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Objectives: To analyse the relation between serum glucose concentration and hospital outcome across the whole spectrum of acute coronary syndromes.Methods: This was a prospective cohort study of 2127 patients presenting with acute coronary syndromes. The patients were stratified into quartile groups (Q1 to Q4) defined by serum glucose concentrations of 5.8, 7.2, and 10.0 mmol/l. The relation between quartile group and major in-hospital complications was analysed.Results: The proportion of patients with acute myocardial infarction increased incrementally across the quartile groups, from 21.4% in Q1 to 47.9% in Q4 (p < 0.0001). The trend for frequency of in-hospital major complications was similar, particularly left ventricular failure (LVF) (Q1 6.4%, Q4 25.2%, p < 0.0001) and cardiac death (Q1 0.7%, Q4 6.1%, p < 0.0001). The relations were linear, each glucose quartile increment being associated with an odds ratio of 1.46 (95% confidence interval (CI) 1.27 to 1.70) for LVF and 1.52 (95% CI 1.17 to 1.97) for cardiac death. Although complication rates were higher for a discharge diagnosis of acute myocardial infarction than for unstable angina, there was no evidence that the effects of serum glucose concentration were different for the two groups, there being no significant interaction with discharge diagnosis in the associations between glucose quartile and LVF (p = 0.69) or cardiac death (p = 0.17). Similarly there was no significant interaction with diabetic status in the associations between glucose quartile and LVF (p = 0.08) or cardiac death (p = 0.09).Conclusion: Admission glycaemia stratified patients with acute coronary syndromes according to their risk of in-hospital LVF and cardiac mortality. There was no detectable glycaemic threshold for these adverse effects. The prognostic correlates of admission glycaemia were unaffected by diabetic status and did not differ significantly between patients with acute myocardial infarction and those with unstable angina. [ABSTRACT FROM AUTHOR]

The article presents a prospective study which investigates the relationship between subsequent fatal ischaemic heart disease (IHD) and psychological characteristics events. The study includes 1408 white men aged 40-64 years without a history of myocardial infarction to finish a Crown-Crisp experiential index form (CCEI). Results show that the associations were independent of social class, age, and known cardiovascular risk factors.

Rationale for the study Endothelial protein C receptor (EPCR) is involved in the regulation of thrombin generation and inflammation. PROCR gene variant rs867186 codes for an amino acid substitution (Ser219Gly) within the membrane spanning region of EPCR. The minor allele of the variant has been identified as functional, and associated with increased shedding of EPCR from the endothelial surface. Previous analysis has also shown increased coagulation activated markers in those with the Gly allele1. Furthermore, while heterozygotes for this variant may be protected from coronary heart disease (CHD), homozygotes had a threefold elevation in CHD risk in a prospective cohort (NPHSII). In a case-control study of CHD (HIFMECH), there was a suggestion that the EPCR genotype interacts with factors present in metabolic syndrome, to increase CHD risk. Methodology NPHSII was analysed to further assess the CHD risk associated with EPCR Ser219Gly in those who have been identified as diabetic, or as having 'metabolic syndrome-tm), during 15 years' follow-up. Results Individuals who were Gly/Gly and had 'metabolic syndrome-tm) had a fourfold increase in CHD risk compared with Ser/Ser (HR=4.72, CI 1.69 to 13.4) p=0.006; or an eightfold increase in risk above those who were Ser/Ser without metabolic syndrome (HR=8.02, CI 2.89 to 22.2) p=0.006. No Gly/Gly individuals without metabolic syndrome had a CHD event. Conclusions Homozygotes for the Gly allele are present at a frequency of ~1%. If the findings in the study can be replicated, the variant would constitute a considerable CHD risk in 1% of diabetics. Replication studies are under way in three further, large prospective cohorts. [ABSTRACT FROM AUTHOR]

OBJECTIVES: To evaluate the impact the National Service Framework (NSF) for coronary heart disease has had on emergency treatment and outcomes in patients presenting with acute coronary syndromes. DESIGN: Retrospective cohort study. SETTING: Coronary care units of two district general hospitals. RESULTS: Data from 3371 patients were recorded, 1993 patients in the 27 months before the introduction of the NSF and 1378 patients in the 24 months afterwards. After the introduction of the NSF in-hospital mortality was significantly reduced (95 patients (4.8%) v 43 (3.2%), p = 0.02). This was associated with a reduction in the development of Q wave myocardial infarction (40.6% v 33.3%, p < 0.0001) and in the incidence of left ventricular failure (15.9% v 12.3%, p = 0.003). The proportion of patients receiving thrombolysis increased (69.4% v 84.7%, p < 0.0001) with a decrease in the time taken to receive it (proportion thrombolysed within 20 minutes 12.1% v 26.6%, p < 0.0001). The prescription of beta blockers (51.9% v 65.8%, p < 0.0001), angiotensin converting enzyme inhibitors (37% v 66.4%, p < 0.0001), and statins (55.2% v 72.7%, p < 0.0001) improved and the proportion of patients referred for invasive investigation increased (18.3% v 27.0%, p < 0.0001). Trend analysis showed that improvements in mortality and thrombolysis were directly associated with publication of the NSF, whereas the improvements seen in prescription of beta blockers and statins were the continuation of pre-existing trends. CONCLUSIONS: In the two years that followed publication of the NSF the initial treatment and outcome of patients presenting with acute coronary syndromes improved. Some of the improvements can be attributed to the NSF but others are continuations of pre-existing trends. [ABSTRACT FROM AUTHOR]

Objectives: To evaluate the impact the National Service Framework (NSF) far coronary heart disease has had on emergency treatment and outcomes in patients presenting with acute coronary syndromes. Design: Retrospective cohort study. Setting: Coronary care units of two district general hospitals. Results: Data from 3371 patients were recorded, 1993 patients in the 27 months before the introduction of the NSF and 1378 patients in the 24 months afterwards. After the introduction of the NSF in-hospital mortality was significantly reduced (95 patients (4.8%) v 43 (3.2%), p = 0.02). This was associated with a reduction in the development of Q wave myocardial infarction (40.6% v 33.3%, p < 0.0001) and in the incidence of left ventricular failure (15.9% v 12.3%, p = 0.003). The proportion of patients receiving thrombolysis increased (69.4% v 84.7%, p < 0.0001) with a decrease in the time taken to receive it (proportion thrombolysed within 20 minutes 12.1% v 26.6%, p < 0.0001 ). The prescription of 13 blockers (51.9% v 65.8%, p < 0.0001), angiotensin converting enzyme inhibitors (37% v 66.4%, p < 0.0001), and statins (55.2% v 72.7%, p < 0.0001) improved and the proportion of patients referred far invasive investigation increased (18.3% v 27.0%, p < 0.0001). Trend analysis showed that improvements in mortality and thrombolysis were directly associated with publication of the NSF, whereas the improvements seen in prescription of β blockers and statins were the continuation of pre-existing trends. Conclusions: In the two years that fallowed publication of the NSF the initial treatment and outcome of patients presenting with acute coronary syndromes improved. Some of the improvements can be attributed to the NSF but others are continuations of pre-existing trends. [ABSTRACT FROM AUTHOR]

Objectives: To determine whether case fatality rates in South Asian (Bangladeshi, Indian and Pakistani) patients with acute myocardial infarction have shown similar declines to those reported for white patients during the past 15 years. Design: Cross-sectional, observational study. Setting: Coronary care unit in east London. Patients: 2640 patients-29% South Asian-admitted with acute myocardial infarction between January 1988 and December 2002. Main outcome measures: Differences over time in rates of in-hospital death, ventricular fibrillation and left ventricular failure. Results: The proportion of South Asians increased from 22% in 1988-92 to 37% in 1998-2002. Indices of infarct severity were similar in South Asian and white patients, with declining frequencies of ST elevation infarction (88.2% to 77.5%, p < 0.0001), Q wave development (78.1% to 56.9%, p <0.0001) and mean (interquartile range) peak serum creatine kinase concentrations (1250 (567-2078) to 1007 (538-1758) IU/l, p < 0.0001) between 1988-92 and 1998-2002. Rates of in-hospital death (13.0% to 9.4%, p < 0.01), ventricular fibrillation (9.2% to 6.0%, p < 0.001) and left ventricular failure (33.2% to 26.5%, p < 0.0001) all declined; these changes did not interact significantly with ethnicity. Odds ratios for the effect of time on risk of death increased from 0.81 (95% CI 0.70 to 0.93) to 1.02 (95% CI 0.87 to 1.21) after adjustment for ethnicity and indices of infarct severity (ST elevation, peak creatine kinase, Q wave development and treatment with a thrombolytic). Conclusions: In the past 15 years, death from acute myocardial infarction among South Asians has declined at a rate similar to that seen in white patients. This is largely caused by reductions in indices of infarct severity. [ABSTRACT FROM AUTHOR]

Objectives: To determine the incremental value of clinical data, troponin T, ST segment monitoring, and heart rate variability for predicting outcome in patients with non-ST elevation acute coronary syndromes.Methods: Prospective cohort study of 304 consecutive patients. Baseline clinical and electrocardiographic data were recorded, serial blood samples were obtained for troponin T assay, and 48 hour Holter monitoring was performed for ST segment and heart rate variability analysis. End points were cardiac death and non-fatal myocardial infarction during 12 months' follow up.Results: After 12 months, 7 patients had died and 21 had had non-fatal myocardial infarction. The risk of an event was increased by troponin T > 0.1 microg/l, T wave inversion on the presenting ECG, Holter ST shift, and a decrease in the standard deviation of 5 minute mean RR intervals. Positive predictive values of individual multivariate risk were low; however, analysis of all multivariate risk markers permitted calculation of a cumulative risk score, which increased the positive predictive value to 46.9% while retaining a negative predictive value of 96.9%.Conclusion: A cumulative approach to risk stratification in non-ST elevation coronary syndromes successfully identifies a group in whom the risk of cardiac death or non-fatal myocardial infarction approaches 50%. [ABSTRACT FROM AUTHOR]

Background: Shortening prehospital delay has been identified as an important means of improving responses to reperfusion treatment. If this increases the risk profile of the population delivered to hospital, it may paradoxically cause a deterioration in hospital mortality. Objective: To examine the interaction between arrival time (time from onset of chest pain to arrival at hospital) and thrombolytic treatment in determining the early outcome of acute myocardial infarction. Methods: Prospective cohort study of 1723 patients with acute myocardial infarction who were potentially eligible for thrombolytic treatment (ST elevation on ECG; arrival time ≤ 12 hours). Results: All patients were eligible for thrombolysis but only 1098 (80%) received it. Patients who did not receive thrombolytic treatment were older (66 (58-73) v 61 (53-70) years, p < 0.001), more commonly female (32.1% v 24.8%, p < 0.01), and had higher frequencies of previous infarction (28.6% v 15.6%, p < 0.001) and left ventricular failure (37.5% v 26.9%, p < 0.01) than patients who received thrombolytic treatment. For the group as a whole, 30 day mortality was 11.7% and was unaffected by arrival time, but in patients who did not receive thrombolysis an arrival time of ≤ 6 hours was associated with significantly higher 30 day mortality than an arrival time of 6-12 hours (24.3% v 2.6%, p = 0.002). Conversely, in patients who did receive thrombolysis an arrival time of ≤ 6 hours was associated with a lower 30 day mortality than an arrival time of 6-12 hours (8.5% v 14.5%, p < 0.02). Conclusions: Shortening prehospital delay in acute myocardial infarction will tend to increase the risk profile of patients presenting to emergency departments. The data presented here indicate that this may increase hospital mortality if underutilisation of thrombolytic treatment among high risk groups is not diminished. [ABSTRACT FROM AUTHOR]

The article reports that traditional myocardial infarction (Ml) has been diagnosed according to the World Health Organization criteria, which emphasizes the importance of the clinical syndrome, electrocardiographic changes, and elevation of long--standing but relatively non-specific markers of myocardial damage such as creatine kinase. In 2000, a Joint European Society of Cardiology and American College of Cardiology committee published a redefinition of MI based upon raised serum concentrations of cardiac troponins. This has led to the inclusion of patients with lower levels of myocardial damage than was previously detectable.

The trandolapril cardiac evaluation investigators reported a male to female ratio of sudden cardiac death in coronary disease of 1.4: 1. The low proportion of female subjects undergoing implantable cardioverter-defibrillator (ICD) implantation is well recognized and these data lead the authors to question whether there could be a sex bias in the referral or prescription of ICD in patients with coronary artery disease (CAD). The authors analysed the characteristics of 514 ICD implants performed between January 1990 and October 2002. Their study indicates that too few females with CAD are referred for an ICD.

The article focuses on a study related to myocardial hypertrophy in Friedreich's Ataxia (FA). FA is the commonest autosomal recessive spinocerebellar ataxia and is associated with cardiomyopathy, which may be hypertrophic or dilated. FA is caused by a triplet expansion in the FA gene. The consequent reduction in frataxin levels, which is a mitochondrial protein, is associated with mitochondrial iron overload, increased sensitivity to oxidative stress, and profound deficit of oxidative phosphorylation. Researchers previously showed that phosphocreatine/ATP in human heart measured by MR spectroscopy is reduced in FA patients irrespective of evidence of cardiomyopathy and increased towards normal by treatment with CoQ1 0 and vitamin E.