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cute aortic dissection presents with various symptoms; that is, pain, nausea, vomiting, hematemesis, cold sweat, syncope, cerebrovascular accident, ischemic peripheral neuropathy, hypertension, congestive heart failure, shock, cardiac arrest, and sudden death. In addition, fever is often associated with acute aortic dissection and in rare cases is persistent so that it becomes difficult to determine whether or not it is associated with acute aortic dissection. A number of such cases have been reported, 1-4 as well as those in which aortic dissection was identified as the cause of an initially unexplained fever. [5][6][7][8][9][10] However, the duration of fever associated with acute aortic dissection is not well known, so the present study was undertaken to investigate the duration of fever associated with acute aortic dissection and to examine the relationship between duration and hematological parameters and reduction in false lumen size. Methods SubjectsDuring the 26-year period from January 1978 to December 2003, 336 patients with acute aortic dissection were admitted to Kinki University Hospital. Of these 57 meeting the following requirements were selected: (1) hospitalization within 1 week after disease onset, (2) treated medically rather than surgically, (3) judged free of infection, ileus, acute renal failure, malignant tumor, collagen disease, drug allergy, etc and (4) followed for 1 month after disease onset. Diagnosis of DissectionContrast-enhanced computed tomography (CT) scans were used to make a definitive diagnosis of aortic dissection. FeverAxillary body temperatures were measured and the highest temperature during the day was considered the body temperature for that day. A diagnosis of fever was made if body temperature was over 37°C. The duration of fever was defined as the period from the onset of fever to the last day on which body temperature was over 37°C during the 1-month follow-up period.The mean duration of fever was calculated for the entire study population. The patients were then divided into 2 groups: those with duration of fever shorter than the mean (Group A: brief fever group) and those with duration of fever equal to or longer than the mean (Group B: extended fever group). Hematological parameters and reduction in false lumen size were compared between these groups. Reduction in False Lumen SizeContrast-enhanced CT images, obtained at admission and 1 month later, were fed into a computer to determine the false lumen reduction ratio, as shown in Fig 1. HematologyWhite blood cell (WBC) and platelet counts, and C-reactive protein (CRP), fibrinogen, fibrin degradation product (FDP), D-dimer, and thrombin -antithrombin III complex (TAT) concentrations were compared between groups. Mean values for the WBC and platelet counts and CRP concentration were calculated for each week, and changes were analyzed at 1, 2, 3 and 4 weeks after admission. For fibrinogen, FDP, D-dimer, and TAT, the means weeks 1-2 and weeks 3-4 were analyzed.Circ J 2007; 71: 766 -771 (Received September 4, 2006; ...

Tsukuba hypertensive mice (THM) are a hypertensive model prepared by mating a transgenic mice with human renin gene and a transgenic mice with human angiotensinogen gene. In the present study, we examined effects of renin-angiotensin system (RAS) on cardiac hypertrophy and renal disorders using Tsukuba hypertensive mice. While THM showed an increase of about 30 mmHg in systolic pressure compared to C57BL/6 mice employed as normal control animals, the increase in blood pressure was not observed in the mice to which either gene was transferred. Urinary volume, water intake volume, urinary albumin excretion, heart to body weight ratio and renal glomerular sclerosis index increased significantly in THM, but none of these parameters showed a significant difference from the C57 mice when they were examined in mice to which either of the genes was transferred. In contrast, when lisinopril was administered to THM, all the parameters decreased significantly without lowering the systolic pressure. From these findings, it was demonstrated that RAS was playing a significant role in cardiac hypertrophy and renal disorders of THM and that lisinopril had inhibitory effects on cardiac hypertrophy and renal glomerular sclerosis by inhibiting RAS.

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Tissue Ang II concentration is more important than hypertension in causing cardiac hypertrophy, and both tissue Ang II level and hypertension are important in causing glomerulosclerosis in THM.