Type 3 SCAD, the least common type, is also due to an intramural hematoma causing coronary stenosis, but the lesions are shorter than as seen in type 2 SCAD, being less than 20 mm in length. Due to the short segment of coronary stenosis in type 3 SCAD, it is often difficult to differentiate type 3 SCAD lesions from coronary stenosis due to atherosclerotic plaques and intra-coronary imaging is often needed to distinguish between the two. Some authors have proposed a fourth designation of SCAD, type 4 SCAD, in which there is a complete intraluminal occlusion of the coronary artery due to any of the  previously mentioned types (Type 1–3). Intracoronary imaging
Intracoronary imaging (ICI), consisting of intracoronary optical coherence tomography (OCT) and intravascular ultrasound (IVUS) can help distinguish SCAD from an atherosclerotic lesion when it is difficult to do so with angiography. ICI techniques provide a direct view of the walls of the coronary artery to confirm SCAD, but may actually worsen the dissection as the probes are inserted into the damaged area. ICI confers a 3.4% risk of iatrogenic dissection in people with SCAD compared to 0.2% risk in the general population. Between the two ICI methods, OCT - a newer technique - has superior spatial resolution than IVUS and is the preferred technique if ICI is required, but the need to inject extra contrast with OCT poses risk for worsening the dissection. Other methods
Some studies propose coronary CT angiography to evaluate SCAD in lower-risk people, with research into the approach ongoing.
Pharmacology
Pharmacodynamics
Zafirlukast is an antagonist of cysteinyl leukotriene receptor 1 (CysLT1), a receptor found throughout the smooth muscle of the lungs, within interstitial lung macrophages (white blood cells that operate in the interstitial space of the lungs), and rarely in epithelial cells. CystLT1 is a receptor for a specific class of leukotrienes that contain the amino acid cysteine. These cysteinyl leukotrienes include leukotriene C4, leukotriene D4, and leukotriene E4, all of which are produced by inflammatory cells like eosinophils, basophils, and macrophages in the lungs. Through their action on CysLT1 these leukotrienes can trigger bronchoconstriction, a state in which the bronchial passages of the lungs constrict, leading to the characteristic, reactive airway symptoms associated with bronchial asthma. The other pro-inflammatory effects of leukotrienes, such as their inhibition of mucus clearance and their stimulation of mucus secretion and edema, are thought to play a role in the characteristic symptoms of allergic rhinitis (also called hay fever). By inhibiting the action of these specific leukotrienes, zafirlukast is thought to exert an anti-inflammatory effect against leukotriene-mediated inflammatory conditions. Pharmacokinetics
Absorption
Zafirlukast is rapidly absorbed into the bloodstream following oral administration, reaching peak plasma levels within 3 hours of taking the dose. The peak plasma level is the maximum concentration of zafirlukast in the blood. Distribution
Zafirlukast is moderately distributed into the bodys tissues, with an apparent steady state volume of distribution of 70 liters. Zafirlukast is highly plasma protein bound, 99% bound to albumin.