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lschaemic heart disease may present as a wide variety of clinical entities including unstable or stable angina pectoris, acute myocardial infarction, and occasionally heart failure. Chronic stable angina is a [...]

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 [...]

Objective: To analyse differences in the presentation and management of Bangladeshi and white patients with Q wave acute myocardial infarction (AMI). Design: Prospective observational study. Setting: East London teaching hospital. [...]

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: [...]

Objectives: To compare serum potassium concentrations in diabetic and non-diabetic patients in the early phase of acute coronary syndromes. Background: Acute phase hypokalaemia occurs in response to adrenergic activation, which [...]

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 [...]

Background: Early discharge after myocardial infarction is safe and feasible. Factors that delay discharge need to be identified in order to improve care and reduce bed occupancy. Objective: To investigate [...]

Coronary artery disease is characterized by reduced blood flow through coronary arteries due to the formation of fatty plaque on vessel walls, with subsequent constriction of the vessel. Ischemia, lack of oxygen supply to the heart muscle, results from low blood flow, and this may cause the pain of angina, or it can not produce symptoms. The factors differentiating 'silent' from painful ischemia are unclear. Ischemia can be diagnosed during treadmill stress testing by changes in the electrocardiograms, which are recordings of the heart's electrical activity. The time between an ischemic episode and onset of anginal pain, the anginal perceptual threshold, may be helpful in studying the mechanisms underlying silent ischemia. The threshold is prolonged in diabetics, particularly in those whose autonomic nerves (which regulate function of organs such as the heart) are damaged. However, the role of nerve damage in nondiabetic patients with silent ischemia is unknown. If nerve-related mechanisms are important, then altered perception of angina would be expected to be greater in the elderly, as autonomic and sensory function declines with age. To better understand silent ischemia, the anginal perceptual threshold was evaluated in 82 nondiabetic men with angina. Electrocardiogram changes suggestive of ischemia were found from 147 to 325 seconds after the start of exercise in 79 patients, and the anginal perceptual threshold ranged from 10 to 64 seconds. Patients' ages weakly but significantly correlated with the threshold, as older patients had longer intervals between onset of electrocardiogram changes and perception of angina. Differences were particularly obvious when the thresholds from patients over 68 years were compared with those from patients under 56 years. Although autonomic nerve function and blood pressure varied with age, as expected, neither were related to the anginal perceptual threshold. The study indicates that altered perception of angina associated with aging is not due entirely to changes in autonomic function. (Consumer Summary produced by Reliance Medical Information, Inc.)

Heart 2003;89:1288-1290 Although C reactive protein is intimately involved with the pathogenic mechanisms that drive acute coronary syndromes, there is no evidence that it is helpful for identifying patient groups [...]

A 47 year old woman was kicked in the sternum by a horse and fell to the ground with brief loss of consciousness. She presented nine hours later with chest [...]

ObjectiveTo determine the changing risk of ventricular fibrillation, the prognostic implications, and the potential long term prognostic benefit of earlier hospital admission, after acute myocardial infarction.DesignProspective observational study.SettingA district general hospital in east London.Patients1225 consecutive patients admitted to a coronary care unit with acute myocardial infarction.Main outcome measuresTime of onset of pain and ventricular fibrillation, and long term survival of patients admitted with acute myocardial infarction.ResultsThe rate of ventricular fibrillation in these hospital inpatients was high in the first hour from onset of pain (118 events/1000 persons/h; 95% confidence interval (CI) 50.7 to 231) and fell rapidly to an almost constant low level by six hours; 27.4% of patients with early ventricular fibrillation died in hospital, compared with 11.6% of those without (p < 0.0001), but mortality in patients who survived to hospital discharge was not altered by early ventricular fibrillation (five year survival: 75.0% (95% CI 60.0% to 84.8%) with ventricular fibrillation v 73.3% (95% CI 69.6% to 76.6%) without ventricular fibrillation).ConclusionsPatients successfully resuscitated from early ventricular fibrillation have the same prognosis as those without ventricular fibrillation after acute myocardial infarction. Faster access to facilities for resuscitation must be achieved if major improvements in the persistently high case fatality of patients after acute myocardial infarction are to be made.

ObjectiveTo examine demographic and clinical characteristics of patients with acute myocardial infarction in order to identify factors affecting the electrocardiographic evolution of injury.MethodsProspective cohort study of 1399 consecutive patients with a first myocardial infarction. Baseline clinical data associated with ST elevation and Q wave development were identified and 12 month survival was estimated.ResultsSmoking had complex effects on the evolution of injury, increasing the odds of ST elevation (odds ratio (OR) 1.61; 95% confidence interval (CI) 1.08 to 2.36), but reducing the odds of Q wave development (OR 0.69, 95% CI 0.49 to 0.96). The effects of previous aspirin treatment were more consistent with reductions in the odds of ST elevation (OR 0.57, 95% CI 0.35 to 0.94) and Q wave development (OR 0.53, 95% CI 0.34 to 0.84). ST elevation and Q wave development were both associated with an adverse prognosis, with estimated 12 month survival rates of 80.6% (95% CI 78.2% to 83.1%) and 80.0% (95% CI 77.5% to 82.5%), respectively, compared with 86.5% (95% CI 81.2% to 91.9%) and 89.9% (95% CI 86.2% to 93.7%) for patients without these ECG changes.ConclusionsThe thrombogenicity of the blood may be a major determinant of infarct severity. Smoking increases thrombogenicity and the likelihood of ST elevation, but because coronary occlusion is relatively more thrombotic in smokers, responses to both endogenous and exogenous thrombolysis are better, reducing the risk of Q wave development. Previous aspirin treatment reduces thrombogenicity, protecting against ST elevation and Q wave development.

ObjectiveTo assess the role of β cell failure in the development of autonomic dysfunction in patients with coronary artery disease. DesignAutonomic function was measured by standard clinical methods and by heart rate variability in 24 type II diabetic and 24 non-diabetic subjects with coronary artery disease. Quantitative estimates of pancreatic β cell function (%β) and insulin resistance were made from basal plasma glucose and insulin concentrations using a computer solved model. Fasting proinsulin levels provided an independent measure of β cell function. ResultsThe circadian rhythm of sympathovagal balance (ratio of low to high frequency spectral components of heart rate variability) was significantly attenuated in patients with below median (%β ≤ 63.3) compared with above median pancreatic β cell function. Multiple measures of autonomic function showed positive associations with %β (low frequency: r = 0.41, p = 0.004; high frequency: r = 0.27, p = 0.07; lying/standing fall in systolic pressure: r = -0.30, p = 0.04) and negative associations with proinsulin (low frequency: r = -0.35, p = 0.03; high frequency: r = -0.36, p = 0.02; standard deviation of RR intervals: r = -0.43, p = 0.007). Associations tended to be stronger in non-diabetic than diabetic patients. In contrast, there was no association between insulin resistance and either autonomic function or the circadian rhythm of sympathovagal balance, regardless of diabetes status. ConclusionsThe data are consistent with the hypothesis that β cell failure plays a pathogenic role in the development of autonomic dysfunction in patients with coronary artery disease.

ObjectivesTo examine the circadian, seasonal, and weekly rhythms of acute myocardial infarction, and to identify subgroups in whom the rhythms are attenuated or absent to provide further information about the mechanisms of the rhythms and the processes responsible for triggering plaque events.Design and settingProspective, observational study in a general hospital.Patients and methods1225 consecutive patients admitted to a coronary care unit with acute myocardial infarction were studied. Admission rates were calculated according to the hour of the day (circadian rhythm), day of the week (weekly rhythm), and month of year (seasonal rhythm). The data were analysed for variations within the whole group and within subgroups.ResultsA weekly rhythm of acute myocardial infarction could not be demonstrated but there was a trend towards higher admission rates at the beginning of the week. However, the time of onset of symptoms showed significant circadian variation for the group as a whole, peaking in the morning (P = 0·006), against an otherwise fairly constant background rate. Subgroup analysis showed complete absence of the circadian rhythm in patients who were diabetic, South Asian, or taking β blockers or aspirin on admission. Significant seasonal variation in admission rates was also demonstrated for the group as a whole with a winter peak and a summer trough (P = 0·009). Again, no seasonal rhythm could be demonstrated in patients who were diabetic, South Asian, or taking β blockers or aspirin on admission.