Electrocardiogram Conduction Research Articles

Analysis of cardiac conduction disorders in adult patients in the early postoperative period after Ozaki surgery

Purpose. To assess the disorders of the cardiac conduction system (CCS) that occurred in the early postoperative period after aortic valve (AV) replacement by the Ozaki method.Methods. The study included 256 patients after a successfully performed Ozaki procedure. Patients with a history of open cardiac surgery, with an implanted pacemaker, with permanent atrial fibrillation, with simultaneous Ozaki surgery with correction of another pathology, in case of repeated surgery on AV in the next six months, with lethal outcome, under the age of 18 years, when it is impossible to analyze the CCS dynamics were excluded. The mean age was 57.9±11.1 years, the male sex was 119 people (46.5%), the body mass index was 29.7±5.5 kg/m2 , diabetes was observed in 40 patients (15.6%), anamnesis of CCS disorders in 10 (3.9%), CCS disorders on the baseline electrocardiogram (ECG) in 32 (12.5%). Conduction abnormalities were assessed according to the anamnesis and the results of daily ECG recording.Results. In the early postoperative period, CCS disorders were registered in 35 patients (13.7%), of whom 27 (10.6%) had their first occurrence, and 8 (3.1%) had previously existed. By the time of discharge, persistent CCS disorders (which occurred for the first time and in the case of progression of pre-existing blocks) remained in 11 (4.3%): 8 (3.1%) had bundle branch blocks, 3 (1.2%) had atrioventricular blocks that required implantation of a permanent pacemaker. Patients with pacemaker had initial conduction abnormalities. The most frequent dysfunction of the CСS was the left bundle branch block (LBBB) (45.5%). We analyzed 14 variables as predictors of the onset or progression of persistent CCS disorders. Two independent predictors were identified - the presence of conduction abnormalities on the baseline ECG and the time of cardiopulmonary bypass. In patients with persistent conduction disturbances in the postoperative period, CCS disorders on the baseline ECG were more common - 36.4% compared with patients without CCS disorders after surgery - 11.4% (p=0.035) and there was a longer duration of cardiopulmonary bypass 140.6±41.1 min. and 122.4±26.1 min. respectively (p=0.03).Conclusion. The most frequent disorder of the conduction was the LBBB. None of the first dysfunctions of CCS led to the implantation of the pacemaker. The presence of initial ECG conduction disturbances and the time of cardiopulmonary

Features of the cardiovascular system in newborns, carrying out the cerebral ischemia

Aim. To identify the features of the function of the cardiovascular system in newborns with cerebral ischemia (CI) of hypoxic origin.
 Materials and methods. In the neurological department of the children's hospital in 64 newborns coming from maternity hospitals with CI, a clinical and instrumental examination confirmed the diagnosis of CI of hypoxic origin after excluding structural damage to cardiomyocytes, infectious, traumatic and dysmetabolic causes of its occurrence; 12.2% of children were diagnosed with CI of easy degree, 81.2% CI of moderate severity; the control group consisted of 24 healthy full-term children, comparable in age. All patients were examined by a pediatric cardiologist with an electrocardiogram (ECG), echocardiographic ultrasound screening assessment of the heart (ECHO-CG), Holter electrocardiogram monitoring, cardiointervalography.
 Results. In newborns, who underwent CI, there is a higher heart rate, more often there is a single supraventricular extrasystole. Bradycardia with heart rate less than 100 beats/min, sino-atrial block II degree, atrioventricular block II degree were recorded only in newborns after CI. According to ECHO-CG data, a hypokinetic type of hemodynamics takes place in newborns with CI. A decrease in cardiac output reflects a narrowing of the adaptive range of its regulation. In every second child with CI, homeostasis is achieved by a sharp overstrain of the autonomic nervous system regulatory systems, which is most likely based on a shift in regulation from the reflex vegetative to the humoral-metabolic type. As the severity of CI progresses, depletion of reserves to support reflex and humoral homeostasis has been established.
 Conclusion. In connection with the revealed clinical and instrumental features of the cardiovascular system, newborns with CI who came under the supervision of pediatricians at children's clinics, at the age of one month, in addition to a neurological examination, an examination of a pediatric cardiologist with an ECG is shown. If, according to ECG data, heart rhythm and conduction abnormalities, fluctuations in the duration of the QT interval are detected, CI and/or HM-ECG are indicated to determine further observation tactics.

Prevalence of abnormalities in electrocardiogram conduction in dialysis patients: a comparative study.

The electrocardiogram (ECG) can aid in identification of chronic kidney disease (CKD) patients at high risk for cardiovascular diseases. Cohort studies describe ECG abnormalities in patients on hemodialysis (HD), but we did not find data comparing ECG abnormalities among patients with normal kidney function or peritoneal dialysis (PD) to those on hemodialysis. We hypothesized that ECG conduction abnormalities would be more common, and cardiac conduction interval times longer, among patients on hemodialysis vs. those on peritoneal dialysis and CKD 1 or 2. Retrospective review of adult inpatients' charts, comparing those with billing codes for "Hemodialysis" vs. inpatients without those charges, and an outpatient peritoneal dialysis cohort. Patients with CKD 3 or 4 were excluded. One hundred and sixty-seven charts were reviewed. ECG conduction intervals were consistently and statistically longer among hemodialysis patients (n=88) vs. peritoneal dialysis (n=22) and CKD stage 1 and 2 (n=57): PR (175±35 vs 160±44 vs 157±22 msec) (p=0.009), QRS (115±32 vs. 111±31 vs 91±18 msec) (p=0.001), QT (411±71 vs. 403±46 vs 374±55 msec) (p=0.006), QTc (487±49 vs. 464±38 vs 452±52 msec) (p=0.0001). The only significantly different conduction abnormality was prevalence of left bundle branch block: 13.6% among HD patients, 5% in PD, and 2% in CKD 1 and 2 (p=0.03). To our knowledge, this is the first study to report that ECG conduction intervals are significantly longer as one progresses from CKD Stage 1 and 2, to PD, to HD. These and other data support the need for future research to utilize ECG conduction times to identify dialysis patients who could potentially benefit from proactive cardiac evaluations and risk reduction.

Prevalence of abnormalities in electrocardiogram conduction in dialysis patients: a comparative study

ABSTRACTBackground: The electrocardiogram (ECG) can aid in identification of chronic kidney disease (CKD) patients at high risk for cardiovascular diseases. Cohort studies describe ECG abnormalities in patients on hemodialysis (HD), but we did not find data comparing ECG abnormalities among patients with normal kidney function or peritoneal dialysis (PD) to those on hemodialysis. We hypothesized that ECG conduction abnormalities would be more common, and cardiac conduction interval times longer, among patients on hemodialysis vs. those on peritoneal dialysis and CKD 1 or 2.Methods: Retrospective review of adult inpatients’ charts, comparing those with billing codes for “Hemodialysis” vs. inpatients without those charges, and an outpatient peritoneal dialysis cohort. Patients with CKD 3 or 4 were excluded.Results: One hundred and sixty-seven charts were reviewed. ECG conduction intervals were consistently and statistically longer among hemodialysis patients (n=88) vs. peritoneal dialysis (n=22) and CKD stage 1 and 2 (n=57): PR (175±35 vs 160±44 vs 157±22 msec) (p=0.009), QRS (115±32 vs. 111±31 vs 91±18 msec) (p=0.001), QT (411±71 vs. 403±46 vs 374±55 msec) (p=0.006), QTc (487±49 vs. 464±38 vs 452±52 msec) (p=0.0001). The only significantly different conduction abnormality was prevalence of left bundle branch block: 13.6% among HD patients, 5% in PD, and 2% in CKD 1 and 2 (p=0.03). Conclusion: To our knowledge, this is the first study to report that ECG conduction intervals are significantly longer as one progresses from CKD Stage 1 and 2, to PD, to HD. These and other data support the need for future research to utilize ECG conduction times to identify dialysis patients who could potentially benefit from proactive cardiac evaluations and risk reduction.

Can Cardiac Conduction System Disease Be Prevented?

Cardiac conduction system disorders on the electrocardiogram (ECG) are common. Left bundle branch block (LBBB) is associated with adverse outcomes, and variants previously considerednormal, suchas rightbundlebranchblock (RBBB),1 left anterior fascicularblock,2orPR intervalprolongation,3may also portend morbidity andmortality. At present, no paradigm to treat ECG conduction abnormalities inpatientswithout cardiomyopathyorheart blockexists. Such conduction abnormalities are associated with hypertension, left ventricular hypertrophy (LVH), and atrial fibrillation, anda linkwith inflammation and fibrosis has been suggested.1-3 Although recentlydescribedgeneticdeterminants for conduction abnormalities4 in some patients argue against treatment, the involvement of modifiable or preventable risk factors in others would make prevention of ECG conduction defects an attractive strategy. In this issue of JAMA Internal Medicine, Dewland et al5 present an important study in this area. The authors hypothesized that the antifibrotic and anti-inflammatory properties of angiotensin-converting enzyme inhibitors or statins may reduce incident conduction abnormalities. To test this hypothesis, they studied the effect of randomized administration of lisinopril vs other antihypertensives and pravastatin vs standard care on the development of ECG conduction abnormalities in high-risk patients with hypertension and moderate hypercholesterolemia in the Antihypertensive Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT).6 They assessed 21 004 individuals 55 years or older with hypertension and at least 1 other cardiac risk factor from 33 357 in the parent trial. They excluded 10 691 patients without serial ECGs or with baseline conduction disease or paced rhythm. They assessed 12-lead ECGs every 2 years for incident ECG conduction abnormalities. During the 5-year follow-up, LBBB was detected in 389 individuals; RBBB, in 570; and any conduction defect, in 1114. Lisinopril was associated with a statistically significant 19% reduction in incident ECG conduction abnormalities compared with chlorthalidone. The reduction in incident LBBB was of borderline statistical significance (adjusted hazard ratio, 0.77; 95% CI, 0.60-1.00; P = .05), and the reduction in incident RBBB was not statistically significant. No differences were found for amlodipine compared with chlorthalidone or for pravastatin compared with usual hyperlipidemia treatment. Left ventricular hypertrophy, male sex, age, smoking, coronary disease, diabetes, and body mass index were associated with incident ECG abnormalities. To our knowledge this is the first report that incident conduction system disease may be prevented by drug therapy, in this case lisinopril. This important observation is consistent with established knowledge that angiotensinconverting enzyme inhibition has salutary effects on inflammation, hypertrophy, and fibrosis. If confirmed in other populations, the ability to prevent conduction system disease could have substantial clinical and research implications. First, the major goal of therapy would likely be to prevent incident LBBB. More specific definition of individuals who may benefit, beyond associations with age and diabetes, may be needed to facilitate such preventive strategies. Second, the authors suggest studies to determine whether pharmacologic treatment can affect existing conduction abnormalities, including the need for pacemaker implantation. It would have been intriguing to study whether patients with existing conduction abnormalities in ALLHAT had a slower progression of disease depending on the randomization limb, if a sufficient number of such patients were present at baseline. Third, the association of lisinopril with reduced incident conduction disease5 was not attributable to blood pressure control. Indeed, lisinopril was significantly less effective than chlorthalidone in reducing blood pressure and preventing major cardiovascular outcomes in ALLHAT.6 One hypothesis that could reconcile this paradox is that lisinopril may cause greater regression in left ventricular mass over time than chlorthalidone or amlodipine, independently of blood pressure, particularly in white individuals.6 This finding suggests that interventions that prevent or treat LVH may prevent conduction system disease. Some limitations of this study should be recognized. Echocardiographic indices were reported in a minority of patients,6 and ECG indices of LVH are less reliable (particularly once conduction abnormalities develop). This limitation should be considered when interpreting the lack of interaction between baseline LVH and antihypertensive treatment randomization. Another limitation is that a large number of patients (n = 10691) were excluded owing to lack of ECGs. Remaining patients were more likely to be white men without diabetes or baseline LVH than the parent ALLHAT cohort. Although this difference does not alter the association of incident ECG conduction abnormalities with comorbidities, it may have introduced differences in baseline comorbidities in subgroups randomized to each antihypertensive. Finally, atrial fibrillation, which is linked with atrial conduction slowing,7 was not reported, and only 2 to 3 ECGs recorded during the 5 years precluded detection of transient conduction abnormalities (such as those caused by medications). However, these effects would likely be minor. In conclusion, Dewland et al5 should be congratulated for this important study from ALLHAT showing that treatment with the angiotensin-converting enzyme inhibitor Author Audio Interview at jamainternalmedicine.com

Clinical Predictors of Pacemaker Implantation in Patients with Syncope Receiving Implantable Loop Recorder with or without ECG Conduction Abnormalities

Implantable loop recorders (ILR) allow prolonged cardiac rhythm monitoring and improved diagnostic yield in syncope patients. Predictive factors for pacemaker (PM) implantation in the ILR population with unexplained syncope have not been adequately investigated. In this single center, retrospective, observational study we investigated factors that predict PM implantation in this population. We retrospectively analyzed our ILR database of patients aged over 18 years who underwent ILR implantation for unexplained syncope between January 2009 and June 2013. Patient case notes were examined for demographics, history, electrocardiogram (ECG) abnormalities, investigations, and events during follow-up. The primary end-point was the detection of a symptomatic or asymptomatic bradycardia requiring PM implantation. During a period of 4.5 years, 200 patients were implanted with ILR for unexplained syncope, of who n = 33 (16.5%) had clinically significant bradycardia requiring PM implantation. After multivariable analysis, history of injury secondary to syncope was found to be the strongest independent predictor for PM implantation (odds ratio [OR]:9.1; P < 0.001; 95% confidence interval [CI]: (3.26-26.81). Other significant predictors included female sex, PR interval > 200msec, and age >75 years. In patients without conduction abnormalities on the ECG, history of injury secondary to syncope was found to be the strongest independent predictor for PM implantation (OR: 8.16; P = 0.00027; 95% [CI]: (2.67-26.27). A history of injury secondary to syncope and female sex were independent predictive factors for bradycardia necessitating PM implantation in patients receiving an ILR for syncope with or without ECG conduction abnormalities.

A Late Presentation of Dynamic ECG Conduction Abnormalities following Blunt Chest Injury

Cardiac abnormalities following blunt chest trauma can range from minor ST changes to arrhythmias, cardiac rupture, cardiogenic shock and death. A normal electrocardiogram (ECG) on presentation does not guarantee the absence of myocardial injury, and with no gold standard test to detect the condition, myocardial contusion is often identified only at autopsy. We describe the late presentation of evolving and dynamic conduction abnormalities on the ECG, including a sinusoidal conduction pattern, in a young trauma patient. This sequence of conduction abnormalities has not previously been observed and we discuss the potential explanations.

The diagnostic and therapeutic aspects of loss-of-function cardiac sodium channelopathies in children

Loss-of-function sodium channelopathies manifest as a spectrum of diseases including Brugada syndrome (BrS) and cardiac conduction disease. To analyze the diagnostic and therapeutic aspects of these disorders in children. Patients aged ≤ 16 years with genetically confirmed loss-of-function sodium channelopathies (SCN5A mutation), presenting with cardiac symptoms, positive family history, and/or abnormal electrocardiogram (ECG), were included. Abnormal ECG consisted of type 1 BrS ECG and/or prolonged conduction intervals (PR interval/QRS duration > 98th percentile for age). Among the cohort (n = 33, age 6 ± 5 years, 58% male subjects, 30% probands), 14 (42%) patients were symptomatic, presenting with syncope (n = 5), palpitations (n = 1), supraventricular arrhythmias (n = 3), aborted cardiac arrest (n = 3), and sudden cardiac death (n = 2). Heart rate was 91 ± 26 beats/min, PR interval 168 ± 35 ms, QRS duration 112 ± 20 ms, and heart-rate corrected QT interval 409 ± 26 ms. Conduction intervals were prolonged in 28 (85%) patients; 6 of these patients also had spontaneous type 1 BrS ECG. Eight fever-associated events occurred in 6 patients; 2 of these were vaccination-related fever episodes. Treatment included aggressive antipyretics during fever in all patients; antiarrhythmic treatment included implantable cardioverter-defibrillator (n = 4), pacemaker (n = 2), and beta-blockers, either alone (n = 3) or in combination with device (n = 2). During follow-up (4 ± 4 years), 2 previously symptomatic patients had monomorphic ventricular tachycardia; there were no deaths. Diagnosis of loss-of-function sodium channelopathies in children relies on cardiac symptoms, family history, and ECG. Fever and vaccination are potential arrhythmia triggers; conduction delay is the commonest finding on ECG. Beta-blockers have a role in preventing tachycardia-induced arrhythmias; implantable cardioverter-defibrillator should probably be reserved for severe cases.

Abstract P344: Prevalence of Conduction Abnormalities in a Systolic Heart Failure Disease Management Population by Race, Ethnicity, and Gender

While there have been several studies evaluating the prevalence of electrocardiogram (ECG) conduction abnormalities such as left bundle branch block (LBBB) and atrial fibrillation (AF) in the general population, there are none currently describing that of the Hispanic population in patients with systolic heart failure. Given the need for examining race and ethnic differences in ECG abnormalities, the primary purpose of this study is to compare the prevalence of ECG abnormalities in three systolic heart failure populations from two indigent heart failure clinics. The study examines EKG difference among three ethnic groups: Caucasians, African-Americans, and Hispanics. We also investigated ECG differences between genders. This is a cross sectional study. A total of 926 patients were enrolled in a systolic heart failure disease management program in two safety net hospitals in Florida and Louisiana. Inclusion criteria was an ejection fraction (EF) &lt; or equal to 40% by echocardiography, and ECGs which were obtained closest to the date of enrollment. Caucasian patients had more atrial fibrillation than African-American patients. Hispanics had more paced rhythm, left bundle branch block and abnormal QT intervals than Caucasian or African-American patients. A QRS interval greater than 120 milliseconds (ms) was less prevalent among African-Americans. ECG conduction abnormalities vary across race, ethnicity, and gender. Adequate medical attention should be addressed to these variations since relevant ECG findings can offer additional guidance for therapeutic interventions, as well as provide important prognostic information and potentially modify morbidity and mortality rates.

Lamotrigine does not prolong QTc in a thorough QT/QTc study in healthy subjects, Dixon et al. 2008; request for publication of PR interval data

Dixon et al. reported the results of the most thorough study of lamotrigine effects on electrocardiogram (ECG) intervals that has been published to date [1]. In this placebo- and moxifloxacin-controlled trial, lamotrigine monotherapy at doses up to 400 mg day−1 was shown to not prolong the QTc interval in healthy subjects. The report stated that additional ECG conduction intervals were measured, including the PR interval and the QRS duration. While QRS duration results were reported in the paper, the PR interval results from the study were neither reported nor discussed. Approved labelling for lamotrigine does not include evidence indicating that lamotrigine has any effect on PR interval [2, 3]; however, the literature contains at least two trials where lamotrigine was reported to be associated with a small increase in mean PR (or PQ) interval in patients with epilepsy. Matsuo et al. reported a mean 5 ms increase in PR interval in epilepsy patients randomized to treatment with lamotrigine [4]. Recently, Saetre et al. reported that lamotrigine was associated with a mean 8.8 ms increase in PQ interval in a group of elderly epilepsy patients treated with a relatively low mean daily lamotrigine dose (∼110 mg day−1, serum concentration ∼2.6 µg ml−1) [5]. Given these findings, a complete reporting of the ECG data, including PR interval, is important for an accurate assessment of the cardiac profile of lamotrigine. The extensive ECG data acquisition and relatively high steady-state plasma concentrations of lamotrigine (9.6 µg ml−1 for the 400 mg day−1 dose group) evaluated in the Dixon et al. trial [1] would provide the specific data needed to determine whether there is an effect of lamotrigine on PR interval. As such, we respectfully request an addendum to this publication that would allow the inclusion of a graphical presentation of PR interval data, such as that used in the report for QRS duration, as well as a quantitative statement of the mean placebo-subtracted change from baseline for PR interval at steady state (Cmax) for the three lamotrigine doses that were studied.

Development of atrio-ventricular block during adenosine infusion and incidence of subsequent pacemaker implantation: A retrospective study

Background Atrio-ventricular (AV) block during adenosine infusion complicates a small percentage of pharmacologic stress tests. The prognostic value of adenosine infusion-related AV block for predicting later conduction disturbances requiring permanent pacemaker (PPM) implantation is not known. Methods Retrospective analysis of the nuclear laboratory electronic data-base identified 125 patients, mean age 66.6 years (y) (SD 12.6), 65% females, who developed transient AV block during adenosine infusion. A control group of 337 consecutive patients mean age 64.4 y (SD 12.5), 63% females, without AV block on adenosine infusion was identified. Both sets of data were entered in the electrophysiology laboratory electronic data-base to identify those patients requiring permanent pacemakers (PPM). Results In the AV block group, 57 patients(46%) had baseline electrocardiogram (ECG) conduction disturbances (included sinus bradycardia, AV block, right or left bundle branch block and non-specific intraventricular conduction delay) versus 80 patients(24%) in the control group (p<0.001). A total of 8 patients received PPM, 50% due to sick sinus syndrome and 50% due to high-degree AV block. In the AV block group, the incidence of PPM implantation due to conduction disturbance was 2.4% (3 patients) by the end of 2.2 y (SD 1.44) after the adenosine infusion versus 1.5%(5 patients) by the end of 2.4 y (SD 0.26) in the control group (NS). The mean age for PPM implantation was 78.3 y (SD 6.3). Interestingly, ischemia localized to the right coronary artery territory was identified in 15 patients (12%) in the AV block group versus 10 patients (3%) in the control group (p<0.001). Conclusions The occurrence of AV block during adenosine infusion did not increase the incidence of conduction disturbances requiring PPM implantation during the time interval studied. Development of AV block during adenosine infusion occurred more frequently in patients with baseline ECG conduction abnormalities. Patients requiring PPM implantation were > 70 y regardless of the AV block status.

Electrocardiographic Effects of Desipramine and 2-Hydroxydesipramine in Children, Adolescents, and Adults Treated with Desipramine

To assess the developmental effects of desipramine (DMI) treatment on the electrocardiogram (ECG), we investigated serum concentrations of DMI ([DMI]), and its major active metabolite 2-hydroxydesipramine ([OHDMI]) and ECG parameters. ECGs and [DMI] and [OHDMI] were analyzed from 50 children, 39 adolescents, and 30 adult psychiatric patients receiving DMI. There were modest overall correlations between [DMI], [OHDMI], or [OHDMI+DMI], and the PR and QRS intervals when data from all 119 subjects were pooled. Within the pediatric age groups there were no significant associations between serum drug levels and heart rate or conduction intervals; and in all subjects with ECG abnormalities, there were some findings of higher [DMI], [OHDMI], and [OHDMI+DMI]. These findings indicate that only modest associations of [DMI] and [OHDMI] with ECG conduction intervals were found, and are not likely to be clinically significant in any of the age groups studied. Compared with adults, children and adolescents do not appear to be at increased risks for ECG changes related to DMI treatment or to circulating concentrations of [DMI] or [OHDMI].