫病、毒血症、尿毒症、药物、过敏反应或营养缺乏,如白肌病(Reef,1985 年)。胸片检查可发现全身心肌肥大和心源性肺水肿,尤其是在雏马身上。由于放射线检查不能可靠地确定心腔大小、心内分流或心脏功能,因此怀疑患有心脏病的患者应进行超声心动图检查。不过,即使进行了超声心动图检查,也很难确定瓣叶病变的病因(即先天性畸形还是后天性疾病)。超声心动图可显示特定的心腔扩大,这取决于哪些瓣膜受到影响。彩色血流多普勒可显示房室瓣处有湍急的反流血流喷射。要全面评估心脏功能,还需要考虑其他因素,但这不在本评论的讨论范围之内。最终,先天性瓣膜发育不良的马患者的长期预后取决于潜在病理和由此导致的反流的严重程度。在轻度病例中,可以达到一定的运动表现水平。但对于导致心脏失代偿和慢性心力衰竭的严重病例,预后一般较差甚至严重。虽然并非所有病例都需要治疗心房颤动,但可根据情况尝试使用利尿剂、正性肌力促进剂和抗心律失常药物进行药物治疗。受影响马驹的尸检结果可能包括受影响的心腔明显增大,瓣膜通常显示融合和/或畸形的瓣叶,腱索缩短(Marr & Bowen, 2010)。如果有条件,建议对瓣膜叶进行组织病理学评估,以确认疑似先天性瓣膜发育不良。有临床意义的先天性瓣膜发育不良虽然在小马驹中罕见,但却是马医师的重要鉴别依据,在评估临床症状模糊的幼马时应加以考虑:Todd Sumerfield:撰稿-原稿。Carl Toborowsky:撰写--审阅和编辑。本评论没有需要报告的资助者。
{"title":"Congenital valvular dysplasia in the horse","authors":"Todd Sumerfield, Carl Toborowsky","doi":"10.1111/eve.14034","DOIUrl":"https://doi.org/10.1111/eve.14034","url":null,"abstract":"<p>In the case report described in this issue, Bell et al. (<span>2024</span>) describe a previously unreported occurrence of aortic, mitral and tricuspid valve dysplasia (TVD) in a 7-month-old, Warmblood-cross colt. The prevalence of congenital heart disease (CHD) in the horse is limited to historical studies that suggest a prevalence of 0.03%–0.2% (Buergelt, <span>2003</span>; Michaëlsson & Ho, <span>2000</span>). Valvular dysplasia appears to make up an even smaller group of CHD in horses, and was identified in only 8/18 foals in one report (Hall et al., <span>2010</span>). The reported numbers likely underestimate total occurrence, as the true numbers include foals with severe cardiac malformations who die during or shortly after birth, as well as clinically silent defects that go undetected. Despite the suspectedly low occurrence of congenital valvular disease, the equine practitioner must still be aware of these conditions and be familiar with the clinical presentation and available diagnostics for detection and management of congenital valvular dysplasia.</p><p>The horse in this report had changes consistent with congenital dysplasia of the aortic, mitral and tricuspid valves. Individual case reports of dysplasia of the mitral valve (Marr & Bowen, <span>2010</span>; McGurrin et al., <span>2003</span>; Schober et al., <span>2000</span>) and mitral and tricuspid valves (Duz et al., <span>2013</span>) in horses have been published. Anecdotal observation of TVD as an isolated congenital defect has also been previously reported by the authors. Most congenital abnormalities of the tricuspid valve in horses are forms of atresia (Hall et al., <span>2010</span>; Krüger et al., <span>2016</span>; Meurs et al., <span>1997</span>), with some investigators suggesting it is among the most common form of equine CHD (Hall et al., <span>2010</span>). Atrioventricular valvular dysplasia can also be a component of complex CHD (Bayly et al., <span>1982</span>; Kohnken et al., <span>2018</span>; van der Luer & van der Linde-Sipman, <span>1978</span>). Dysplasia of the aortic valve has been described as an isolated abnormality (Clark et al., <span>1987</span>; Taylor et al., <span>2007</span>), as well as in combination with other CHD (Michlik et al., <span>2014</span>).</p><p>The clinical signs of valvular dysplasia tend to manifest early in life, particularly when disease is severe. The clinical presentation of horses with CHD varies greatly based on disease severity. Most foals diagnosed with one or more forms of valvular dysplasia present with lethargy, exercise intolerance, failure to thrive, dyspnoea, cyanosis or syncope within the first days to weeks of life (Scansen, <span>2019</span>). Clinical signs are often nonspecific, which can complicate diagnosis and delay management. Recognition of disease requires that the practitioner consider CHD as a differential. Abnormal cardiac auscultation is often the first diagnostic that triggers suspicio","PeriodicalId":11786,"journal":{"name":"Equine Veterinary Education","volume":"36 11","pages":"568-570"},"PeriodicalIF":0.8,"publicationDate":"2024-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/eve.14034","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142404802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}