Disclosures Spontaneous Coronary Artery I have nothing to disclose - - PDF document

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Spontaneous Coronary Artery Dissection

Jeffrey Zimmet, MD, PhD Associate Professor of Medicine, UCSF Director, Cardiac Catheterization Laboratory, SFVAMC

Disclosures

I have nothing to disclose

SCAD: Major points

■ It’s not just related to pregnancy ■ It is an under-recognized cause of

acute coronary syndrome

■ If you don’t suspect it, you can

easily miss it

■ The “classic” angiographic

appearance represents only a fraction of cases – need to know the alternative types

SCAD: Major Points

■ Invasive coronary

angiography is still the mainstay of diagnosis

■ Intravascular imaging with

IVUS or OCT is an important adjunct in equivocal cases

■ CT can be helpful but often

misses the diagnosis, especially in smaller vessels

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SCAD: Major points

■ Many cardiologists won’t recognize

the non-pathognomonic forms on coronary angio

■ The principles of management are

primarily a product of expert

• pinion

SCAD – What is it?

■ The non-traumatic and non-iatrogenic

separation of the coronary arterial walls, creating a false lumen

■ It is an under-recognized and often-

missed cause of acute coronary syndrome

■ It is uncommon, but not as rare as once

thought.

How does it occur?

Two primary theories:

■ Intimal tear

◆ The primary event is a tear or

rupture of the intima, allowing pressurized blood to enter the subintimal space

■ Medial hemorrhage

◆ The primary event is the

rupture of vasa vasorum

Intimal tear vs Medial hemorrhage

◆Leads to “classic” appearance

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SCAD: Epidemiology

■

Female preponderance: recent series estimate 92- 95% of cases when atherosclerotic causes were excluded

■

Association with pregnancy and the peripartum period

■

Recent series estimate that SCAD accounts for between 1 and 4% of acute coronary syndromes

■

Should be strongly considered in younger women without CAD RFs presenting with ACS

■

However, older women not excluded. In recent case series, over half of patients were > 50 years

• ld and 62% were post-menopausal

Predisposing factors

■

Strong association with fibromuscular dysplasia (FMD) – present in >70% of SCAD patients who are screened

Predisposing factors

■

Pregnancy (once thought to comprise a large proportion of cases; now ~5%)

■

Hormonal therapy

■

Connective tissue disorders:

• Marfan syndrome
• Loeys-Dietz syndrome
• Ehler-Danlos syndrome
• cystic medial necrosis
• alpha-1 antitrypsin deficiency
• polycystic kidney disease

SCAD - Precipitating factors

■

Intense emotional stress

■

Weight lifting and isometric exercises

■

Valsalva-like activities: childbirth, coughing, vomiting, bowel movement

■

Sympathomimetic drugs, including cocaine and methamphetamines

■

Note that the same stresses can precipitate classic atherosclerotic MI/plaque rupture

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Clinical Presentation

■

Most present with chest pain and positive cardiac enzymes (96% of the largest published series of 196 pts)

■

Long period from symptom-onset to presentation is the norm -- average of 1.1 days in the same series

■

1/3 of patients had unstable symptoms (ongoing pain or stuttering/recurrent pain) prior to cardiac cath

■

A significant proportion present as STEMI

■

A small proportion present with ventricular arrhythmia, cardiogenic shock, or SCD

Diagnosis by angiography

■ Classification proposed by J Saw in

Catheter Cardiovasc Interv in 2014

◆ Type I: classic angiographic appearance

(pathognomonic) of multiple lumens

◆ Type II: diffuse narrowing in the absence of

• atherosclerosis. Often long and smooth,

affecting mid to distal segments of arteries

◆ Type III: mimicks atherosclerotic disease

Diagnosis by angiography

■ Type I: classic angiographic appearance

(pathognomonic) of multiple lumens

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■ Type I: classic angiographic appearance

(pathognomonic) of multiple lumens

■ Type II: diffuse narrowing in the absence of

• atherosclerosis. Often long and smooth,

affecting mid to distal segments of arteries

◆Saw J, et al J Am Coll Cardiol. 2016 Jul 19;68(3):297-312 ■ Type III: mimicks atherosclerotic disease

Diagnosis by angiography

■

Screening for renal and iliac FMD at the time of coronary angiography may be useful, due to strong association of FMD with SCAD

■

Acute plaque rupture (in arteriosclerotic coronary disease) may appear angiographically identical

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Diagnosis by OCT and IVUS

■

Definitive diagnosis of SCAD

■

Risks of placing wire in false lumen, or propagating the dissection.

Diagnosis by OCT and IVUS

◆normal ◆dissection

Diagnosis by OCT Diagnosis by OCT

◆Antoniucci D, et al, Eur Heart 11(12):1130-1134.

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Increased suspicion for SCAD in:

■

Myocardial infarction in young women (especially age ≤50)

■

Absence of traditional cardiovascular risk factors

■

Little or no evidence of typical atherosclerotic lesions in coronary arteries

■

Peripartum state

■

History of fibromuscular dysplasia

■

History of relevant connective tissue disorder or systemic inflammatory condition (e.g. Marfan’s, SLE, cystic medial necrosis, etc, etc).

■

Recent intensive exercise or emotional stress

SCAD Management

■ All based on expert opinion from

case series

■ No randomized trials

SCAD Management

Beta blockers

◆ Probably beneficial ◆ Almost universally recommended ◆ Reduce shear stress ◆ Beneficial in tolerating ischemia ◆ Reduce ventricular arrhythmia

SCAD Management – Antiplatelet therapy

■

Reduction of false lumen thrombus burden

■

Treatment of prothrombotic environment when intimal tear is present (not all SCAD)

■

Aspirin: generally considered important in both short- and long-term treatment

■

Clopidogrel: Controversial

◆ Often given in combination with ASA for 1-12 months

after presentation

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SCAD – gpIIb/llla inhibitors

■

Glycoprotein IIb/IIIa inhibitors (abciximab, eptifibatide, tirofiban)

◆ generally not recommended. Greater propensity

for bleeding, and potential to extend the dissection

SCAD - Thrombolytics

■

Generally considered to be contraindicated

■

Multiple reports of clinical worsening, extension of intramural hematoma and dissection

■

In one retrospective series of 87 patients with SCAD who received thrombolytics, 52 had clinical worsening

■

Multiple individual case reports of benefit of thrombolytics, due to lysis of false lumen thrombi and improvement in true lumen compression

■

Balance of evidence suggests they should be avoided

SCAD - Anticoagulants

■ Heparin/LMWH is generally given up to the

point of angiography for ACS management

■ Risk of extending the dissection ■ Risk is balanced by potential benefit of

improving flow in the true lumen, and improving compression by false lumen thrombus

■ Most recommend discontinuation of heparin

• nce the diagnosis is made; however, there is

not general agreement on this point

■ Contrast with carotid dissection

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SCAD – adjunctive pharmacology

■ ACE inhibitors

◆ No data ◆ Generally given when there are other

indications, such as LV dysfunction or hypertension

SCAD – adjunctive pharmacology

■ Statins

◆ No good data ◆ tend to be given post MI, regardless of etiology ◆ one small retrospective study suggested high rate of

recurrence of SCAD with statin use

◆ another study reported high statin use with low

recurrence rate

◆ bottom line: give them to patients with

• hyperlipidemia. Use in others is just a guess

SCAD - Revascularization

Conservative therapy is generally recommended if possible

■

Conservatively-treated patients often heal

■

Multiple prospective series with planned repeat angiography

■

have demonstrated that spontaneous dissections most

• ften heal with conservative management: 73% (43 of 59

cases); 90% (79 of 88); and 97% (29 of 30)

■

almost all repeat imaging performed more than 1 month after presentation shows healing, although multiple individual cases show residual dissection on repeat late angio

SCAD – Conservative therapy

■

In published case series, patients who were initially treated conservatively had a small likelihood of progression requiring revascularization: 3.5% in the Vancouver series, and 10% in the Mayo clinic series.

■

Most recurrence occurs in the first several days. Patients treated conservatively should be monitored for 3-5 days in the hospital.

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Factors favoring mechanical revascularization

■ Ongoing chest pain or ischemia despite

medical therapy

■ Dissection involving the left main ■ Cardiogenic shock ■ Recurrent ventricular arrhythmias

SCAD - Revascularization

CABG:

■

Should be considered for left main dissection or anatomy unsuitable for PCI

■

Or as rescue strategy for unsuccessful PCI

SCAD – PCI concerns

Unique challenges of PCI in SCAD:

■

Risk of guide catheter dissection

■

Wire can track into the false lumen

■

Compression of the intramural hematoma by stents can propagate the dissection, rather than fixing it

■

Common variants involve dissection into distal branches that are too small for stenting

■

Compression of the true lumen by hematoma can lead to stent undersizing, setting up a milieu for downstream stent malapposition

PCI Strategies in SCAD

■ Risk of guide catheter dissection

◆ Consider femoral access for better guide control ◆ Selection of less-supportive guide catheters

■ Wire can track into the false lumen

◆ Use IVUS to confirm wire location

■ Compression of the intramural hematoma by

stents can propagate the dissection, rather than fixing it

◆ Extend stents up to 1 cm proximal and distal to the

dissection

◆ Consider stenting the proximal and distal edges first,

followed by the mid portion

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Stenting Pitfalls in SCAD: the “squeegee effect” PCI Strategies in SCAD

■ Common variants involve dissection into distal

branches that are too small for stenting

◆ Reports of successful decompression of the false

lumen with cutting balloon angioplasty

■ Compression of the true lumen by hematoma

can lead to stent undersizing, setting up a milieu for downstream stent malapposition and increasing risk for stent thrombosis

◆ Consider repeat cath with IVUS after SCAD healing

for patients who receive stents

Low Success Rates for PCI in SCAD

■ Vancouver series of 168 patients ◆ Successful PCI in just 64% ◆ 12% required urgent CABG ◆ 6% acute stent thrombosis ◆ 57% had extension of dissection during PCI ■ Mayo Clinic cohort of 189 patients ◆ 47% PCI success ◆ 13% required emergent CABG

PCI Success Rates in SCAD

■ Italian series of 134 patients ◆ 72% PCI success ◆ 9% urgent CABG ◆ 5% acute stent thrombosis

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◆SCAD of the LAD Artery With Intramural Hematoma A 40-year-old woman presented 10 days

after a third-trimester miscarriage with troponin-positive non–ST-segment elevation myocardial infarction.

◆Katherine C. Michelis et al. JACC 2014;64:1033-1046

Longer-Term Management

■ Aspirin and beta blockade are the only nearly-

universal medications. Many get clopidogrel.

■ ACE-I for patients with LV dysfunction ■ Statins controversial; universal only for

patients with other indications

■ Cardiac rehabilitation geared towards SCAD

◆ Low weight threshold of 20 lbs ◆ Lower target heart rate and BP thresholds

■ Advise against continued hormone therapy in

those patients

■ Advise against future pregnancy (recurrence

rate thought to be high, but this is based on a 7-patient series)

Prognosis

■ In-hospital mortality relatively low, at under

5% in more-recent series

■ Recurrence rates are significant, with

recurrence in ~15% at 2 years and as high as 27% at 4 years (most recurrence is early).

■ In the largest prospectively-followed cohort of

280 patients, at a median followup of 2.3 years

◆ MACE was 20.4% ◆ Recurrent SCAD was 12.2%

Wrap up

■

SCAD is an infrequent but increasingly-recognized cause of ACS

■

Preponderance in women, especially of younger age

■

Can occur in the peripartum period, although the majority of cases occur outside of this group

■

Also associated with physical and emotional stress, FMD, and with connective tissue disorders

■

Diagnosed by cardiac cath; often missed

■

Conservative therapy is favored when possible

■

Aspirin and beta blockade for short- and long-term therapy

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◆Thank You