Rapidly progressive symptom development of pulmonary arterial hypertension: a case report of Trousseau syndrome.

Trousseau syndrome is most commonly defined as a hypercoagulability syndrome associated with mucin-producing adenocarcinoma. We report here a rare case of Trousseau syndrome presenting as pulmonary arterial hypertension. The patient complained of cough and increasing exertional dyspnea. Rapidly progressive symptom development of pulmonary arterial hypertension accompanied by right heart failure was observed, and the patient died on hospital day 2. An autopsy revealed Krukenberg tumors on both ovaries and a signet-ring cell gastric carcinoma. In the lungs there was tumor embolism with signet-ring cells to some extent, but the peripheral pulmonary arteries were occupied primarily by pulmonary embolism with platelets, fibroblasts, and fibrotic organized thrombi.

Evidence for the therapeutic potential of ex vivo expanded human endothelial progenitor cells using autologous serum.

BACKGROUND: Transplantation of endothelial progenitor cell (EPC) augments angiogenesis in animal models of tissue ischemia. Although it is desirable to use expanded autologous EPCs for therapeutic angiogenesis in the clinical arena, a major obstacle is the limitation of the EPC expansion technique without using animal-derived serum such as fetal bovine serum (FBS). To overcome this issue, the possibility of human EPC (hEPCs) expansion using autologous serum (AS) culture was investigated. METHODS AND RESULTS: Peripheral blood mononuclear cells were isolated from healthy volunteers by density-gradient centrifugation and culture-expanded in medium containing either FBS or AS. In vitro angiogenic functions, such as differentiation, migration and tube formation, were not significantly different between hEPCs cultured with FBS and AS. Next, we investigated whether transplantation of hEPCs would augment angiogenesis in unilateral hind limb ischemia using nude mice. The ratio of ischemic/normal limb blood flow and tissue capillary density in mice receiving hEPCs cultured with either FBS or AS significantly increased as compared with control mice receiving PBS alone. The ischemic/normal limb blood flow ratio and histological capillary density were not significantly different between hEPCs cultured with FBS and AS. CONCLUSIONS: hEPCs can be culture-expanded in medium containing AS. Moreover, the angiogenic functions of such hEPCs are almost identical to those of hEPCs cultured with FBS. Ex vivo expanded hEPCs using AS seems to be useful for future clinical therapeutic angiogenesis.

Upregulation of renal eNOS by high-sodium diet facilitates hypertension in doxorubicin-treated rats through enhanced oxidative stress.

It is known that renal nitric oxide (NO) is an important controller of urinary sodium excretion. A defect in the kidney's NO system could cause salt-sensitive hypertension. Since it has been demonstrated that doxorubicin binds to the reductase domain of endothelial NO synthase (eNOS) and generates superoxide in vitro, we tested our hypothesis that a high-sodium diet would upregulate the expression of eNOS and enhance oxidative stress in the kidney of doxorubicin-treated rats, resulting in a facilitation of hypertension. At 4 weeks after treatment with doxorubicin in Sprague-Dawley rats, the systolic blood pressure significantly increased only in the high-sodium diet group. The expressions of eNOS protein in the renal cortex and medulla were significantly higher in high-sodium groups than in normal-sodium groups, regardless of doxorubicin treatment. In rats treated with doxorubicin, a biomarker of oxidative damage 8-hydroxy-2'-deoxyguanosine (8-OHdG) immunohistological staining of renal tissues showed strong staining of the proximal and distal tubules. In particular, rats with doxorubicin in the high-sodium diet group demonstrated a significant increase in urinary exertion of 8-OHdG as well as more prominently stained tubules against 8-OHdG antibody, but markedly lower urinary NO(x) excretion than in rats without doxorubicin, even than in the untreated, low-sodium group. In conclusion, these results indicate that the oxidative stress induced by doxorubicin impairs NO production in the kidney. As such, doxorubicin treatment appears to contribute to the development of salt-sensitive hypertension through reductive activation of upregulated eNOS by a high-sodium diet instead of NO production.

Reduction of early elastic recoil by cutting balloon angioplasty as compared to conventional balloon angioplasty.

BACKGROUND: Restenosis after successful balloon angioplasty remains problematic. Early elastic response after angioplasty is significant when considering the possible development of restenosis. The purpose of this study was to compare early elastic recoil within 10 minutes after successful percutaneous transluminal coronary angioplasty and early lumen loss at 24 hours after angioplasty in a cutting balloon group and a conventional balloon group. METHODS: Extent of early elastic recoil was quantitatively measured as the difference of mean balloon diameter at maximal inflation pressure and minimal luminal diameter after angioplasty in 82 cutting balloon-treated lesions and 51 conventional balloon-treated lesions. RESULTS: Reference diameter and balloon/artery ratio were similar between the cutting balloon and conventional balloon groups (2.89 0.47 mm vs. 2.88 0.60 mm; 1.19 0.11 vs. 1.19 0.13, respectively). Early elastic recoil after angioplasty was significantly smaller in the cutting balloon than the conventional balloon group (0.96 0.40 mm vs. 1.12 0.37 mm, respectively; p = 0.04). Also, the mean amount of lumen loss from 10 minutes after angioplasty to 24 hours after was significantly smaller in the cutting balloon than the conventional balloon group (0.08 0.28 mm vs. 0.20 0.33 mm, respectively; p = 0.02). CONCLUSION: There is significantly less early elastic recoil in the cutting balloon angioplasty than in the conventional balloon angioplasty group. The efficacy of cutting balloon continues 24 hours after angioplasty.