Regression of left ventricular hypertrophy and improvement of diastolic function in hypertensive patients treated with telmisartan

Mattioli, Anna Vittoria; Zennaro, Mauro; Bonatti, Silvia; Bonetti, Lorenzo; Mattioli, Giorgio

doi:10.1016/j.ijcard.2003.10.018

Cited by 49 publications

(42 citation statements)

References 32 publications

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“…However, there are few trials of pharmacologic and nonpharmacologic anti-hypertensive therapy, including salt restriction, that use LVH modification as the primary endpoint that also includes substantial numbers of subjects with severely impaired renal function (85)(86)(87). Nonpressure overload factors would not be expected to be affected by conventional antihypertensive therapy.…”

Section: What Are the Key Principles Of Management Of Lvh In Ckd And mentioning

confidence: 99%

Left Ventricular Mass in Chronic Kidney Disease and ESRD

Glassock

Pecoits‐Filho

Barberato

2009

Clinical Journal of the American Society of Nephrology

324

279

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Chronic kidney disease (CKD) and ESRD, treated with conventional hemo-or peritoneal dialysis are both associated with a high prevalence of an increase in left ventricular mass (left ventricular hypertrophy [LVH]), intermyocardial cell fibrosis, and capillary loss. Cardiac magnetic resonance imaging is the best way to detect and quantify these abnormalities, but M-Mode and 2-D echocardiography can also be used if one recognizes their pitfalls. The mechanisms underlying these abnormalities in CKD and ESRD are diverse but involve afterload (arterial pressure and compliance), preload (intravascular volume and anemia), and a wide variety of afterload/preload independent factors. The hemodynamic, metabolic, cellular, and molecular mediators of myocardial hypertrophy, fibrosis, apoptosis, and capillary degeneration are increasingly well understood. These abnormalities predispose to sudden cardiac death, most likely by promotion of electrical instability and re-entry arrhythmias and congestive heart failure. Current treatment modalities for CKD and ESRD, including thrice weekly conventional hemodialysis and peritoneal dialysis and metabolic and anemia management regimens, do not adequately prevent or correct these abnormalities. A new paradigm of therapy for CKD and ESRD that places prevention and reversal of LVH and cardiac fibrosis as a high priority is needed. This will require novel approaches to management and controlled interventional trials to provide evidence to fuel the transition from old to new treatment strategies. In the meantime, key management principles designed to ameliorate LVH and its complications should become a routine part of the care of the patients with CKD and ESRD.

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Section: What Are the Key Principles Of Management Of Lvh In Ckd And mentioning

confidence: 99%

Left Ventricular Mass in Chronic Kidney Disease and ESRD

Glassock

Pecoits‐Filho

Barberato

2009

Clinical Journal of the American Society of Nephrology

324

279

View full text Add to dashboard Cite

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“…those who have not had any previous episodes of AF, and those with paroxysmal or persistent AF who either do not need any antiarrhythmic therapy, or those with persistent AF who do require anti-arrhythmic therapy to maintain sinus rhythm following cardioversion). [16][17][18][19] Telmisartan has the longest half-life of any ARB (approximately 24 hours) 20 and has been shown to reduce left ventricular hypertrophy (LVH) in clinical studies of hypertensive patients, [21][22][23][24] as well as in the ONgoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial (ONTARGET) and Telmisartan Randomized AssessmeNt Study in ACE-I iNtolerant subjects with cardiovascular Disease (TRANSCEND) cardiovascular (CV) outcomes, although no reduction in new-onset AF was found. [25][26][27] The purpose of the present study was to assess the efficacy of an antihypertensive therapeutic dose of telmisartan (80 mg once daily) as compared with that of the β-blocker carvedilol (25 mg once daily), which has been shown to have clinically important anti-arrhythmic properties, [28][29][30][31][32] for the prevention of AF recurrence in a population of hypertensive patients with a recent history of AF and who were in sinus rhythm and who did not require anti-arrhythmic therapy.…”

Section: Introductionmentioning

confidence: 99%

A multicentre, randomized study of telmisartan versus carvedilol for prevention of atrial fibrillation recurrence in hypertensive patients

Galzerano

Michele

Paolisso³

et al. 2012

J Renin Angiotensin Aldosterone Syst

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Introduction: Atrial remodelling, leading to atrial fibrillation (AF), is mediated by the renin-angiotensin-aldosterone system. Methods: Mild hypertensive outpatients (systolic/diastolic blood pressure 140-159/90-99 mmHg) in sinus rhythm who had experienced ≥ 1 electrocardiogram (ECG)-documented AF episode in the previous six months received randomly telmisartan 80 mg/day or carvedilol 25 mg/day. Blood pressure and 24-hour ECG were monitored monthly for one year; patients were asked to report symptomatic AF episodes and to undergo an ECG as early as possible. Results: One hundred and thirty-two patients completed the study (telmisartan, n=70; carvedilol, n=62

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“…39 Increased left atrial pump function represents a compensatory mechanism in hypertensive patients with LVH. The LVH regression observed by Mattioli et al 27 in hypertensive patients treated with telmisartan for 1 year also brought about a reduction in left atrial size and volume, and improvement in atrial performance. 40 In addition, there was an improvement in the early to atrial filling ratio.…”

Section: Effect On Left Atrial Volume and Functionmentioning

confidence: 71%

“…27 These reductions in blood pressure were accompanied by a time-dependent, significant reduction in LVMI from 119 ± 7 to 109 ± 3 g/m 2 (P < 0.001) (Fig. 2), determined using twodimensional echocardiography, over the 12-month study period.…”

Section: Clinical Evaluation Of Telmisartan Effect On Lvh Regression mentioning

confidence: 81%

Pre-Clinical and Clinical Experience of Telmisartan in Cardiac Remodelling

Verdecchia

2005

J Int Med Res

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Epidemiological studies have established that left ventricular hypertrophy (LVH) is an independent risk factor for cardiovascular and cerebrovascular morbidity and mortality. In turn, hypertension is a well-established risk factor for LVH. Ambulatory blood pressure monitoring has shown that 24-h mean ambulatory blood pressure is a particularly powerful predictor of LVH, being superior to casual clinic blood pressure measurements

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Regression of left ventricular hypertrophy and improvement of diastolic function in hypertensive patients treated with telmisartan

Cited by 49 publications

References 32 publications

Left Ventricular Mass in Chronic Kidney Disease and ESRD

Left Ventricular Mass in Chronic Kidney Disease and ESRD

A multicentre, randomized study of telmisartan versus carvedilol for prevention of atrial fibrillation recurrence in hypertensive patients

Pre-Clinical and Clinical Experience of Telmisartan in Cardiac Remodelling

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