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CTO Manual Online cases: 6 , 19 , 103
PCI Manual Online cases: 4 , 9 , 11 , 14 , 19 , 27 , 31 , 35 , 40 , 41 , 42 , 43 , 44 , 45 , 50 , 54 , 57 , 58 , 61 , 66 , 78 , 83 , 84 , 87 , 94
Acute coronary syndromes encompass ST-segment elevation acute myocardial infarction (STEMI), non-ST-segment elevation acute myocardial infarction, and unstable angina. STEMI patients require immediate reperfusion to minimize the infarct size and decrease mortality.
Given urgency to restore the patency of the culprit vessel in STEMI patients, there is often limited time for planning. Nevertheless, the key components of planning remain essential, such as knowledge of prior revascularization procedures (e.g., STEMI in a patient with prior stenting could be due to stent thrombosis; knowledge of bypass graft anatomy is particularly important in prior CABG patients as it may expedite diagnostic angiography), cardiac function (risk of developing cardiogenic shock is higher in ACS patients who already have decreased ejection fraction) comorbidities (such as renal failure, diabetes, and need for future surgery), and medications that have been administered.
STEMI in postpartum patients may be due to spontaneous coronary dissection (SCAD, Section 22.1 ). STEMI in women who have recently had a stressful event may be due to stress cardiomyopathy (takotsubo), but coronary angiography often needs to be performed to exclude other possible etiologies.
Monitoring is of critical importance in ACS patients, as they are more likely to develop hemodynamic instability and arrhythmias. Often accelerated idioventricular rhythm and ST-segment normalization are indications of successful reperfusion in STEMI patients.
Potent antithrombotic medication administration (both anticoagulation and antiplatelet) is critical for treating thrombotic lesions, to minimize the risk of thrombus expansion or new thrombus formation. Antiplatelet treatment may be best achieved with more potent and rapidly acting oral P2Y12 inhibitors (such as prasugrel and ticagrelor), sometimes in combination with an intravenous antiplatelet agent, such as a glycoprotein IIb/IIIa inhibitor or cangrelor (for cases with large thrombus burden or for bailout in case of thrombotic complications). Anticoagulation is most commonly achieved with unfractionated heparin .
If glycoprotein IIb/IIIa (GP IIb/IIIa) receptor antagonists or cangrelor are being used, heparin is given at a dose of 50–70 U/kg IV bolus to achieve an activated clotting time (ACT) of 200–250 seconds (Hemochron device). When GP IIb/IIIa receptor antagonists or cangrelor are not being used, 70–100 U/kg bolus of unfractionated heparin is recommended with an ACT goal of 300–350 seconds (Hemochron device) .
Radial access is generally preferred over femoral access in ACS patients, especially those with STEMI, given multiple prior studies that have shown lower bleeding risk and lower mortality with radial access , although the SAFARI-STEMI trial did not show any difference in clinical outcomes with femoral vs. radial access . Femoral access is preferred in prior CABG patients, in many of whom graft engagement can be challenging using radial access. Moreover, timing is important in STEMI patients: if vessel engagement is challenging through radial access causing delays in reperfusion (such as in patients with arteria lusoria) , prompt conversion to femoral access is indicated, since “time=muscle.”
Vessel engagement is performed as outlined in Chapter 5: Coronary and Graft Engagement .
In STEMI patients it is often debated whether angiography of both the suspected culprit and the nonculprit vessels should be performed before performing PCI or whether the target vessel should be immediately engaged with a guide catheter with immediate PCI of the culprit lesion.
Immediate engagement of the suspected culprit vessel can shorten door-to-balloon time by 8–13 minutes . However, if the culprit lesion is in the RCA and PCI is done without knowledge of the left coronary anatomy, outcomes may be suboptimal, as some patients may have significant left main or multivessel CAD and may: (1) require hemodynamic support; or (2) be best served with CABG to improve their long-term outcomes, hence balloon angioplasty only of the culprit lesion may be preferable without stent implantation.
A recommended approach to coronary vessel engagement in STEMI patients is shown in Fig. 20.1 .
The goal of diagnostic angiography in ACS patients is to identify the culprit lesion(s), and define the overall coronary anatomy, so that the optimal revascularization strategy can be selected.
Identification of the ACS culprit lesion(s) is often easy on diagnostic angiography (vessel occlusion with thrombus), but can sometimes be challenging. The following parameters can help identify the culprit lesion ( PCI Manual Online cases 9 , 11 , 42 , 50 , 56 , 78 , 87 ):
Electrocardiogram.
Slow antegrade flow.
Luminal haziness, suggestive of thrombus.
Collateral flow.
Occlusion of distal branches, suggestive of prior coronary embolism.
Left ventriculography (can reveal area of hypokinesis or suggest alternative diagnoses, such as takotsubo cardiomyopathy).
Intravascular imaging with optical coherence tomography (OCT), revealing plaque rupture or erosion and thrombus.
Transthoracic echocardiography that can reveal areas of hypokinesis/akinesis and can also help with diagnosis of mechanical complications, such as ventricular rupture, ventricular septal defect, and papillary muscle rupture.
In some cases a culprit lesion cannot be identified, because the presenting symptoms are not due to ischemia (such as in takotsubo cardiomyopathy).
In other cases, the culprit lesion may not be angiographically apparent. Intravascular imaging with OCT can help determine if a culprit lesion is present.
In cases where it remains unclear what the culprit lesion(s) are, subsequent magnetic resonance imaging can help detect the area of myocardial injury and infer what the culprit lesion(s) and vessel(s) are .
Complete revascularization (either at the time of emergent PCI or staged) is recommended for ST-segment elevation myocardial infarction patients, given the results of the COMPLETE trial . In patients with cardiogenic shock culprit-only PCI is recommended in the acute setting based on the results of the CULPRIT-SHOCK trial .
Wiring in ACS patients is performed as described in Chapter 8 : Wiring. A specific challenge for wiring (and also lesion preparation and stenting) is the presence of intracoronary thrombus, in part because the distal vessel may be poorly or not at all visible, since collaterals may not have had enough time to form . Moreover, it may be impossible to determine whether there is angulation within the occluded segment, or whether the guidewire has entered into side branches. In case of guidewire exit from the vessel subsequent advancement of a balloon can result in perforation ( PCI Manual Online case 45 ), further complicating an already high-risk clinical presentation.
Workhorse guidewire
To minimize the risk of perforation, initial wiring through an acute complete thrombotic occlusion is usually attempted with soft workhorse guidewires without hydrophilic tip coating. Occasionally advancement of the guidewire alone will result in restoration of some antegrade flow, that can facilitate subsequent wiring attempts and management of intracoronary thrombus.
Hydrophilic coated guidewires
If a soft workhorse guidewire fails to advance through the occlusion, then a soft guidewire with hydrophilic tip coating can be used (such as the Sion or BMW Universal, see Section 30.7.1 ).
Polymer-jacketed guidewires.
Filterwire or Spider ( Section 30.8 ). Although these devices are currently only approved for use in SVGs in the United States, they may capture thrombi liberated during thrombectomy, balloon angioplasty, and stenting) ( PCI Manual Online case 61 , 66 ).
If crossing with workhorse (with or without hydrophilic coating, Section 30.7.1 ) guidewires fails, soft polymer-jacketed guidewires, such as the Fielder FC or Sion black (Asahi Intecc, Nagoya, Japan, Section 30.7.2 ) are often used next. Escalation to stiffer polymer-jacketed guidewires (such as the Pilot 200) should be avoided, if possible, as it increases the risk of perforation, but may be needed in some challenging lesions .
Guidewire advancement over a microcatheter or a small balloon (1.0–1.5 mm in diameter) can also be useful for crossing by increasing support and allowing guidewire exchanges without losing wire position.
Occasionally advancing a knuckled guidewire ( PCI Manual Online case 54 ) may help advance through areas of tortuosity with low (although not zero) risk of perforation, but may require strong guide catheter support, for example, by using a guide catheter extension.
If the location of the guidewire tip is uncertain after advancing it through an occlusion, it may be best to not advance a balloon but attempt to clarify the guidewire position first. If there is absolutely no antegrade flow after wiring, obtaining a second arterial access and performing contralateral injection may help clarify guidewire position through collateral filling of the occluded vessel. Injecting contrast through an over-the-wire balloon or microcatheter should be avoided, as it carries risk of extending a subintimal dissection if the microcatheter or balloon tip is in the subintimal space. Use of intravascular ultrasound can often aid in confirming intraluminal placement of the guidewire. Careful “dottering” of the thrombotic lesion with a low-profile short balloon may also be performed, however it is not a reliable strategy to confirm true lumen guidewire position; sometimes, it may restore enough flow to confirm guidewire location.
Sometimes, wiring may fail because the lesion being crossed is not the culprit lesion for the acute event (it may be a chronic total occlusion). Alternatively some patients may have more than one culprit lesion. Repeat review of the angiogram (and of prior angiograms if available) and correlation of the electrocardiographic and angiographic findings may be helpful in such cases. Intravascular imaging (especially with OCT, which is the best imaging modality for detecting intracoronary thrombus) can be especially helpful in cases with unclear or multiple potential culprit lesions, as presence of thrombus or ulceration within a lesion strongly suggests it is a culprit. Thrombus aspiration can clarify the anatomy distal to the occlusion, and help clarify if the guidewire is in a side branch or in the main vessel.
A unique characteristic of ACS lesions is intracoronary thrombus that can be managed as outlined in Fig. 20.2 .
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