Coarctation of aorta is strongly asssociated with bicuspid aortic valves. This is a risk factor for infective endocarditis. Aneurysm of a sinus of Valsalva is a rare defect with a prevalence of 0.09% and is associated in 10% of cases with bicuspid aortic valves and less frequently with coarctation of aorta and atrial septal defect. The association of coarctation of aorta with an atrial septal defect is rare. This is the first case reported in Puerto Rico of an adult patient with coarctation of aorta in association with a ruptured aneurysm of a sinus of Valsalva and an atrial septal defect. The patient is a 22 year old male with coarctation of aorta diagnosed since childhood, who was admitted at the Cardiovascular Center of Puerto Rico due to infective endocarditis secondary to teeth infection (caused by Streptococcus mitis) and signs of congestive heart failure. Upon evaluation with transthoracic and transesophageal echocardiograms, he was found to have coarctation of aorta in aortic isthmus, aortic root dilatation, bicuspid aortic valve with vegetation, severe aortic and tricuspid regurgitation, aneurysm of non coronary sinus of Valsalva with perforation to right atrium, biatrial enlargement and dilated right ventricle. Successful antibiotherapy of endocarditis was achieved. Afterwards, surgical replacement of aortic valve and ascending aorta and closure of non coronary sinus of Valsalva aneurysm was done. A secundum atrial septal defect was found and was also closed. Color photographic registration of the findings confirmed at surgery was obtained. Surgical correction of coarctation of aorta was postponed for a future time. The patient had a successful postsurgical recovery and was discharged home with anticoagulation treatment.
Carbon monoxide (CO) is endogenously produced from the degradation of heme, in a reaction that is catalyzed by heme oxygenase (HO). Systemic blockade of HO acutely decreases neural HO activity, and this increases arterial pressure in a manner that is reversed by CO microinjections into the nucleus tractus solitarii (NTS) of the brain stem; such findings are the original evidence that endogenous CO in the NTS serves as a tonic vasodepressor. Whilst the NTS coordinates the balance and distribution of sympathetic and parasympathetic influences on the cardiovascular system, the actions of the endogenous CO on these autonomic components have not been explored. The purpose of the current study was to identify the sympathetic and parasympathetic influences that contribute to the vasoregulatory actions of the endogenous CO system. Towards this end, male Sprague-Dawley rats were fitted with chronic femoral catheters and permitted four days recovery before conducting awake experiments. The acute blood pressure effects of an HO inhibitor, zinc deuteroporphyrin 2,4-bisglycol (ZnDPBG), were examined in animals pretreated with atropine, prazosine or propranolol to block the muscarinic, ␣1or -adrenergic receptors, respectively. Administration of ZnDPBG (45 µmol/kg, IP) increased arterial pressure from 123 Ϯ 2 to 133 Ϯ 3 mm Hg (p < .05) but did not affect heart rate. The actions of ZnDPBG were not affected by pretreatment with atropine (50 mg/kg, IP) but were abolished by pretreatment with prazosine (5 mg/kg, IP). In addition, pretreatment with a beta-blocker, propranolol (15 mg/kg, IP), resulted in an abbreviated pressor response to ZnDPBG. Immunohistochemical staining and Western blot analysis confirmed that HO is present in both the NTS and adrenal medulla, but complementary experiments revealed that ZnDPBG treatment did not affect circulating levels of epinephrine. This study shows that HO is present in NTS and that the actions of ZnDPBG are independent of parasympathetic changes. While HO is present in the adrenal medulla and the pressor effect of ZnDPBG apparently arises from enhanced sympathetic tone, the HO inhibitor does not increase plasma levels of epinephrine. These findings suggest that inhibition of heme-derived CO in the NTS leads to activation of peripheral sympathetic neurons and that the consequent pressor effect arises from ␣1-adrenergic-mediated vasoconstriction and 1-adrenergic-mediated increases in cardiac performance.
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