Diastolic Dysfunction


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Diastolic Dysfunction

  1. 1. DIASTOLIC DYSFUNCTION AMONG ELDERLYWITH DIABETES MELLITUS Dr Doha Rasheedy Assistant lecturer of geriatric medicine Geriatrics Intensive care unit Geriatric medicine department Ain Shams University
  2. 2.  Nearly half of HF patients have normal LV systolic function (diastolic dysfunction). Diastolic dysfunction is a major contributor to hospital admissions among elderly population. Associated with high morbidity and mortality. .(Zile and Brustaert, 2002)
  3. 3.  Diastolic dysfunction is abnormality of diastolic distensibility, filling, or relaxation of the left ventricle. When clinical syndrome of heart failure develop it is called Diastolic heart failure . (Aurigemma and Gaash,2004)
  4. 4.  The mechanical abnormalities in diastole are caused mainly by ventricular relaxation (impaired lusiotrophy ) and/or  ventricular stiffness.
  5. 5. Aging and diastolic function
  6. 6. Aging is an independent risk for diastolic dysfunction because:↓Speed of LV relaxation with age, even in the absence of cardiovascular disease dt:  ↓levels or activity of the sarcoplasmic reticulum calcium ATP-ase pump (SERCA) .  ↑levels or activity of phospholamban (the naturally occurring SERCA-inhibitory protein). (Garcia, 2000)
  7. 7. ↑ LV stiffness with age dt: ↑ collagen cross-linking, ↑ connective tissue matrix  ↑smooth muscle content (myocyte hypertrophy) to compansate for apoptosis  loss of elastic fibers (Garcia, 2000)
  8. 8.  Diabetes mellitus can affect cardiac structure and function in the absence of hypertension and coronary artery disease, a condition called diabetic cardiomyopathy. Diastolic dysfunction has been described as an early sign of this diabetic cardiomyopthy preceding the systolic dysfunction. (Boudina and Abel, 2007)
  9. 9. The pathogenesis of diabetic cardiomyopathy: Several hypotheses have been proposed:1- Advanced glycation:  Of interstitial proteins such as collagen, which results in myocardial stiffness.  Of SERCA protein lead to decreased its activity and prolonged cardiac relaxation (Hayat et al., 2004) 2-Endothelial dysfunction
  10. 10.  3-Activation of the Renin-Angiotensin- aldosterone System: (RAAS)  oxidative damage  cardiomyocyte and endothelial cell apoptosis. (Boudina and Abel, 2007) 4- Increased Oxidative Stress: hyperglycemia result in excess formation of mitochondrial reactive oxygen spieces (ROS)  (NO) level  myocardial inflammation with myocardial collagen deposition and fibrosis. (Young et al., 2002)
  11. 11.  5-Autonomic dysfunction 6-Mitochondrial Dysfunction  oxidative phosphorylation capacity.   ATP production. 7-Inflammatory dysfunction  expression of nuclear factor kB triggers for a cascade of pro-inflammatory cytokines which induce collagen synthesis and fibrosis. (Boudina and Abel, 2007)
  12. 12.  8-Altered Substrate Metabolism (Metabolic Cardiomyopathy):  glucose and lactate metabolism and fatty acid (FA) metabolism .  FA uptake > oxidation rates in the heart →lipid accumulation in the myocardium that may promote lipotoxicity.  Lipid intermediates such as ceramide promote apoptosis of cardiomyocytes. (Boudina and Abel, 2007)
  13. 13. Diagnosis of Diastolic heart failureIs based on three criteria: Clinical features of heart failure, particularly left heart failure; A normal ejection fraction (over 50%); Evidence of abnormal left ventricular relaxation, filling, diastolic distensibility or diastolic stiffness.
  14. 14. Assessment of Diastolic function 1-Cardiac catheterisation with simultaneous pressure and volume measurements (invasive). 2-Isovolumic relaxation time (IVRT) A normal IVRT is about 70±12 ms, about 10ms longer in those over forty If its prolonged, it indicates poor myocardial relaxation. 3-Transmitral inflow (E/A; E wave deceleration) 4-pulmonary venous inflow (atrial flow reversal) Pulmonary vein Doppler (Garcia, 2000) 5-Tissue Doppler imaging (Satpathy and Mishra,2006)
  15. 15. Patterns of Left Ventricular Diastolic Filling (Aurigemma and Gaash,2004)
  16. 16. Management
  17. 17. Prevention Primary prevention of diastolic heart failure includes smoking cessation and aggressive control of hypertension, hypercholesterolemia, and coronary artery disease. Lifestyle modifications such as weight loss, smoking cessation, dietary changes, limiting alcohol intake, and exercise are equally effective in preventing diastolic and systolic heart failure. (Satpathy and Mishra,2006)
  18. 18. Management The goals of treating diastolic dysfunction :  normalizing blood pressure.  promoting regression of left ventricular hypertrophy.  preventing tachycardia.  maintaining atrial contraction .(Zile and Brustaert, 2002)
  19. 19.  Diuretics may improve dyspnea (Watch for excessive preload reduction, stroke volume) Nitrates Treat and prevent myocardial ischemia. .(Zile and Brustaert, 2002)
  20. 20. Calcium channel blockers Decrease cytoplasmic calcium concentration and allow myocardial relaxation. Reduce blood pressure. Reducing myocardial ischemia. Regression of left ventricular hypertrophy. Slowing the heart rate. .(Zile and Brustaert, 2002)
  21. 21. Beta blockers Slowing heart rate . Reducing blood pressure Reduce myocardial ischemia Promoting regression of left ventricular hypertrophy. Antagonizing the excessive adrenergic stimulation during heart failure. Beta blockers have been independently associated with improved survival in patients with diastolic heart failure .(Zile and Brustaert, 2002)
  22. 22. Angiotensin converting enzyme (ACE) inhibitors, Angiotensin (AT) receptor antagonists, and Aldosterone antagonists Block neurohormonal activation. Promote regression of hypertrophy and prevent myocardial fibrosis. Reduce the congestive state. .(Zile and Brustaert, 2002)
  23. 23. Maintain atrial contraction Cardioversion of atrial fibrillation. Sequential atrioventricular pacing. Beta-blockers. Calcium-channel blockers. Radiofrequency ablation modification ofatrioventricular node and pacing. (Aurigemma and Gaash,2004)
  24. 24. Digoxin Positive inotropic agents (such as digoxin) are generally not recommended in the treatment of patients with isolated diastolic HF, because left ventricular ejection fraction is preserved. Digoxin had no effect on all-cause or cause specific mortality or CV hospitalizations. (Aurigemma and Gaash,2004)
  25. 25. Alagebrium chloride Alagebrium chloride is known to reduce the pathological condition through breaking AGE cross-links. However, there has been little assessment regarding the impact of alagebrium on AGE-dependent signaling or restoring structural physiology of human heart. (Seo et al.,2008)
  26. 26. Future consideration There is ongoing clinical trial SERCA Gene Therapy Trial This study is not yet open for participant recruitment.
  27. 27. Summary Diastolic Dysfunction is common in elderly diabetic patients. Diastolic Dysfunction is multifactorial. Non invasive imaging techniques can be used for diagnosis. At this time, further studies are needed to determine optimal treatment strategies
  28. 28. THANK YOU