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Ann Thorac Surg 2003;76:917-919
© 2003 The Society of Thoracic Surgeons
a Department of Cardiothoracic Surgery, Harper University Hospital, Wayne State University, Detroit, Michigan, USA
Accepted for publication February 14, 2003.
* Address reprint requests to Dr Baciewicz, 3990 John R, Suite 2102, Detroit, MI, USA48201
e-mail: fbaciewi{at}dmc.org
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Introduction |
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A recent large study of different HAART regimens in severely immunosuppressed HIV-infected persons, with an average entry CD4+ cell count of 40 cells/mm3, showed that only one-third of these patients had died a median of 3.5 years after initiation of HAART [2]. Previous suggestions that HIV-infected patients with CD4+ cell counts less than 100 to 200/mm3 did poorly postoperatively were from an era before HAART, and may have been confounded by poor nutritional status or poor functional status in these individuals at the time of surgery.
Because there is risk of inoculation with the human immunodeficiency virus type I (HIV-1), cardiac surgeons, nurses, anesthesiologists, and perfusionists have refused to participate in cardiac surgery on infected patients. Although the risk of acquiring HIV from a needle stick is only 0.3% [3], there are multiple opportunities given the technical nature of cardiac surgery to become infected.
Recent reports have detailed coronary bypass and valve replacements in patients with HIV [4–5]. This case report presents a patient with HIV who was operated on in October 1997 for a type I aortic dissection. This report is being provided to present a detailed and successful outcome of a patient with type I aortic dissection and HIV.
The patient is a 57-year-old homosexual man with a history of HIV infection who presented with a 2-day complaint of sudden onset of numbness and coolness in the right lower extremity. The patient denied any back pain, chest discomfort, or shortness of breath. He gave a history of hypertension and coronary artery disease. He had a myocardial infarction in 1997.
His physical examination revealed a blood pressure of 190/120 mm Hg in both upper extremities. A grade II/VI aortic insufficiency murmur was appreciated. There were decreased pulses in the right groin. Posterior tibial and dorsalis pulses were absent on the right side. There were palpable pulses at the left common femoral, popliteal, and dorsalis pedis.
The chest roentgenogram showed a normal-sized thoracic aorta. There was a normal pericardial silhouette. The patient underwent a chest computed axial tomographic scan that showed an aortic dissection beginning in the ascending aorta and extending to both iliac arteries.
The white blood cell count was 8,500 with 14% lymphocytes. His absolute CD4+ count was 390/mL3. There was no detectable viral load by HIV RNA polymerase chain reaction.
The patient was taken emergently to the operating room. A type I dissection was noted starting just above the right coronary artery. The dissection had been present for several days by inspection. The dissection involved the superior and inferior aspects of the transverse aortic arch. The aortic valve was resuspended. During a 32-minute period of hypothermic circulatory arrest with retrograde cerebral perfusion, hemi-arch replacement of the transverse arch was performed. The intima and adventitia of the aortic root and the transverse arch were reapproximated before placement of the 32-mm Hemashield graft (Boston Scientific Medi-tech, Wayne, NJ). The patient had a previous coronary arteriogram revealing a 40% left anterior descending lesion. The patient was weaned from cardiopulmonary bypass without difficulty. The postoperative electrocardiogram was unchanged. A vein patch was used to repair the defect in the left common femoral artery, which was the arterial cannulation site.
Postoperatively, the patient was hemodynamically stable. There was a Doppler pulse in the left dorsalis pedis, and postoperatively there was now a palpable right dorsalis pedis pulse. Postoperatively, the patient was neurologically intact.
On the morning of the first postoperative day it was noted that the patient’s previously palpable right dorsalis pedis pulse and the left dorsalis pedis Doppler pulse had disappeared. An arteriogram was obtained that revealed a normal-sized ascending and transverse aortic arch. There was dissection distal to the left subclavian artery. There was decreased flow to the right lower extremity and flow to the left lower extremity was by collaterals only. The patient was referred for percutaneous fenestration and stenting. The fenestration was performed in the distal abdominal aorta. Stents were placed in both the left and right iliac arteries. Following the fenestration and stenting procedure there were palpable left and right dorsalis pedis pulses. The left lower extremity range of movement was decreased as compared with the right.
The patient was transferred to the step-down unit on his fourth postoperative day. He made steady progress and was restarted on his antiviral medications on the fourth postoperative day. He was discharged on his eleventh postoperative day. His pre-discharge echocardiogram showed excellent cardiac function. The patient walked with assistance at the time of discharge. His discharge medications included Septra DS, Vasotec, Lopressor, Mycostatin swish and swallow, Norvir (600 mg twice a day), and Lamivudine (150 mg twice a day).
Subsequent magnetic resonance imaging studies for up to three and a half years later have revealed a normal-sized ascending, transverse, descending thoracic, and abdominal aorta. The residual dissection in the thoracic aorta is unchanged from the initial postoperative study. The white blood cell count was 3,900 with an absolute CD4+ count 276/mL3, and the viral titer was nondectectable.
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Because the dissection extended into the left subclavian artery and it involved the superior aspect of the transverse arch, the axillary arteries were not used for arterial in-flow. His postoperative lower extremity ischemia was managed with interventional techniques [6], although an operative approach could have been used.
The HIV and aquired immunodeficiency disease syndrome is now a suppressible, chronic infection, which can be managed with highly active antiretroviral therapy, even patients with initial severe immunocompromised and CD4+ cell depletion typically demonstrate impressive immune restoration as a result of HAART. In fact, the risk of death or opportunistic infection even in HIV-infected patients who previously had CD4+ cell counts less than 200 cells/mm3 is very low if the patients demonstrated a rise in CD4+ cell count to more than 200 cells/mm3 [2].
Because of these findings we have offered surgical repair to patients whose cardiac prognosis is worse than that of their immune condition. The mortality with acute type I dissection is 50% within 48 hours, thus having a higher mortality risk than from HIV infection. Certainly, we believe that HIV-infected persons with CD4+ cell counts more than 200/mm3 can be offered a surgical option; many HIV-infected persons with CD4+ cell counts more than 100/mm3 who are otherwise good surgical candidates (ie, good functional performance status, good cardiopulmonary function, good nutritional status) are also likely to do well postoperatively. We routinely seek input from our infectious disease colleagues in making these decisions.
There are approximately 1 million people in the United States infected with HIV. Recent publications have demonstrated that multi-drug anti-retroviral therapies have improved life expectancy in patients with HIV infection. With improved life expectancy, these patients may require cardiac surgery intervention for valvular or coronary artery disease.
Satisfactory results have been achieved in patients who have undergone cardiac surgery for endocarditis. The operative mortality has ranged from 0% to 30%. These patients have had higher morbidity and mortality than the general population for the same procedure [5]. Given their depressed immune status these patients are more likely to have infectious complications develop. This subgroup of patients has an increased risk of pneumonia and a prolonged ventilator course because of lung colonization with Pneumocystis carinii.
In our institution, the patient’s P carinii prophylaxis and antiretroviral therapy are restarted as soon as possible after operation. In addition, our most experienced operating room and intensive care unit personnel are involved in the patient’s care.
This case report demonstrates that type I aortic dissection can be repaired in an HIV infected patient with an acceptable hospital length of stay and without unacceptable risk to involved hospital personnel. We propose that type I aortic dissection repair be performed in AIDS patients with CD4+ counts greater than 200/mL3 as their cardiac mortality outweighs their immune mortality.
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