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Chronic coronary arterial occlusions

Histologic specimens of chronic coronary arterial occlusions with (A) large central neovascular channels (arrow) or (B) extensive media/adventitial collaterals. [Pg.539]

Sharkey SW, Murakami MA, Smith SA, Apple FS. Canine myocardial creatine kinase isoenzymes after chronic coronary artery occlusion. Circulation 1991 84 333-40. [Pg.1669]

Development of novel antianginal therapy has suffered from the lack of predictive animal models. Some of the more interesting newer approaches include direct measurement of myocardial oxygen tension.electrocardiographic analysis in normal 5.>W> and diseased hearts,4-7 regional vascular resistance studies, blood flow distribution 9>50 and functional evaluation in normal hearts5l as well as in animals subjected to chronic coronary artery occlusion.52,53 The clinical predictability of these models remains undetermined. [Pg.44]

El Gendi H, Violaris AG, Foale R, Sharma HS, Sheridan DJ. Endogenous, local, vascular endothelial growth factor production in patients with chronic total coronary artery occlusions further evidence for its role in angiogenesis. Heart 2002 87(2) 158-159. [Pg.361]

The most common reason for failure of a chronic total occlusion is inability to cross with aguidewire. The pathologic basis for this has been studied (15-17). Srivatsa et al, (15) evaluated the histologic correlates of angiographic total coronary artery occlusion in an autopsy series of 61 patients with... [Pg.538]

Fig. 13.1 Phosphorylated c-Ski expression in cytosolic fraction of cells in post-MI rat heart. In post-MI rat hearts with chronic large myocardial infarction, phosphorylated c-Ski expression was noted in the cytosol of cells populating the infarct scar (predominantly myofibroblasts) and the remnant heart (mixed cytosolic fraction from myocytes and nonmyocytes). Hearts were sampled at different times after surgical ligation of coronary artery occlusion and Western analysis was carried out to assess phosphorylated c-Ski expression. Trends in -fold protein expression (target band intensity corrected for loading) are shown in curves. Fig. 13.1 Phosphorylated c-Ski expression in cytosolic fraction of cells in post-MI rat heart. In post-MI rat hearts with chronic large myocardial infarction, phosphorylated c-Ski expression was noted in the cytosol of cells populating the infarct scar (predominantly myofibroblasts) and the remnant heart (mixed cytosolic fraction from myocytes and nonmyocytes). Hearts were sampled at different times after surgical ligation of coronary artery occlusion and Western analysis was carried out to assess phosphorylated c-Ski expression. Trends in -fold protein expression (target band intensity corrected for loading) are shown in curves.
Cardiac MRI may have a role in risk stratification for SCD due to its ability to detect myocardial scar. The use of gadolinium, which accumulates in infarcted tissue, has allowed delayed enhancement MRI to detect scar burden. Early experiments in dog models performed by coronary artery occlusion compared acute and chronic infarcts to pathologic specimens of the dog heart postmortem (89,90). Delayed enhancement MRI was remarkably accurate in imaging the infarcted tissue in comparison to the pathologic specimen. The spatial extent of hyperenhancement was the same as the spatial extent of myocyte necrosis at every stage post-MI. Reversible ischemia did not show delayed gadolinium uptake. Thus, delayed enhancement MRI can distinguish between reversible and irreversible injury, and... [Pg.15]

Acute coronary syndromes most often result from a physical disruption of the fibrous cap, either frank cap fracture or superficial endothelial erosion, allowing the blood to make contact with the thrombogenic material in the lipid core or the subendothelial region of the intima. This contact initiates the formation of a thrombus, which can lead to a sudden and dramatic blockade of blood flow through the affected artery. If the thrombus is nonocclusive or transient, it may either be clinically silent or manifest as symptoms characteristic of unstable angina. Importantly, if collateral vessels have previously formed, for example, due to chronic ischemia produced by multi vessel disease, even total occlusion of one coronary artery may not lead to an acute myocardial infarction. [Pg.226]

Degertekin M, Sonmez K, Gencbay M, et al. Heparin-coated stent implantation in chronic total occlusion. 3rd International Congress on Coronary Artery Disease, Lyon, France, Oct 2-5, 2000 67. [Pg.262]

Suero JA, Marso SR Jones PG, et al. Procedural outcomes and long term survival among patients undergoing percutaneous coronary intervention of a chronic total occlusion in native coronary arteries a 20 year experience. JACC 2001 38 409-414. [Pg.541]

Rahel BM, Laarmen GJ, Suttorp MJ, et al. Primary stenting of occluded native coronary arteries II—rationale and design of the PRISON II study a randomized comparison of bare metal stent implantation with Sirolimus-eluting stent implantation for the treatment of chronic total coronary occlusions. Am Heart J 2005 I49 el-e3. [Pg.542]

Both acute coronary syndromes (ACSs) and infarcts in chronic phase affect, as a result of the occlusion of the corresponding coronary artery, one part of the two zones into which the heart can be divided (Figure 1.14A) (1) the inferolateral zone, which encompasses all the inferior wall, a portion of the inferior part of the septum and most of the lateral wall (occlusion of the RCA or the LCX) (2) the anteroseptal zone, which comprises the anterior wall, the anterior part of the septum and often a great part of inferior septum and part of the mid-lower anterior portion of lateral wall (occlusion of the LAD). In general, the LAD, if it is large, as is seen in over 80% of cases, tends to perfuse not only the apex but also part of the inferior wall (Figures 1.1 and 1.14). [Pg.18]

Therefore, in chronic patients it is impossible to know the exact degree of occlusion of the coronary artery culprit of ACS in this moment, although, probably, it can be predicted what the type and location of the occlusion that produced the MI were. For example, a case of proximal occlusion to D1 and SI of LAD (Figure 2.3A) after treatment presented an ECG of non-complete occlusion of LAD, encompassing the septal branches, but not the diagonal... [Pg.287]


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Coronary arteries occlusion

Coronary artery

Coronary artery disease chronic occlusions

Coronary occlusions

Occlusion

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