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Spontaneous Coronary Artery Dissection – A Wolf in Sheep’s Clothing

Written by Joseph Kummer, MD, Bryan Heart Cardiologist

Contemporary management of Acute Coronary Syndromes (ACS) involves comprehensive therapies derived from an abundance of scientific evidence. These are generally designed to treat acute rupture of an intracoronary atheromatous plaque. However, there are several “wolves in sheep’s clothing” that mimic a plaque rupture event in clinic presentation but involve a very different pathologic event. One such entity is Spontaneous Coronary Artery Dissection (SCAD). A recent review article in The New England Journal of Medicine regarding this topic was very informative and I will highlight the issues discussed.1 It is very important to recall that not all myocardial infarctions are due to atherosclerosis, even in the setting of a typical clinical presentation for a plaque-rupture event. SCAD is a great example of this.

Other examples include:

  • Takotsubo Cardiomyopathy
  • Coronary Vasospasm
  • Myocarditis
  • Pericarditis
  • Infiltrative or Toxic Injury
  • Arteritis
  • Myocardial Contusion

Many of these, including SCAD, can present with:

  • Acute, typical anginal chest pain
  • ST segment changes (Elevation or Depression), and
  • Elevated cardiac Troponin

Hence, these diseases often meet all criteria for a ST-segment Elevation Myocardial Infarction (STEMI) or a non-STEMI. Not surprisingly, we initially treat them as such and discover only later, after further diagnostic investigation, that there was no plaque-rupture process as originally suspected.

What is Spontaneous Coronary Artery Dissection SCAD?       

The pathogenesis, diagnostic criteria, and management of SCAD have been much more clearly elucidated in the past few years. It seems that SCAD is following a similar path to Takotsubo Cardiomyopathy which was first officially described and had diagnostic criteria established about 20 years ago. After Takotsubo Cardiomyopathy was defined, the number of diagnosed cases increased exponentially for several years thereafter. Of course, it has always existed, but it wasn’t until it had a name and diagnosis that we could describe what we had been seeing since the dawn of coronary angiography. Likewise, SCAD is now well described and recognized. As such, we have made great strides in understanding this disease and learning how to approach our therapeutic interventions.

SCAD is therefore increasingly recognized as a cause of myocardial injury, but it remains a relatively uncommon event in absolute terms. The inciting pathophysiologic insult is still not fully understood. We do know that the primary cause of myocardial injury involves an intramural hematoma within a coronary artery. There is often an associated intimal tear of the artery, involving separation of the artery’s intima from the media. Historically, the primary process was thought to be the tear of the intima, but increasingly, this tear is thought to be secondary to a spontaneous hematoma in the media of the artery.  This may result from rupture of the vasa vasorum. As the intramural hematoma expands, an acute coronary syndrome may be caused either by direct luminal compression or the ensuing development of an intimal tear from the expanding hematoma.

Who does SCAD impact?

SCAD is very unique in its demographic focus. It is important to know that it can occur in persons of either sex and at any age starting in adolescence. However, the vast majority occur in a very narrow demographic. Specifically, 90% of cases occur in women who are 47 to 53 years old.

Only about 1% of ACSs are thought to be due to SCAD. Even though it’s rare overall, about one-fourth to one-third of ACS cases in females 50 years or younger are due to this. About 15-20% of pregnancy or peri-partum ACSs are caused by SCAD.

What causes SCAD?

There are several postulated mechanisms regarding the cause of this event. There are many associations, including emotional and physical stress, stimulant drugs, pregnancy, etc. Valsalva maneuvers from vomiting, retching, isotonic exercise, etc. have been associated. Thus far there is no clear association with other systemic inflammatory disorders, and widespread inflammatory changes are not typically seen in pathologic specimens from SCAD. Genetic testing has not shown a universal abnormality, but inconsistent associations have been seen with several other genetic mutations associated with a variety of vascular disorders. At this time, genetic screening is generally not indicated for patients with SCAD or their relatives.

Fibromuscular Dysplasia and SCAD

However, there is a very strong association with fibromuscular dysplasia (FMD). In fact, it is estimated that over half of patients with SCAD have evidence of non-coronary artery abnormalities seen in FMD. These may include:

  • Aneurysm
  • Tortuosity or
  • Dissection of arteries in multiple sites, including:
    • Cervical
    • Visceral or
    • Peripheral vessels

It is unclear whether SCAD is essentially a subtype of FMD or if there is simply an association between the two diseases. Regardless, the strong association with FMD suggests an underlying arteriopathy as a predisposing mechanism in the pathogenesis of SCAD.

Diagnosing SCAD      

SCAD presents with ST-segment Elevation in up to 50% of cases, and chest pain typical of angina is almost always present. Cardiogenic shock and ventricular tachycardia are infrequently seen and can lead to death. There are no particular characteristics of the initial history and physical, lab data, nor EKG abnormalities that differential SCAD from a typical plaque-rupture MI. Therefore, coronary angiography is necessary to determine whether emergent coronary revascularization is needed for an acute atherosclerotic event.

For patients without acute ST-segment Elevation, Cardiac CT Angiography can be an excellent method of confirming the diagnosis. Since patients with SCAD are often younger females with relatively few comorbidities, their coronary calcium burden is often low. The lack of calcific disease of the coronary arteries often allows for excellent visualization of the coronary artery lumen as well as potentially dissection flaps or an intramural hematoma. This can of course exclude a culprit atheromatous coronary lesion.

It should be noted that invasive coronary angiography carries significant risk in this disease. Introduction of a catheter and direct injection of contrast dye into an artery with an acute dissection flap runs the risk of extending the dissection. Cardiac CT angiography obviously avoids this risk. Likewise, attempts to open the artery with angioplasty and stenting are notoriously challenging. Angioplasty and stent deployment are often unsuccessful due to the fragility of the vessel and difficulty cannulating the proper lumen when a false lumen exists. Therefore, percutaneous coronary artery intervention is usually not advised in a relatively stable patient. Intracoronary ultrasound is often very helpful with confirming the diagnosis via visualization of a dissection flap and hematoma, but this likewise involves significant risk of propagation of the dissection.

Management of SCAD  

It is estimated that over 80% of patients with SCAD can be successfully managed with medical therapy alone.  As opposed to an acute MI caused by a plaque-rupture event, the majority of arteries affected by SCAD will actually heal on their own. Complete resolution of the dissection flap over time is often seen with conservative therapy. Therefore, percutaneous or surgical revascularization efforts should be reserved for patients with high-risk features, such as refractory chest pain, cardiogenic shock, ventricular arrhythmias, or high-risk anatomic lesions such as severe left main coronary artery obstruction.

Patients should be monitored in the hospital for 3-5 days to observe for any recurrent ischemic symptoms, as the dissection and/or hematoma may propagate. Chest pain in SCAD is treated with the same anti-anginals that are used for coronary arterial disease (beta-blockers, nitrates, ranolazine, etc.). Control of blood pressure is important. Note that imaging of peripheral arteries with full-body CT or MR angiography is indicated in all these patients to look for fibromuscular dysplasia.

Due to the potential risk of increased intramural hemorrhage, aggressive anticoagulation therapy is generally not recommended. Most patients are prescribed daily aspirin at discharge, but the role of dual anti-platelet therapy remains a source of investigation. Expert consensus states that dual anti-platelet therapy may be considered for at least the short-term and potentially for up to a year following an MI from SCAD. At least one study suggested a significant decrease in the recurrence of SCAD in patients treated with beta-blockers after an initial event.

Mortality from SCAD is fairly low at only 1-2%, but recurrent ischemic events occur in almost 20% of patients, often within the first few days of the initial event. Patients should be referred to cardiac rehabilitation after discharge. This has been shown to be beneficial for both the physical as well as the psychological aspects of this often surprising and traumatizing event.

The Future of SCAD   

Now that SCAD is a well-defined clinical entity, we have greatly expanded our understanding of its pathophysiology, management, and prognosis. As such, we will hopefully continue to make significant advances in recognizing and treating this potentially serious cause of myocardial injury that often affects relatively young, healthy individuals.       

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If at any time Bryan Heart can be of assistance with the screening or an assessment of a patient, please call us at 402-483-3333.


 Source:

  1.  Spontaneous Coronary-Artery Dissection. Kim ES. N Eng J Med. 2020;383:2358-70.
kummer joseph

About Joseph Kummer, MD

Joseph Kummer, MD, is a cardiologist at Bryan Heart. Kummer is a graduate of The University of Nebraska Medical Center College of Medicine. He completed his residency at Northwestern Memorial Hospital and fellowship at Henry Ford Hospital. Kummer is certified by the American Board of Internal Medicine in Cardiovascular Disease and fellow of the American College of Cardiology

View Dr. Kummer’s physician profile

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