Читать книгу Practical Cardiovascular Medicine - Elias B. Hanna - Страница 223

Epicardial (macrovascular) vasospasm is definitely diagnosed on coronary angiography when the following three features occur, spontaneously or with provocation:^{6,120,121,122}

 Focal or diffuse vasospasm leading to ≥75% dynamic luminal reduction. One study used a 90% cutoff¹²²

 ST-segment elevation or depression

 Reproduction of the patient’s symptoms

Microvascular vasospasm is diagnosed when ST-segment changes and symptoms occur with provocation, without any visualized spasm.⁶ An additional feature of microvascular spasm is a slow coronary flow (delayed TIMI frame count) without epicardial obstruction.

When present spontaneously, vasospasm is frequently confused with a true fixed obstruction; the diagnosis of vasospasm is made when the stenosis improves to <50% with intracoronary NTG administration. While it is reasonable to administer NTG whenever any coronary stenosis is seen, to rule out a dynamic component before any PCI, vasospasm is particularly suspected when the stenosis is concentric with smooth borders. Conversely, ostial spasm occurring at the catheter tip does not have a diagnostic value. The dose of intracoronary NTG is 50-200 mcg- studies suggest no further coronary dilatation with doses beyond 200 mcg.

Vasospasm may be provoked with intracoronary ergonovine, or safer yet, slow intracoronary acetylcholine boluses (very quick offset). Angiographic vasospasm without symptoms or ECG changes is suspicious but not diagnostic of vasospastic angina.

Although acetylcholine provocation is safe, it is not routinely performed at many institutions. The diagnosis is presumptive in a patient with the following triple combination: rest angina or effort angina, no angiographic CAD, and documentation of transient ST changes on stress ECG or ambulatory ECG. ST changes being infrequently documented, provocative testing is preferably performed and alters chronic management.¹²²

In vessels with normal endothelial function, acetylcholine induces the synthesis of NO and coronary vasodilatation. In vessels with endothelial dysfunction, the endothelium cannot generate NO, hence acetylcholine directly acts as a vasoconstrictor.