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

Article Figures & Data

Figures

  • Figure 1
    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

Tables

  • 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)

  • 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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