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Biomedical subjects

P Loh

Publications and source records attributed to P Loh.

At least 19 recordsLinked to original sources
PubMed2002

Electrophysiologic investigation in Brugada syndrome; yield of programmed ventricular stimulation at two ventricular sites with up to three premature beats.

INTRODUCTION: Numerous reports on the inducibility of ventricular tachyarrhythmias (VT) in patients with atypical right bundle branch block and right precordial ST-elevation (Brugada syndrome) are based on multicentre studies that have used different stimulation protocols. Therefore, we prospectively investigated the inducibility of VT in these patients using a uniform protocol. METHODS: In 41 consecutive patients (29 males) showing a pattern of right bundle branch block and ST-elevation, programmed ventricular stimulation was performed in the right ventricular apex with up to three premature stimuli at sinus rhythm and at four different paced cycle lengths (500, 430, 370, and 330 ms) until refractoriness was reached or reproducible induction of a sustained (>30s) VT occurred. If a VT was not reproducibly inducible, the same protocol was repeated in the right ventricular outflow tract. RESULTS: A history of life-threatening events defined as syncope (n=17) or aborted sudden cardiac death (n=13) was present in 30 patients (73%); 11 individuals were asymptomatic. Inducibility (68%) was similar between symptomatic (n=21, 70%) and asymptomatic patients (n=7, 64%). In 16 (39%) patients, VT were reproducibly inducible. If patients were only stimulated in the right ventricular apex, inducibility rate decreased to 39%. If only two premature beats at two sites were used it was as low as 32%. The mean coupling intervals of the second and third premature stimuli inducing sustained VT were short: 189+/-21 ms vs 186+/-22 ms, respectively. Forty-four percent of all patients (i.e. 64% of the inducible patients) had inducible VT only with coupling intervals shorter than 200 ms. CONCLUSIONS: The stimulation protocol markedly influences the extent of inducibility of VT in patients with right bundle branch block and ST-segment elevation. These findings question the significance of previous multicentre studies using different stimulation protocols and should have implications for further studies.

Adult↗
PubMed2001

Brugada syndrome and supraventricular tachyarrhythmias: a novel association?

INTRODUCTION: The Brugada syndrome is a distinct form of idiopathic ventricular fibrillation characterized by a unique ECG pattern consisting of a right bundle branch block-like aspect and ST segment elevation in leads V1 to V3. As a high induction rate of ventricular tachyarrhythmias has been reported in Brugada syndrome, we hypothesized that this also may be true for supraventricular tachycardias in these patients. METHODS AND RESULTS: Between January 1995 and December 2000, we identified 35 consecutive patients with Brugada syndrome; 26 had a history of cardiac arrest or syncope and 9 were asymptomatic. All patients underwent electrophysiologic study, including an atrial and ventricular stimulation protocol. Ten patients (29%) were found to have supraventricular tachyarrhythmias (SVT) in addition to the Brugada syndrome. These 10 patients presented with aborted sudden cardiac death (n = 3) and/or a family history of sudden cardiac death (n = 4), syncope (n = 4), or primarily with a Brugada typical ECG, a positive family history, and palpitations (n = 2). Eight of them underwent genetic testing, but only 1 had a mutation in the SCN5A gene. In 6 patients, an AV nodal reentrant tachycardia was easily and reproducibly inducible. Two patients had clinical documented and inducible episodes of an atrial tachycardia (1 in addition to an AV nodal reentrant tachycardia). One patient had paroxysmal atrial fibrillation alternating with sinus rhythm, and 2 patients with accessory pathways were identified. CONCLUSION: This is the first description of an association of the Brugada syndrome with SVT. Thus, the arrhythmogenic substrate in Brugada syndrome may not be restricted to the ventricular level. Palpitations in this syndrome should raise the possibility of SVT. Conversely, in patients with SVT and aborted sudden cardiac death or syncope not related to SVT, the Brugada syndrome should be considered a possible additional electrophysiologic abnormality.

Adult↗
PubMed2001

Analysis of the cat eye syndrome critical region in humans and the region of conserved synteny in mice: a search for candidate genes at or near the human chromosome 22 pericentromere.

We have sequenced a 1.1-Mb region of human chromosome 22q containing the dosage-sensitive gene(s) responsible for cat eye syndrome (CES) as well as the 450-kb homologous region on mouse chromosome 6. Fourteen putative genes were identified within or adjacent to the human CES critical region (CESCR), including three known genes (IL-17R, ATP6E, and BID) and nine novel genes, based on EST identity. Two putative genes (CECR3 and CECR9) were identified, in the absence of EST hits, by comparing segments of human and mouse genomic sequence around two solitary amplified exons, thus showing the utility of comparative genomic sequence analysis in identifying transcripts. Of the 14 genes, 10 were confirmed to be present in the mouse genomic sequence in the same order and orientation as in human. Absent from the mouse region of conserved synteny are CECR1, a promising CES candidate gene from the center of the contig, neighboring CECR4, and CECR7 and CECR8, which are located in the gene-poor proximal 400 kb of the contig. This latter proximal region, located approximately 1 Mb from the centromere, shows abundant duplicated gene fragments typical of pericentromeric DNA. The margin of this region also delineates the boundary of conserved synteny between the CESCR and mouse chromosome 6. Because the proximal CESCR appears abundant in duplicated segments and, therefore, is likely to be gene poor, we consider the putative genes identified in the distal CESCR to represent the majority of candidate genes for involvement in CES.

Abnormalities, Multiple↗
PubMed2001

Fine particulate matter and polycyclic aromatic hydrocarbon concentration patterns in Roxbury, Massachusetts: a community-based GIS analysis.

Given an elevated prevalence of respiratory disease and density of pollution sources, residents of Roxbury, Massachusetts, have been interested in better understanding their exposures to air pollution. To determine whether local transportation sources contribute significantly to exposures, we conducted a community-based pilot investigation to measure concentrations of fine particulate matter (particulate matter < 2.5 microm; PM(2.5)) and particle-bound polycyclic aromatic hydrocarbons (PAHs) in Roxbury in the summer of 1999. Community members carried portable monitors on the streets in a 1-mile radius around a large bus terminal to create a geographic information system (GIS) map of concentrations and gathered data on site characteristics that could predict ambient concentrations. Both PM(2.5) and PAH concentrations were greater during morning rush hours and on weekdays. In linear mixed-effects regressions controlling for temporal autocorrelation, PAH concentrations were significantly higher with closer proximity to the bus terminal (p < 0.05), and both pollutants were elevated, but not statistically significantly so, on bus routes. Regressions on a subset of measurements for which detailed site characteristics were gathered showed higher concentrations of both pollutants on roads reported to have heavy bus traffic. Although a more comprehensive monitoring protocol would be needed to develop robust predictive functions for air pollution, our study demonstrates that pollution patterns in an urban area can be characterized with limited monitoring equipment and that university-community partnerships can yield relevant exposure information.

Cities↗
PubMed2000

A patient with "atrial torsades de pointes".

A patient with long QT syndrome and a history of palpitations underwent electrophysiologic study. Runs of polymorphic self-terminating atrial tachyarrhythmias were easily induced and occurred spontaneously several times. Atrial monophasic action potential (MAP) durations were prolonged at short pacing cycle lengths. Premature high right atrial extrastimuli prolonged MAP durations in the low right atrium, resulting in an inverse electrical restitution curve, and increased dispersion of repolarization. MAP morphology showed gradually increasing early afterdepolarizations. When the arrhythmia was initiated, a new action potential reproducibly emerged from these afterdepolarizations. To the knowledge of the authors, this is the first reported case of "atrial torsades de pointes" in a patient.

Action Potentials↗
PubMed1999

Reentrant pathway during ventricular echoes is confined to the atrioventricular node : high-resolution mapping and dissection of the triangle of koch in isolated, perfused canine hearts.

Background-During ventricular echoes, reentrant excitation is supposed to involve 2 functionally distinct pathways in the atrioventricular (AV) nodal area. The exact pathway of reentrant excitation is unknown. The objectives of this study were to analyze electrical activity in the AV nodal area after ventricular stimulation and during ventricular echoes and to assess the role of perinodal atrial tissue in AV nodal reentry. Methods and Results-In 16 isolated, blood-perfused canine hearts, multiterminal electrodes were used to map electrical activity in Koch's triangle after ventricular stimulation and during ventricular echoes. The subendocardial cell layers were chemically destroyed in 3 hearts. Incisions in the posterior approach to the compact node were made in 6 hearts. The apex of the triangle of Koch was surgically dissociated from the perinodal atrial tissue in 5 hearts. Retrograde atrial activation occurred via 2 distinct endocardial exit sites. Ventricular echoes could be induced in all hearts irrespective of the atrial activation pattern. Simultaneous retrograde activation of both exit sites often preceded reciprocation. Ventricular echoes were demonstrable after chemical destruction of the endocardium and after surgical dissociation of the perinodal atrial tissue from the AV node. Conclusions-Our data show that the reentrant pathway during ventricular echoes is confined to the AV node. The tissue that connects the node to the endocardial exit sites has to be excluded from the reentrant circuit responsible for single echoes.

Action Potentials↗
PubMed1999

Double component action potentials in the posterior approach to the atrioventricular node: do they reflect activation delay in the slow pathway?

OBJECTIVES: The aim of the study was to elucidate the mechanism of double component action potentials in the posterior approach to the atrioventricular (AV) junctional area. BACKGROUND: Double component action potentials are often associated with activation delay and therefore might be a marker of the location of the so-called slow pathway. METHODS: The AV junction was scanned for double component action potentials in Langendorff perfused pig and dog hearts, using conventional microelectrode recordings. Characteristics of these action potentials were investigated during basic and premature stimulation and cooling of the anterior approach to the node. RESULTS: During basic stimulation, double component action potentials were recorded in 19 out of 20 hearts. In 74% of these cases, the second component occurred before the His deflection. During premature stimulation this percentage was 50%, while delay between the two components always increased. In 80% of the cases, the amplitude of the two components became <20 mV during progressive shortening of the coupling interval. The first component was generated by activation in superficial layers, the second one by activation in deeper layers. Cooling of the anterior region revealed that the second component was caused by activation arriving from the anterior region. CONCLUSIONS: Double component action potentials in the posterior approach to the AV node are generated by the asynchronous arrival of wave fronts in different, weakly coupled layers or by the summation of asynchronously arriving wave fronts. They are not always associated with activation delay in the slow pathway.

Action Potentials↗
PubMed1998

Anisotropic conduction in the triangle of Koch of mammalian hearts: electrophysiologic and anatomic correlations.

OBJECTIVES: The purpose of this study was to characterize anisotropy in the triangle of Koch by relating electrophysiology with anatomy. BACKGROUND: Atrioventricular (AV) node fast and slow pathway characteristics have been suggested to be due to nonuniform anisotropy in the triangle of Koch. METHODS: During atrial pacing, we determined the electrical activity within the triangle of Koch by multichannel mapping in 11 isolated hearts from pigs and dogs. Orientation of fibers was determined in nine hearts. RESULTS: Fibers were parallel to the tricuspid valve annulus (TVA) in the posterior part of the triangle of Koch. In the midjunctional area, the direction of the fibers changed to an orientation perpendicular to the TVA. During stimulation from posterior and anterior sites, activation proceeded parallel to the TVA at a high conduction velocity (0.5 to 0.6 m/s). During stimulation from sites near the coronary sinus, a narrow zone of slow conduction occurred in the posterior part of the triangle of Koch where activation proceeded perpendicular to the fiber orientation. Above and below this zone, conduction was fast and parallel to the annulus. After premature stimulation, conduction delay in the triangle of Koch increased by 4 to 21 ms; in contrast, the AH interval increased by 80 to 210 ms. CONCLUSIONS: Data support the concept of anisotropic conduction in the triangle of Koch. Activation maps correlated well with the arrangement of superficial atrial fibers. Comparison of conduction delay in the triangle of Koch and AH delay after premature stimulation disproves that anisotropy in the superficial layers plays an important role in slow AV conduction.

Animals↗
PubMed1998

Origin of heat-induced accelerated junctional rhythm.

INTRODUCTION: The application of high-frequency current to the AV junctional area results in a temperature rise in the myocardium and may cause accelerated junctional rhythm (AJR). The aim of the study was to characterize heat-induced AJR in an in vitro animal model. METHODS AND RESULTS: Studies were performed in isolated perfused pig and rabbit hearts. Using a small heating probe, we could induce AJR from a discrete area located in the middle of the triangle of Koch, which was smaller than the area from which RF energy application could elicit AJR. Histology showed that the heat-sensitive area was located over, or close to, the compact AV node. It did not correspond with the areas where double potentials were found or with the site(s) of earliest atrial activation during VA conduction. Microelectrode recordings revealed that AJR arose in nodal-type cells. Heat increased the slope of the phase 4 depolarization and shortened the action potential duration. Two types of AJR were observed: the first one was regular and the second one showed irregularity in the intervals. Interaction of multiple foci and the presence of conduction block between the foci and the His bundle caused the irregularity of the His-His intervals during the second type of AJR. CONCLUSION: AJR observed during heat and RF application in the AV nodal area results from the effect of heat on AV nodal cells with underlying pacemaker activity. The heat-sensitive area is located over, or very close to, the compact AV node.

Action Potentials↗
PubMed1998

'Para' AV nodal re-entry tachycardias.

Aim AV node, para AV nodal, and parahisian areas are usually not clearly defined in the literature. Radiofrequency catheter ablation in these areas may be deleterious to normal AV conduction. The purpose of this contribution is to discuss the anatomy in these areas in relation to outcome an AV conduction disturbances after radiofrequency ablation. Guidelines for therapeutic management of AV nodal re-entry tachycardia and tachycardias with involvement of a parahisian pathway, will be discussed.

Atrioventricular Node↗
PubMed1997

Electrical activity in Koch's triangle.

The authors have conducted several experimental studies of the cellular electrophysiology of the atrioventricular (AV) node employing the Langendorff-blood perfused heart of both dogs and pigs. Two types of experiments are described: experiments showing that cells with electrophysiological characteristics of typical nodal cells can be found outside Koch's triangle; and mapping experiments during the induction of ventricular echo beats in an attempt to delineate the reentrant circuit thought to underlie AV nodal reentry.

Animals↗
PubMed1996

Atrioventricular junctional tissue. Discrepancy between histological and electrophysiological characteristics.

BACKGROUND: Previous work has demonstrated that cells with AV nodal-type action potentials are not confined to Koch's triangle but may extend along the AV orifices. The aim of this study was to examine the histological and electrophysiological characteristics of this tissue. METHODS AND RESULTS: Studies were performed in isolated, blood-perfused dog and pig hearts. Microelectrode recordings revealed cells with nodal-type action potentials around the tricuspid and mitral valve rings. These cells were found within 1 to 2 mm of the valve annuli. A zone of cells with intermediate action potentials, approximately 1 cm wide, separated cells with nodal-type action potentials from cells with atrial-type action potentials in the body of the atria. In cells with nodal-type action potentials, adenosine caused a reduction in action potential amplitude (49 +/- 2 versus 33 +/- 2 mV, mean +/- SE; P < .001), upstroke velocity (2.5 +/- 0.2 versus 2.0 +/- 0.2 V/s, P < .05), and duration (150 +/- 4 versus 96 +/- 8 ms, P < .001). The light microscopic appearance of AV junctional cells was similar to that of myocytes in the body of the atrium. A polyclonal antibody raised against connexin-43 bound to atrial and ventricular tissue but not to the AV junctional tissue or AV nodal region. The absence of connexin-43 correlated with the sites of cells with nodal-like action potentials. With pacing techniques, the AV junctional tissue in the region of the posterior AV nodal approaches could be electrically dissociated from atrial, AV nodal, and ventricular tissue. AV nodal echoes were induced with ventricular pacing in three dog hearts. In each case, retrograde conduction was through the slow pathway, and anterograde conduction was through the fast pathway. During echoes, activation of AV junctional cells preceded atrial activation during retrograde slow pathway conduction, but these cells were not activated during anterograde fast pathway conduction. CONCLUSIONS: AV junctional cells around both annuli are histologically similar to atrial cells but resemble nodal cells in their cellular electrophysiology, response to adenosine, and lack of connexin-43. The light microscopic appearance of AV junctional cells is a poor guide to their action potential characteristics. The AV junctional cells in the posterior AV nodal approaches appear to participate in slow pathway conduction. These cells may be the substrate of the slow "AV nodal" pathway.

Action Potentials↗
PubMed1996

Electrophysiologic and extracellular ionic changes during acute ischemia in failing and normal rabbit myocardium.

The incidence of ventricular arrhythmias is higher in failing hearts than in control hearts, especially during acute ischemia. Electrophysiological and extracellular ionic changes during acute ischemia in normal and failing rabbit myocardium were assessed. Heart failure was induced in rabbits by combined volume and pressure overload. In perfused papillary muscles, the onset of electrical uncoupling and changes in action potential duration and conduction velocity during acute ischemia were determined. In Langendorff-perfused rabbit hearts the changes in extracellular potassium concentration ([K+]o) and pH during acute global ischemia were studied. In perfused papillary muscles, during the first 10 min of ischemia, action potential duration at 80% of repolarization decreased more in preparations from failing than from control hearts (from 174 to 104 ms and from 156 to 119 ms respectively (P < 0.001)). Conduction velocity was significantly lower in failing hearts during ischemia (P < 0.005). The onset of electrical uncoupling was similar in failing and control hearts (mean +/- S.E.M., 17 +/- 1 and 15 +/- 1 min respectively, n.s.). Langendorff-perfused hearts [K+]o, after 10 min of ischemia, was 11.0 +/- 0.4 mM in failing and 9.5 +/- 0.3 mM in control hearts (P < 0.01), while the change in pH was the same. After pretreatment with glibenclamide, an ATP sensitive K+ channel blocker, [K+]o reached lower values after 10 min of ischemia in both failing (8.8 +/- 0.5 mM) and control hearts (7.2 +/- 0.4 mM). During ischemia, action potential duration shortening is more pronounced and conduction velocity is lower in failing myocardium than in control myocardium. [K+]o reaches higher values during acute ischemia in failing compared with normal myocardium. These changes are not caused by an earlier activation of IK.ATP. Increased spatial dispersion in electrophysiological parameters and [K+]o over the ischemic border in failing hearts may explain the higher propensity for reentrant arrhythmias during acute regional ischemia in failing hearts.

Action Potentials↗
PubMed1996

Electrophysiology of the A-V node in relation to A-V nodal reentry.

During A-V nodal reentry the impulse is supposed to travel through two distinct pathways in the A-V nodal junction, called slow and fast pathways. Clinically, catheter ablation of these pathways has been very successful in abolishing A-V nodal reentrant tachycardias. So-called double potentials have been used as a marker for the slow pathway, and the occurrence of accelerated junctional rhythms (AJR) following ablation is an indicator of successful destruction of the slow pathway. In Langendorff, blood-perfused porcine and canine hearts, extensive mapping of extracellular potentials, combined with microelectrode recordings, was carried out to answer the following questions: 1) what is the origin of double extracellular potentials? 2) what causes post-ablation AJR? 3) what is the activation pattern of the AV junction during ventricular echoes? 1) Two types of double potentials were found: a low-frequency component followed by a high-frequency deflection, the LH potential was caused by asynchronous activation of the sinus septum above the coronary sinus and the region between the coronary sinus orifice and tricuspid annulus, where the L component is a far field potential. HL potentials (high-frequency deflection followed by a low frequency component) were caused by asynchronous activation of atrial cells and cells with AV nodal characteristics at the same location. These cells were present around the entire tricuspid annulus, and were not part of the compact node. The proximity of LH potentials to the slow pathway is probably serendipity, HL potentials could represent the slow pathway. 2) Two types of AJR could be initiated both by application of radiofrequency energy and by heat: a regular rhythm that progressively accelerated and an irregular rhythm. The discrete sites where heat application induced AJR did not correlate with areas showing double potentials, nor with exit regions during ventricular pacing. They were close to the compact node and the underlying mechanism was accelerated phase 4 depolarization in single or multiple foci, the latter accounting for irregular AJR. The association between presence of AJR and successful slow pathway ablation is probably also serendipity. 3) During ventricular pacing, two separate areas of earliest atrial activity were found. When ventricular echoes were induced by premature stimulation, the retrograde impulse activated both atrial exit sites and still returned in the ventricles as an echo. Thus, no evidence was found that atrial tissue forms part of the reentrant circuit.

Animals↗
PubMed1992

[Value of 24-hour blood pressure measurement in patients with arterial hypertension, left heart enlargement and increased cardiac risk].

Non-invasive 24-h blood pressure and a 24-h electrocardiogram were recorded in 45 normotensive and 97 matched, untreated, hypertensive subjects, with and without echocardiographic signs of left-ventricular hypertrophy and without signs of coronary artery disease. Forearm vascular resistance was calculated from mean blood pressure and postischemic blood flow, which was measured by venous plethysmography. Systolic ambulant 24-h blood pressure exhibited the closest correlation with left-ventricular mass index in hypertensives (r = 0.48; p less than 0.001). No relation could be found between blood-pressure fall overnight and left-ventricular hypertrophy. Blood-pressure variability was significantly higher in hypertensive subjects. Furthermore, systolic 24-h blood pressure significantly correlated with the rate of ventricular arrhythmias in hypertensives. Casual blood pressure exhibited no comparable correlations. A significant close correlation between 24-h blood pressure and vascular resistance was identified in hypertensives. Furthermore, left-ventricular mass index and vascular resistance were correlated (in hypertensives: r = 0.32; p less than 0.01). This finding speaks for a parallel development of total peripheral resistance and left-ventricular hypertrophy in essential hypertension. The close relationships between ambulatory 24-h blood pressure, left-ventricular hypertrophy, ventricular arrhythmias, and vascular resistance demonstrates the high diagnostic and, possibly, the prognostic value of long-term blood-pressure measurement.

Adult↗