PCI complications: coronary vasospasm

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: : Anum Ijaz M.B.B.S., M.D.[2]

Overview

Coronary vasospasm can be induced by percutaneous coronary intervention (PCI) secondary to endothelial denudation and nitric oxide loss. The main goal of the treatment is to reverse angioplasty-induced vasospasm. The initial treatment is intracoronary vasodilatation with calcium channel blockers and/or nitrates, which should be given slowly when using guiding catheters. Therapies for vasospasm will usually take effect within seconds to one minute. The current definition of epicardial coronary spasm is a greater than 90% reduction in coronary artery diameter following intracoronary acetylcholine relative to the post-nitroglycerin baseline, accompanied by reproduction of the patient's symptoms and ischemic ST segment deviation.

Classification

Focal coronary spasm

Focal coronary spasm is limited to a localized segment of the coronary artery.

Multifocal coronary spasm

Multifocal coronary spasm involves several localized segments of the same coronary artery.

Multivessel coronary spasm

Multivessel coronary spasm involves several coronary arteries.

Pathophysiology

• Coronary vasospasm can be induced by PCI secondary to endothelial denudation and nitric oxide loss.
• Some cases are catheter-induced which is caused by a contact of a catheter without balloon deployment. Catheter-induced coronary vasospasm is usually short-lived.
• Catheter-induced coronary vasospasm is most prone to occur at the ostium of the right coronary artery (RCA). The left main is less susceptible to ostial spasm.
• Non-selective beta-blockade can worsen coronary spasm through unopposed alpha-adrenergic vasoconstriction; this is the mechanistic basis for avoiding beta-blockers periprocedurally in a patient with demonstrated vasospasm.

Differential Diagnosis

• The differential diagnosis of coronary spasm during PCI includes abrupt closure due to dissection or thrombus formation.

Epidemiology and Demographics

• Coronary vasospasm can occasionally be induced by PCI.
• Rotablator cases are more prone to coronary vasospasm. The reported incidence of rotablator cases with coronary vasospasm ranges anywhere from 4 to 36%.
• A Cochrane systematic review found that patients undergoing rotational atherectomy were approximately nine times more likely to develop angiographically detectable vasospasm than those undergoing balloon angioplasty alone.
• A 2023 retrospective acute coronary syndrome registry (n=283) reported vasospasm during rotational atherectomy in 15.4% of cases performed at low burr speed (130,000-150,000 rpm) versus 6.9% at high burr speed (160,000-220,000 rpm); lower burr speed was associated with more vasospasm while higher burr speed was associated with more slow flow.

Risk factors

• Smoking is a risk factor for coronary vasospasm, and is the most prominent risk factor for vasospastic angina.
• Rotational atherectomy is a procedural risk factor for coronary vasospasm.
• Recurrent coronary vasospasm is itself a risk factor for the later development of fixed atherosclerotic coronary stenosis requiring PCI; in a cohort of 3,556 patients with vasospastic angina, documented vasospasm was independently associated with subsequent PCI, with a lower 10-year PCI-free survival (97.4% vs 98.4%, p=0.002).

Natural History, Complications and Prognosis

• Coronary vasospasm can lead to life-threatening arrhythmias, depending on the vessel that is involved. Specifically, right coronary artery spasm can lead to sinus arrest or complete heart block, while left anterior descending artery spasm can lead to ventricular tachycardia or fibrillation. Multivessel spasm can also lead to ventricular arrhythmias.
• The right coronary artery ostium is prone to catheter-induced spasm, giving the appearance of an ostial lesion on angiography. Pre-treatment with 200 mcg of IC nitroglycerin should be administered prior to intervention of this area.
• Patients who have coronary artery disease in addition to coronary vasospasm have an overall worse prognosis.
• Survivors of cardiac arrest attributable to coronary vasospasm are at high risk of recurrence, particularly with inadequate medical therapy; calcium channel blockers suppress episodes, whereas beta blockers may trigger arrhythmia. ICD placement should be considered in survivors of sudden cardiac arrest with vasospastic/variant angina, because vasodilator therapy may not be fully protective.
• In a provocative-testing series of patients with MINOCA and vasomotor abnormalities, the overall arrhythmic complication rate among those with a positive provocation test was 5.4%.

Diagnosis

• Physicians should suspect coronary vasospasm if ST segment elevation is detected in patients experiencing angina, and if the ECG completely returns to baseline upon resolution of symptoms.
• The definitive diagnosis of coronary vasospasm is made angiographically by demonstration of reduction of luminal diameter in a discrete segment of the vessel, which is proven to be reversible.
• Reversibility may be demonstrated by previous or subsequent enlargement of luminal diameter, often after the administration of intracoronary vasodilators.
• The current quantitative diagnostic definition of epicardial coronary spasm is a greater than 90% reduction in coronary diameter following intracoronary acetylcholine relative to the post-nitroglycerin baseline, accompanied by reproduction of the patient's symptoms and ischemic ST segment deviation (COVADIS/2023 AHA/ACC Chronic Coronary Disease guideline criteria). This distinguishes epicardial spasm from microvascular spasm, in which ischemic ECG changes and angina occur with less than 90% epicardial constriction.

Treatment

Choices of Treatment

Intracoronary Vasodilator

Intracoronary vasodilators should be given slowly through guiding catheters with side holes to maximize the delivery into the artery with minimal dispersal through the catheter side holes.

• Intracoronary nitroglycerin 100-300 mcg. Generally well tolerated and have an additive effect.
• Intracoronary calcium channel blockers. Generally well tolerated, have an additive effect, and have a small risk of transient heart block.
  • Diltiazem 0.5-2.5 mg/min, up to 5-10 mg
  • Verapamil 100 mcg/min, up to 1.0-1.5 mg
  • Nicardipine 100-300 mcg
  • Nifedipine 10 mg sublingual (SL)
• Intracoronary nitroprusside 100-300 mcg

Systemic Vasodilators

• Nifedipine 10 mg sublingual
• Atropine 0.5 mg IV. Particularly useful in the setting of hypotension or bradycardia.

Device Related Treatments

• Removal of interventional hardware with guide wire in place to minimize mechanical provocation. This strategy may minimize distal vessel spasm.
• Repeat prolonged (2-5 min) PTCA at low pressure (1-4 atmospheres). May mechanically "break" vasospasm.
• Stenting. May improve focal spasm, but may simply propagate the site of spasm to a location proximal or distal to the stent within the vessel, so it should be avoided if possible.

Medications to Avoid

• Non-selective beta blockers should be avoided in the setting of active coronary vasospasm because unopposed alpha-adrenergic tone can aggravate spasm.

Distinguishing Refractory Vasospasm from No-Reflow and Dissection

Abrupt vessel closure during PCI may result from vasospasm, no-reflow, or focal dissection, and distinguishing among these determines management.

• Vasospasm should be treated with nitroglycerin, intracoronary "flush cocktails" (adenosine, nitroprusside, nicardipine, or verapamil), atropine, fluid boluses, or vasopressors for hemodynamic support.
• No-reflow should be treated with a "flush cocktail" of adenosine, nitroprusside, nicardipine, or verapamil, with or without abciximab, selectively delivered distally to the occlusion.
• For abrupt vessel closure of unknown mechanism, distal contrast injection with a microcatheter should differentiate no-reflow from focal dissection before escalating to stenting.

Step by Step Treatment Approach

• Therapeutic treatment of PCI-induced vasospasm should be performed in this order (step-wise fashion):

• Before initiating pharmacologic therapy, hemodynamic stability should be assessed; unstable patients require hemodynamic support (vasopressors, inotropes, intra-aortic balloon pump, or left ventricular assist device), and guidewire position should be confirmed to be in the true lumen.
• Initial step is intracoronary vasodilatation with IC calcium channel blockers and/or nitrates, which should be given slowly when using guiding catheters with side holes to avoid dispersal of the drug through the holes instead of into the coronary artery.
• If one agent is unsuccessful, combined therapy should be implemented as these medications have an additive effect. Be mindful for heart block with CCB therapy.
• IV atropine can be useful if there is associated hypotension of bradycardia.
• Should medical therapy fail, remove all hardware and leave the guide wire in place to maintain position. This may minimize distal vessel spasm.
• Repeat prolonged PTCA for 2-5 minutes at low pressures (1-4 atmospheres).
• Stenting should be a last ditch option, and used if above measures have failed, as it may lead to propagation of spasm to a new location. Refractory vasospasm may be indicative of dissection, which is also an indication for stenting.
• This stepwise approach aligns with the broader abrupt-vessel-closure algorithm, which treats by mechanism: vasospasm with vasodilators and atropine, dissection with stenting, and no-reflow with a distal flush cocktail.

Areas of Uncertainty

• The role of long-acting nitrates in preventing coronary vasospasm remains disputed because of nitrate tolerance, even though short-acting or intracoronary nitrates are clearly effective acutely.
• The optimal rotational atherectomy burr speed to minimize vasospasm while avoiding slow flow is unsettled and is based on single-center retrospective data only.

Assessment of Response to Therapy

Therapies for vasospasm will usually take effect within seconds to one minute. Anticipated outcomes include:

• Resolution of the coronary vasospasm
• Resolution of the ECG changes (ST depression or elevation)
• Resolution of symptomatic angina and other symptoms, if present