Influences of White-Coat Hypertension and White-Coat Effect on the Left Ventricular Mass and Diastolic Function

BACKGROUND: Overstimation of blood pressure(BP) by clinic measurements occur in about 20 to 30% of subjects(white-coat hypertension) who may, consequently, be misdiagnosed as hypertensives and received unnecessary medications. The clinical significance of white-coat hypertension and its effects on the cardiovascular wystem have not been studied systematically.This study was designed to evaluate the influences of white-coat hypertension and white-coat effect, defined as difference between clinic and ambulatory BP, on the LV mass and diastolic function. METHODS: LV mass index was calculated and LV systolic and diastolic function were assessed by the analysis of mitral and pulmonary venous flow velocity in 45 untreated essential hypertensives and 20 normotensives(NT). Ambulatory BP monitoring classified hypertensives as white-coat hypertensives(WCHT,n=20) and sustained hypertensives(SHT, n=25). RESULTS: 1) Left ventricular systolic indices were not different among the three groups. 2) Left ventricular mass inedx of WCHT(114.5+/-36.3g/m2) was similar to that of SHT(115.6+/-34.9g/m2) and was significantly greater than that of NT(86.5+/-37.7g/m2)(p<0.05). 3) Some of left ventricular diastolic parameters(isovolumic relaxation time, E/A ratio, A velocity, pulmonary systolic fraction, ratio of systolic to diastolic forward flow velocity) of WCHT and SHT were significantly different from those of NT(p<0.05), but there were no differences between two hypertensive groups. 4) Even though both systolic and diastolic white-coat effect in WCHT were significantly greater than those of SHT(o<0.05),white-coat effect did not influence on the left ventricular mass or function in both groups. CONCLUSION: An increased left ventricular mass and diastolic dysfunction in WCHT suggests that white-coat hypertension could not be considered as an entirely innocuous clinical condition.

Induction of Embryonal Teratocarcinoma Cell(P19 cell) to Differentiate into Smooth Muscle Cell

BACKGROUND: Understanding the regulatory mechanisms of the smooth muscle cells differentiation is one of the central issues in researches of atherogenesis where smooth muscle cells undergo dedifferentiation and regain embryonic phenotype. Smooth muscle myosin heavy chain isoforms(SM1,SM2) are important molecular markers to define the stage of smooth muscle cell differentiation. METHODS: In order to establish an in vitro model of smooth muscle cell differentiation using a pluripotent murine embryonal teratocarcinoma cell line(P19 cell), we first isolated cDNA clone of mouse SM1 and then tried various chemicals to induce P19 cells to differentiate into smooth muscle cells, The expression of Sm1 and alpha-smooth muscle actin was examined using RNase protection assay, Western blotting and indirect immunofluorescence. RESULTS: In the presence of luM retinoic acid, a small proportion of P19 cells could be in duced to differentiate into smooth muscle cells expressing SM1 as well as alpha-smooth muscle actin since day 8 after treatment. By blocking the Brain-2 expression, thus inhibiting neuronal differentiation, we could obtain more abundant differentiated smooth muscle cells. Sequential immunofluorescencc demonstrated that it took weveral days for smooth muscle myosin heavy chain to organize completely in differentiation smooth muscle cells. On the other hand, 10nM retinoic acid, 1% dimethyl sulfoxide or 2mM hexamethylene bisacetamide could not indduce P19 cell to differentiate to smooth muscle cells. CONCLUSION: In conclusion, P19 cells can be induced to differentiate into smooth muscle cells and this in vitro system will be useful in understanding the regulation of SM1 gene expression as well as of angiogenesis.

A Case of Left Ventricular Rupture and Complete Rupture of both Papillary Muscles Following Blunt Chest Trauma

Blunt chest trauma can cause various types of cardiac injuries such as myocardial contusion,cardiac ruptrue, valvular or papillary muscle injuries, and pericardial or coronary artery injuries. Complete rupture of both papillary muscles accompanied by left ventricular(LV) rupture following blunt chest trauma to our knowledge has not been previously reported. A 40-year-old female was referred because of severe dyspnea and anterior chest pain which occured immedicately after blunt chest trauma. Echocardiography demonstrated a moderate pericardial effusion as well as rupture of both papillary muscle with severe mitral regurgitation. Hemopericardium and a complets tear of the anterolateral papillary muscle at the mid portion were observed. The posteromedial papillary muscle was totally transected at the attachment site of LV wall and accompanied by external rupture of left ventricle at that site. Mitral valve replacement and primary repair of LV ruptrue was performed successfully. In the case we report, complete rupture of both papillary muscles developed after blunt chest trauma and LV rupture occurred as the papillary muscle was torn from the LV wall.