The effects of coronary revascularization by percutaneous transluminal coronary angioplasty or coronary bypass grafting, or both, on survival were evaluated in 81 patients with cardiogenic shock complicating acute myocardial infarction. Thirty-two patients had successful revascularization and 49 patients had unsuccessful or no revascularization. Revascularization was achieved by coronary angioplasty in 22 patients, coronary bypass surgery in 2 and angioplasty followed by bypass surgery in 8. No significant differences were noted between the two groups with regard to baseline clinical or hemodynamic variables. Intraaortic balloon counterpulsation was employed in 27 (84%) of the 32 patients in the group with revascularization and in 19 (39%) of the 49 patients without revascularization (p = 0.0006). The in-hospital survival was significantly better in the patients with--18 (56%) of 32--than in the patients without revascularization--4 (8%) of 49 (p less than 0.0001). At a mean follow-up period of 21 +/- 15 months, this survival difference persisted--16 (50%) of 32 patients with revascularization survived versus 1 (2%) of 49 patients without revascularization (p less than 0.0001). The mean time from the onset of shock to revascularization differed significantly between survivors (12.4 +/- 15 h) and nonsurvivors (58.5 +/- 93 h) in the group with revascularization (p = 0.0004). In the revascularization group, the in-hospital survival rate was 77% (17 of 22) when revascularization was performed within 24 h but only 10% (1 of 10) when it was performed after 24 h (p = 0.0006).(ABSTRACT TRUNCATED AT 250 WORDS)
The effect of empiric antiarrhythmic therapy with quinidine and procainamide on long-term mortality was examined in 209 patients with coronary artery disease resuscitated after out-of-hospital cardiac arrest. The antiarrhythmic agent used was determined by the patient's private physician without knowledge of the study ambulatory electrocardiogram. Of the 209 patients, procainamide was prescribed in 45 (22%), quinidine in 48 (23%) and no antiarrhythmic therapy in 116 (55%). Digoxin therapy was initiated in 101 patients. The 2-year total survival rate for the quinidine, procainamide and nontreated patients was 61, 57 and 71% (p less than 0.05), and for sudden death was 69, 69 and 89% (p less than 0.01), respectively. These observations suggest that empiric antiarrhythmic therapy in survivors of out-of-hospital cardiac arrest did not affect total mortality and was associated with an increased frequency of sudden death.
The human leukocyte antigen (HLA) genes may play a role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) and its progressive form, non-alcoholic steatohepatitis (NASH). The aim of this study was to assess the association of HLA class I and II alleles with NASH and its histological features.
Deoxyribonucleic acid (DNA) was extracted from 140 subjects (85 biopsy-proven NAFLD and 55 controls) and genotyped for HLA (-A, -B, -C, -DR1, -DR3, -DQ, and -DP). Liver biopsies were assessed for presence of NASH, degree of fibrosis and inflammation. Multivariate analysis was performed to assess associations between HLA genes and different histologic features of NAFLD.
Our data for HLA class I showed that HLA-C∗4 was associated with lower risk for histologic NASH and HLA-C∗6 was protective against portal fibrosis. Conversely, HLA-B∗27 was associated with high-grade hepatic steatosis, while HLA-A∗31 was associated with increased risk for advanced fibrosis. Among HLA class II alleles, HLA-DQA1∗01 was associated with lower risk for NASH while HLA-DRB1∗03 was associated with increased risk for NASH.
Our findings indicate that HLA class I and II gene polymorphism may be associated with susceptibility to NASH, fibrosis and other pathologic features and may be involved in the pathogenesis of NAFLD.
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