Percutaneous coronary intervention (PCI) in the left main coronary artery can be challenging for many reasons:
Severe ischemia and hemodynamic instability : the left main provides blood flow to most of the myocardium, hence coronary flow compromise during the procedure can result in hypotension, cardiogenic shock, or cardiac arrest.
Anatomic complexity: the left main can have ostial disease, body disease, and/or bifurcation disease (the bifurcation is involved in >80% of left main lesions undergoing PCI ). Lesions in the left main body are the easiest to treat.
It is important to review prior coronary angiograms and operative reports, to answer questions, such as:
Is there also disease or occlusion of the right coronary artery?
Are there visible collaterals from the right coronary artery to the left system?
Is the left main protected by an aorto-coronary bypass graft?
Is there severe calcification that may require atherectomy?
Additional clinical information, such as left ventricular function and baseline hemodynamic status, clinical presentation and comorbidities, is vital to help assess procedural risk and to determine the need for hemodynamic support. Right heart catheterization can help assess filling pressures and cardiac output, determine the need for hemodynamic support prior to the intervention, and monitor hemodynamics during the procedure.
Monitoring is performed as described in Chapter 2 : Monitoring. Careful monitoring is especially important in patients with left main disease due to risk of rapid hemodynamic deterioration. If hypotension develops, early use of vasopressors (such as norepinephrine) is encouraged to prevent rapid hemodynamic deterioration. Defibrillation pads should ideally be placed on the patient to allow prompt treatment in case of ventricular arrhythmia or fibrillation.
Medications are administered as described in Chapter 3 : Medications.
Either femoral or radial artery access can be used for left main PCI. Femoral artery may be preferred in patients with highly complex anatomy. Larger guides (7 or 8 French) provide more support and are preferred for left main bifurcation PCI.
Left main engagement can be challenging in patients with ostial left main lesions, as severe pressure dampening can occur causing extensive ischemia. Careful monitoring of the pressure waveform is needed, followed by prompt disengagement in case of dampening before any hemodynamic deterioration or vessel injury occurs.
Larger guides (7 or 8 French) provide more support and allow some bifurcation stenting techniques, such as V-stenting (Section 188.8.131.52).
Side hole guides should not be used for engaging the left main (with the exception of left main chronic total occlusions), as they may mask pressure dampening leading to profound ischemia. Side hole catheters are particularly dangerous in patients with short left main because the guide catheter might completely obstruct the ostium of the circumflex with a seemingly normal pressure waveform ( Fig. 17.1 ).
As described in Chapter 15 : Ostial Lesions ( Section 15.1.5 ) in cases of severe left main ostial disease a guidewire (and often a balloon mounted on the wire) should be inserted and advanced to the tip of the guide catheter prior to engagement, to facilitate immediate wiring (and ballooning) upon engagement.
Intermittently disengage the guide catheter to alleviate ischemia. Use of the independent-hand technique (Section 9.5.8, Fig. 9.5 and Fig. 15.4 ) or the floating wire technique ( Section 15.1.5 , Fig. 15.3 ) can facilitate guide manipulations.
Avoid contrast injections while pressure is dampened to minimize the risk of left main ostial dissection that can be catastrophic. If a dissection occurs, disengage the guide and perform only cautious contrast injections from a distance to clarify the situation without enlarging the dissection. Also prepare for stent implantation to seal the dissection entry.
Avoid prolonged contrast injections if the patient has a left dominant coronary circulation or a total occlusion of the right coronary artery, as they can cause hypotension.
Angiographic evaluation of left main disease has limitations: although it is usually adequate for left main lesions with ≥70% diameter stenosis, there is significant interobserver variability for 30–70% lesions . The high variability of the visual assessment stems from the lack of reference segment due to the short length and usually diffuse disease of the left main. The most appropriate views to visualize the left main bifurcation are RAO-caudal, AP-caudal, and LAO-caudal (“spider”) views. The LAO-cranial or AP-cranial views are the most reliable for accurate aorto-ostial positioning of the proximal stent edge. The ostium of the left main is usually oval, therefore orthogonal views are important for proper assessment. The high anatomical and pathological variability of left main disease makes functional assessment or intravascular imaging essential for assessing intermediate left main lesions.
Selecting target lesion(s)
As described in Chapter 7 : Selecting Target Lesion(s), decision about revascularization in patients with left main disease are challenging and depend on several factors:
Clinical presentation (stable vs acute coronary syndrome).
Coronary anatomy (extent and complexity) and ability to provide complete revascularization.
Left ventricular function.
Comorbidities, such as diabetes.
In general the choice of revascularization strategy in patients with left main disease who are good surgical candidates and do not have diabetes, depends on overall CAD complexity. Patients with complex CAD (such as patients with high [≥33] Syntax score) who are good surgical candidates usually benefit more from CABG, whereas those with low (0–22) or intermediate (23–32) Syntax score derive similar benefit from either CABG or PCI . This, however, remains an area of continued controversy with some studies showing better outcomes with CABG. The ultimate decision should be made by a heart team taking into account the patient’s preference and comorbidities.
An algorithm about left main revascularization is shown in Fig. 17.2 .