J-Tc间期延长对冠心病诊断的价值

评价J-Tc间期延长在冠心病诊断中的价值,对5组人的Q-Tc间期和J-Tc间期进行了比较,结果表明CLBBB组,心肌病组和非冠心病的左室肥厚劳损组的Q-Tc间期明显长于正常组,而J-Tc间期却与正常组相近。冠心病的慢性冠状动脉功能不全组及急性心肌梗死(AMI)充分发展期组Q-Jc及J-Tc间期均明显长于正常组。认为J-Tc间期是慢性冠状动脉功能不全及AMI发展期的可靠诊断指标。     

糖尿病性植物神经病变的QT间期延长:心脏猝死的一种可能原因

现已发现各种疾病中QT间期异常与心脏猝死有关,尽管导致QT间期缩短或延长的机理尚不明确,但植物神经张力对QT间期的影响已被公认.本文研究伴有不同程度植物神经病变的糖尿病人在安静时(平卧、坐位和站立)和活动时(Velsalva动作)QT间期的变化。病人和方法:将糖尿病人(年龄42±12岁)分     

J-Tc间期在冠心病诊断中的价值

为评价J-Tc间期对冠心病的诊断价值,对6组人的Q-Tc间期和J-Tc间期进行了比较,结果表明即肺心病组、CLBBB组、心肌病组和非冠心病的左室肥厚、劳损组的Q-Tc间期明显长于正常组,J-Tc间期却与正常组相近。冠心病组的慢性冠不全组及AMI充分发展期组Q-Tc及J-Tc间期均明显长于正常组。故认为J-Tc间期是慢性冠不全病及AMI发展期的可靠诊断指标。     

慢性丙型肝炎后肝硬化患者心电图改变与Child-Pugh分级相关性

目的探讨慢性丙型肝炎(CHC)后肝硬化患者心电图改变与Child-Pugh分级和肝硬化性心肌病(CCM)之间的关系。方法设立健康对照组(51例)、CHC组(45例)、CHC后肝硬化组(51例)。CHC后肝硬化组按照Child-Pugh分级标准又分为Child-Pugh A级14例,Child-Pugh B级20例,Child-Pugh C级17例。所有病例使用日本光电心电图机ECG-1550P标准12导联同步心电图机记录、测量、分析心电图,比较各组心电图改变的差异及与Child-Pugh分级和CCM发病的关系。结果1心电图异常:CHC后肝硬化组心电图异常率为72.55%,总心电图异常例次112,平均每例患者有2.20次异常心电图;健康对照组、CHC组心电图异常率分别为1.96%、6.66%,均为轻微异常心电图。2CHC后肝硬化主要心电图异常种类:Q-T间期延长(28/51,54.90%),ST-T改变(27/51,52.94%),肢导低电压(17/51,33.33%),说明3种异常心电图组合较为常见。3CHC后肝硬化组患者心电图异常组合与Child-Pugh分级之间的关系:Child-Pugh A级Q-Tc间期延长0例(0/14),ST-T改变1例(1/14),肢导低电压1例(1/14);Child-Pugh B级Q-Tc间期延长13例(13/20),ST-T改变11例(11/20),肢导低电压5例(5/20);Child-Pugh C级Q-T间期延长15(15/17),ST-T改变15例(15/17),肢导低电压11例(11/17)。结论 CHC后肝硬化患者存在多种心电图异常,其中以Q-Tc间期延长、ST-T改变、肢导低电压为主,出现3种心电图异常组合且肝功能为Child-Pugh B级、ChildPugh C级,且并发CCM,对判断CHC后肝硬化预后具有重要提示作用。     

七氟醚诱导对老年人Q—T间期的影响

目的 评估七氟醚诱导对老年人Q-T间期的影响.方法 40例行择期手术的老年患者,ASAⅠ～Ⅱ级,年龄65～75岁,术前心电图无异常,随机分为两组,A组(七氟醚组, n=20),B组(异丙酚组,n=20).分别于麻醉前、诱导后2、5、10、30 min行心电图检查,记录心率(HR)、Q-T间期,计算Q-Tc.结果 诱导5 min后七氟醚组Q-T间期和Q-Tc显著延长(P＜0.05);异丙酚组Q-T间期有降低趋势,但无统计学意义(P ＞0.05).结论 七氟醚诱导使老龄患者Q-T间期延长,在临床应用中应引起重视.     

肝硬化患者心电图Q—Tc间期延长的临床意义

目的探讨肝硬化患者Q-Tc间期变化及相关影响因素。方法检测125例肝硬化患者与50例非肝硬化患者心电图Q-Tc、凝血酶原时间（PT）、血清白蛋白（Alb）、血清总胆红素（TBil）、血清钾、血清钙、丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）、γ-谷氨酰转肽酶（GGT）和碱性磷酸酶（ALP）等指标,组间比较Q—Tc的变化及肝功能、不同Child分级间Q-Tc异常率,采用单因素直线相关回归分析探讨Q-Tc与各项相关指标的关系。结果肝硬化组Q-Tc为（440±15）ms,非肝硬化组为（405±13）ms,两组比较P〈O．001;以Q-Tc≥440ms为异常,肝硬化组异常率为37．90％（47／125）,非肝硬化组为12．00％（6／50）,两组比较P〈0．001。肝硬化组中ChildC级的Q-Tc异常率为72．50％（25／34）,B级为41．50％（19／45）,A级为28．37％（13／46）;A级与C级比较P〈0．01。单因素直线相关回归分析结果显示,Q-Tc与Child积分呈正相关,相关系数r=0．31（P〈0．01）;与腹水程度呈正相关,相关系数r=0．24（P〈0．05）;与血清总胆红素（TBil）呈正相关,相关系数r=0．23（P〈0．05）。结论肝硬化存在Q-Tc异常延长,病因是多因素性的,随肝硬化病情加重,Q-Tc异常率升高。Q-Tc延长是引起室性心律失常的常见诱因,可能也是肝硬化患者出现猝死的原因之一。     

陈旧性心肌梗塞患者Q-Tc延长与室性心律失常的关系

本文分析139例OMI患者的DCG和常规ECG资料,以探讨Q-Tc间期延长与室性心律失常的关系,发现有复杂室性心律失常者47例,Q-Tc的均值为0.426±0.039秒;而非复杂室性心律失常者92例,Q-Tc均值0.403±0.047秒(P<0.005)。Q-Tc≥0.440秒者34例,其中18例(52.9％)有复杂室性心律失常;Q-Tc<0.440秒者105例,仅29例(27.6％)有复杂室性心律失常(P<0.001)。结果表明OMI患者若Q-Tc延长则易发生复杂室性心律失常。     

急性心肌梗塞J—Tc间期延长与住院期猝死的关系

急性心肌梗塞(AMI)时由于心室肌复极延迟,致 Q-Tc 和 J-Tc 间期延长,临床研究已证实,AMI 时 Q-Tc 间期延长可诱发致命性心律失常,且是心原性猝死的危险因素。J-Tc 间期能更好地反映心室肌复极状况,其与 AMI住院期猝死的关系,目前尚无报道。作者分析测定255例 AMI 患者的心电图 J-Tc 间期,初步探讨 AMI 时 J-Tc 间期延长与住院期猝死的关系。对象和方法1.观察对象 1984年1月—1992年6月入 CCU 治疗 AMI 的患者291例(均按     

2型糖尿病患者胃动力学与植物神经病变关系的探讨

目的研究胃动力障碍及植物神经病变与2型糖尿病(DM2)的关系。方法采用半流质核素胃排空试验对129例DM2患者的胃动力进行了研究,同时还用Ewing法对心血管植物神经功能、用B超对膀胱残余尿量、用神经病星对外周神经进行定量测定。结果糖尿病胃排空延迟发生率为62.02％。植物神经病变呈弥漫性分布,随病程延长而加重。胃动力异常者,其植物神经病变发生率较胃动力正常者显著增高。结论DM2胃动力异常及植物神经病变发生率均明显增高,二者显著相关。故早期进行胃排空试验,并同时对其它植物神经功能进行测定,对糖尿病胃及神经并发症的早期防治有重要意义。     

糖尿病心脏植物神经功能障碍与尿流率测定的关系及其临床意义

根据心脏植物神经功能试验，将５０例糖尿病患者分为功能正常组（Ⅰ组）１１例，轻度异常组（Ⅱ组）１８例，重度异常组（Ⅲ组）２１例。尿流率测定结果表明三组排尿量（Ｖ）、最大尿流率（ＭＦＲ）及平均尿流率（ＡＰＲ）均低于对照组。Ⅱ组的ＭＦＲ和ＡＦＲ低于Ⅰ组，Ⅲ组最低。最大尿流率时间（ＭＦＲＴ）和排尿总时间（ＶＴ）在Ⅱ、Ⅲ组中延长。三组ＭＦＲ的异常发生率分别为３６．４％、６１．１％和９５．２％；ＡＦＲ为２７．２％、４４．４％和８５．７％；ＶＴ为１８．２％、２７．８％和６１．９％。揭示心脏植物神经功能异常者大多有尿流率异常，病程长、病情重及伴有其他并发症者尤为显著。     

Relationship Between Autonomic Function and Progression of Renal Disease in Diabetic Proteinuria: Clinical Correlations and Implications for Blood Pressure Control

The objective off this study was to test the relationship between neurologic and microvascular complications of type 1 diabetes mellitus. It was hypothesized that the mechanisms operative in autonomic dysfunction seen in diabetic patients with microangiopathy play a role in the rapidity of progression to renal failure. Twenty-six type 1 diabetic patients with proteinuria were studied with computerized monitoring of heart rate variation during timed ventilation, assumption of upright posture, and Valsalva maneuver and with 24-h ambulatory blood pressure monitoring at baseline. Renal function was evaluated over the ensuing 12 months of intensive insulin therapy. Blood pressure was treated so as to achieve consistent 24-h readings < 140/90 mm Hg. Angiotensin converting enzyme inhibitors were the preferred antihypertensive agents. Serial serum creatinine concentrations were compared using repeated measures analysis of variance. Over 12 months there were no significant serum creatinine changes for any autonomic test group with normal results at baseline. Groups with abnormal autonomic results at baseline demonstrated statistically significant increases in serum creatinine over 12 months compared to their baseline. Of the tests, Valsalva separated groups of patients with similar degrees of baseline renal impairment. Each of the sympathetic plus Valsalva combinations demonstrated a significant difference in progression of serum creatinine increase over 12 months. In each instance, if both sympathetic and Valsalva results were abnormal, there was a statistically significant increase in serum creatinine over 12 months when compared to groups in which one or both test results were normal. There is a relationship between autonomic function and the progression of renal dysfunction. The inability to vary the heart rate to a Valsalva maneuver identifies a degree of parasympathetic dysfunction that permits unopposed sympathetic tone, heralding more rapid renal destruction. A simple inexpensive bedside laboratory test discerned a relatively low-risk group of diabetic patients with proteinuria that demonstrated no deterioration in renal function over 12 months. When the Valsalva maneuver was markedly abnormal the presence of a mean arterial pressure > 100 mm Hg was associated with a greater likelihood of rapid renal deterioration. This group at higher risk of renal deterioration should undergo aggressive lowering of mean arterial blood pressure to <95 mm Hg.     

QT prolongation on the electrocardiogram in diabetic autonomic neuropathy

Patients with Type 1 diabetes and autonomic neuropathy have an increased risk of sudden death for which the mechanism remains obscure. Prolongation of the QT interval on the electrocardiogram may occur with sympathetic dysfunction and is also associated with ventricular arrhythmia and sudden death. We have therefore measured the QT interval in patients with Type 1 diabetes with normal, borderline, and definitely abnormal autonomic function tests and in non-diabetic control subjects. The maximum QT interval was measured on 12-lead electrocardiograms recorded at rest and then plotted against the RR interval. The QT interval was above the upper 95% limit for the non-diabetic control subjects in 5 diabetic patients with abnormal autonomic function tests (33%), but in no cases with normal or borderline tests. Multivariate analysis confirmed that autonomic score contributed significantly (p less than 0.025) to the variance in QT interval. The raw Valsalva ratio alone also contributed significantly to the variance in QT interval (p = 0.025). Heart rate variability, heart rate response to standing, age, sex, and the presence of symptoms of autonomic neuropathy did not contribute significantly.     

Ventricular arrhythmias and Q-Tc interval during stress-ECG

Q-T prolongation is well-known to be related to ventricular arrhythmias in a number of clinical circumstances. The purpose of this study was to determine whether heart rate corrected Q-T interval (QTc) may indicate susceptibility to ventricular arrhythmias during stress testing. QTc was determined at rest, during submaximal and maximal bicycle work load in normals and patients with remote myocardial infarction, documented coronary artery disease (CAD) and in a group of patients with different cardiac diseases and premature ventricular beats during exercise testing (PVC). Ventricular arrhythmias were graded according to Lown. Q-Tc interval significantly increased in all groups of those patients having complex ventricular arrhythmias (Lown greater than or equal to III). In patients with ischemic S-T segment depression during stress testing, QTc was only lengthened if complex ventricular arrhythmias were present. Q-Tc lengthening in stress testing is assumed to be associated with occurrence of ventricular premature beats rather than ischemia. There is evidence that abnormal repolarization due to imbalance of the autonomic nervous system induces ventricular arrhythmias. Monitoring of Q-Tc interval during stress testing is warranted and may be useful to predict future cardiac events such as sudden cardiac death.     

Exertional myocardial ischemia in diabetes: a quantitative analysis of anginal perceptual threshold and the influence of autonomic function

Patients with diabetes are prone to silent myocardial infarction and silent exertional ischemia. Although the mechanism is not clear, it may reflect a specific impairment of the sensory innervation of the heart. To test this hypothesis, anginal perceptual threshold was measured in 32 diabetic patients and 36 nondiabetic control patients, all of whom had typical exertional angina. Anginal perceptual threshold was defined as the time from onset of 0.1 mV ST depression to the onset of chest pain during treadmill stress electrocardiography. Although ST depression occurred earlier in the diabetic than in the nondiabetic group (111 +/- 82 versus 216 +/- 162 s, p less than 0.005), the anginal perceptual threshold in the diabetic group was delayed by a mean of 86 s (149 +/- 76 versus 63 +/- 59 s, p less than 0.001), with 95% confidence intervals of 53 to 119 s. Autonomic function tests were abnormal in the diabetic group, and in both groups regression analyses (using a third order polynomial) showed marked prolongations of anginal perceptual threshold as the heart rate responses to the Valsalva maneuver decreased to below the normal range (r = 0.5, p less than 0.001). There was a similar though less pronounced relation between anginal perceptual threshold and the heart rate responses to deep breathing (r = 0.3, p less than 0.02). These data suggest that prolongation of the anginal perceptual threshold may be caused by autonomic neuropathy involving the sensory innervation of the heart. To test sensory function, median nerve conduction studies were performed in 19 patients (10 diabetic and 9 nondiabetic).(ABSTRACT TRUNCATED AT 250 WORDS)     

Relationship Between Autonomic Function and Plasma Fibrinogen,Viscosity, and Elements of Fibrinolytic Activity in Diabetic Nephropathy

Twenty-three insulin-dependent diabetics with proteinuria (3.3 g/day: range 0.3 to 8.9) and azotemia (creatinine clearance: 58 mL/min, range 30 to 112) were tested for 24-h mean arterial blood pressure; instantaneous heart rate variations to a computerized protocol involving timed ventilation, assumption of upright posture, and Valsalva maneuver; plasma fibrinogen, viscosity, fibrinolytic activity, and plasminogen activator inhibitor. These were to test the hypothesis that autonomic dysfunction is associated with altered concentrations of plasma fibrinogen, fibrinolytic activity, viscosity, and plasminogen activator inhibitor. We have previously shown the absence of a correlation between level of blood pressure, clinical and standard laboratory testing, and the results of the autonomic function testing protocol used in this study. In this group of patients, plasma fibrinogen concentration was correlated (positively) with mean arterial pressure and (negatively) with heart rate variation in response to the Valsalva maneuver. The greater the mean arterial pressure or the worse the Valsalva results, the higher the plasma fibrinogen concentration. In addition, patients with one or no abnormal autonomic function tests had a mean fibrinogen of less than 400 mg/dL compared to the group of patients with two or more abnormal tests who had a mean fibrinogen of 500 mg/dL. In patients with demonstrated parasympathetic abnormalities, postural heart rate variation testing also discerned a differential in plasma fibrinogen. Lower concentration of plasminogen activator inhibitor throughout the day, and greater fibrinolytic activity in the morning were also noted to be present in patients with abnormal heart rate response to the Valsalva maneuver. We conclude that there are relationships between high blood pressure, autonomic function, and hemostatic factors favoring thrombogenesis that may be related by common mechanisms and treatments in the diabetic with kidney disease.     

Rapid autonomic tone regulation of atrioventricular nodal conduction in man

The changes in P-P intervals and atrioventricular nodal (AVN) conduction during the Valsalva maneuver were studied in 17 patients. In spite of a significant decrease in the sinus P-P interval during phase II of the maneuver (733 +/- 143 to 520 +/- 86 msec, p less than 0.005) and prolongation during phase IV (884 +/- 171 msec, p less than 0.01), there was no change in the AH interval (control: 78 +/- 15: phase II: 76 +/- 15: phase IV: 72 +/- 14 msec, N.S.). In six patients consecutive P-P intervals during phase II were recorded in solid-state memory and were used to trigger pacing of the high right atrium at rest. This showed a significant increase in the AH interval (75 +/- 10 to 123 +/- 45 msec, p less than 0.05). Valsalva maneuver during constant rate atrial pacing resulted in a significant decrease in the AH interval during phase II (115 +/- 36 to 80 +/- 15 msec, p less than 0.001). During phase IV there was prolongation of the AH interval (156 +/- 58 msec) but in 11 patients (61%) a variable degree of Wenckebach periodicity appeared. Thus autonomic tone modulates the changes in AVN conduction induced during physiologic heart rate variation, resulting in maintenance of adequate 1:1 AVN conduction.     

Assessment of cardiovascular tests in the diagnosis of diabetic autonomic neuropathies

Eight tests for cardiovascular reflex function were evaluated in a group of 140 diabetic patients. The sensitivity, reproducibility and normal values of each test were previously assessed in a group of 70 normal controls. The measure of the R-R interval variation during six cycles of deep breathing (expiration/inspiration ratio) proved to be the most sensitive test, and was selected for screening. The Valsalva ratio, the bradycardia/tachycardia ratio post-standing and the blood pressure response to standing and to sustained handgrip served as a confirmatory test of autonomic neuropathy and were related to the severity of the lesion. The R-R interval variation during one deep breathing cycle, the post-standing tachycardia, and the R-R 30/15 standing ratio proved to be of little or not value in assessing cardiovascular neuropathy. Cardiovascular autonomic neuropathy was diagnosed in 38.5% of our diabetic population, predominantly in patients with other clinical evidence of autonomic neuropathy. In a few asymptomatic patients, abnormal cardiovascular responses were the first evidence of autonomic lesion.     

Spectrum of dysautonomia in mitral valvular prolapse

PURPOSE: Symptoms suggesting altered autonomic regulation of cardiovascular function have been noted in some patients with mitral valvular prolapse (MVP) but may also occur in patients with other disorders. We evaluated cardiovascular responses to autonomic stimuli in 118 patients with symptoms of dysautonomia, 78 of whom had MVP, and 40 of whom did not, to determine if unique patterns of these responses distinguished patients in one symptomatic subgroup from another. SUBJECTS AND METHODS: The responses of patients to standing, quantitated Valsalva maneuver, facial immersion in ice water, and administration of isoproterenol, phenylephrine, and tyramine were compared with those in 12 asymptomatic patients with MVP and 23 normal volunteers. RESULTS: Constitutional, cardiovascular, and neuropsychiatric symptoms occurred with similar frequency in the two symptomatic patient groups. The most common pattern of abnormal responses in symptomatic patients with or without MVP was (1) an increased heart rate and elevated plasma norepinephrine levels while supine and then while standing quietly for five minutes, (2) an exaggerated increase in heart rate during phase II of Valsalva, (3) a diminished bradycardic response during phase IV of Valsalva, and (4) an exaggerated heart rate response to administration of isoproterenol. The increased heart rate during Valsalva, but not the exaggerated sensitivity to isoproterenol, was correlated with the magnitude of the chronotropic response to standing only in symptomatic patients with MVP. Exaggerated hypertensive overshoot during phase IV of Valsalva was observed in only a few symptomatic patients. No consistent pattern of these abnormalities, however, was noted in any of the patient subgroups. Hemodynamic responses to autonomic stimuli in asymptomatic MVP patients were generally indistinguishable from those observed in normal subjects. CONCLUSION: These findings suggest that abnormal cardiovascular responses to autonomic stimuli may occur in any patient with symptoms of dysautonomia regardless of the presence or absence of MVP and that the pattern of these abnormal responses may be diverse. It is therefore important to characterize the pattern of altered autonomic regulation of cardiovascular function in each patient when considering mechanistic implications or making therapeutic decisions about these patients.     

Detection of silent myocardial ischemia in diabetes mellitus

The prevalence of silent myocardial ischemia and its relation to autonomic dysfunction and pain threshold was studied in 58 men with diabetes mellitus and without cardiac symptoms. All patients underwent 48-hour ambulatory electrocardiographic monitoring and exercise testing after assessment of their autonomic function and pain threshold. Silent myocardial ischemia, defined as greater than or equal to 1 mm of ST-segment depression on either exercise testing or ambulatory electrocardiographic monitoring, was corroborated by exercise-induced reversible defect(s) on tomographic thallium scintigraphy. Autonomic function was assessed by heart rate response to: (1) Valsalva maneuver, (2) deep breathing, and (3) upright posture, as well as by diastolic blood pressure response to sustained handgrip and systolic blood pressure response to upright posture. Autonomic dysfunction was defined as greater than or equal to 2 abnormal responses. Pain threshold measurements were performed using electrical cutaneous stimulation of both forearms. Of the 58 diabetic patients, 21 were found to have autonomic dysfunction (36%). Silent myocardial ischemia was detected in 10 patients (17%), and was significantly more frequent in patients with than without autonomic dysfunction (38 vs 5%, p = 0.003). There was no difference in the electrical pain threshold or tolerance in subjects with and without silent myocardial ischemia. It is concluded that silent myocardial ischemia in asymptomatic diabetic men occurs frequently and in association with autonomic dysfunction, suggesting that diabetic neuropathy may be implicated in the mechanism of silent myocardial ischemia.     

Clinical and instrumental diagnosis of autonomic neuropathy in insulin-dependent diabetes

Summary The authors report a study of the relationship between symptomatic autonomic neuropathy and the response to simple cardiovascular autonomic tests (Valsalva maneuver, handgrip-test, detection of postural hypotension), in a large series of insulin-dependent diabetics (IDD). Symptoms of autonomic neuropathy were referred by 28 out of 130 IDD, prevalence and severity showed a clear relationship with the duration of diabetes. Only 4 out of 36 patients examined showed a pathologic response to the handgrip-test, while an abnormal Valsalva maneuver was evident in 24 out of 113 IDD. The data show that while the recognition of symptoms indicating a widespread autonomic derangement is rather easy, the diagnosis of autonomic neuropathy may be more difficult in the presence of mild or unspecific symptoms. The Valsalva maneuver exhibited the higher frequency of abnormal responses suggesting that the parasympathetic cardiovascular regulation may be impaired earlier than the sympathetic one. This early subclinical autonomic neuropathy may be due to metabolic or functional factors. Even if clinical consequences of an autonomic derangement of cardiovascular regulation may be serious, in our opinion subclinical impairment, being detectable in a large proportion of patients within the first year of disease, is unlikely to have a short-term severe prognostic value.