Electrocardiographic and vectorcardiographic findings in asymptomatic young men with primary T-wave abberations in the electrocardiogram. Relationship to sympatho-adrenal activity at rest and during different stress tests

Summary. Twelve asymptomatic men aged 18–19 years with flat, notched or inverted precordial T waves without concomitant ST depression (group T) were compared to thirteen age-matched controls with normal electrocardiograms (group C). Orthogonal leads, spatial vectorcardiography and sympatho-adrenal activity, as reflected by plasma catecholamines, were studied at rest and during mental stress (Stroop's colour word conflict test), isometric exercise (hand grip) and a cold pressor test. The groups had similar heart volumes and physical work capacity. Group T showed higher resting supine systolic blood pressure (140±15 mmHg vs. 121±8 mmHg, P<0·001) and plasma noradrenaline (1·82±0·79 nmol 1^-1vs. 1·25±0·49 nmol 1<sp>^-1, P<0·05) whereas heart rate, diastolic blood pressure and plasma adrenaline were similar in the two groups at rest. Increases in diastolic blood pressure and plasma adrenaline were larger in group T in connection with each of the stressful provocations. The magnitude of the T-wave aberrations in the electrocardiogram and the orthogonal leads in the vectorcardiogram as well as the spatial QRS-T angle were positively correlated to the plasma noradrenaline levels at rest. Changes of the T-wave aberrations in connection with stress were variable. The changes were positively correlated to heart rate and adrenaline during mental stress, to adrenaline during isometric exercise and to heart rate and noradrenaline during cold provocation. The present study demonstrates increased sympathetic tone at rest and increased reactivity in connection with stress in otherwise healthy young subjects selected on the basis of T-wave aberrations often considered as indicative of organic heart disease. The findings suggest that the T-wave aberrations were caused by increased sympathetic discharge.     

Assessment of systolic and diastolic function in heart failure using ambulatory monitoring with acoustic cardiography

INTRODUCTION. The circadian variation of heart function and heart sounds in patients with and without heart failure (HF) is poorly understood. We hypothesized HF patients would exhibit less circadian variation with worsened cardiac function and sleep apnea. METHODS. We studied 67 HF patients (age 67.4 ± 8.2 years; 42% acute HF) and 63 asymptomatic control subjects with no history of HF (age 61.6 ± 7.7 years). Subjects wore a heart sound/ECG/respiratory monitor. The data were analyzed for sleep apnea, diastolic heart sounds, and systolic time intervals. RESULTS. The HF group had significantly greater prevalence of the third heart sound and prolongation of electro-mechanical activation time, while the control group had an age-related increase in the prevalence of the fourth heart sound. The control group showed more circadian variation in cardiac function. The HF subjects had more sleep apnea and higher occurrence of heart rate non-dipping. CONCLUSIONS. The control subjects demonstrated an increasing incidence of diastolic dysfunction with age, while systolic function was mostly unchanged with aging. Parameters related to systolic function were significantly worse in the HF group with little diurnal variation, indicating a constant stimulation of sympathetic tone in HF and reduction of diurnal regulation.     

Assessment of systolic and diastolic function in heart failure using ambulatory monitoring with acoustic cardiography

Abstract

Introduction. The circadian variation of heart function and heart sounds in patients with and without heart failure (HF) is poorly understood. We hypothesized HF patients would exhibit less circadian variation with worsened cardiac function and sleep apnea. Methods. We studied 67 HF patients (age 67.4 ± 8.2 years; 42% acute HF) and 63 asymptomatic control subjects with no history of HF (age 61.6 ± 7.7 years). Subjects wore a heart sound/ECG/respiratory monitor. The data were analyzed for sleep apnea, diastolic heart sounds, and systolic time intervals. Results. The HF group had significantly greater prevalence of the third heart sound and prolongation of electro-mechanical activation time, while the control group had an age-related increase in the prevalence of the fourth heart sound. The control group showed more circadian variation in cardiac function. The HF subjects had more sleep apnea and higher occurrence of heart rate non-dipping. Conclusions. The control subjects demonstrated an increasing incidence of diastolic dysfunction with age, while systolic function was mostly unchanged with aging. Parameters related to systolic function were significantly worse in the HF group with little diurnal variation, indicating a constant stimulation of sympathetic tone in HF and reduction of diurnal regulation.     

Influence of age, the autonomic nervous system and anxiety on QT-interval variability

As QT variability increases and heart rate variability diminishes, the QT variability index (QTVI) - a non-invasive measure of beat-to-beat fluctuations in QT interval on a single ECG lead - shows a trend towards positive values. Increased QT variability is a risk factor for sudden death. Aging lengthens the QT interval and reduces RR-interval variability. In the present study we investigated the influence of aging and the autonomic nervous system on QT-interval variability in healthy subjects. We studied 143 healthy subjects, and divided them into two age ranges (younger and older than 65 years). For each subject we measured two QTVIs: from the q wave to the end of the T wave (QTeVI) and to the apex of the T wave (QTaVI). Both indexes were calculated at baseline and after sympathetic stress. In 10 non-elderly subjects, both QTVIs were determined after beta-adrenoreceptor blockade induced by intravenous infusion of propranolol or sotalol. The QTVI was higher in elderly than in younger subjects (P<0.001). QTVIs obtained during sympathetic stress remained unchanged in the elderly, but became more negative in the younger group (P<0.05). QTeVI and QTaVI at baseline were correlated positively with age (P<0.01) and anxiety scores (P<0.05), but inversely with the low-frequency spectral power of RR-interval variability (P<0.001). QTVIs were higher in subjects with higher anxiety scores. In younger subjects, sotalol infusion increased both QTVIs significantly, whereas propranolol infusion did not. In conclusion, aging increases QT-interval variability. Whether this change is associated with an increased risk of sudden death remains unclear. The association of abnormal QT-interval variability with anxiety and with reduced low-frequency spectral power of heart rate variability merits specific investigation. In healthy non-elderly subjects, acute sympathetic stress (tilt) decreases the QTVI. beta-Adrenoreceptor blockade inhibits this negative trend, thus showing its sympathetic origin. Because a negative trend in QTVI induced by sympathetic stress increases only in younger subjects, it could represent a protective mechanism that is lost with aging.     

Do elderly patients with an excessive fall in blood pressure on standing have evidence of autonomic failure?

1. Blood pressure, heart rate and plasma catecholamine responses were examined in two groups of elderly subjects distinguished by blood pressure responses to standing. Subjects in the control group showed a fall of less than 15 mmHg in systolic blood pressure on standing; subjects in the orthostatic hypotension group had falls of more than 20 mmHg systolic and 10 mmHg diastolic blood pressure on standing. 2. The heart pressure response on standing showed no significant difference between the two groups. 3. The orthostatic hypotension patients had lower plasma noradrenaline concentrations than the control patients (P less than 0.01) in the supine position, but during 10 min standing there was no significant difference in noradrenaline levels between the groups, and the percentage increase of noradrenaline levels in the orthostatic hypotension group was greater (P less than 0.05) than in the control group. 4. In the supine position, diastolic blood pressure was higher (P less than 0.05) in the orthostatic hypotension group than in the control group. 5. We conclude that impairment of baroreceptor function is not involved in most cases of orthostatic hypotension in the elderly, nor is there reduction of sympathetic nervous activity. We suggest that mechanical changes or adrenoreceptor dysfunction are more likely to be important factors in orthostatic hypotension in the elderly.     

Significant changes in systolic blood pressure post vectored upper cervical adjustment vs resting control groups: a possible effect of the cervicosympathetic and/or pressor reflex

OBJECTIVE: To determine whether a vectored adjustment of the atlas in patients identified as demonstrating signs of upper cervical joint dysfunction would cause lowering of blood pressure in comparison with resting controls. DESIGN: Test 1: controlled clinical trial with a treatment (adjustment) group and a control (resting) group. Test 2: controlled clinical trial with subjects serving as their own controls. SETTING: Private chiropractic practice. PARTICIPANTS: Test 1: Forty established patients demonstrating signs of upper cervical subluxation/joint dysfunction and 40 established patients without such signs. Test 2: Thirty established patients demonstrating signs of upper cervical subluxation/joint dysfunction. INTERVENTION: Specific, vectored upper cervical (atlas) adjustment or similarly positioned resting. MAIN OUTCOME MEASURES: Prerest, postrest, and postadjustment systolic, diastolic, and pulse rates as recorded through use of a digital oscillometric sphygmomanometer. RESULTS: In test 1, subjects receiving adjustment had a significant (P <.001) decrease in systolic blood pressure whereas resting subjects did not. Intergroup comparison of the treatment (adjustment) and control (resting) groups demonstrated a significant difference (P <.001). A greater pre/post drop in systolic pressure was associated with greater age and higher initial systolic pressure. In test 2, the pre/postrest change in systolic blood pressure was not significant. The systolic blood pressure changed significantly (P <.001) from postrest readings to postadjustment readings. CONCLUSION: The results indicate that palpation and vectored atlas adjustment causes a significant decrease in systolic blood pressure in patients with putative upper cervical subluxation/joint dysfunction in comparison with resting controls. Similar results were also demonstrated when subjects acted as their own controls. The lack of randomization, blinding, and a manipulated control group are factors that weaken these findings. The sudden drop in systolic pressure is proposed to be due to stimulation of the cervicosympathetic reflex or moderation of muscle tone and elimination of the effects of the pressor reflex.     

Effects of beta-adrenergic blockade on verapamil-responsive and verapamil-irresponsive sustained ventricular tachycardias.

To assess effects of beta-adrenergic blockade on ventricular tachycardia (VT) of various mechanisms, electrophysiology studies were performed before and after intravenous infusion of propranolol (0.2 mg/kg) in 33 patients with chronic recurrent VT, who had previously been tested with intravenous verapamil (0.15 mg/kg followed by 0.005 mg/kg/min infusion). In the verapamil-irresponsive group, 10 patients (group IA) had VT that could be initiated by programmed ventricular extrastimulation and terminated by overdrive ventricular pacing, and 11 patients (group IB) had VT that could be provoked by isoproterenol infusion (3-8 micrograms/min) but not by programmed electrical stimulation, and that could not be converted to a sustained sinus rhythm by overdrive ventricular pacing. Notably, in the group IA patients, all 10 patients had structural heart disease (coronary arteriosclerosis or idiopathic cardiomyopathy); beta-adrenergic blockade accelerated the VT rate in one patient but exerted no effects on the VT rate in the remaining 9 patients, and VT remained inducible in all 10 patients. By contrast, in the group IB patients, 7 of the 11 patients had no apparent structural heart disease; beta-adrenergic blockade completely suppressed the VT inducibility during isoproterenol infusion in all 11 patients. There were 12 patients with verapamil-responsive VT (group II). 11 of the 12 patients had no apparent structural heart disease. In these patients, the initiation of VT was related to attaining a critical range of cycle lengths during sinus, atrial-paced or ventricular-paced rhythm; beta-adrenergic blockade could only slow the VT rate without suppressing its inducibility. Of note, 14 of the total 33 patients had exercise provocable VT: two in group IA, five in group IB, and seven in group II. Thus, mechanisms of VT vary among patients, and so do their pharmacologic responses. Although reentry, catecholamine-sensitive automaticity, and triggered activity related to delayed afterdepolarizations are merely speculative, results of this study indicate that beta-adrenergic blockade is only specifically effective in a subset group (group IB) of patients with VT suggestive of catecholamine-sensitive automaticity.     

Changes in autonomic cardiovascular control in mid-pregnancy

Summary. Spectral analysis of heart rate variability was used to study autonomic nervous control in mid-pregnancy. Fifty women (age 22–36 years) with singleton pregnancies (mean duration of gestation 27.7 weeks) and 39 non-pregnant female controls (age 21–39 years) were studied using controlled breathing and orthostatic tests. During spontaneous breathing the overall heart rate variability was lower in pregnant subjects indicating a decreased parasympathetic tone at rest. The decreased parasympathetic tone probably counts for the increased heart rate in pregnancy. The parasympathetic efferent capacity of autonomic cardiac control was found to be similar in pregnant and non-pregnant subjects, as no difference was seen during controlled breathing in periodic heart rate variability between the groups. Standing up caused a similar change in low frequency and mid-frequency bands in both groups, but high frequency heart rate variability increased in pregnant subjects and decreased in the controls indicating an increased sympathetic tone at rest in mid-pregnancy.     

Beta blockade by oral propranolol and labetalol

beta-Adrenergic blockade after single, oral doses of labetalol or propranolol was evaluated in a double-blind, placebo-controlled study by an isoproterenol sensitivity test and handgrip exercise in 10 healthy men. The tests were performed with subjects resting in a supine position. At the doses used, there was no effect on heart rate and blood pressure in either the resting position or in the isometric exercise phase. It is possible that exercise-induced changes in blood pressure and heart rate were reduced by higher vagal tone in this young group tested in the supine position. Isoproterenol increased heart rate and reduced diastolic blood pressure in a dose-dependent manner. The dose of isoproterenol at which heart rate increased 25 bpm above the resting rate (CD25; 1.36 +/- 0.18 microgram) was of the order of that at which diastolic blood pressure fell 25 mm Hg from baseline (HD25; 1.07 +/- 0.07 microgram). There was a significant positive correlation between CD25 and HD25 in the 10 subjects. Propranolol and labetalol induced a dose-dependent, parallel shift to the right in the dose-response curves of isoproterenol effects on heart rate and diastolic blood pressure, indicating that both drugs are nonselective, competitive antagonists of beta-adrenergic receptors. On the average, propranolol was 17 and 19 times more potent than labetalol in antagonizing the chronotropic and hypotensive actions of isoproterenol, respectively.     

Modification by Beta-Adrenergic Blockade of the Circulatory Responses to Acute Hypoxia in Man

In 17 healthy men, beta-adrenergic blockade reduced significantly the tachycardia and the elevation of cardiac output associated with inhalation of 7.5% oxygen for 7 to 10 minutes.Hypoxia did not increase plasma concentrations of epinephrine or norepinephrine in six subjects. Furthermore, blockade of alpha and beta receptors in the forearm did not modify the vasodilation in the forearm induced by hypoxia, providing pharmacologic evidence that hypoxia of the degree and duration used was not associated with an increase in the concentrations of circulating catecholamines in man.Part of the increase in cardiac output and heart rate during acute hypoxia in man is produced by stimulation of beta-adrenergic receptors, probably by cardiac sympathetic nerves. The mechanism of the vasodilation in the forearm during hypoxia remains uncertain.     

Digital arterial tone in hypertensive subjects

Summary. The digital arterial tone has been measured in 12 consecutively referred hypertensive subjects before and after 8 weeks treatment with propranolol. Similar measurements were performed in 12 normotensive, age-matched controls. The study showed uniformly, that the digital arterial tone increased with falling local temperature applied at the digits (measured at 30, 20, 15, 10 and 5^o C). Among the untreated hypertensive subjects the digital arterial tone was significantly higher compared to normotensive controls. After treatment with propranolol a significant increase in digital arterial tone was demonstrated, and most pronounced among the patients complaining of tendency to cold fingers. Additional body-cooling increased arm and finger systolic blood pressure significantly, but not the digital arterial tone. The frequent Raynaud-like symptoms in patients treated with non-selective beta-adrenoreceptor blocking drugs seem to be due to blockade of peripheral beta-II adrenergic receptors giving rise to more pronounced alpha-mediated vasoconstriction.     

Adrenergic control of circulating lymphocyte subpopulations. Effects of congestive heart failure, dynamic exercise, and terbutaline treatment

The current studies were undertaken to explore the relationship between enhanced sympathetic nervous activity and lymphocyte subset distribution in three settings: congestive heart failure, dynamic exercise, and beta-adrenergic agonist treatment. We compared the number and subset distribution of circulating lymphocytes in 36 patients with congestive heart failure and 31 age-matched control subjects. The number of circulating lymphocytes was lower in heart failure than in control. This was due to a reduction in Tsuppressor/cytotoxic and natural killer cells without significant alteration of Thelper cells. The extent of the alteration was similar in patients with idiopathic and ischemic heart failure, but the reduction was more pronounced in patients with New York Heart Association class III-IV than in class I-II. The plasma catecholamine elevation in heart failure was also independent of etiology but more pronounced in the more severely ill patients. We also assessed lymphocyte subsets after acute stimulation of sympathetic activity by dynamic exercise and after treatment with the beta-adrenergic agonist terbutaline. Dynamic exercise until exhaustion increased the number of circulating lymphocytes in healthy controls and heart failure patients in a subset-selective manner. By contrast, a 7-d treatment with terbutaline caused a reduction in the circulating number of lymphocytes in some subsets that was identical to that seen in heart failure patients. We conclude that prolonged sympathetic activity reduces the number of circulating lymphocytes by a beta-adrenergic mechanism. Such alterations might be involved in the pathophysiology of heart failure and other disease states involving increased activity of the sympathetic nervous system.     

Interaction between autonomic tone and the negative chronotropic effect of adenosine in humans

Prior studies have demonstrated that sympathetic tone may influence the effects of adenosine on His-Purkinje automaticity, and that enhanced vagal tone may influence its effects on the sinus node. However, the interaction between autonomic tone and the effects of adenosine on the sinus node in humans remains unknown. Therefore, this study was designed to investigate the interaction between different states of autonomic tone and the bradycardiac response of the sinus node to adenosine. In 11 patients without structural heart disease who underwent a clinically indicated electrophysiology procedure, the sinus cycle length was measured before and after a 12-mg bolus of adenosine in the baseline state, during an infusion of 2 mcg/min of isoproterenol, after the administration of 0.2 mg/kg of propranolol, and again after the administration of 0.04 mg/kg of atropine. Adenosine significantly lengthened the sinus cycle length in the baseline state (760 +/- 165 vs 909 +/- 188 ms, P < 0.05), during isoproterenol infusion (516 +/- 67 vs 766 +/- 146 ms, P < 0.05), after propranolol (850 +/- 153 vs 914 +/- 143 ms, P < 0.05) and after the combination of propranolol and atropine (662 +/- 76 vs 801 +/- 121 ms, P < 0.05). The degree of lengthening in sinus cycle length was significantly greater (P < 0.05) during isoproterenol infusion (253 +/- 157 ms, or 51% +/- 40%) than in the baseline state (149 +/- 85 ms, or 20% +/- 12%), after propranolol (68 +/- 53 ms, or 8% +/- 8%), and after propranolol and atropine (140 +/- 110 ms, or 21% +/- 18%). The negative chronotropic effect of adenosine is influenced by autonomic tone. The effect of adenosine on the sinus node is accentuated by beta-adrenergic stimulation and unaffected by beta-adrenergic blockade or combined beta-adrenergic and cholinergic blockade.     

The central hypotensive effect of clonidine. Studies in tetraplegic subjects.

A single oral dose of 300 microng of clonidine lowered systolic blood pressure by 20 +/- 4 mm Hg and diastolic blood pressure by 13 +/- 4 mm Hg in five healthy normotensive subjects (controls). Heart rate fell from 56 +/- 2 to 52 +/- 2 beats/min. In six tetraplegic subjects with physiologically complete chronic cervical spinal cord transection above the level of the sympathetic outflow, the same dose of clonidine did not significantly lower either systolic or diastolic blood pressure. Heart rate fell from 67 +/- 4 to 53 +/- 2 beats/min. Peak plasma concentrations of clonidine, measured by mass fragmentography, and elimination of the drug from plasma were similar in tetraplegic and control subjects and there was no difference in the incidence of the principal side effects of clonidine--sedation and dry mouth. Although the number of subjects studied is small, the absence of a fall in blood pressure after clonidine in the tetraplegic subjects suggests that the hypotensive action of clonidine in man is dependent on intact descending bulbospinal pathways and is mediated by withdrawal of sympathetic tone and provides direct evidence that some antihypertensive drugs may lower blood pressure in man by a direct action on the brain.     

Qualitative and quantitative analysis of portal Doppler waveform and a novel factor of portal pulsatility: Systolic spike wave

Background We attempted to identify the physiologic circumstances associated with the portal Doppler waveform. Method The subjects were 98 patients: 42 had cirrhosis; 23, hepatitis; and 33, no liver disorder. We measured right portal venous peak velocity, minimum velocity, and hepatic arterial peak systolic velocity. Portal venous pulsatility was calculated as portal venous minimum velocity divided by portal venous peak velocity. We analyzed portal waveforms both qualitatively and quantitatively. Results Portal Doppler waveforms were classified as nonphasic, monophasic, biphasic, biphasic including spike wave, and triphasic. Portal waveforms were phasic in 84 subjects who had a mild systolic dip during the arterial systolic period. Markedly portal pulsatility (portal venous pulsatility<0.6) was present in only 7 subjects. A systolic spike wave corresponding to a hepatic arterial peak systolic wave was detected in 48 subjects. Hepatic arterial peak systolic velocity was significantly higher in the group with spike wave than in the group without it. Conclusion Although portal pulsatility is generally attributed to multiple factors, the present study has pointed out a new factor; transmission via the hepatic artery through the portal vein vasa vasorum. Hepatic venous drainage and hepatic arterial blood flow influence portal waveform.     

Mechanism of the postural vasoconstrictor response in the human foot

1. The mechanism of postural vasoconstriction in the skin of the foot was examined in 102 healthy subjects by using laser Doppler flowmetry. 2. In 45 subjects, when one foot was lowered 50 cm below heart level and the other foot kept horizontal, blood flow was progressively reduced in the dependent foot (by 79%) with a concomitant, but less pronounced, reduction in flow in the horizontal foot (by 18%), indicating that a central mechanism is involved. After lumbar sympathetic blockade (in 10 patients with epidural anaesthesia), the flow in the horizontal foot remained virtually constant, indicating that the central component is mainly mediated via efferent sympathetic nerves, whereas the postural fall in flow in the dependent foot, though partially attenuated, was preserved, indicating that a local mechanism is mainly involved. 3. On lowering one foot below heart level in 12 subjects, there was a small but significant reduction in systolic and mean arterial pressures during the first minute of dependency. During the fourth minute, systolic pressure decreased, diastolic pressure and heart rate increased, but the mean arterial pressure was maintained. 4. In 19 subjects postural vasoconstriction was nearly abolished during local nervous blockade (lignocaine 3.7 x 10(-4)-7.4 x 10(-2) mol/l), indicating that the local mechanism mediating the vasoconstriction is mainly neurogenic in nature. However, there was still a small fall (19%) in flow in the dependent foot during blockade, probably indicating a minor contribution of a local myogenic mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrocardiogram of young diabetic subjects

Standard 12-lead electrocardiogram patterns were studied in 100 Type I diabetic subjects aged 15-40 years and in 100 control subjects of the same age. Neither study group had evidence of clinical ischaemic heart disease or other systemic diseases which might affect cardiac function. The diabetic subjects had higher heart rates, lower electrocardiographic voltages and more T wave inversions than the controls. The diabetic women had longer QT intervals corrected for heart rate than the control women. The R-R interval variability (mean +/- S.D.) in the ECG was smaller in the diabetic subjects than in the controls (13 +/- 11 vs. 17 +/- 11%, p less than 0.05). Its magnitude was related to the heart rate variation in deep breathing, a measure of autonomic nervous function (r = 0.54, n = 50). The diabetic subjects with vagal autonomic neuropathy had an R-R interval variability of only 0-6%. The standard electrocardiograms of young asymptomatic diabetic subjects appear to differ in many respects from the those of healthy subjects in the same age group. The differences may reflect the presence of preclinical diabetic cardiovascular complications at an early age. A small or absent R-R interval variability helps to select patients for closer evaluation of autonomic function.     

组织多普勒成像技术评估慢性房颤患者左室壁运动

目的 应用组织多普勒成像技术（DTI）探讨慢性房颤患者的室壁运动特点,为临床诊治提供重要的信息,方法,将研究分为三组,A组为18例正常对照,B组为15例心房大小正常的房颤患者,C组为16例心房扩大的房颤患者,所有患者均无严重瓣膜病或节段性室壁运动异常,采用HP SONOS 5500超声显像仪和脉冲DTI,分别在心尖四腔心切面和胸骨旁长轴切面测定左室侧壁和后壁收缩期峰值速度（VS）,舒张期峰值速度（VE）,心电图QRS波起始至收缩期峰值速度的平均时间T1,心电图QRS波起始至舒张期峰值速度的平均时间T2,平均心率为R－R,结果 （1）A组正常人均有舒张早期和晚期两个波峰（E峰和A峰）,B组和C组房颤患者均只有一个舒张期波峰（E峰）,（2）A组与B组这间的DTI测值差异均无显著性意义（均为P＞0．05）,（3）C组左室侧的VS显著小于A组（P＜0．05）,C组左室后壁的VS,VE均显著大于A组（P均＜0．05）,C组侧壁的T1／（R－R）^1/2,Ts/(R-R)1/2显著高于A组（P均＜0．05）,C组后壁的T1／（R－R）^1/2,T2/(R-R)^1/2与A组比较差异无显著性意义（P均＞0．05）,结论 左房增大的房颤患者左室壁在长轴方向收缩活动减弱,舒张期峰值速度延迟,在短轴方向舒缝活动增强,DTI技术能精确地定量分析房颤患者的室壁活动,可成为评价房颤患者心肌舒缩功能的无创伤性新方法。     

Management of sympathetic overactivity in tetanus with epidural bupivacaine and sufentanil: experience with 11 patients.

OBJECTIVE: To determine the efficacy and safety of epidural bupivacaine and sufentanil for the management of sympathetic overactivity in tetanus. DESIGN: Retrospective case review. SETTING: Sixteen-bed surgical intensive care unit in a tertiary care centre. PATIENTS: All patients referred to the unit during a 63-month period with the diagnosis of tetanus were included in the study. MEASUREMENTS AND MAIN RESULTS: All patients (n = 11) had severe tetanus and developed sympathetic overactivity, which was managed by epidural blockade. Three patients died, but there were no fatalities directly attributable to sympathetic overactivity. Before epidural blockade, the average difference between the mean maximum and mean minimum systolic blood pressures was 78 +/- 28 (so) mm Hg. After blockade, this difference was reduced to 38 +/- 15 (so) mm Hg (p < .0001). Similar significant reductions in diastolic blood pressure and heart rate were observed. The mean hourly infusion doses of bupivacaine and sufentanil were 17 mg and 21 microg, respectively. Midazolam was the principal adjunctive sedative agent and was used in all patients (mean dose, 9 mg/hr). Additional pharmacologic agents were necessary in two patients in whom epidural blockade alone was insufficient to control sympathetic overactivity. One patient developed renal failure and there were no instances of pneumothorax. One patient developed an epidural abscess of probable hematogenous origin, which was successfully treated without neurologic sequelae. CONCLUSIONS: Epidural blockade is effective in controlling sympathetic overactivity and the associated complications (renal failure, cardiac injury, and sudden death). Although a serious complication occurred in one patient, the efficacy of the technique deserves further validation.     

Autonomic Nervous System Function in Migraine Without Aura

Autonomic nervous system functions were studied in 13 females with migraine without aura during headache-free intervals, using physiological, pharmacological and biochemical methods. Heart-rate in the resting condition and blood pressure rises in the cold-face and isometric handgrip tests were higher than in controls. Normal cardiovascular responses to the Valsalva manoeuvre and to noradrenaline infusion suggest that the baroreflex arc is intact. Normal heart rate responses to the Valsalva manoeuvre, to the cold-face test and to deep breathing confirmed a normal cardiac parasympathetic function. Clonidine infusion showed a sedative and depressor effect and an inhibition of plasma NA similar to those occurring in controls, suggesting a normal central sympathetic tone. As a whole, the physiological, pharmacological and biochemical tests were consistent with a non-specific sympathetic hyperactivity, but do not confirm any impairment of the autonomic control of the cardiovascular system in migraine patients in headache-free intervals.