Impaired baroreflex control of vascular resistance and heart rate in acute myocardial infarction.

The baroreflex control of vascular resistance and heart rate was studied in 11 patients to determine whether it is impaired in patients with acute myocardial infarction. Reflex forearm vasoconstriction in response to lower body negative pressure at 40 mm Hg was less in the early convalescent phase (mean seven days) than in the late convalescent phase (mean 41 days). Pressor as well as vasoconstricting responses to the cold pressor test did not differ between the early and late convalescent phases. The slope of the regression line relating systolic blood pressure and the RR interval during a transient rise in blood pressure produced by intravenous phenylephrine was appreciably reduced in the early convalescent phase of myocardial infarction. These results suggest that baroreflex control of vascular resistance and heart rate is impaired in patients with acute myocardial infarction.     

Enalaprilat augments arterial and cardiopulmonary baroreflex control of sympathetic nerve activity in patients with heart failure

Objectives. This study sought to determine the effects of enalaprilat on reflex control of sympathetic nerve activity.Background. Angiotensin-converting enzyme inhibitors decrease mortality in patients with congestive heart failure. Their efficacy appears to be related importantly to antiadrenergic effects, the mechanism for which has not been determined. Because baroreflexes tonically inhibit sympathetic outflow, and baroreflexes are blunted in heart failure, we hypothesized that these agents reduce sympathetic activity by augmenting baroreflexes.Methods. We assessed baroreflex control sympathetic nerve activity and heart rate in patients with congestive heart failure and in control subjects before and after enalaprilat (0.02 mg/kg body weight intravenously). Arterial baroreflexes were perturbed by bolus administration of sodium nitroprusside and phenylephrine. Cardiopulmonary baroreflexes were perturbed by lower body negative pressure and head-down tilt. Muscle sympathetic nerve activity was recorded by microneurography.Results. Enalaprilat decreased systolic blood pressure in patients with heart failure and control subjects. Sympathetic nerve activity increased in control subjects but decreased in patients with heart failure after enalaprilat despite reductions in central venous pressure in this group. Baroreflex control of sympathetic nerve activity was unchanged by enalaprilat in control subjects. In patients with heart failure, both arterial and cardiopulmonary baroreflex control of sympathetic nerve activity was enhanced by enalaprilat. Baroreflex control of heart rate was unchanged by enalaprilat in either group.Conclusions. Enalaprilat augments both arterial and cardiopulmonary baroreflex control of sympathetic activity in heart failure. These augmented inhibitory influences are associated with a reduction in sympathetic outflow and may contribute to the beneficial effects of angiotensin-converting enzyme inhibitors in heart failure.     

Effects of exercise training on the heart rate variability and QT dispersion of patients with acute myocardial infarction.

Heart rate variability (HRV) reflects the autonomic tone of the heart, and QT dispersion reflects the regional inhomogeneity of ventricular repolarization. The purpose of the present study was to determine the effects of early exercise training on HRV and QT dispersion in patients with acute myocardial infarction (AMI). Forty patients (mean age: 59 years) with AMI were randomized to training rehabilitation (group Tr, n=20) or conventional rehabilitation (group C, n=20). Two weeks after AMI, group Tr underwent 10 min of exercise using a bicycle ergometer (80% of anaerobic threshold) twice a day. At the end of the second and fourth weeks, 12-lead and 24-h Holter ECGs were recorded. QT intervals were measured and corrected using Bazett's formula (QTc), and QTc dispersion (QTcd) was defined as the difference between maximum and minimum QTc. HRV was accessed by the high-frequency component (HF: 0.15-0.40 Hz) of the HRV power spectrum (parasympathetic activity) and the ratio of low frequency (0.04-0.15 Hz) to HF (L/H ratio: sympathetic activity). In group Tr, HF increased (82.5 to 131.1 ms2), the L/H ratio decreased (3.9 to 2.6), and QTcd decreased (77.2 to 57.2 ms). In group C, none of the indices changed. It was concluded that early exercise training improves sympathovagal balance and decreases QTcd, and may reduce the arrhythmogenic substrate following AMI.     

β—受体阻滞剂早期治疗对急性心肌梗死患者心率变异的影响

目的 研究早期使用β－受体阻滞剂对急民生心肌梗死患者心率变异的影响。方法 ４４例急性心肌梗死患者入院后随机分为β－受体阻滞剂治疗组（１８例）和对照组（２６例）。治疗组于即刻给予氨酰心安（１２．５～２５ｍｇ／天）,或美多心安（２５～５０ｍｇ／天）,余两组治疗相同,入院后１０～１４天行２４小时动态心电图检查,分别析时域指标ＳＮＤＤＳＤＡＮＮｒＭＳＳＤＰＮＮ５０,散点图指标ＶＬＩ,ＶＡＩ的变化,用配对ｔ     

Diet associated with exercise improves baroreflex control of sympathetic nerve activity in metabolic syndrome and sleep apnea patients

Sleep and Breathing - We tested the hypothesis that (i) diet associated with exercise would improve arterial baroreflex (ABR) control in metabolic syndrome (MetS) patients with and without...     

Insulin in the brain increases gain of baroreflex control of heart rate and lumbar sympathetic nerve activity

Chronic central administration of insulin increases the gain of baroreflex control of heart rate, but whether baroreflex control of the sympathetic nervous system is similarly affected is unknown. The sites and mechanisms by which brain insulin influences the baroreflex are also unclear. Therefore, the present study tested the hypothesis that acute infusion of insulin into the brain ventricles of urethane-anesthetized rats increases gain of baroreflex control of heart rate and lumbar sympathetic nerve activity and that this action is gender specific. Furthermore, to identify the location within the brain that mediates these effects, insulin was infused into either the lateral ventricle or the fourth ventricle. Lateral ventricular insulin infusion increased the gain of baroreflex control of heart rate (2.1+/-0.3 to 4.0+/-0.6 bpm/mm Hg; P<0.05) and sympathetic activity (2.3+/-0.3% to 4.8+/-1.1% control/mm Hg; P<0.05) within 60 to 90 minutes; however, the increase in heart rate gain was similar in males and females. Increases in the maximum of baroreflex control of heart rate (395+/-10 to 452+/-13 bpm; P<0.05) and of sympathetic activity (156+/-13% to 253+/-22% control; P<0.05) were also observed. In contrast, fourth ventricular insulin infusion failed to alter baroreflex function. In conclusion, increases in brain insulin act acutely in the forebrain to enhance gain of baroreflex control of heart rate and lumbar sympathetic nerve activity.     

Effect of exercise training on heart rate recovery in patients post anterior myocardial infarction

Background

Regular exercise training has been shown to reduce mortality, improve functional capacity; and control the risk factors in myocardial infarction (MI) patients. Heart rate recovery (HRR) is a strong independent mortality predictor in patients with previous MI.

Determination of exercise training heart rate in patients on beta-blockers after myocardial infarction.

BACKGROUND: In patients with coronary artery disease, the target intensity-level of exercise training is usually based on a training heart rate that aims to be close to the upper level of metabolic aerobic exercise. AIM: We intended to evaluate whether a training heart rate calculated with the Karvonen formula after a conventional exercise test is comparable with the heart rate at the anaerobic threshold in patients after myocardial infarction treated with beta-blockers and if not to propose a new formula. METHODS AND RESULTS: In this multicenter prospective study, 115 consecutive beta-blocked patients recovering from myocardial infarction performed a cardiopulmonary exercise test to determine the anaerobic threshold. The training heart rate determined by the Karvonen formula was compared with the heart rate at the anaerobic threshold in a derivation sample (n=58) and a validation sample (n=57) of patients. The Karvonen training heart rate was significantly lower than the heart rate at the anaerobic threshold (91+/-5 versus 102+/-17 bpm, P<0.0001) in the first sample of patients and this difference was clinically relevant in 40% of patients. Thus, a 'modified Karvonen training heart rate', equal to 0.8xx(maximum heart rate-resting heart rate)+resting heart rate, was calculated by linear regression in the derivation sample and prospectively assessed in the validation sample. The modified Karvonen training heart rate was closer to the heart rate at the anaerobic threshold than the Karvonen training heart rate, and the difference between the modified Karvonen training heart rate and the heart rate at the anaerobic threshold was clinically relevant in only 5% of patients. CONCLUSION: The Karvonen formula underestimates the heart rate at the anaerobic threshold in beta-blocked patients, which may lead to undertraining of patients with coronary artery disease; we propose another formula more adapted to these patients.     

Differential effects of captopril and nicardipine on baroreflex control of sympathetic nerve activity and heart rate in renal hypertension.

OBJECTIVE: To test the hypothesis that an angiotensin I converting enzyme inhibitor and a calcium channel blocker have different effects on the arterial baroreflex in renal hypertension. DESIGN AND METHODS: We examined the baroreflex control of renal sympathetic nerve activity and heart rate before and after blood pressure was reduced by a similar magnitude (11 +/- 1 mmHg) with intravenous captopril or nicardipine in two-kidney, one clip hypertensive (mean arterial pressure 92 +/- 2 mmHg, n = 12) and normotensive rabbits (mean arterial pressure 75 +/- 1 mmHg, n = 9) in the conscious state. Data obtained during activation and deactivation of baroreceptors were analysed with logistic function curves, and the maximum slope of the curve was taken as the sensitivity of the baroreflex. RESULTS: The maximum slopes of the curves relating mean arterial pressure to renal sympathetic nerve activity and to the heart rate in hypertensive rabbits were significantly smaller than the maximum slopes in normotensive rabbits. In renal hypertensive rabbits, the maximum slope of the mean arterial pressure-renal sympathetic nerve activity curve was increased with captopril compared with that with vehicle. In contrast, the maximum slope of the mean arterial pressure-heart rate curve was increased with nicardipine compared with that with vehicle. CONCLUSIONS: Our data indicating that the baroreflex control of renal sympathetic nerve activity was improved by captopril and that baroreflex control of the heart rate was potentiated by nicardipine suggest that these classes of antihypertensive agents had differential effects in conscious hypertensive rabbits.     

Acute effect of captopril administration on baroreflex sensitivity in patients with acute myocardial infarction

Depressed baroreflex sensitivity (BRS) after acute myocardialinfarction (AMI) is considered an indication of decreased vagaland/or increased sympathetic tone. To determine the effect ofangiotensin converting enzyme inhibitors (ACEI) on BRS afterAMI we studied 27 patients with a first Q wave AMI, no signsof heart failure and no history of arterial hypertension ordiabetes mellitus. An additional group of10 patients with thesame clinical characteristics served as controls. On the 5thday after the onset of AMI, three consecutive boluses of phenylephrinewere given intravenously and baseline BRS was taken as the meanslope of the linear regression lines of RR intervals over systolicblood pressure. QT interval was also measured and correctedaccording to Bazett's formula (QTc). Consequently, a singleoral dose of captopril 50 mg or placebo was given to treatmentor control group patients, respectively; BRS and QTc were reassessedlh later. One hour after captopril administration BRS increasedfrom 5.95±2.80 to 9.14±3.46ms.mmHg^–1 (P<0.0001);QTc increased from 414±46 to 425± 46 ms (P<0.0001),systolic blood pressure decreased from 125±19 to 115±15mmHg (P=0.0002), while heart rate did not change significantly.Baseline BRS was correlated only with age (r= 0.74, P<0.0001).In the control group, 1 h after placebo, no difference was observedin any variable compared to baseline. Captopril appears to improveBRS immediately in the early phase of AMI.     

Effect of exercise training on heart rate variability in patients with new-onset left ventricular dysfunction after myocardial infarction

BACKGROUND: Cardiac rehabilitation with exercise training alters sympathovagal control of heart rate variability (HRV) toward parasympathetic dominance in patients after acute myocardial infarction (MI). However, its effects on HRV in patients after MI with new-onset left ventricular dysfunction are yet unknown. We aimed to investigate the effects of 8 weeks of supervised, high-intensity exercise training on time- and frequency-domain measures of HRV in this selected patient population. METHODS AND RESULTS: Twenty-five men with an acute MI and a low ejection fraction were randomly assigned to enter or not to enter a training program in a regional rehabilitation center. HRV was evaluated before and after 1 and 2 months of training and at 12 months. Maximal exercise testing with respiratory gas exchange was performed at baseline and after training. Resting heart rate decreased (P <. 01) and the percentage of R-R intervals differing >50 ms from the preceding one (pNN50) increased (P <.05) after training. The standard deviation of R-R intervals (SDRR) tended to increase, but frequency-domain indexes remained unchanged. There was a significant decrease in SDRR (P <.05) and high-frequency power (P <.01) at 12 months in untrained patients. Exercise time increased by 38% and maximal oxygen uptake increased by 29% in the training group (P <. 01). CONCLUSIONS: Despite beneficial effects on clinical variables, exercise training did not markedly alter HRV indexes. A significant decrease in SDRR and high-frequency power in the control group suggests an ongoing process of sympathovagal imbalance in favor of sympathetic dominance in untrained patients after MI with new-onset left ventricular dysfunction.     

急性心肌梗塞患者心率变异性的分析

目的 探讨急性心肌梗塞患者的心纺变异性。方法 对３４例急性心肌梗塞（ＡＭＩ）患者及３０例正常对照者２４小时动态心电图进行分析,通过计算机人工确认窦性心博后,经计算机处理,算出心率变异（ＨＲＶ）的时域和频域的各项指标。结果 ＡＭＩ组与对照组的平均心动周期标准差（ＳＤＮＮ）、相邻Ｒ－Ｒ间期之差的均方根值（rＭＳＳＤ）、相邻 Ｒ－Ｒ间期差值〉５ｍｓ的百分比（ＰＮＮ５０）、低频（ＬＦ）、高频（ＨＦ）及ＬＦ／     

Early alterations of the baroreceptor control of heart rate in patients with acute myocardial infarction

Experimental coronary occlusion is accompanied by an acute impairment of the baroreceptor-heart rate reflex. This study was planned to determine whether this impairment also occurs in humans. In 30 patients admitted to a coronary care unit for an anterior (n = 14) or inferior (n = 16) transmural myocardial infarction (MI), we measured 1) the increase in RR interval induced by stimulating carotid baroreceptors through progressive reductions in neck chamber pressure, 2) the increase in RR interval induced by stimulating arterial baroreceptors through intravenous boluses of phenylephrine, and 3) the reduction in RR interval induced by deactivating arterial baroreceptors through intravenous boluses of nitroglycerin. Measurements were performed 49.5 +/- 2.4 hours (mean +/- SEM) after the MI. The results were compared with those of five age-matched patients admitted to the coronary care unit for chest pain and found free from ischemic heart disease. The sensitivity of the carotid baroreceptor-heart rate reflex (slope of the linear regression of RR interval over neck pressure changes) was markedly less in MI than in control patients (3.8 +/- 0.5 vs. 5.9 +/- 0.6 msec/mm Hg, p less than 0.05), the reduction being similar in patients with anterior and inferior MI. This was the case also for the baroreflex sensitivity measured by the phenylephrine and the nitroglycerin methods (slope of the linear regression of RR interval over systolic blood pressure changes). However, 10.2 +/- 0.3 days later, the baroreflex sensitivity measured by all three methods increased significantly (p less than 0.05 or 0.01) and became similar to that of control subjects, which showed no significant change from the early to the late period after admission into the coronary care unit. Thus, MI is accompanied by an acute marked impairment of the baroreceptor control of the heart in humans, and this is the case both for an anterior and an inferior MI. The impairment is largely transient in nature, however, and a clear-cut recovery of the baroreflex can be seen a few days later.     

Association of anxiety with reduced baroreflex cardiac control in patients after acute myocardial infarction

Background Although depression has been associated with increased mortality in patients after acute myocardial infarction (AMI), little is known about the effects of depression on autonomic nervous system control of heart rate. This study evaluated whether depression is associated with impaired baroreflex sensitivity (BRS) in patients with AMI. Methods Two hundred four hospitalized patients with AMI were evaluated 6 ± 3 (mean ± SD) days after AMI. BRS was assessed using cross-spectral analysis to measure baroreceptor-mediated R-R interval oscillations. Depression was determined using the Diagnostic Interview Schedule, and severity of depressive symptoms was measured with the Beck Depression Inventory. In order to adjust for possible differences in anxiety, we also measured state anxiety using the Spielberger State Anxiety Inventory. Results Depression was not significantly related to BRS. However, anxiety was significantly related to low BRS in multivariate analysis, after the potentially confounding variables of age, blood pressure, and respiratory frequency were controlled for. Comparison of groups with high and low anxiety (on the basis of a median split of state anxiety scores) showed that BRS was reduced by approximately 20% in the patients with the higher anxiety scores (4.7 ± 3.2 ms/mm Hg vs 5.7 ± 3.3 ms/mm Hg, P < .05), after adjustment for differences in age, blood pressure, and respiratory frequency. Conclusions High levels of anxiety, but not depression, are associated with reduced vagal control in patients after AMI. (Am Heart J 2002;143:460-6.)     

The effect of intravenous amiodarone on heart rate in patients with acute myocardial infarction or ischemia and sinus tachycardia

The effect of intravenous (IV) amiodarone (300 mg) on heart rate was investigated in 22 patients with acute myocardial infarction (18) or ischemia (4) and sinus tachycardia. There were 11 men and 11 women (age range, 48 to 83 years; mean, 63.5). Amiodarone IV slowed the mean heart rate from 109 +/- 14 beats/min to 94 +/- 15 beats/min (p less than 0.0005). There was a linear correlation between the initial heart rate (preamiodarone) and the final heart rate (postamiodarone), (r = 0.6930, p less than 0.0005). Most of the patients with initial heart rates higher than the mean maintained relatively high heart rates (above the mean), while most patients with lower initial heart rates showed low heart rates (below the mean) after amiodarone administration. Patients in Killip class 1 showed a significant reduction in heart rate after receiving amiodarone, from a mean of 105 +/- 10 to 88 +/- 11 beats/min (p less than 0.01). Patients in Killip class 2 also had reduced heart rates (118 +/- 14 to 81 +/- 39 beats/min), but these changes were not statistically significant. Of the three patients in Killip class 3 to 4, the heart rate slowed by 10 beats/min in one, while in the remaining two no changes were observed. There were no significant side effects from the administration of amiodarone.     

Effects of long-term exercise training on autonomic control in myocardial infarction patients

Autonomic dysfunction, including baroreceptor attenuation and sympathetic activation, has been reported in patients with myocardial infarction (MI) and has been associated with increased mortality. We tested the hypotheses that exercise training (ET) in post-MI patients would normalize arterial baroreflex sensitivity (BRS) and muscle sympathetic nerve activity (MSNA), and long-term ET would maintain the benefits in BRS and MSNA. Twenty-eight patients after 1 month of uncomplicated MI were randomly assigned to 2 groups, ET (MI-ET) and untrained. A normal control group was also studied. ET consisted of three 60-minute exercise sessions per week for 6 months. We evaluated MSNA (microneurography), blood pressure (automatic oscillometric method), heart rate (ECG), and spectral analysis of RR interval, systolic arterial pressure (SAP), and MSNA. Baroreflex gain of SAP-RR interval and SAP-MSNA were calculated using the α-index. At 3 to 5 days and 1 month after MI, MSNA and low-frequency SAP were significantly higher and BRS significantly lower in MI patients when compared with the normal control group. ET significantly decreased MSNA (bursts per 100 heartbeats) and the low-frequency component of SAP and significantly increased the low-frequency component of MSNA and BRS of the RR interval and MSNA. These changes were so marked that the differences between patients with MI and the normal control group were no longer observed after ET. MSNA and BRS in the MI-untrained group did not change from baseline over the same time period. ET normalizes BRS, low-frequency SAP, and MSNA in patients with MI. These improvements in autonomic control are maintained by long-term ET. These findings highlight the clinical importance of this nonpharmacological therapy based on ET in the long-term treatment of patients with MI.     

心率水平对急性心肌梗死患者长期预后的影响

目的:观察急性心肌梗死(AMI)患者出院时心率水平与预后的关系。方法:连续入选2003年至2004年我院AMI患者904例,随访728例,根据出院时心率水平分为55～70次/min(A组)、71～80次/min(B组)、81～90次/min(C组)及>90次/min(D组)4组,随访4.5年。结果:1.随出院时心率水平的增加,3～4年时左心室射血分数(LVEF)明显降低,D组及C组因心力衰竭再次心肌梗死,心绞痛再住院率及1年、2年及3年病死率显著高于A组与B组,差异有统计学意义(P<0.05)。2.多因素分析结果显示出院时心率水平是随访期间再住院率及病死率的独立影响因素(OR=1.645,95%CI:1.390～3.018,P=0.005)。结论:过快的心率是AMI患者死亡及再住院的强预测因子,对AMI患者应严格控制心率,从而改善预后。