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Ann Thorac Surg 2004;78:e67-e68
© 2004 The Society of Thoracic Surgeons
a Department of Cardiac Pathology, Institut Mutualiste Montsouris, Paris, France
Accepted for publication February 6, 2004.
* Address reprint requests to Dr Le Bret, Department of Cardiac Pathology, Institut Mutualiste Montsouris, 42 Boulevard Jourdan, 75014 Paris, France
emmanuel.lebret{at}imm.fr
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Introduction |
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A 31-year-old white man was referred to our institution for severe isolated thoracic pain.
The patient's history revealed that, because of dyspnea and cyanosis, the diagnosis of aortopulmonary window was established at 17 years of age but that closure of the defect was not considered because of irreversible pulmonary hypertension. Heart-lung transplantation was proposed to the patient but was refused by the family. After that, he was lost to follow-up.
On admission in the intensive care unit (ICU), the thoracic pain had almost disappeared, the systemic arterial pressure was 120/80 mm Hg with a heart rate of 85 per minute, and all pulses were present and symmetric. Neither a systolic nor diastolic murmur could be heard. Electrocardiography showed sinus rhythm, right bundle branch block, and severe right ventricular hypertrophy. A chest roentgenogram showed a large left hilar mass, suggesting dilatation of the pulmonary artery (Fig 1). Transthoracic echocardiography showed a very large dilatation of the ascending aorta (58 mm) and the absence of shunt through the window due to isosystemic pulmonary hypertension. No pericardial effusion, aortic insufficiency, or intraluminal flap was noted. Spiral computed tomography demonstrated the presence of two separate semilunar valves and a huge aortopulmonary window almost forming a single aortopulmonary trunk (Fig 2) from which the two branches of the pulmonary artery originated. A large hematoma was noted around the pulmonary artery without evidence of pericardial effusion.
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Postmortem examination confirmed the presence of a large aortopulmonary window starting just above the left coronary ostium and extending up to the origin of both pulmonary arteries. A dissection was discovered on the trunk of the pulmonary artery at the junction with the aorta. The false lumen extended posteriorly and was almost totally occupied by fresh thrombus. No reentry site was noted. A complete rupture 2 cm in diameter was present on the left side of the dissected arterial wall.
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Although arterial dissection commonly occurs in the aorta in patients with a history of systemic hypertension, it is unusual in the pulmonary artery. Pulmonary dissection occurs in both sexes with a slight female predominance (1/1.2). The dissection is usually located on the pulmonary trunk (72%) followed by the intrapulmonary arteries (10%) A recent review of 52 cases of pulmonary artery dissections [1] reported that 75% dissections developed in patients with underlying pulmonary hypertension either primary (20%) or secondary to cardiac diseases [1, 2]. Congenital malformations are mostly responsible for secondary pulmonary hypertension [3], but it has been observed in hereditary disorders [4], acquired valvular lesion, and chronic pulmonary diseases (tuberculosis and syphilis) [1].
According to the literature [1–6], dissection always occurs at the site of maximal dilatation of the artery. In contrast to aortic dissection and because of the thinness and fragility of the external layer, the high pressure inside the false lumen tends to favor rupture of the free wall rather than tearing the intimal flap and opening a reentry site. For this reason the mortality rate after pulmonary arterial dissection is extremely high and no aneurysmal chronic dissection has ever been described.
Our observation raises the main issue of surgical treatment of pulmonary dissection and its ultimate rupture. Obviously no time was lost between admission to the ICU, echocardiography, and computed tomography. It is unlikely that the maneuvers and mobilization during the computed tomographic scan led to the rupture of the dissection, although this possibility cannot be excluded. However, it was hardly possible to confirm the diagnosis without this examination.
More importantly, because of the nature of the lesion and the size and the fragility of the pulmonary trunk, one may wonder how the pulmonary trunk could have been replaced even in the absence of massive hemorrhage. In the face of such a complication and with the moribund patient in cardiac arrest, any kind of surgical repair proved impossible. Even though surgical repair could have been possible, the presence of irreversible pulmonary hypertension would most likely have led to the impossibility of weaning the patient from cardiopulmonary bypass and eventually to his death.
Pulmonary artery dissection is a very rare entity. In most cases, the diagnosis is made after rupture of the pulmonary artery into the pericardium, leading to massive tamponade and severe clinical deterioration or death. When associated with major irreversible pulmonary hypertension, it generally results in an intractable anatomic and pathophysiologic condition and literally places the medical and surgical team at an absolute therapeutic dead end.
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This article has been cited by other articles:
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  A. T. Yetman and T. Graham The dilated aorta in patients with congenital cardiac defects. J. Am. Coll. Cardiol., February 10, 2009; 53(6): 461 - 467. [Abstract] [Full Text] [PDF]
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 K. Imanaka, T. Matsuoka, K. Abe, M. Nishimura, and S. Kyo Acute Stanford Type B Dissection and Cardiac Tamponade: Rupture From Around Ductus Arteriosus Ann. Thorac. Surg., July 1, 2007; 84(1): 278 - 280. [Abstract] [Full Text] [PDF]
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