atherosclerotic and ischemic heart disease n.
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Atherosclerotic and Ischemic Heart Disease

Atherosclerotic and Ischemic Heart Disease

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Atherosclerotic and Ischemic Heart Disease

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  1. Atherosclerotic and Ischemic Heart Disease Howard L. Sacher, D.O. Long Island Cardiology and Internal Medicine

  2. Pathophysiology • Classification of vascular injury is divided into 3 types: • Type I functional alteration • Type II  Endothelial and Intimal damage, the internal elastic lamina is preserved • Type III  Deep injury involving the intima and media. The lamina is not preserved

  3. After Type I injury the endothelium’s ability to release intrinsic relaxing substances

  4. Proposed scenario of EDRF and Endothelin during ischemic syndromes

  5. ACh decreases as risk factors increase, decreasing the smooth muscles’ ability to relax

  6. Smooth Coronary artery segment that shows EDRF dependent dilation to ACh will also dilate with exerciseBut when evaluating coronary segments that where irregular and stenosed, they did not show EDRF dependent dilation to ACH. These did not dilate with exercise

  7. Adenosine • Thought to act on the coronary vasculature by stimulating the Adenosine A2 receptors on the smooth muscles. • Adenosine crosses the endothelial barriers to stimulate the Endothelial Independent Pathway for vasodilatation

  8. The hypokinetic inferior and akinetic apical wall is shown to improve several months after revascularization

  9. Who benefits from Diagnostic testing from this last graph? • A Pt with a low pre-test probablity of disease will continue to have a low likelihood of disease regardless of a (-) test • A Pt with a high pre-test probability of disease will continue to have a high likelihood of disease regardless of a (-) test • Diagnostic testing is most beneficial for those Pt’s with intermediate probability for disease

  10. Normal MIBI – uniform tracer uptake globally on SA slices

  11. Normal VLA slices

  12. Normal HLA slices of the same patient

  13. Patient with Basilar Septal ischemia evidenced by decreased tracer uptake at STR with increased uptake at RST

  14. Pt also has some apical thinning

  15. With a completely reversible Septal wall toward the Anterior segments of the ventricle on HLA

  16. Ischemia that is a result of Stress is dynamic with cascade of events, pain and ECG changes are seen late in the game

  17. Moral of story is to revascular for the greatest reduction in long term mortality

  18. Patient has significant multivessel disease – MIBI reveals a inferior wall infarction with septal and anterior wall ischemia. Areas of the inferoseptal walls may also reveal some peri-infarct ischemia

  19. Most important factor in Myocardial Oxygen demand is Heart Rate • 2nd Most important factor is Left Ventricular Wall Tension • LVWT is related to mean pressure during systole, LV volume and contractility • Inc. LVWT = Inc resistance to coronary flow with concomitant Inc. in O2 demand

  20. Hint: know thisTrinitrogylcerin and Isosorbide are directly active as -ONO2. -ONO2 is then converted to nitric oxide which acts both pre and post synaptically to vasodilate