Prognostic significance of hypertension and albuminuria for early mortality after acute myocardial infarction

The motile enterococci with the vanC gene have intrinsic low-level resistance to vancomycin, but have not been implicated in a nosocomial outbreak. We determined the colonization rate of motile enterococci in hospitalized and nonhospitalized patients. Perianal or stool specimens were cultured in Enterococcosel broth supplemented with 6 micrograms of vancomycin per mL. Rapid motility and pigment tests were performed on all enterococci isolated. A total of 82 motile and/or pigmented enterococci were isolated from 679 patients for a colonization rate of 12.1%. There were 43 Enterococcus gallinarum, 32 Enterococcus casseliflavus, 4 Enterococcus flavescens, and 3 Enterococcus mundtii identified. The E. gallinarum vancomycin MIC90 was 32 micrograms/mL and the E. casseliflavus vancomycin MIC90 was 8 micrograms/mL.     

In-hospital and follow-up mortality of patients with acute myocardial infarction

Patients with definite acute MI who were admitted to Songkla University Hospital between 1982 and 1990 were studied. The 195 patients and 202 admissions were nearly equally distributed between these 65 and older versus those younger than 65. Three quarters were males. The in-hospital mortality was 19.5 per cent and 76.3 per cent of the deaths were from heart failure. Neither age nor gender determined the mortality once corrected for the Killip's staging. There was no difference in mortality when comparing Q versus non-Q MI, anterior versus inferior wall MI or males versus females. One hundred and thirty-eight patients could be followed for and average of 27.1 months. First year mortality was 11 per cent and the first 2 years was 14 per cent. The in-hospital mortality, representing the prethrombolytic era, appeared to be similar to values reported from the Thai and Western literature. The predominance of death from heart failure rather than from arrhythmia may be a consequence of delayed admission whence arrhythmic death had already occurred or patients will seek hospital advice only if highly symptomatic.     

Influence of cigarette smoking on rate of reopening of the infarct-related coronary artery after myocardial infarction: a multivariate analysis

OBJECTIVES: This study sought to determine whether the reopening of the infarct-related vessel is related to clinical characteristics or cardiovascular risk factors, or both. BACKGROUND: In acute myocardial infarction, thrombolytic therapy reduces mortality by restoring the patency of the infarct-related vessel. However, despite the use of thrombolytic agents, the infarct-related vessel remains occluded in up to 40% of patients. METHODS: We studied 295 consecutive patients with an acute myocardial infarction who underwent coronary angiography within 15 days (mean [+/- SD] 6.7 +/- 3.2 days) of the onset of symptoms. Infarct-related artery patency was defined by Thrombolysis in Myocardial Infarction trial flow grade > or = 2. Four cardiovascular risk factors--smoking, hypertension, hypercholesterolemia and diabetes mellitus--and eight different variables-age, gender, in-hospital death, history of previous myocardial infarction, location of current myocardial infarction, use of thrombolytic agents, time interval between onset of symptoms, thrombolytic therapy and coronary angiography--were recorded in all patients. RESULTS: Thrombolysis in current smokers and anterior infard location on admission were the three independent factors highly correlated with the patency of the infarct-related vessel (odds ratios 3.2, 3.0 and 1.9, respectively). In smokers, thrombolytic therapy was associated with a higher reopening rate of the infard vessel, from 35% to 77% (p < 0.001). Nonsmokers did not benefit from thrombolytic therapy, regardless of infarct location. CONCLUSIONS: These observational data, if replicated, suggest that in patients with acute myocardial infarction, thrombolytic therapy may be most effective in current smokers, whereas nonsmokers and ex-smokers may require other management strategies, such as emergency percutaneous transluminal coronary angioplasty.     

Falling hospital mortality for acute myocardial infarction in Quebec hospitals

OBJECTIVE: To present in-hospital mortality trends for acute myocardial infarction (AMI). DESIGN: Observational study using the Quebec administrative hospital database, which records all hospitalizations for AMI, for the period 1986 to 1996. RESULTS: From 1986 to 1996, the case fatality rate for AMI decreased from 18.4% to 12.7% despite an increase in the total number of admissions, due to an ageing population. Men and women have had similar yearly mortality reductions--7.6% versus 7.4%, respectively--although the absolute case fatality rate remains significantly higher for women. The mortality reduction for men was constant over the decade, while the decline for women was more pronounced over the last five years. Improving case fatality rates were also observed in the elderly and again were most evident from 1991 to 1996. CONCLUSIONS: These data show a sharp decline in case fatality rates for AMI patients treated in Quebec hospitals from 1986 to 1996, suggesting that treatment advances observed in clinical trials are being applied at a population level. While improved survival has been observed in all patient groups, the data suggest that the part of the decline in mortality may be due to increased penetration of proven treatment strategies in women and the elderly.     

Free nor-adrenaline and adrenaline excretion in relation to complications in acute myocardial infarction

The authors report on the clinical data, operating technique, postoperative complications, and late results in a series of 31 epidermoid and 21 dermoid cysts of the central nervous system.     

Patients treated by cardiologists have a lower in-hospital mortality for acute myocardial infarction

Local anesthetics suppress excitability by interfering with ion channel function. Ensheathment of peripheral nerve fibers, however, impedes diffusion of drugs to the ion channels and may influence the evaluation of local anesthetic potencies. Investigating ion channels in excised membrane patches avoids these diffusion barriers. We investigated the effect of local anesthetics with voltage-dependent Na+ and K+ channels in enzymatically dissociated sciatic nerve fibers of Xenopus laevis using the patch clamp method. The outside-out configuration was chosen to apply drugs to the external face of the membrane. Local anesthetics reversibly blocked the transient Na+ inward current, as well as the steady-state K+ outward current. Half-maximal tonic inhibiting concentrations (IC50), as obtained from concentration-effect curves for Na+ current block were: tetracaine 0.7 microM, etidocaine 18 microM, bupivacaine 27 microM, procaine 60 microM, mepivacaine 149 microM, and lidocaine 204 microM. The values for voltage-dependent K+ current block were: bupivacaine 92 microM, etidocaine 176 microM, tetracaine 946 microM, lidocaine 1118 microM, mepivacaine 2305 microM, and procaine 6302 microM. Correlation of potencies with octanol:buffer partition coefficients (logP0) revealed that ester-bound local anesthetics were more potent in blocking Na+ channels than amide drugs. Within these groups, lipophilicity governed local anesthetic potency. We conclude that local anesthetic action on peripheral nerve ion channels is mediated via lipophilic drug-channel interactions. IMPLICATIONS: Half-maximal blocking concentrations of commonly used local anesthetics for Na+ and K+ channel block were determined on small membrane patches of peripheral nerve fibers. Because drugs can directly diffuse to the ion channel in this model, these data result from direct interactions of the drugs with ion channels.     

Secondary prevention practices after acute myocardial infarction in a large city hospital

Increasingly, health care workers are being threatened and physically attacked by the people they are trying to help. What can physicians do to protect themselves and their coworkers?     

'Rescue' after failed thrombolysis for acute myocardial infarction

Prompt restoration of coronary artery patency in acute myocardial infarction is associated with substantial improvements in morbidity and mortality. The pivotal role of thrombolysis and aspirin in achieving these goals is well established. However, despite the success of thrombolytic therapy in large trials, clinical assessment in individual patients often suggests that reperfusion has not occurred after initial therapy. This review considers the validity of such bedside predictions and discusses whether such patients should be managed differently.     

Emergency coronary artery bypass grafting after acute myocardial infarction. What influences early postoperative mortality?

Chicken gamma-enolase cDNA was cloned and its sequence and tissue-specific expression were analyzed. The cDNA, consisting of 2273 bp of nucleotides, was composed of 86 bp of the 5'-noncoding region, 1305 bp of an open reading frame encoding a protein of 434 amino acids and 882 bp of the 3'-noncoding region. The deduced amino acid sequence showed higher homology (more than 90%) to those of mammalian gamma-enolases than to those of chicken alpha- or beta-enolases. Northern blot analysis has revealed that the mRNA for gamma-enolase (2.3 kb) is expressed in the brain and, to much less but significant extents, in the pituitary and adrenal gland of the chicken.     

Comparison of mortality from acute myocardial infarction between 1979 and 1992 in a geographically defined stable population

This study documents mortality from acute myocardial infarction (AMI), in hospital and at 1 year, for each of 3 selected 1-year periods in a stable community over a 13-year period beginning in 1979 and continuing into the thrombolytic era, to detect any changes occurring in conjunction with the introduction of new therapies. Every patient with AMI occurring in a geographically defined stable community (Hamilton, Ontario, Canada) in 3 1-year periods (1979 to 1980 [n = 816], 1986 to 1987 [n = 816], and 1991 to 1992 [n = 831]) was identified and clinically characterized by standardized criteria. Subsequent in-hospital and 1-year survival were ascertained prospectively. The 3 cohorts were similar in prognostic factors. Mean age was progressively greater over the study period from 63 years in 1979 to 1980, to 67 years in 1991 to 1992 (p = 0.02). There was no change in in-hospital mortality rates from 1979 to 1980 (17%) and 1986 to 1987 (16%). However, from 1986 to 1987 and 1991 to 1992, in-hospital mortality decreased from 16% to 9% (p < 0.001) and 1-year mortality decreased from 26% to 19% (p < 0.001). For patients who survived the hospital phase of AMI, 1-year mortality did not change and was between 11% and 12% in each of the 3 study periods. From 1986 to 1987 and 1991 to 1992, there was an increase in the use of thrombolytic therapy from 5% to 44% of patients. The acute use of aspirin increased from 30% to 88% and the acute use of beta blockers increased from 19% to 48% of patients. The observed increase in use of these agents could account for half of the actual mortality reduction observed. This prospective population-based survey demonstrates improved in-hospital survival after AMI associated with increased use of established effective therapies between 1987 and 1992. The 1-year mortality of hospital survivors of AMI was unchanged throughout the period of study, remaining at 11% to 12%.     

C-reactive protein as a predictor of cardiac rupture after acute myocardial infarction

Although cardiac rupture is the second most common cause of death after ventricular failure in acute myocardial infarction, no diagnosis has ever been made before an episode of clinical compromise, and no significant predictive factors have been described. This study was designed to determine whether high serum C-reactive protein (CRP) levels could predict the incidence of subacute cardiac rupture after acute myocardial infarction. Nine consecutive patients with cardiac rupture were compared retrospectively with 28 consecutive control patients without rupture after acute myocardial infarction. In the rupture group, peak serum CRP levels increased rapidly and markedly after infarction, reaching more than 20 mg/dl on day 2, and persisted at high levels compared with those in the control group. However, the time course and levels of serum creatine phosphokinase were not significantly different between the two groups. High serum CRP levels ( > 20 mg/dl) had a high diagnostic sensitivity (89%) and specificity (96%) for cardiac rupture. Patients with persistently high serum CRP levels, particularly above 20 mg/dl, might have high probability of occurrence of sub-acute cardiac rupture after acute myocardial infarction.