RESUMO
Electrocardiographic changes frequently occur after severe physical or emotional stress. Such changes can mimic acute ST-segment elevation myocardial infarction with elevated serum cardiac-specific markers (CK-MB, Troponin I), segmental wall motion abnormalities, and myocardial dysfunction. Several reports, however, have found that coronary angiography revealed no significant stenosis. We present a 70-yearold female with a traumatic subdural hematoma testing positive for cardiac enzymes, and ECG changes suggestive of acute ST-segment elevation myocardial infarction. Such a case, however, fits the diagnostic parameters of Tako-tsubo cardiomyopathy, or Tako-tsubo syndrome; even though its etiology, pathophysiology, diagnosis, and treatment remain uncertain. Tako-tsubo syndrome is characterized by a distinctive form of systolic dysfunction that predominantly affects the distal LV chamber, but a favorable outcome with appropriate medical therapy is expected. Because of its unusual nature and favorable prognosis, it is clear that Tako-tsubo syndrome is an important affliction that should be recognized by any emergency department.
Assuntos
Feminino , Humanos , Constrição Patológica , Angiografia Coronária , Eletrocardiografia , Emergências , Hematoma Subdural , Hidrazinas , Infarto do Miocárdio , Prognóstico , Estresse Psicológico , Cardiomiopatia de Takotsubo , TroponinaRESUMO
BACKGROUND: The angiotensin-converting enzyme (ACE) has a major role in the degradation of bradykinin, tachykinin, substance P which are associated with bronchial hyperresponsiveness and inflammation. The other role of ACE is the genesis of angiotensin II which causes bronchial smooth muscle contraction. The deletion polymorphism of ACE gene(DDtype) may be related to the high serum level of ACE. OBJECTIVE: We studied to evaluate an association between the insertion /deletion polymorphism of the ACE gene and asthma, and its severity. Materials and methods: Sixty asthmatic patients and 44 healthy controls were enrolled. Severity of asthma was classified by the guideline of NHLBI/WHO workshop. The ACE genotypes of all the subjects were determined by polymerase chain reaction. RESULTS: The distribution of ACE genotypes were not significantly different between healthy controls and asthma group (p)0.05). In asthmatic patients, the genetic polymorphism was similar between different severity groups (p) 0.05). Conchcsion: It is suggested that I/D polymorphism of the ACE gene may not be associated with development of asthma. The severity of asthma may not be influenced by I/D polymorphism of the ACE gene.