ABSTRACT
In December 2007, a woman was involved in a traffic accident. At first, her vital signs were normal, but electrocardiogram showed ST-segment elevation in the inferior leads. She was diagnosed as a blunt chest trauma-induced myocardial infarction. Her right coronary angiography showed total occlusion. She underwent an emergency coronary artery bypass surgery; 64-multi-detector-row computed tomography (64-MDCT) demonstrated an intravascular protruding lesion, which suggested subintimal hematoma. One month later, repeat coronary angiogram showed spontaneous recanalization, and 64-MDCT showed no discontinuous vessel wall. Coronary artery occlusion secondary to blunt chest trauma is rare, and it's even rarer to have spontaneous recanalization.
Subject(s)
Accidents, Traffic , Coronary Occlusion/diagnosis , Thoracic Injuries/diagnosis , Wounds, Nonpenetrating/diagnosis , Coronary Occlusion/etiology , Coronary Occlusion/surgery , Female , Humans , Remission, Spontaneous , Thoracic Injuries/complications , Thoracic Injuries/surgery , Wounds, Nonpenetrating/complications , Wounds, Nonpenetrating/surgery , Young AdultABSTRACT
OBJECTIVE: Endothelial progenitor cells (EPCs) play an important role in the self-healing of a vascular injury by participating in the reendothelialization that limits vascular remodeling. We evaluated whether prostaglandin I(2) plays a role in the regulation of the function of EPCs to limit vascular remodeling. METHODS AND RESULTS: EPCs (Lin(-)cKit(+)Flk-1(+) cells) were isolated from the bone marrow (BM) of wild-type (WT) mice or mice lacking the prostaglandin I(2) receptor IP (IP(-/-) mice). Reverse transcription-polymerase chain reaction analysis showed that EPCs among BM cells specifically express IP. The cellular properties of EPCs, adhesion, migration, and proliferation on fibronectin were significantly attenuated in IP-deficient EPCs compared with WT EPCs. In contrast, IP agonists facilitated these functions in WT EPCs, but not in IP-deficient EPCs. The specific deletion of IP in BM cells, which was performed by transplanting BM cells of IP(-/-) mice to WT mice, accelerated wire injury-mediated neointimal hyperplasia in the femoral artery. Notably, transfused WT EPCs, but not IP-deficient EPCs, were recruited to the injured vessels, participated in reendothelialization, and efficiently rescued the accelerated vascular remodeling. CONCLUSIONS: These findings clearly indicate that the prostaglandin I(2)-IP system is essential for EPCs to accomplish their function and plays a critical role in the regulation of vascular remodeling.
Subject(s)
Endothelium, Vascular/metabolism , Epoprostenol/metabolism , Mesenchymal Stem Cells/metabolism , Neovascularization, Physiologic/physiology , Animals , Cell Adhesion , Cell Movement , Cell Proliferation , Endothelium, Vascular/pathology , Fibronectins/metabolism , Hyperplasia/metabolism , Hyperplasia/pathology , Mesenchymal Stem Cells/pathology , Mice , Mice, Knockout , Models, Animal , Receptors, Epoprostenol/genetics , Receptors, Epoprostenol/metabolism , Signal Transduction/physiology , Tunica Intima/injuries , Tunica Intima/metabolism , Tunica Intima/pathologyABSTRACT
We describe a case of Brugada syndrome, in which recurrent syncope with convulsive seizures was induced after antidepressant treatment. The patient had been treated with five kinds of psychotropic drugs. The twelve-lead ECG after the syncope exhibited an RSR'-pattern in the precordial leads, however, a coved type ST-segment elevation was induced by a pilsicainide test. Although ventricular fibrillation was not induced in the electrophysiologic study, an ICD implantation was considered as the recommended therapy since Brugada syndrome unmasked by antidepressants could not be ruled out. The possible contribution of antidepressants to Brugada type ST-segment changes is discussed.
Subject(s)
Antidepressive Agents, Tricyclic/adverse effects , Brugada Syndrome/chemically induced , Brugada Syndrome/diagnosis , Adult , Brugada Syndrome/physiopathology , Diagnosis, Differential , Humans , MaleABSTRACT
A 66 year-old man was introduced to our hospital because of multiple infiltrative pulmonary shadows on February, 2001. We diagnosed bronchiolitis obliterans with organizing pneumonia (BOOP) from the clinical and bronchoalveolar lavage fluid (BALF) findings, and initiated oral steroid therapy. Since the abnormal chest shadows disappeared, the dose of steroid was decreased and maintained at 10 mg/day. In August 2001, multiple infiltrative shadows returned, and we therefore increased the steroid dose to 30 mg/day. The expanding infiltrative shadows were then joined by new multiple nodular shadows. The bronchioalveolar lavage fluid revealed small bodies of cryptococcus species. A positive result for anti-cryptococcus antigen was also obtained from the serum. We then diagnosed pulmonary cryptococcosis without meningitis. Therapy was started with anti-mycotic agents including amphotericin-B, flucytosine and fluconazole, which proved successful. This case of opportunistic cryptococcus infection in an immunocompromized patient, which responded to anti-mycotic therapy, is reported.
