老年人运动诱发心律失常

运动有益健康 ,然而不适当的运动则有害健康 ,甚至可促发疾病。作者对老年人运动诱发心律失常进行了观察。1　对象与方法1.1　对象　患者 32 (男 2 9,女 3)例 ,年龄 6 0～ 89(73± 6 )岁。既往病史中有高血压病 13例 ,冠心病 12例 ,肺心病 1例 ,无明确心脏病史者 6例。诱发心律失常的运动方式 :跑步者 15例 ,打拳者 12例 ,骑自行车者 3例 ,搬重物者 2例。1.2　方法　在安静状态下均有常规心电图记录 ,有心律失常者 3例。运动诱发心律失常均有即刻心电图记录或心电监护结果。运动前后心律失常率的比较用 χ2 检验。原发疾病诊断以《实用内科…     

遗传性心律失常综合征

心源性猝死是引起猝死的重要原因.约有10%～20%的心源性猝死患者没有器质性心脏改变[1],其中大部分为青年人.这类患者的共同特点是在运动、情绪激动或噪音刺激等情况下易诱发恶性室性心律失常而致晕厥甚至猝死.引起心律失常的原因多是编码心肌离子通道的基因发生异常改变,使得动作电位不同时相的离子通道功能改变而导致心室肌早或晚复极异常.这类疾病主要包括:Brugada综合征(Brugada syndrome),长Q-T间期综合征(long QT syndrome,LQTS),短QT间期综合征(short QT syndrome,SQTS),儿茶酚胺敏感多形性室速(catecholaminergic polymophic ventricular tachycardia,CPVT)等,统称为遗传性心律失常综合征,现就近期相关研究进展综述如下.     

平板运动试验诱发心律失常的特点分析

目的:分析平板运动试验诱发心律失常的特点。方法:选择1654例患者应用标准Bruce方案进行次极量或极量平板运动试验,同步监测12导联心电图和血压,记录运动前、运动中及恢复期的心电图和血压。结果:运动试验阳性304例,阴性1350例;运动诱发心律失常共234例,诱发率14.1%;阳性者心律失常60例(60/304,19.7%),明显高于阴性者174例(174/1350,12.9%,P0.01)。运动诱发偶发室早146例(8.8%),明显多于偶发房早52例(3.1%,P0.05)。运动诱发的心律失常185例(79.1%)在运动中和/或恢复期前期(前3min)出现,多于恢复后期(后3min)出现的49例(20.9%,P0.05)。运动诱发的心律失常在恢复期前期(前3min)/或恢复期后期(后3min)消失的(80.3%,188/234)明显多于超过6min消失的(19.7%,46/234,P0.05)。其中1例持续性室性心动过速者通过用药才能消失。结论:运动试验阳性者易诱发心律失常,以室性心律失常最为常见。运动诱发的心律失常多在运动中和/或恢复期前期出现,且大多可在恢复期消失,但有些严重的心律失常较难消失。     

平板运动试验诱发心律失常的特点及对原有心律失常的影响

目的探讨平板运动试验诱发心律失常的特点,以及对原有心律失常的影响。方法对4643例患者应用标准Bruce方案进行次极量平板运动试验,同步监测血压和12导联心电图,记录运动前、运动中及恢复期的血压和心电图。结果运动前原有心律失常176例,运动诱发心律失常504例。心律失常的发生与性别无关(P=0.318),运动试验阳性者心律失常发生率(20.8%)明显高于阴性者(13.8%),P<0.001。在运动中发生的心律失常多于恢复期,但无统计学意义(P>0.05)。运动前原有心律失常在运动中消失的比例室性心律失常(66.7%)明显多于房性心律失常(34.0%),P=0.002;而运动诱发的房性和室性心律失常多在恢复期消失(分别为73.08%和66.47%)。结论运动诱发的心律失常以室性心律失常最为常见,且大多可在恢复期消失,因此应高度重视恢复期的心电监测(至少10min)。     

食管心房调搏12830例分析

目的探讨经食管心房调搏(trans-esophageal atrial pacing,TEAP)对心律失常的诊断价值。方法对我院26年来临床有反复心悸、头晕、短暂晕厥症状的12 830例患者的食管心房调搏检查结果进行分析,了解不同心律失常的发生情况。结果心律失常的诱发率为61.23%,室上性心动过速的诱发率(50.35%)明显高于室速(1.23%);两者比较,差异有统计学意义(P<0.05)。经食管心房调搏超速抑制成功终止99.83%的室上速,失败占0.15%(患者自行要求终止,未列入统计范畴)。两者比较,差异有统计学意义(P<0.05)。全部患者在检查中均未出现严重并发症。结论经食管心房调搏诱发和抑制室上速是有效的无创性方法,可为临床进一步治疗提供可靠依据,值得大力推广与广泛应用。     

行为应激诱发心律失常的研究进展

行为应激是诱发心律失常的一个重要原因。尤其与室颤(VF)和心源性猝死(SCD)的心肌电稳定性改变有着十分密切的关系.然而,心理应激诱发心律失常的机制尚未完全阐明。随着医学模式的转变,对行为应激诱发心律失常的机制和早期预测预防的研究越来越受到人们的重视。本文就应激诱发心律失常的机制进行综述。一、历史回顾与实验方法早期应用动物的心肌损伤模型进行应激与心律失常的因果关系的研究。显然.这一研究方法并不适用。实验动物的应激心理特征与临床病人完全不同。研究发现SCD多由     

96例晕厥患者的病因分析

目的对晕厥患者进行病因分析,寻找晕厥诊疗方向。方法选择2014年1月1日~2016年12月21日以晕厥收入我院神经内科的患者96例,分析患者的病因构成。结果所有患者中,神经介导的反射性晕厥50例,占52.1%,体位性低血压及直立不耐受综合征性晕厥31例,占32.3%,心源性晕厥如心律失常、冠状动脉粥样硬化性心脏病、肺栓塞等引起的10例,占10.4%。非晕厥5例,占5.2%。结论晕厥的主要病因是神经介导的反射性晕厥,其次为体位性低血压晕厥、心源性晕厥;需重视神经系统疾病引起的晕厥病因的查找;对病因进行危险分层有助于降低潜在的风险。     

动态心电图在不明原因晕厥诊断中的价值

目的探讨动态心电图(Holter)在不明原因晕厥诊断中的应用价值。方法对146例不明原因的晕厥患者进行24小时Holter检查。全部患者经病史、体检、常规心电图和体位性低血压试验等均未发现晕厥的直接原因。结果146例患者经Holter检查,55例(37.67%)出现心律失常,25例(17.12%)出现晕厥发作,22例(15.06%)晕厥发作与心律失常有关。尤其与心电图RR间期有一定的相关性。25例晕厥患者中,RR间期≥3.0秒者共57次,其中31次发生晕厥;而RR间期<3.0秒者256次,无1例发生晕厥(P<0.01)。结论一些不明原因晕厥的发作与心律失常有关。Holter检查对不明原因晕厥的病因诊断仍然是一种有价值的工具。     

314例患者运动试验中室性心律失常分析

运动试验是诊断冠心病并判断其预后的常用辅助方法之一 ,运动不仅可以诱发心肌缺血 ,还可诱发各种类型的心律失常。运动试验中室性心律失常与心肌缺血之间是否有关目前报道甚少。本文分析了314例活动平板运动试验并同期进行了冠脉造影的患者 ,对在平板运动试验中中伴发室性心律失常者进行研究 ,探讨心肌缺血与室性心律失常之间的关系 ,现报道如下。资料与方法病例选择　选择我院 1996年 1月～ 2 0 0 2年 3月临床诊断或疑诊为冠心病而先后进行活动平板运动试验和冠脉造影 (CoronaryAngiography ,CAG)检查的患者 314例 ,患者平均年龄 5 2± …     

29例心源性晕厥患者动态心电图分析

目的 研究心源性晕厥患者的心律失常发生情况与高危心电图的具体表现.方法 对29例疑为心源性晕厥的患者进行24 h动态心电图监测.结果 29例患者均发生了较严重的心律失常,晕厥15例,R-R间期小于3.0s者无晕厥表现,R-R间期大于3.0s者出现晕厥表现.结论 心律失常尤其是慢性心律失常是造成心源性晕厥的主要原因,一般具有器质性心脏病的患者进行动态心电图检查,可以获得可靠的病因,并进行针对性的治疗.     

Familial clustering of lone atrial fibrillation in patients with saddleback-type ST-segment elevation in right precordial leads.

AIMS: We recently identified a large family with a high prevalence of lone atrial fibrillation (AF) and saddleback-type ST-segment elevation in leads V(1-3), without a history of ventricular arrhythmias or syncope. On the basis of this finding, we studied whether there is a relationship between saddleback ST-elevation and lone AF. METHODS AND RESULTS: We examined 168 (mean age 50+/-8 years, 130 males) lone AF patients and 541 (mean age 50+/-6 years, 274 males) healthy subjects. The prevalence of saddleback ST-elevation was higher in the lone AF group than the control group (10 vs. 0.4%, P<0.001). None had a coved-type ST-elevation in baseline ECG or during drug challenge with ajmaline or flecainide (n=13), a family history of sudden cardiac death, ventricular tachyarrhythmias, syncope, or any other features diagnostic to the Brugada syndrome. Familial clustering of lone AF (i.e. AF in >30% of first-degree relatives) was more common among the subjects with saddleback ST-elevation (24 vs. 7%, P=0.03). CONCLUSION: Saddleback-type ST-segment elevation is a relatively common finding among patients with lone AF. The familial clustering of the disorder indicates that genetic factors may be involved in the pathogenesis of the ECG abnormality and lone AF in these patients.     

特发性室性心律失常的射频消融

目的特发性室性心律失常（IVA）是指不伴有明显器质性心脏病的室性心动过速（室速）或室性早搏（室早）,约占所有室性心律失常的10％左右。本文系统分析925例IVA病例,探讨IVA的临床、电生理和射频消融的特点。方法本文回顾性分析了从1994年3月至2009年2月,925例IVA患者的临床特点,射频消融治疗的过程和结果。925例病人,男性500例,女性425例,平均年龄（36．65±14．81）岁。临床证实为IVA患者,并且排除了器质性心脏病。在停用抗心律失常药物5个半衰期后,进行电生理检查和射频消融治疗。结果特发性右心室室性心律失常（IRVA）516例,特发性左心室室性心律失常（ILVA）409例,IRVA多发生于女性,发病的平均年龄40岁,大多数表现为频发室早伴有反复单形室性心动过速,出现黑喙症状为14．3％;ILVA多发生于男性,发病的平均年龄33岁,多表现为持续性室速,出现黑矇症状为5．9％。IRVA有486例（94．2％）起源于右心室流出道,而在右心室流出道起源的室速／室早里,又以起源于间隔面的多见,占78％左右,起源于游离壁的占10％左右,其余的12％起源于二者之间的部位。射频消融多采用寻找心内膜最早激动点结合起搏标测来寻找合适的靶点。ILVA最多见的类型是左心室特发室速（ILVT）,有272例（66．5％）,ILVT主要起源于左后分支区域,也可以起源于左前分支区域和临近希氏束部位。主要用激动顺序标测结合浦肯野电位的方法确定消融靶点。IRVA的516例患者射频消融即刻成功率为89．3％。ILVA射频消融即刻成功率为93．7％。结论IVA患者虽然没有器质性心脏病,但是伴有多种临床症状,少部分病人甚至出现黑矇、晕厥,应积极行射频消融治疗,预防出现心室颤动危及生命。     

Effects of sympathetic activation on ventricular ectopic beats in subjects with and without evidence of organic heart disease

In a selected group of 10 apparently healthy subjects and 22 patients with organic heart disease, all with frequent ventricular ectopic beats on Holter monitoring, we assessed the influence of sympathetic activation by comparing the arrhythmogenic effects of a symptom-limited bicycle exercise stress test and 90 degree head up tilt. Tilting reduced ventricular arrhythmias in the normal subjects (-48 +/- 18% from 9 +/- 2 beats min-1, P less than 0.05). Exercise stress testing caused small and insignificant changes in arrhythmias during the early (50-75 W) phases and an almost complete suppression of ventricular ectopic beats in the final stages (-99 +/- 1%, P less than 0.01). In six of the 10 subjects, ventricular arrhythmias reappeared in the early recovery phase. In the 22 patients with organic heart disease, tilting increased ventricular ectopic beats (43 +/- 17% from 9 +/- 3 beats min-1, P less than 0.05); augmented repetitive forms in 12 patients (179 +/- 88% from 1.4 +/- 0.6 per 3 min) and produced repetitive forms in six of the 10 remaining patients who did not show repetitive forms during control conditions. Exercise stress testing caused a marked increase in ectopic activity in the early phase (84 +/- 35%) while the response during the maximal phase of exercise as well as during recovery was related to the effort capabilities. Arrhythmias were increased in 12 patients with limited exercise duration and were reduced in 10 patients with good exercise tolerance. These data indicate that sympathetic activation has different effects on ventricular arrhythmias depending on the clinical setting and that tilting is a useful maneuver to evaluate the arrhythmogenic effects of increased sympathetic activity.     

Arrhythmia Detection by Patient and Auto-Activation in Implantable Loop Recorders

AIMS: The Reveal Plus implantable loop recorder offers additional automatic detection of arrhythmias that may not be symptomatic. We evaluated the clinical utility of this function compared with standard patient activation. METHODS: Over an 18 month period, 50 consecutive patients (age 54 +/- 20 years; 24 male) with unexplained dizziness, palpitations and/or syncope had ILR activations which were downloaded for analysis. Patient and auto-activation were analysed with respect to arrhythmia detection and the impact on management of patients was examined. RESULTS: Patient symptoms were syncope in 72% and non-syncope (dizziness and/or palpitations) in 28%. There were 181 patient activation events with 16% showing symptomatic arrhythmia leading to a positive diagnosis in 8 patients. Of 682 auto-activations, detection was appropriate in 17% and inappropriate in 83% (undersensing in 76% and oversensing in 24%). In 8 patients clinically relevant arrhythmia was detected by patient activation alone. In 4 of these patients, further arrhythmia was detected by auto-activation. No patient had important arrhythmia detected only by auto-activation. CONCLUSION: Automatic detection of asymptomatic arrhythmia did not appear to improve the diagnostic utility of the ILR in our series. The large number of stored inappropriate auto-activation events limits the ability of this function to detect clinically relevant arrhythmia. Symptom-rhythm correlation using the patient activation function remains clinically useful in patients with unexplained syncope or palpitation.     

Value of the isoprenaline test in arrhythmogenic heart diseases

The sympathetic nervous system seems to play a major role in the genesis of ventricular arrhythmias. The authors studied this adrenergic factor prospectively by exercise stress testing and intravenous isoprenaline in 107 patients referred for evaluation of arrhythmias or symptoms thought to be due to arrhythmias: 30 patients had morphologically normal hearts (15 ventricular extrasystoles, 15 bursts of ventricular tachycardia); 55 patients had dilated cardiomyopathy and 22 had probable or proven arrhythmogenic right ventricular dysplasia. Exercise testing was carried out with 30 watt increments every 3 minutes. Ventricular tachycardia was induced in 6 patients with apparently normal hearts (17%), 13 patients with dilated cardiomyopathy (31%) and 7 patients with arrhythmogenic right ventricular dysplasia (40%). Isoprenaline was infused for 3 minutes at a dose of 8-12 g/min: ventricular tachycardia was induced in 7 patients with apparently normal hearts (24%) and 23 patients with dilated cardiomyopathy. In some patients presenting with syncope, an arrhythmogenic response to isoprenaline was the only abnormality detected by the study protocol. An arrhythmia was induced by isoprenaline in 17 of the 18 patients with confirmed right ventricular dysplasia (94%), 12 of whom had sustained mono or polymorphic ventricular tachycardia. Two of these patients did not have significant right ventricular wall motion abnormalities. Four asymptomatic subjects related to patients with right ventricular dysplasia underwent the isoprenaline test; bursts of ventricular tachycardia were recorded in 3 of them. Polymorphic ventricular tachycardia was specifically associated with cardiac disease. The maximum heart rate attained by exercise testing (148 +/- 19/min) was higher than that attained with isoprenaline (148 +/- 22/min).(ABSTRACT TRUNCATED AT 250 WORDS)     

Inducible ventricular flutter and fibrillation predict for arrhythmia occurrence in coronary artery disease patients presenting with syncope of unknown origin

INTRODUCTION: Ventricular fibrillation and ventricular flutter (cycle length < or = 230 msec) induced at electrophysiologic studies are thought to be nonspecific findings in patients presenting with syncope of unknown origin. However, there are limited data on the prognosis of these patients in long-term follow-up. METHODS AND RESULTS: We followed 274 consecutive patients with coronary artery disease presenting with syncope or presyncope who underwent electrophysiologic studies from January 1992 to June 1999 and assessed the risk of subsequent arrhythmias stratified by the electrophysiologic result at the time of their presentation with syncope. Ventricular fibrillation was induced in 23 patients (8%); ventricular flutter in 24 (9%), sustained ventricular tachycardia in 41 (15%); and nonsustained ventricular tachycardia 42 (15%). In 37 +/- 25 months of follow-up, there have been ventricular arrhythmias in 34 patients, including 3 (13%) of 23 who had induced ventricular fibrillation, and 7 (30%) of 24 with induced ventricular flutter, compared to 13 (32%) of 41 with sustained ventricular tachycardia, 7 (17%) of 42 with nonsustained ventricular tachycardia, and only 4 (3%) of 144 noninducible patients (P < 0.001 for induced ventricular fibrillation and ventricular flutter vs noninducible patients). The inducibility of ventricular fibrillation and ventricular flutter were independent risk factors for arrhythmia occurrence in follow-up. CONCLUSION: Ventricular fibrillation and ventricular flutter induced at electrophysiologic studies have prognostic significance for arrhythmia occurrence in patients presenting with syncope. These induced arrhythmias may not be as nonspecific as previously thought and treatment should be considered for these patients.     

Effects of sympathetic activation on ventricular ectopic beats in subjects with and without evidence of organic heart disease

In a selected group of 10 apparently healthy subjects and 22patients with organic heart disease, all with frequent ventricularectopic beats on Holter monitoring, we assessed the influenceof sympathetic activation by comparing the arrhythmogenic effectsof a symptom-limited bicycle exercise stress test and 90°head up tilt. Tilting reduced ventricular arrhythmias in thenormal subjects (–48±18% from 9±2 beatsmin^-1, P<0.05). Exercise stress testing caused small andinsignificant changes in arrhythmias during the early (50–75W) phases and an almost complete suppression of ventricularectopic beats in the final stages (–99±1%, P<0.01).In six of the 10 subjects, ventricular arrhythmias reappearedin the early recovery phase. In the 22 patients with organicheart disease, tilting increased ventricular ectopic beats (43±17%from 9±3 beats min^-1, P<0.05); augmented repetitiveforms in 12 patients (179±88% from 1.4±0.6 per3 min) and produced repetitive forms in six of the 10 remainingpatients who did not show repetitive forms during control conditions.Exercise stress testing caused a marked increase in ectopicactivity in the early phase (84±35%) while the responseduring the maximal phase of exercise as well as during recoverywas related to the effort capabilities. Arrhythmias were increasedin 12 patients with limited exercise duration and were reducedin 10 patients with good exercise tolerance. These data indicatethat sympathetic activation has different effects on ventriculararrhythmias depending on the clinical setting and that tiltingis a useful manoevre to evaluate the arrhythmogenic effectsof increased sympathetic activity.     

Implantable defibrillator event rates in patients with unexplained syncope and inducible sustained ventricular tachyarrhythmias: a comparison with patients known to have sustained ventricular tachycardia

OBJECTIVES

To assess the clinical significance of inducible ventricular tachyarrhythmias among patients with unexplained syncope.

BACKGROUND

Induction of sustained ventricular arrhythmias at electrophysiology study in patients with unexplained syncope and structural heart disease is usually assigned diagnostic significance. However, the true frequency of subsequent spontaneous ventricular tachyarrhythmias in the absence of antiarrhythmic medications is unknown.

METHODS

In a retrospective case-control study, the incidence of implantable cardiac defibrillator (ICD) therapies for sustained ventricular arrhythmias among patients with unexplained syncope or near syncope (syncope group, n = 22) was compared with that of a control group of patients (n = 32) with clinically documented sustained ventricular tachycardia (VT). Sustained ventricular arrhythmias were inducible in both groups and neither group received antiarrhythmic medications. All ICDs had stored electrograms or RR intervals. Clinical variables were similar between groups except that congestive cardiac failure was more common in the syncope group.

RESULTS

Kaplan-Meier analysis of the time to first appropriate ICD therapy for syncope and control groups produced overlapping curves (p = 0.9), with 57 ± 11% and 50 ± 9%, respectively, receiving ICD therapy by one year. In both groups, the induced arrhythmia was significantly faster than spontaneous arrhythmias, but the cycle lengths of induced and spontaneous arrhythmias were positively correlated (R = 0.6, p < 0.0001). During follow-up, three cardiac transplantations and seven deaths occurred in the syncope group, and two transplantations and five deaths occurred in the control group (36-month survival without transplant 52 ± 11% and 83 ± 7%, respectively, p = 0.03).

CONCLUSIONS

In patients with unexplained syncope, structural heart disease and inducible sustained ventricular arrhythmias, spontaneous sustained ventricular arrhythmias occur commonly and at a similar rate to patients with documented sustained VT. Thus, electrophysiologic testing in unexplained syncope can identify those at risk of potentially life-threatening tachyarrhythmias, and aggressive treatment of these patients is warranted.     

Low recurrence of syncope in patients with inducible sustained ventricular tachyarrhythmias treated with an implantable cardioverter-defibrillator.

AIMS: To determine the effectiveness of the implantable cardioverter defibrillator (ICD) in preventing recurrence of syncope in patients with structural heart disease, previously unexplained syncope and inducible ventricular arrhythmias. METHODS: Thirty-eight patients with syncope, structural heart disease and inducible arrhythmias had an ICD implanted. All ICDs delivered antitachycardia pacing and shocks of adjusted energy. Detection and therapy were programmed according to uniform criteria. RESULTS: The mean age of the patients was 63+/-11 years and most of them were male (36/38). After a mean follow-up of 28+/-15 (4-61) months, six patients died and one underwent heart transplantation. Syncope recurred in three patients, but in none of them was it caused by an arrhythmic event. In 18 patients, 113 episodes of ventricular tachycardia/ventricular fibrillation were detected and appropriately treated by the ICD. The mean time from implant until first appropriate therapy was 18+/-14 months. The actuarial probability of receiving appropriate therapy was 20% and 42% at 12 and 24 months, respectively. CONCLUSIONS: In patients with unexplained syncope, structural heart disease and inducible arrhythmias, ICD prevents syncope associated with arrhythmic events. Frequent effective use of antitachycardia pacing and shocks of adjusted energy seem essential to this aim.     

Prognostic determinants in hypertrophic cardiomyopathy. Prospective evaluation of a therapeutic strategy based on clinical, Holter, hemodynamic, and electrophysiological findings.

BACKGROUND. Patients with hypertrophic cardiomyopathy (HCM) frequently have arrhythmias and hemodynamic abnormalities and are prone to sudden death and syncope. An important need exists for improved risk stratification and definition of appropriate investigation and therapy. METHODS AND RESULTS. The relation of 31 clinical, Holter, cardiac catheterization, and electrophysiological (EP) variables to subsequent cardiac events in 230 HCM patients was examined by multivariate analysis. Studies were for cardiac arrest (n = 32), syncope (n = 80), presyncope (n = 52), ventricular tachycardia (VT) on Holter (n = 36), a strong family history of sudden death (n = 9), and palpitations (n = 21). Nonsustained VT on Holter was present in 115 patients (50%). Sustained ventricular arrhythmia was induced in 82 patients (36%). Seventeen cardiac events (eight sudden deaths, one cardiac arrest, and eight syncope with defibrillator discharges) occurred during a follow-up of 28 +/- 19 months. The 1-year and 5-year event-free rates were 99% and 79%, respectively. Two variables were significant independent predictors of subsequent events: sustained ventricular arrhythmia induced at EP study (beta, 3.5; p = 0.002) and a history of cardiac arrest or syncope (beta, 2.9; p less than 0.05). Only two of 66 patients without symptoms of impaired consciousness had a cardiac event (3-year event-free rate, 97%). In contrast, nonsustained VT on Holter was associated with a worse prognosis only in patients with symptoms of impaired consciousness: 11 of 79 symptomatic patients with VT on Holter (14%) had events versus only four of 85 symptomatic patients without VT on Holter (5%) (p = 0.057). Notably, none of 51 patients without symptoms of impaired consciousness in whom VT was not induced at EP study had a cardiac event. CONCLUSIONS. In HCM, VT on Holter is of benign prognostic significance in the absence of symptoms of impaired consciousness and inducible VT, and sustained VT induced at EP study, especially when associated with cardiac arrest or syncope, identifies a subgroup at high risk for subsequent cardiac events.