β-Blocker Effects on Respiratory Sinus Arrhythmia and Baroreflex Gain in Normal Subjects

Pitzalis, Maria Vittoria; Mastropasqua, Filippo; Massari, Francesco; Passantino, Andrea; Totaro, Paolo; Forleo, Cinzia; Rizzon, Paolo

doi:10.1378/chest.114.1.185

Cited by 31 publications

(23 citation statements)

References 44 publications

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“…An ancillary observation of the present investigation deals with the changes in heart rate variability after atenolol, which, to some extent, were expected. Previous studies have shown an increase in the HF power of RR variability after chronic 5,[35][36][37][38] or acute 8 -10 ␤-blockade in healthy subjects, although not consistently. 12 In the present study, we report a shift of cardiac sympathovagal balance toward a parasympathetic predominance, as indicated by increased HF RR and decreased LF RR spectral components, expressed in normalized units.…”

Section: Cogliati Et Al Msna Variability and Acute ␤-Blockade 2789mentioning

confidence: 79%

Acute β-Blockade Increases Muscle Sympathetic Activity and Modifies Its Frequency Distribution

et al. 2004

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Background-The possible mechanisms by which ␤-adrenergic antagonists may act on the neural regulation of the cardiovascular system are still elusive. Recent studies reported a marked increase of postganglionic muscle sympathetic nerve activity (MSNA) after acute ␤-blockade associated with unchanged values of arterial blood pressure and baroreflex sensitivity. We tested the hypothesis that acute ␤-blockade might also alter the oscillatory characteristics of MSNA, thus decreasing its effectiveness on peripheral vasoconstriction. Methods and Results-In 11 healthy volunteers, ECG, MSNA, arterial pressure, and respiration were recorded before and after atenolol (0.05 mg/kg IV bolus) administration. The frequency distribution of RR interval, MSNA, systolic arterial pressure (SAP), and respiratory variability was assessed by spectrum and cross-spectrum analysis. Spontaneous baroreflex sensitivity (␣-index) and plasma catecholamines (high-performance liquid chromatography) were measured. Atenolol induced a significant increase in RR interval (14.3Ϯ1.6%) with no changes in systolic and diastolic arterial pressure. MSNA increased (42Ϯ13% from 18Ϯ2 bursts per minute). The low-frequency (LF) component of RR and MSNA variability decreased (Ϫ44Ϯ7% and Ϫ24Ϯ5%, respectively), whereas the high-frequency (HF) component increased (163Ϯ55% and 34Ϯ11%, respectively), expressed in normalized units. Spectral coherence, an index of oscillatory coupling, decreased between LF RR and LF MSNA , whereas it increased between HF MSNA and HF Resp . SAP variability, ␣-index, and plasma catecholamines remained unchanged. Conclusions-Atenolol induced a change in MSNA frequency distribution reflecting a stronger respiratory coupling. This shift toward high frequency, despite an increase in MSNA, may lead to a less efficient sympathetic vasomotor modulation.

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Section: Cogliati Et Al Msna Variability and Acute ␤-Blockade 2789mentioning

confidence: 79%

Acute β-Blockade Increases Muscle Sympathetic Activity and Modifies Its Frequency Distribution

et al. 2004

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“…A spectral decomposition algorithm 23 was used to measure the centered frequency and the area below the spectral peaks in the respiratory band (near 0.27 Hz). The respiratory oscillations in the R-R interval (ie, RSA) and SBP (ie, Ludwig waves, SBP-HF) spectra were identified by means of cross-spectral analysis 24 (expressed in ms 2 and mm Hg 2 , respectively).…”

Section: Spectral Analysismentioning

confidence: 99%

“…To assess the relations between signals in the respiratory band, we performed autoregressive bivariate spectral analyses between the R-R intervals and RESP (R-R-RESP), SBP and RESP (SBP-RESP), and R-R intervals and SBP (R-R-SBP) as in previous studies 24,25 by use of the squared coherence function (K 2 ) to evaluate the phase stability between the oscillations of 2 signals (range: 0, no relation to 1, close relation) at any frequency and phase function (⌽; range Ϫ180°to ϩ180°). When ⌽ was negative, the first signal was considered as following the second, and vice versa.…”

Section: Cross-spectral Analysismentioning

confidence: 99%

Respiratory Systolic Pressure Variability During Atrial Fibrillation and Sinus Rhythm

et al. 1999

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Abstract-Previous studies have found that respiratory variations of ventricular response in atrial fibrillation are infrequent and inconsistent. This asynchrony between heart rate and respiration may characterize the physiological mechanisms coupling heart rate and systolic blood pressure oscillations in the respiratory band. The aim of this study was to evaluate whether synchronous variations in systolic blood pressure and respiration depend on a simultaneous change in heart rate. Univariate and bivariate spectral analyses were made of the R-R interval, systolic blood pressure, and respiratory signals during controlled respiration (16 breaths/min) in 24 patients with atrial fibrillation before and after efficacious electrical cardioversion and in 24 age-and sex-matched control subjects. During atrial fibrillation, the spectral coherence between respiration and heart rate was low (0.18Ϯ0.03), but there was a high level of coherence between respiration and systolic blood pressure (0.67Ϯ0.05). After cardioversion, the coherence between respiration and heart rate increased to 0.86Ϯ0.04, whereas the geometric mean values of the concomitant respiratory systolic blood pressure oscillations decreased by 72% (from 21.1 to 5.9 mm Hg 2 , PϽ0.001), which was similar to that observed in the control group (5.7 mm Hg 2 ). These results confirm the inconsistent effect of respiration on heart rate response during atrial fibrillation and demonstrate that respiratory sinus arrhythmia is not a prerequisite for systolic blood pressure oscillations but may play an antioscillatory role in respiratory systolic blood pressure variability, which is probably mediated by arterial baroreflex mechanisms. (Hypertension. 1999;34:1060-1065.) Key Words: arrhythmia Ⅲ blood pressure Ⅲ heart rate T he clinical hallmark of atrial fibrillation (AF) is an irregular ventricular rhythm. Few studies have investigated the respiratory oscillations of ventricular rhythm during AF, 1-3 and only 2 4,5 have made use of spectral analysis. These last 2 studies reported the presence of respiratory arrhythmia during AF in a small percentage of patients, but none measured respiration as a factor of analysis.The mechanisms underlying the origin of respiratory sinus arrhythmia (RSA) are still debated, but 2 main and not mutually exclusive theories have been put forward: One considers it to be the effect of cycling respiratory stimulation on arterial baroreceptors (the "peripheral" theory), and the other emphasizes the direct role of central respiratory drive (the "central" theory). Bivariate spectral analyses may quantify the relations between the heart period (R-R interval) and systolic blood pressure (SBP) but do not build causality between 2 signals: The spontaneous relation between the R-R interval and SBP fluctuations is a closed loop, and crossspectral analysis is unable to separate the mechanical R-R-SBP feedforward by baroreflex feedback from SBP to R-R. 6 A number of methods 7-11 and models 12-15 for exploring the fundamental relations between R-R and SBP o...

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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: 95%

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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β-Blocker Effects on Respiratory Sinus Arrhythmia and Baroreflex Gain in Normal Subjects

Cited by 31 publications

References 44 publications

Acute β-Blockade Increases Muscle Sympathetic Activity and Modifies Its Frequency Distribution

Acute β-Blockade Increases Muscle Sympathetic Activity and Modifies Its Frequency Distribution

Respiratory Systolic Pressure Variability During Atrial Fibrillation and Sinus Rhythm

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

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