Pathophysiology of Coronary Microvascular Dysfunction

Transcription

1 Pathophysiology of Coronary Microvascular Dysfunction Cheol Woong Yu, MD, PhD Cardiology Department Division of Internal Medicine Korea University Anam Hospital.

2 Etiologies of Chest Pain without obstructive CAD

3 History of terminology.. In 1967, Likoff et al. cohort of patients with angina pectoris and electrocardiographic abnormalities of myocardial ischemia but normal-appearing epicardial coronaries on angiography and first suggested a possible coronary microvascular disorder. In 1973, Kemp in editorial first used the term Syndrome X commenting on group X in a study of patients with angina and normal coronary angiograms In 1985, Cannon and Epstein Recommend the term microvascular angina Dysfunction of small intramural prearteriolar coronary arteries might be the pathogenetic cause of this syndrome

4 Camici et al,n Engl J Med 2007;356: Normal coronary system Intramyocardial oxygen consumption metabolite in myocardium Endothelial dependent dilatation dilation of arteriole R in overall network and Pr in distal preaterioles shear stress and triggers flow dependent dilation of larger preateriole and conductance arteries

5 Pathogenic mechanisms of CMD Type 1: in the absence of myocardial diseases and obstructive CAD Microvascular remodelling Endothelial dysfunction Smooth muscle dysfunction Type 2: in myocardial diseases without obstructive CAD Microvascular remodelling Smooth muscle dysfunction Extramural compression Reduced diastolic perfusion time (increased intramyocardial pressure or tissue oedema) Vascular wall infiltration Vascular rarefaction Perivascular fibrosis Type 3: in obstructive CAD Endothelial dysfunction Smooth muscle dysfunction Luminal obstruction (microembolization) Type 4: iatrogenic Luminal obstruction (microembolization by plaque and thrombus debris) Autonomic dysfunction

6 European Heart Journal (2014) 35, F. Crea et al. European Heart Journal (2014) 35,

7 Remodelling of coronary arterioles medial wall thickening, mainly owing to smooth muscle hypertrophy and increased collagen deposition, with variable degrees of intimal thickening

8 Hypertrophic cardiomyopathy Myocardial ischaemia, due to severe CMD Well-established pathophysiological feature. Structural abnormalities of the small intramural coronary arteries, medial hypertrophy, intimal hyperplasia, and decreased luminal size

9 A variable combination of abnormal vasodilation

10 CMD from abnormal extravascular pressure

11 Aortic stenosis Angina episodes are reported by about half of the patients with a severe degree of aortic stenosis despite of normal epicardial coronary arteries Cause of CMD (i) reduced time of diastolic coronary filling (ii) increased LV diastolic filling pressure and intramyocardial pressure during diastole, both contributing to impairment of perfusion selectively in the subendocardium (iii) reduced capillary density (iv) a low coronary perfusion pressurewhen compared with intracavitary pressure (v) Increased intramyocardial systolic pressure and delay in myocardial relaxation at the end of systole, which further reduces time of coronary filling and perfusion

12 Takotsubo syndrome Postulated mechanism: Catecholamine Cardiotoxicity, Multivessel Epicardial Coronary Artery Spasm, microvascular dysfunction CMR: subendocardial necrosis with delayed enhancement Impaired coronary perfusion and severe myocardial metabolic abnormalities in patients with takotsubo cardiomyopathy

13 Risk factor Pathogenesis F. Crea et al. European Heart Journal (2014) 35,

14 Coronary microvascular obstruction owing to platelet microemboli from eroded coronary atherosclerotic plaque in a patient who died from an acute coronary syndrome

15 Different Regions of Microvascular Flow After Acute Reperfused STEMI MVO size%lv, infarct size%lv, and EF are well known prognostic factor after reperfused STEMI and well assessed by cardiac magnetic resonance imaging. Several studies demonstrated that MVO size has the best prognostic value of all CMR parameters. Bekkers SC, et al. J Am Coll Cardiol 2010;55: As a result,treatment strategies, including both pharmacological and non-pharmacological strategies have begun to target MVO. However, there is currently a few definitive proof that any agent or intervention at the time of reperfusion reduces MVO and thus results in improved prognosis.

16 Infarct tissue: an area of hyperenhancement on LGE images MVO : an area of hypoenhancement within the hyperenhanced infarct tissue.

17 Impact of coronary microvascular function on long-term cardiac mortality in patients with acute STEMI