Sinus valsalva aneurysm on cardiac CT angiography: Assessment and detection

Authors


  • JM Troupis MBBS, FRANZCR; A Nasis MBBS (Hons), FRACP; S Pasricha MBBS, FRANZCR; M Patel MBChB; AH Ellims MBBS (Hons), FRACP; S Seneviratne MBBS, FRACP.
  • Conflict of interest: None declared.

Correspondence

Dr Mihir Patel, Diagnostic Imaging, Monash Medical Centre, Southern Health, 208/148 Wells Street, South Melbourne, Vic 3205, Australia.

Email: mihirp97@yahoo.co.nz

Summary

After the advent of ECG gated cardiac CT angiography (CCTA) there has been significant improvement in image quality of the ascending aorta. As a result the sinuses of valsalva are readily assessable. Sinuses of valsalva aneurysm can cause significant dysfunction of the aortic root and annulus and can be congenital or acquired. The aneurysm most commonly originates from the right coronary sinus. Complications related to sinuses of valsalva aneurysm can cause chest pain and can be life threatening. The cardiac imager should actively assess the sinuses of valsalva in every CCTA study.

As cardiac CT angiography (CCTA) has developed into a readily accessible and useful tool for the exclusion of obstructive coronary artery disease in the acutely unwell patient with chest pain,[1] cardiac imagers are being exposed to images with significant improvement in visibility of the ascending aorta.[2]

The aortic root, which is seen on CCTA, includes the aortic annulus, sinus of valsalva and the sinotubular junction. Sinuses of valsalva aneurysm (SVA) can lead to significant dysfunction of the aortic root and annulus and may be life threatening.[3] As such, they should be carefully assessed in anyone with either ischaemic-type chest pain, or alternatively, dissection-type symptoms.

Definition

The sinuses of valsalva are three focal expansions that form the walls of the aortic root. The right coronary artery arises from the right sinus and the left coronary artery arises from the left sinus, with the left sinus lying slightly more superiorly than the right sinus[4]

SVA is defined as dilatation or enlargement of one or more of the aortic sinuses between the aortic valve annulus and the sinotubular junction[4]

Prevalence

The incidence ranges from 0.1 to 3.5% of all congenital heart defects[5] with proposed prevalence of 0.09% in the general population.[6]

Causes

The acquired SVA is more common than the congenital and most often is caused by weakness at the junction of the aortic media and the annulus fibrosis, due to congenital deficiency of elastic lamellae with separation of the media in the sinus from the media adjacent to the aortic valve annulus.

Acquired SVA are associated with infections (syphilis, TB), atherosclerosis, connective tissue disorders or trauma.[7-9] There is usually elastic connective tissue degeneration as the associated underlying weakness of the wall of the sinus.

Differential diagnosis

Aortic root dissection can be differentiated due to the presence of a dissection flap, which may be in close apposition to the sinus and in particular at the sinotubular junction.

Measurement

The dimensions of the aortic root are best measured within the plane of the aortic valve and during diastole to achieve accurate results. The three lengths are obtained in a perpendicular orientation, from the apex of each sinus to the opposite wall. The longest diameter is used to determine the presence of dilatation, and the relative severity, if more than one sinus is abnormal (Fig. 1). Traditionally accepted partition values for upper limits of normal for aortic root dimensions by sex are shown in Table 1.[10]

Figure 1.

Series of views (oblique coronal, oblique axial and oblique axial with measurements) confirming asymmetrical aneurysmal change involving the non-coronary cusp (3.9 cm; body surface area of 1.9 m2).

Table 1. Traditionally accepted values of upper limits of normal diameters for sinotubular junction, sinuses of valsalva and aortic valve annulus, according to sex without normalizing to body surface area
Measurement levelMen (cm)Women (cm)
Sinotubular junction3.63.2
Sinuses of valsalva4.03.6
Aortic valve annulus3.12.6

For further accuracy, 98% specificity is attained by use of an upper normal limit of 2.1 cm/m2 (normalized for body surface area) for aortic diameter at the sinuses of Valsalva in both men and women.[10] The influence of sex has been shown to be neutralized when diameter is indexed to body surface area.

Aneurysms originate most commonly in the right coronary sinus, less frequently from the non coronary sinus and only rarely from the left coronary sinus.[11]

Potential complications

Aortic regurgitation complicates SVA in 30–40%[4, 5, 12]

Ruptures occur in 34% of patients.

Fistulas predominantly occur from the right sinus of valsalva to the right ventricle and may cause either right or left heart failure from obstruction of the ventricular outflow tract. The anatomic location determines the likely cardiac chamber involvement with uncommon involvement of all cardiac chambers or extra cardiac perforations having been reported.[12]

Other complications may include myocardial ischaemia due to kinking or compression of the coronary ostia. Thrombus formation within the dilated sinus has the potential to embolise.

Surgical threshold

Surgical repair is the mainstay of treatment of both ruptured and unruptured SVA and is associated with a 10-year survival rate of 90%.[13, 14] For symptomatic, unruptured SVA, the indications for surgery include malignant arrhythmias, infective endocarditis, coronary artery compression and outflow tract obstruction. The 2010 American Guidelines on Thoracic Aortic Disease suggests treatment of SVA similar to aortic aneurysm with consideration for surgical repair in the setting of symptomatic aneurysm, size greater than 5.5 and 4.5 cm without and with genetic connective tissue disorder respectively, and growth rate >0.5 cm/year (Fig. 2).[15]

Figure 2.

A 44-year-old man requiring a CCTA for the exclusion of obstructive coronary artery disease, prior to surgery for a dilated aortic root. Markedly aneurysmal non coronary sinus on a background of mildly aneurysmal right coronary and left coronary sinuses. Patient non-coronary sinus increased in size from 5.5 cm to 6 cm (transverse diameter) in 12 months on trans-oesophageal echocardiogram. Subsequently he underwent aortic root replacement.

Conclusion

SVA are potentially life threatening conditions that can now be readily identified on CCTA. The cardiac imager should exclude sinuses of valsalva aneurysm in all patients undergoing CCTA for exclusion of obstructive coronary artery disease.

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