coronary microvascular dysfunction

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coronary microcirculation-microvascular angina

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coronary microvascular dysfunction

  1. 1. ?Coronary microcirculation Coronary microvascular dysfunction Angina with normal coronary arteries, a continuous dilemma * Cardiac syndrome X : 1973 * Microvascular angina : 1985 Can we open the “black box” ? Finding the missing piece to the puzzle
  2. 2. • Coronary Microcirculation • Classification of CMVD • Pathophysiologic mechanisms • Clinical presentation • Assessment • Management Coronary microvascular dysfunction(CMVD) Much discussed but little understood
  3. 3. What we can see is only 5% of the total coronary tree.
  4. 4. Coronary blood flow is driven by the pressure difference between the aorta and the capillary bed and modulated further by various physical and neural factors, which affect the microcirculation. Moreover, the different compartments of the microcirculation are influenced by one main physiological mechanism to control their vascular tone with cardiac metabolism as the final determining factor.
  5. 5. Impaired CFR Microvascular Angina
  6. 6. • Coronary Microcirculation • Classification of CMVD • Pathophysiologic mechanisms • Clinical presentation • Assessment • Management Coronary microvascular dysfunction(CMVD) Much discussed but little understood
  7. 7. Clinical setting Risk factors Microvascular angina Type 1 : in the absence of myocardial diseases and obstructive CAD Hypertrophic cardiomyopathy Dilated cardiomyopathy Anderson-Fabry’s disease Amyloidosis Myocarditis Aortic stenosis Type 2 : in myocardial diseases Stable angina Acute coronary syndrome Type 3 : in obstructive CAD PCI CABG Type 4 : iatrogenic Classification of coronary microvascular dysfunctionSecondaryCMVD
  8. 8. • Coronary Microcirculation • Classification of CMVD • Pathophysiologic mechanisms • Clinical presentation • Assessment • Management Coronary microvascular dysfunction(CMVD) Much discussed but little understood
  9. 9. Main pathogenetic mechanisms Endothelial dysfunction SMC dysfunction Vascular remodelling Type 1 : in the absence of myocardial diseases and obstructive CAD Vascular remodelling SMC dysfunction Extramural compression Luminal obstruction Type 2 : in myocardial diseases Endothelial dysfunction SMC dysfunction Luminal obstruction Type 3 : in obstructive CAD Luminal obstruction Autonomic dysfunction Type 4 : iatrogenic Pathophysiologic mechanisms of coronary microvascular dysfunction
  10. 10. • Coronary Microcirculation • Classification of CMVD • Pathophysiologic mechanisms • Clinical presentation • Assessment • Management Coronary microvascular dysfunction(CMVD) Much discussed but little understood
  11. 11. Coronary microvascular dysfunction(CMVD) ‘microvascular angina’ (MVA) Primary *CMVD in the absence of myocardial diseases and obstructive CAD Secondary *CMVD in myocardial diseases *CMVD in obstructive CAD * Iatrogenic CMVD
  12. 12. Primary ‘microvascular angina’ Stable Predominant effort angina Unstable Acute rest angina Largely investigated formPoorly investigated
  13. 13. Primary ‘Microvascular angina’ Typical Angina Evidence of stress-induced Myocardial ischemia Normal coronary angiogram
  14. 14. ST-segment depression Perfusion defects in antero- lateral wall of the LV at peak exercise. Myocardial perfusion scintigraphy in a patient with typical effort angina and normal coronary arteries Evidence of stress-induced myocardial ischemia
  15. 15. * IC acetylcholine (ACH) constriction * IC nitroglycerin (NTG) dilation Spasm of epicardial coronaries on acetylcholine provocation should be excluded.
  16. 16. • Coronary Microcirculation • Classification of CMVD • Pathophysiologic mechanisms • Clinical presentation • Assessment • Management Coronary microvascular dysfunction(CMVD) Much discussed but little understood
  17. 17. The classical ischemic cascade, triggered by coronary vasospasm and/or epicardial stenosis.
  18. 18. The alternative ischemic cascade, triggered by coronary microvasculature dysfunction(CMVD).
  19. 19. Diagnostic challenge Epicardial CAD CMVD Assessment of CMVD is primarily functional and not anatomic. RWMAs (Stress echo) + VE - VE CFR Distribution of myocardial ischemia - Diffuse - Patchy
  20. 20. FFR and CFR: What Do They Investigate? FFR: Specific for epicardial disease CFR : Affected by both epicardial and microcirculatory disease (cannot distinguish between the two)
  21. 21. Pa Pd FFR = Pd /Pa (during hyperemia) = 58/79 = 0.73 0 Pa Pd Baseline HyperemiaAdenosine IC 100 80 60 40 20 FFR
  22. 22. FFR threshold for ischemia FFR No ischemia Yes ischemia 1.00 0.8 0.00 FFR < 0.8  inducible ischemia FFR > 0.8  no inducible ischemia
  23. 23. CFR
  24. 24. Coronary flow velocity profile obtained with tranthoracic Doppler of LAD: in diastole the flow velocity is higher than in systole.
  25. 25. LAD:mid & distal
  26. 26. FFR > 0.80FFR ≤ 0.80 Diagnosis Non-flow-limiting stenosis Preserved microvascular function Treatment Medical therapy, no PCI Diagnosis Flow-limiting stenosis Preserved microvascular function Treatment PCI CFR >2.0 Diagnosis Non-flow-limiting stenosis CMVD Treatment Medical therapy, no PCI Diagnosis Flow-limiting stenosis CMVD Treatment PCI CFR <2.0
  27. 27. LevelClassRecommendations CIIaExercise or dobutamine echo should be considered in order to establish whether RWMAs occur in conjunction with angina and ST-changes. CIIbTransthoracic doppler echo of the LAD with measurement of diastolic CBF following iv adenosine and at rest may be considered for non invasive measurement of CFR CIIbIC acetylcholine and adenosine with Doppler measurements may be considered during coronary arteriography, if the arteriogram is visually normal, to assess endothelium dependent and non-endothelium CFR and detect microvascular/epicardial vasospasm. Investigation in patients with suspected CMVD 2013 ESC guidelines on the management of stable coronary artery disease
  28. 28. • Coronary Microcirculation • Classification of CMVD • Pathophysiologic mechanisms • Clinical presentation • Assessment • Management Coronary microvascular dysfunction(CMVD) Much discussed but little understood
  29. 29. Old anti-anginals Short acting nitrate - sublingual Beta-blockers Long-acting nitrates Calcium channel blockers DHP Amlodipine Non-DHP Diltiazem and Verapamil Limited effect in coronary microcirculation
  30. 30. Main anti-ischemic effectsDrugs Improvement of left ventricular relaxation and diastolic function during ischemia Ranolazine Reduction of heart rateIvabradine Vasodilation through ATP/K-channel opening and nitrate-like effects Nicorandil Improved cardiac metabolism during ischemiaTrimetazidine Newer anti-anginals
  31. 31. Main anti-ischemic effectsDrugs Improved endothelial function; antagonism of angiotensin II ACE inhibitors Improvement of endothelial functionStatins Redistribution of coronary blood flow towards ischemia areas Xanthines Anti-α vasoconstrictor effectsα-antagonists Improvement of endothelial functionEstrogens (Post-menopausal (women Additional drugs
  32. 32. Anti-angina effectsTherapy Inhibition of visceral pain transmissionImipramine Non-pharmacological Treatments : Modulation of pain transmission and processing; modulation of ischemic sympathetic effects Spinal cord stimulation Improvement of endothelial function; development of coronary microvessels Enhanced external counterpulsation Training effect; reduction of sympathetic tone Rehabilitation programs Improvement of pain tolerance; reduction of anxiety Psychologic interventions Additional alternative therapies proposed for patients with refractory microvascular angina
  33. 33. Spinal cord stimulation Enhanced external counterpulsation
  34. 34. LevelClassRecommendations BIIt is recommended that all patients receive secondary prevention medications including aspirin and statins. BIß-blockers are recommended as a first line treatment BICalcium antagonists are recommended if ß-blockers do not achieve sufficient symptomatic benefit or are not tolerated. BIIbACE inhibitors or nicorandil may be considered in patients with refractory symptoms BIIbXanthine derivatives or nonpharmacological treatments such as neurostimulatory techniques may be considered in patients with symptoms refractory to the above listed drugs. 2013 ESC guidelines on the management of stable coronary artery disease Treatment in patients with MVA
  35. 35. Key Take-Home Points
  36. 36. Underlying pathophysiology is heterogenous. This is responsible for nonuniform response to different diagnostic tests and therapeutic approaches.
  37. 37. This appears to be insufficient because ischaemia-related symptoms frequently recur and these patients incur in relatively large health-care costs, in addition to the major adverse cardiac events. Existing guidelines focus on symptom management and current clinical practice on ‘reassurance’.
  38. 38. Definition and classification of microvascular angina
  39. 39. Stepwise therapeutic approach to patients with microvascular angina.
  40. 40. Thank You

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