cardiovascular remodeling and it's prevention

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cardiovascular remodeling and it's prevention,hypertension,anti hypertensive drugs

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cardiovascular remodeling and it's prevention

  1. 1. Good Afternoon<br />
  2. 2. ROLE OF DRUGS IN <br />PREVENTING THE REMODELING <br />OF CARDIOVASCULAR SYSTEM IN FOLLOW UP OF HF PATIENT<br />ROLE OF DRUGS IN <br />PREVENTING THE REMODELING <br />OF CARDIOVASCULAR SYSTEM IN FOLLOW UP OF HF PATIENT<br /> PRESENTED BY- <br /> SUBRATA DAS<br /> ASISH BARUI<br />
  3. 3. HEART FAILURE<br />Definition- This is a clinico-pathological condition in which<br />heart cannot maintain adequate cardiac output to meet the<br />Metabolic demand of the tissue in response to normal <br />venous reterurn<br />
  4. 4. PATHOPHYSIOLOGY<br /><ul><li>Cardiac injury –> depressed cardiac function poor tissue perfusion
  5. 5. Cardiac output must increase
  6. 6. Activation of neurohormonal axis
  7. 7. Norepi, AVP, angiotensin II, endothelin
  8. 8. Chronic NH release is dysfunctional
  9. 9. Alterations in HR, contractility
  10. 10. Myocardial hypertrophy and ischemia</li></li></ul><li>Neurohormonal changes<br />
  11. 11.
  12. 12. CHF Vicious Cycle<br />LOW CARDIAC OUT PUT<br />Increased Preload<br />Increased Afterload <br />Norepinephrine<br />Increased Salt<br />Vasoconstriction<br />Renal Blood Flow<br />Renin<br />Angiotension I<br />Angiotension II<br />Aldosterone<br />
  13. 13. Circulating and local (tissue) RAS influence on the cardiovascular system<br />Circulating RAS<br />Short-term effects<br />Local RAS<br />Long-term effects<br />Intraglomerular hypertension<br />Sodium/water reabsorption via aldosterone secretion<br />Vascular hypertrophy<br />by Increase production of growth factors &<br />extracellular matrix<br />ANGIOTENSIN II<br />Vasoconstriction<br />Positive chronotropic effects/ arrhythmogenic effects<br />Myocardial hypertrophy<br />Heart<br />Heart<br />
  14. 14. Myocardial inadequacy<br />Renal hypoxia<br />Reduced cardiac output<br />Angiotesinogen<br />Central Sympathetic stimulation<br />Digitalis <br />Bradykinin<br />Angiotensin I<br />-blocker<br />ACE inhibitor<br />Angiotensin II<br />AT1-blocker<br />AT2Receptor<br />AT1Receptor<br />Sympathetic stimulation<br />Cardiovascular remodeling<br />-blocker<br />Vasodilatation<br />Natriuresis<br />Extracellular matrix degradation<br />Angioedema<br />Hypertension<br />Aldosterone<br />Transforming growth factor <br />Plasminogen activator<br /><ul><li>Myocyte apoptosis
  15. 15. Hypertrophy
  16. 16. Focal myocardial necrosis</li></li></ul><li>ACE INHIBITORs<br />ACE inhibitors interfere with the renin-angiotensin system by inhibiting the enzyme that is responsible for the conversion of angiotensin I to angiotensin II. <br />However, because ACE inhibitors also inhibit kininase II, they may lead to the upregulation of bradykinin, which may further enhance the beneficial effects of angiotensin suppression. <br />ACE inhibitors stabilize LV remodeling, improve symptoms, reduce hospitalization, and prolong life<br />
  17. 17. DRUGS & DOSE<br />
  18. 18. βBlockers<br /><ul><li>Beta blocker block central sympathetic stimulation which activate the RAS &</li></ul> sympathetic stimulation by angiotensin II <br /><ul><li>The beneficial affect due to antagonism of ventricular wall stress enhancing,</li></ul> apoptosis promoting and pathological remodeling effects of excess sympathetic <br /> activity<br /><ul><li>It improve patient symptoms, prevent hospitalization, and prolong life
  19. 19. The only contraindication is severe decompensate CHF</li></li></ul><li>DigitalisMechanism of Action<br />+ve inotropic effect by ↑ intracellular Ca & enhancing actin-myosin cross bride formation (binds to the Na-K ATPase -> inhibits Na pump -> ↑ intracellular Na -> ↑ Na-Ca exchange<br />Vagotonic effect<br />Arrhythmogenic effect<br />
  20. 20. CONCLUSION<br />Myocardial & vascular remodeling is sing of progressive heart failure <br />Prevention of remodeling is proven benefit using ACE inhibitor, beta blocker & digitalis.<br />
  21. 21. Thank You….<br />
  22. 22. QUESTIONS?<br />

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