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Vasospasm – Case 1

Clinical Presentation

  • 73-year-old male who presented with chest pain (CCS Class II).

Past Medical History

  • HTN, HLD, DM, CAD s/p 2-Vessel CABG and Multiple PCI’s, Hypothyroidism, CKD
  • LVEF 19%

Clinical Variables

  • Stress MPI: Mild anteroseptal and posterolateral scarring.

Medications

  • Home Medications: Aspirin, Ticagrelor, Carvedilol, Atorvastatin, Isosorbide Mononitrate, Furosemide, Sacubitril-Valsartan, Dulaglutide, Insulin, Levothyroxine, Ranitidine, Allopurinol
  • Adjunct Pharmacotherapy: Ticagrelor, Bivalirudin

Pre-procedure EKG

Angiograms

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Right coronary artery (RCA) angiography
  • 50-60% distal RCA stenosis
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Right coronary artery (RCA) angiography

  • 50-60% distal RCA stenosis
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Left coronary artery angiography

  • patent intervention sites in the left circumflex (LCx) coronary artery
  • total occlusion of the mid left anterior descending (LAD) coronary artery
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Saphenous vein graft (SVG) to D2 bypass graft angiography

  • 80-90% in-stent restenosis lesion.
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Left internal mammary artery (LIMA) to LAD bypass graft angiography

  • 80-90% LAD lesion distal to the LIMA anastomosis.
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Pre-dilatation of the lesion in the LAD, distal to the LIMA anastomosis with a Mini Trek 2.0/12mm balloon.

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Cutting balloon angioplasty of the lesion in the LAD, distal to the LIMA anastomosis with a Wolverine 2.5/6mm balloon.

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Positioning of an Xience Sierra 2.75/12mm in the LAD, distal to the LIMA anastomosis.

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8 of 13

Post-dilatation of the stent placed in the LAD, distal to the LIMA anastomosis with a NC Emerge 3.0/8mm balloon.

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Retraction of the wire and the balloon into the LIMA.

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Angiography of the LIMA to LAD bypass graft showing multiple discreet focal lesions, concerning for combined spasm and pseudo-stenosis.

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The wire was retracted into the proximal LIMA. Angiography shows persistence of multiple discreet focal lesions and improvement of others confirming a combination of spasm and pseudo-stenoses.

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Intra-graft vasodilators were given and majority of the focal lesions are no longer present.

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Final angiography of the LIMA to LAD. The wire is removed and the focal lesions are no longer present.

Post-procedure EKG

Case Overview

  • Underwent intervention of the LAD distal to the LIMA to LAD anastomosis.
  • After successful intervention of the LAD, the wire and balloon were retracted back into the LIMA.
  • Angiography showed presence of multiple focal lesions which were concerning for combined spasm and pseudo-stenosis.
  • The wire was further retracted with improvement in some of the lesions distal to the wire; however, many of the focal lesions persisted.
  • Intra-graft vasodilators were given and the focal lesions resolved.
  • Troponin-I peaked at 0.03 ng/mL and CK-MB peaked at 1.8 ng/mL.
  • Patient was discharged home the next day without further sequelae.

Learning Objectives

  • What is the likely explanation or reason why the complication occurred?
    • Pseudo-stenosis is also known as accordion effect and concertina phenomenon. It occurs when coronary equipment (i.e. coronary guidewire, stent etc.) causes mechanical distortion (folding/pleating) of a coronary artery along its long axis, and it presents as a filling defect.
    • Coronary Spasm: the most common cause of intra-procedure coronary spasm is guidewire or balloon/stent manipulation. Catheter-induced spasm which usually involves the RCA ostium more often than the LCA ostium, and typically is within 2cm of the catheter tip. Cases where rotational atherectomy is used are more prone to coronary spasm. Coronary spasm occurs because of endothelial denudation and nitric oxide loss.
  • How could the complication have been prevented?
    • Use a less supportive/stiff coronary guidewire.
    • Vasodilators should be given prophylactically and for treatment of coronary spasm, especially when performing ostial RCA and LCA interventions.
  • Is there an alternate strategy that could have been used to manage the complication?
    • It is reasonable and safer to diagnose pseudo-stenosis while leaving a guidewire within the coronary artery, and withdrawing it gradually until its radio-opaque (floppy) segment rests equally on either side of the suspect lesion. However, this technique is usually not feasible when there are multiple discreet lesions. If this technique fails, focal defect is located in the distal segment of a large vessel, reduced coronary flow with ongoing chest pain and EKG changes, or if there are multiple discreet lesions, then use a transit exchange catheter to remove the coronary guidewire. Place the exchange catheter distally over the guidewire and the remove the guidewire. This usually allows the vessel to return to its natural contour, resolving the pseudo-stenosis. It is important to position the exchange catheter distal as possible before removing the coronary guidewire because once the wire is removed, the vessel tortuosity will be restored and some position will be lost when reintroducing the wire. The guidewire can be exchanged, for a less supportive wire that will better conform to the artery contour if needed.
    • Step by step algorithm for management of coronary spasm:
      • 1st: Intra-coronary/intra-graft vasodilators should be given slowly through a catheter, especially if using a guide catheter with side holes to maximize delivery into the artery. If one agent is unsuccessful, give combined therapy as CCB and nitrates have additive effect. We use the following agents and administer them intra-coronary/intra-graft:
        • Nitroglycerin 100-200 mcg, Verapamil 100-200 mcg, Nicardipine 100-200 mcg
      • 2nd: If medical therapy fails, remove hardware without losing coronary guidewire position to minimize mechanical provocation.
      • 3rd: If persists, consider performing prolonged (2-5 min) PTCA at low pressure (1-4 atm).
      • 4th: In rare cases, a stent can be placed if above measures fail. Placement of a stent should be avoided as much as possible because it may propagate the spasm in either direction of the stent. Remember, refractory spasm may be indicative of dissection, which is also treated with a stent.
    • Intra-coronary/intra-graft imaging with IVUS/OCT may be used to help elucidate the etiology of a focal lesion.
  • What are the important learning points?
    • If a new lesion appears while performing a procedure an operator has to consider a broad differential which includes coronary spasm, thrombus, dissection, plaque shift, and pseudo-stenosis.
    • Coronary spasm is classified as:
      • Focal coronary spasm : involves a single localized segment of a single coronary artery
      • Multifocal coronary spasm: involves multiple localized segments of the same coronary artery
      • Multivessel coronary spasm: involves segment(s) of more than one coronary artery
    • Coronary spasm may appear benign but can lead to life-threatening arrhythmias and conduction abnormalities. Prognosis is worse in patients who have combined CAD and coronary spasm.
    • Definitive diagnosis of coronary spasm is made angiographically when there is a luminal narrowing in a segment of a vessel that is shown to be reversible, typically with administration of intracoronary vasodilators.
    • If there is a new focal lesion after introduction of coronary equipment, remember to review the initial acquisitions and follow the algorithm above. Often times both a spasm and pseudo-stenosis can present simultaneously, and both IC vasodilators and removal of coronary equipment is necessary for the filling defect to resolve. However, if there is concern for dissection or thrombus, wire position should NOT be lost.
Educational Content

ABRUPT VESSEL CLOSURE (AVC)

  • AVC is the commonest major complication of PCI8
  • Incidence: 0.3% [used to be 3% in pre-stent era]9
  • Risk factors:10
    • Proximal vessel tortuosity
    • Diffuse lesion
    • Pre-existing thrombus
    • Degenerated vein graft
    • Extremely angulated lesion
    • Unstable angina
    • Multivessel disease
    • Female gender
    • Chronic renal failure
  • Common causes:10
    • Coronary dissection
    • Intracoronary thrombus formation
    • Native thrombus (or atheroma) embolization
    • Air injection
    • Coronary no-reflow
    • Coronary vasospasm

In the current DES era, commonest causes of AVC are stent edge dissection and acute stent thrombosis. However, the cause is indeterminate in almost 50% of patients.9

  • Classification of coronary perforation: As per the National Heart, Lung and Blood Institute scheme, types A–F classification remains useful to describe the severity of luminal injury:11
Type AMinor radiolucency within the coronary lumen without dye persistence
Type BParallel tracks or double lumen separated by a radiolucent area during angiography without dye persistence
Type CExtraluminal, persisting extravasation of contrast
Type DSpiral luminal filling defects
Type EPersistent lumen defect with delayed antegrade flow
Type FFilling defect accompanied by total coronary occlusion
  • Prevention:
    • Maintain ACT > 300 throughout procedure
    • Make sure interface is free of air
    • Avoid high-pressure balloon dilatation or stenting
    • Avoid unnecessary post-dilatation and very long stents
    • Use distal protection devices in vein graft PCI
    • Be careful when retrieving delivery after stent implantation
    • Avoid geographical miss during stenting
    • Avoid aggressive post-dilatation at the stent edges
    • Be careful while positioning wire distal tip in tortuous vessel
  • Management: Abrupt closure results in acute ischemia manifesting as ECG changes, hypotension, bradycardia, chest pain and ventricular arrhythmias. The first step is to identify the underlying cause of AVC and then treat it accordingly.
    • Immediate priority should be to ensure intraluminal position of coronary guidewire and, if in doubt, an over-the-wire balloon catheter or Twin-Pass or other microcatheter should be advanced distal into the target vessel to allow minimal contrast media injection and confirm wire position.
    • If intraluminal guidewire position is confirmed, the most likely mechanism underlying AVC is dissection or intraluminal thrombus. Prompt balloon

inflation should be attempted to establish antegrade flow. If flow returns immediately after balloon inflation the likely cause of AVC is dissection and urgent stenting is useful for stabilizing.

    • If the distal flow after balloon inflation is sluggish (TIMI 0 or 1), the likely cause of AVC is distal thromboembolism. Using a Twin-Pass or microcatheter to administer distal vasodilators can help reestablish flow.
    • If initial contrast agent injection reveals guidewire position within a false lumen, careful exploration of the occluded segment using a second guidewire must be performed.
    • Aspiration thrombectomy and Glycoprotein IIb/IIIa antagonists may be helpful if acute closure is due to

thrombus. Control of anticoagulation is of paramount importance to avoid thrombotic occlusion of stented artery. ACT should be measured every ~30 minutes to keep ACT > 300 throughout the procedure and dose of anticoagulation is adjusted accordingly. If ACT is not reaching therapeutic levels consider resistance to anticoagulant and a possible reason for suspected thrombus formation causing AVC.

    • Intravenous fluids, vasopressors, inotropes and intra-aortic balloon pump (IABP) should be considered for unstable hemodynamics.
    • Emergency CABG should be considered if patient have persistent AVC depending on the location of the occlusion, patient’s clinical condition and assessment of risks and benefits.

Coronary slow flow/no-reflow phenomenon

Slow flow/No-reflow is an acute reduction in coronary flow (TIMI grade 0–1) in a patent vessel with absence of dissection, thrombus, spasm, or high-grade residual stenosis at the original target lesion.12 The underlying mechanism is complex and not completely understood, but some proposed mechanisms include distal embolization of calcium, plaque or thrombus and microvascular spasm caused by release of vasoconstrictor substances like serotonin and thromboxane, oxidative stress, and reperfusion injury.13 Clinical and lesion characteristics associated with higher incidence of no-reflow include left ventricular systolic serotonin and thromboxane, oxidative stress,and reperfusion injury.13 Clinical and lesion characteristics associated with higher incidence of no-reflow include left ventricular systolic dysfunction or hemodynamic instability, long calcified lesions, ostial lesions, chronic total occlusion of right coronary artery, thrombotic lesions, and vein graft lesions. Use of rotational atherectomy is also associated with a higher incidence of no-reflow.
Prevention
    • Direct stenting whenever feasible
    • Use of distal embolic protection devices for vein graft interventions.
    • Aspiration thrombectomy in STEMI cases if there is large thrombus burden
    • For cases involving rotational atherectomy, the use of rota flush, small

initial burr sizes, shorter rotablation runs, avoiding drops in rotations per minute (RPMs), and prevention of hypotension/bradycardia

Management: Coronary no re-flow must be immediately differentiated from AVC due to dissection as placement of stent in a vessel with no reflow may worsen the situation. Exclusion of dissection, thrombus, spasm, or high-grade residual stenosis at the original target lesion suggests no-reflow.
    • Stabilize hemodynamics with medications/intra-aortic balloon pump (IABP)
    • IC verapamil (100–200 μg)
    • IV adenosine (10–20 μg)
    • IC nitroprusside (50–200 μg)
    • Moderately forceful injection of blood or saline through the manifold
    • GPIIb/IIIa agents, IV cangrelor may also be helpful

Air Embolism

Intracoronary air embolism is a potentially lethal but rare complication. It could result in hypotension, hemodynamic collapse, cardiac arrest, and in rare cases death. Coronary air embolism is almost always iatrogenic. It occurs mostly when
    • Catheters are not adequately aspirated and flushed
    • During introduction or withdrawal of a guidewire, balloon catheter or other interventional devices
    • Do not connect the manifold to the catheter with the flush running. This may lead to an air embolism if the catheter already has a column of air inside it.
    • Draw back at least 2 cc of blood into the injection syringe and make sure that the interface is free of air prior to injection.
    • Inject some dye into the ascending aorta prior to engaging left main.
    • Always ensure that all the catheters and tubings are aspirated, flushed and free of air.
    • Take adequate care when prepping stents or balloons and ensure that the syringe tip is facing downwards.
    • Always inject with the syringe tip facing downwards
  • Do not connect the manifold to the catheter with the flush running. This may lead to an air embolism if the catheter already has a column of air inside it.
  • Draw back at least 2 cc of blood into the injection syringe and make sure that the interface is free of air prior to injection.
  • Inject some dye into the ascending aorta prior to engaging left main.
  • Always ensure that all the catheters and tubings are aspirated, flushed and free of air.
  • Take adequate care when prepping stents or balloons and ensure that the syringe tip is facing downwards.
  • Always inject with the syringe tip facing downwards

Treatment

    • Put patient on 100% oxygen.
    • Flush air free saline vigorously into the coronary arteries. Aspirate blood and air column via guide catheter and reinject saline forcefully back into coronary arteries.
    • Administer IV phenylephrine 200 μg for hypotension. Repeat, as needed every minute. If significant hypotension or hemodynamic collapse is present, push IV 1 cc epinephrine (1:10,000 dilution).
    • Intracoronary injection of vasodilators (adenosine, nitroprusside, verapamil) may be attempted.
    • Supportive measures should be instituted (IABP for persistent hypotention) and patient admitted to intensive coronary care unit for further monitoring

Coronary Vasospasm

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. It is usually short-lived and is most prone to occur at the ostium of the right coronary artery (RCA). The left main is less susceptible to ostial spasm
    • Rotablator cases are more prone to vasospasm
Diagnosis
    • Coronary vasospasm is detected by presence of EKG changes of ST segment elevation in association with angina, and then EKG 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 reversible by the administration of intracoronary vasodilators.
Treatment
    • Initial step is intracoronary vasodilatation with IC calcium channel blockers and/or nitrates [nitroglycerin 100-300 mcg, verapamil 100 mcg/min, up to 1.0-1.5 mg, nicardipine 100-300 mcg, nitroprusside 100-300 mcg]
    • IV atropine can be useful if there is associated hypotension of bradycardia
    • If vasospasm persists, remove all hardware and leave the guide wire in place to maintain position. This may

If vasospasm persists, 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 reserved in cases if all the 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


Abrupt Vessel Closure Summary

  • Dissection
    • Minor dissections - usually heal without clinical sequelae, no treatment required
    • Major dissections - repeated prolonged low-pressure balloon [distal vessel], stenting [Proximal/mid vessel segment or impaired flow due to dissection]
  • Thromboembolism
    • Twin-Pass or microcatheter to administer vasodilators distally
    • Check ACT to keep > 300. Consider starting IV Cangrelor or bailout GPIs
    • Balloon dilatation and/or thrombus aspiration in case of stent thrombosis
    • Stenting on case of thrombosis in in unstented vessel segment
  • No-reflow
    • Intracoronary Adenosine, Nitroprusside, Nicardipine, Verapamil, or GPI’s
    • A transit catheter or over-the-wire balloon should be used to deliver the vasodilators to the distal microvasculature
    • Insertion of IABP to improve flow
  • Air embolism
    • Start 100% oxygen
    • Flush air free saline vigorously into the coronary arteries. Aspirate blood via guide catheter and reinject forcefully back into coronaries
    • IV phenyl epinephrine or epinephrine as needed
    • Intracoronary injection of vasodilators
  • Vasospasm
    • Intracoronary Nitroglycerin, Adenosine, Nitroprusside, Nicardipine, or Verapamil
    • IV fluid bolus and/or atropine as needed
    • Remove all hardware and leave the guide wire in place to maintain position
    • Repeat prolonged PTCA for 2-5 minutes at low pressures (1-4 atmospheres)
  • Unknown etiology
    • Maintain wire position distally and pass a microcatheter distally to inject contrast
    • If flow distally, problem at site of vessel closure and needs to be investigated
    • If no flow distally, consider no reflow and give IC vasodilators


References

  1. de Feyter P.J., de Jaegere P.P.T., Murphy E.S., Serruys P.W. (1992) Abrupt coronary artery occlusion during percutaneous transluminal coronary angioplasty. Am Heart J 123:1633–1642.
  2. Francesco Giannini, Luciano Candilio, Satoru Mitomo, Neil Ruparelia, Alaide Chieffo, Luca Baldetti, Francesco Ponticelli, Azeem Latib, Antonio Colombo. Practical Approach to the Management of Complications During Percutaneous Coronary Intervention. J Am Coll Cardiol Intv. 2018 Sep, 11 (18) 1797-1810.
  3. Klein L. (2005) Coronary complications of percutaneous coronary interventions: a practical approach to the management of abrupt closure. Catheter Cardiovasc Interv 64:395–401.
  1. Huber MS, Mooney LF, Madison J, et al. Use of a morphologic classification to predict clinical outcome after dissection from coronary angioplasty. Am J Cardiol 1991;68:467–71.
  2. Rezkalla S.H., Kloner R.A. (2002) No-reflow phenomenon. Circulation 105:656–662.
  3. Piana R., Paik G., Moscucci M., et al. (1994) Incidence and treatment of “no-reflow” after percutaneous coronary intervention. Circulation 89:2514–8.
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