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Influences of Dry Weight Adjustment Based on Bioimpedance Analysis on Ambulatory Blood Pressure in Hemodialysis Patients.

Jung Ho SHIN ; Chae Rim KIM ; Moonki HONG ; Su Hyun KIM ; Suk Hee YU

Journal of the Korean Society of Hypertension.2012;18(4):166-175. doi:10.5646/jksh.2012.18.4.166

BACKGROUND: Hypertension is a common problem for hemodialysis patients and is associated with an increased cardiovascular mortality. We analyzed ambulatory blood pressure (ABP) in hemodialysis patients and investigated if an adjustment of dry weight can be used to control blood pressure. METHODS: ABP was measured for twenty-four hours after hemodialysis. A bioimpedance Analysis (BIA) was conducted. Patients were divided into two groups by the edema index. A normohydration (NH) group included patients with the edema index less than 0.40, and an overhydration (OH) group included patients with the edema index 0.40 or more. We accordingly adjusted the dry weight based on BIA results. RESULTS: Thirty-six patients were recruited, comprising twenty-two men and fourteen women. In regard to the ABP, 24-hour systolic and diastolic blood pressures were 140.2 +/- 19.7 mm Hg and 79.0 +/- 10.6 mm Hg, respectively. There was a significant association between 24-hour systolic blood pressure and the edema index (r = 0.501, p = 0.002). Twenty four-hour systolic blood pressure was significantly different between the NH and OH groups (median value, 132.0 vs. 150.5 mm Hg; p = 0.008). In OH group, after adjustment of the dry weight, the edema index was decreased from 0.411 +/- 0.009 to 0.389 +/- 0.047 and office systolic blood pressure was also decreased from 144.7 +/- 32.7 mm Hg to 125.3 +/- 15.4 mm Hg in OH group (p = 0.028 and p = 0.018, respectively). CONCLUSIONS: The edema index obtained by the bioimpedance analysis is significantly correlated with 24-hour systolic blood pressure in hemodialysis patients. Also, an adjustment of dry weight can be used to control blood pressure in hemodialysis patients.
Blood Pressure ; Blood Pressure Monitoring, Ambulatory ; Edema ; Female ; Humans ; Hypertension ; Male ; Renal Dialysis

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Determinants of Follow-up Changes of Brachial Ankle Pulse Wave Velocity in Korean Women.

Dae Young KIM ; Sung Yeol KONG ; Sung Ja LEE ; Ha Do SONG ; Eun Jin HAN ; Ji Hoon YANG ; Ji Yeon KIM ; Dong Hyun LEE ; Hyun Ho SHIN

Journal of the Korean Society of Hypertension.2012;18(4):154-165. doi:10.5646/jksh.2012.18.4.154

BACKGROUND: Pulse Wave Velocity (PWV) correlates well with arterial distensibility and stiffness and is a useful approach for evaluating the severity of systemic arteriosclerosis in adults. In addition, measurement of brachial-ankle PWV (baPWV) has been commonly reported as a simple, noninvasive, and practicable method. Arterial stiffness assessed by PWV could predict cardiovascular morbidity and mortality. In this study, we investigated the association between the changes of baPWV and cardiovascular risk factors in Korean women using data from follow-up evaluations. METHODS: The subjects were 626 women (age, 47.2 +/- 8.2) in whom we measured baPWV and cardiovascular risk factors at baseline and about one year later. Arterial stiffness was evaluated by baPWV and biological parameters were evaluated on the same day. We retrospectively analyzed the relationships between changes of baPWV and those other factors. All analyses were performed with SPSS ver. 20.0 and p-values < 0.05 were considered significant. RESULTS: In correlation analysis, changes of baPWV were affected by changes in systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure, total cholesterol, high density lipoprotein-cholesterol, and low density lipoprotein-cholesterol. Multiple regression analysis of relationship between changes of baPWV and other associated variables shows that improvement of baPWV was significantly positively associated with changes of SBP and hemoglobin A1c (HbA1c), and worsening of baPWV was significantly negatively associated with changes of DBP, age, and SBP in sequence. CONCLUSIONS: In improvement of baPWV, decreases of SBP and HbA1c and in worsening of baPWV, increases of DBP, age, and SBP were significant factors in Korean women.
Adult ; Animals ; Ankle ; Arteriosclerosis ; Blood Pressure ; Cholesterol ; Female ; Follow-Up Studies ; Hemoglobins ; Humans ; Pulse Wave Analysis ; Retrospective Studies ; Risk Factors ; Vascular Stiffness

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Altered Regulation of Endothelin, Atrial Natriuretic Peptide, and Nitric Oxide Systems in Angiotensin II-induced Hypertension.

Eun Hui BAE ; Chang Seong KIM ; Joon Seok CHOI ; Seong Kwon MA ; Jong Un LEE ; Soo Wan KIM

Journal of the Korean Society of Hypertension.2012;18(4):146-153. doi:10.5646/jksh.2012.18.4.146

BACKGROUND: The present study aimed to determine the changes of endothelin (ET), nitric oxide, and atrial natriuretic peptide (ANP) systems in the kidney and aorta in angiotensin (Ang) II-induced hypertension. METHODS: Male Sprague-Dawley rats were used. Ang II (100 ng.min-1.kg-1) was infused through entire time course. Fourteen days after beginning the regimen, aorta and kidney were taken. The protein expression of nitroc oxide synthase (NOS) was determined by semiquantitative immunoblotting. The mRNA expression of components of ET, NOS, ANP system was determined by real-time polymerase chain reaction. RESULTS: Hypertension was developed in the experimental group. mRNA expression of ET-1 in the aorta and kidney was increased. The protein expression of endothelial NOS (eNOS) was decreased in the aorta, while that of inducible NOS and neuronal NOS remained unaltered. mRNA expression of ANP, natriuretic peptide type (NPR)-A, and NPR-C was not changed in the aorta. CONCLUSIONS: Based on these results, it seems that in Ang II-induced hypertensive rats, increased expression of ET-1 in the aorta and kidney, and decreased eNOS expression in the aorta contribute to the pathogenesis of hypertension.
Angiotensin II ; Angiotensins ; Animals ; Aorta ; Atrial Natriuretic Factor ; Endothelins ; Humans ; Hypertension ; Immunoblotting ; Kidney ; Male ; Neurons ; Nitric Oxide ; Rats ; Rats, Sprague-Dawley ; RNA, Messenger

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Changing Concept of Hypertensive Heart Disease.

Joong Wha CHUNG

Journal of the Korean Society of Hypertension.2012;18(4):137-145. doi:10.5646/jksh.2012.18.4.137

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.
Animals ; Apoptosis ; Biomarkers ; Collagen ; Cytokines ; Dilatation ; Echocardiography ; Fibroblasts ; Heart ; Heart Diseases ; Humans ; Hypertension ; Hypertrophy ; Magnetic Resonance Imaging ; Molecular Imaging ; Myocardium ; Myocytes, Cardiac ; Myofibroblasts ; Track and Field ; Ventricular Remodeling

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Effects of Bosentan Treatment on Angiotensin Converting Enzyme in Monocrotaline Induced Pulmonary Hypertension Rats.

Sung Jin KIM ; Ji Hae CHA ; Hae Ryun LEE ; Young Mi HONG

Journal of the Korean Society of Hypertension.2011;17(1):28-36. doi:10.5646/jksh.2011.17.1.28

BACKGROUND: Pulmonary artery hypertension is characterized by persistent increase of vascular resistance, and is associated with right ventricle failure. We investigated changes of plasma renin, serum aldosterone, angiotensin converting enzyme (ACE) concentrations, ACE gene expressions and protein contents after bosentan treatment. METHODS: Six-week-old male Sprague-Dawley rats were divided into three groups: control (C) group, monocrotaline (M) group, and bosentan (B) group. Groups M and B were subcutaneously administered with 60 mg/kg of monocrotaline. In group B, 20 mg/kg/day of bosentan was administered by gavage twice a day. The rats were sacrificed after 1, 5, 7, 14, and 28 days. Changes of ACE gene expressions were analyzed by reverse transcription-polymerase chain reaction. Also, plasma renin, serum aldosterone, and ACE levels were measured. RESULTS: Serum aldosterone levels were significantly increased in group M compared with group C and significantly decreased after bosentan treatment on day 28. Serum ACE concentrations were significantly decreased compared with group M after bosentan treatment on day 28. Gene expressions of ACE were significantly increased in group M compared with group C on day 5 and significantly decreased after bosentan treatment on day 7 and 14. ACE protein contents significantly increased in group M compared with group C in week 2 and 4. It significantly decreased after bosentan treatment in week 2. CONCLUSIONS: The renin-angiotensin system is associated with pulmonary artery hypertension. To investigate the effects of bosentan on the renin-angiotensin system in pulmonary artery hypertension, further studies on the effects of bosentan according to different doses are required in the future.
Aldosterone ; Angiotensins ; Animals ; Gene Expression ; Heart Ventricles ; Humans ; Hypertension ; Hypertension, Pulmonary ; Male ; Monocrotaline ; Peptidyl-Dipeptidase A ; Plasma ; Pulmonary Artery ; Rats ; Rats, Sprague-Dawley ; Renin ; Renin-Angiotensin System ; Sulfonamides ; Vascular Resistance

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Effects of Angiotensin II and Shear Stress Interaction on Vascular Inflammation.

Sung Hyun CHOI ; Eun Hye PARK ; Yujin OH ; Sang Hong BAEK

Journal of the Korean Society of Hypertension.2011;17(1):17-27. doi:10.5646/jksh.2011.17.1.17

BACKGROUND: Angiotensin II (AngII) and abnormal oscillatory shear stress are highly associated with vascular inflammation including atherosclerosis. However, it is poorly understood how interactions between AngII and shear stress in human aortic endothelial cells (HAEC) are involved in mechanisms by which cellular adhesion molecules are expressed. The purpose of this study was to improve that understanding. METHODS: AngII (10(-7)M for 6 hr) and two-types of shear stress treatments were used: laminar shear stress (LS: unidirectional, 12 dynes/cm2) and oscillatory shear stress (OS: bi-directional, 5 dynes/cm2, 1 Hz) in HAEC. Immunoblotting was used to detect expression of cellular adhesion molecules markers such as vascular cell adhesion molecule 1 (VCAM1) and intercellular adhesion molecule 1 (ICAM1). RESULTS: AngII significantly increased VCAM1 and ICAM1 expression in HAEC that had been reduced due to pretreatment with telmisartan. AngII-LS co-stimulation and AngII-OS co-stimulation significantly increased VCAM1 and ICAM1 expression in HAEC. The expression levels of VCAM1 and ICAM1 were also, significantly reduced when pretreated with telmisartan. However, VCAM1 and ICAM1 expression were significantly reduced under LS and OS stimulation. CONCLUSIONS: Telmisartan may modulate the expressions of VCAM1 and ICAM1 via different types of shear stress in HAEC that are activated by AngII.
Angiotensin II ; Angiotensins ; Atherosclerosis ; Benzimidazoles ; Benzoates ; Endothelial Cells ; Humans ; Immunoblotting ; Inflammation ; Intercellular Adhesion Molecule-1 ; Vascular Cell Adhesion Molecule-1

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How Much Do We Lower the Blood Pressure in Hypertensive Patients with Diabetes?.

Dong Kyu JIN ; Seung Jin LEE

Journal of the Korean Society of Hypertension.2011;17(1):10-16. doi:10.5646/jksh.2011.17.1.10

Hypertension is an independent risk factor of atherosclerotic cardiovascular disease. Diabetes multiplies the risk when combined. Therefore, it is crucial for the doctors to control the blood pressure (BP) properly in hypertensive patients with diabetes. And then, how much do we lower the BP? Several guidelines recommend target BP levels to minimize the risk under the basis of so many experimental and observational studies. But, we must consider several factors to properly apply the guidelines in the clinical fields. First, diabetes is not a uniform but a diverse disease. From asymptomatic microvascular disease to macrovascular cardiovascular disease, diabetic clinical findings are so different. So we must define where the patients stand in long diabetic road, and what the patients want to us. Second, because more people are becoming health-conscious, more people take the aspirin, lipid-lowering agents and other medications. It's means that interpretation of the results of recent studies is more difficult than previous, old studies. Third, measuring the BP in the hospital is really reflect the ambulatory BP? Now, it's too early to conclude that the one is more better than the other. From the next study, we can consider the use of ambulatory, home BP monitoring combined with hospital BP measuring. Finally, although BP lowering-effects are similar, all anti-hypertensives do not have same effect in diabetic patients. For example, angiotensin converting enzyme-inhibitor is more superior than calcium channel blocker in patients with heart failure. So, we must consider what type of drug used in the study.
Angiotensins ; Antihypertensive Agents ; Aspirin ; Blood Pressure ; Calcium Channels ; Cardiovascular Diseases ; Heart Failure ; Humans ; Hypertension ; Risk Factors

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The Appropriate Interpretation of Recent Clinical Trials: How to Read RCT in the Era of Advertizing-based Medicine.

Iwao KUWAJIMA

Journal of the Korean Society of Hypertension.2011;17(1):1-9. doi:10.5646/jksh.2011.17.1.1

Although evidence-based medicine (EBM) has changed medical therapy from experience- or experiment-based medicine to the modern science-based medicine, nowadays it seems to be used as a tool of advertizing strategy of industries. Clinical trial is a fundamental component of EBM and it costs very much and are mostly conducted by the financial support of pharmaceutical industries at a tremendous expense. If anticipated results for the sponsor were not shown in the trial, a "spin" has been used to mislead readers as if positive results for test drugs or devices were obtained by emphasizing subgroup analysis, or searching favorable endpoint by post-hoc analysis. Clinical trials on angiotensin receptor blocker (ARB) are continuing succession of defeat all over world except two Japanese clinical trials, JIKEI HEART and KYOTO HEART studies. However, in both trials, subjective soft endpoints, such as angina pectoris or congestive heart failure were used despite of prospective randomized, open labeled, blinded endpoint design. In the era of advertizing-based medicine, It is important to read clinical trial data with critical view points.
Angina Pectoris ; Angiotensins ; Asian Continental Ancestry Group ; Drug Industry ; Evidence-Based Medicine ; Financial Support ; Heart ; Heart Failure ; Humans

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Obesity Increases Blood Pressure Variability during the Night.

Hong Ju AN ; Wan KIM ; Chung KANG ; Dong In NAM ; Il Hyung JUNG ; Hoon KANG ; Sang Sun LEE ; Ho Yeong SONG ; Sang Cheol CHO ; Won Yu KANG ; Sun Ho HWANG

Journal of the Korean Society of Hypertension.2014;20(1):1-7. doi:10.5646/jksh.2014.20.1.1

BACKGROUND: Previous studies have reported that obesity increases heart rate variability. Body mass index (BMI) has been reported to affect blood pressure variability (BPV) over 24 hours. However, the diurnal variation in the effect of BMI on BPV has not been evaluated. This study aimed to clarify the diurnal variation in the effect of BMI on BPV. METHODS: A total of 2,044 patients were consecutively enrolled in this study, and the data were analyzed retrospectively. All patients underwent 24-hour ambulatory blood pressure monitoring. We divided patients into two groups according to BMI (non-obese group: n = 1,145, BMI < 25; obese group: n = 899, BMI > or = 25). We compared BPV during daytime and nighttime between the non-obese and obese groups. We also evaluated the impact of BMI on BPV by multivariate regression analysis. RESULTS: On univariate regression analysis, there was no significant difference in BPV during daytime (systolic BP [SBP] variability: 20.7 vs. 21.7, p = 0.511; diastolic BP [DBP] variability: 16.8 vs. 17.5, p = 0.539). However, both SBP variability (13.8 vs. 17.6, p = 0.009) and DBP variability (11.7 vs. 14.3, p = 0.042) during nighttime were affected significantly by BMI. After adjusting other compounding variables (age > 60 years, current smoking habit, hypertension, diabetes mellitus, and use of calcium channel blockers and renin-angiotensin-aldosterone system blockers), multivariate analysis showed that BMI was an independent factor associated with increase in BPV during the night (SBP variability: p = 0.039; DBP variability: p = 0.034). CONCLUSIONS: Obesity increased BPV during nighttime.
Blood Pressure Monitoring, Ambulatory ; Blood Pressure* ; Body Mass Index ; Calcium Channel Blockers ; Diabetes Mellitus ; Heart Rate ; Humans ; Hypertension ; Multivariate Analysis ; Obesity* ; Renin-Angiotensin System ; Retrospective Studies ; Smoke ; Smoking

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A Case of Renovascular Hypertension Controlled by Renal Autotransplantation.

Eunyoung LEE ; Youn Kyung KEE ; Jungyoen LEE ; In Mee HAN ; Jae Il SHIN ; Myoung Soo KIM ; Sungha PARK

Journal of the Korean Society of Hypertension.2013;19(2):63-69. doi:10.5646/jksh.2013.19.2.63

Renovascular hypertension caused by renal artery stenosis is an uncommon but curative cause of hypertension in children. We report a case of recurrent severe hypertension caused by renovascular hypertension. After recurrence of hypertension after redo percutaneous transluminal renal angioplasty, the blood pressure was finally controlled by renal autotransplantation. This case demonstrates the importance of considering renovascular hypertension as a cause of severe hypertension in children. Also, renal autotransplantation should be considered as a viable treatment option for treatment of renovascular hypertension that is recurrent after renal angioplasty.
Angioplasty ; Blood Pressure ; Child ; Humans ; Hypertension ; Hypertension, Renovascular* ; Recurrence ; Renal Artery ; Renal Artery Obstruction ; Transplantation*

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