ABSTRACT
Resumo Coarctação da aorta abdominal é uma causa rara de claudicação de membros inferiores e hipertensão refratária. O tratamento é complexo e exige conhecimento de diversas técnicas de reconstrução vascular. Apresentamos um caso de coarctação ao nível das artérias renais, seu tratamento e revisão da literatura. Paciente feminina, 65 anos, com hipertensão refratária desde os 35 anos, utilizando cinco medicações anti-hipertensivas em dose máxima. Pressão arterial média de 260/180mmHg e claudicação incapacitante (menos de 20 metros) bilateral. Angiotomografia computadorizada demonstrou coarctação de aorta justarrenal de 4 mm de maior diâmetro, calcificação circunferencial no local da estenose e tortuosidade da aorta infrarrenal. Foi submetida a tratamento híbrido, com ponte ilíaco-birrenal e implante de stent Advanta V12 no local da estenose. A paciente evoluiu satisfatoriamente e, 60 dias depois da cirurgia, apresentava-se com uma pressão arterial de 140/80mmHg, em uso de apenas duas medicações anti-hipertensivas e sem claudicação.
Abstract Coarctation of the abdominal aorta is a rare etiology of intermittent claudication and refractory hypertension. Treatment is complex and requires knowledge of several vascular reconstruction techniques. We report a case of aortic coarctation at the level of the renal arteries, describing its treatment and presenting a literature review. Female patient, 65 years old, with refractory hypertension since the age of 35, using five antihypertensive medications at maximum doses. Blood pressure was 260/180mmHg and she had disabling claudication (less than 20 meters). Computed tomography angiography showed a 4mm coarctation in the juxtarenal aorta, with circumferential calcification at the stenosis site, and tortuous infrarenal aorta. Hybrid repair was performed with an iliac-birenal bypass and implantation of an Advanta V12 stent at the stenosis site. The patient's postoperative course was satisfactory, she was free from claudication, and her blood pressure 60 days after surgery was 140/80mmHg, taking two antihypertensive medications.
Subject(s)
Humans , Female , Aged , Aortic Coarctation/surgery , Aortic Coarctation/complications , Aorta, Abdominal , Aortic Coarctation/diagnosis , Renal Artery , Stents , Angioplasty, Balloon , Hypertension, Renovascular/surgery , Hypertension, Renovascular/etiology , Intermittent Claudication/surgery , Intermittent Claudication/etiologyABSTRACT
AIM: To observe the dynamic changes of myocardial collagen metabolism in pressure-overloaded rats.METHODS: The pressure-overloaded rat model was established by partial abdominal aortic coarctation.The rats underwent surgery but not constrictive were used as sham-operated control group.The rats were euthanized at 3, 4, 8 and 12 weeks.The body mass, heart mass and left ventricular mass were weighed, and the heart mass index (HMI) and left ventricle mass index (LVMI) were calculated.Masson trichrome staining was used on the myocardial sections, alkaline hydrolysis was used to detect the content of myocardial hydroxyproline (HYP), and the serum levels of procollagen type I carboxy-terminal peptide (PICP), procollagen type III amino-terminal peptide (PIIINT), and collagen C telopeptide type I (CTX-I) were also measured.RESULTS: Compared with sham-operated control group, the collagen deposition was evident, and collagen volume fraction (CVF) was increased significantly in model group (P<0.01), which further increased over time.HMI, LVMI and HYP significantly increased in model group (P<0.05), and HYP showed a tendency to increase over time.In addition, the serum concentration of PICP was increased significantly in model group, and the difference was significant at 4, 8 and 12 weeks (P<0.05).The serum concentration of PIIINP was increased significantly, but CTX-I was lowered significantly in model group (P<0.01).CONCLUSION: In the state of pressure overload, myocardial collagen metabolism is in disorder, and myocardial fibrosis is the major pathological change, which further increases over time.
ABSTRACT
AIM:To investigate the expression of poly(ADP-ribose) polymerase-2 (PARP-2) during rat car-diac hypertrophy in vitro and in vivo, and to explore the effects of PARP-2 on the cardiac hypertrophy.METHODS:Ab-dominal aortic coarctation ( AAC) was performed to establish a model of pressure overload-induced cardiac hypertrophy in SD rats.The expression of PARP-2 at mRNA and protein levels in the myocardium was determined by real-time PCR and Western blot.The hypertrophy model of the cardiomyocytes was induced by treating the cells with angiotensinⅡ( AngⅡ) . PARP-2 was knocked down by siRNAs in neonatal rat cardiomyocytes and the cardiomyocyte hypertrophy was evaluated by measuring the mRNA levels of ANF, BNP, and β-MHC and the cellular surface area.RESULTS: The expression of PARP-2 at mRNA and protein levels was both increased in the AAC rats as compared with those in the sham animals.The expression of PARP-2 at mRNA and protein levels was also increased in a time-and concentration-dependent manner in AngⅡ-induced hypertrophy model of the cardiomyocytes.In the neonatal rat cardiomyocytes, knockdown of PARP-2 ex-pression by siRNA attenuated AngⅡ-induced cardiac hypertrophy of the cardiomyocytes, indicating that endogenous PARP-2 played a positive regulatory role in cardiac hypertrophy.CONCLUSION:The mRNA and protein levels of PARP-2 in-crease in the in vitro and in vivo models of cardiac hypertrophy.Knockdown of PARP-2 protects cardiomyocytes from hyper-trophy.
ABSTRACT
The middle aortic syndrome (MAS) is rare (about 0.5-2% of all the cases of aortic coarctation) vascular disorder characterized by severe narrowing in the descending thoracic aorta, abdominal aorta, or both. It can be congenital or acquired due to several conditions.MAS may present clinically as uncontrolled hypertension, abdominal angina or lower limb claudication. Surgical treatment is effective in controlling symptom and improves life expectancy.