Some studies have shown a higher risk of acute stent thrombosis with bivalirudin vs. UFH, which may be offset by extending the bivalirudin infusion 1–4 hours after PCI. Being an anticoagulant, bivalirudin is best compared to UFH, not the combination UFH + GPI. In fact, contrary to the design of older trials, the decision to add GPI should not be based on the anticoagulant used.59
Bivalirudin is administered as an intravenous infusion during PCI. On admission, patients may receive UFH with a switch to bivalirudin during PCI. The switch to bivalirudin is safe.174
Appendix 5. Difference between plaque rupture and plaque erosion
A vulnerable plaque is characterized by a lipid-rich necrotic core that is surrounded by a thin fibrous cap and infiltrated by inflammatory cells, especially metalloproteinase-rich macrophages (called thin-cap fibroatheroma). The thin cap ruptures, especially at the shoulders/margins of the plaque where the stress is highest, and leads to thrombus formation. Plaque rupture is, thus, characterized by a ruptured cap and a thrombus in continuity with a necrotic core. The ruptured cap is identified as a flap on IVUS or OCT. Most plaque ruptures are non-occlusive and silent, contributing to a stair-step progression of coronary stenosis. Stable CAD stenoses are frequently multiple layers of healed plaque ruptures. On IVUS, heavy atherosclerosis and compensatory vessel expansion (positive remodeling) often indicate prior episodes of plaque rupture and a vessel that has expanded to its limit, risking a more symptomatic rupture (the plaque is running out of energy supply).
Plaque erosion, on the other hand, is characterized by thrombus formation over a thick cap that has not ruptured (no communication with the necrotic core), or over a fibrointimal plaque rich in smooth muscle cells without a necrotic core (fibrotic plaque).175-177 Plaque erosion is responsible for ~25% of MIs, more so in women, especially young female smokers (< 50 years old). Compared with plaque rupture, plaque erosion occurs, on average, on less stenotic lesions.
Plaque rupture leads to the complex eccentric morphology and overhanging borders on angiography. Conversely, plaque erosion has an uncomplicated angiographic morphology with smooth borders.
Appendix 6. Spontaneous coronary artery dissection
Spontaneous coronary artery dissection (SCAD) is a split of a coronary artery wall without atheroma, resulting from either a bleeding inside the media or an intimal tear. SCAD is the cause of up to 4% of MIs; however, it is under-diagnosed and may be the cause of up to 35% of MIs in women ≤50 years of age. It most frequently involves the media, leading to a long smooth stenosis > 30 mm (average 46 mm) without a flap or stain, mimicking the smooth appearance of vasospasm or plaque erosion (this is called intramural hematoma or SCAD type 2, ~70% of SCADs). Less frequently, it involves the intima, in which case a flap or stain is seen angiographically (called SCAD type 1, ~30% of SCADs). The intimal flap being absent in 70% of patients, spontaneous coronary dissection is suspected in a woman with a smooth, long lesion non-responsive to NTG and non-calcified, mimicking a “long refractory vasospasm” (Figure 1.10). IVUS or OCT may be used to confirm the diagnosis by showing a large “blood-speckled” hypodense (dark) mass behind the intima, pushing the intact and relatively thin intima into the lumen; yet, IVUS or OCT is not routinely recommended as any coronary manipulation may propagate the dissection.178 SCAD has the following additional features:178-182
Typically involves the mid-to-distal coronary segments, most commonly the LAD, and may involve multiple coronary arteries (~10-20%). Proximal or left main involvement is rare (~8%), hence shock is rare.
Occurs overwhelmingly in women (95%), mainly young and middle-age women (like coronary erosion), but is also seen in women >50, with one large registry suggesting that the mean age of women affected by SCAD is 61;179 it may rarely be seen in men.
Presents as NSTEMI (~60%) or STEMI (~40%).
Is highly associated with coronary tortuosity (78%), including corkscrew coronary arteries, and peripheral fibromuscular dysplasia. The same collagen fragility that predisposes to wall disruption also facilitates coronary elongation.
Is often initiated by intense exercise (especially isometric), heavy lifting, or intense Valsalva (including vomiting). Intense emotional stress may also be a trigger.
Treatment: PCI vs conservative management- Spontaneous coronary dissection has a relatively high complication rate during PCI, which results from wiring the false lumen or balloon-induced hematoma propagation distally or proximally toward the left main. In fact, PCI failure or complications are seen in 50-70% of the cases and emergency CABG is required for complications in 13% of the cases!178-183 Even coronary engagement and contrast injections are associated with a risk of ostial or left main dissection, including hydraulic dissection. Indeed, dissection complicates 3.4 % of diagnostic angiographies and up to 8% of intracoronary imaging studies. As opposed to plaque rupture or erosion, the overwhelming majority of spontaneous coronary dissections spontaneously heal on follow-up angiography ≥ 35 days (70-97%), justifying conservative management in patients without active ischemia, without total occlusion, and with TIMI 2 or 3 flow. The diagnosis being solely based on angiographic lesion morphology and context, some operators may feel uneasy observing tight stenoses without definite diagnostic confirmation; as such, IVUS may be used in equivocal cases, the patient is closely monitored for 5-7 days, and the diagnosis is eventually confirmed retrospectively by repeating coronary imaging at 6 weeks to show healing (CT or coronary angiography). Conservative treatment consists of aspirin, clopidogrel, and beta-blocker therapy, along with 5-7 days of inpatient monitoring. Some degree of antithrombotic therapy is required to prevent thrombosis of the compressed true lumen. Too much antithrombotic therapy, however, risks extending the false lumen hematoma; hence, only antiplatelet therapy is typically used, not anticoagulation.181,182
In patients with ongoing STEMI, total occlusion, or hemodynamic compromise, PCI is justified: low-pressure balloon dilatation may be tried as a stand-alone strategy to re-establish flow, avoiding long stenting in a pathology that will heal on its own. CABG is an option in left main or multivessel SCAD; CABG is hampered by distal vessel involvement and by a high rate of graft closure (70%) on long-term follow-up, as native disease regresses.183
Progression and follow-up:
SCAD almost always heals, yet acute extension may be seen in ~5-10% of cases in the first week, before eventual healing; thus, ECG signs of ongoing or recurrent ischemia may justify repeat coronary angiography or CT. Note that persistent pain, by itself, does not necessarily imply ischemia, as the dissection process may be painful by itself.Figure 1.10 NSTEMI in a healthy 47-year-old woman. Chest pain started during kick boxing. Several features suggest SCAD type 2 and argue against performing PCI: (1) long smooth disease >30 mm with no calcification (arrows), (2) tortuous, elongated coronary arteries, (3) distal disease, (4) woman <60 years. The flow was TIMI 2 and she was not having ongoing angina, so conservative management was adopted. Intravascular imaging was avoided.
Instead of repeating coronary angiography, coronary CT may be used to document SCAD healing 6 weeks later; it may also be used in patients with recurrent symptoms, to rule out proximal SCAD extension that would warrant intervention. CT is not a great initial diagnostic modality as it is insensitive for distal SCAD of small vessels <2.5 mm.
In-hospital and long-term survival is very favourable in non-pregnancy SCAD (0 to 2% in-hospital mortality, 0% mortality in the Canadian SCAD registry).183 Yet, one series suggests a high mortality, higher than traditional MI, mainly when PCI is attempted or in women older than 60.179 Also, there is a 10-30% risk of recurrence at 1-3 years, and 30% at 5 years. Recurrence is reduced with: β-blockers (2/3 reduction), avoidance of emotional and physical triggers, such as heavy lifting>30-50 pds, Valsalva, and hormonal therapy.
SCAD