Evaluation of Importance of Central Effects of Atenolol and Metoprolol Measured by Heart Rate Variability During Mental Performance Tasks, Physical Exercise, and Daily Life in Stable Postinfarct Patients

Tuininga, Ype S.; Crijns, Hjgm; Brouwer, Jan; Berg, Maarten P. van den; Veld, A. J. Man In't; Mulder, G.; Lie, Ki

doi:10.1161/01.cir.92.12.3415

Cited by 59 publications

(43 citation statements)

References 36 publications

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“…The goal of treatment with atenolol will be a > 20% decrease in the mean heart rate, which reflects adequate beta blockade. 28,29 The average starting dose of losartan will be 0.4 mg/kg and the daily dose will be increased as tolerated by ∼0.4 mg/kg in each subsequent cycle to a maximum daily dose of between 1.0 and 1.4 mg/kg, not to exceed 100 mg.…”

Section: Study Treatmentsmentioning

confidence: 99%

Rationale and design of a randomized clinical trial of β-blocker therapy (atenolol) versus angiotensin II receptor blocker therapy (losartan) in individuals with Marfan syndrome

Lacro

Dietz

Wruck

et al. 2007

American Heart Journal

207

161

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Background-Cardiovascular pathology, including aortic root dilation, dissection, and rupture, is the leading cause of mortality in patients with Marfan syndrome (MFS). The maximal aortic root diameter at the sinuses of Valsalva is considered the best predictor of adverse cardiovascular outcome. Although advances in therapy have improved life expectancy, affected individuals continue to suffer cardiovascular morbidity and mortality. Recent studies in a FBN1-targeted mouse model of MFS with aortic pathology similar to that seen in humans showed that treatment with losartan normalized aortic root growth and aortic wall architecture.

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Section: Study Treatmentsmentioning

confidence: 99%

Rationale and design of a randomized clinical trial of β-blocker therapy (atenolol) versus angiotensin II receptor blocker therapy (losartan) in individuals with Marfan syndrome

Lacro

Dietz

Wruck

et al. 2007

American Heart Journal

207

161

View full text Add to dashboard Cite

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“…Studies of situations in which mental or physical stress induces a reduction of HRV give support to this point of view (11,14). On the contrary, interventions that reduce the sympathetic outflow may induce an increase in HRV; this is the case for pharmacological maneuvers (15), some relaxation techniques (16)(17)(18) and, hypothetically, physical training (19). Conversely, a sedentary life style may induce a reduction in parasympathetic outflow paralleled by an increase in sympathetic outflow (20).…”

Section: Introductionmentioning

confidence: 96%

Relative influence of age, resting heart rate and sedentary life style in short-term analysis of heart rate variability

Migliaro

Contreras

Bech

et al. 2001

Braz J Med Biol Res

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In order to assess the relative influence of age, resting heart rate (HR) and sedentary life style, heart rate variability (HRV) was studied in two different groups. The young group (YG) consisted of 9 sedentary subjects aged 15 to 20 years (YG-S) and of 9 nonsedentary volunteers (YG-NS) also aged 15 to 20. The elderly sedentary group (ESG) consisted of 16 sedentary subjects aged 39 to 82 years. HRV was assessed using a short-term procedure (5 min). R-R variability was calculated in the time-domain by means of the root mean square successive differences. Frequency-domain HRV was evaluated by power spectrum analysis considering high frequency and low frequency bands. In the YG the effort tolerance was ranked in a bicycle stress test. HR was similar for both groups while ESG showed a reduced HRV compared with YG. Within each group, HRV displayed a negative correlation with HR. Although YG-NS had better effort tolerance than YG-S, their HR and HRV were not significantly different. We conclude that HRV is reduced with increasing HR or age, regardless of life style. The results obtained in our short-term study agree with others of longer duration by showing that age and HR are the main determinants of HRV. Our results do not support the idea that changes in HRV are related to regular physical activity.

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“…Similarly, recent evidence by Ablad et al (2007) obtained in anaesthetized rabbits suggested that β-blockers are acting centrally to increase cardiac vagal tone. In contrast, there are data obtained in normal human subjects 20,21 and in post-MI patients 22,23 indicating that the effects of β-blockers on vagal tone are likely to be due to their peripheral actions.…”

Section: Heart Failure Autonomic Control Of the Heart And Metoprololmentioning

confidence: 94%

Beneficial Effect of the Central Nervous System β-Adrenoceptor Blockade on the Failing Heart

Gourine

Bondar

Spyer

et al. 2008

Circulation Research

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Heart failure patients are routinely given ␤-adrenoceptor antagonists (␤-blockers), although the mechanism(s) underlying their beneficial effects is not fully resolved. It is not entirely clear how long-term application of negative inotropic compounds improves cardiac performance, slows remodeling processes, and decreases mortality. All ␤-blockers, which produce a beneficial effect in heart failure, have in common a high degree of lipophilicity and, therefore, have the ability to cross the blood-brain barrier. Here, we show that blockade of ␤-adrenoceptors directly in the brain (chronic intracerebroventricular administration of metoprolol) attenuates the progression of left ventricular remodeling in a rat model of myocardial infarction-induced heart failure. These results provide the first direct evidence that the action of certain ␤-blockers in the brain could contribute to their beneficial effect on the failing heart. M ortality associated with heart failure (HF) still remains high, despite considerable achievements in medical therapy, device technology, and cardiac surgery. The use of ␤-adrenoceptor (␤-AR) antagonists (␤-blockers) pioneered in the 1970s for the treatment of arterial hypertension became one of the most important advances in HF therapy. 1,2 The efficacy of 3 ␤-blockers, bisoprolol, carvedilol, and metoprolol, in HF treatment have been demonstrated in large placebo-controlled clinical trials. [3][4][5] These studies have revealed a reduction in the number of deaths from worsening HF in patients treated with carvedilol and metoprolol resulting from an improvement in left ventricular (LV) function and a delayed progression of LV remodeling. 3,4 In contrast, bisoprolol decreased mortality mainly by preventing sudden cardiac death, 5 whereas several ␤-blockers (eg, bisindolol and others) have been found to be insufficiently effective to be used in HF therapy. 2 A number of mechanisms explaining variable effects of ␤-blockers in HF patients have been proposed (including polymorphism in the genes encoding ␤-ARs, modulation of systemic neurohormonal activity, antagonism of the toxic actions of norepinephrine on the myocardium, favorable effects on myocardial energetics, etc). 2,6,7 Interestingly, it appears that the ␤-blockers, which produce a beneficial effect in HF, all have in common a high degree of lipophilicity and, as a result, have the ability to cross the blood-brain barrier. 2,8 Beneficial actions of certain lipophilic ␤-blockers in preventing ventricular fibrillation have already been attributed to their possible action within the brain. 9 We, therefore, suggested that the favorable effects of ␤-blockers in HF may be attributable, at least in part, to their central nervous system (CNS) effects. To test this hypothesis, we infused metoprolol (a ␤ 1 -blocker widely used in HF therapy) directly into the brain and determined the effect of this treatment on the progression of LV remodeling after myocardial infarction (MI) in rats. Materials and MethodsMI in rats was induced using a permanen...

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Evaluation of Importance of Central Effects of Atenolol and Metoprolol Measured by Heart Rate Variability During Mental Performance Tasks, Physical Exercise, and Daily Life in Stable Postinfarct Patients

Cited by 59 publications

References 36 publications

Rationale and design of a randomized clinical trial of β-blocker therapy (atenolol) versus angiotensin II receptor blocker therapy (losartan) in individuals with Marfan syndrome

Rationale and design of a randomized clinical trial of β-blocker therapy (atenolol) versus angiotensin II receptor blocker therapy (losartan) in individuals with Marfan syndrome

Relative influence of age, resting heart rate and sedentary life style in short-term analysis of heart rate variability

Beneficial Effect of the Central Nervous System β-Adrenoceptor Blockade on the Failing Heart

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