Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dilated Cardiomyopathy (DCM) is associated with many diseases. By means of epidemiologic, clinical and invasive diagnostic techniques, the etiology of DCM is identified almost in 50% of the cases. Chronic infection with Trypanosoma cruzi is recognized as a cause of DCM in Latin America. A blind study of 40 cases of DCM explores the electrovectorcardiographic data obtained in chronic chagasic cardiomyopathy (CCC). Twenty one of 40 patients fulfilled epidemiologic and seroimmunologic criteria for CCC, 19 had DCM. There were not differences between these groups in regard to sex or age. Patients suffering DCM had in addition diabetes mellitus, systemic hypertension or ischemic heart disease. Those with CCC had not comorbid diseases in 50% of the cases. Arrhythmias and conduction blocks were equally recognized in both groups, as well as ECG evidence of injury or necrosis (p > 0.05). However, ECG signs of subepicardial ischemia were a dominant feature in patients with CCC and normal epicardial coronary arteries (p < 0.05). Probably this finding is due to a small vessels damage, a pathogenic mechanism proposed in CCC.
 ...
PMID:[Vector electrocardiographic findings in chronic Chagas cardiomyopathy]. 965 83

Chronic infection and inflammation have recently been implicated as important etiologic agents for atherosclerosis in general and, in particular, ischemic heart disease. Several agents have been suggested as possible candidates for the chronic inflammation including cytomegalovirus, Helicobacter pylori and Chlamydia pneumoniae. We hypothesized that a vascular infection with C. pneumoniae may induce a chronic inflammatory reaction in the host vascular tissue and activated inflammatory cells may express inflammatory mediators such as cyclooxygenase-2 (COX-2) and matrix metalloproteinases (MMPs). At first, we evaluated the relationship between C. pneumoniae infection and atherosclerosis indirectly by serologic study, and then, to confirm our hypothesis, we performed an immunohistochemical study of atherosclerotic plaques. The seropositive rate of anti-Chlamydia pneumoniae IgG was higher in the disease group (Group I, 59.8%, n = 254) than in the negative control group (Group III, 47.4%, n = 97) (p = 0.041), but the anti-Chlamydia pneumoniae IgA was not different in seropositivity between the two groups (Group I, 64.6%; Group III, 57.7%). The simultaneous seropositive rates of both IgG and IgA were 56.7% in Group I and 43.3% in Group III (p = 0.033). In subgroups without the conventional risk factors of atherosclerosis, these findings were more prominent. Furthermore, we performed immunohistochemical staining on the atherosclerotic aortic tissues obtained from patients that were seropositive to C. pneumoniae (n = 5), by using antibodies to C. pneumoniae, COX-2, and MMP-9. The immunoreactivity for COX-2 and MMP-9 increased in the atherosclerotic plaques itself, predominantly in the surrounding area of immunoreactive C. pneumoniae. These findings support our hypothesis and C. pneumoniae may participate in a pathogenetic mechanism for atherogenesis or progression of atherosclerosis. The present study may open a promising perspective concerning future therapeutic trials of chronic inflammation related atherogenesis under pathophysiological conditions.
 ...
PMID:Serologic and histopathologic study of Chlamydia pneumoniae infection in atherosclerosis: a possible pathogenetic mechanism of atherosclerosis induced by Chlamydia pneumoniae. 1095 85