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  • 1
    Electronic Resource
    Electronic Resource
    Human Histopathology of Electroanatomic Mapping After Cooled-Tip Radiofrequency Ablation to Treat Ventricular Tachycardia in Remote Myocardial Infarction (2005)
    350 Main Street , Malden , MA 02148-5018 , USA , and 9600 Garsington Road , Oxford OX4 2DQ , UK . : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 16 (2005), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Introduction: Catheter ablation of ventricular tachycardia (VT) in remote myocardial infarction (MI) often requires excessive mapping procedures. Documentation of the electrical substrate via electrogram amplitude may help to identify regions of altered myocardium resembling exit areas of reentrant VTs. Methods and Results: A patient with multiple symptomatic monomorphic VTs (biventricular ICD, remote MI) underwent electroanatomic substrate mapping (CARTO™) for VT ablation. Regions of scar (bipolar electrogram amplitudes ≤0.5 mV), normal myocardium (≥1.5 mV), and “altered” myocardium (0.5–1.5 mV) were identified. Ablation was directed to regions with “altered” myocardium based on pace map correlation. After ablation the clinical VT did not reoccur. The patient died due to worsening of heart failure 7 days afterward. During postmortal evaluation specified sites of electroanatomic mapping were correlated to histopathological findings. Annotated scar areas were documented to consist of areas with massive fibrosis (≥80% of mural composition). Ablations were found to span through regions with intermediate fibrosis (21–79%) mapped as “altered” myocardium. Ablation produced transmural coagulation necrosis of mesh-like fibrotic tissue with interspersed remnants of myocardial cells up to a maximum depth of 7.0 mm. Subendocardial intramural bleedings were universal findings 7 days after ablation. Conclusions: Electroanatomic substrate mapping for VT ablation sufficiently identified regions of scar and normal myocardium. Regions with bipolar electrogram amplitudes between 0.5 and 1.5 mV were found to correlate to areas of “intermediate” fibrosis (21–79%) with only remnant strands of myocardial cells and were identified as target region for ablation. Cooled-tip endocardial radiofrequency ablation lead to transmural coagulation necrosis up to a depth of 7.0 mm.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8167.2005.40826.x
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  • 2
    Electronic Resource
    Electronic Resource
    Influence of the Pacing Rate on the Atrioventricular Conduction Time During Aerobic and Anaerobic Exercise: Basic Concepts for a Dromotropically Controlled Rate Responsive Pacemaker (1999)
    Oxford, UK : Blackwell Publishing Ltd
    Pacing and clinical electrophysiology 22 (1999), S. 0 
    Details
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The dromotropic pacemaker concept needs a rate responsive algorithm in which the pacing rate is controlled by the atrioventricular conduction time (AVCT). To develop basic concepts for such a rate responsive algorithm, the influence of the pacing rate on the AVCT was investigated. Seven patients (62 ± 7.8 years) with sick sinus syndrome and intact atrioventricular conduction underwent two cardiopulmonary exercise tests (CPX) on a treadmill. According to the determination of the anaerobic threshold (AT) and the patients maximum capacity in the first incremental CPX the work rate for two exercise levels below and above the AT were chosen for the second constant workload CPX. The calculation of the optimal pacing rate (HRopt) was based on the oxygen uptake (VO2) during exercise after reaching steady-state conditions. According to the increase of the V2 from 14.8 ± 2.3 mL/min per kilogram during aerobic work (38.3 ± 16.0 W) to 19.4 ± 4.7 mL/min per kilogram during anaerobic work (80.6 ± 32.3 W), the HRopt was calculated to be 98.6 ± 6.9 beats/min and 116.4 ± 4.7 beats/min. Starting from HRopt, the pacing rate was increased (overpacing) and decreased (underpacing) by about 5 beats/min every minute. At optimal pacing rate the AVCT decreased significantly from 233.0 ± 30.5 ms during aerobic work and to 226.4 ± 27.3 ms during anaerobic work (P 〈 0.05). Whereas overpacing induced a significant prolongation of the AVCT during aerobic work (4.17 ± 1.78 ms per 10 beats/min) and anaerobic work (3.84 ± 1.60 ms per 10 beats/min), underpacing yielded a significant shortening of the AVCT by about 4.49 ± 2.64 ms per 10 beats/min during aerobic work and 4.75 ± 1.87 ms per 10 beats/min during anaerobic work (P 〈 0.01). The slopes of the regression lines of the relationship between AVCT and pacing rate were not significantly different. Based on the reciprocal relationship of heart rate (HR) and AVCT, basic concepts may be established for a dromotropic rate responsive algorithm.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8159.1999.tb00411.x
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  • 3
    Electronic Resource
    Electronic Resource
    Effects of (−)-Phenylephrine on force of contraction in the presence of cocaine and hydrocortisone in cat papillary muscle (1984)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 328 (1984), S. 90-93 
    Details
    ISSN: 1432-1912
    Keywords: Extraneuronal uptake ; Neuronal uptake ; (−)-Phenylephrine ; Cat papillary muscle ; Alpha-adrenoceptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The positive inotropic effect of (−)-phenylephrine, in the presence of propranolol, was studied after inhibition of neuronal and extraneuronal uptake in isolated papillary muscles from reserpine-pretreated cats. An inhibition of extraneuronal uptake with hydrocortisone influenced the effect of (−)-phenylephrine neither when present alone nor in the presence of cocaine (additional inhibition of neuronal uptake). An inhibition of neuronal uptake with cocaine caused a small but significant increase in the potency of (−)-phenylephrine. We conclude that in cat ventricular cardiac muscle the extraneuronal compartment is apparently neither a “site of loss” nor a “site of gain” for (−)-phenylephrine with respect to force of contraction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00496113
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  • 4
    Electronic Resource
    Electronic Resource
    Angiographically undetected plaque in the left main coronary artery (1997)
    Springer
    The international journal of cardiovascular imaging 13 (1997), S. 293-299 
    Details
    ISSN: 1573-0743
    Keywords: coronary plaque ; intracoronary ultrasound ; left main coronary artery
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The absence of angiographic findings despite significant coronary artery disease has been previously described. Possible explanations for the limitation of plaque detection by angiography include compensatory vessel enlargement in face of intracoronary plaque formation, the lack of reference segments in diffuse atherosclerosis as well as technical limitations. Intracoronary ultrasound (ICUS) imaging provides the possibility of direct plaque visualization. We studied angiographically normal left main coronary arteries (LMCA) in 72 patients prior to diagnostic angiography or therapeutic interventions using ICUS (30 MHz). ICUS images were continuously recorded and recalled from memory for morphometric analysis. Lumen area, plaque area and the total vessel area were determined by computer software. ICUS imaging revealed atherosclerotic plaque in 55 of the 72 patients with angiographically normal LMCA (76%). The average plaque area stenosis was 22±12% (range 3–44%). Total vessel area showed a significant direct correlation with plaque area, indicating compensation of coronary plaque formation. The average percent change in plaque area (difference between maximal and minimal plaque area within the LMCA) was 11±19%, indicating a diffuse pattern. Measurement of change in lumen area (difference between maximal and minimal lumen area within the LMCA) revealed an average value of 6±7%. Lumen area of the LMCA was 15.9±3.2 mm2 in patients with and 17.2±1.9 mm2 without atherosclerotic plaque (n.s.). Thus, the lack of angiographic changes despite advanced plaque formation in the LMCA could be explained by compensatory vessel enlargement and by diffuse distribution of plaque in the vessel; true lumen narrowings overlooked by angiography seem not to account for the failure of angiography to detect plaque.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1005784908117
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