Pattern of instent neointimal formation compared to native atherosclerosis in the coronary bifurcation lesions: volumetric intravascular ultrasound analysis / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>No clinical study has systematically analyzed and compared circumferential neointimal and plaque distribution of stent neointimal proliferation and in native atherosclerotic plaques. This study aimed to investigate and compare the pattern of instent neointimal formation and native atherosclerosis in the coronary bifurcation lesions by volumetric analysis using systematic intravascular ultrasound (IVUS).</p><p><b>METHODS</b>We examined bifurcation lesions in native coronary artery (plaque group, n = 102) and stented bifurcations at 9-month follow-up (neointima group, n = 51) using volumetric IVUS analysis of both the main vessel (MV) and side branch (SB). Three 5-mm segments were analyzed; the proximal MV (MVp), distal MV (MVd) and SB ostium (SBo). For each segment, volumetric analysis was performed in each of four quadrants (divided according to the branch takeoff and the geometric center of the lumen); carinal, epicardial, abcarinal, and myocardial. The eccentricity index was defined as the ratio of the abcarinal plaque (or neointimal) volume to the carinal plaque (or neointimal) volume.</p><p><b>RESULTS</b>The plaque distribution differed significantly between the four quadrants, with the largest in the abcarinal quadrant, followed by the myocardial, epicardial, and carinal quadrants. The distribution of neointima was similar in the MV, but the four quadrants in the SB did not differ significantly. The eccentricity indices of both the MVd (P < 0.001) and SBo (P = 0.001) were significantly higher for the plaque group than the neointima group.</p><p><b>CONCLUSIONS</b>The distribution of neointimal proliferation seems to have a similar pattern to that of atherosclerotic plaque in native coronary arteries, particularly in the main vessel, but the trend is less prominent.</p>

Dose-dependent Effect of Benidipine in Patients with mild moderate Hypertension

BACKGROUND AND OBJECTIVES: This study was designed to evaluate the appropriate dose and dose-dependent effect of benidipine hydrochloride, a Ca+ +/- channel blocker, in patients with mild-moderate essential hypertension. Material and MethodsBenidipine was administered in 2 mg, 4 mg and 8 mg once daily with 1 month interval in 41 hypertensive patients with diastolic blood pressure over 90 mmHg and systolic blood pressure from 140 to 210 mmHg. Blood pressure, heart rate, subjective symptoms and adverse effects were checked every 4 weeks after benidipine administration. Laboratory examinations were performed before and after benidipine administration. RESULTS: The dose-dependent, antihypertensive effect of benidipine was evaluated in 41 patients. The blood pressure significantly reduced from 166+/-15 mmHg/103+/-7 mmHg to 13815 mmHg/88+/-11 mmHg at 12 weeks administration of benidipine and overall effective rate was 95%. The systolic and diastolic blood pressure was reduced significantly in proportion to dose of benidipine (p<0.0001). Antihypertensive effect was prominent at 4mg of benidipine. The heart rate was not affected by benidipine. No significant laboratory changes were observed. CONCLUSION: Benidipine has a dose-dependent effect in the treatment of mild-moderate hypertension, and the dosage to be needed may be 4mg or more for sufficient antihypertensive effect.

CAG Repeat Expansions in the Patients with Mood Disorder / 신경정신의학

OBJECTIVES: The genetic facotrs have been suggested for the etiology of mood disorders but the mode of inheritance is complex. Increased severity and an earlier onset of the bipolar and major depressive disorder over generations within families(Anticipation) were reported. In order to test the hypothesis that trinucleotide repeat expansions underlie the genetic basis of Bipolar and major depressive disorders, we have analyzed the extent of CAG reapeats in genomic DNA from mood disorder patients. METHODS: 55 bipolar disorder, 67 major depressive disorder patients were recruited according to the DSM-III-R criteria. 89 normal controls were recruited from the medical personnel, students and the visitors to the health services center who had no history of psychiatric illness and show normal profile of MMPI. The genomic DNA of patients and controls was analyzed by use of the(CTG) 17 oligonucleotide and the repeat expansion detection(RED) method. The Mann-Whitney U test was used to compare the distribution of the number of CAG repeats among the groups. RESULTS: when the bipolar disorder, major depressive disorder patients were compared with the control group, no significant differences were observed. CONCLUSION: Our results do not support the hypothesis that expanding CAG repeats are causing the observed genetic anticipation in bipolar disorders and major depressive disorders.