Management of Microvascular Angina Pectoris

Gaetano A. Lanza; Rossella Parrinello; Stefano Figliozzi

Disclosures

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

In This Article

Clinical Characteristics and Diagnosis

In the modern era of invasive cardiology, more than 50 % of patients undergoing coronary angiography for non-acute chest pain are found to have normal or near normal coronary arteries.[3]

While, in several clinical studies, these patients have been assessed as a unique cohort, it should instead be realized that they actually constitute a heterogeneous group, of which patients with MVA, as defined above, are only a well selected subset who need careful identification and specific assessment.

Chest pain caused by CMVD is often indistinguishable from that caused by obstructive CAD. However, some clinical and diagnostic findings may suggest a microvascular origin of angina.[4] Thus, in contrast with obstructive CAD, patients with MVA are more often women, with an average age of symptom onset around 50–55 years. Persistence of a dull pain sensation after stopping efforts and a poor or slow response to short-acting nitrates is very suggestive of MVA. Accordingly, failure of short-acting nitrates to improve the ischemic threshold during an exercise stress test[5] is also a clue to MVA.

A further finding highly suggestive of MVA is the lack of left ventricular wall motion abnormalities at ECG stress test in spite of the induction of typical angina and ischemic ECG changes.[6] The reason that MVA patients, in contrast with CAD patients, do not usually display contractile abnormalities likely resides in the fact that CMVD is patchily distributed across the myocardial wall. Thus, contractile dysfunction in the small myocardial regions with CMVD can be obscured by the normal, or even enhanced, myocardial contraction of interposed myocardial areas.[7]

In clinical practice, the diagnosis of MVA is mainly based on the exclusion criterion of the absence of obstructive CAD at angiography in patients with typical effort angina and evidence of myocardial ischemia on noninvasive investigation, as described above. However, a definite diagnosis might be achieved by documenting the presence of CMVD. This can be obtained by measuring the changes in coronary blood flow (CBF) in response to vasodilator and/or vasoconstrictor stimuli.

This can more precisely and completely be achieved with invasive methods (e.g., intracoronary Doppler recording), although several non-invasive methods are also now available to valuably assess coronary microcirculation, including positron emission tomography, cardiovascular magnetic resonance, and transthoracic Doppler echocardiography (TTDE).[8] However, non-invasive investigation only allows the reliable assessment of coronary microvascular dilation, whereas demonstration of selective enhanced coronary microvascular constriction would require invasive investigation.[8]

Although more advanced methods can be required in some patients, in daily practice CMVD can in most cases be revealed by measuring CBF response to dilator stimuli in the left anterior descending coronary artery by TTDE. In patients with typical angina and normal coronary arteries, a CBF increase<2.0 during adenosine administration and/or <1.6 during cold pressor test can be considered diagnostic for CMVD.[8]

Of note, while MVA is taken into account when invasive coronary angiography is normal in patients with angina and evidence of myocardial ischemia, in some patients who present clinical findings strongly suggestive of MVA (see above), the exclusion of obstructive CAD might be obtained by non-invasive computed tomography coronary angiography, which has a high negative predictive value and can avoid the small, but definite, risk of invasive coronary angiography in most cases.[9]

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