横井 博厚

Previous studies have shown highly effective lowering of blood pressure with thiazide diuretics in combination with angiotensin receptor blockers. However, thiazide diuretics may cause the development of diabetes and abnormal lipid metabolism. Little is known as to whether dysmetabolic potential of thiazide diuretics could be neutralized when adding angiotensin receptor blockers. This study consisted of 26 patients with essential hypertension. Patients were randomized to 24 weeks of treatment with either candesartan, 12 mg monotherapy (n = 13, group A), or hydrochlorothiazide (HCTZ), 6.25 mg in combination with candesartan, 8 mg (n = 13, group B). Before and after treatment, we assessed glucose and lipid profiles including adiponectin, resistin, and active glucagon-like peptide-1 (GLP-1) levels. At baseline, there were no differences in age, body mass index, systolic blood pressure (SBP), and diastolic blood pressure (DBP), as well as plasma levels of hemoglobin A1c, insulin, low-density lipoprotein cholesterol, triglycerides, adiponectin, resistin, and active GLP-1 between the two groups. There were significant reductions in SBP (from 152 +/- 10 mmHg at baseline to 134 +/- 12 mmHg after treatment) and DBP (from 84 +/- 5 mmHg at baseline to 71 +/- 8 mmHg after treatment) in group A. There were also significant reductions in SBP (from 148 +/- 10 at baseline to 128 +/- 7 mmHg after treatment) and DBP (from 90 +/- 9 at baseline to 74 +/- 12 mmHg after treatment) in group B. There were no differences in reduction of SBP or DBP after 24 weeks of treatment between the two groups. There were no changes of the glucose and lipid profiles, including adiponectin, resistin, insulin, and active GLP-1 levels after 24 weeks of treatment in both groups. A low dose of HCTZ in combination with candesartan reduces blood pressure effectively without adverse effects on the glucose and lipid profiles. Therefore, the combination of thiazide diuretics and angiotensin receptor blockers could assist patients in achieving long-term control of blood pressure with good tolerability.

Previous studies have shown highly effective lowering of blood pressure with thiazide diuretics in combination with angiotensin receptor blockers. However, thiazide diuretics may cause the development of diabetes and abnormal lipid metabolism. Little is known as to whether dysmetabolic potential of thiazide diuretics could be neutralized when adding angiotensin receptor blockers. This study consisted of 26 patients with essential hypertension. Patients were randomized to 24 weeks of treatment with either candesartan, 12 mg monotherapy (n = 13, group A), or hydrochlorothiazide (HCTZ), 6.25 mg in combination with candesartan, 8 mg (n = 13, group B). Before and after treatment, we assessed glucose and lipid profiles including adiponectin, resistin, and active glucagon-like peptide-1 (GLP-1) levels. At baseline, there were no differences in age, body mass index, systolic blood pressure (SBP), and diastolic blood pressure (DBP), as well as plasma levels of hemoglobin A1c, insulin, low-density lipoprotein cholesterol, triglycerides, adiponectin, resistin, and active GLP-1 between the two groups. There were significant reductions in SBP (from 152 +/- 10 mmHg at baseline to 134 +/- 12 mmHg after treatment) and DBP (from 84 +/- 5 mmHg at baseline to 71 +/- 8 mmHg after treatment) in group A. There were also significant reductions in SBP (from 148 +/- 10 at baseline to 128 +/- 7 mmHg after treatment) and DBP (from 90 +/- 9 at baseline to 74 +/- 12 mmHg after treatment) in group B. There were no differences in reduction of SBP or DBP after 24 weeks of treatment between the two groups. There were no changes of the glucose and lipid profiles, including adiponectin, resistin, insulin, and active GLP-1 levels after 24 weeks of treatment in both groups. A low dose of HCTZ in combination with candesartan reduces blood pressure effectively without adverse effects on the glucose and lipid profiles. Therefore, the combination of thiazide diuretics and angiotensin receptor blockers could assist patients in achieving long-term control of blood pressure with good tolerability.

Background: Mechanisms of the pseudonormalization (PN) of the transmitral flow (TMF) velocity pattern have been mainly attributed to left ventricular diastolic function. Purpose: To assess the influence of left atrial (LA) function on the PN with two-dimensional tissue tracking technique. Methods: The subjects consisted of 21 healthy volunteers and 70 patients with various cardiac diseases. Images of one cardiac cycle in the apical four-chamber view were stored by the HIVISION 900 (Hitachi Medico, Chiba, Japan). The LA volume (LAV) loop was created using two-dimensional tissue tracking technique and LAV index (LAVI) at a given cardiac phase was calculated. A preload of 90. mmHg was applied using a customized lower body positive pressure (LBPP) system. Patients were divided into the PN group (n= 18) with their early diastolic TMF velocity (E) increased and late diastolic TMF velocity (A) decreased, and the non-(N)-PN group (n= 52) with both E and A wave velocities increased by BPP. Results: (1) During LBPP, the LAVImax in both the groups increased significantly. (2) In the N-PN group, the LAVIpass (p&lt 0.001), LAVIact (p&lt 0.01), and LAVItotal (p&lt 0.0001) increased significantly. The dV/dts (p&lt 0.0001) and dV/dtE (p&lt 0.0001) increased significantly with an increase in the dV/dtA. On the other hand, there was no change in those parameters except LAVIpass (p&lt 0.05) and dV/dtE (p&lt 0.05) significantly increased in the PN group. (3) As a result, the LAVImin was significantly greater in the PN group than in the N-PN group (p&lt 0.0001) during LBPP. The ratio of E velocity to early diastolic mitral annular velocity (E/E') during LBPP was significantly greater in the PN group than in the N-PN group (p&lt 0.0001). Conclusions: The lack of an increase in active LA emptying volume in response to an increase of preload leads to elevated LA pressure and the pseudonormalization of the TMF velocity pattern in patients with various cardiac diseases. © 2013 Japanese College of Cardiology.