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PubMed1987

Deposits of eosinophil granule proteins in cardiac tissues of patients with eosinophilic endomyocardial disease.

Eosinophilic endomyocardial disease is a complication of the hypereosinophilic syndrome and of several other disorders associated with high blood eosinophil counts. Eosinophil granule proteins may be involved in the development of these lesions. This multi-centre study investigated whether these proteins could be demonstrated within the cardiac tissues of eighteen patients with eosinophilic endomyocardial disease. Serial sections of tissue taken at necropsy or at cardiac biopsy were stained for eosinophil major basic protein by indirect immunofluorescence and for eosinophil cationic protein, eosinophil protein-X, and activated eosinophils by means of alkaline-phosphatase-linked monoclonal antibodies. Activated eosinophils and secreted eosinophil granule proteins were most evident within the necrotic and later stage thrombotic lesions and were found mainly within the areas of acute tissue damage in the endocardium and in the walls of small blood vessels. These findings suggest that eosinophil granule proteins are involved in cardiac injury, producing muscle damage and vascular injury which lead to the development of endomyocardial fibrosis.

Acute Disease↗
PubMed2001

Improved 3-D-echocardiographic endocardial border delineation using the contrast agent FS069 (Optison) transesophageal studies in a porcine model.

3-D echocardiography has the potential for quantitative assessment of regional wall motion. However, the 3-D procedures used to date do not provide the same spatial and temporal resolution as 2-D echocardiography, which results in problems with border delineation of the endocardium. There are, as yet, few studies testing if the use of contrast agent can improve endocardial definition in the 3-D data set. FS069 (Optison) was used for the first time for this purpose in the present study. A total of 12 mechanically-ventilated pigs were examined by transesophageal 3-D echocardiography, 1. using fundamental imaging and 2. following left-atrial injection of FS069 (Optison). The left ventricle was analyzed using an 18-segment model. Score with the value 0 (not visible), 1 (moderately visible) and 2 (well defined) were used to rate endocardial definition. All segments were assessed both end-diastolic and end-systolic. Various LV regions were examined by grouping segments (anterior/lateral/inferior and basal/mid-ventricular/apical). Using the contrast agent, the proportion of nonvisible segments fell diastolic from 40 (18.5%) to 15 (6.9%), and systolic from 26 (12.0%) to 11 (5.1%). The proportion of well defined segments increased diastolic from 62 (28.7%) to 108 (50%) and systolic from 73 (33.8%) to 123 (56.9%). The mean visibility score increased diastolic from 1.10 +/- 0.68 to 1.43 +/- 0.62 (p < 0.001), systolic from 1.22 +/- 0.64 to 1.52 +/- 0.59 (p < 0.001). The benefit was greatest in regions where the visibility score was lowest without contrast: in the area of the lateral wall and systolic near the apex. In conclusion, the use of FS069 (Optison) results in significantly better endocardial delineation in the 3-D data set. This could be important in future for the 3-D echocardiographic assessment of regional wall motion.

Albumins↗
PubMed2001

Myocardial viability assessment by endocardial electroanatomic mapping: comparison with metabolic imaging and functional recovery after coronary revascularization.

OBJECTIVES: The objective of this study was to compare electroanatomic mapping for the assessment of myocardial viability with nuclear metabolic imaging using positron emission computed tomography (PET) and with data on functional recovery after successful myocardial revascularization. BACKGROUND: Animal experiments and first clinical studies suggested that electroanatomic endocardial mapping identifies the presence and absence of myocardial viability. METHODS: Forty-six patients with prior (> or =2 weeks) myocardial infarction underwent fluorine-18 fluorodeoxyglucose (FDG) PET and Tc-99m sestamibi single-photon emission computed tomography (SPECT) before mapping and percutaneous coronary revascularization. The left ventricular endocardium was mapped and divided into 12 regions, which were assigned to corresponding nuclear regions. Functional recovery using the centerline method was assessed in 25 patients with a follow-up angiography. RESULTS: Regional unipolar electrogram amplitude was 11.0 mV +/- 3.6 mV in regions with normal perfusion, 9.0 mV +/- 2.8 mV in regions with reduced perfusion and preserved FDG-uptake and 6.5 mV +/- 2.6 mV in scar regions (p < 0.001 for all comparisons). At a threshold amplitude of 7.5 mV, the sensitivity and specificity for detecting viable (by PET/SPECT) myocardium were 77% and 75%, respectively. In infarct areas with electrogram amplitudes >7.5 mV, improvement of regional wall motion (RWM) from -2.4 SD/chord +/- 1.0 SD/chord to -1.5 SD/chord +/- 1.1 SD/chord (p < 0.01) was observed, whereas, in infarct areas with amplitudes <7.5 mV, RWM remained unchanged at follow-up (-2.3 SD/chord +/- 0.7 SD/chord to -2.4 SD/chord +/- 0.7 SD/chord). CONCLUSIONS: These data suggest that the regional unipolar electrogram amplitude is a marker for myocardial viability and that electroanatomic mapping can be used for viability assessment in the catheterization laboratory.

Aged↗
PubMed1985

Encircling endocardial incision interrupts efferent vagal-induced prolongation of endocardial and epicardial refractoriness in the dog.

The purpose of this study was to test the hypothesis that vagal efferent nerves travel in the left ventricular subendocardium in a base to apex direction. Efferent vagal stimulation during constant background isoproterenol infusion prolonged left ventricular endocardial and epicardial effective refractory periods in a control state and after a left ventriculotomy performed while dogs were supported by cardiopulmonary bypass. After a 2 mm deep endocardial circumferential incision, efferent vagal stimulation still prolonged the effective refractory period at an endocardial site basal to the encircling endocardial incision, but no longer prolonged the effective refractory period at the endocardium or immediately overlying epicardium apical to the incision. Interpretation of these data suggests that efferent vagal fibers travel in the superficial subendocardium of the canine left ventricle in a base to apex direction, penetrating upward to innervate the epicardium. Conceivably, a lesion such as a subendocardial myocardial infarction could selectively interrupt efferent vagal innervation, leaving sympathetic innervation unopposed. This may be a source of some arrhythmias.

Animals↗
PubMed1986

Beta-adrenergic receptor properties of canine myocardium: effects of chronic myocardial infarction.

To determine the effects of chronic myocardial infarction on beta-adrenergic properties of canine myocardium, the hearts of nine mongrel dogs were studied 3 weeks after acute myocardial infarction. Infarction was produced by ligating the left anterior descending coronary artery in five dogs and the circumflex artery in four dogs. The heart was divided into normal and infarct zones (either anterior or posterior, depending on the vessel ligated) and marginal zones (septal and lateral), each zone being subdivided into epicardial and endocardial portions. Myocardial blood flow (microsphere technique) was markedly reduced in the infarct zone. In eight endocardial infarct samples after left anterior descending ligation, the maximal number (+/- SD) of binding sites assessed by 125I-iodocyanopindolol was 3.9 +/- 1.9 pmol/mg deoxyribonucleic acid (DNA) and was reduced from normal endocardial values (9.7 +/- 9.4 pmol/mg DNA, p less than 0.05). The dissociation constant (Kd), which is a measure of the affinity of the iodinated antagonist for the receptor, did not differ (304 +/- 222 versus 338 +/- 219 pM, p = NS). In the epicardium, the maximal number of beta-adrenergic receptors was also reduced (p less than 0.05), without a change in Kd. In the lateral and septal zones neither the maximal number of binding sites nor Kd values differed from those of normal endocardium. In nine endocardial infarct zones, (-)-isoproterenol-stimulated adenylate cyclase activity was reduced compared with control (34,870 +/- 29,430 versus 88,660 +/- 63,640 pmol/mg DNA/30 minutes, p less than 0.01), but the ratio of (-)-isoproterenol-stimulated to maximal (sodium fluoride-stimulated) adenylate cyclase activity was unchanged between normal and infarct zones.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1986

Quantitative assessment of regional left ventricular motion using endocardial landmarks.

In this study the hypothesis is tested that the motion pattern of small anatomic landmarks, recognizable at the left ventricular endocardial border in the contrast angiocardiogram, reflects the motion of the endocardial wall. To verify this, minute metal markers were inserted in the endocardium of eight pigs with a novel retrograde transvascular approach. Marker motion was subsequently recorded with roentgen cinematography and compared with the motion of the landmarks on the endocardial contours detected from the contrast ventriculogram with an automated contour detection system. Linear regression analysis of the directions of the systolic metal marker and endocardial landmark pathways yielded a correlation coefficient of 0.86 and a standard error of the estimate of 10.3 degrees. Landmark pathways were also measured in 23 normal human left ventriculograms. Normal left ventricular endocardial wall motion during systole, as observed in the 30 degrees right anterior oblique view, is characterized by a dominant inward transverse motion of the opposite anterior and inferoposterior walls and a descent of the base toward the apex. The apex itself is almost stationary. On the basis of these observations, a widely applicable model for the assessment of left ventricular wall motion is described in mathematical terms.

Animals↗
PubMed1999

Enhanced endocardial visualization with noncontrast harmonic imaging during stress echocardiography.

The diagnostic value of echocardiography hinges on the reader's ability to adequately visualize the endocardium of the left ventricle. This study was designed to evaluate the potential benefit of noncontrast harmonic imaging to enhance endocardial visualization. Eighty consecutive outpatients who underwent treadmill stress echocardiography were randomly assigned to either fundamental or harmonic imaging. The echoes were interpreted by 2 experienced readers. Compared with fundamental imaging, harmonic imaging of tissue improved the overall endocardial visualization score by 35% and 21% for readers 1 and 2, respectively (P <.001). Harmonic imaging also reduced the percentage of nondiagnostic segments by one half (P <.01). In patients undergoing treadmill stress echo, harmonic imaging offers a clinically significant improvement in endocardial visualization.

Echocardiography↗
PubMed1999

Assessment of regional wall motion abnormalities with real-time 3-dimensional echocardiography.

Accurate characterization of regional wall motion abnormalities requires a thorough evaluation of the entire left ventricle (LV). Although 2-dimensional echocardiography is frequently used for this purpose, the inability of tomographic techniques to record the complete endocardial surface is a limitation. Three-dimensional echocardiography, with real-time volumetric imaging, has the potential to overcome this limitation by capturing the entire volume of the LV and displaying it in a cineloop mode. The purpose of this study was to assess the feasibility of using real-time 3-dimensional (RT3D) echocardiography to detect regional wall motion abnormalities in patients with abnormal LV function and to develop a scheme for the systematic evaluation of wall motion by using the 3-dimensional data set. Twenty-six patients with high-quality 2-dimensional echo images and at least 1 regional wall motion abnormality were examined with RT3D echocardiography. For 2-dimensional echocardiography, wall motion was analyzed with a 16-segment model and graded on a 4-point scale from normal (1) to dyskinetic (4), from which a wall motion score index was calculated. Individual segments were then grouped into regions (anterior, inferoposterior, lateral, and apical) and the number of regional wall motion abnormalities was determined. The RT3D echocardiogram was recorded as a volumetric, pyramid-shaped data set that contained the entire LV. Digital images, consisting of a single cardiac cycle cineloop, were analyzed off-line with a computerized display of the apical projection. Two intersecting orthogonal apical projections were simultaneously displayed in cineloop mode, each independently tilted to optimize orientation and endocardial definition. The 2 planes were then slowly rotated about the major axis to visualize the entire LV endocardium. Wall motion was then graded in 6 equally spaced views, separated by 30 degrees, yielding 36 segments per patient. A higher percentage of segments were visualized with 2-dimensional versus RT3D echocardiography (97% vs 83%, respectively, P <.001). With the use of the 2-dimensional echocardiographic results as the standard, RT3D echocardiography detected 55 (96%) of 57 regional wall motion abnormalities. Analysis of the RT3D echocardiograms resulted in 3 false-negative and 5 false-positive findings. The total number of regional wall motion abnormalities was correctly classified by RT3D echocardiography in 19 (73%) of 26 patients. RT3D echocardiography detected 11 of 13 anterior, 19 of 20 inferoposterior, 9 of 9 lateral, and 15 of 15 apical wall motion abnormalities. An excellent correlation was found between the 2 techniques for assessment of the regional wall motion score index (r = 0.89, P <.001). This initial clinical study demonstrates the feasibility and potential advantages of RT3D echocardiography for the assessment of regional LV function. Compared with 2-dimensional echocardiography, this new method permits recording of the entire LV in a single beat, allowing the extent and location of the regional wall motion abnormalities to be determined.

Cardiomyopathy, Dilated↗
PubMed1999

Demonstration of penetrating intramyocardial coronary arteries with high-frequency transthoracic echocardiography and Doppler in human subjects.

Characterization of intramyocardial coronary artery flow may offer insight into the spectrum of coronary physiology. The purposes of this study were to test the feasibility of detection and measurement of intramyocardial coronary artery flow by using high-frequency transthoracic ultrasound and to evaluate the hemodynamic and morphologic differences in intramyocardial coronary arteries between patients with echocardiographically normal myocardium and patients with diseased myocardium. In 116 subjects (age 58 +/- 19 years; male:female 67:49; 58 normal [control subjects], 40 with left ventricular hypertrophy [LVH], 18 with systolic left ventricular dysfunction [cardiomyopathy, CM]), we examined the myocardium just beneath the apical impulse window at a depth of 3 to 5 cm by using a 6- or 7-MHz centerline frequency transducer. For color Doppler examination, a special preset coronary program with a low Nyquist limit (12 to 20 cm) was used. After obtaining linear color signals, the width and length, peak and mean diastolic pulsed Doppler flow velocities, diastolic velocity time integrals, and percent duration of diastolic Doppler flow were measured. The number of linear color flow signals per square centimeter was counted in 520 different cardiac cycles, and the angles formed by their inner curvature was measured with a graduated protractor. We identified color flow Doppler signals within the myocardium having a mean width of 1.1 +/- 0.4 mm and flow direction from epicardium to endocardium in 104 (89. 7%) subjects and spectral Doppler signals in 74 (63.8%) subjects. In 33 (45.8%) subjects, only diastolic flow was detected and in 39 (54. 2%) subjects, diastolic flow was predominant with systolic reversal. Peak and mean diastolic flow velocities and velocity time integrals of spectral Doppler signal in control subjects were 26.2 +/- 8.6 cm/s, 19.0 +/- 6.3 cm/s, and 9.5 +/- 2.7 cm, respectively. There were no significant differences in width and density of linear color flow signals among the 3 groups. The color flow signals in the LVH and CM groups had a narrower angle of inner curvature (P <.005 for LVH, P <.05 for CM, respectively), and their spectral Doppler signals showed significantly higher diastolic velocities and shorter diastolic flow duration (P <.005 for LVH, P <.05 for CM, respectively) than those of the control subjects. Detection and measurement of flow signals consistent with penetrating intramyocardial coronary arteries are feasible in a high percentage of subjects by use of high-frequency transthoracic ultrasound. The findings in patients with LVH and CM suggest that there are distinct hemodynamic and morphologic departures from those with normal left ventricles that may be a consequence of disordered myocardial perfusion in diseased myocardium.

Blood Flow Velocity↗
PubMed2002

Expression of mOb1, a novel atypical 73 amino acid K50-homeodomain protein, during mouse development.

We report the initial characterization of mOb1 (Odd homeoBox 1), which encodes an atypical 73 amino acid K50-homeodomain protein localised in the cytoplasm and absent from nuclei during mouse development. Conserved orthologues were present in man, rat, cow, pig and chicken, but not in fish, amphibians or invertebrates. Temporo-spatial patterns of mOb1 transcript and mOb1 protein expression were coincident in developing mouse embryos. Cardiac expression was first observed at E8.25 in linear heart tube myocardium and briefly in both horns of the sinus venosus. Myocardial expression peaked at E13.5, where after it diminished and was not detectable above background by adulthood. At no stage was expression observed in endocardium, endocardial cushion tissue, the coronary arteries or great vessels. At E13.5 and E15.5, mOb1 expression broadened to include skeletal muscle, stratified epithelium (upper aerodigestive tract and skin), epithelium of developing airways, vibrissae, midbrain/hindbrain junction, meninges, mesenchymal cellular condensations that preceded cartilage formation and chondrocytes.

Amino Acid Sequence↗
PubMedDate not supplied

Distribution of cardiac nerves in patients with diabetes mellitus: an immunohistochemical postmortem study of human hearts.

BACKGROUND: Autonomic neuropathy and functional cardiac denervation are complications of diabetes mellitus (DM). It is unknown if DM patients show histopathologic evidence of cardiac denervation. METHODS AND RESULTS: Nine sites were sampled at fixed distances from the atrioventricular valves from 27 postmortem hearts. Sections were stained with antibodies to S100 protein and to neurofilament (NF). Samples were visualized by light microscopy using the avidin-biotin peroxidase technique. The amount of cardiac nerves was graded blindly using semiquantitative methods according to the following criteria: Grade 0=presence of nerves in the epicardium only; Grade 1=strictly perivascular nerves; Grade 2=Grade 1 and nerve sprouts between myocardial cells sporadically; Grade 3=Grade 2 and nerve sprouts throughout the myocardium and endocardium. Specimens were divided into four groups. Control group consisted of patients with neither myocardial infarction (MI) nor DM. Experimental groups consisted of MI (n=7), MI with DM (n=6), and DM without MI (n=8). Average age of all patients was 57.3+/-15.7 years. No age differences existed among groups. Heterogeneous nerve distribution existed in all groups. S100-positive nerve density for control, MI, DM and MI, and DM without MI are 1.95+/-0.40, 1.66+/-0.54, 1.54+/-0.37, and 1.81+/-0.14, respectively (P=ns). NF-positive nerve density in the same groups were 1.10+/-0.18, 1.31+/-0.24, 1.13+/-0.12, and 1.19+/-0.42, respectively (P=ns). No differences in nerve densities between anterior and inferoposterior sections of the left ventricle existed. CONCLUSION: In postmortem human hearts, cardiac nerve distribution was heterogeneous among normal, MI, and DM patients. No evidence of cardiac denervation in patients with DM was demonstrated.

Autonomic Nervous System↗
PubMed2003

Counter intuitive relations between in vivo RF lesion size, power, and tip temperature.

BACKGROUND: Radiofrequency (RF) lesion size in vitro is positively correlated with applied power and catheter tip temperature. However, the relation between RF lesion size, power, and tip temperature in vivo remains unclear. We hypothesized that due to flow, anatomy and tip contact effects in vivo, increased tip temperature would be inversely related to applied power and RF lesion size. METHODS: RF lesions were created on the endocardium of 16 pigs using 5, 6, and 7 Fr catheters. The ablation generator was set to achieve a temperature of 70 degrees C. RF lesions were created in different regions of the heart so as to encompass a wide range of blood flow and catheter movement conditions. RF lesions were measured acutely (DIMEN, mm) and correlated with average power applied (POWER, W), and average tip temperature (TEMP, degrees C). The POWER and TEMP relation was also examined. RESULT: For TEMPs below 55 degrees C, the power output from the generator was typically maximized at 50 W. At TEMPs above 55 degrees C, POWER decreased exponentially with increasing TEMP (POWER = 50 - exp(-((41-TEMP)/7)), r = 0.98, p < 0.05). Further, DIMEN tended to be inversely related to TEMP (Slope: -0.07 +/- 0.04, r = -0.15, p = 0.07); but, was positively related to POWER (Slope: 0.04 +/- 0.02, r = 0.23, p < 0.05). These relations varied by tip size and estimated local blood flow characteristics. CONCLUSION: In vivo, variable tissue contact and flow yield DIMEN-POWER-TEMP relations opposite to those found in vitro. These counterintuitive results suggest that maximum in vivo RF lesion size is achieved when power is maximized at tip temperatures between 50 and 60 degrees C.

Animals↗
PubMed1985

d-Sotalol: a new potent class III anti-arrhythmic agent.

We have compared the effect of a new drug d-sotalol which has minimal beta-blocking action with the parent (beta-blocking) compound dl-sotalol on monophasic action potential (MAP) duration in open-chested dogs. In seven experiments d-sotalol was administered in intravenous bolus doses of 1.5, 3 and 6 mg/kg given at 10 min intervals. In a further seven experiments dl-sotalol was administered using the same dosage regimen. The animals were anaesthetized with chloralose and urethane. Atrioventricular block was created by injection of the bundle of His with 0.1 ml of 40% formalin in order to ensure capture by ventricular pacing. After prior beta-blockade with propranolol (0.25 mg/kg), simultaneous epicardial and endocardial MAP were recorded at paced heart rates of 100 and 150 beats/min after each bolus injection. d-Sotalol and dl-sotalol showed similar prolongation of MAP duration (measured at 90% repolarization) in both endocardial and epicardial recording at both paced heart rates. These results show that the dextro-isomer of sotalol possesses similar class III action to the parent compound and that this action is homogeneous with respect to left ventricular endocardium and epicardium at heart rates of 100 beats/min and 150 beats/min over a wide dose range. d-Sotalol may be a useful anti-arrhythmic agent in man.

Action Potentials↗
PubMed1996

Cardiac myxoma is rich in factor XIIIa positive dendrophages: immunohistochemical study of four cases.

Cardiac myxoma is an enigmatic tumour thought to arise from primitive cardiac mesenchymal cells. Factor XIIIa+ dendrophages are tissue histiocytes that are active in tissue repair and thrombosis. To explore whether factor XIIIa+ dendrophages play a role in cardiac myxoma morphogenesis, we stained four cases with an antiserum against coagulation factor XIIIa (FXIIIa). We also used antibodies recognizing CD34, CD31, and S-100 protein. Samples of valvular endocardium from 12 and 16 week fetuses and two adult autopsies were compared with the four myxomas. All cardiac myxomas had rounded and dendritic FXIIIa+ cells admixed with more numerous CD34+ spindle and stellate myxoma cells. The CD34+ cells formed multicellular syncytia and capillary sprouts. Many of these syncytial structures also expressed CD31 and, to a lesser extent, S-100 protein, strongly in two cases and more focally in two. Fetal subendocardium was composed of CD34+ stellate fibroblast-like cells invested with scattered FXIIIa+ histiocytes; no S-100+ cells were detected. Our findings confirm that cardiac myxomas are composed of CD34+ primitive subendocardial cells. These cells show a capacity for CD31+ endothelial differentiation. In cardiac myxoma, the CD34+ myxoma cells are accompanied by numerous FXIIIa+ dendrophages, the presence of which suggests abnormal organizing thrombus-like differentiation in cardiac myxoma morphogenesis.

Antigens, CD34↗
PubMed2001

Prichard's structures of the fossa ovalis are not histogenetically related to cardiac myxoma.

AIMS: Cardiac myxomas are neoplasms of unknown histogenesis. They are thought to arise from hypothetical subendothelial vasoformative reserve cells or from primitive cells which reside in the fossa ovalis and surrounding endocardium. In 1951 Prichard described a kind of microscopic endocardial structure with a predilection for the interatrial septum, which were suggested to be related to cardiac myxomas. To confirm the existence of Prichard's structures and to clarify their role in the genesis of cardiac myxomas, we examined histologically the fossa ovalis and we performed an immunohistochemical study of the endocardial abnormalities that were found. METHODS AND RESULTS: A prospective histological study of 100 interatrial septa and an immunohistochemical study of three out of the 12 endocardial abnormalities that were detected, as well as of four conventional cardiac myxomas were accomplished. Antibodies were used to vimentin, CD31, CD34, alpha-smooth muscle actin, S100 protein, thrombomodulin, calretinin and c-kit (CD117), a tyrosine kinase growth factor receptor for stem cell factor usually expressed by embryonic/fetal endothelium. Structures similar to the ones described by Prichard were found in 12% of septa, most of them in the left side of the fossa ovalis. The hearts with these structures were from patients 10 years older than the ones without them (72 +/- 10 versus 62 +/- 16 years, P=0.006). Immunohistochemically the cells comprising Prichard's structures were positive for vimentin, CD31, CD34 and thrombomodulin, and negative for alpha-smooth muscle actin, S100 protein, calretinin and c-kit. Therefore these cells seem to be mature endothelial cells, but not primitive multipotential mesenchymal cells. Furthermore, these cells were not found in the atrial tissue from the bases of any of the conventional cardiac myxomas. CONCLUSIONS: Our study suggests that there is no apparent relation between Prichard's structures and cardiac myxomas, and that Prichard's minute endocardial deformities are age-related phenomena.

Actins↗
PubMed2001

Cycle length-associated modulation of the regional dispersion of ventricular repolarization in a canine model of long QT syndrome.

Previous tridimensional activation mapping showed that the development of functional conduction block at the onset of torsades de pointes was regionally heterogeneous; conduction block was frequently observed in the LV and the interventricular septum (IVS) but not in the RV, in the canine anthopleurin-A (AP-A) model of long QT syndrome (LQTS). This may be related to the distribution of myocytes with M celllike electrophysiological characteristics. To better understand the regional difference of arrhythmogenicity in LQTS, the authors investigated cycle length related modulation of ventricular repolarization among three different layers: the endocardium (End), mid-myocardium (Mid), and epicardium (Epi) of the LV and RV and at two different areas: the Epi and septum (Sep) in the IVS. The LQT3 model was produced by AP-A in dogs. Using constant pacing and single premature stimulation (S1S2), the ventricular repolarization pattern was analyzed from 256 unipolar electrograms. Activation-recovery intervals (ARIs) were used to estimate local repolarization. In seven experiments, AP-A increased regional ARI dispersion to 88.1 +/- 36.0 ms in the LV, to 72.9 +/- 35.7 ms in the IVS, and to 23.0 +/- 8.7 ms in the RV at the pacing cycle length (CL) of 1,000 ms. Development of the large ARI dispersion was due to greater ARI prolongation at the Mid site in the LV and at Sep site in the IVS. As the S1S2 interval was shortened, regional ARI dispersion decreased gradually, and finally, ARI dispersion showed a reversal gradient of repolarization between the Mid and Epi sites in the LV and between the Sep and Epi sites in the IVS. Two factors contributed to create the reversal gradient of repolarization: (1) a difference in restitution kinetics at the Mid site in the LV and at the Sep site in the IVS, characterized by a larger delta ARI and slower time constant (tau), and (2) a difference in diastolic intervals at each site resulting in different input to restitution at the same CL. However, the RV showed small alteration in the transmural dispersion of repolarization in the S1S2 protocol. S2 created heterogeneous functional conduction block in the LV and IVS but not in the RV. In the LQT3 model, the arrhythmogenicity of torsades de pointes is primarily due to dispersion of repolarization in the LV and IVS because of prominent distribution of M cells. The RV seems to participate passively in reentrant excitation during torsades de pointes.

Animals↗
PubMed2002

Focal atrial tachycardia originating from the musculature of the coronary sinus.

Focal atrial tachycardias originate predominantly from the right atrium along the crista terminalis and less commonly from the left atrium. Successful catheter ablation usually can be performed via an endocardial approach. We report the case of a 34-year-old patient in whom a focal atrial tachycardia was successfully ablated 4 cm within the coronary sinus after extensive mapping of the left atrial endocardium and coronary sinus using the three-dimensional CARTO mapping system. Rarely, atrial tachycardia can originate from the coronary sinus musculature and require ablation inside the coronary sinus.

Adult↗
PubMed2003

Use of electrogram characteristics during sinus rhythm to delineate the endocardial scar in a porcine model of healed myocardial infarction.

INTRODUCTION: Substrate-based catheter ablation of postmyocardial infarction (post-MI) ventricular tachycardia necessitates electroanatomic definition of the scarred endocardium. We sought to determine whether electrogram criteria during sinus rhythm could identify the location and extent of the myocardial scar by electroanatomic mapping. METHODS AND RESULTS: A porcine model of healed MI was generated by injecting agarose microspheres into the mid left anterior descending coronary artery. At least 4 weeks post-MI, the animals (n = 24) underwent detailed left ventricular endocardial electroanatomic mapping using a 4-mm-tip catheter (BioSense-Webster, Inc.). Based upon mapping data in normal animals, infarcted tissue was defined as bipolar electrogram amplitude < 1.5 mV and electrogram duration > or = 50 msec. Radiofrequency ablation lesions (2-10 per animal) were placed to tag the endocardial borders of the electroanatomic mapping-defined scar. The area of the scar defined by abnormal voltage amplitude was 25.9 +/- 15.4 cm2 (range 6.9-60.5). This area correlated well with that defined as scar by the electrogram duration criteria (26.4 +/- 16 cm2). Of those points remote from the infarct with falsely low voltage amplitude resulting from presumed poor catheter-tissue contact, 94% were correctly identified as normal when using the electrogram duration criteria. Late potentials were observed predominantly along the borders of the infarcted myocardium. The radiofrequency lesions placed to tag the scar borders were located along the scar periphery during gross pathologic examination. CONCLUSION: During normal sinus rhythm, both bipolar electrogram voltage amplitude and electrogram duration criteria are able to help differentiate normal from scarred myocardial tissue. Using these criteria, a detailed reconstruction of the endocardial scar can be rendered by electroanatomic mapping of the heart.

Animals↗