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Review

Coronary microvascular dysfunction: Considerations for diagnosis and treatment

Benita Tjoe, MD, Lili Barsky, MD, Janet Wei, MD, Bruce Samuels, MD, Babak Azarbal, MD, C. Noel Bairey Merz, MD and Chrisandra Shufelt, MD, MS
Cleveland Clinic Journal of Medicine October 2021, 88 (10) 561-571; DOI: https://doi.org/10.3949/ccjm.88a.20140
Benita Tjoe
Barbra Streisand Women’s Heart Center, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA
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Lili Barsky
Barbra Streisand Women’s Heart Center, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA
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Janet Wei
Barbra Streisand Women’s Heart Center, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA; Investigator, Women’s Ischemia Trial to Reduce Events in Nonobstructive CAD (WARRIOR) ; Investigator, Women’s Ischemia Syndrome Evaluation (WISE)
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Bruce Samuels
Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA
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Babak Azarbal
Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA
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C. Noel Bairey Merz
Director, Barbra Streisand Women’s Heart Center, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA; Investigator, Women’s Ischemia Trial to Reduce Events in Nonobstructive CAD (WARRIOR) ; Investigator, Women’s Ischemia Syndrome Evaluation (WISE)
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Chrisandra Shufelt
Associate Director, Barbra Streisand Women’s Heart Center, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA; Investigator, Women’s Ischemia Trial to Reduce Events in Nonobstructive CAD (WARRIOR) ; Investigator, Women’s Ischemia Syndrome Evaluation (WISE)
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    Figure 1

    The effects of acetylcholine (ACH) and adenosine (ADE) on the smooth muscle of the coronary vasculature. ACH binds to the muscarinic receptor (M3), stimulating the release of calcium (Ca2+) into the vascular smooth muscle cell, which drives nitric oxide (NO) formation for vasodilation and also drives contraction for vasoconstriction. ADE stimulates the conversion of adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP), leading to inhibition of calcium influx and induction of nitric oxide formation, both of which result in vasodilation.

    A2a = adenosine receptor; AC = adenylate cyclase; ACh = acetylcholine; ADE = adenosine; ATP = adenosine triphosphate; Ca2+ = calcium; cAMP = cyclic adenosine monophosphate; cGMP = cyclic guanosine monophosphate; eNOS = endothelial nitric oxide synthase; GTP = guanosine triphosphate; iNOS = inducible nitric oxide synthase; M3 = muscarinic receptor; NO = nitric oxide; PKA = protein kinase activation; PKG = guanosine monophosphate-dependent protein kinase; sGC = soluble guanylate-cyclase

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    TABLE 1

    Invasive coronary function testing in patients with INOCA: Three medications

    Drug administeredResultsDiagnosis
    1. AdenosineCoronary flow reserve < 2.5Nonendothelial-dependent microvascular dysfunction
    2. Acetylcholine< 50% increase in coronary blood flowEndothelial-dependent microvascular dysfunction
    < 5% increase in coronary artery diameterEndothelial-dependent macrovascular dysfunction
    > 90% decrease in coronary artery diameter
    Chest pain and ischemic ST-segment changes on electrocardiography
    Epicardial coronary spasm
    Chest pain and ischemic ST-segment changes on electrocardiography in the absence of significant epicardial coronary vasoconstrictionMicrovascular coronary spasm
    3. Nitroglycerin< 20% increase in coronary artery diameterNonendothelial-dependent macrovascular dysfunction
    • INOCA = ischemia and no obstructive coronary artery disease (ie, < 50% stenosis)

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    TABLE 2

    Treatments for coronary microvascular dysfunction based on the pathway identified by invasive coronary function testing

    Endothelial dysfunction
    Angiotensin-converting enzyme inhibitor
    Angiotensin receptor blocker
    Statin
    L-arginine
    Cardiac rehabilitation
    Enhanced external counterpulsation
    Nonendothelial dysfunction
    Angiotensin-converting enzyme inhibitor
    Beta-blocker
    Alpha-/beta-blocker
    Ranolazine
    Ivabradine
    Phosphodiesterase-5 inhibitor
    Vasospasm
    Calcium channel blocker
    Nitrate
    Nociceptive abnormality
    Tricyclic antidepressant
    Spinal cord stimulation
    Cognitive behavior therapy
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Cleveland Clinic Journal of Medicine: 88 (10)
Cleveland Clinic Journal of Medicine
Vol. 88, Issue 10
1 Oct 2021
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Coronary microvascular dysfunction: Considerations for diagnosis and treatment
Benita Tjoe, Lili Barsky, Janet Wei, Bruce Samuels, Babak Azarbal, C. Noel Bairey Merz, Chrisandra Shufelt
Cleveland Clinic Journal of Medicine Oct 2021, 88 (10) 561-571; DOI: 10.3949/ccjm.88a.20140

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Coronary microvascular dysfunction: Considerations for diagnosis and treatment
Benita Tjoe, Lili Barsky, Janet Wei, Bruce Samuels, Babak Azarbal, C. Noel Bairey Merz, Chrisandra Shufelt
Cleveland Clinic Journal of Medicine Oct 2021, 88 (10) 561-571; DOI: 10.3949/ccjm.88a.20140
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  • Article
    • ABSTRACT
    • TINY VESSELS, BIG EFFECTS
    • RISK FACTORS AND CLINICAL PRESENTATION OF MICROVASCULAR DYSFUNCTION
    • CORONARY FUNCTION TESTING
    • OTHER DIAGNOSTIC APPROACHES
    • DRUG AND NONDRUG THERAPIES
    • KNOWLEDGE GAPS REMAIN
    • FUTURE DIRECTIONS
    • HOPE FOR STRONG GUIDELINES LIES IN ONGOING CLINICAL TRIALS
    • DISCLOSURES
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