Even afterwards, SCAD has a high recurrence risk at 30% within 10 years, often at a different site than the initial lesion - meaning that stents placed in the location of the first lesion may not protect against a second. Given the lack of consensus on the cause of SCAD, prevention of future SCAD may include medical therapy, counseling about becoming pregnant again (for those who had pregnancy-associated SCAD), or avoidance of oral contraceptives - as they contain estrogen and progesterone. Epidemiology
SCAD is the most common cause of heart attacks in pregnant and postpartum women. Over 90% of people who develop SCAD are women. It is especially common among women aged 43–52. With angiography and improved recognition of the condition, diagnosis of SCAD has improved since the early 2010s. While prior studies had reported a SCAD prevalence of less than 1% in patients presenting with acute coronary syndrome, more recent data suggests the prevalence of SCAD in acute coronary syndrome patients may be between 2-4%. History
SCAD was first described in the year 1931, at postmortem examination, in a 42-year-old woman. Due to a lack of recognition and diagnostic technology though, SCAD literature until the 21st century included only case reports and series. With the recent advent of coronary angiography and intracoronary imaging, recognition and diagnosis of SCAD has greatly increased, especially in the 2010s. See also
Dissection (medical)
Aortic dissection
Kounis syndrome

References
External links

"Spontaneous Coronary Artery Dissection Postpartum"
"Spontaneous-Coronary-Artery-Dissection-Case-Series-and-Review"
Farber disease (also known as Farbers lipogranulomatosis, acid ceramidase deficiency, "Lipogranulomatosis", and ASAH1-related disorders) is an extremely rare, progressive, autosomal recessive lysosomal storage disease caused by a deficiency of the acid ceramidase enzyme. Acid ceramidase is responsible for breaking down ceramide into sphingosine and fatty acid. When the enzyme is deficient, this leads to an accumulation of fatty material (called ceramide) in the lysosomes of the cells, leading to the signs and symptoms of this disorder. Signs and Symptoms
The symptoms of Farber disease develop over time. The onset of symptoms and how quickly they progress vary from person to person.The most common symptoms include:
Bumps under the skin located at pressure points and joints, also called subcutaneous nodules, lipogranulomas, or granulomas
Swollen, painful joints with progressive limitation of range of motion resulting in contracture
Hoarse voice/cryOther symptoms observed in some individuals with Farber disease include:
Respiratory disease, e.g. lung infections, labored breathing, respiratory distress
Central nervous system disease, e.g. developmental delay, muscle weakness, seizures
Systemic inflammation
Failure to thrive
Bone disease, e.g. erosion of bone near joints, osteoporosis, peripheral osteolysis
Enlarged liver (hepatomegaly)
Eye disease, e.g. cherry-red spot, corneal opacities

Genetics
Farber disease is caused by variants in the ASAH1 gene. This gene codes for the acid ceramidase enzyme. Individuals with Farber disease have two copies of this gene that are not functioning properly leading to the enzyme deficiency. Over 73 different gene variants have been reported to cause Farber disease. No definitive genotype-phenotype correlations are known.Farber disease is inherited in an autosomal recessive manner.