![Cardiovascular Anatomy ,[object Object]](https://image.slidesharecdn.com/ap3-090930162426-phpapp02/85/ap3-1-320.jpg)
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- 17. Heart Wall Figure 20.4
- 18. Cardiac Chambers
- 23. Structural Differences between the Left and Right Ventricles Figure 20.7a-c
- 25. Valves of the Heart Figure 20.8a
- 30. Heart Casts - Muscle Removed
- 31. Left Main LAD Diagonal Septal perforators Circumflex Left atrial branch Obtuse Marginal
- 33. Conus branch Sinus node branch Acute Marginal Posterior descending artery Left ventricular branch RV branch
- 34. RAO Circumflex LAD Diagonal Septal
- 35. LAD
- 36. Evolution of fibrous plaque LDL Monocyte endothelium Cell adhesion factors Foam Cells 1 1. LDL enters 2. & Oxidizes 3. Monocytes adhere & 4. cross intima become macrophages macrophage 5. Macrophages Eat Fat become Foam cells 6. muscle cells multiply & 7. enter intima 8. Muscle cells die & harden plaque -Calcium develops
- 38. Fuster V, et al. N Eng J Med 1992;326:311-318. 2. Photos courtesy of Boehringer Ingleheim International GmbH, by Lennart Nilsson Braunwald E, et al. 2002 http://www.acc.org/clinical/guidelines/unstable/unstable.pdf
Notas do Editor
- These are casts of human coronary arteries and ventricles with the muscle dissolved away. So, what we see are the interior contents of the chambers and vessels as on an angiogram. Note the color legend. Each persons coronary arrangement is different, especially the crux area which determines coronary dominance. This model is fairly normal, except here the diagonals arise perpendicularly to the LAD. From Hurst, Atlas of the Heart.
- Schematic of the evolution of the atherosclerotic plaque. Accumulation of lipoprotein particles in the intima. The modification of these lipoproteins is depicted by the darker color. Modifications include oxidation and glycation. Oxidative stress including products found in modified lipoproprotiens can induce local cytokine elaboration. The cytokines thus induce increased expression of adhesion molecules for leukocytes that cause their attachment and chemoattractant molecules that direct their migration into the intima. Blood monocytes, on entering the artery wall in response to chemoattractant cytokines such as monocyte chemoattractant protein 1 (MCP-1), encounter stimuli such as macrophage colony stimulating factor (M-CSF) that can augment their expression of scavenger receptors. Scavenger receptors mediate the uptake of modified lipoprotein particles and promote the development of foam cells. Macrophage foam cells are a source of mediators such as further cytokines and effector molecules such as hypochlorous acid, superoxide anion (02-), and matrix metalloproteinases. Smooth muscle cells in the intima divide, and other smooth muscle cells migrate into the intima from the media. Smooth muscle cells can then divide promoting extracellular matrix accumulation in the growing atherosclerotic plaque. In this manner, the fatty streak can evolve into a fibrofatty lesion. In later stages, calcification can occur (not depicted) and fibrosis continues, sometimes accompanied by smooth muscle cell death (including programmed cell death, or apoptosis), yielding a relatively acellular fibrous capsule surrounding a lipid-rich core that may also contain dying or dead cells and their detritus. LDL = low-density lipoprotein; IL-1 = interleukin-1.