Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3737_Библиотеки_им_академика_М_И_Перельмана

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The sinuses of Valsalva can be identied as small dilatations in the aortic wall just above each cusp of the aortic valve, precisely between the annulus and Sino tubular (ST) junction. They allow aortic valve opening during systole without occlusion of coronary artery ostia [1]. Defect in aortic wall resulting in outpouching protrusion into nearby cardiac chambers is known as Sinus of Valsalva Aneurysm (SOVA). SOVA was rst described by Hope in 1839. Edward and Burchell’s reported that SOVAs are secondary to failure of the aortic media to fuse with the heart during prenatal development. The estimated incidence varies between 0.09 up to 0.96% [2–5]. Ethnicity plays

an important role in this variable incidence. Chue etal. [6] reported ve times higher incidence of ruptured SOVA (RSOVA) in Far Eastern patients than in Westerns.

Embryologically, SOVA forms rst as a blind diverticulum secondary to pressure forces on the aortic root [7]. Thus, congenital defects potenti­ating these pressure forces can lead to develop­ment of a SOVA [1]. SOVA is either congenital or acquired. Whether congenital or acquired, SOVA is a consequence of weakness of the elastic lam­ina at the junction of the aortic media and the annulus brosis [8]. Congenital ones are seen in connective tissue disorders such as Marfan syn­drome [9] or Ehlers-Danlos syndrome [10–14]. Also, there are several congenital defects com­monly associated with SOVA.For example, ven­tricular septal defects (VSDs), with or without aortic regurgitation have been reported in 12% and up to 78% of SOVA patients [15, 16], most commonly with aneurysm of right coronary sinus. Aortic valve abnormalities such as bicus­pid aortic valve has been reported in at least 10% of SOVA patients [9, 15].

notable difference in distribution is thought to be related to the role of outlet septum defects in the genesis of SOVAs. The right coronary cusp of aortic valve adjoins a big part of the outlet sep­tum, while left coronary cusp does not originate from the outlet septum [17].

Usually asymptomatic, but occasionally, continu­ous murmur can be heard due to the ow in and out of the intact aneurysmal pouch [18]. Unruptured lesions can result in signicant arrhythmias including ventricular tachycardia, atrial brillation, and complete heart block through extension into the interventricular sep­tum and compression of the atrioventricular (AV) node and His bundle [18]. Cases of coronary artery compression secondary to compression of coronary ow by unruptured SOVA have been reported [19]. SOVA can uncommonly cause RVOT obstruction. Rarely (Fig.1), thrombus for­mation within the SOVA can lead to thromboem­bolic cerebrovascular accidents Fig.2 [20].

failure. Sudden cardiac death can result from tamponade, ischemia, arrhythmia and/or conduc­tion issues [22].

Both ruptured and unruptured SOVAs have non­specic clinical presentation. As shown in our case, clinical presentation and even initial diag­nostic evaluation may not easily lead to proper diagnosis. Therefore, multi-modality imaging is of crucial role in establishing precise diagnosis and guiding management.

On frontal lm, SOVA may manifest as bulging of the aorta to the right of caval shadow. Ruptured

Transcatheter Aortic Valve implantation/replace­ment (TAVI/TAVR) suggested sinus-to­commissure method which means measuring from the commissure to the opposite sinus. This method generally results in 2mm smaller SOV mean diameter compared to the sinus-to-sinus method [29]. The typical SOVA can be seen on CT as thin walled-out pouching in proximity to the wall of aorta. If disconnected from the aortic wall, once should suspect ruptured SOVA [27]. The main disadvantages of MDCT are radiation exposure, low temporal resolution, and lack of