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Interact CardioVasc Thorac Surg 2009;9:141-143. doi:10.1510/icvts.2009.205849 © 2009 European Association of Cardio-Thoracic Surgery
Aortic dissection due to sildenafil abuse
a Department of Cardiology, Bursa Acibadem Hospital, Bursa, Turkey Received 20 February 2009; received in revised form 3 April 2009; accepted 6 April 2009
*Corresponding author. Bursa Yuksek
This report deals with a 28-year-old male patient, admitted with a type A aortic dissection, potentially related to the use of sildenafil. In the literature, we found only two other potentially sildenafil-related cases of aortic dissections, one type A and one type B. In our patient, a bicuspid aortic valve and an ascending aortic aneurysm were other underlying anomalies that could have led to the aortic dissection.
Key Words: Sildenafil; Aortic dissection
Aortic dissection is one of the most dramatic diseases that cardiovascular surgeons have encountered since the first detailed description suggested by Morgagni in 1761 [1]. Acute aortic dissection is defined as blood present between the layers of the aortic wall (false lumen), outside the true lumen, as a result of the decomposition of the media. The separation in the media is in 95% of the cases caused by the blood flowing through a tear in the intima (intimal tear or flap), while in 5% of the cases the cause is bleeding within the media (intramural hematoma). According to some series, the aortic dissection might be undetected up to 38% during the initial evaluation and a considerable number of patients are diagnosed during postmortem evaluations [2]. Early diagnosis and surgical treatment are essential in acute type A and in complicated type B aortic dissections. That surgical results are more acceptable is mostly the consequence of recently applied retrograde or anterograde cerebral perfusion techniques, hemostatic and anti-fibrinolytic agents such as aprotinin, biological binding agents, and albumin and collagen-coated grafts. The most frequent etiologic factors are reported to be chronic systemic hypertension, hereditary connective tissue diseases and congenital aortic valve diseases (bicuspid and unicuspid aorta). In this case, we present a type A dissection following use of sildenafil.
A 28-year-old male patient with no known history of cardiac problems was taken to the emergency service for sudden chest pain and fainting  2 h after the use of 50 mg sildenafil – without any sexual intercourse involved. The patient had been using sildenafil in intervals for approximately a year, without any doctor prescriptions and no adverse effects had occurred. The patient was not using any other medicines regularly. The patient was not known to have any other disease. Apart from a daily consumption of approximately three packages of cigarettes, he did not have a history of stimulant use. In the emergency service, the patient was conscious, complained of severe chest pain; the physical examination revealed tachycardia and severe diastolic murmur in the aortic focus. No characteristics were detected in the respiratory sounds of both lungs. The abdominal examination did not reveal any characteristics and bilateral femoral pulses were present. The ECG of the patient showed findings of left ventricular hypertrophy. The transthoracic echocardiography revealed a dissection phlep reaching out to the valves in the ascending aorta, and the patient had a moderate – severe aortic failure (due to a cusp involvement) and a bicuspid aorta. The valve opening was sufficient and no gradients were detected on the aortic valve. The other cardiac structures were normal as much as they were observed. The ascending aorta diameter was 6.13 cm. The patient underwent a computed tomography angiography (CTA) immediately. The tomography detected an intimal phlep in the ascending aorta, beginning from the level of aortic valve and ending in the level of left subclavian artery (De Bakey type II) (Figs. 1 and 2). In the segments analyzed by the CTA-scan of the patient, no other vascular aneurysms were detected. The patient was immediately taken into operation. (After the patient applied to the emergency service, the preparations were completed in the first 2 h and the patient was taken under the operation.)
During the operation, the Bentall procedure was applied; no complications developed at the postoperative stage and the patient left the clinic without any problems. In the pathological analysis applied on the aneurysmal segment removed after the operation, no collagen tissue disorders (Marfan, Ehlers-Danlos, etc.) were discovered.
In the literature, we came across a total of two similar cases, one with a post-sildenafil type A aortic dissection and the other being a type B dissection after the use of cocaine and sildenafil. We found out in our case that type A aortic dissection formation is associated with the sildenafil use. Moreover, the patient had bicuspid aorta and secondary ascending aortic aneurysm [3, 4]. As a result of the autopsies done on 186 patients who died of aortic dissection, bicuspid and unicuspid aortic valve were found in 7–13% and 1.1%, respectively. Edwards et al. detected a congenital aortic valve anomaly of 9% in the dissection series involving 119 cases and ending in death [5]. Bicuspid aortic valve is an independent risk factor for progressive aortic dilatation, aneurysm formation and dissection. Vascular complications may develop without any valve dysfunctions. In fact, in >50% of young patients with a bicuspid aortic valve, aortic dilatation was detected by echocardiography. The patients with a bicuspid aortic valve have a 9-fold risk of dissection [6]. In cases with acute aortic dissection, the most significant pre-disposing factor is uncontrolled hypertension. Our case did not have a history of hypertension and at the time of his acceptance to the hospital, his blood pressure values were at normotensive limits. The point that should be highlighted in this case is that sildenafil use, independent of changes in the aorta pressure, can trigger an aortic dissection. Indeed, in the study carried out in 2005 by Kocakoc et al., sildenafil use is suggested to render no significant change on Doppler and aorta velocities [7]. Based on these studies, we can conclude that sildenafil does not have a substantial effect on the aorta pressure. Sildenafil decreases aortic ‘stiffness’ in humans. In vitro studies show sildenafil has vasorelaxant properties in rat aorta. Probably, due to this impact, sildenafil use can trigger intimal tearing, and this impact can be more apparent [8]. Again in the study conducted on pulmonary arteries, it is stated that without changing pulmonary artery or systemic blood pressure, it increases the pulmonary flow and that it proliferates pulmonary smooth muscle cells. Based on all these grounds, especially with an underlying pathology, sildenafil use can make the aorta wall more sensitive and can trigger the dissection [3]. Although our case involves risk factors for an aortic dissection, the fact that as soon as sildenafil reaches up to the peak plasma level, a dissection table is formed suggesting a relation between sildenafil and dissection. Because dissection occurs in the critical time interval between the peak plasma concentration time and half-life of sildenafil and because the patient has no history of any triggering factor (mechanical stress, trauma etc.), sildenafil is thought to trigger the dissection.
The patients for whom sildenafil use is suitable should undergo not only an examination for coronary artery disorder but also the diseases that will affect the aorta; physical examination should definitely be accompanied by an echocardiographic examination.
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Abstract
1. Introduction
