Pre-Clinical and Clinical Experience of Telmisartan in Cardiac Remodelling

Verdecchia, Paolo

doi:10.1177/14732300050330s103

Cited by 8 publications

(4 citation statements)

References 43 publications

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“…Both the drugs displayed antihypertensive effects successfully, however, no clinically significant insulin resistance effect was observed for azilsartan and telmisartan [28]. Verdecchia reported that telmisartan is effective in reversing cardiac remodelling through improving the left ventricular and left atrial functions in hypertensive patients [29]. Alongside cardiac health improvement, telmisartan was reported to have an impact on the growth of small abdominal aortic aneurysms [30].…”

Section: Discussionmentioning

confidence: 99%

Clinical data analysis of telmisartan for hypertension management in Indian population

Kumar¹

2021

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It is of interest to evaluate the clinical characteristics, treatment patterns, clinical effectiveness, and safety of telmisartan as a monotherapy or as part of combination therapy in Indian adults (>18 years old) with hypertension. All patients were receiving telmisartan as monotherapy, or as a combination therapy for hypertension management. Demographics, risk factors, existing comorbidity, and ongoing medical therapies were retrieved from the patients’ medical records. A total of 8607 patients with hypertension (median age, 51.0 years) were part of the study. The gender distribution suggested, 5534(64.3%) patients were male, and 3073 (35.7%) were female patients. The excess salt intake (39.0%) was the most common risk factor according to the results. The analysis revealed telmisartan dual therapy (57.9%) as the most prescribed therapy, followed by monotherapy (32.5%), and triple therapy (9.6%). Further, telmisartan 40mg (21.3%) and telmisartan 40mg plus amlodipine 5mg (17.6%) were the most commonly prescribed therapies. The data suggested that only 17.2% of patients required dose titration. The mean systolic blood pressure (SBP) and diastolic blood pressure (DBP) (mmHg) were significantly decreased with monotherapy (mean change: 19.8 [15.1] mmHg and 8.8[8.2] mmHg), dual therapy (mean change: 23.7 [16.6] mmHg and 10.3[8.5] mmHg), and triple therapy (mean change: 28.6 [19.0] mmHg and 12.1[10.8] mmHg) after the treatment (P<0.001). A total of 98.4% of the patients were compliant, and 97.6% achieved the target blood pressure goal with telmisartan-based therapy. There were 157 adverse events reported altogether. The Physicians’ global evaluation of efficacy and tolerability showed the majority of the patients receiving telmisartan-based therapy on a good to excellent scale. Telmisartan used as a monotherapeutic agent or as a part of combination therapy was successful and effective in reducing blood pressure and achieving the blood pressure target. Irrespective of the patient’s age, duration, and stages of hypertension, the study resulted in a good to excellent scale in efficacy and tolerability in the Indian patients having hypertension.

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Section: Discussionmentioning

confidence: 99%

Clinical data analysis of telmisartan for hypertension management in Indian population

Kumar¹

2021

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“…These results demonstrate that LVH induced by pressure overload can be prevented by telmisartan. While taking away the pressure overload was possibly the primary mechanism, hemodynamic independent effects could likely involve as well in such prevention by telmisartan [3,23,26] and other drugs that also target renin-angiotensin system [23,24].…”

Section: Discussionmentioning

confidence: 99%

Left ventricular hypertrophy induced by abdominal aortic banding and its prevention by angiotensin receptor blocker telmisartan—a proteomic analysis

et al. 2010

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Cardiac hypertrophy is frequently caused by pressure overload (i.e., high blood pressure or hypertension) and can lead to heart failure. The major objective of the present study was to investigate the proteomic changes in response to the development of left ventricular hypertrophy (LVH) induced by abdominal aortic banding (AB) and its prevention by antihypertensive treatment with angiotensin II receptor blocker (ARB) telmisartan. One week after AB and Sham surgery, rats were assigned into three groups: SHAM-control, aortic banding without treatment (AB-Ctrl) and aortic banding with telmisartan treatment (AB-Telmi; 5mg/kg/day for 8 weeks). Echocardiography, hemodynamics, and pathology were performed to assess LVH. Left ventricular myocardium was sampled. The analysis of proteomic proteins from myocardium was performed by two-dimensional gel electrophoresis and MALDI-TOF-MS. In AB-Ctrl, heart rate, systolic arterial blood pressure, diastolic blood pressure, left ventricular end systolic pressure, interventricular septal thickness at diastole, posterior wall thickness in diastole, heart weight (HW) and HW/body weight (BW) were increased, indicating that both hypertension and LVH developed. Telmisartan prevented hypertension and LVH. Concurrently, among numerous proteins, there were 17 that were differentially expressed among hypertrophic hearts, normal hearts, and the hearts where hypertrophic response was suppressed by ARB treatment. Primarily, proteins involved in cell structure, metabolism, stress and signal transduction exhibited up-regulations in LVH, providing cellular and molecular mechanism for hypertrophic development. These changes were prevented or greatly attenuated by telmisartan regimen. Interestingly, antioxidative-related heat shock protein 2 was detected neither in SHAM-Ctrl nor in AB-Ctrl, but in AB-Telmi. LVH is accompanied by series changes of protein expression. Both LVH and proteomic changes can be prevented by blockade of renin-angiotensin system with telmisartan. These protein alterations may constitute mechanistic pathways leading to hypertrophy development and experimental targets for novel therapeutic strategy.

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“…Animals subjected to TAC were treated with GGD (1.5 g/kg), telmisartan (Tel, 8 mg/kg, as a positive control), or tap water (as a vehicle control) by oral gavage for 4 weeks. Telmisartan, an angiotensin II receptor blocker, has been shown to suppress cardiac hypertrophy and collagen deposition induced by pressure overload both in patients and in animal models [ 8 , 9 ].…”

Section: Methodsmentioning

confidence: 99%

The Effects of Guizhi Gancao Decoction on Pressure Overload‐Induced Heart Failure and Posttranslational Modifications of Tubulin in Mice

Chen

Zhao

Tian

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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Guizhi Gancao Decoction (GGD), a traditional Chinese medical recipe, has been widely used in the treatment of cardiovascular diseases in China for centuries. The present study was carried out to determine whether GGD exerts direct protective effects against pressure overload-induced heart failure. Moreover, we investigated whether GGD affects tubulin expression and posttranslational modifications. We demonstrated that GGD ameliorated TAC caused cardiac hypertrophy by gravimetric and echocardiography analysis in C57BL/6 mice. We found that GGD abrogated TAC-induced myocardium fibrosis by Masson's staining and collagen volume fraction (CVF) analysis. By using pressure-volume hemodynamic measurements, we found that GGD prevented TAC-induced cardiac systolic and diastolic dysfunction. Immunoblotting and immunofluorescent analysis revealed that GGD abrogated TAC-induced detyrosination and acetylation abnormalities on microtubules. Our present study demonstrated potential therapeutic effects of GGD against pressure overload-induced heart failure.

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Pre-Clinical and Clinical Experience of Telmisartan in Cardiac Remodelling

Cited by 8 publications

References 43 publications

Clinical data analysis of telmisartan for hypertension management in Indian population

Clinical data analysis of telmisartan for hypertension management in Indian population

Left ventricular hypertrophy induced by abdominal aortic banding and its prevention by angiotensin receptor blocker telmisartan—a proteomic analysis

The Effects of Guizhi Gancao Decoction on Pressure Overload‐Induced Heart Failure and Posttranslational Modifications of Tubulin in Mice

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