Influence Of Beta-blockade Research Articles

The influence of beta-blockade on the hemodynamic effects of levosimendan in elderly (>= 70 years) patients with acutely decompensated systolic heart failure

The purpose of this study was to evaluate the influence of chronic beta-blockade on the hemodynamic parameters in elderly (>or= 70 years) patients with acutely decompensated systolic heart failure treated with levosimendan. Eighteen patients with acutely decompensated systolic heart failure (8 on chronic beta-blockade) were included in this study. Inclusion criteria were symptoms and signs of acute heart failure in the presence of: a) left ventricular ejection fraction < 0.35; b) cardiac index < 2.5 l/min/m2, c) pulmonary capillary wedge pressure > 15 mmHg; and d) systolic blood pressure between 90 and 110 mmHg. After completion of baseline hemodynamic measurements, a levosimendan intravenous infusion was started (initial loading dose given as an infusion of 24 microg/kg over 10 minutes, followed by a continuous infusion of 0.1 microg/kg/min for 24 hours). At the end of levosimendan infusion hemodynamic measurements were repeated. Demographic characteristics as well as baseline systolic and diastolic blood pressure were not significantly different between patients not receiving beta-blockers (Group A) and those under beta-blockade (Group B), whereas heart rate was significantly lower in the latter. Treatment with levosimendan was associated with an increase in the cardiac index and a decrease in wedge pressure in both groups (Group A: 43.8% and 33%; p < 0.001 vs. baseline; Group B: 17.72% and 17.5%, p < 0.001 vs. baseline, respectively). Peripheral and pulmonary resistance significantly decreased in both groups (31% vs. 15%, p < 0.001 and 44.5% vs. 25%, p < 0.001, respectively). Thus, the beneficial hemodynamic effects of levosimendan are maintained in elderly patients with acute decompensated systolic heart failure treated with beta-blockers.

The prognostic value of the heart rate response during exercise and recovery in patients with heart failure: Influence of beta-blockade

Background The heart rate increase during exercise (ΔHR) and heart rate recovery (HRR) have demonstrated prognostic value in several investigations, but its application in the heart failure (HF) population is limited, particularly in a beta-blocked (BB) cohort. Methods Five-hundred and twenty subjects with HF underwent cardiopulmonary exercise testing to determine peak oxygen consumption (VO 2), the minute ventilation/carbon dioxide production (VE/VCO 2) slope, ΔHR and HRR at 1 min (HRR 1). Results There were 79 cardiac-related deaths during the tracking period. A HRR 1 threshold of </≥ 16 beats/min was a significant prognostic marker in the overall group (hazard ratio: 4.6, 95% CI: 2.8–7.5, p < 0.001) as well as no-BB (hazard ratio: 9.1, 95% CI: 4.1–20.2, p < 0.001) and BB (hazard ratio: 2.9, 95% CI: 1.6–5.4, p < 0.001) subgroups. The ΔHR was a significant univariate predictor in the overall group and no-BB subgroup only. Multivariate Cox regression analysis revealed HRR 1 was the strongest prognostic marker (chi-square: 39.9, p < 0.001). The VE/VCO 2 slope (residual chi-square: 21.8, p < 0.001) and LVEF (residual chi-square: 9.6, p = 0.002) were also retained in the regression. Conclusions These results indicate that HRR maintains prognostic value in HF irrespective of BB use. The routine inclusion of HRR in the prognostic assessment of patients with HF may be warranted.

Abstract 3038: Influence Of Beta-blockade On Mitral Regurgitant Volume In Patients With Degenerative Mitral Valve Prolapse

Introduction: Beta-blockers may be indicated for treatment of hypertension or atrial arrhythmias in patients with degenerative mitral valve prolapse (MVP) and moderate-severe mitral regurgitation (MR). However the influence of beta-blockade on the mitral regurgitant volume is uncertain. Methods: The influence of metoprolol on regurgitant volume was studied in 25 asymptomatic patients with moderate-severe MR due to MVP in a randomized double-blind cross over study. Metoprolol or placebo were titrated by an independent investigator according to symptoms, blood pressure and resting heart rate (mean dose 119mg, range 23.75 to 195mg/day). Severity of MR was assessed by cardiac magnetic resonance imaging (MRI) and echo-Doppler after 10 –14 days on each treatment. Regurgitant fraction was calculated using MRI from the difference between stroke volume by LV volumetry and aortic forward flow by phase contrast analysis. Results. Conclusion: Although metoprolol decreased heart rate and systolic blood pressure it does not influence the mitral regurgitant volume in patients with degenerative mitral valve prolapse.

724 Influence of beta-blockade on results of low-dose dipyridamole echocardiography tests for myocardial viability

724 Influence of beta-blockade on results of low-dose dipyridamole echocardiography tests for myocardial viability

Effect of Beta-Blockade on Postexercise Oxygen Uptake Kinetics in Patients with Chronic Heart Failure

Background: Beta-blocking agents have recently been demonstrated to improve survival in chronic heart failure (CHF), but a debate exists regarding the influence of beta-blockade on exercise capacity in these patients. The time delay for oxygen uptake to return to baseline after exercise (VO₂ recovery kinetics) has been shown to be related to the severity of CHF, skeletal muscle metabolic abnormalities and prognosis. We performed the present study to determine the effect of beta-blockade on VO₂ recovery kinetics in patients with CHF. Methods: Twenty-five patients with CHF were randomized to 6 months of bisoprolol (n = 10, ejection fraction = 27 ± 6%) or placebo (n = 15, ejection fraction = 25 ± 5%) therapy. Bisoprolol dosage was titrated in accordance with the Cardiac Insufficiency Bisoprolol Study protocol. Before and after the study period, oxygen uptake kinetics in recovery from maximal exercise were calculated and expressed as the slope of a single exponential relation between oxygen uptake and time during the first 3 min of recovery. Results: Resting and maximal heart rates were reduced after bisoprolol therapy, by 17 (p < 0.05) and 14 (p = 0.08) beats/min, respectively. Maximal oxygen uptake was unchanged in the bisoprolol (19.0 ± 4.9 vs. 19.9 ± 4.3 ml/kg/min) and placebo (18.9 ± 3.6 vs. 19.4 ± 3.6 ml/kg/min) groups. The time constants in recovery were reduced by modest and insignificant amounts in both groups (127.2 ± 41 vs. 112.6 ± 27 s for bisoprolol and 119.5 ± 55 vs. 97.3 ± 31 s for placebo). The time constant in recovery was poorly related to peak VO₂ (r = –0.10). Conclusion: In patients with CHF, beta-blockade does not influence exercise capacity or oxygen uptake recovery kinetics. While this study confirms the suppression of sympathetic drive which has been shown to have beneficial effects in CHF, these results suggest that beta-blockade has minimal effects on indices of exercise tolerance, including VO₂recovery time.

The QRS score: a promising new exercise score for detecting coronary artery disease based on exercise-induced changes of Q-, R- and S-waves: a relationship with myocardial ischaemia.

Recently, a new exercise test criterion diagnosing coronary artery disease was proposed, based on a composite of changes in Q-, R- and S-waves: the QRS score. We compared this new criterion with conventional ST-segment depression and other compositions of Q-, R- and S-wave changes in patients and normals and related the QRS score to reversible thallium-201 scintigraphic defects and ST-segment depression as markers for ischaemia. The influence of beta-blockade on the QRS score was also studied. The study population consisted of 155 persons with 53 normals (group I) and 102 patients with documented coronary artery disease (group II). Another 20 patients (group III) with proven coronary artery disease and a positive exercise test by ST-segment criteria were studied for the influence of beta-blockade on the QRS score. A symptom-limited exercise protocol according to the modified Bruce protocol was used. For the QRS score, Q-, R- and S-wave amplitudes which could be recovered immediately were subtracted from pretest values: delta Q, delta R, delta S respectively. The score was calculated by the formula: (delta R - delta Q - delta S)AVF + (delta R - delta Q - delta S)V5. Using a cut-off point of > 5 as normal, the QRS score resulted in a sensitivity of 88.2%, a specificity of 84.8% and a predictive accuracy of 87.1%. For ST-segment depression these values were 54.9%, 83% and 64.5% respectively (P < 0.001 compared to the QRS score). Predictive accuracies of changes in Q-, R- and S-waves in leads AVF and V5 separately, combinations of changes and combining the two leads, resulted-with the exception of solitary S-wave changes-in predictive accuracies higher than those of ST-segment depression, but all were lower than the QRS score. We found a significant correlation between the QRS score, the summed ST-segment depression (P < 0.004) and the extent of reversible thallium-201 defects (P < 0.001). Applying Bayes' theorem, the combination of an abnormal QRS score and ST-segment depression resulted in the highest post-test risk for coronary artery disease and a normal QRS score without ST-segment depression in the lowest post-test risk. The QRS score and the maximal ST-segment depression changed significantly under the influence of beta-blockade (P < 0.02 and P < 0.001 respectively). Our data suggest that an abnormal QRS score reflects myocardial ischaemia. Furthermore, for the interpretation of the exercise test, the combined analysis of ST-segments and the QRS score is of value for the prediction of the presence or absence of coronary artery disease and its follow-up.

Influence of beta-blockade on ejection fraction, ANP, and cGMP in patients after myocardial infarction

Influence of beta-blockade on ejection fraction, ANP, and cGMP in patients after myocardial infarction

Influence of beta blockade on exercise capacity and heart rate response after human orthotopic and heterotopic cardiac transplantation

It has been reported that use of β blockers may not be safe after cardiac transplantation because the denervated hearts may be largely dependent on circulating catecholamines to increase cardiac output. Therefore, the effects of intravenous propranolol were studied during maximal treadmill exercise in 7 patients with heterotopic and 6 with orthotopic cardiac transplantations. An average decrease of about 15% in exercise duration (p < 0.001), a 34% reduction in systolic blood pressure increase (p < 0.05) and a 40% attenuation in heart rate increase (p <0.001) were observed after β blockade. In patients with heterotopic transplantation, β blockade produced similar effects on heart rate m the denervated donor hearts and the innervated recipient hearts during and after mild exercise. During peak exercise, β blockade attenuated the rate to a greater extent in the donor hearts. Although the denervated donor heart is more sensitive to β blockade than the innervated recipient heart during exercise, no adverse effects were observed. Beta-blocker therapy should be considered for cardiac transplant patients if longer-term studies confirm their safe use in these patients.

Does beta adrenergic blockade influence the prognostic implications of post-myocardial infarction exercise testing?

The influence of beta blockade on the ability of ST depression, during pre-discharge exercise testing, to predict coronary anatomy and subsequent complications was studied in 300 consecutive post-infarct patients, 125 of whom underwent cardiac catheterisation. At the time of exercise 62 patients were taking a beta blocker. The exercise test had a higher sensitivity in predicting multivessel disease in patients who were not taking beta blockers than in patients who were (95% v 76%). beta Blockade did not, however, influence the ability of the test to identify patients at risk of subsequent cardiac events (sensitivity 84% and 85% respectively). These results suggest that it is not necessary to stop treatment with beta blockers before predischarge exercise testing of patients who have had an acute myocardial infarction.

Influence of beta blockade and intrinsic sympathomimetic activity on hemodynamics, inotropy and respiration at rest and during exercise

The degree of intrinsic Sympathomimetic activity (ISA) is reported to influence the effects of β blockade at rest, but the effects during exercise are not well documented. Heart rate, blood pressure and left ventricular (LV) function (as assessed by systolic time intervals) were measured at rest and during upright bicycle exercise as well as with flow-volume spirometry at rest in 13 healthy volunteers. The measurements were performed before and 4 and 24 hours after a single oral dose of pindolol (10 mg), nadolol (80 mg) and acebutolol (400 mg) in a double-blind, randomized, crossover manner. All drugs reduced heart rate, but nadolol had the most pronounced and longest bradycardic effect at rest. Diastolic blood pressure was only slightly influenced by the drugs, whereas systolic pressure was significantly lower compared with control values, especially during exercise (p < 0.001). Neither preejection period (PEP) nor LV ejection time (LVETc) was changed at rest after pindolol, but PEP increased and LVETc decreased significantly after nadolol (p < 0.05 for PEP and p < 0.01 for LVETc) and acebutolol (p < 0.05 for both). During exercise, PEP and LVET were significantly longer after all 3 drugs compared with control values. Only nadolol, which lacks ISA, significantly decreased expiratory flow values (p < 0.05). Thus, unlike the other β blockers, pindolol (with strong ISA) did not depress LV function at rest, while during exercise all 3 β blockers had equal adverse effects. The degree of ISA appears to be important in determining the hemodynamic effects of β-blocking drugs.

Physical training under the influence of beta-blockade in rats. III. Effects on muscular metabolism.

Rats were trained by daily running exercises for 7 weeks. In addition, one group of rats was trained under the influence of propranolol, while another group received daily injections of propranolol only. None of the treatments used had influence on the activities of myocardial enzymes: 3-hydroxyacyl-CoA - dehydrogenase (HADH), succinate dehydrogenase (SDH), malate dehydrogenase (MDH), and citrate synthase (CS) which were assayed for estimating oxidative capacity, or lactate dehydrogenase (LDH) which was used as a measure of anaerobic capacity. Training without propranolol resulted in elevated activities of the oxidative enzymes in M. extensor digitorum and in M. soleus. The corresponding changes in the rat group trained with propranolol always were much smaller, despite an equal amount of training. Only the trend for lowered activity of LDH was observable in skeletal muscle of the rat groups trained both with and without propranolol. Long-term beta-blockade alone did not induce enzymatic changes. It is concluded that a functioning sympathetic nervous system is necessary for the adaptive responses of muscular metabolism to training. Blockade of the sympathetic influence during exercise periods also hampers the training-induced responses.

Role of the Systemic Vasculature in the Hemodynamic Response to Changes in Plasma Ionized Calcium

Hemodynamic consequences of sustained (one hour) hypocalcemia and hypercalcemia (plasma ionized calcium concentration [Ca++] maintained approximately 60% below or above normal, encompassing the clinical range) were studied and the influence of beta blockade on these hemodynamic alterations examined in 16 anesthetized, closed-chest dogs. Alterations in [Ca++] were associated with directionally similar changes in mean arterial pressure, whereas on the average cardiac output remained unchanged. Thus, the peripheral vasculature played an important role in the hemodynamic response to alterations in [Ca++]. The state of beta adrenergic activity was an important determinant of the hemodynamic response to hypocalcemia. Prior to beta blockade, hypocalcemia was associated with decreased systemic vascular resistance, whereas after beta blockade with propranolol hydrochloride, systemic vascular resistance was not different from control except at the five-minute observation period, and cardiac output and stroke volume fell.

Physical training under the influence of beta-blockade in rats. II: Effects on vascular reactivity

Rats were treated by daily swimming or running exercises for 7 weeks. One group of rats was also trained under the influence of propranolol, while another group received daily propranolol injections only. The rat groups trained without beta blockade maintained a higher tail skin temperature when exposed to 5 degrees C after the 7-week training period. This phenomenon was not observable in the animals having received their training under the influence of beta-blockade. Both rat groups trained without beta-blockade showed increased vasodilatatory response to isoprenaline, as judged from a higher elevation of the tail skin temperature in response to the drug. This response was absent in the animal group having performed its training periods under the influence of propranolol. After the injection of phenylephrine the trained rats had a higher tail skin temperature than did the controls or propranolol-treated rats. The present results suggest an elevated sensitivity of beta 2-adrenoceptors and/or decreased sensitivity of alpha-adrenoceptors in trained rats. It is suggested that for the development of these changes repeated activation of the sympathetic nervous system by exercise periods is needed. That is why they are preventable if the training is performed under the influence of beta-blockade.

Extracellular potassium activity changes in the canine myocardium after acute coronary occlusion and the influence of beta-blockade

Extracellular potassium activity before and after coronary occlusion was measured in the canine heart by means of potassium-selective surface electrodes. In the ischaemic myocardium potassium activity rapidly increased from a preocclusion value of 3.2 +/- 0.3 mmol.litre-1 to 10 +/- 0.6 mmol.litre-1 within the first 5 min and to about 11.3 +/- 0.5 mmol.litre-1 after 10 min of ischaemia (range from 9.5 to 14.5 mmol.litre-1). Following the initial 10 min of ischaemia no further increase was measured. In the non-ischaemic area potassium activity remained constant. Acute beta-blockade significantly attenuated the initial rate of increase in potassium activity; however, beta-blockade did not influence maximal values of extracellular potassium activity measured after occlusion. Lowering of heart rate by vagal stimulation did not modify the pattern of increase in potassium during acute ischaemia. Following ventricular fibrillation, a slow but continuous rise in potassium activity was found. These results demonstrate that extracellular potassium activity in the acutely ischaemic myocardium is considerably higher than indicated by the technique of coronary vein sampling and is in the range necessary for the development of re-entrant arrhythmias in the early phase after coronary occlusion.

Physical training under the influence of beta blockade in rats: effect on adrenergic responses.

Rats were trained by daily swimming or running exercises with and without daily propranolol injections. Both training methods resulted in cardiac enlargement, but only swimming exercise caused hypertrophy of the brown adipose tissue. These changes were antagonized by beta blockade. The size of the adrenals reflected the stress of the treatments, but other known stress parameters, such as the size of the thymus or sexual organs dit not. Only swimming training without beta blockade sensitized the rats to the calorigenic action of noradrenaline. The cooling rate of the rats in water, when taking into account the insulative capacity of the body, was decreased in swimming-trained as well as in propranolol-treated rats but increased in running-trained rats. The latter two changes may be due to circulatory alterations, while the delayed body cooling in swimming-trained rats probably results from increased heat production capacity. Training-induced resting bradycardia and enhanced tachycardic response to isoprenaline were observable only in the animal groups trained without beta blockade. The pressor response to noradrenaline tended to be higher in the trained groups and the propranolol-treated group than in the controls and was smaller in the animal groups trained under the influence of beta blockade. On the other hand, the hypotonic response to isoprenaline was smaller in the propranolol-treated and running-trained animals. The results emphasize the importance of the sympathetic nervous system in the adaptation of an organism to physical training.

The renin-angiotensin-aldosterone system in hypertension: its biochemistry and applications.

SummaryThe biochemical action of renin on its substrate (angiotensinogen) leads to the formation of angiotensin I which is converted by angiotensin converting enzyme (kininase II) into the vasoactive peptide angiotensin II which has many biological functions. Another angiotensin converting enzyme (tonin) forms angiotensin II directly from renin substrate.Indirect means of assessing the plasma renin level have been developped such as plasma renin activity (PRA) and renin concentration assayed after acidification of the plasma to pH 3.3 (PRC3.3). The PRA and PRC3.3 determinations give concordant findings in normal subjects on a regular and a low sodium diet and in hypertensive patients on a regular diet and/or after sodium-volume depletion. The relationship between PRA or PRC3.3 on the one side and urinary sodium excretion, age or plasma aldosterone concentration on the other side is of the same magnitude. However PRA and PRC3.3 determinations can give discordant findings in conditions such as influence of beta-blockade, effect of exercise, renal vein plasma renin levels, infusion of saralasin and females on oral contraceptives.The diagnostic and prognostic value of plasma renin determinations are also reported: hyperaldosteronism, renovascular hypertension, predictive value of renin determinations in the hypotensive effect of beta-blockers or diuretics, renin secreting tumors and renin as risk factor for stroke and heart attack.

Calorigenic responses to cold of rats after prolonged infusion of norepinephrine.

ARTICLESCalorigenic responses to cold of rats after prolonged infusion of norepinephrineAC Hsieh, and JC WangAC Hsieh, and JC WangPublished Online:01 Jul 1971https://doi.org/10.1152/ajplegacy.1971.221.1.335MoreSectionsPDF (673 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited BySympathoadrenal SystemCold acclimation increases physiological responsiveness to intraventricular injection of β-endorphin in pentobarbital anaesthetized rats12 January 2009 | International Journal of Peptide and Protein Research, Vol. 24, No. 1Cold acclimation increases physiological responsiveness to intraventricular injection of β-endorphin in pentobarbital anaesthetized rats. 1. Cardiovascular functions12 January 2009 | International Journal of Peptide and Protein Research, Vol. 23, No. 4Endurance training augments the stimulatory effect of epinephrine on oxygen consumption in perfused skeletal muscleActa Physiologica Scandinavica, Vol. 120, No. 4Nonshivering thermogenesisBrain Research Bulletin, Vol. 12, No. 2Autonomic Regulation of ThermogenesisTemperature responses of rats to treadmill exercise, and the effect of thermoregulatory capacityActa Physiologica Scandinavica, Vol. 115, No. 1Physical training under the influence of beta-blockade in rats. II: Effects on vascular reactivityEuropean Journal of Applied Physiology and Occupational Physiology, Vol. 42, No. 3Physical training under the influence of beta blockade in rats: Effect on adrenergic responsesEuropean Journal of Applied Physiology and Occupational Physiology, Vol. 41, No. 3Effects of cold-acclimation on β-adrenergic receptors of rabbit carotid arteryGeneral Pharmacology: The Vascular System, Vol. 10, No. 3Metabolic and cardiovascular responses to prolonged noradrenaline load and their antagonism by beta blockade in the ratActa Physiologica Scandinavica, Vol. 104, No. 4Changes in interscapular brown adipose tissue of the rat during perinatal and early postnatal development and after cold acclimation VI. Effect of hormones and ambient temperatureInternational Journal of Biochemistry, Vol. 5, No. 1Lipid metabolism during cold-exposure and during cold-acclimationLipids, Vol. 7, No. 5Changes in interscapular brown adipose tissue of the rat during perinatal and early postnatal development and after cold acclimation. V. Adenyl cyclase, cyclic amp, protein kinase, phosphorylase, phosphorylase kinase, and glycogenInternational Journal of Biochemistry, Vol. 3, No. 14 More from this issue > Volume 221Issue 1July 1971Pages 335-337 Copyright & PermissionsCopyright © 1971 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1971.221.1.335PubMed5555805History Published online 1 July 1971 Published in print 1 July 1971 Metrics

Throxine and noradrenaline on noradrenaline sensitivity, cold resistance, and brown fat.

Throxine and noradrenaline on noradrenaline sensitivity, cold resistance, and brown fat.

Role of the sympathicoadrenal system in the hemodynamic response to exercise in dogs.

ARTICLESRole of the sympathicoadrenal system in the hemodynamic response to exercise in dogsE Ashkar, JJ Stevens, and BA HoussayE Ashkar, JJ Stevens, and BA HoussayPublished Online:01 Jan 1968https://doi.org/10.1152/ajplegacy.1968.214.1.22MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByThe Autonomic Nervous SystemEffects of hypoxia on catecholamine and cardiorespiratory responses in exercising dogsRespiration Physiology, Vol. 61, No. 2Effect of prolonged physical training on the histochemically demonstrable catecholamines in the sympathetic neurons, the adrenal gland and extra-adrenal catecholamine storing cells of the ratJournal of the Autonomic Nervous System, Vol. 10, No. 2Physical training under the influence of beta blockade in rats: Effect on adrenergic responsesEuropean Journal of Applied Physiology and Occupational Physiology, Vol. 41, No. 3Role of adrenaline in gas exchanges and respiratory control in the dog at rest and exerciseRespiration Physiology, Vol. 30, No. 3Effect of chemical sympathectomy on coronary flow and cardiovascular adjustment to exercise in dogsPflügers Archiv, Vol. 341, No. 4Effect of Prolonged Physical Training on the Catecholamine Levels of the Heart and the Adrenals of the RatActa Physiologica Scandinavica, Vol. 82, No. 2Untersuchungen über die Kollateralenentwicklung am gesunden Herzen nach körperlichem Training More from this issue > Volume 214Issue 1January 1968Pages 22-27 Copyright & PermissionsCopyright © 1968 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1968.214.1.22PubMed5634529History Published online 1 January 1968 Published in print 1 January 1968 Metrics