Spontaneous coronary artery dissection (SCAD) is an uncommon but dangerous condition in which one of the arteries that supply the heart spontaneously develops a blood collection, or hematoma, within the artery wall. This leads to a separation and weakening of the walls of the artery. SCAD is a major cause of heart attacks in young, otherwise healthy women without known risk factors. While the exact cause is not yet known, SCAD is likely related to changes that occur during and after pregnancy, as well as other diseases. These changes lead to the dissection of the wall which restricts blood flow to the heart and causes symptoms. SCAD is often diagnosed in the cath lab with angiography, though more advanced confirmatory tests exist. While the risk of death due to SCAD is low, it has a relatively high rate of recurrence leading to further heart attack-like symptoms in the future. It was first described in 1931. Signs and symptoms
SCAD often presents like a heart attack in young to middle-aged, healthy women. This pattern usually includes chest pain, rapid heartbeat, shortness of breath, sweating, extreme tiredness, nausea, and dizziness. A minority of people with SCAD may also present in cardiogenic shock (2-5%), ventricular arrhythmias (3-11%), or after sudden cardiac death. Pregnancy- and postpartum-associated SCAD generally have worse outcomes compared to other cases. Causes
Risk factors include pregnancy and the postpartum period. Evidence suggests that estrogen- and progesterone-related vascular changes affect the coronary arteries during this period, contributing to SCAD.
Hay fever in Japan is caused primarily by sugi (Cryptomeria japonica) and hinoki (Chamaecyparis obtusa) tree pollen. "Allergy friendly" trees include: female ash, red maple, yellow poplar, dogwood, magnolia, double-flowered cherry, fir, spruce, and flowering plum. Grasses (Family Poaceae): especially ryegrass (Lolium sp.) and timothy (Phleum pratense). An estimated 90% of people with hay fever are allergic to grass pollen. Weeds: ragweed (Ambrosia), plantain (Plantago), nettle/parietaria (Urticaceae), mugwort (Artemisia Vulgaris), Fat hen (Chenopodium), and sorrel/dock (Rumex)Allergic rhinitis may also be caused by allergy to Balsam of Peru, which is in various fragrances and other products. Genetic factors
The causes and pathogenesis of allergic rhinitis are hypothesized to be affected by both genetic and environmental factors, with many recent studies focusing on specific loci that could be potential therapeutic targets for the disease. Genome-wide association studies (GWAS) have identified a number of different loci and genetic pathways that seem to mediate the bodys response to allergens and promote the development of allergic rhinitis, with some of the most promising results coming from studies involving single-nucleotide polymorphisms (SNPs) in the interleukin-33 (IL-33) gene. The IL-33 protein that is encoded by the IL-33 gene is part of the interleukin family of cytokines that interact with T-helper 2 (Th2) cells, a specific type of T cell. Th2 cells contribute to the bodys inflammatory response to allergens, and specific ST2 receptors, also known as IL1RL1,  on these cells bind to the ligand IL-33 protein.