Читать книгу Practical Cardiovascular Medicine - Elias B. Hanna - Страница 230

In a patient with a coronary total occlusion, the presence of coronary collaterals does not imply that the occlusion is chronic. Underdeveloped intercoronary channels often pre-exist in normal individuals before the occurrence of the coronary occlusion; coronary occlusion or severe stenosis leads to widening of these channels within the first 24 hours, followed by progressive enlargement and maturation of the collateral wall. Mature collaterals that approximate the size of a side branch and provide grade 3 filling of the recipient artery require ≥2 weeks to form, often ≥12 weeks.^144,145

Basic collateral filling may be seen in acute MI. In fact, half of patients with acute MI develop collateral flow in the first 6 hours, while all patients develop collaterals within 24 hours.¹⁴⁵ More mature collaterals may be seen early in MI if it was preceded by a chronic, severe coronary stenosis (e.g., ≥90% chronic stenosis). Grade 3 collaterals suggest an occlusion that is at least several weeks old, but do not rule out the possibility of acute occlusion on top of a chronic, subtotally occlusive stenosis. Intercoronary collaterals are angiographically graded as follows (Rentrop classification): grade 1 = side branch filling of the recipient occluded artery, without visualization of the body of the recipient artery; grade 2 = partial, faint filling of the body of the recipient artery; and grade 3 (mature collaterals) = complete filling of the recipient artery or presence of a large, continuous collateral the size of a side branch. Nitric oxide promotes collateral growth; traditional risk factors, particularly diabetes, may impede the development of collaterals.

Mature collateral flow may provide up to 50% of the native antegrade flow, and thus may drastically reduce ischemia.¹⁴⁶ Chronic total occlusions (CTOs) most often develop slowly, allowing collaterals to develop and allowing normal function of the subtended myocardium at rest. While a CTO is almost always associated with stress-induced ischemia, the degree of ischemia depends on the size of the territory and the maturity of collaterals.¹⁴⁷

CTO is defined as a total occlusion that is >3 months old without any antegrade filling (true CTO), or with faint antegrade filling through microchannels (functional CTO). CTO is distinguished from an acute or recent occlusion by the clinical presentation and the ECG (stable angina in CTO, recent ACS or MI in recent occlusion). A small subset of CTOs may be the long-term remnant of an old, non-recanalized MI. The duration of the CTO is gauged by the date of worsening of angina or the date of an old MI. Bridging collaterals, which are fine collateral vessels that form a caput medusae around the CTO, usually imply an old occlusion >3 months old and a reduced PCI success rate. This fine bridging network is sometimes confused with intra-CTO microchannels (functional CTO), yet the two entities have radically opposite implications: the former implies a low PCI success rate, while the latter implies a high PCI success rate.

After successful PCI of a CTO, a considerable fraction (50%) of the collateral function is immediately lost through spasm and is non-recruitable should acute reocclusion occur.¹⁴⁵ The patient may have a stable CTO for years; however, if a CTO is recanalized with PCI then acutely reoccludes, an acute MI will ensue, even if reocclusion occurs as early as a few hours or days after recanalization. This is due to: (i) early loss of collateral flow (spasm early on, anatomic involution later on), (ii) distal embolization from the upstream thrombosis, which occludes the microcirculation and any patent collaterals (similar to early SVG thrombosis). Yet sometimes, when reocclusion occurs early, collateral flow may be quickly recruited and may limit MI size.