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From the Departments of *Cardiothoracic Anesthesia, and Cardiothoracic Surgery, University-Hospital of Udine, Udine, Italy.
Address correspondence and reprint requests to Luigi Vetrugno, Department of Cardiothoracic-Anesthesia, University-Hospital of Udine, 33100 Udine, Italy. Address e-mail to vetrugnoluigi{at}katamail.com.
A previously healthy 35-year-old man was transferred to our intensive care unit with severe dyspnea, hypotension, and a history of atypical chest pain. The patient’s clinical condition appeared to be rapidly deteriorating, showing signs cerebral hypoperfusion, in that he was somnolent yet responsive on presentation.
Pulmonary inspiratory rales were heard over all lung areas of auscultation and harsh continuous murmurs were heard over the precordium. His systemic blood pressure was low (80/40 mm Hg) and his heart rate was elevated (100 bpm with sinus rhythm).
His medical and clinical history revealed no infection, cardiac disease, or chest trauma. Because the clinical signs and hemogasanalysis were indicative of imminent sudden respiratory failure, tracheal intubation was preformed. Transesophageal echocardiography (TEE), as opposed to transthoracic echocardiography, was then performed, which provides high-resolution images, multiple scan planes, and an accurate assessment of cardiac and aortic pathology.1
A midesophageal four-chamber TEE view at 0 degrees rotation showed a moderately depressed left ventricular function (ejection fraction of about 40%) and what appeared to be a third anomalous chamber between the right and left ventricle (Fig. 1 top left). A midesophageal aortic valve (AV) long axis view showed a pulsating aneurysmal outpouching off of the aortic root (5 cm x 10.5 cm) that completely dissected the interventricular septum (Fig. 1 top right). The aortic insufficiency appeared to be secondary to structural abnormality of the right coronary cusp, possibly secondary to decreased support of the cusp as a result of the location of the sinus of valsalva aneurysm (SVA) (Video clips 1 and 2; please see video clips available at www.anesthesia-analgesia.org). This brisk bidirectional flow finding was interpreted as a SVA originating from the right coronary cusp and extending through the entire interventricular septum. Given its large size and extension to the interventricular septum, it was unclear from TEE findings whether the aneurysm had ruptured.
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Advancing the probe to the transgastric mid short axis view at 0 degrees rotation showed that the right ventricle was small and flattened (Fig. 1 bottom). It appeared that the cause of hypotension was probably the inflow/outflow obstruction of the right ventricle from the SVA (Video clips 1 and 2).
Cardiac catheterization confirmed a normal coronary artery tree and the presence of the SVA originating from the right sinus (Video clips 1 and 2). The patient was prepared and underwent emergency surgery, at which time intraoperative TEE confirmed our preoperative findings. It is clear that TEE in this case allowed for accurate detection of an unexpected severe abnormality, altering diagnosis and surgical strategy. During surgery, aortotomy revealed that the aneurysm orifice (2.5 cm x 1.5 cm) was located in the right coronary sinus (Fig. 2). The AV appeared to be tricuspid, with a right hypoplastic coronary cup and an abnormal noncoronary redundant flap located at the base of the aortic annulus.
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A considerable amount of bio-glue was injected in the aneurysm orifice, which was then sealed with a composite Dacron patch of autologous pericardium tissue. The AV was also replaced with a St. Jude 21 mm mechanical bi-leaflet prosthesis valve. The patient was weaned from cardiopulmonary bypass and TEE confirmed good surgical results. The patient had an uneventful postoperative course with cardiac function recovery.
Studies have shown that about 83% of cases of SVA that extend into the interventricular septum originate in proximity to the right coronary sinus of Valsalva.2 Right coronary sinus aneurysms usually rupture into the right ventricle, whereas noncoronary cusp aneurisyms tend to rupture into the right atrium.3 Studies have reported that an SVA that extends into the interventricular septum is possible, and is usually due to an intramural rupture of a congenital aneurysm with subsequent formation of a pulsating aneurysmal outpouching off of the aortic root that extends into the tissue of the interventricular septum. A coexisting ventricular septal defect can usually be seen, which tends to be located right below the aneurysm. This association is mainly due to a structural abnormality in the distal bulbar septum.4 Secondary causes of SVA include surgery, trauma, bacterial endocarditis, syphilis, tuberculosis, and Behcet’s disease.5
The prevalence SVA that requires surgical repair accounts for <1% of cardiac pathologies. The most common coexisting lesion is a double committed ventricular septal defect, which can be seen in up to 60% of patients with a right sinus aneurysm. Aortic regurgitation frequently occurs, which is most likely due to the lack of supporting tissue and sagging of the aortic cusps.1
The complications of SVA are numerous and heterogeneous (depending on localization), and can include rupture into a adjacent cardiac chamber, vascular compression, alteration in cardiac electrical conduction, abnormal vascular coagulation leading to thrombosis and emboli, etc. Numerous signs and symptoms of SVA include heart palpitation (due to atrial fibrillation, ventricular tachycardia, complete heart block, etc.), general fatigue, exertional dyspnea, syncope, infectious endocarditis. Most SVAs, however, tend to be silent and are discovered serendipitously.
TEE correctly showed that the complete inflow/ outflow obstruction of the right ventricle of our patient was due to the compression from the aneurysm and excluded other pathologies with similar clinical presentation (i.e., aortic dissection, cardiac tamponade, valve insufficiency or ischemia, etc).
Rosenberger et al.6 recently reported a similar case, in which complications were due to an SVA obstructing the right ventricular outflow tract. To the best of our knowledge, our case differs (inpatient age and type of SVA) from others, in that it deals with a young patient having an exceptionally large unruptured SVA that dissected the interventricular septum, and that TEE proved to be extremely essential in the clinical management of the patient.
ACKNOWLEDGMENTS
We thank Dr. Mark Zeppieri for the revision of the manuscript.
Footnotes
Accepted for publication December 19, 2007.
This article has supplementary material on the Web site: www.anesthesia-analgesia.org.
REFERENCES
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