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Myocardial Remodeling

Myocardial Remodeling. Class two Ding Ma, Nan Li, Jin Zhou, Huan Luo, Lan Mi, Han Yan. Case 4. A 71-year old male Complains : 15-years history of paroxysmal chest pain, increasing for 5 hours, associated with dyspnea and unable to lie flat. 15 years ago. 10 years later. 2-year history.

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Myocardial Remodeling

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  1. Myocardial Remodeling Class two Ding Ma, Nan Li, Jin Zhou, Huan Luo, Lan Mi, Han Yan

  2. Case 4 • A 71-year old male • Complains: 15-years history of paroxysmal chest pain, increasing for 5 hours, associated with dyspnea and unable to lie flat

  3. 15 years ago 10 years later 2-year history He has pain at the front of his heart after fatigue, exercise or when he is humoursome Discontinuous paroxysmal chokey and suffocation Case 4 cont. As a result of fatigue and humoursome, he suddenly had a server pain at the front of his heart.

  4. 3 1 2 He took Suxiao Jiuxin Wan 2 times, 16 granules in all, but the symptom didn’t become unrelieved. The man was sent to the emergency at 2am and taken examinations At 11pm of the day before he was sent to the hospital, without obvious inducement, he suddenly had a server pain at the front of his heart while lying on the bed at rest. The pain radiated to the left shoulder and limb associated with chokey, suffocation, sudation except nausea, vomiting, fever and cough. Case 4 cont.

  5. ECG DRUG Change Timeworn inferior myocardial infarction V3-6, ST↓0.05-0.2mv CK-MB（+） CTn(-) Myo(-) 1 hour ago, the patient sat up changing his clothes and complained breathless. Later on, he could not lie flat and then had sudation and dyspnea. The symptom could be slightly unrelieved after taking KeSai and GTN. Case 4 cont.

  6. Hypertension for 7-8 years; BPmax=220/110mmHg. Taking Xin tong dingto maintain BP at 160-170/90-100mmHg. BP Serum cholesterol is a litter higher. Blood Lipid Deny of previous history of diabetes, hepatitis and tuberculosis. No history of being sensitive to any drugs. History Case 4 cont.

  7. Assistant Test Chest radiograph: far-grained.Radiographic cardiomegaly Serum cholesterol: TG:181mg/dl (normal<150mg/dl) T-CHO:211mg/dl (normal<220mg/dl) LDL-C: 154mg/dl (normal<140mg/dl) HDL-C:42mg/dl (normal>36mg/dl) Test Cont.T Test cont. Med.Test Rales. HR=120/min, normal rhythm, no cardiacs at all valve areas. Abdomen is soft, couldn’t touch liver and spleen, there is no swelling in either lower legs. Temperature: 36.2℃ Respirations: 16/min Pulse: 120/min BP: 190/100mmHg In his right senses, sit up state, rapid respiration, low-grade of cyanose of the lip. No neck vein distention, no cardiomegaly, Case 4 cont.

  8. Case 4 cont. Hyperlipidemia Coronary heart disease Acute anterior myocardial infarction Hypertension Diagnose Timeworn inferior myocardial infarction Acute left-side heart failure

  9. Question • What happened to the heart after infarction during these 10 years that kept him in a stable state? Compensatory Mechanism

  10. Agenda Early remodeling in 72h 1 Late remodeling after 72h 2

  11. Adaptive responses -Starling -Perturbations in circulatory hemodynamics Infarct expansion matrix metalloproteinases (MMPs) released →degeneration of collagen Early remodeling

  12. Cardio-myocyte Collagen Infarct MMP Necrosis LV expansion Degeneration Activation Expansion Hypotonicity of the wall

  13. Leading to… Neurohormonal activation Cytokines Activation of RAS Myocardial stretch Late remodeling Late remodeling

  14. Signal pathway of Gq α1 receptor of myocyte hypotrophy →hypotrophy → hypothophy ANP →inhibition of hypotrophy NE and AngⅡ →ET-1 → Neurohormonal activation Myocardial infraction → activation of sympathetic nerve system → β1receptor of juxtaglomerular apparatus →release of renin →AngⅡ↑ promotes the presynaptic release of NE blocks its reuptake, increases catecholamine synthesis, potentiates the postsynaptic action of NE release of NE→

  15. Hypotrophy

  16. AT1 receptor → AngⅡ↑ AngⅡ↑ PKC Calcium-dependent activation of tyrosine kinase ↓ Myocardial stretch Mechanical stretch → fetal gene program Early genes → time-dependent increase in protein synthesis

  17. hypotrophy in noninfarcted myocardium local AngⅡ↑ Ang gene expression &increased local ACE activity local RAS in the noninfarcted myocardium Serine proteases Activation of RAS

  18. Cytokines Necrotic myocytes macrophages macrophages fibroblasts → → TGF-β１ fibroblast proliferatin fibroblasts →myofibroblasts → NO↑ ACE↑ Vascular permeability ↑ INF-γ macrophages → local AngⅡ↑ → synthesis of collagen types 1 and 3 myofibroblasts

  19. AngⅡ G protein pathway Up-regulation gene expression Cardiomyocyte hypotrophy In short Cardiac remodeling

  20. Summary

  21. Reference • Hiroyuki Tsutsui. Mitochondrial Oxidative Stress and Heart Failure. The Japanese Society of Internal Medicine. 2006.DOI:10.2169/internalmedicine.45.1765 • William C. Stanley, Fabio A. Recchia, etc. Myocardial Substrate Metabolism in the Normal and Failing Heart. 2005. Physiol Rev 85:1093-1129 • A. D. Struthers. Pathophysiology of Heart Failure Following Myocardial Infarction. 2005;91;14-16 • Hiroyuki Morita, Jonathan Seidman, etc. Genetic Causes of Human Heart Failure. The Journal of Clinical Investigation. 2005. Volume115 Number3 • Jun REN, Cindy X FANG. Small Guanine Nucleotide-binding Protein Rho and Myocardial Function.2005. Acta Pharmacologica Sinica. Volume 26 Page 279  • Da-yue DUAN2, Luis LH LIU,etc. Functional role of anion channels in cardiac diseases. Acta Pharmacologica Sinica. 2005. Volume 26 Page 265

  22. Thank You ! www.themegallery.com

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