The SCAD is a rare cause of acute coronary syndrome or sudden cardiac death, specifically associated with pregnancy or the postpartum period in young women [8, 9]. It is defined as a non-atherosclerotic and non-traumatic separation of the arterial wall layers, resulting in the development of a false lumen which can cause significant collapse of the true lumen [1]. The short-term mortality rate is relatively high, reaching approximately 38%. However, the long-term outcome is favorable after surviving from the initial event [9]. Pregnancy-associated SCAD is associated with more severe symptoms than general SCAD. It is known to occur frequently during the first month of the postpartum period and is more commonly observed among multiparous women, particularly those over the age of 30 [10]. It often involves multivessel coronary arteries involving LAD [8]. The main diagnostic method in patients suspicious of acute coronary syndrome due to coronary dissection is coronary angiography, which should be performed as soon as possible [11]. There are currently no optimal treatment guidelines for pregnancy-associated SCAD. Conservative therapy may be considered for benign cases. Percutaneous coronary intervention should be applied to patients with ongoing ischemia, those with hemodynamic instability, or those with focalized single vessel with significant flow limitations. In cases of left main or multivessel proximal LAD involvement with hemodynamic instability, the consideration of coronary artery bypass grafting surgery should be taken into account [1, 11]. The overall prognosis is determined in accordance with the amount of viable myocardium, the extension of the dissection, and the overall clinical status [8].

The RCVS is an uncommon clinical condition, with a higher prevalence observed in young women during the puerperium period, reported to be around 7–9%. This condition is characterized by recurrent thunderclap headaches with or without other neurological symptoms, along with reversible multifocal cerebral vasoconstriction of medium-sized cerebral vessels [2]. The acute headache may be accompanied by vomiting, nausea, photophobia, phonophobia, and in some cases, seizures [12]. The diagnosis of RCVS is based on consistent clinical characteristics, physical examination, and neurovascular imaging with CT or MRA, revealing multifocal cerebral vasoconstrictions [2, 4, 13]. Furthermore, it is recommended to undergo a follow-up imaging test to demonstrate complete or at least significant improvement of vasoconstriction [12, 14]. Approximately 25–33% of patients may experience complications such as seizures, ischemic stroke, brain hemorrhage, and posterior reversible encephalopathy syndrome according to previous reports [2, 12]. The majority of patients with RCVS show a self-limiting course, resulting in full recovery or only a few sequelae. The symptom of a headache usually improves within 3 weeks, while vasoconstriction in imaging tests typically improves within 3 months [2, 12, 15]. The patients require close monitoring for potential complications and, if experiencing symptoms, they should receive prompt medical treatment, which may include analgesia, antiepileptics, and antiemetics if necessary. Nimodipine, among the CCBs, is the preferred medication for relieving headaches. Additionally, verapamil and nicardipine may be considered as alternative medications [16, 17].

The etiologies of concurrent pregnancy-associated SCAD and RCVS remain unclear in this case. One possible explanation may be physiological adaptation following pregnancy. There are reports suggesting that vascular shear stress increases in the end of pregnancy due to a 30–50% increase in plasma volume, which consequently leads to an increase in cardiac output. During labor, active Valsalva efforts may partly contribute to sympathetic overactivity and stress in coronary and cerebral vessels, potentially precipitating SCAD with RCVS [1, 2, 10, 14]. Furthermore, pregnancy induces changes in the levels of progesterone and estrogen, which are elevated during the term and rapidly decrease during the postpartum period. The hormonal changes may affect the vascular endothelium, which has hormone receptors [18]. In addition, exposure to high levels of hormones during pregnancy may result in the degeneration of vessel walls, leading to impairments in arterial tone, vascular cells, and endothelial function [1,2,3]. However, the exact mechanisms have yet to be clearly identified.

Several cases of extracerebral vascular involvement in RCVS have been previously described, including associations with carotid artery dissection or renal artery spasms. While there have been only a few reports of coronary vasospasm with RCVS, it is well known that cardiac involvement is extremely rare in RCVS [19,20,21]. On the other hand, SCAD with extracoronary involvement is well correlated with vascular abnormalities such as aneurysm, pseudoaneurysm, fibromuscular dysplasia, and dissection. However, there is no mention of RCVS [22, 23]. The simultaneous existence of both diseases may pose a risk to patients and lead to various complications. Therefore, receiving a quick diagnosis followed by appropriate treatment will lead to a positive outcome.