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coronary microcirculation-microvascular angina
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Coronary Microvascular Dysfunction – An Update
Magdy El-MasryProf. of Cardiology
Tanta University,Egypt
?Coronary microcirculationCoronary 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
• Coronary Microcirculation
• Classification of CMVD
• Pathophysiologic mechanisms
• Clinical presentation• Assessment • Management
Coronary microvascular dysfunction(CMVD) Much discussed but little
understood
What we can see is only 5% of the total coronary tree.
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.
Impaired CFR
Microvascular Angina
• Coronary Microcirculation• Classification of CMVD• Pathophysiologic mechanisms• Clinical presentation• Assessment • Management
Coronary microvascular dysfunction(CMVD) Much discussed but little
understood
Clinical settingRisk factorsMicrovascular angina
Type 1 : in the absence of myocardial diseases and obstructive CAD
Hypertrophic cardiomyopathyDilated cardiomyopathyAnderson-Fabry’s diseaseAmyloidosisMyocarditisAortic stenosis
Type 2 : in myocardial diseases
Stable anginaAcute coronary syndrome
Type 3 : in obstructive CAD
PCICABG
Type 4 : iatrogenic
Classification of coronary microvascular dysfunctionS
econ
dary
C
MV
D
• Coronary Microcirculation• Classification of CMVD• Pathophysiologic mechanisms• Clinical presentation• Assessment • Management
Coronary microvascular dysfunction(CMVD) Much discussed but little
understood
Main pathogenetic mechanisms
Endothelial dysfunctionSMC dysfunctionVascular remodelling
Type 1 : in the absence of myocardial diseases and obstructive CAD
Vascular remodellingSMC dysfunctionExtramural compressionLuminal obstruction
Type 2 : in myocardial diseases
Endothelial dysfunctionSMC dysfunctionLuminal obstruction
Type 3 : in obstructive CAD
Luminal obstructionAutonomic dysfunction
Type 4 : iatrogenic
Pathophysiologic mechanisms of coronary microvascular dysfunction
• Coronary Microcirculation• Classification of CMVD• Pathophysiologic mechanisms• Clinical presentation• Assessment • Management
Coronary microvascular dysfunction(CMVD) Much discussed but little
understood
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
Primary ‘microvascular angina’
Stable
Predominant effort angina
Unstable
Acute rest angina
Largely investigated formPoorly investigated form
Primary ‘Microvascular angina’
Typical Angina Evidence of stress-induced Myocardial ischemia
Normal coronary angiogram
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
* IC acetylcholine (ACH) constriction* IC nitroglycerin (NTG) dilation
Spasm of epicardial coronaries on acetylcholine provocation should be
excluded.
• Coronary Microcirculation• Classification of CMVD• Pathophysiologic mechanisms• Clinical presentation• Assessment • Management
Coronary microvascular dysfunction(CMVD) Much discussed but little
understood
The classical ischemic cascade, triggered by coronary vasospasm and/or epicardial stenosis.
The alternative ischemic cascade, triggered by coronary microvasculature dysfunction(CMVD).
Diagnostic challengeEpicardial
CAD
CMVD
Assessment of CMVD is primarily functional and not anatomic.
RWMAs(Stress echo)
+ VE
- VE
CFR
Distribution of myocardial ischemia - Diffuse- Patchy
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)
Pa
Pd
FFR = Pd /Pa (during hyperemia) = 58/79 = 0.730
Pa
Pd
Baseline HyperemiaAdenosine IC
100
80
60
40
20
FFR
FFR threshold for ischemia
FFR
Noischemia
Yes ischemia
1.00 0.8 0.00
FFR < 0.8 inducible ischemia FFR > 0.8 no inducible ischemia
CFR
Coronary flow velocity profile obtained with tranthoracic Doppler of LAD: in diastole the flow velocity is higher than in systole.
LAD:mid & distal
FFR > 0.80 FFR ≤ 0.80DiagnosisNon-flow-limiting stenosisPreserved microvascular function
TreatmentMedical therapy, no PCI
DiagnosisFlow-limiting stenosisPreserved microvascular function
Treatment PCI
CFR >2.0
DiagnosisNon-flow-limiting stenosis
CMVD
TreatmentMedical therapy, no PCI
DiagnosisFlow-limiting stenosis
CMVD
Treatment PCI
CFR <2.0
Diagnosis and Treatment Based on Fractional Flow Reserve and Coronary
Flow Reserve Values
Level Class RecommendationsC IIa Exercise or dobutamine echo should be considered in
order to establish whether RWMAs occur in conjunction with angina and ST-changes.
C IIb Transthoracic 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
C IIb IC 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
• Coronary Microcirculation• Classification of CMVD• Pathophysiologic mechanisms• Clinical presentation• Assessment • Management
Coronary microvascular dysfunction(CMVD) Much discussed but little
understood
Old anti-anginalsDRUG CLASS VASODILATION HEART RATE MYOCARDIAL
CONTRACTILITY
Short acting
nitrate -
sublingual
Beta-blockers
Long-acting
nitrates
Calcium channel
blockers
DHP Amlodipine Non-DHP Diltiazem and Verapamil
Limited effect in coronary microcirculation
Main anti-ischemic effects Drugs
Improvement of left ventricular relaxation and diastolic function during ischemia
Ranolazine
Reduction of heart rate Ivabradine
Vasodilation through ATP/K-channel opening and nitrate-like effects
Nicorandil
Improved cardiac metabolism during ischemia Trimetazidine
Newer anti-anginals
Main anti-ischemic effects DrugsImproved endothelial function; antagonism of angiotensin II
ACE inhibitors
Improvement of endothelial function Statins
Redistribution of coronary blood flow towards ischemia areas
Xanthines
Anti-α vasoconstrictor effects α-antagonists
Improvement of endothelial function Estrogens(Post-menopausal
(women
Additional drugs
Anti-angina effects TherapyInhibition of visceral pain transmission Imipramine
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
Spinal cord stimulation
Enhanced external counterpulsation
Level Class RecommendationsB I It is recommended that all patients receive secondary
prevention medications including aspirin and statins.B I ß-blockers are recommended as a first line treatmentB I Calcium antagonists are recommended if ß-blockers
do not achieve sufficient symptomatic benefit or are not tolerated.
B IIb ACE inhibitors or nicorandil may be considered in patients with refractory symptoms
B IIb Xanthine 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
Key Take-Home Points
Underlying pathophysiology is heterogenous.
This is responsible for nonuniform response to different diagnostic tests and therapeutic approaches.
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’.
Definition and classification of microvascular angina
Stepwise therapeutic approach to patients with microvascular angina.
Thank You