Sudden cardiac death and left ventricular ejection fraction during long-term follow-up after acute myocardial infarction in the primary percutaneous coronary intervention era: results from the HIJAMI-II registry.

OBJECTIVE: To determine the incidence of sudden cardiac death (SCD) according to left ventricular ejection fraction (LVEF) in survivors of myocardial infarction (MI) in the primary percutaneous coronary intervention (PCI) era. DESIGN: A multicentre observational prospective registered cohort study. SETTING: 18 medical centres in Japan. PATIENTS: 4122 consecutive patients (mean age 66 (SD 12) years, 73.7% male) with acute MI, who were discharged alive. MAIN OUTCOME MEASURES: The primary end-point was SCD, and a secondary end-point was death from any cause. RESULTS: Patients were categorised into three groups: LVEF >40% (n = 3416), LVEF < or =40% and >30% (n = 507) and LVEF < or =30% (n = 199). Among all patients, 77.8% received PCI and 3.7% received coronary artery bypass graft surgery. During an average follow-up of 4.1 years, SCD was 1.2% and mortality was 13.1%. Patients with LVEF < or =30% and LVEF < or =40% and >30% were at increased risk for SCD (HR 5.99, 95% CI 2.73 to 13.14, p<0.001, HR 3.37, 95% CI 1.74 to 6.50, p<0.001, respectively), and mortality (HR 3.85, 95% CI 2.96 to 5.00, p<0.001, HR 2.06, 95% CI 1.66 to 2.57, p<0.001, respectively), compared to patients with LVEF >40%. Kaplan-Meier estimates of SCD in patients with LVEF < or =30% were 2.9%, 5.1% and 5.1% at 1, 3 and 5 years, respectively. CONCLUSION: There is a low incidence of SCD in survivors of MI in the primary PCI era, although LVEF is a predictor of increased risk for SCD.

Decrease in expression of the master operon of flagellin synthesis in a dnaA46 mutant of Escherichia coli.

We examined the expression of the fliC, fliA and fihD genes in the dnaA46 mutant. In Northern blot analysis, the amounts of fliC, fliA, and flhD mRNA decreased in the dnaA46 mutant growing at 37 degrees C but not at 28 degrees C. The promoter activity of each gene also decreased in this mutant at 37 degrees C. The decrease in expression of the flh D gene was not related to the cAMP-catabolite activator protein (CAP) pathway. We tentatively conclude that DnaA protein is involved in the expression of the flhD gene by a mechanism independent of the cAMP-CAP pathway.

Control by phosphatidylglycerol of expression of the flhD gene in Escherichia coli.

We reported elsewhere that mutation in the pgsA gene, responsible for the synthesis of phosphatidylglycerol, repressed the synthesis of flagellin and caused the loss of motility of Escherichia coli (Tomura et al., FEBS Letters 329, 287-290, 1993). We now describe evidence for a decrease in promoter activity of the flhD gene, a master gene for flagellum synthesis, in the pgsA3 mutant. We constructed a plasmid with a promoter region of the flhD gene connected with the structure region of the lacZ gene. The activity of beta-galactosidase in the extract prepared from the pgsA3 mutant harboring the fusion plasmid was 30% of that in the wild type cells. This result means that phosphatidylglycerol is likely to be required for the initiation of transcription of the flhD gene. We also found that the motility-less phenotype of the mutant was partially suppressed by elevating incubation temperature. This suppression is caused by restoration of transcription of the flhD gene by high temperature. As the content of phosphatidylglycerol did not increase by elevating incubation temperature, we proposed that this suppression is caused by alternation of a physical structure of phospholipid bilayers in cytoplasmic membranes.

[Investigation of etiologies for acute renal failure due to rhabdomyolysis in 5 patients].

We experienced 5 cases of acute renal failure due to rhabdomyolysis during the last two years and investigated those etiologies. Diagnosis of rhabdomyolysis was established by the detection of elevated serum creatine phosphokinase, myoglobin, aldolase, myoglobinuria as well as by the clinical course. The respective underlying illness of the 5 cases were grand mal seizures, infection (high fever), heat stroke, diabetes mellitus with hyperosmolar nonketotic coma and cerebral infarction treated by barbiturate. In this investigation, however, any single cause was not enough as the etiologies of rhabdomyolysis. There were multiple factors responsible to rhabdomyolysis in each case, such as hypokalemia, hypophosphatemia, shock, arteriosclerosis, etc. Some cases could not be classified as traumatic or non-traumatic rhabdomyolysis. Thus, in one case, acute renal failure due to rhabdomyolysis induced by the combination of grand mal seizures and serum potassium/phosphate depletion. 2 cases recovered without hemodialysis. 3 cases died in multiple organ failure, included a case treated by hemodialysis. We conclude that acute renal failure due to rhabdomyolysis induced easily by numerous diseases and early diagnosis is recommended.

Immune response against hamster erythrocytes in the low-responder mouse strains. XI. Strain difference in the effects of various microbial adjuvants.

Enhancing and suppressing effects of microbial adjuvants were studied in female mice of the C3H/He, AKR and SL strains. Propionibacterium acnes, Bordetella pertussis, BCG and yeast cell wall (YCW) were chosen as adjuvants. As antigens, we chose hamster erythrocytes (HRBC) which proved to be a weak antigen for mice. Adjuvants were given on day --7, day 0 or day 3, and HRBC were injected on day 0. The results were as follows. 1) P. acnes facilitated IgM and IgG antibody production in AKR mice and suppressed IgM antibody production in SL mice, when given on day --7. When P. acnes was given on day 0, they suppressed IgM antibody production in all of the strains used. 2) When B. pertussis was given on day 0, it exhibited enhancing effects on IgG antibody production in all of the strains and a suppressing effect on IgM antibody production in SL mice. 3) BCG suppressed IgM antibody production in all strains when given on day 0. 4) YCW showed no influence on antibody production in any combination used in this work. 5) SL mice were very sensitive to suppressing effects by adjuvants. Strain differences in the expression of enhancing and suppressing effects by adjuvants appear to be under some control independent of antigen-specific immune response genes.