Short PR Interval Research Articles

Lown-Ganong-Levine Syndrome in a 3-Month-Old Infant with Isolated Left Ventricular Noncompaction

This report describes a 3-month-old boy with isolated left ventricular noncompaction admitted to a medical facility due to heart failure and dysrhythmia. His electrocardiogram showed a short PR interval and a normal QRS complex after abortion of supraventricular tachycardia in favor of Lown-Ganong-Levine syndrome or enhanced atrioventricular nodal conduction.

Clinical presentation and treatment of atrial fibrillation in Wolff-Parkinson-White syndrome

A case of Wolff-Parkinson-White syndrome with atrial fibrillation (AF) is reported in a patient who presented with syncope, tachycardia, and hypotension. The electrocardiogram (ECG) showed a fast irregular rhythm with wide polymorphic QRS tachycardia without the QRS twisting around the isoelectric baseline, diagnostic of AF and Wolff-Parkinson-White syndrome. The patient did not respond to intravenous amiodarone. Elective cardioversion restored sinus rhythm, and the ECG showed a wide QRS complex, short PR interval, and delta wave, indicating the presence of an accessory pathway and pre-excitation. AF was easily induced during the electrophysiologic study, requiring electrical cardioversion for severe hypotension. Successful radiofrequency ablation of the accessory pathway completely prevented further inducible AF. The patient no longer had any evidence of pre-excitation on ECG and remained symptom-free with no medications for 11 months.

Electrophysiological characteristics associated with symptoms in pacemaker patients with paroxysmal atrial fibrillation

The purpose of this study is to identify the electrophysiological factors affecting symptoms in paroxysmal atrial fibrillation (PAF) using patients with paroxysmal atrial fibrillation and pacemakers with advanced atrial fibrillation (AF) diagnostics. Seventy-nine patients (age 71.0 +/- 8.2, 54.4% male) with symptomatic PAF and AF burden of 1% to 50% with DDDRP pacemakers implanted were assessed for 6 months. Patients recorded symptom onset and duration and these were correlated with device-derived electrophysiological data. Of 2,638 AF episodes, 333 were symptomatic and 2,305 asymptomatic, with 194 non-atrial tachyarrhythmia symptomatic episodes giving a sensitivity of 12.6% and a positive predictive value of 63.2% for specific AF symptoms. Symptomatic AF episodes were 3.8 times more common diurnally than nocturnally (p < 0.001). Diurnally, symptomatic AF was significantly associated with a shorter AF cycle length (CL; p = 0.04), faster ventricular rate (p = 0.004), shorter PR interval (p < 0.001), faster preceding heart rate (p = 0.001) and increased early recurrence of AF (p < 0.04). Nocturnally, a significantly longer AF CL (p = 0.04) and PR interval (p < 0.001) prior to AF onset predicted symptomatic AF. Symptoms in PAF are predicted by changes in AF episode duration, ventricular rate during AF, preceding sinus heart rate, AV nodal conduction and AF cycle length but not ventricular irregularity. Excess diurnal sympathetic tone and excess nocturnal vagal tone predispose to symptomatic PAF. These findings may have relevance for therapies for symptom control of PAF.

Cx30.2enhancer analysis identifies Gata4 as a novel regulator of atrioventricular delay

The cardiac conduction system comprises a specialized tract of electrically coupled cardiomyocytes responsible for impulse propagation through the heart. Abnormalities in cardiac conduction are responsible for numerous forms of cardiac arrhythmias, but relatively little is known about the gene regulatory mechanisms that control the formation of the conduction system. We demonstrate that a distal enhancer for the connexin 30.2 (Cx30.2, also known as Gjd3) gene, which encodes a gap junction protein required for normal atrioventricular (AV) delay in mice, is necessary and sufficient to direct expression to the developing AV conduction system (AVCS). Moreover, we show that this enhancer requires Tbx5 and Gata4 for proper expression in the conduction system, and Gata4(+/-) mice have short PR intervals indicative of accelerated AV conduction. Thus, our results implicate Gata4 in conduction system function and provide a clearer understanding of the transcriptional pathways that impact normal AV delay.

When headaches are not neurological: an unusual presentation of Ebstein's anomaly

A 16-year-old male was admitted following a loss of vision. Baseline observations demonstrated SpO2 80% on air, tachycardia of 180 beats per minute (bpm) and hypotension of 90/50 mmHg. He reported bilateral visual disturbance while sitting in bed together with breathlessness, chest discomfort and dizziness but had not had palpitation or syncope. He had been prescribed propranolol for recurrent migraines of increasing frequency with similar visual disturbances, nausea and vomiting but with no perceived benefit. He was otherwise well, a non-smoker who drank minimally and denied recreational drug use. On examination, the jugular venous pressure was elevated but there were no other cardiorespiratory findings of note. Arterial blood gas analysis revealed profound hypoxia and a compensated metabolic acidosis. A 12-lead electrocardiogram demonstrated a supraventricular tachycardia with broad QRS (Figure 1). Carotid sinus massage and intravenous adenosine had no effect. Electrolyte levels were abnormal (potassium 2.7 mmol/litre, magnesium 0.45 mmol/litre, corrected calcium 1.60 mmol/litre) and a central venous line was inserted to allow electrolyte replacement. During this procedure, he spontaneously reverted to sinus rhythm at a rate of 70 bpm. A repeat electrocardiogram showed sinus rhythm with normal axis but T wave inversion in the inferior leads and evidence of pre-excitation with a short PR interval and classical delta waves (Figure 2). As a result, Wolff–Parkinson–White syndrome was diagnosed. The chest radiograph showed an abnormal, globular cardiac silhouette (Figure 3). Following return to sinus rhythm, the blood pressure and acid–base status normalized. Routine transthoracic echocardiography demonstrated Ebstein's anomaly with an associated atrial septal defect and small membranous ventricular septal defect.

Echocardiographic optimization of the atrioventricular and interventricular intervals during cardiac resynchronization

An optimized atrioventricular (AV) interval can maximize the benefits of cardiac resynchronization therapy (CRT). If programmed poorly, it may curtail beneficial effects of CRT. AV optimization will not convert non-responder to responder, but may convert under-responder to improved status. There are many echocardiographic techniques for AV optimization but there is no universally accepted gold standard. The optimal AV delay varies with time, necessitating periodic re-evaluation. As the optimal AV delay may lengthen on exercise, a rate-adaptive AV delay should not be routinely programmed. Intra- and interatrial conduction delays may require AV junctional ablation when AV optimization is impossible in patients with a poor clinical response. Fusion with the spontaneous QRS complex may be acceptable on a trial basis to seek a better clinical response or with a short PR interval. Routine VV optimization is presently controversial but programming may prove beneficial in some patients with a suboptimal CRT response where no cause is found. It may partially compensate for less than optimal left ventricular (LV) lead position and may correct for heterogeneous ventricular activation including a prolonged LV latency interval and slow conduction (scarring) near the LV pacing site. VV timing is generally programmed using the aortic velocity-time integral, and long-term variations of the optimal value necessitate periodic re-evaluation.

Re-examination of the Electrocardiogram in Boys With Duchenne Muscular Dystrophy and Correlation With Its Dilated Cardiomyopathy

Duchenne muscular dystrophy (DMD) results in dilated cardiomyopathy (DC). Characteristic electrocardiographic (ECG) changes include short PR interval, right ventricular hypertrophy (RVH), prolonged QTc interval, and prominent Q waves in leads I, aVL, V5, and V6 or in leads II, III, aVF, V5, and V6. We re-examined the prevalence and correlation of ECG changes with DC in DMD. Electrograms of 115 patients with DMD were evaluated. DC was defined as an echocardiographic ejection fraction<55%. PR interval and RVH were based on age-based normal values. Abnormal Q waves were >or=4 mm. Abnormal QTc interval was >or=450 ms. ST-segment depression was defined as >0.5 mm. Fisher's exact test evaluated significant differences between groups and logistic regression determined whether number of ECG changes predicted DC. Forty had DC. No significant differences existed between the number of ECG changes in DC and non-DC groups (p=0.279). Distribution of findings included short PR interval (43%), RVH (37%), prominent Q waves in leads V5 (34%) and V6 (33%), prominent Q waves in leads I, aVL, V5, and V6 (3, 1 with DC), prominent Q waves in leads II, III, aVF, V5, and V6 (9, 4 with DC), long QTc interval (0), ST depression (2, 1 with DC), and flat/biphasic ST segments (38, 15 with DC). In conclusion, ECG changes are similar in patients with DMD regardless of presence of DC. Previously reported characteristic ECG changes are seen in a minority of DMD cases. The most common findings are short PR interval and RVH. Prominent Q waves in leads II, III, aVF, V5, and V6 are more likely.

Abstract 3470: Deletion of Glycogen Synthase Kinase-3α (GKS-3α) Causes a Glycogen Storage Cardiomyopathy

Background: GSK-3 and its targets play critical roles in a wide array of processes including development and cancer. In mammalian cells there are two isoforms, α and β. GSK-3β is purported to be a negative regulator of cardiac hypertrophy, but this is based solely on over-expression approaches, and virtually nothing is known of the functions of GSK-3α. Methods: We generated mice deleted for GSK-3α. Heart development, as well as postnatal cardiac growth, glycogen metabolism, morphology, physiology, and ECG conduction invervals were examined. Age-matched wild type (WT) mice served as controls. Results: Heart development was normal, consistent with full compensation by GSK-3β for loss of GSK-3α during development. However, echocardiographic LV mass (in mg) was significantly increased in the KO compared to WT: 187.95 ± 35.05 vs 143.52 ± 23.94*. Heart weight (HW, mg) and HW/body weight ratio were also significantly increased in the KO: 186.73 ± 15.3* and 4.96 ± 0.38* for KO (n = 19); 146.33 ± 14.92 and 4.12 ± 0.27 for WT (n = 10). Thus deletion of GSK-3α leads to significant cardiac hypertrophy with aging. The underlying mechanism appears to be marked glycogen deposition seen with both Periodic acid-Schiff staining and transmission electron microscopy. Although LV function as assessed by echocardiography was normal at 4 months of age, invasive hemodynamic evaluation demonstrated a depressed response to isoproterenol infusion. ECG revealed a significantly shortened PR interval without pre-excitation. Conclusions: We demonstrate for the first time a striking isoform-specific role for GSK-3α in the heart, and that role is as a critical regulator of glycogen metabolism. Deletion of GSK-3α leads to a glycogen storage cardiomyopathy, sharing some features with that seen with mutations in AMP-activated protein kinase. These data suggest the possibility that mutations in, or alterations in activity of, GSK-3α could account for some cases of hypertrophic cardiomyopathy. (*, P &lt; 0.01, KO vs. WT)

Short PR Interval in the Absence of Preexcitation: A Characteristic Finding in a Patient with Fabry Disease

Fabry disease (FD) is a rare lysosomal storage disease characterized by intracellular deposition of glycosphingolipids that can involve various organs including the heart. Here, we report the finding of a short PR interval in a patient with FD and recurrent syncope associated with short atrial-His (A-H) and His-ventricular (H-V) intervals in the absence of preexcitation. While electrocardiographic abnormalities are not uncommon among FD patients, there have been few reports on electrophysiological studies performed on these patients. The exact mechanism for the short A-H and H-V intervals remains unclear, but they may result from accelerated conduction in the AV node-His-Purkinje system.

Clinical Use of Electrocardiography in Adults With Congenital Heart Disease

The prevalence of adult congenital heart disease (ACHD) has risen markedly over the past 2 decades, with the number of adults now rivaling the number of children with severe defects.1 This is, perhaps, not surprising given that current care allows nearly 90% of infants born with heart defects to thrive into their adult years.1,2 This remarkable triumph is tempered, however, by the realization that early interventions were reparative and not curative. Numerous complications may surface years after uneventful childhood courses, justifying vigilant clinical follow-up throughout adulthood. The 12-lead ECG remains an invaluable cornerstone in the clinical appraisal of adults with congenital heart disease that, in certain circumstances, provides diagnostic and/or prognostic information. The present review imparts a clinical perspective to ECG interpretation in ACHD, emphasizing practical and pathogenomonic findings in the more frequently encountered congenital defects in adults. Anatomic features of the conduction system relevant to ECG findings in ACHD are summarized, including variations in the location of the sinus node, atrioventricular (AV) node, and His-Purkinje system. Thereafter, pertinent ECG features are highlighted for common subtypes of ACHD (Table). Examples are provided throughout for illustration. View this table: Table. Typical ECG Features in Common Forms of ACHD ### Sinus Node In the morphologically normal heart, a crescent-shaped sinus node is characteristically located epicardially along the lateral aspect of the superior cavoatrial junction. It generates a P-wave axis typically between 15° and 75°. Most patients with ACHD have normally positioned atrial chambers, called atrial situs solitus, with normal sinus node location. The position of the sinus node may, however, vary with the atrial chambers and their appendages. #### Juxtaposition of the Atrial Appendages In juxtaposition of the atrial appendages, both appendages are on the same side of the arterial pedicle rather than each being ipsilateral to its respective atrium. Left juxtaposition, with left-sided atrial appendages, frequently accompanies tricuspid atresia and has …

Genetic Wiring Diagram of the Cardiac Conduction System

In 1906, Tawara published his treatise, recently translated from German to English,1 on the anatomy of the cardiac conduction system, which he elucidated through painstaking dissection and histological examination. In the following decades, the conduction system was generally understood and studied in anatomic and physiological terms. Most molecular biology focused on the genes and proteins that generate or propagate the cardiac action potential. Unlike other tissues and organs, including the heart, little was known about its embryonic development, even though the anatomic form of the conduction system is clearly relevant to its function. Until recently, developmental biology was hampered by the lack of a working model of how the conduction system forms, reagents, and methods. This situation has changed significantly since Gourdie and Mikawa2 reported their seminal observations in 1995. In an elegant series of chick embryo experiments, their laboratories proved that a developing node or fiber in the central and peripheral conduction systems forms by recruitment of adjacent multipotent myocytes.2,3 The murine conduction system develops by the same process of accretion.4 Soon afterward, Berul et al,5 Morley et al,6 and Baker et al7 described their applications of intracardiac electrophysiology and optical mapping to study normal and abnormal conduction in the mouse, thus opening the door for experimental genetics and developmental biology. Article p 2535 The inductive patterning of tissues is a central theme in development. In the chick embryo, endothelin-1 is secreted by the coronary arterioles to induce …

Early repolarization associated with accelerated atrioventricular conduction (short PR interval) and incomplete right bundle branch block: postulated mechanisms

A 36-year-old male patient, who was admitted with atypical chest pain and had normal physical examination and laboratory findings, including on an echocardiogram and a maximal exercise treadmill/thallium test, is described. His electrocardiograms (ECGs) revealed ST-segment elevation in leads V 1 through V 1, suggestive of early repolarization variant (ERPV); in addition, there was evidence of accelerated atrioventricular conduction (short PR interval) and incomplete right bundle branch block (IRBBB). It is postulated that these 2 features represent ECG “correlates” of ERPV, which is characterized by accelerated repolarization and depolarization, and are due to a rapid conduction through all or some component(s) of the atria/AV-node/Hiss bundle/left bundle branch/left ventricle “chain,” leading to a short PR interval and early and accelerated activation of the left ventricle, with resultant IRBBB. In addition to this being a case report, it constitutes a speculation that all the noted ECG findings are related and occurred in the context of ERPV; in all scientific fairness, it is possible that the accelerated atrioventricular conduction and IRBBB could have also occurred in a patient who happened to have ERPV. Finally, the occasional occurrence of morbidity and mortality in a patient with ERPV does not mitigate (at least until we know more) the time-honored belief that the ERPV is, after all, a benign ECG variant.

A familial form of conduction defect related to a mutation in the PRKAG2 gene

We describe four members of the same family with a very similar ECG pattern characterized by conduction defects (right bundle branch block, frequent left anterior hemiblock, atrial hypertrophy, and sometimes severe nodal dysfunction) contrasting with a short PR interval. Significant clinical events were reported only after 60 years of age. A mutation in the gamma2 subunit of the AMP activated protein kinase gene (PRKAG2) was identified in the four members of the family, with an autosomal dominant inheritance. The phenotype observed in this family appears different from that previously described as associated with this gene as neither left ventricular hypertrophy nor Wolff-Parkinson-White syndrome was present. These findings extend the phenotype associated with the PRKAG2 gene and emphasize an additional cause of familial conduction defect.

Percutaneous Epicardial Mapping and Ablation of a Posteroseptal Accessory Pathway

A 20-year-old man with no past medical history experienced a syncopal episode. He was found to be pulseless, and cardiopulmonary resuscitation was initiated. When emergency medical service arrived, rhythm strip showed an irregular wide-complex tachycardia consistent with preexcited atrial fibrillation with cycle length as short as 180 ms (333 beats per minute) (Figure 1A). He was defibrillated successfully into sinus rhythm. A 12-lead ECG showed sinus rhythm with PR interval of 110 ms, delta waves and pseudo-infarct pattern in the inferior leads consistent with a posteroseptal accessory pathway (Figure 1B). He was referred to us for an electrophysiology study. Figure 1. A, Rhythm strip of patient during the cardiac arrest, showing irregular wide-complex tachycardia very suggestive of preexcited atrial fibrillation. B, 12-lead ECG after resuscitation. The short PR interval, delta wave and pseudo-infarct pattern in the inferior leads are consistent with the presence of a manifest accessory pathway (Wolff-Parkinson-White Syndrome). During the procedure, extensive mapping in the right atrium, the coronary sinus (CS) and its branches, and the left atrium (via transseptal approach) was performed. A CS angiogram showed the presence of a diverticulum. The area of earliest ventricular …

Cardiovascular Manifestations in Fabry Disease: A Clinical and Echocardiographic Study

This study reviews the clinical and echocardiographic findings in a cohort of Fabry patients (n=12) and compares echocardiographic findings to normal controls. Almost all patients had extracardiac manifestations. Five out of 12 patients had cardiovascular symptoms. Nine out of 12 patients had left ventricular hypertrophy (LVH) on the electrocardiogram (ECG) and one patient had short PR interval. Three patients had epicardial coronary disease. Four patients had 'rat-tail' appearance on left ventriculogram. Six patients who had myocardial biopsy showed extensive vacuolation of the myocytes on light microscopy and concentric, myelinoid lamellar cytoplasmic inclusion bodies on electron microscopy. On echocardiography, LV mass was significantly increased in the Fabry group compared to normal controls. Traditional parameters of diastolic function including peak E velocity, peak A velocity and deceleration time were no different to normal controls. The IVRT was significantly prolonged in the Fabry subjects. The PV atrial reversal duration exceeded that of mitral A wave duration in the Fabry group. The septal E' velocity with Doppler tissue imaging (DTI) was significantly lower in the Fabry group than the normal controls. Fabry disease should be considered in the differential diagnosis in patients with unexplained LVH and late onset hypertrophic cardiomyopathy. Extracardiac manifestations are common.

Down syndrome associated with hypothyroidism and chronic pericardial effusion: echocardiographic follow-up.

We present a 39-year-old male patient with Down syndrome who was evaluated for fatigue, palpitations and bouts of cyanosis. Physical examination showed features of trisomy-21(Down syndrome), with a slow pulse rate, distant cardiac sounds and absent apex beat. He had normal jugular venous pressure without pulsus paradoxus. The ECG showed QRS microvoltage and flattened P and T segments. The 48-hour ambulatory ECG depicted normal sinus rhythm with intermittent short PR interval without tachyarrhythmias. The chest Xray revealed cardiomegaly without pulmonary venous congestion. Although serial transthoracic echocardiographic examination demonstrated pericardial effusion with features of tamponade, there were no overt signs of clinical cardiac tamponade. Biochemically, the serum thyroxine of 3 pmol/l (normal 10 to 25) and thyroid-stimulating hormone of 160 mU/l (normal 0.20 to 4.20)) were compatible with hypothyroidism. The patient was treated with L-thyroxine sodium daily, which was gradually increased to 0.125 mg daily. Within a few months he lost weight and became more alert; furthermore, the symptoms of hypothyroidism and the pericardial effusion resolved. It can be concluded that Down syndrome may be associated with hypothyroidism and pericardial effusion. These were alleviated following hormone replacement. Regular evaluation of thyroid function tests is important in Down syndrome. (Neth Heart J 2007;15:67-70.).

Questioning Guidelines in the ECG Puzzler

My colleague and I use AACN’s “9 features” (those that appear in the ECG Puzzler column) in a basic ECG course we teach to nurses working in the intensive care and telehealth units in our hospital. However, we’ve been wondering about some discrepancies in the column. The first deals with heart rate. Although the ECG Puzzler states that “normal” heart rate is “60–90 beats per minute,” the literature (including AACN’s literature) states that a normal rate is 60 to 100/min.The second problem is with PR interval. According to the ECG Puzzler, a short PR interval is one that is less than 0.08 seconds. However, the literature seems to disagree on this measurement, instead suggesting that a short PR interval is less than 0.12 seconds.The next point is about QTc and T waves. We would suggest that both of these features could include a check box that reads “cannot determine” for cases in which neither is discernible because of distortion.Similarly, ST segments could include a check box that reads “flat,” because this has been identified as an abnormality of concern in the literature.Our thanks to these authors for their letters. First let’s deal with points the letters have in common.Yes, it’s true that sinus rhythm historically has been defined as 60 to 100/min. However, physiologically and clinically speaking, sinus rhythm in the resting adult is specifically 44 to 84/min for men and 50 to 90/min for women.1,2As for the PR interval, it is normally between 0.12 and 0.20 seconds; therefore, we’ve made a correction to the column beginning with this issue. A QRS duration greater than 0.12 seconds does suggest an intraventricular conduction delay. However, given that it is often difficult to determine exactly where the QRS begins and ends, precise measurements are difficult to ensure. And so, to improve the specificity of identifying a wide QRS in the ECG Puzzler column, the criterion of “greater than 0.12 seconds” (3 small boxes) has been applied.We concur with Ms Walden that tachycardia is greater than 100/min rather than 120/min. We also agree that there are numerous characteristics of ventricular tachycardia easily applied to a resting 12-lead ECG (eg, QRS axis). Ms Walden is not incorrect in her assessment, but the 4 signs of ventricular tachycardia she outlines are correct only with a particular ECG waveform; for the ECG waveform in our example, Ms Walden’s criteria are not helpful. Also, our overall interpretation was not incorrect; that is, we called it ventricular tachycardia. Because our column only provided a short dual-lead ECG strip typically found in clinical practice, many additional ECG criteria cannot be applied. It is for this reason that we focus on criteria that can be applied, such as QRS width and morphology.We agree that it is important for the patient to have a cardiac evaluation—that is why we introduced the final paragraph with the word however in italics to emphasize the point. A comprehensive list of possible cardiac procedures (eg, resting ECG, serial ECG, Holter ECG, serum biomarkers, C-reactive protein level, echocardiography, stress test, angiogram, computed tomography scan, magnetic resonance images) is beyond the scope of the ECG Puzzler column. For the sake of brevity, then, we simply used “and so on.”The letter from Kilbourne and Sorenson raises 2 other points. Yes, “cannot determine” is not a fixed option for measures of QTc and T wave, but depending on the scenario presented in the ECG Puzzler we have added it as an option. Although notable, “flat” ST segments are nondiagnostic; in other words, they do not definitively identify a diagnosis. Given that the focus of our column is clinical, however, we prioritized true ST-segment deviation that meets diagnostic criteria.

Adverse remodeling of cardiac cholinergic innervation and pacemaker dysfunction in Gαq overexpressing mice

Cardiac-selective overexpression of Gαq leads first to cardiac hypertrophy and then to marked systolic dysfunction and blunted β-adrenergic response. Unlike clinical heart failure, Gαq overexpressors also exhibit a reduced heart rate. To address this discrepancy, we evaluated cardiac cholinergic innervation in Gαq overexpressors at 6 months of age. Resting HR, chronotropic response to right vagal stimulation (VS) and effect of atropine (5 mg/kg, i.p.) were determined by EKG analysis in mice anesthetized with 2% isoflurane. Compared to control mice, overexpressors had a lower resting HR and shorter PR interval (25±3 vs 65±11 ms, n=6-7, P<0.01). VS caused a robust, frequency-dependent bradycardia in control mice with 20Hz stimuli reducing HR by 81±2% to 84±19 bpm. Chronotropic response to VS was absent or blunted in transgenic mice. Transgenic responders exhibited a higher threshold for stimulation-evoked bradycardia and smaller responses. Stimulation at 20Hz decreased HR by 20±4% to 132±12 bpm (n=4). Atropine increased heart rate by 114±23 bpm in control mice but did not affect HR significantly in overexpressors. Immunohistochemical analysis of atrial tissue sections revealed a much lower density of cholinergic nerves in Gαq mice compared to nontransgenic controls. We conclude that chronic Gαq overexpression by cardiac myocytes produces an intrinsic pacemaker defect and causes adverse remodeling of cardiac cholinergic neurons. Supported by grants from AHA and HL075265.

Short PR interval and catecholaminergic polymorphic ventricular tachycardia - typical or accidental association?

Short PR interval and catecholaminergic polymorphic ventricular tachycardia - typical or accidental association?

Bradycardia-dependent block in the accessory pathway in a patient with alternans Wolff-Parkinson-White syndrome

Although the intermittent preexcitation in the WolffParkinson-White (WPW) syndrome is a well-known phenomenon manifested by abrupt loss of delta wave from 1 beat to the next on the electrocardiogram (ECG), the occurrence of WPW syndrome on alternate beats during regular cardiac rhythm has been observed occasionally on rhythm strips. -5 We report a case of probable bradycardiadependent block in the accessory pathway in a patient with alternans WPW syndrome during regular sinus rhythm. A 57-year-old woman presented to the hospital with a 12-lead ECG recorded during a routine examination for arterial hypertension. She denied history of episodes of tachycardia and was receiving captopril. The patient’s initial physical examination, biochemical profile, and chest x-ray were all normal. The admission ECG (Fig. 1) showed regular sinus rhythm at 95 beats/min and 2 different types of QRS complexes on alternate beats: (a) a narrow QRS complex (0.08 second) showing PR interval of 0.16 seconds and a negative T wave in the inferior leads (arrows), and (b) a wide QRS complex (0.12 seconds) revealing short PR interval of 0.10 to 0.11 seconds and WPW conduction with upright delta wave in lead V2 to V6, I, and aVL (type B). There was also RR interval alternans. The shorter RR interval of 580 milliseconds was followed by a broad QRS complex with WPW pattern, and the longer RR interval of 680 milliseconds was followed by a normal conduction. In the precordial leads, alternans WPW syndrome was followed by a premature ventricular contraction (asterisk). The subsequent long compensatory pause of 880 milliseconds terminated with a narrow QRS complex (suggesting bradycardia-dependent block in the bypass tract), which begun another episode of alternans WPW syndrome. The next ECG obtained several minutes later revealed normal ventricular conduction, with disappearance of the wide QRS complex characteristics of WPW syndrome. Alternans WPW could not be induced either spontaneously or/nor