Review: Cardioprotective effects of telmisartan in uncomplicated and complicated hypertension

Quartı-Trevano, Fosca; Mancia, Giuseppe

doi:10.3317/jraas.2008.017

Cited by 14 publications

(13 citation statements)

References 79 publications

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“…Vascular stiffening causes an increase in the amplitude and early return of the reflected wave during systole, with augmentation of the central systolic BP and a resultant increase in AI [18] . Furthermore, the carotid IMT represents structural changes like wall thickening and the formation of atherosclerotic plaques, which are correlated with a greater incidence of atherosclerosis in the coronary circulation and other large arteries [19] . Telmisartan has been shown to cause an insignificant reduction in AI [18] and significant decreases in both BNP [20] and IMT [21] .…”

Section: Discussionmentioning

confidence: 99%

Effects of Telmisartan on Arterial Stiffness Assessed by the Cardio-Ankle Vascular Index in Hypertensive Patients

Kinouchi¹,

Ichihara

Sakoda³

et al. 2010

Kidney Blood Press Res

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Background/Aims: This study was conducted to determine the effect of telmisartan on the cardio-ankle vascular index (CAVI), a novel blood pressure (BP)-independent marker for arterial stiffness in hypertensive patients. Methods: One hundred consecutive hypertensive patients were randomly assigned either to a group treated with calcium channel blocker (CCB)-based therapy or a group treated with telmisartan-based therapy. Clinical and biological parameters were then measured before and 12 months after the start of this study. Results: CAVI, the logarithm of urinary albumin excretion, and BP were reduced significantly after telmisartan-based therapy. The decreases in 24-hour diastolic BP and daytime systolic BP associated with telmisartan-based therapy were significantly greater than those associated with CCB-based therapy. Both therapies significantly and similarly decreased the clinical BP, 24-hour systolic BP, daytime diastolic BP and serum levels of low-density lipoprotein cholesterol. No significant differences in the metabolic parameters were observed between the two therapies. Conclusion: Telmisartan-based therapy had beneficial effects on arterial stiffness assessed by CAVI, albuminuria, 24-hour BP and metabolism compared with CCB-based therapy. Since these markers are known to influence the future risk of cardiovascular events, telmisartan could be a useful drug for hypertensive patients.

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Section: Discussionmentioning

confidence: 99%

Effects of Telmisartan on Arterial Stiffness Assessed by the Cardio-Ankle Vascular Index in Hypertensive Patients

Kinouchi¹,

Ichihara

Sakoda³

et al. 2010

Kidney Blood Press Res

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“…Losartan did not inhibit monocrotalineinduced RV hypertrophy (14), while candesartan prevented it (15). Telmisartan, a 5th generation AT1R blocker, is used for the treatment of hypertension and has cardioprotective effects (16). However, little is known about the effects of telmisartan on RV hypertrophy.…”

Section: Introductionmentioning

confidence: 99%

Effects of Telmisartan on Right Ventricular Remodeling Induced by Monocrotaline in Rats

et al. 2009

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Abstract. The present study investigated whether telmisartan, an angiotensin II type 1 receptor antagonist, has cardioprotective effects on monocrotaline-induced right ventricular (RV) remodeling in rats. Six-week-old male Wistar rats were divided into control group (CONT), monocrotaline (60 mg/ kg, i.p.)-treated group (MCT), monocrotaline (60 mg/ kg, i.p.) + telmisartan (3 mg/kg per day, p.o.)-treated group (MCT+TEL), and telmisartan (3 mg/kg per day, p.o.) alonetreated group (TEL). Hearts were excised after echocardiography examinations at day 25. Significant increase in RV weight and histologically remarkable fibrosis in RV sections were observed in MCT. Tricuspid annular plane systolic excursion, a parameter for RV systolic function, significantly decreased in MCT. These RV hypertrophy, fibrosis, and dysfunction were inhibited in MCT+TEL. In MCT, the acceleration time/ejection time ratio of pulmonary artery flow velocity, an index of pulmonary hypertension, significantly decreased. This decrease was not affected in MCT+TEL. In MCT, expressions and activities of matrix metalloproteinase (MMP)-2 and MMP-9, which play a critical role in cardiac remodeling, significantly increased in the RV. In MCT+TEL, these increases in expressions and activities were inhibited. MCT showed about 2-fold increase in transforming growth factor-β1 expression compared with CONT, and such an increase was not decreased in MCT+TEL. There were no significant changes of these parameters in TEL compared with CONT. These results suggest that telmisartan could attenuate the monocrotaline-induced RV remodeling through improvements of RV hypertrophy, fibrosis, dysfunction, and inhibition of MMPs.

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“…In 2002, the LAARS study enrolled 280 hypertensive patients that were randomized to receive losartan (50 mg) or atenolol (50 mg) for 24 months and demonstrated a significant annual IMT decrease of 0.038±0.004 mm in the losartan group (2). Similarly, Tedesco et al demonstrated a significant IMT regression after 24 months of losartan treatment (3).…”

Section: To the Editormentioning

confidence: 99%

“…We believe that telmisartan has different properties for targeting vascular failure. Recently, Grassi et al (2) reported that telmisartan 1) is effective in favoring the regression of cardiac and vascular organ damage, 2) reduces arterial stiffness and improves vascular distensibility and 3) reverses the endothelial dysfunction typical of the hypertensive state, particularly when complicated by chronic kidney disease (CKD) or metabolic syndrome. Telmisartan Randomized Assessment Study in ACE-I Intolerant Patients with Cardiovascular Disease (TRANSCEND) Investigators (3) have reported that telmisartan was well tolerated in patients unable to tolerate angiotensin-converting enzyme (ACE) inhibitors, and that it modestly reduced the risk of the composite outcome of cardiovascular death, myocardial infarction, or stroke.…”

Section: Response To: Telmisartan and Carotid Intimamedia Thickness Rmentioning

confidence: 99%

Response to: Telmisartan and Carotid Intima-Media Thickness Regression: A Class Effect of Angiotensin-Receptor Blockers?

2008

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compared the renovascular effects of telmisartan and amlodipine in hypertensive patients with chronic kidney disease and mild renal insufficiency. Among other results, a significant increase in carotid intima-media thickness (IMT) was demonstrated in the amlodipine group after 12 months of treatment as compared to baseline values. In the telmisartan group, however, the investigators found a significant IMT regression; as they commented, it remains to be determined whether this regression is specific to telmisartan or constitutes a class effect of angiotensin-II receptor blockers (ARBs).Previous studies on the effect of ARBs on IMT have yielded conflicting results. In 2002, the LAARS study enrolled 280 hypertensive patients that were randomized to receive losartan (50 mg) or atenolol (50 mg) for 24 months and demonstrated a significant annual IMT decrease of 0.038±0.004 mm in the losartan group (2). Similarly, Tedesco et al. demonstrated a significant IMT regression after 24 months of losartan treatment (3). Moreover, Olsen et al. (4) and Sonoda et al. (5) showed that losartan resulted in a significant IMT decrease (0.83±0.11 to 0.79±0.16 mm and 0.87±0.14 to 0.79±0.16 mm, respectively) in hypertensive patients within 3 and 1 years of treatment, respectively. In contrast, losartan failed to induce a significant IMT regression within 12 months of treatment in a study by UchiyamaTanaka et al. (6).As in the losartan trials, studies on the effect of candesartan on IMT have yielded conflicting results. Ariff et al. (7) and Ono et al. (8) demonstrated that candesartan leads to a significant IMT reduction of 0.05 mm and 0.13 mm within 12 and 24 months respectively. However, these findings were not confirmed by Ichihara et al., who showed that IMT remained unchanged when candesartan was added in patients already receiving calcium channel blockers (9). Similarly, candesartan did not induce a significant IMT regression in a study by Tomás et al. (10). However, this study was underpowered to identify a beneficial effect of candesartan on IMT since it involved a small sample size (n= 34) and lasted only 3 months.Valsartan has been shown not to induce IMT regression. In a recent article by Okura et al., did not influence IMT after 24 months of treatment (11). Similar results were demonstrated in a study by Kosch et al., but that study followed patients for only 3 months (12). On the other hand, treatment with irbesartan in the SILVHIA study resulted in a significant IMT reduction compared with atenolol, which was used as control (13).The conflicting results of the aforementioned studies raise serious concerns as to whether the beneficial effect of telmisartan on IMT shown by Nakamura et al.(1) can be considered a class effect of ARBs. We believe that further studies are necessary to clarify this issue.

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Review: Cardioprotective effects of telmisartan in uncomplicated and complicated hypertension

Cited by 14 publications

References 79 publications

Effects of Telmisartan on Arterial Stiffness Assessed by the Cardio-Ankle Vascular Index in Hypertensive Patients

Effects of Telmisartan on Arterial Stiffness Assessed by the Cardio-Ankle Vascular Index in Hypertensive Patients

Effects of Telmisartan on Right Ventricular Remodeling Induced by Monocrotaline in Rats

Response to: Telmisartan and Carotid Intima-Media Thickness Regression: A Class Effect of Angiotensin-Receptor Blockers?

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