Anatomy and Pathology of Large Coronary Vessels

Author(s):  
A. V. G. Bruschke ◽  
B. Buis
Keyword(s):  
Author(s):  
D. E. Philpott ◽  
A. Takahashi

Two month, eight month and two year old rats were treated with 10 or 20 mg/kg of E. Coli endotoxin I. P. The eight month old rats proved most resistant to the endotoxin. During fixation the aorta, carotid artery, basil arartery of the brain, coronary vessels of the heart, inner surfaces of the heart chambers, heart and skeletal muscle, lung, liver, kidney, spleen, brain, retina, trachae, intestine, salivary gland, adrenal gland and gingiva were treated with ruthenium red or alcian blue to preserve the mucopolysaccharide (MPS) coating. Five, 8 and 24 hrs of endotoxin treatment produced increasingly marked capillary damage, disappearance of the MPS coating, edema, destruction of endothelial cells and damage to the basement membrane in the liver, kidney and lung.


Author(s):  
Masahiro Ono ◽  
Kaoru Aihara ◽  
Gompachi Yajima

The pathogenesis of the arteriosclerosis in the acute myocardial infarction is the matter of the extensive survey with the transmission electron microscopy in experimental and clinical materials. In the previous communication,the authors have clarified that the two types of the coronary vascular changes could exist. The first category is the case in which we had failed to observe no occlusive changes of the coronary vessels which eventually form the myocardial infarction. The next category is the case in which occlusive -thrombotic changes are observed in which the myocardial infarction will be taken placed as the final event. The authors incline to designate the former category as the non-occlusive-non thrombotic lesions. The most important findings in both cases are the “mechanical destruction of the vascular wall and imbibition of the serous component” which are most frequently observed at the proximal portion of the coronary main trunk.


1972 ◽  
Vol 191 (3) ◽  
pp. 241-244
Author(s):  
Rolf Andersson ◽  
Stig Holmberg ◽  
Nils Svedmyr ◽  
Gunnar Åberg
Keyword(s):  

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
W Phanthawimol ◽  
Y Komatsu ◽  
M Hattori ◽  
Q.J Naeemah ◽  
S Shimoo ◽  
...  

Abstract Background Catheter ablation of LV summit VT can be challenging due to possible subepicardial or intramural site of origin and its close proximity to the major coronary vessels. Objective Local electrograms monitoring inside LV summit communicating vein potentially defines arrhythmogenic substrates and facilitates ablation from the adjacent anatomical structures. Results We experienced two cases of LV summit VT with epicardial local abnormal ventricular activities (Epi-LAVA) recorded from distal bipolar electrode of the 2F microcatheter in communicating vein close to the superior portion of LV summit. During sinus rhythm, Epi-LAVA displayed isolated late fractionated potentials in the first case but had initial fractionated potentials fused with terminal portion of far-field ventricular signals and late isolated potentials exhibiting 2:1 conduction in the second case. Epi-LAVA represented earliest ventricular signals during VT in both cases. Pace mapping at Epi-LAVA sites yielded single QRS morphology with excellent pacemap score and induced VT. Our strategy was to perform ablation at the facing site of Epi-LAVA aiming to eliminate the potentials transmurally. Radiofrequency (RF) energy was applied above and under the left coronary cusp opposite to Epi-LAVA sites using 3.5-mm tip open-irrigation catheter with a power of 30–35 W for 60 seconds under real-time intracardiac echocardiograhic guidance. VT was slowed and terminated in 1 second. Repeat ablation delayed and completely abolished Epi-LAVA followed by noninducibility of VT. Anatomical proximity of the left coronary cusp semilunar insertion and subepicardial or intramural site of origin possibly dictates successful ablation. Epi-LAVA from coronary vein mapping serve as a new landmark of the ablation target with a measurable procedural endpoint. Conclusion Elimination of epicardial substrates with RF energy application at the left coronary cusp can be a novel strategy for LV summit VT ablation. Funding Acknowledgement Type of funding source: None


Life Sciences ◽  
1996 ◽  
Vol 58 (24) ◽  
pp. 2225-2232 ◽  
Author(s):  
J.M. Price ◽  
J.F. Cabell ◽  
A. Hellermann
Keyword(s):  

2008 ◽  
Vol 295 (2) ◽  
pp. H482-H490 ◽  
Author(s):  
Christina Kolyva ◽  
Jos A. E. Spaan ◽  
Jan J. Piek ◽  
Maria Siebes

A novel single-point technique to calculate local arterial wave speed ( SPc) has recently been presented and applied in healthy human coronary arteries at baseline flow. We investigated its applicability for conditions commonly encountered in the catheterization laboratory. Intracoronary pressure (Pd) and Doppler velocity ( U) were recorded in 29 patients at rest and during adenosine-induced hyperemia in a distal segment of a normal reference vessel and downstream of a single stenosis before and after revascularization. Conduit vessel tone was minimized with nitroglycerin. Microvascular resistance (MR) and SPc were calculated from Pd and U. In the reference vessel, SPc decreased from 21.5 m/s (SD 8.0) to 10.5 m/s (SD 4.1) after microvascular dilation ( P < 0.0001). SPc was substantially higher in the presence of a proximal stenosis and decreased from 34.4 m/s (SD 18.2) at rest to 27.5 m/s (SD 13.4) during hyperemia ( P < 0.0001), with a concomitant reduction in Pd by 20 mmHg and MR by 55.4%. The stent placement further reduced hyperemic MR by 26% and increased Pd by 26 mmHg but paradoxically decreased SPc to 13.1 m/s (SD 7.7) ( P < 0.0001). Changes in SPc correlated strongly with changes in MR ( P < 0.001) but were inversely related to changes in Pd ( P < 0.01). In conclusion, the single-point method yielded erroneous predictions of changes in coronary wave speed induced by a proximal stenosis and distal vasodilation and is therefore not appropriate for estimating local wave speed in coronary vessels. Our findings are well described by a lumped reservoir model reflecting the “windkesselness” of the coronary arteries.


Sign in / Sign up

Export Citation Format

Share Document