Electrocardiogram Conduction Abnormalities Research Articles

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.

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.

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.

Relation of CTG expansion and clinical variables to electrocardiogram conduction abnormalities and sudden death in patients with myotonic dystrophy

We prospectively followed 63 patients with myotonic dystrophy (DM) after establishing diagnosis of DM for an average 8 years in an attempt to detect conduction disturbances (by electrocardiography and/or Holter monitoring) and sudden cardiac events (sudden death, cardiac syncope) and correlate them to potential predicting factors (CTG repeat expansion in the myotonin protein kinase gene and several clinical variables: clinical type and duration of DM, age and sex). Twenty-six patients developed conduction disturbances, five patients died suddenly, and two patients experienced cardiac syncope necessitating urgent implantation of pacemaker. Analysis showed no significant correlation between conduction disturbances and/or cardiac events and CTG expansion. Furthermore, no correlation was found with type of DM, whereas conduction disturbances and sudden cardiac events correlated with patients' age, duration of disease and male sex. Results on our cohort of DM patients show that CTG expansion has no role in predicting neither conduction abnormalities nor sudden death. It seems that risk of sudden death increases with duration of disease and age, and that risk is higher in male patients.

Contrast agent-induced cardiac arrhythmias in rats: Lesions and mechanisms of injury

Other than minor contraindications, no known meaningful health risks have been reported during the use of microbubble ultrasound echogenic contrast imaging agents in the United States. At this meeting, we have reported on electrocardiogram conduction abnormalities in rat hearts exposed to pulsed ultrasound following intravenous injection of a contrast agent. Rats had no meaningful conduction abnormalities when exposed to ultrasound alone or contrast agent alone but developed premature atrial and ventricular complexes and polymorphic ventricular tachycardia when a contrast agent was administered and the heart was exposed to pulsed ultrasound. When ultrasound exposure was concluded, cardiac arrhythmias ceased but reoccurred when ultrasound exposure was resumed. Acute multifocal coagulative necrosis of cardiac rhabdomyocytes was observed microscopically in myocardium of rats exposed to ultrasound following injection of a contrast agent. Because cardiac arrhythmias were induced only when a contrast agent interacted with ultrasound during exposure, the presence of myocardial lesions alone did not appear sufficient to serve as foci for ectopic electrical activity. These results suggest that a microbubble contrast agent through its biomechanical interactions with pulsed ultrasound has the potential to induce conduction abnormalities leading to potentially hazardous cardiac arrhythmias. [Work supported by NIH Grant No. HL58218.]

Contrast agent-induced cardiac arrhythmias in rats: Exposimetry and clinical findings

Other than minor contraindications, no known meaningful health risks have been reported following the use of microbubble ultrasound echogenic contrast imaging agents in the United States. Recently, a report from the Netherlands has documented premature ventricular contractions during triggered second harmonic imaging of a contrast agent for myocardial perfusion in healthy male volunteers. Because of this report, we designed a study to characterize electrocardiogram conduction abnormalities in rat hearts exposed to pulsed ultrasound following injection of a contrast agent. We used a focused f/1 3.1-MHz, transducer that had in situ (at the heart) peak rarefactional and compressional pressures of 15.9 MPa and 36.1 MPa, respectively, 1.7-kHz PRF, 1.2-μs pulse duration, and MI of 5.8. Rats had no meaningful conduction abnormalities when exposed to ultrasound alone or contrast agent alone but developed premature atrial and ventricular complexes and polymorphic ventricular tachycardia when a contrast agent was administered intravenously and the heart exposed to pulsed ultrasound. When ultrasound exposure was concluded, cardiac arrhythmias ceased but reoccurred when ultrasound exposure was resumed. These results suggest that a microbubble contrast agent through its biomechanical interactions with pulsed ultrasound has the potential to induce conduction abnormalities leading to potentially hazardous cardiac arrhythmias. [Work supported by NIH Grant No. HL58218.]