Читать книгу Practical Cardiovascular Medicine - Elias B. Hanna - Страница 226

Microvascular dysfunction has two forms, both reflective of endothelial dysfunction:

1 Microvascular spasm, which is part of the spectrum of coronary vasospasm

2 Impaired capacity to vasodilate the microcirculation and increase myocardial flow during exercise (<2.5 x increase)

It is diagnosed by either one of the following:

(1) Provocative coronary testing with acetylcholine, seeking ST-segment and chest pain response

(2) Demonstration of impaired coronary microvascular dilation and coronary flow reserve after adenosine (<2.5× increase in coronary flow, measured with a coronary flow wire).^6,127–129

(3) Slow angiographic flow in the absence of CAD (“coronary slow flow phenomenon”).

LVEDP is frequently elevated and may be the consequence or the cause of impaired coronary flow. Along those lines, microvascular dysfunction may be secondary to left ventricular hypertrophy.¹²⁹

The diagnosis of vasospasm or microvascular dysfunction is often made presumptively in a patient with chest pain, documented ST changes or convincing ischemia on stress testing, and no significant CAD. While the stress test is sometimes considered falsely positive (e.g., artifact), patients with convincing angina and ischemic ECG or imaging defects most likely have microvascular dysfunction, or, less frequently, macrovascular spasm. Indeed, one study has found a correlation between impaired coronary response to acetylcholine and ischemic defects on nuclear testing,¹²⁸ and another found an increased prevalence of abnormal stress testing (77%) in patients with abnormal vasomotion.¹³⁰ Yet, stress imaging with echo or SPECT is not very sensitive; stress imaging with PET or MRI is preferred to detect abnormal vasodilatory reserve. Unlike nuclear SPECT imaging, nuclear PET can quantify the absolute myocardial flow, both at rest and after stress and their ratio (<2-2.5 is abnormal).

Microvascular dysfunction is mostly prevalent in women, while epicardial vasospasm is nearly as prevalent in men as in women.^120,121 In ACOVA and in 2 other large studies, ~20% of men with chest pain and unobstructed coronary arteries had microvascular dysfunction, and ~20% had macrovascular spasm; ~70% of women had abnormal vasomotor response (microvascular dysfunction ~40%; macrovascular spasm ~30%).^6,120,121 The prevalence of microvascular dysfunction actually increases with age (mean age 58-64).

In macrovascular spasm, pain is predominantly a resting pain, while in microvascular dysfunction, pain is predominantly exertional or mixed resting/exertional (70%). ^120-122

β-blockers, CCBs, nitrates, ranolazine, statins, and ACE-Is have been used for this syndrome with a variable success rate. Unlike in macrovascular spasm, β-blockers are recommended and were first-line treatment in CorMicA trial; ¹²² they are efficacious via a reduction of exertional myocardial O2 demands, as in obstructive CAD, not via a direct microvascular effect. Nitrates are not microvascular dilators but lessen ischemia through preload reduction. Ranolazine appears to be particularly effective in reducing angina and improving myocardial flow, via improving diastolic relaxation.¹³¹ In one study of microvascular dysfunction, L-arginine, a precursor of NO available as an over-the-counter supplement, significantly improved myocardial flow.¹³²