The Experts below are selected from a list of 372 Experts worldwide ranked by ideXlab platform
Kazuomi Kario - One of the best experts on this subject based on the ideXlab platform.
-
comparative effects of valsartan plus Cilnidipine or hydrochlorothiazide on nocturnal home blood pressure
Journal of Clinical Hypertension, 2021Co-Authors: Takeshi Fujiwara, Naoko Tomitani, Hiroshi Kanegae, Satoshi Hoshide, Kazuomi KarioAbstract:We tested our hypothesis that, in hypertensive patients with higher nocturnal home systolic blood pressure (HSBP) at baseline, a valsartan/Cilnidipine (80/10 mg) combination would reduce nocturnal HSBP more markedly than a valsartan/hydrochlorothiazide (80/12.5 mg) combination. Patients measured their nocturnal HSBP over three nights prior to study randomization and at the end of treatment. Sixty-three and 66 patients comprised the valsartan/Cilnidipine and valsartan/hydrochlorothiazide groups; their respective baseline nocturnal HSBP values were 124.3 ± 15.6 and 125.8 ± 15.2 mm Hg (P = .597). Nocturnal HSBPs were significantly reduced from baseline in both groups. Although the valsartan/hydrochlorothiazide group exhibited a significantly greater reduction in nocturnal HSBP compared to the valsartan/Cilnidipine group (-5.0 vs. -10.0 mm Hg, P = .035), interaction between the treatment groups and the baseline nocturnal HSBP levels for the changes in nocturnal HSBP after the treatment periods was significant (P = .047). The BP-lowering effect of valsartan/Cilnidipine was more dependent on baseline nocturnal HSBP than that of valsartan/hydrochlorothiazide.
-
comparative effects of valsartan plus either Cilnidipine or hydrochlorothiazide on home morning blood pressure surge evaluated by information and communication technology based nocturnal home blood pressure monitoring
Journal of Clinical Hypertension, 2018Co-Authors: Takeshi Fujiwara, Naoko Tomitani, Hiroshi Kanegae, Kazuomi KarioAbstract:The authors tested the hypothesis that a valsartan/Cilnidipine combination would suppress the home morning blood pressure (BP) surge (HMBPS) more effectively than a valsartan/hydrochlorothiazide combination in patients with morning hypertension, defined as systolic BP (SBP) ≥135 mm Hg or diastolic BP ≥85 mm Hg assessed by a self-measuring information and communication technology-based home BP monitoring device more than three times before either combination's administration. This was an 8-week prospective, multicenter, randomized, open-label clinical trial. The HMBPS, which is a new index, was defined as the mean morning SBP minus the mean nocturnal SBP, both measured on the same day. The authors randomly allocated 129 patients to the valsartan/Cilnidipine (63 patients; mean 68.4 years) or valsartan/hydrochlorothiazide (66 patients; mean 67.3 years) combination groups, and the baseline HMBPS values were 17.4 mm Hg vs 16.9 mm Hg, respectively (P = .820). At the end of the treatment period, the changes in nocturnal SBP and morning SBP from baseline were significant in both the valsartan/Cilnidipine and valsartan/hydrochlorothiazide groups (P < .001): -5.0 vs -10.0 mm Hg (P = .035) and -10.7 vs -13.6 mm Hg (P = .142), respectively. HMBPS was significantly decreased from baseline in both groups (P < .001), but there was no significant difference between the two groups: 14.4 mm Hg vs 14.0 mm Hg, respectively (P = .892). Valsartan/Cilnidipine could not significantly suppress HMBPS compared with valsartan/hydrochlorothiazide. Large-scale randomized controlled studies are needed to assess how reducing HMBPS will affect future cardiovascular outcomes. The information and communication technology-based home BP monitoring device may become an alternative to ambulatory BP monitoring, which has been a gold standard to measure nocturnal BP and the morning BP surge.
-
the relationship between a blunted morning surge and a reversed nocturnal blood pressure dipping or riser pattern
Journal of Clinical Hypertension, 2017Co-Authors: Takeshi Fujiwara, Naoko Tomitani, Keiko Sato, Ayako Okura, Noriyuki Suzuki, Kazuomi KarioAbstract:The authors sought to determine the association between the blunted morning blood pressure (BP) surge and nocturnal BP dipping of the "riser" pattern in 501 patients with hypertension enrolled in the ACHIEVE-ONE (Ambulatory Blood Pressure Control and Home Blood Pressure [Morning and Evening] Lowering by the N-Channel Blocker Cilnidipine) trial. The patients' sleep-trough morning BP surge and prewaking surge were calculated and then classified according to their nocturnal systolic BP reduction pattern as extreme dippers, dippers, nondippers, and risers. The prevalence of the riser pattern was significantly higher in both the lowest sleep-trough morning BP surge decile and the prewaking surge decile (blunted surge group) compared with the remaining deciles (56.0% vs 10.4% [P<.0001] and 59.2% vs 10.2% [P<.0001], respectively). The riser pattern was a significant determinant of both blunted sleep-trough morning BP surge (odds ratio, 73.3; P<.0001) and blunted prewaking surge (odds ratio, 14.8; P<.0001). The high prevalence of the riser pattern in patients with blunted morning BP surges may account for the cardiovascular risk previously reported in such patients.
Akira Takahara - One of the best experts on this subject based on the ideXlab platform.
-
Selectivity of Ca2+ channel blockers for dilator actions on the isolated lower esophageal sphincter and aorta from rats
Elsevier, 2018Co-Authors: Akira Takahara, Shuhei Nozaki, Akane Ishiguro, Kaori Okamura, Xin Cao, Megumi Aimoto, Yoshinobu NagasawaAbstract:We compared dilator actions of representative four Ca2+ channel blockers on the isolated lower esophagus sphincter (LES) and thoracic aorta from rats. Verapamil, diltiazem, nifedipine and Cilnidipine suppressed KCl-induced contractions of LES and thoracic aorta in a concentration-dependent manner. The order of selectivity for LES, which was calculated as ratio of IC50 value for thoracic aorta divided by that for LES, was diltiazem > verapamil > nifedipine > Cilnidipine. These results suggest that diltiazem more preferentially dilates the LES whereas Cilnidipine is expected to have lower potential risk of gastroesophageal dysfunction during the antihypertensive therapy. Keywords: Ca2+ channel blockers, Lower esophagus sphincter, Thoracic aort
-
Cilnidipine a new generation ca2 channel blocker with inhibitory action on sympathetic neurotransmitter release
Cardiovascular Therapeutics, 2009Co-Authors: Akira TakaharaAbstract:Cilnidipine is a unique Ca(2+) channel blocker with an inhibitory action on the sympathetic N-type Ca(2+) channels, which is used for patients with hypertension in Japan. Cilnidipine has been clarified to exert antisympathetic actions in various examinations from cell to human levels, in contrast to classical Ca(2+) channel blockers. Furthermore, renoprotective and neuroprotective effects as well as cardioprotective action of Cilnidipine have been demonstrated in clinical practice or animal examinations. After the introduction of nifedipine as an antihypertensive drug, many Ca(2+) channel blockers with long-lasting action for blood pressure have been developed to minimize sympathetic reflex during antihypertensive therapy, which have been divided into three groups; namely, first, second, and third generation based on their pharmacokinetic profiles. Since Cilnidipine directly inhibits the sympathetic neurotransmitter release by N-type Ca(2+) channel-blocking property, the drug can be expected as fourth generation, providing an effective strategy for the treatment of cardiovascular diseases.
-
the n and l type calcium channel blocker Cilnidipine suppresses renal injury in dahl rats fed a high sucrose diet an experimental model of metabolic syndrome
Nephron Physiology, 2005Co-Authors: Tomoyuki Konda, Akira Takahara, Azusa Enomoto, Junko Matsushita, Toshiki MoriyamaAbstract:Background/Aims: The L/N-type calcium channel blocker (CCB) Cilnidipine has been demonstrated to suppress progressive renal disease in a variety of experimental models, but the char
Guichard Jean-baptiste - One of the best experts on this subject based on the ideXlab platform.
-
Determinants of atrial remodeling and its proarrhythmic effect in atrial fibrillation
2019Co-Authors: Guichard Jean-baptisteAbstract:Rationnel et objectif : La fibrillation atriale (FA) est la pathologie rythmique supra-ventriculaire la plus fréquente. Le remodelage atrial, électrique ou structurel, conduit au développement de la cardiomyopathie atriale. L’objectif est de caractériser les déterminants du remodelage atrial à l’étage supra-ventriculaire dans la FA.Principaux résultats :Le premier axe de recherche a permis d’objectiver le remodelage induit par le flutter atrial (FLA) chronique à l’aide d’un modèle chronique canin. Le FLA cause un remodelage atrial électrique mais non structurel. L’ablation du FLA diminue significativement la durée mais pas la vulnérabilité à présenter des arythmies supra-ventriculaires.Le second axe de recherche a permis de caractériser le rôle différentiel de l’arythmie atriale de la réponse ventriculaire rapide en cas de FA dans le développement du remodelage atrial. De plus, il existe un effet synergique au niveau du remodelage atrial de l’arythmie atriale et de la fréquence ventriculaire élevée en cas de FA, au niveau du processus fibrotique notamment.Le troisième axe de recherche a permis d’objectiver le rôle de la Cilnidipine, un inhibiteur calcique de type N et L, dans la limitation du remodelage atrial en cas de FA chronique, à l’aide d’un modèle aigü et chronique canin, que ce soit sur son versant électrique, structurel et autonome.Conclusion – Différents facteurs, tels que le flutter atrial, l’arythmie atriale et ventriculaire en cas de FA, ont été caractérisés comme déterminants du remodelage atrial. A contrario, la modulation d’un des déterminants du remodelage atrial, le système nerveux autonome, permet de de limiter le remodelage atrial secondaire à la FA.Rational : Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. Atrial remodeling, whether electrical or structural, leads to the development of atrial cardiomyopathy. The aim of the thesis was to characterize the determinants of atrial remodeling, and their proarrhythmic effect in AF.Main results :The first part of the thesis focused on the characterization of the atrial remodeling induced by sustained atrial flutter (AFL) in a chronic canine model AFL caused electrical remodeling but no structural. In addition, AFL ablation significantly reduced arrhythmia duration but not AF vulnerability.The second part of the thesis characterized the differential role of atrial arrhythmia and ventricular response in AF-induced atrial remodeling. Lone atrial arrhythmia and lone high-rate ventricular response induced atrial remodeling. In addition, there was a synergistic effect on atrial remodeling of combined atrial arrhythmia and high ventricular rate, especially regarding fibrosis.The third part of the thesis studies the ability of Cilnidipine, an N- and L-type calcium channel blocker, to alter autonomic, electrical and structural remodeling associated with chronic AF, in a subacute and chronic dog model. Cilnidipine’s electrical and structural anti-remodeling properties were associated with suppression of the changes in autonomic tone caused by AF.Conclusion - This work provides new insights into the mechanisms involved in AF-related atrial remodeling and introduces novel preventive approaches
-
Déterminants du remodelage atrial et de son effet pro-arythmique dans la fibrillation atriale
2019Co-Authors: Guichard Jean-baptisteAbstract:Rationnel et objectif - La fibrillation atriale (FA) est la pathologie rythmique supra-ventriculaire la plus fréquemment diagnostiquée. Le remodelage atrial, qu’il soit électrique ou structurel, conduit à la mise en place et au développement de la cardiomyopathie atriale. La cardiomyopathie atriale est responsable de différentes complications : d’une part mécaniques conduisant à l’augmentation du risque thrombo-embolique et de l’insuffisance cardiaque, d’autre part électriques conduisant à différentes arythmies atriales dont la FA. L’objectif du présent travail est de caractériser les déterminants du remodelage atrial et de leur effet pro-arythmique à l’étage supra-ventriculaire dans la FA. Principaux résultats – Le premier axe de recherche a permis d’objectiver le remodelage induit par le flutter atrial (FLA) chronique à l’aide d’un modèle chronique canin. Le FLA est à l’origine d’un remodelage atrial électrique avec une augmentation de la vulnérabilité à développer de la FA et une diminution des périodes réfractaires effectives (PRE). Cependant, le FLA n’induit pas de remodelage structurel avec notamment l’absence d’augmentation de la durée de FA, de diminution des vitesses de conduction et d’augmentation du processus fibrotique atrial. À noter que la FA chronique, en présence d’un substrat anatomique de FLA, présente des caractéristiques électrophysiologiques originales, en terme de durée de cycle et de d’arythmie et de sa stabilité. De plus, l’ablation du FLA permet de diminuer significativement la durée mais pas la vulnérabilité à présenter des arythmies supra-ventriculaires. Le second axe de recherche a permis de caractériser le rôle différentiel de l’arythmie atriale de la réponse ventriculaire rapide en cas de FA dans le développement du remodelage atrial. Nos travaux ont caractérisé le remodelage atrial induit par l’arythmie atriale isolée en cas de FA : d’une part électrique via la diminution des PRE et l’augmentation de la vulnérabilité ; d’autre part structurel via la diminution des vitesses de conduction et les anomalies des canaux sodiques, des jonctions communicantes et du processus fibrotique. La réponse ventriculaire rapide isolée induit également un remodelage atrial à type d’augmentation de la vulnérabilité, de diminution des vitesses de conduction, d’anomalies modérées du processus fibrotique et des canaux sodiques. À noter une dégradation modérée de la fonction systolique ventriculaire gauche. Cependant, ce remodelage atrial est significativement différent du remodelage induit par l’insuffisance cardiaque. De plus, il existe un effet synergique au niveau du remodelage atrial de l’arythmie atriale et de la fréquence ventriculaire élevée en cas de FA, au niveau du processus fibrotique notamment. Le troisième axe de recherche a permis d’objectiver le rôle de la Cilnidipine, un inhibiteur calcique de type N et L, dans la limitation du remodelage atrial en cas de FA chronique, à l’aide d’un modèle aigü et chronique canin. Nos travaux ont caractérisé l’action anti-remodelante de la Cilnidipine au niveau électrique, via la limitation de la diminution des PRE, de l’augmentation de la vulnérabilité atriale et de la durée de FA. D’autre part, la Cilnidipine semble limiter le remodelage atrial, ce qui est objectivé par la normalisation des vitesses de conduction, de l’expression des canaux sodiques, des jonctions communicantes et de la fibrose tissulaire. La Cilnidipine, contrairement aux inhibiteurs calciques de type L tels que la nifédipine, possède une activité anti-remodelante via la modulation de l’activité du système nerveux autonome. Conclusion – Différents facteurs, tels que le flutter atrial, les fréquences atriales et ventriculaires en cas de FA, ont été caractérisés comme déterminants du développement du remodelage atrial. A contrario, la modulation d’un des déterminants du remodelage atrial, le système nerveux autonome via la Cilnidipine, permet de de limiter le remodelage atrial secondaire à la FA. Ce travail fournit de nouvelles données sur les mécanismes impliqués dans le remodelage atrial lié à la FA et introduit de nouvelles approches préventives au développement de la FA.Rational and objective - Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. Atrial remodeling, whether electrical or structural, leads to the development of atrial cardiomyopathy. The atrial cardiomyopathy results in various complications: on one hand, mechanical with an increased thromboembolic risk and heart failure, and on the other hand electrical prdeisposing to atrial arrhythmias including AF. The aim of the thesis was to characterize the determinants of atrial remodeling, and their proarrhythmic effect in AF. Main results - The first part of the thesis focused on the characterization of the atrial remodeling induced by sustained atrial flutter (AFL) in a chronic canine model in order to characterize the interrelationship between AF and AFL. AFL caused electrical remodeling, including increased AF vulnerability and decreased effective refractory periods (ERPs). However, failed to influence AF duration, atrial conduction velocities and fibrosis. Chronic AF in the presence of an anatomical substrate for AFL led to specific AF characteristics, in terms of cycle length and its variability. In addition, AFL ablation significantly reduced arrhythmia duration but not AF vulnerability. The second part of the thesis characterized the differential role of atrial arrhythmia and ventricular response in AF-induced atrial remodeling. We characterized the atrial remodeling induced by lone atrial arrhythmia in AF, with AV-block to prevent high ventricular rate: on the one hand electrical via decreased ERP, reduced expression of sodium channels and gap junctions, which increased AF vulnerability; on the other hand, structural fibrosis which contributed to conduction slowing. Lone high-rate ventricular response also induced atrial remodeling involving increased AF vulnerability, decreased atrial conduction velocities, moderate abnormalities of fibrosis and sodium channel downregulation. In addition, there was a synergistic effect on atrial remodeling of combined atrial arrhythmia and high ventricular rate, especially regarding fibrosis. Thus, atrial tachyarrhythmia and rapid ventricular response during AF produce distinct atrial remodeling; both can contribute to the arrhythmogenic substrate. These results provide new insights into the determinants of AF-related remodeling and provide novel considerations for ventricular rate-control. The third part of the thesis studies the ability of Cilnidipine, an N- and L-type calcium channel blocker, to alter autonomic, electrical and structural remodeling associated with chronic AF, in a subacute and chronic dog model. We found that the Cilnidipine inhibits the electrophysiological, autonomic and structural consequences of AF-related remodeling and the AF-associated increase in AF-vulnerability and AF-duration; in contrast, the highly selective L-type calcium channel blocker nifedipine had no protective effects. The protective effects of Cilnidipine on the remodeling consequences of short-term AF were principally manifested by reductions in AF-induced ERP-abbreviation. With longer-term AF, Cilnidipine also attenuated conduction-velocity reductions, protecting against AF-induced fibrosis and downregulation of sodium-channel and connexin subunits. Cilnidipine’s anti-remodeling properties were associated with suppression of the changes in autonomic tone caused by AF. Conclusion - Thus, we have shown 1) the distinct remodeling phenotypes produced by the closely related atrial re-entrant arrhythmias AFL and AF, as well as the interaction when they co-exist; 2) the specific contributions of the atrial rhythm and ventricular rate consequences of AF and how they interact; and 3) the ability of autonomic outflow inhibition by blocking N-type Ca2+-channels to prevent both electrical and structural components of AF-induced profibrillatory remodeling. This work provides new insights into the mechanisms involved in AF-related atrial remodeling and introduces novel preventive approaches
-
Déterminants du remodelage atrial et de son effet pro-arythmique dans la fibrillation atriale
HAL CCSD, 2019Co-Authors: Guichard Jean-baptisteAbstract:Rational : Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. Atrial remodeling, whether electrical or structural, leads to the development of atrial cardiomyopathy. The aim of the thesis was to characterize the determinants of atrial remodeling, and their proarrhythmic effect in AF.Main results :The first part of the thesis focused on the characterization of the atrial remodeling induced by sustained atrial flutter (AFL) in a chronic canine model AFL caused electrical remodeling but no structural. In addition, AFL ablation significantly reduced arrhythmia duration but not AF vulnerability.The second part of the thesis characterized the differential role of atrial arrhythmia and ventricular response in AF-induced atrial remodeling. Lone atrial arrhythmia and lone high-rate ventricular response induced atrial remodeling. In addition, there was a synergistic effect on atrial remodeling of combined atrial arrhythmia and high ventricular rate, especially regarding fibrosis.The third part of the thesis studies the ability of Cilnidipine, an N- and L-type calcium channel blocker, to alter autonomic, electrical and structural remodeling associated with chronic AF, in a subacute and chronic dog model. Cilnidipine’s electrical and structural anti-remodeling properties were associated with suppression of the changes in autonomic tone caused by AF.Conclusion - This work provides new insights into the mechanisms involved in AF-related atrial remodeling and introduces novel preventive approaches.Rationnel et objectif : La fibrillation atriale (FA) est la pathologie rythmique supra-ventriculaire la plus fréquente. Le remodelage atrial, électrique ou structurel, conduit au développement de la cardiomyopathie atriale. L’objectif est de caractériser les déterminants du remodelage atrial à l’étage supra-ventriculaire dans la FA.Principaux résultats :Le premier axe de recherche a permis d’objectiver le remodelage induit par le flutter atrial (FLA) chronique à l’aide d’un modèle chronique canin. Le FLA cause un remodelage atrial électrique mais non structurel. L’ablation du FLA diminue significativement la durée mais pas la vulnérabilité à présenter des arythmies supra-ventriculaires.Le second axe de recherche a permis de caractériser le rôle différentiel de l’arythmie atriale de la réponse ventriculaire rapide en cas de FA dans le développement du remodelage atrial. De plus, il existe un effet synergique au niveau du remodelage atrial de l’arythmie atriale et de la fréquence ventriculaire élevée en cas de FA, au niveau du processus fibrotique notamment.Le troisième axe de recherche a permis d’objectiver le rôle de la Cilnidipine, un inhibiteur calcique de type N et L, dans la limitation du remodelage atrial en cas de FA chronique, à l’aide d’un modèle aigü et chronique canin, que ce soit sur son versant électrique, structurel et autonome.Conclusion – Différents facteurs, tels que le flutter atrial, l’arythmie atriale et ventriculaire en cas de FA, ont été caractérisés comme déterminants du remodelage atrial. A contrario, la modulation d’un des déterminants du remodelage atrial, le système nerveux autonome, permet de de limiter le remodelage atrial secondaire à la FA
Toshio Ogihara - One of the best experts on this subject based on the ideXlab platform.
-
renoprotective effect of n type ca channel blockade in diabetic nephropathy
Journal of Diabetes and Its Complications, 2007Co-Authors: Tomomi Fujisawa, Hiroshi Ikegami, Shinsuke Noso, Yoshihisa Hiromine, Yumiko Kawabata, Masanori Nishino, Kazuaki Asano, Toshio OgiharaAbstract:Abstract Objective This study aimed to investigate the renoprotective effect on diabetic nephropathy of a novel class of Ca 2+ channel blocker, Cilnidipine, that inhibits both L-type and N-type Ca 2+ channels; a conventional L-type Ca 2+ channel blocker was substituted with Cilnidipine in type 2 diabetic patients with albuminuria. Methods Urinary albumin index (UAI), serum creatinine, and blood pressure were measured in 38 outpatients with type 2 diabetes receiving amlodipine, an L-type Ca 2+ channel blocker, in addition to an angiotensin I converting enzyme inhibitor and/or an angiotensin type 1 receptor blocker. Amlodipine was then substituted with Cilnidipine, and the same parameters were measured after 3 months. Results Although blood pressure was not significantly changed after substitution with Cilnidipine, log-transformed UAI was significantly decreased ( P =.004) with a mean reduction of 28% [95% confidence interval (CI)=11–42]. Serum creatinine was significantly ( P =.04) increased (from 0.82±0.22 to 0.86±0.23 mg/dl). When the subjects were divided into two groups according to the change in serum creatinine, UAI change was significant only in those with an increase in serum creatinine, who exhibited a mean reduction of UAI of 39% (95% CI=16–56, P =.005), but not in those without an increase in serum creatinine, whose mean reduction of UAI was 18% (95% CI=−12 to 40, P =.2). Conclusions In patients with diabetic nephropathy, blocking N-type Ca 2+ channels with a new class of Ca 2+ channel blocker resulted in a significant reduction in albuminuria, suggesting a renoprotective effect of N-type Ca 2+ channel blockade, even when combined with renin–angiotensin inhibition.
Takeshi Fujiwara - One of the best experts on this subject based on the ideXlab platform.
-
comparative effects of valsartan plus Cilnidipine or hydrochlorothiazide on nocturnal home blood pressure
Journal of Clinical Hypertension, 2021Co-Authors: Takeshi Fujiwara, Naoko Tomitani, Hiroshi Kanegae, Satoshi Hoshide, Kazuomi KarioAbstract:We tested our hypothesis that, in hypertensive patients with higher nocturnal home systolic blood pressure (HSBP) at baseline, a valsartan/Cilnidipine (80/10 mg) combination would reduce nocturnal HSBP more markedly than a valsartan/hydrochlorothiazide (80/12.5 mg) combination. Patients measured their nocturnal HSBP over three nights prior to study randomization and at the end of treatment. Sixty-three and 66 patients comprised the valsartan/Cilnidipine and valsartan/hydrochlorothiazide groups; their respective baseline nocturnal HSBP values were 124.3 ± 15.6 and 125.8 ± 15.2 mm Hg (P = .597). Nocturnal HSBPs were significantly reduced from baseline in both groups. Although the valsartan/hydrochlorothiazide group exhibited a significantly greater reduction in nocturnal HSBP compared to the valsartan/Cilnidipine group (-5.0 vs. -10.0 mm Hg, P = .035), interaction between the treatment groups and the baseline nocturnal HSBP levels for the changes in nocturnal HSBP after the treatment periods was significant (P = .047). The BP-lowering effect of valsartan/Cilnidipine was more dependent on baseline nocturnal HSBP than that of valsartan/hydrochlorothiazide.
-
comparative effects of valsartan plus either Cilnidipine or hydrochlorothiazide on home morning blood pressure surge evaluated by information and communication technology based nocturnal home blood pressure monitoring
Journal of Clinical Hypertension, 2018Co-Authors: Takeshi Fujiwara, Naoko Tomitani, Hiroshi Kanegae, Kazuomi KarioAbstract:The authors tested the hypothesis that a valsartan/Cilnidipine combination would suppress the home morning blood pressure (BP) surge (HMBPS) more effectively than a valsartan/hydrochlorothiazide combination in patients with morning hypertension, defined as systolic BP (SBP) ≥135 mm Hg or diastolic BP ≥85 mm Hg assessed by a self-measuring information and communication technology-based home BP monitoring device more than three times before either combination's administration. This was an 8-week prospective, multicenter, randomized, open-label clinical trial. The HMBPS, which is a new index, was defined as the mean morning SBP minus the mean nocturnal SBP, both measured on the same day. The authors randomly allocated 129 patients to the valsartan/Cilnidipine (63 patients; mean 68.4 years) or valsartan/hydrochlorothiazide (66 patients; mean 67.3 years) combination groups, and the baseline HMBPS values were 17.4 mm Hg vs 16.9 mm Hg, respectively (P = .820). At the end of the treatment period, the changes in nocturnal SBP and morning SBP from baseline were significant in both the valsartan/Cilnidipine and valsartan/hydrochlorothiazide groups (P < .001): -5.0 vs -10.0 mm Hg (P = .035) and -10.7 vs -13.6 mm Hg (P = .142), respectively. HMBPS was significantly decreased from baseline in both groups (P < .001), but there was no significant difference between the two groups: 14.4 mm Hg vs 14.0 mm Hg, respectively (P = .892). Valsartan/Cilnidipine could not significantly suppress HMBPS compared with valsartan/hydrochlorothiazide. Large-scale randomized controlled studies are needed to assess how reducing HMBPS will affect future cardiovascular outcomes. The information and communication technology-based home BP monitoring device may become an alternative to ambulatory BP monitoring, which has been a gold standard to measure nocturnal BP and the morning BP surge.
-
the relationship between a blunted morning surge and a reversed nocturnal blood pressure dipping or riser pattern
Journal of Clinical Hypertension, 2017Co-Authors: Takeshi Fujiwara, Naoko Tomitani, Keiko Sato, Ayako Okura, Noriyuki Suzuki, Kazuomi KarioAbstract:The authors sought to determine the association between the blunted morning blood pressure (BP) surge and nocturnal BP dipping of the "riser" pattern in 501 patients with hypertension enrolled in the ACHIEVE-ONE (Ambulatory Blood Pressure Control and Home Blood Pressure [Morning and Evening] Lowering by the N-Channel Blocker Cilnidipine) trial. The patients' sleep-trough morning BP surge and prewaking surge were calculated and then classified according to their nocturnal systolic BP reduction pattern as extreme dippers, dippers, nondippers, and risers. The prevalence of the riser pattern was significantly higher in both the lowest sleep-trough morning BP surge decile and the prewaking surge decile (blunted surge group) compared with the remaining deciles (56.0% vs 10.4% [P<.0001] and 59.2% vs 10.2% [P<.0001], respectively). The riser pattern was a significant determinant of both blunted sleep-trough morning BP surge (odds ratio, 73.3; P<.0001) and blunted prewaking surge (odds ratio, 14.8; P<.0001). The high prevalence of the riser pattern in patients with blunted morning BP surges may account for the cardiovascular risk previously reported in such patients.