Some case reports and case series suggest associations with autoimmune inflammatory diseases, but there have not been larger studies to explore this relationship. Underlying heritable conditions such as fibromuscular dysplasia and connective-tissue disorders (e.g., Marfan syndrome, Ehlers–Danlos syndrome, and Loeys–Dietz syndrome) are associated with SCAD, but SCAD otherwise lacks a significant genetic component. SCAD triggers may include severe physical or emotional stress, but many cases have no obvious cause. Pathophysiology
SCAD symptoms are the result of a restriction in the size of the affected coronary artery. The dissection leads to a collection of blood, or hematoma, between the layers of the artery wall. The hematoma does not carry oxygen to the heart muscle but instead forms a "false lumen" that restricts the flow of blood through the "true lumen" to the heart muscle. As yet, there is no consensus on why the hematoma develops in the first place.The restriction limits the availability of oxygen and nutrients to the heart muscle, or myocardium. As a result, the myocardium continues to demand oxygen but is not adequately supplied by the coronary artery. This imbalance leads to ischemia, damage, and eventually death of myocardium, causing a heart attack (myocardial infarction). Diagnosis
Given the demographics of SCAD, it is important to maintain a high index of suspicion for the condition in otherwise low-risk women presenting with symptoms of acute coronary syndrome. Initial evaluation may show ECG changes of ST elevation, like heart attacks due to other causes.
Statins are not recommended in the treatment post-SCAD (in the absence of other indications for statins) as the myocardial infarctions in SCAD are not the result of atherosclerotic plaques. Cardiac rehabilitation is recommended for all patients after myocardial infarction due to SCAD and is associated with a reduction in anginal symptoms increased psychological well-being. Dual antiplatelet therapy should be started after percutaneous coronary intervention (stents) is used to treat SCAD and continued for at least 1 year afterwards. Dual antiplatelet therapy during the acute phase and for at least 1 year after medically treated SCAD may be also used, based on expert consensus.Physical stress is associated with SCAD recurrence but there are no heart rate, blood pressure or weight exercise parameters that are established in those with SCAD. In general, it is recommended that those with SCAD avoid isometric exercise, high intensity endurance training, exercising to the point of exhaustion and activities involving a prolonged Valsalva to reduce the risk of SCAD recurrence.After addressing the SCAD, people are often treated with typical post-heart attack care, though people who are pregnant may need altered therapy due to the possibility of some teratogenic cardiac medications affecting fetal development. Depending on the clinical situation, providers may screen for associated connective tissue diseases. Prognosis
People with SCAD have a low in-hospital mortality after treatment. However, the lesion may worsen after leaving the hospital within the first month. One study suggested a 1.2% mortality rate following SCAD but a 19.9% risk for either death, heart attacks, or strokes.