Baseline 12-lead Electrocardiogram Research Articles

Prolonged QRS Duration in Lead V2 and Risk of Life-Threatening Ventricular Arrhythmia in Patients With Brugada Syndrome

Brugada syndrome is an inherited disorder that predisposes some patients to sudden cardiac death. It is not well established which Brugada syndrome patients are at risk of life-threatening arrhythmias. We investigated whether standard 12-lead electrocardiograms (ECG) can identify such patients. The subjects were 35 men with Brugada syndrome (mean age, 50.1 ± 12.4 years). Documented ventricular fibrillation or aborted sudden cardiac arrests were judged to be related to the Brugada syndrome. Ten patients (mean age, 49.6 ± 14.9 years) were symptomatic, and 25 (mean age, 50.3 ± 11.5 years) were asymptomatic. We determined the PR interval, QRS duration, and QT interval from baseline 12-lead ECG leads II and V2 as well as the J point elevation amplitude of lead V2. The QRS interval was measured from QRS onset to the J point in leads II and V2. The only significant difference between the symptomatic and asymptomatic patients was the QRS duration measured from lead V2. The mean QRS interval was 129.0 ± 23.9 ms in symptomatic patients versus 108.3 ± 15.9 ms in asymptomatic patients (P = 0.012). A QRS interval in lead V2 ≥ 120 ms was found to be a possible predictor of a life-threatening ventricular arrhythmia and/or syncope (P = 0.012). Prolonged QRS duration as measured on a standard 12-lead ECG is associated with ventricular arrhythmia and could serve as a simple noninvasive marker of vulnerability to life-threatening cardiac events in patients with Brugada syndrome.

Twelve-lead electrocardiogram monitoring of subjects before and after voluntary exposure to the Taser X26

Objectives The Taser (Taser International, Scottsdale, Ariz) uses high-voltage electricity to incapacitate subjects. We sought to evaluate cardiac rhythm changes during deployment of the Taser on healthy volunteers. Methods This prospective study was performed on 32 healthy volunteer subjects receiving a Taser X26 discharge. The subjects had baseline 12-lead electrocardiogram (ECG) monitoring performed immediately before and within 1 minute after the Taser discharge. Changes in cardiac rhythm, morphology, and interval duration were evaluated. Descriptive statistics and paired-sample t test comparisons are reported. Results All 32 subjects had an interpretable 12-lead ECG obtained before and after the Taser activation, although 1 subject's post–PR interval could not be determined. The mean age and body mass index were 33 years and 26.5 kg/m 2, respectively. Overall, there was a significant increase in heart rate (2.4; 95% confidence interval [CI], 0.0-4.9) and a decrease in PR interval (−6.5; 95% CI, −9.7 to −3.3). When stratified by sex, only the PR interval in men significantly decreased (−5.9; 95% CI, −9.2 to −2.5). There were significant changes in heart rate (4.0; 95% CI, 1.3-6.7), PR interval (−6.0; 95% CI, −11.3 to −0.7), and QT interval (−18.8; 95% CI, −33.2 to −4.3) among those with a normal body mass index, and in PR interval among those who were overweight/obese (−6.7; 95% CI, −10.8 to −2.5). None of the statistically significant differences between ECG measures were clinically relevant. Conclusions There were no cardiac dysrhythmia and interval or morphology changes in subjects who received a Taser discharge based on a 12-lead ECG performed immediately before and within 1 minute after a Taser activation.

Heart rate turbulence and death due to cardiac decompensation in patients with chronic heart failure

As treatment strategies for patients with chronic heart failure (HF) become more sophisticated, identifying patients at high risk of death and predicting mode of death is important. The aim of this study was to explore the potential utility of heart rate turbulence (HRT) to identify patients with HF at high risk of death. In a prospective study, 553 ambulant outpatients age 63+/-10 with symptoms of HF and evidence of cardiac dysfunction were recruited. All patients underwent 24-h Holter ECG recordings, which were analysed for arrhythmias, heart rate variability and HRT a measurement that is thought to quantify cardiac autonomic regulatory mechanisms. Baseline chest radiograph, biochemistry and 12-lead electrocardiograms were also obtained. In patients with HRT measurements at 5 years follow up, 146 patients had died, 59 due to decompensated HF. Independent predictors of death from decompensated HF at 5-year follow up (Cox proportional hazard model) were HRT slope (HR for 10% increment 0.84, 95% CI 0.77-0.91), serum sodium (HR for 10% increment 0.75, 95% CI 0.62-0.91) and serum creatinine (for 10% increment HR 1.14, 95% CI 1.08-1.19) all P<0.01. These 3 variables combined had excellent discrimination between patients dying of decompensated HF and other patients, C-statistic=0.82. In patients with mild-to-moderate HF, HRT slope is an independent predictor of death due to decompensated HF. HRT may have the potential to help tailor therapy in this patient group.

Electrocardiographic Findings and Incident Coronary Heart Disease Among Participants in the Atherosclerosis Risk in Communities (ARIC) Study

The associations of many electrocardiographic (ECG) abnormalities at rest with incident coronary heart disease (CHD) are not completely established, and whether individual ECG abnormalities convey similar risk across gender and race is uncertain. We studied the independent association of several ECG findings with incident CHD, testing for effect modification by gender and race, in a large, population-based, prospective cohort study. Findings from the baseline 12-lead electrocardiograms in 1987 to 1989 were classified according to the Minnesota Code in 12,987 black and white men and women, aged 45 to 64 years, who were initially free of CHD and the use of specific cardiac medications. The incidence of CHD was ascertained through 2000. After adjustment for multiple cardiovascular risk factors, the ECG findings that had the highest hazard rate ratios (HRRs) for incident CHD, when considered singly, were left ventricular hypertrophy with ST-T strain pattern in white men (HRR 6.50) and in black women (HRR 2.31) and, in the whole cohort, major (HRR 2.27) and minor (HRR 2.47) ST depression and major T-wave abnormalities (HRR 2.12). Statistically significant associations were also found in the whole cohort for minor Q waves and left ventricular hypertrophy by the Cornell definition, but not for a prolonged QTc interval, major ventricular conduction defects, or ST elevation. In conclusion, several 12-lead ECG findings were independently associated with incident CHD in middle-aged adults. With only a few exceptions, the associations were similar for blacks and whites.

The efficacy of azimilide in the treatment of atrial fibrillation in the presence of left ventricular systolic dysfunction: Results from the Azimilide Postinfarct Survival Evaluation (ALIVE) trial

ObjectivesThe purpose of this study was to assess the effect of oral azimilide dihydrochloride (AZ) 100 mg versus placebo on the onset, termination, and prevalence of atrial fibrillation (AF) in a subpopulation of patients in the Azimilide Postinfarct Survival Evaluation (ALIVE) trial. BackgroundPrevious clinical trials have demonstrated the antiarrhythmic effects of AZ in patients with AF. Azimilide was investigated for its effects on mortality in patients with depressed left ventricular (LV) function after recent myocardial infarction (MI) and in a subpopulation of patients with AF. MethodsA total of 3,381 post-MI patients with depressed LV function were enrolled in this randomized, placebo-controlled, double-blind study of AZ 100 mg on all-cause mortality. A total of 93 patients had AF on the baseline 12-lead electrocardiogram (ECG). An additional 27 patients developed AF after initially being in sinus rhythm at randomization. These patients were identified through 12-lead ECGs obtained during routine visits at week 2, months 1, 4, 8, and 12. ResultsPatients with AF at baseline had a higher mortality than those without AF (p = 0.0006). Among AF patients, there was no difference in mortality between AZ patients and placebo patients (p = 0.82). Fewer AZ patients developed AF than placebo patients (p = 0.04). More AZ patients than placebo patients converted to sinus rhythm, but this difference did not achieve statistical significance (p = 0.076). Over one-year follow-up, more AZ patients were in sinus rhythm than placebo patients (p = 0.04). ConclusionsAzimilide was safe and effective AF therapy in patients with depressed LV function after an MI.

Does shock wave lithotripsy of renal stones cause cardiac muscle injury? A troponin I-based study

Objectives To investigate whether shock wave lithotripsy (SWL) causes cardiac muscle injury that alters the levels of troponin I plasma, a cardio-specific enzyme shown to be useful in diagnosing cardiac muscle injury because of its high specificity. Methods Patients treated by SWL for renal stones participated in the study. They had undergone a baseline 12-lead electrocardiogram (ECG) a few days earlier. One day after SWL, they were queried about any chest discomfort, blood was drawn for evaluation of troponin I and creatine kinase with isoenzymes (CK-MB), and an ECG was carried out. Results Thirty-two patients (21 men and 11 women, mean age ± SD 51.0 ± 10.6 years) comprised the study group. Fourteen SWL treatments were on the right side and 18 on the left. The mean number of shock waves was 2859 ± 202. The mean time to evaluation after SWL was 22.3 ± 1.3 hours. None of the patients reported chest discomfort. The mean value was 6.6 ± 9.2 mU/mL for CK-MB and 0.02 l ± 0.04 ng/mL for troponin I. No ECG changes suggestive of myocardial injury were evident. None of the 5 patients who experienced ventricular extrasystoles during SWL had any evidence of cardiac muscle injury. Conclusions We evaluated the symptoms, perioperative ECG changes, and cardiac troponin I and CK-MB plasma levels in patients who underwent SWL for renal stones and did not identify any myocardial damage. Troponin I plasma levels were not elevated after this procedure and, therefore, remain suitable for evaluation of patients complaining of chest pain after SWL.

Value of the electrocardiogram in predicting left ventricular enlargement and dysfunction after myocardial infarction

Purpose To identify electrocardiographic predictors of left ventricular enlargement or persistent dysfunction following a myocardial infarction. Methods Baseline and predischarge 12-lead electrocardiograms (ECGs) from 272 patients with anterior myocardial infarction who were enrolled in the Healing and Early Afterload Reducing Therapy trial were evaluated and related to echocardiographic data obtained at baseline and day 90. ST-segment elevation, QRS score, and number of negative T waves were assessed at both time points. The majority of patients (87%; n = 237) received reperfusion therapy. Multivariate models were used to adjust for potential confounders, including maximal creatine kinase level and ejection fraction at baseline. Results None of the baseline electrocardiographic variables independently predicted ventricular enlargement or recovery of function. In contrast, the sum of ST- and maximum ST-segment elevation, and the number of leads with ST-segment elevation ≥1 mm in the predischarge ECG, were independent predictors of ventricular enlargement from baseline to day 90. Each lead with ST-segment elevation ≥1 mm was associated with 3.5 mL of ventricular enlargement (95% confidence interval [CI]: 1.6 to 5.5 mL; P <0.0001). Similarly, the sum of ST-segment elevation (odds ratio [OR] = 0.78; 95% CI: 0.69 to 0.89; P <0.0001), the maximum ST-segment elevation (OR = 0.25; 95% CI: 0.13 to 0.45; P <0.0001), and the number of leads with ST-segment elevation ≥1 mm (OR = 0.58; 95% CI: 0.45 to 0.74; P <0.0001) were independently associated with a lower likelihood of recovery of function at day 90. Conclusion Predischarge ECG may be a useful tool for early identification of patients at risk of ventricular enlargement and persistent dysfunction following myocardial infarction.

Increased QT dispersion in patients with Prinzmetal's variant angina and cardiac arrest.

We sought to compare QT dispersion in patients presenting with Prinzmetal's variant angina complicated by cardiac arrest or syncope and patients with uncomplicated variant angina. Despite the usually benign course of treated Prinzmetal's variant angina, a proportion of vasospastic angina patients develop ventricular arrhythmias and sudden death in association with coronary spasm. Increased QT dispersion has been suggested to increase susceptibility to ventricular arrhythmias in patients with coronary artery spasm. We studied 25 consecutive patients (mean age 58 years; 14 men) with classical Prinzmetal's variant angina and documented coronary artery spasm. None of the patients had coronary artery stenoses < or =40%. Five patients had suffered a documented cardiac arrest, two had recurrent syncope and 18 had no arrhythmic events or syncopal episodes. In all patients QT dispersion (QT maximum-QT minimum in every ECG lead) was measured on the baseline 12-lead electrocardiogram at study entry using a digitising board. Mean (+/-S.D.) QT dispersion of study patients was 62.3+/-19.5 ms. QT dispersion in patients with cardiac arrest and syncope (79.4+/-17.3 ms) was significantly higher compared to patients with no such events (56.3+/-16.9 ms), (95% CI 7.5-38.8, P=0.005). No significant clinical, biochemical or angiographic differences were found between patients with and those without cardiac arrest or syncope. QT dispersion is increased in patients with Prinzmetal's variant angina complicated by cardiac arrest and syncope compared to patients without such events. Increased QT dispersion may be both a substrate for sudden cardiac death and a marker of risk in patients with Prinzmetal's variant angina.

Comparable Bronchodilation with Hydrofluoroalkane-134a (HFA) Albuterol and Chlorofluorocarbons-11/12 (CFC) Albuterol in Children with Asthma

This was an open-label, parallel group, randomized, age-stratified, multicenter study designed to compare the safety and efficacy of regular use of albuterol formulated in hydrofluoroalkane-134a (HFA albuterol) and albuterol formulated in chlorofluorocarbons-11/12 (CFC albuterol) in children with asthma. Children age 4-11 years using a short-acting inhaled beta2-agonist for 6 months to manage stable asthma, and with a prestudy forced expiratory volume in 1 sec (FEV1) of >50% predicted after withholding short-acting inhaled beta2-agonists for at least 6 hr, an increase in FEV1 ≥ 12% within 30 min after two puffs of CFC albuterol, and the capability to comply with medication withholding requirements were eligible for study entry. After screening evaluation, patients entered a minimum 7-day run-in period. On study day 1 spirometry and a baseline 12-lead electrocardiogram (ECC) were performed, pulse and blood pressure were measured, and patients self administered two puffs of their randomized study drug, either HFA albuterol or CFC albuterol. Serial spirometry was performed over 6 hr after study drug dosing. Pulse and blood pressure were measured just prior to each spirometry and a 12-lead ECG was performed at 60 min postdose. Patients took two puffs of their study drug four times a day for 4 weeks. At study week 4, study day 1 procedures were repeated. Patients maintained a daily diary of morning (a.m.) and evening (p.m.) peak expiratory flow (PEF), daytime asthma symptom scores, nighttime asthma sleep disturbance scores, and study drug use. Demographics and baseline characteristics of the 63 patients randomized to HFA albuterol (33) and CFC albuterol (30) were similar. No significant differences were found between the HFA albuterol and CFC albuterol treatment groups for any of the primary or secondary FEV, efficacy variables either at study day 1 or study week 4. No significant differences were noted between treatment groups for a.m. and p.m. PEF, individual asthma symptom scores, nighttime asthma sleep disturbance scores, and rescue study drug use over the 4-week study. No significant differences were found between the two treatment groups for change from predose in heart rate, systolic and diastolic blood pressure, and 12-lead ECG intervals at either study day 1 or study week 4. Adverse event reporting was similar for the two treatment groups. In this study, with regular use of HFA albuterol in children with asthma, there was a similar safety profile and comparable bronchodilator efficacy as with CFC albuterol.

Analysis of cardiac arrhythmias during dobutamine pharmacologic stress testing in nuclear cardiology as related to the presence or absence of baseline arrhythmias

Background. Intravenous dobutamine is an acceptable pharmacologic stress agent for evaluation of myocardial ischemia, but it has the undesirable side effect of precipitating cardiac arrhythmias. All patients are susceptible to the arrhythmogenic potential of dobutamine. However, the presence of a baseline arrhythmia creates additional concern about proceeding with a pharmacologic dobutamine stress test. The purpose of this study was to evaluate cardiac arrhythmias during dobutamine stress as they relate to the presence or absence of baseline arrhythmias in patients undergoing radionuclide myocardial perfusion imaging. Methods and Results. Data from 486 consecutive dobutamine stress tests in nuclear cardiology were reviewed retrospectively. Baseline and stress electrocardiographic monitoring and 12-lead electrocardiograms were used for classification of arrhythmias. For patients without baseline arrhythmias, the estimated probability of having nonsustained ventricular tachycardia with dobutamine stress was 4.0% (16 of 403), as compared with 15.7% (13 of 83) for patients with baseline arrhythmias ( p < 0.001). Three of the 403 patients (0.7%) and 2 of the 83 patients (2.4%) had their study terminated because of ventricular tachycardia ( p > 0.05). Conclusions. The probability of having nonsustained ventricular tachycardia with dobutamine stress testing was significantly greater in patients who had baseline arrhythmias than in those who had no arrhythmias at baseline. Although termination of the study because of ventricular tachycardia was not statistically significant between these two groups, patients with baseline cardiac arrhythmias should be considered at higher risk for the development of nonsustained ventricular tachycardia during dobutamine stress testing than patients who have no baseline arrhythmia.

Performance of the signal-averaged electrocardiogram: Relation to baseline QRS duration

Analysis of the duration and terminal components of the filtered QRS complex on the signal-averaged electrocardiogram (ECG) has been widely used for the detection of late potentials. Although filtered QRS duration is strongly related to 12-lead QRS duration, the relation of performance of the signal-averaged ECG to baseline QRS duration has not been critically examined. To examine the relation of test performance of the signal-averaged ECG to 12-lead QRS duration and to test the hypothesis that the difference between filtered and baseline 12-lead QRS duration would reflect more accurately the presence of late potentials than would analysis of the filtered QRS alone, we evaluated signal-averaged and 12-lead ECGs in 144 normal subjects and in 132 patients who were examined by electrophysiologic study and of whom 45 had inducible sustained monomorphic ventricular tachycardia. The signal-averaged ECG was considered positive by standard late potential criteria when the filtered vector QRS duration was >114 msec and either the root-mean-square voltage of the terminal 40 msec of the filtered QRS was <20 μV or the low-amplitude signal of the terminal filtered QRS was >38 msec. A new signal-averaged ECG criterion for the presence of late potentials was developed in the 144 normal subjects on the basis of the difference between the longest filtered QRS duration in any of the orthogonal leads and QRS duration on the baseline 12-lead ECG (“the QRS difference”), which was adjusted by regression analysis for the decreasing QRS difference found with increasing baseline QRS duration. Among patients who underwent electrophysiologic study, performance of standard late potential criteria was highly dependent on underlying 12-lead QRS duration: when subgrouped according to a median QRS duration of 92 msec on the routine ECG, patients with longer QRS durations had significantly lower specificity (61% vs 96%; p = 0.0001) and higher sensitivity (71% vs 36%; p < 0.05) than did those with shorter QRS durations. The new regression-based QRS difference criteria had specificity (96% vs 92%; p not significant [NS]) equivalent to that of standard late potential criteria in the normal subjects, and when applied to the 132 patients who underwent electrophysiologic study, analysis of the QRS difference significantly improved specificity (89% vs 79%; p < 0.05) with no loss in sensitivity (58% vs 60%; p NS). In addition, performance of the regression-based QRS difference criteria was less dependent on 12-lead QRS duration than was performance of standard late potential criteria, with similar specificity (83% vs 93%; p NS) and a trend toward higher sensitivity (65% vs 43%; p NS) at QRS durations >92 msec. These data demonstrate that test performance of standard late potential criteria is highly dependent on baseline QRS duration, However, new signal-averaged ECG criteria that can be derived on the basis of the difference between standard and filtered QRS duration improve accuracy of the signal-averaged ECG, are less dependent on 12-lead QRS duration, and are independent of terminal QRS root-mean-square voltage and low-amplitude-signal magnitude measurements.

Behavior of a respiratory rate-responsive pacemaker during and after cardiac surgery

DVANCES IN pacemaker technology now allow devices to increase their paced rates in response to information from biologic sensors.’ Previous case reports have described unexpected adverse device behavior related to sensor activation during surgery in the presence of these “rate-responsive” devices. 2-5 In this report, a patient with a minute ventilation-sensing device who underwent coronary artery bypass surgery had sensor and device function assessed during the operation. The device estimates minute ventilation by calculating thoracic impedance from measurements of voltage obtained during a low energy current application (1 mA, 7.6 usec, 18 Hz) delivered between the extrathoracic pulse generator and the proximal pole of the intrathoracic bipolar pacemaker electrode. It was hypothesized that the marked changes in thoracic impedance consequent to chest opening would affect sensor behavior. In addition, the effects of cautery and mechanical ventilation settings on device sensor function were observed in a prospective manner. A 65year-old woman was admitted for urgent coronary revascularization because of unstable angina. Three months previously, she received a Telectronics Meta II VU-R 1204H minute volume monitoring rate-responsive pacemaker (Denver, CO) for episodes of symptomatic bradycardia with fatigue. Her predominant rhythm was sinus with normal atrioventricular conduction. Her baseline 12-lead electrocardiogram showed evidence of old inferior infarction. Device telemetry preoperatively revealed that all beats were sensed with no evidence of paced beats. In order to maintain a stable baseline for the sensor, the device was in a “WI + adapt” mode for the 2 hour period before the operation. In this mode, the device obtains sensor data but does not adjust the paced rate. The sensitivity of the sensor or “rate-response factor” was 18 with an upper rate of 120 beats/min and a minimum rate of 60 beats/min. The patient was anesthetized using a moderate-dose fentanyl and benzodiazepine technique. With the sternum open, the pacemaker was interrogated. This showed sensing only with no paced beats. During electrocautery, high frequency (> 10 Hz) continuous interference was detected and appropriately led to no more than two to three beats of temporary asynchronous (noise reversion mode) pacing. WI-R pacing was then instituted at the preoperative rateresponse settings. The device immediately showed sensing only. There was no evidence of a change in paced rate consequent to sensor activation with the chest open (Fig 1 A).