Management of Microvascular Angina Pectoris

Gaetano A. Lanza; Rossella Parrinello; Stefano Figliozzi


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

In This Article

Abstract and Introduction


Microvascular angina (MVA) is defined as angina pectoris caused by abnormalities of small coronary arteries. In itsmost typical presentation, MVA is characterized by angina attacks mainly caused by effort, evidence of myocardial ischemia on non-invasive stress tests, but normal coronary arteries at angiography. Patients with stable MVA have excellent long-term prognoses, but often present with persistent and/or worsening of angina symptoms. Treatment of MVA is initially based on standard anti-ischemic drugs (betablockers, calcium antagonists, and nitrates), but control of symptoms is often insufficient. In these cases, several additional drugs, with different potential anti-ischemic effects, have been proposed, including ranolazine, ivabradine, angiotensin-converting enzyme (ACE) inhibitors, xanthine derivatives, nicorandil, statins, alpha-blockers and, in perimenopausal women, estrogens. In patients with 'refractory MVA', some further alternative therapies (e.g., spinal cord stimulation, pain-inhibiting substances such as imipramine, rehabilitation programs) have shown favorable results.


The term microvascular angina (MVA) is generally used to indicate angina episodes caused by abnormalities of resistance coronary artery vessels, which, in contrast with large conductive epicardial vessels, cannot be visualized on coronary angiography because of their small dimensions (diameter <500 lm). Accordingly, MVA is usually suspected when angina symptoms occur in patients showing normal coronary arteries on angiography.[1]

Coronary microvascular alterations may occur and cause angina in several cardiac or systemic diseases, including cardiomyopathy, obstructive coronary artery disease (CAD), and in patients who have undergone coronary revascularization [2], as a result of their underlying etio-pathogenicmechanisms (secondaryMVA).However, inmany cases,MVAconstitutes the only clinical problem of the patient, thus becoming a distinct clinical entity (primary MVA) (Fig. 1).[1]

Figure 1.

Definition and classification of microvascular angina (MVA). In patients with sufficiently typical chest pain and normal coronary arteries, MVA is diagnosed after careful exclusion of other (cardiac and non-cardiac) causes. MVA can occur either in the absence of any other cardiac disease (primary MVA) or in the context of specific cardiac diseases (secondary MVA). This article focuses on primary MVA

In its most typical and largely investigated form, primary MVA is characterized by stable-effort angina, STsegment depression on electrocardiogram (ECG), or other evidence of myocardial ischemia during exercise or pharmacological stress test, and detection of normal coronary arteries on angiography, in the absence of any evidence of other significant cardiac or systemic disease, a clinical picture also usually known as cardiac syndrome X.[1]

Coronary microvascular dysfunction (CMVD) can also be responsible for an acute form of primary MVA, usually characterized by chest pain occurring at rest, suggesting an acute coronary syndrome. However, this form has been poorly investigated, in both pathophysiological and clinical aspects[1] (Fig. 1).

In this article, we briefly review the main pathophysiological and clinical characteristics of primary stable MVA (subsequently simply named MVA). We then review in more detail the therapeutic tools proposed for the treatment of these patients.