PDF(Pubmed)
Abstract：
UNASSIGNED: The aetiology of secondary complete atrioventricular blocks includes ischaemia, cardiac sarcoidosis, electrolyte imbalance, drug use, rheumatic fever, and infections such as Lyme disease and endocarditis. Diagnosis is important since some of these causes are reversible. Although several studies have reported on aortic valve calcification causing complete atrioventricular blocks, no study has described improvement of complete atrioventricular blocks by removal of the calcification.
UNASSIGNED: A 42-year-old man with syncope had a Mobitz type II atrioventricular block, an alternating bundle branch block, and severe aortic stenosis. We identified a 10 s paroxysmal complete atrioventricular block with pre-syncope and performed pacemaker implantation. Electrocardiography-gated computed tomography confirmed that the calcification had reached the muscular septum. 18F-fluorodeoxyglucose-positron emission tomography (FDG-PET) revealed significant FDG uptake with high CT value of calcification in basal interventricular septum. The calcification in the septum was removed carefully, and aortic valve replacement was performed. The atrioventricular conduction capacity improved post-surgery. During the 1-year follow-up, the patient reported dramatic improvement in exercise capacity. We also noted an improvement of <0.1% in the right ventricular pacing burden.
UNASSIGNED: Complete atrioventricular blocks occur in patients with aortic stenosis accompanied by severe calcification of the aortic valve, which are visualized comprehensively by echocardiography. Electrocardiography-gated computed tomography and FDG-PET enabled detailed evaluation of the extent of calcification and pre- and post-operative tissue inflammation. Hence, we suspected that the calcification in the septum was causing complete atrioventricular block. Moreover, clinicians should recognize that aortic valve calcification with aortic stenosis can cause complete atrioventricular blocks.
UNASSIGNED: A 42-year-old man with syncope had a Mobitz type II atrioventricular block, an alternating bundle branch block, and severe aortic stenosis. We identified a 10 s paroxysmal complete atrioventricular block with pre-syncope and performed pacemaker implantation. Electrocardiography-gated computed tomography confirmed that the calcification had reached the muscular septum. 18F-fluorodeoxyglucose-positron emission tomography (FDG-PET) revealed significant FDG uptake with high CT value of calcification in basal interventricular septum. The calcification in the septum was removed carefully, and aortic valve replacement was performed. The atrioventricular conduction capacity improved post-surgery. During the 1-year follow-up, the patient reported dramatic improvement in exercise capacity. We also noted an improvement of <0.1% in the right ventricular pacing burden.
UNASSIGNED: Complete atrioventricular blocks occur in patients with aortic stenosis accompanied by severe calcification of the aortic valve, which are visualized comprehensively by echocardiography. Electrocardiography-gated computed tomography and FDG-PET enabled detailed evaluation of the extent of calcification and pre- and post-operative tissue inflammation. Hence, we suspected that the calcification in the septum was causing complete atrioventricular block. Moreover, clinicians should recognize that aortic valve calcification with aortic stenosis can cause complete atrioventricular blocks.
摘要：
■继发性完全性房室传导阻滞的病因包括缺血，心脏结节病,电解质不平衡，吸毒,风湿热,以及莱姆病和心内膜炎等感染。诊断很重要，因为其中一些原因是可逆的。尽管有一些研究报道了主动脉瓣钙化导致完全房室传导阻滞，没有研究描述通过清除钙化可以改善完全性房室传导阻滞.
■一名42岁晕厥患者患有MobitzII型房室传导阻滞，交替的束分支块，和严重的主动脉瓣狭窄.我们确定了10s前晕厥的阵发性完全性房室传导阻滞，并进行了起搏器植入。心电图门控计算机断层扫描证实钙化已到达肌间隔。18F-氟脱氧葡萄糖-正电子发射断层扫描（FDG-PET）显示FDG明显摄取，基底室间隔钙化的CT值较高。小心地去除隔膜中的钙化，并进行了主动脉瓣置换术.术后房室传导能力改善。在为期一年的随访中，患者报告运动能力显著改善.我们还注意到右心室起搏负荷的改善<0.1%。
■主动脉瓣狭窄伴主动脉瓣严重钙化的患者会发生完全房室传导阻滞，通过超声心动图全面可视化。心电图门控计算机断层扫描和FDG-PET可以详细评估钙化程度以及手术前后组织炎症。因此，我们怀疑隔膜钙化导致了完全房室传导阻滞.此外，临床医生应认识到主动脉瓣钙化伴主动脉瓣狭窄可引起完全性房室传导阻滞.
■一名42岁晕厥患者患有MobitzII型房室传导阻滞，交替的束分支块，和严重的主动脉瓣狭窄.我们确定了10s前晕厥的阵发性完全性房室传导阻滞，并进行了起搏器植入。心电图门控计算机断层扫描证实钙化已到达肌间隔。18F-氟脱氧葡萄糖-正电子发射断层扫描（FDG-PET）显示FDG明显摄取，基底室间隔钙化的CT值较高。小心地去除隔膜中的钙化，并进行了主动脉瓣置换术.术后房室传导能力改善。在为期一年的随访中，患者报告运动能力显著改善.我们还注意到右心室起搏负荷的改善<0.1%。
■主动脉瓣狭窄伴主动脉瓣严重钙化的患者会发生完全房室传导阻滞，通过超声心动图全面可视化。心电图门控计算机断层扫描和FDG-PET可以详细评估钙化程度以及手术前后组织炎症。因此，我们怀疑隔膜钙化导致了完全房室传导阻滞.此外，临床医生应认识到主动脉瓣钙化伴主动脉瓣狭窄可引起完全性房室传导阻滞.
