ABSTRACT
Spontaneous coronary artery dissection (SCAD) is often revealed by an acute coronary syndrome classified then as a MINOCA. The typical patient is a female patient with no or few cardiovascular risk factor. Our work aims to illustrate the effectiveness of medical treatment in patients with SCAD. Case Report: We report a case of a 56-year-old female patient who was admitted after 3 days of infarct-like thoracic pain related to an anterior extended ST-elevation myocardial infarction. The coronarography showed a SCAD of the left anterior descending coronary artery. The patient was discharged under medical treatment. Six weeks later, coronarography showed a perfused coronary artery. Discussion: Most cases of SCAD present as acute coronary syndrome. Coronary angiography remains the 'first-line' examination. The use of endocoronary imaging such as IVUS and optical coherence tomography is necessary in case of diagnostic doubt (especially in SCAD type 2 and 3). The optimal management of SCAD remains unclear. A conservative approach should be the preferred strategy. Conclusion: SCAD should be considered in any young woman presenting with suspicious chest pain with positive troponin. The diagnosis is initially angiographic and may require endocoronary imaging for greater accuracy. Conservative treatment remains the best option.
ABSTRACT
The human bladder urothelium (BU) and bladder urothelial cells (BUCs) play an important role in the normal functioning of bladder including bladder storage. Current evidence in interstitial cystitis (IC) supports multiple abnormalities in bladder urothelial physiology. These data have come primarily from human studies. The discovery of a novel protein termed the antiproliferative factor (APF) uniquely expressed by IC BUCs is extremely important. APF induces increased permeability of normal BUCs grown in culture. Furthermore, APF regulates expression of other cytokines, including upregulating heparin-binding epidermal growth factor-like growth factor and downregulating epidermal growth factor by BUCs. These cytokine abnormalities were also related to increases in purinergic (adenosine triphosphate) signaling, which could mediate increased bladder sensation. Recent studies of uroplakins, which are specialized proteins expressed only in the apical urothelial cells, suggest that uroplakins play a role in the barrier function of the BU. It is also conceivable that alterations in uroplakins may result in bladder symptoms related to increased permeability or decreased protective function. As the body of knowledge about BU and BUC function increases, novel therapies targeting urothelial cells should become clinically feasible.
