先天性左心室流出道梗阻的外科治疗

目的 :总结先天性左室流出道梗阻 (LVOTO)的外科治疗经验。方法 :分析我科 1998年 1月至 2 0 0 3年 7月 33例先天性LVOTO接受手术治疗的患者临床资料。年龄 1～ 5 5岁 ,平均 (14 9± 10 2 )岁。其中主动脉瓣膜狭窄 10例 (30 3% ) ;主动脉瓣下狭窄 18例 (5 4 5 % ) ;主动脉瓣上狭窄 3例 (9 1% ) ;复合狭窄 2例 (6 1% )。有合并畸形者 2 3例 (6 9 7% ) ,心内膜炎 2例 (6 1% )。主动脉瓣置换 7例 (2 1 2 % ) ,升主动脉加宽 3例 (9 1% ) ,主动脉根部和升主动脉加宽 2例 (6 1% )。对主动脉瓣换瓣的患者常规华法令抗凝治疗 ,并监测凝血酶原时间和国际标准指数。结果 :全组无早期死亡 ;随访 3～ 4 1个月 ,平均 (13 2± 6 8)个月 ,4例患者残留轻度梗阻 (12 2 % ) ;晚期死亡 1例 (3 0 % )术后 18个月死于感染性心内膜炎 ;其余患者恢复良好。结论 :对不同类型的先天性LVOTO选择合适的手术方式、同期处理合并畸型、加强术后随访是提高先天性LVOTO外科治疗疗效的关键。     

房间隔封堵器脱落致左室流出道梗阻1例

患者,女,32岁。主诉因活动后胸闷、心悸5年入院。入院检查:患者一般情况良好,胸骨左缘2、3肋间闻及2～3级收缩期杂音,肺动脉瓣第2音亢进、分裂。心脏超声示:中央型房间隔缺损,直径20mm,肺动脉压力估侧35mmHg(1mmHg=0.133kPa)。入院后各项检查未发现明显手术禁忌。在局麻下行介入封堵术,术中超声进一步明确诊断无误后选择26mmAmplatzer房间隔封堵器,输送、释放过程顺利,超声检查未见明显分流。遂完全释放,使输送导丝与封堵伞分离。释放后观察过程中,患者突然出现剧烈胸痛、头晕、大汗、心率加快、视物不清等症状,急行床旁超声检查,发现封堵…     

肥厚梗阻性心肌病与二尖瓣病变及二尖瓣反流

目的:探讨左心室流出道梗阻对二尖瓣叶及二尖瓣反流的影响。方法:采用数字化超声心动图技术分析左心室流出道梗阻患者二尖瓣前叶形态结构及二尖瓣反流的特点。结果:68例左心室流出道梗阻患者,其中2例二尖瓣前叶赘生物形成合并穿孔,66例二尖瓣前叶近瓣缘部分轻度增厚。全部患者均有明显二尖瓣前叶收缩期前向运动(SAM)及二尖瓣偏心反流。结论:左心室流出道梗阻可引起二尖瓣前叶病变。左心室流出道梗阻患者二尖瓣前叶SAM可导致二尖瓣反流。     

左右心室流出道疏通及二尖瓣替换治疗肥厚性梗阻型心肌病

肥厚性梗阻型心肌病同时有左右室流出道梗阻及二尖瓣病变者手术治疗较为复杂。作者近来遇见一例。经手术治疗 ,取得较好效果 ,特报道如下 :　　患者李× ,女 ,30岁 ,已婚 ,云南昆明人 ,因活动后心慌 ,气短 ,心前区痛及反复晕厥 3年 ,症状日渐加重 ,经当地医院药物治疗无效 ,有家族史 ,于 2 0 0 1年 11月 9日入院。体检 :血压 10 4ｍｍＨｇ/6 0ｍｍＨｇ ,心律齐 ,70ｒ/ｍｉｎ ,胸左 2～ 4肋间至心尖部闻及 3/Ⅵ级收缩期吹性杂音。Ｘ线心脏像 :两肺轻度淤血 ,Ｃ/Ｔ0 5 6。心电图 :左心室肥厚劳损。彩色多普勒超声心动图 :左心房扩大 ,室间隔…     

二尖瓣副瓣及主动脉瓣下隔膜共同导致左室流出道梗阻外科治疗一例

左室流出道梗阻在先天性心脏病中发病率相对较低,本文报道一例二尖瓣副瓣及主动脉瓣下隔膜共同导致左室流出道梗阻的罕见病例。13岁男性被发现二尖瓣副瓣起自主动脉二尖瓣幕帘,呈囊袋状,并有独立腱索连接至前外侧乳头,左室收缩期与主动脉瓣下隔膜共同导致左室流出道重度狭窄。通过手术切除二尖瓣副瓣及主动脉瓣下隔膜,梗阻成功解除,术后复查手术效果良好。     

经导管二尖瓣钳夹系统解除左心室流出道梗阻治疗肥厚型梗阻性心肌病的应用现状及前景

肥厚型心肌病是年轻人心脏猝死的常见原因,在各个年龄段均有较高的发病率和死亡率。近年来针对其复杂的分子以及病理生理机制的治疗发展迅猛,同时结构性的治疗手段也引起广泛重视。经导管二尖瓣钳夹系统解除左心室流出道梗阻,是近年新兴的治疗手段。根据目前文献,经导管二尖瓣钳夹系统对梗阻症状的解除与传统室间隔心肌切除术和介入酒精消融术一样确切有效,且围术期并发症更少。该治疗方案适用于手术风险高,不能耐受外科或是介入消融的患者,以及曾接受过外科或介入消融治疗后依然有梗阻的患者,尤其适用于隐匿梗阻性患者。目前相关临床研究尚缺乏远期预后的数据,仍需要更大规模的研究才能对其确切的疗效以及远期预后进行明确评估。     

经胸超声心动图判断左心室流出道梗阻对经皮主动脉瓣置换术的意义

目的：比经皮主动脉瓣置换术（TAVI）是高危主动脉瓣病变患者的有效治疗手段。本研究通过TAVI合并左心室流出道梗阻（LVOTO）的特殊病例,探讨经胸超声心动图（TTE）术前及术后诊断LVOTO对于TAVI的临床意义。方法：2018年7月至2020年6月间,于我院接受经股动脉TAVI手术的主动脉瓣狭窄患者226例。对接受TAVI患者在围术期进行左心室流出道（LVOT）形态及流速探查。结果：共6例患者出现LVOTO。2例患者TAVI手术的术前发现LVOTO,其室间隔基底段呈明显乙状室间隔,SAM征阳性,术后其LVOTO未见缓解。3例患者术前LVOT的流速正常,术后即刻出现LVOTO,其左心室室壁明显增厚,运动增强,左心室容积偏小,术后SAM阳性,经控制血压及心率治疗后,LVOTO缓解,流速恢复正常。1例患者术前LVOT流速正常,术后LVOT流速正常,左心室腔中部的中位LVOT出现流速明显增快,经治疗后缓解。结论：进行TAVI手术的患者多表现为左心室室壁增厚,左心室容积偏小,室间隔形态改变,易于出现LVOTO。TTE是检出LVOTO的有效手段,应于术前仔细探查,术后注意监测。     

高血压病左心室肥厚与冠脉狭窄关系的研究

目的　探讨高血压病患者年龄和左室肥厚（ＬＶＨ）对冠脉狭窄的影响。方法　分析９７ 例原发性高血压病患者的超声心动图和冠脉造影的资料,观察年龄和ＬＶＨ与冠脉狭窄间的关系。结果　１－ 老年高血压病患者冠脉狭窄的程度明显高于非老年患者;２－ 伴ＬＶＨ 的高血压病患者冠脉狭窄发生率高于无ＬＶＨ者。结论　伴ＬＶＨ 的老年高血压病患者冠脉狭窄发生率高且冠脉狭窄重。     

肥厚性心肌病伴流出道梗阻的心电图表现及与彩超的对比分析

肥厚型心肌病 (ＨＣＭ)临床上较多见 ,其主要表现为室间隔与左室后壁的异常增厚 ,伴流出道梗阻则是其一种特殊类型。它是以非对称性肥厚和心室腔变小为特征的心肌病变。我院 1999年 5月～ 2 0 0 2年 8月确诊的肥厚性梗阻型心肌病 (ＨＯＣＭ)共 3 2例 ,进行了心电图及彩超检查 ,现报告如下。1　资料与方法3 2例均系住院患者 ,其中男 18例 ,女 14例 ,年龄 2 2～ 5 9(平均 41)岁。入院后均行心电图及彩超检查。心电图用福田ＦＣＰ - 410 1型 12道同步记录仪。彩超检查采用美国ＡｃｕｓｏｎＡｓｐｅｎ彩色多普勒显像仪 ,探头频率 3ＭＨｚ。2　结…     

左室流出道肌性梗阻的外科治疗

本文观察了8例肥厚性梗阻型心肌病患者经手术治疗前后的血液动力学变化,其中5例术中经食管超声检查。结果表明,对肥厚性梗阻型心肌病患者施行室间隔部分切除术后,左室流出道明显增宽,压力阶差明显降低,二尖瓣反流程度减轻,晕厥及心力衰竭症状明显改善,无手术死亡。术中经食管超声心动图技术对手术准确切除肥厚的室间隔以及解除左室流出道梗阻是有帮助的。     

Transient left ventricular outflow tract obstruction with systolic anterior motion of the mitral valve: A stunning cause

Left ventricular outflow tract obstruction (LVOTO) and systolic anterior motion (SAM) of the mitral valve may have various etiologies, of which hypertrophic cardiomyopathy is the most common. More rarely, an acute coronary syndrome, myocardial stunning, and takotsubo cardiomyopathy may give rise to LVOTO and SAM. Here, we present a 70‐year‐old female patient with a non‐ST‐elevation acute coronary syndrome treated with percutaneous coronary intervention. Echocardiography the day after, because of dyspnea and hypotension, revealed apical akinesia, LVOTO, and SAM, which proved completely reversible after treatment with a β‐blocker and a 2‐month follow‐up period. It was concluded that postischemic apical stunning had caused LVOTO and SAM.     

Significant left ventricular outflow tract obstruction secondary to systolic anterior motion in a patient without hypertrophic cardiomyopathy: An echocardiographic study

Dynamic left ventricular outflow tract obstruction (LVOTO) can be hemodynamically significant and can adversely affect the heart and quality of life. It is caused by systolic anterior motion (SAM) of the anterior mitral valve into the LVOT. The mechanism underlying SAM has been an area of special interest. However, SAM occurrence in the absence of septal hypertrophy is exceedingly uncommon. Here we present a case of a young male patient who sought medical care with a complaint of exertional dyspnea, New York Heart Association functional Class 2–3, and was found to have SAM and severe LVOTO at rest without hypertrophic cardiomyopathy. Continuous wave Doppler signal showed a peak velocity of 4.96?m/s along the LVOT, with a pressure gradient at rest of 98.44?mmHg, calculated using the modified Bernoulli equation. The patient is not known to have any medical conditions, nor had a family history of cardiac condition or sudden death. Trans-thoracic echocardiography showed concentric remodeling of the LV without hypertrophy. Trans-esophageal echocardiography was performed for further assessment of the anatomy. The anterior mitral leaflet (AML) and posterior mitral leaflet (PML) lengths were 3.7?cm and 1.3?cm, respectively (normal AML?<?3?cm; normal PML?<?1.5?cm). In our patient, the LVOTO is significant enough to result in a decreased cardiac output, which explains the symptoms experienced, due to which he developed concentric remodeling. The only finding in this patient explaining SAM is an elongated AML.     

An accessory mitral valve leaflet causing left ventricular outflow tract obstruction and associated with severe aortic incompetence

This case report describes a 20-year-old woman with Turner's syndrome who presented with reduced effort tolerance limited by dyspnea. She had previously been on pediatric cardiology follow-up for congenital subvalvular aortic stenosis first diagnosed at age 7. Unfortunately she defaulted after two visits before any intervention could be done. Transthoracic echocardiography demonstrated severe aortic incompetence (AI) with a membrane-like structure in the left ventricular outflow tract (LVOT). The mean pressure gradient across the LVOT on continuous wave Doppler was 41 mmHg. The membranous interventricular septum appeared aneurysmal and it was observed that the "subaortic membrane" had a connection to the anterolateral papillary muscle via a strand of chordal tissue. Further images were captured using two-dimensional and three-dimensional transthoracic and transesophageal echocardiography (iE33, Philips Medical Systems, Andover, MA, USA). After a review of the literature it was concluded that this appeared to be an accessory mitral valve (AMV) leaflet causing LVOT obstruction associated with AI. AMV tissue is a rare congenital malformation causing LVOT obstruction. Because it is so unusual, it may not be immediately recognizable even in a high volume echocardiography laboratory. The clue which helped with the diagnosis was the strand of chordal tissue which connected the mass to the papillary muscle. This anomaly is often associated with LVOT obstruction.     

Patients with mild hypertensive heart disease and left ventricular outflow tract obstruction: treatment with angiotensin II antagonists

Systolic anterior motion of the mitral leaflet (SAM) combined with obstruction at the left ventricular (LV) outflow tract is often observed on echocardiography in elderly hypertensive patients with severe concentric LV hypertrophy. We experienced, however, two patients with mild hypertension who had an ejection systolic murmur, SAM, and LV outflow tract obstruction with a pressure gradient of 46 and 45mmHg, respectively, despite very mild symmetric hypertrophy of LV wall (12mm) by echocardiography. Treatment with angiotensin II type 1 receptor blocker improved intraventricular obstruction and LV hypertrophy in both patients. Left ventricular outflow tract obstruction should be suspected in hypertensive patients with mild LV hypertrophy, particularly in those with an ejection systolic murmur. Angiotensin II antagonists could be considered as the treatment of choice for such patients.An erratum to this article can be found at     

Malaligned bioprosthetic valve causing left ventricular outflow tract obstruction

Left ventricular outflow tract obstruction resulting from strut impingement upon the interventricular septum is a rare complication of bioprosthetic mitral valve insertion. Obstruction is more likely to develop when a small, high profile prosthetic valve is inserted into a patient with a small outflow tract. The likelihood of this complication may be reduced by appropriate modification of surgical technique.     

Critical left ventricular outflow tract obstruction due to accessory mitral valve tissue

Left ventricular outflow tract (LVOT) obstruction due to anomalous tissue tag arising from the mitral valve is a rare congenital cardiac anomaly. It generally becomes symptomatic during the first decade of life as exercise intolerance, chest pain, or syncope at effort. To date, only a few cases of critical systemic obstruction due to isolated mitral valve anomaly in neonates have been reported. We report the case of a neonate who was a few hours old and was referred in severe clinical condition due to critical left ventricular outflow obstruction resulting from an anomalous tissue tag of mitral valve origin.     

Haemodynamic effects of acute intravenous metoprolol in apical ballooning syndrome with dynamic left ventricular outflow tract obstruction

Takotsubo syndrome, also called apical ballooning syndrome, is a clinical entity characterized by transient hypokinesis, akinesis, or dyskinesis of the left ventricular mid‐segments with or without apical involvement, and without obstructive coronary lesions. The contemporary presence of left ventricular outflow tract obstruction (LVOTO), systolic anterior motion of the anterior mitral leaflet, and acute mitral regurgitation might explain the worsening of the heart failure or the occurrence of cardiogenic shock in some patients with apical ballooning syndrome. The use of β‐blockers should improve the LVOTO gradient by reducing basal hypercontractility, increasing left ventricular filling and size, and reducing heart rate. However, clear evidence of the direct haemodynamic effects of β‐blockers is still lacking. We present a case of apical ballooning syndrome complicated by dynamic LVOTO, treated with metoprolol.     

Mechanisms,pathophysiology, and diagnostic imaging of left ventricular outflow tract obstruction following mitral valve surgery and transcatheter mitral valve replacement

Left ventricular outflow tract obstruction is a serious complication of mitral valve surgery (repair and replacement) and transcatheter mitral valve replacement. An appreciation of the various mechanisms which cause outflow obstruction in these settings is critical to avoiding this complication and to initiating appropriate treatment. This article discusses the mechanisms, pathophysiology, and imaging of left ventricular outflow tract obstruction which can arise following insertion of a variety of mitral valve prosthetics.     

An unusual cause of left ventricular outflow tract obstruction

Left ventricular outflow tract obstruction (LVOTO) has been reported with bio-prosthetic and mechanical mitral valves (MV), though it is more common with the former. The obstruction can be dynamic or fixed. We hereby report a case of fixed LVOTO following bio-prosthetic MV replacement (MVR).     

Effects of systolic anterior motion of the mitral valve on haemodynamics: Evaluation by a direct method

We evaluated the effects of systolic anterior motion systolicanterior motion of the mitral valve on cardiac haemodynamics.Seven adult mongrel dogs in which systolic anterior motion-septalcontact was observed after dobutamine administration were used.To exclude the effects of left ventricular function and morphology,a stone removal basket catheter was placed in the left ventricularoutflow tract, and haemodynamics were compared with the basketclosed and opened. The basket was opened five times in three dogs not showing systolicanterior motion-septal contact, but the basket itself did noteffect the haemodynamics. In the seven dogs that showed systolicanterior motion-septal contact without left ventricular hypertrophy,the basket was opened a total of 33 times in the presence ofvarious degrees of systolic anterior motion-septal contact.After opening the basket, systolic anterior motion was reducedechocardiographically, and sign (P<0·01) changes wereobserved in the left ventricle-aorta pressure gradient (from68 ± 22 to 25 ± 15 mmHg), the systolic ejectionperiod (from 146 ± 19 to 135 ± 16 ms), and thestroke volume (SV; from 9·4 ± 2·9 to 10·1± 3·3 ml). After basket inflation, aortic pressureand aortic flow waveforms changed but the peak pressure andflow velocity did not. The temporal distribution of left ventricularejection also definitely changed after the basket was opened.No changes were observed in the peak dp/dt, peak negative dp/dt,time constant, left ventricular end-diastolic pressure, or leftatrial pressure. These observations in this animal model ofsystolic anterior motion without left ventricular hypertrophysuggest that. (1) there is no potential for generation of anintra-cavity gradient in the absence of systolic anterior motionof the mitral valve, so that (2) systolic anterior motion narrowedthe left ventricular outflow tract and, consequently, producedthe pressure gradient, decreased the SV, changed the aorticpressure and blood flow waveforms, prolonged the systolic ejectionperiod, and affected the left ventricular ejection dynamics,and that (3) the basket catheter is useful because it allowsthese assessments in the same heart with a nearly fixed leftventricular contractility, at least in our animal model.