Immediate
a Only bivalirudin inhibits fibrin-bound thrombin. Heparin and fondaparinux cannot act on fibrin-bound thrombin. Bivalirudin has not been studied in advanced renal failure (in ACUITY trial) but is not absolutely contraindicated.
b If only one SQ dose was provided before PCI, give additional 0.3 mg/kg IV during PCI. SQ enoxaparin is not well studied in patients > 150 kg, where the 1 mg/kg dose is associated with a marked increase in bleeding risk compared to patients with a normal body weight. AT III, antithrombin III.
IV Bivalirudin. As opposed to UFH, bivalirudin does not activate platelets and inhibits both free and clot-bound thrombin. Bivalirudin is short-acting (half-life 25 min), which is both an advantage (bleeding reduction) but also an ischemic hazard, particularly in patients who have not received timely clopidogrel. Femoral-access studies suggested that bivalirudin is associated with less major bleeding than UFH (MATRIX), but this was partially due to higher GPI use in the UFH arm. A radial-access study with balanced and limited GPI use (VALIDATE-SWEDEHEART) showed an ischemic and bleeding risk identical to UFH.173 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
