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At least 145 records · Page 8Linked to original sources
PubMed2005

Release of endothelin-1 from human endocardium after radiofrequency catheter ablation and coronary angioplasty: comparative results.

BACKGROUND: Plasma levels of endothelin-1 (ET-1) increase after coronary angioplasty (PTCA) due to endothelial injury during the procedure. ET-1 has been found in human endocardial and myocardial cells. It is not known whether ET-1 increases after thermal injury induced by radiofrequency catheter ablation (RFA). METHODS: We determined plasma ET-1 levels at baseline, immediately after, and at 2 and 6 h post-procedure in 31 patients undergoing PTCA and 16 patients undergoing RFA. Patients subjected to diagnostic coronary angiography (n=15) or electrophysiology study (n=13) served as controls. RESULTS: Compared to baseline, ET-1 levels increased significantly immediately post-PTCA (55.1+/-20.1 vs. 42.7+/-14.9 pg/ml, p<0.01) and at 2 h post-RFA (98.0+/-11.7 vs. 53.0+/-17.4 pg/ml, p<0.01) and returned to baseline measurements at 2 h post-PTCA and 6 h post-RFA. There was no change of ET-1 levels in the control groups. ET-1 kinetics curve was significantly higher post-RFA compared to post-PTCA (p<0.001). ET-1 immediately post-PTCA correlated with total pressure-time product applied for balloon inflation during the procedure (r=0.56, p<0.01). There was no correlation between ET-1 levels and the number of RFA applications. No patient developed ischemia post-PTCA. There were no complications or arrhythmia recurrences post-RFA. CONCLUSION: Endocardial thermal injury incurred during RFA is another mechanism of endothelin increase apart from mechanical injury of the coronary endothelium during PTCA and represents further evidence for the existence of the peptide in human endocardial endothelial and myocardial cells. ET-1 increase is delayed and more pronounced post-RFA compared to post-PTCA. Despite that, it does not seem to have any clinical impact in the immediate post-RFA period.

Arrhythmias, Cardiac↗
PubMed2006

Substrate mapping to detect abnormal atrial endocardium with slow conduction in patients with atypical right atrial flutter.

OBJECTIVES: The purpose of this study was to investigate the relationship between the abnormal substrate and peak negative voltage (PNV) in the right atrium (RA) with atypical flutter. BACKGROUND: The impact of a local abnormally low voltage electrogram on the local activation pattern and velocity of atrial flutter (AFL) remains unclear. METHODS: Twelve patients with clinically documented AFL were included to undergo noncontact mapping of the RA. The atrial substrate was characterized by the: 1) activation mapping; 2) high-density voltage mapping; and 3) conduction velocity along the flutter re-entrant circuit. The normalized PNV (i.e., the relative ratio to the maximal PNV) in each virtual electrode recording was used to produce the voltage maps of the entire chamber. The protected isthmus was bordered by low voltage zones. RESULTS: Atypical AFL of the RA was induced by atrial pacing in 12 patients, including 10 upper loop re-entry and 2 RA free wall re-entry flutter. These protected isthmuses were located near the crista terminalis. The mean width of the protected isthmus was 1.7 +/- 0.3 cm and mean voltage at the isthmus was -0.91 +/- 0.39 mV. The conduction velocities within these paths were significantly slower than outside the path (0.30 +/- 0.18 m/s vs. 1.14 +/- 0.41 m/s, respectively; p = 0.004). The ratiometric PNV of 37.6% of the maximal PNV had the best cut-off value to predict slow conduction, with a high sensitivity (92.3%) and specificity (85.7%). CONCLUSIONS: Characterization of the RA substrate in terms of the unipolar PNV is an effective predictor of the slow conduction path within the critical isthmus of the re-entrant circuit.

Adult↗
PubMed1999

Evaluation of extent of shortening versus velocity of shortening at the endocardium and midwall in hypertensive heart disease.

To assess the incremental value of velocity of shortening velocity parameters compared with simpler, more widely used, extent of shortening parameters in compensated left ventricular hypertrophy, we studied 52 patients with left ventricular hypertrophy and 63 age-matched controls. Velocity parameters did not provide incremental information beyond that obtained by extent of shortening parameters.

Aged↗
PubMed2004

Electromechanical properties of Purkinje fiber strands isolated from human ventricular endocardium.

BACKGROUND: Abnormalities in the regulation of intracellular Ca2+ were observed in cardiac cells obtained from failing human hearts. However, the electromechanical properties and pharmacologic responses of human ventricular Purkinje fibers have not been well characterized. METHODS: Strands of free-running Purkinje fibers and/or trabecular muscle fibers with a diameter of around 1.5 mm were removed from the endocardial surface of ventricles obtained from 16 transplant recipient hearts. Action potential (AP) was detected by conventional microelectrode techniques and twitch force by a force-displacement transducer. RESULTS: The human Purkinje fiber strands as revealed by histologic examination were composed of Purkinje cells and the surrounding ventricular muscle cells. In well-polarized Purkinje fibers (mean +/- SE of maximum diastolic potential [MDP] = -85 +/- 1 mV) showing fast-response AP (Phase 0 Vmax >100 V/sec), the cardiotonic agents isoproterenol and strophanthidin (1 to 2 micromol/liter) accelerated the slope of diastolic depolarization and induced delayed afterdepolarization but not spontaneous APs. Steady-state contraction and the post-rest potentiation of contraction (PRPC) were similar in both Purkinje fibers and ventricular muscles, but inotropic agents induced tachyarrhythmia only in Purkinje fibers. In partially depolarized Purkinje fibers (MDP <-70 mV) with slow-response AP, isoproterenol and/or strophanthidin readily induced automatic and triggered rhythms. CONCLUSIONS: Accumulation of excessive cytosolic Ca2+ in the presence of cardiotonic agents could lead to tachyarrhythmias in Purkinje fibers, but rarely in ventricular muscles of failing human hearts.

Adult↗
PubMed2001

Mannose-receptor-mediated clearance of lysosomal alpha-mannosidase in scavenger endothelium of cod endocardium.

Mannose-receptor-mediated clearance of circulating glycoproteins was studied in Atlantic cod (Gadus morhua). Distribution studies with radioiodinated and fluorescently labelled ligands showed that cod liver lysosomal alpha-mannosidase and yeast invertase were rapidly eliminated from blood via a mannose specific pathway in liver parenchymal cells and endocardial endothelial cells of atrium and ventricle. Asialo-orosomucoid, a galactose-terminated glycoprotein, was cleared by liver only. In vitro studies were performed with primary cultures of atrial-endocardial endothelial cells (AEC), incubated at 12 degrees C in a serum free medium. Cod AEC endocytosed mannose-terminated glycoproteins (125I-alpha-mannosidase, 125I-invertase, 125I-mannan, 125I-ovalbumin and unlabelled lysosomal alpha-mannosidase), whereas 125I-asialo-orosomucoid was not recognised. Uptake of radiolabelled mannose-terminated ligands was inhibited 80-100% in the presence of excess amounts of mannan, invertase, D-mannose, L-fucose or EGTA. Our results suggest that the cod endocardial endothelial cells express a specific Ca(2+)-dependent mannose receptor, analogous to the mannose receptor on mammalian macrophages and liver sinusoidal endothelial cells.

Animals↗
PubMed1999

Electrophysiologic and blood-flow responses in the endocardium and epicardium to disopyramide and MS-551 during myocardial ischemia in the dog.

The aim of this study was to determine whether a quantitative relation exists between changes in regional myocardial blood flow (RMBF) and those in electrophysiologic determinants recorded via left ventricular endocardial and epicardial bipolar electrograms after administration of disopyramide (DP) and a class III antiarrhythmic drug, MS-551 (MS), during myocardial ischemia in the dog. Dogs were given DP (1 mg/kg, i.v., n = 14), MS (1 mg/kg, i.v., and 0.1 mg/kg/min, d.i.v., n = 13), or saline (n = 12). The effective refractory period (ERP) was determined by an S1-S2 extrastimulus method, and RMBF by a nonradioactive microsphere technique. The duration of regional electrograms (DRE) was measured as an indicator of conduction time in the myocardium. DP blunted ischemia-induced shortening of ERPs and lengthened DREs at the endocardial and epicardial sites, with a greater effect seen epicardially (p < 0.01 each). DP reduced RMBF, especially at the endocardial surfaces of the ischemic zone (p < 0.05). MS prolonged ERPs at the endocardial and epicardial sites in the ischemic and normal zones (p < 0.05-0.01), but there were no significant differences between the two sites. MS prolonged DREs (p < 0.05), but the magnitude of the prolongation of the DREs was similar to the values in the control group. MS had no effects on RMBF. DP treatment prolonged DREs at both sites in the ischemic zone more markedly than MS or saline treatment (p < 0.01 each). DP reduced RMBF at the endocardial site of the ischemic zone more markedly than MS or saline (p < 0.05 in each). Accordingly, MS prolonged ERPs, but did not increase disparities between endocardial and epicardial sites in the ischemic myocardium, whereas DP had a greater ERP-prolonging effect at the epicardial site than at the endocardial site. DP reduced endocardial RMBF more markedly than epicardial RMBF. These observations suggest that differences in ERPs between endocardial and epicardial ischemic myocardium caused by DP treatment are not due to the difference in RMBF reduction between the two tissue layers, and that DP and MS do not affect the same population of ion channel(s) when ERPs are prolonged.

Animals↗
PubMed1994

Numerical model for radio-frequency ablation of the endocardium and its experimental validation.

A theoretical model for the study of the radio-frequency (RF) ablation technique is presented. The model relies on a finite-element time-domain calculation of the temperature distribution in a block of tissue, resulting from the flow of RF (< 1MHz) electrical current. A thermal damage function is used to calculate the extent of the lesion on the basis of the temperature elevation and the duration of exposure. This work extends the model proposed by Haines [1] by including a more realistic and variable geometry, the cooling effect of the blook flow and a transient analysis. Furthermore, the nonlinearity caused by the temperature dependence of the tissue properties is also considered. The complexity of the model being appreciable, an experiment demonstrating its validity is also described. While remaining workable, the experiment is sophisticated enough to lead to convincing conclusions. It consists in measuring the temperature distribution and the time-dependent electrode resistance during "ablation" of a tissue-equivalent material. Various electrode configurations and electrical excitations are investigated. In all cases, the experimental results agree reasonably well with the numerical calculations. This confirms that the model is accurate for the investigation of RF ablation.

Catheter Ablation↗