Management of Microvascular Angina Pectoris

Gaetano A. Lanza; Rossella Parrinello; Stefano Figliozzi


Am J Cardiovasc Drugs. 2014;14(1):31-40. 

In This Article

Pathophysiologic Mechanisms

The mechanisms responsible for CMVD in patients with stable MVA are likely multiple and heterogeneous. As discussed above, a reduced CBF response to direct arteriolar dilator agents (adenosine, dipyridamole, papaverine), suggesting abnormalities of smooth muscle cell relaxation, has been shown in several studies.[10–12] An impairment of endothelium-dependent coronary microvascular dilatation has also been reported in many patients.[11–13]

Furthermore, an enhanced response to constrictor stimuli has also been described in some studies [14–16], and the contribution to CMVD of increased vasoconstriction is also supported by the increased plasma levels of endothelin-1 in the coronary sinus during atrial pacing.[17]

The causes responsible for CMVD in stable MVA are also heterogeneous. Traditional cardiovascular risk factors probably play a pathogenic role, but they do not seem to explain most cases.[12] Accordingly, several other causes have been proposed to be involved, including increased adrenergic activity,[18] increased insulin resistance,[19] low-grade inflammation[20] and, in female patients, estrogen deficiency.[21]

It should be highlighted that a subset of patients with MVA present an increased painful perception of usually innocuous cardiac stimuli, as intracardiac catheter manipulation, heart chamber electrical stimulation, or simple intracardiac saline or contrast medium injection more easily cause chest pain [22,23]. This increased pain sensitivity may significantly contribute to determining the severity of symptoms and may constitute a therapeutic target in some patients.