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정중화,Jeong, Jung-Hwa 사단법인 한국당뇨협회 2005 당뇨 Vol.188 No.-
' 고혈압을 조절 및 치료를 받게되면 합병증이 발생되지 않는가? 하는 질문에 대한 현재까지의 많은 연구에 의하면, 고혈압을 적절히 치료하면 모든 형태의 합병증이 예방될 수 있음이 증명되었고, 일단 합병증이 발생된 환자라도 치료를 적극적으로 하면 재발하거나 또 다른 합병증으로 진행되는 것을 막을 수 있다고 알려져 있다.
흰쥐에서 아톨바스타틴과 딜티아젬의 약물동태학적 상호작용
정중화,김현용,최준식 한국임상약학회 2007 한국임상약학회지 Vol.17 No.1
The purpose of this study was to investigate the effect of atorvastatin on the pharmacokinetics of diltiazem (15 mg/kg) after oral administration of diltiazem with or without atorvastatin (0.5, 1.5 and 3.0 mg/kg) in rats. Coadministration of atorvastatin increased significantly (p<0.05, 3.0 mg/kg) the plasma concentration-time curve (AUC) and the peak concentration of diltiazem compared to the control group. The total plasma clearance (CL/F) of diltiazem was decreased significantly (p<0.05, 3.0 mg/kg) compared to the control group. The relative bioavailability (RB%) of diltiazem was increased from 1.14- to 1.49-fold. Coadministration of atorvastatin did not significantly change the elimination rate constant , terminal half-life and the time to reach the peak concentration of diltiazem. Based on these results, we can make a conclusion that the significant changes of these pharmacokinetic parameters might be due to atorvastatin, which possesses the potency to inhibit the metabolizing enzyme (CYP3A4) in the liver and intestinal mucosa, and also inhibit the P-glycoprotein (P-gp) efflux pump in the intestinal mucosa.
특발성 확장심근병증과 비대심근병증에서 심실재분극의 차이
정중화 朝鮮大學校 附設 醫學硏究所 2007 The Medical Journal of Chosun University Vol.32 No.2
Background and Objectives: Experimental studies have suggested that variability between the ECG leads in measurement of QT intervals and QT dispersion reflects spatial and temporal inhomogeneity of left ventricular recovery times, Previous clinical studies of QT dispersion have shown that it is increased in patients with hypertrophic cardiomyopathy (HCM), the long QT syndrome, myocardial infarction and idiopathic dilated cardiomyopathy (IDCM). We investigated difference of ventricular repolarization between IDCM and HCM through difference of the QT dispersion and QT variables. Methods: From january 2005 until September 2006, 25 patients with IDCM and 23 patients with HCM were prospectively enrolled in this study at the Chosun University Hospital. Inclusion criteria were left ventricular ejection fraction <50%, left ventricular diastolic dimension >=55mm in the IDCM and left ventricular wall thickness <=13 mm in the HCM. Results: The intraventricular septal thickness (IVST:17.17±2.87, p<0.001) increased in the HCM more than IDCM. End-diastolic left ventricular dimension diastolic (LVDd: 63.00±7.70, p<0.001) was increased in the IDCM. The EF (31.92±10.65, p<O.OOl) and FS (15.64±5.77, p<0.001) were decreased in the IDCM. The QTd, QTc did not differ significantly between IDCM and HCM. But QTcd differ significantly between IDCM and HCM. In the analysis of limb lead and frontal lead, QTc-F (QTc in the Frontal lead) correlate with LVDd in patients with IDCM and all QT variables in the frontal leads correlate with IVST in patients with HCM. In the IDCM, QTd-L, QTcd-L was prolonged more than QTd-F, QTcd-F. In contrast, QT variables of frontal leads were prolonged more than that of limb leads, Conclusion: Our study shows that QTd increased in the IDCM and HCM. But the results of QT interval analysis did not differ among the IDCM and HCM except QTcd, QTcd-L. All QT variables correlate with LV wall thickness in patients with HCM. Therefore the inhomogeneity of ventricular refractoriness in the HCM was influenced by the LV wall thickness. The inhomogeneity of ventricular refractoriness in the IDCM was influenced by LVDd in the analysis of QTc-F.
정중화 朝鮮大學校 附設 醫學硏究所 2009 The Medical Journal of Chosun University Vol.33 No.S
Resistant hypertension is a common problem in clinical practice. About one-third of hypertensive patients is not controlled properly and some portion of this group is may assigned to resistant hypertension. Hypertension is one of the most prevalent and powerful contributors to cardiovascular diseases. The poor outcomes associated with poor blood pressure control may be exacerbated by inadequate usage of antihypertensive drugs. Understanding of underlying pathophysiology will introduce you to a hemodynamic-based approach. This review will show you that resistant hypertension is not an impregnable disease. If you find the inside of this issue, you can control resistant hypertension accordingly.
정중화 대한고혈압학회 2012 Clinical Hypertension Vol.18 No.4
Arterial hypertension leads to both structural and functional changes of the heart. Hypertensive heart disease (HHD) is characterized by complex changes in myocardial structure (e.g., enhanced cardiomyocyte growth, excessive cardiomyocyte apoptosis, accumulation of interstitial and perivascular collagen fibers, disruption of endomysial and perimysial collagen network) that cause the remodeling of the myocardium. In the 1970s, hypertrophic growth of cardiomyocytes is compensatory to reduce wall stress on the ventricular wall imposed by pressure overload. Recent data from animal studies suggest that inhibition of ventricular hypertrophy was not associated with ventricular dilatation or reduced wall motion despite elevated wall stress. The genetic complexity (gene-gene and/or gene-environment interactions) may modulate left ventricular mass and transcriptional regulators are participated in pathologic myocardial growth. Many hormones and cytokines lead to a profibrotic and inflammatory environment. Excess of ventricular collagen in hypertensive patients is the result of both increased collagen synthesis by fibroblasts and stimulated myofibroblasts, and unchanged or decreased collagen degradation by matrix metalloproteinase. Several biochemical markers of myocardial remodeling will prove to be useful. The development of noninvasive methods like echoreflectivity, cardiac magnetic resonance imaging, speckle tracking echocardiography, and cardiac molecular imaging would enable broader application. Meta-analysis showed that there was a significant difference among medication classes in decreasing left ventricular mass.