Prevalence of factor V Leiden (APCR) and other inherited thrombophilias in young patients with myocardial infarction and normal coronary arteries

Objective—To investigate the role of activated protein C resistance (APCR, factor V Leiden) in coronary artery thrombosis.
Methods—The prevalence of APCR and of congenital deficiencies of antithrombin III, protein C, protein S, plasminogen, and factor XII was investigated in adult patients under 45 years of age with acute myocardial infarction. The results were compared with those of a group of 53 age and sex matched control subjects.
Results—Among 75 patients under the age of 45 years who were admitted from November 1994 to April 1996 for acute myocardial infarction, 22 (29.3%) had normal coronary arteriography (group I) and 53 (70.7%) had significant coronary artery disease (group II). Inherited thrombophilia was more often found in group I (4/22, 18.2%) than in group II (4/53, 7.5%) but the difference was not significant (F test: p = 0.22). The prevalence of APCR was 9.1% (2/22) in group I, 3.8% (2/53) in group 2 (p = 0.57), and 3.8% (2/53) in the normal control group (p = 0.57).
Conclusions—The prevalence of congenital thrombophilias, including APCR, does not seem to be increased in young patients with myocardial infarction and normal coronary angiograms, compared with young patients with coronary atherosclerosis and with normal control subjects. However, the statistical power of the study is too low to detect a significant difference and these results are published to allow a meta-analysis of this problem in the future.

Keywords: myocardial infarction; factor V Leiden; coagulation factors; inherited thrombophilia     

Myocardial infarction in young people with normal coronary arteries

Myocardial infarction occurring in young people with angiographically normal coronary arteries is well described but the pathophysiology of this condition remains unknown. Coronary artery spasm in association with thrombus formation and minimal atheromatous disease or spontaneous coronary artery dissection are possible causes. Two young men presented with severe chest pain after acute alcohol intoxication and each sustained an extensive anterior myocardial infarction. Investigations including intravascular ultrasound showed no evidence of atherosclerotic coronary artery disease. Coronary artery spasm associated with acute alcohol intoxication as well as a prothrombotic state and endothelial damage related to cigarette smoking may be mechanisms leading to acute myocardial infarction in these cases. Acute myocardial infarction occurs in young persons with normal coronary arteries and the diagnosis should be considered in young patients presenting with severe chest pain, particularly those abusing cocaine or alcohol, so that reperfusion therapy can be initiated promptly.

Keywords: myocardial infarction;  coronary vasospasm;  alcohol;  intravascular ultrasound     

Reduction in treatment delay by paramedic ECG diagnosis of myocardial infarction with direct CCU admission

Objectives—To establish the feasibility of training paramedics to diagnose acute myocardial infarction by ECG before hospital admission and whether direct paramedic coronary care admission, arranged by very high frequency (VHF) radio communication with the coronary care unit (CCU), would reduce delay of thrombolysis treatment.
Design—Prospective controlled study.
Setting—District general hospital CCU and a local district ambulance paramedic service.
Patients—124 patients with ECG evidence of myocardial infarction or ischaemia admitted directly to the CCU by the paramedic service were compared with 123 patients admitted by the emergency department and subsequently transferred to the CCU.
Main outcome measures—ECG diagnostic accuracy by paramedics, and interval durations for CCU admission and thrombolysis.
Results—ECG diagnostic accuracy by the paramedics was 87.5% in the training phase and 92% in admission. The total call to thrombolysis interval was reduced from 154 to 93 minutes and the "door to needle" interval was reduced from 97 to 37 minutes.
Conclusions—Trained paramedics can reliably diagnose myocardial infarction by ECG. The use of a direct admission procedure, by a VHF radio link to the CCU, substantially reduces the time interval for thrombolytic treatment after acute myocardial infarction.

Keywords: myocardial infarction;  electrocardiogram;  thrombolysis;  paramedic     

Segmental wall motion abnormalities alter vulnerability to ventricular ectopic beats associated with acute increases in aortic pressure in patients with underlying coronary artery disease

Objective—To evaluate whether patients with coronary artery disease are susceptible to pressure related ventricular arrhythmias, and if so to identify possible risk factors.
Design—Interventional study.
Methods—Metaraminol was given to 43 patients undergoing coronary arteriography for ischaemic heart disease to increase their aortic pressure, provided their systolic blood pressure was < 160 mm Hg and they were in sinus rhythm, without any ventricular ectopic activity (or with fewer than six ventricular ectopic beats a minute) during a five minute control period.
Results—During the metaraminol infusion, systolic aortic pressure rose from 131 (15) to 199 (12) mm Hg (mean (SD)). Ventricular ectopy appeared (or ventricular ectopic beats increased by > 100%) in 13/43 patients. Ventricular ectopy was not related to age, sex, presence of hypertension, history of myocardial infarction, use of β blockers, positive exercise test, number of vessels diseased, or heart rate change during metaraminol infusion. There was a strong relation between the appearance of ventricular arrhythmia and segmental wall motion abnormalities: 1/19 (5.3%, 95% confidence interval 0.1% to 26.0%) without abnormality; 2/12 (16.7%, 2.1% to 48.4%) with hypokinesia; and 10/12 (83.3%, 51.6% to 97.1%) with akinesia or dyskinesia, χ² = 22.7, p < 0.001). Ejection fraction was also a significant but not independent risk factor.
Conclusions—Patients with segmental wall motion abnormalities are predisposed to ventricular ectopic beats during an increase in systolic aortic pressure. This could be explained by associated electrophysiological inhomogeneity. The presence of mechanical inhomogeneity, as may occur in postinfarction akinesia or dyskinesia, may affect the aortic pressure above which ventricular arrhythmias appear.

Keywords: mechanoelectrical feedback;  segmental wall motion;  akinesia;  dyskinesia;  ventricular ectopic beats;  arrhythmias     

Incidence of Factor V Leiden in Patients with Acute Myocardial Infarction

The genetic defect of coagulation factor V known as factor V Leiden produces a resistance to degradation by activated protein C (APC) and increases the risk of venous thromboembolism. The data on arterial thrombosis associated with APC resistance are still not clearly defined. We conducted a study in patients presenting with acute myocardial infarction (MI) to assess whether factor V Leiden increases the risk of arterial thrombosis. We studied 109 patients who had a diagnosis of acute MI (69 males and 40 females, aged 25–91 years), and 112 controls. The study population was identified by characteristic ECG changes and elevation of serum CK-MB, whereas the control subjects were anonymous healthy blood donors with no known history of coronary artery disease. Blood samples from the patients and controls were analyzed for the factor V Leiden mutation by DNA analysis, using the polymerase chain reaction. Heterozygous factor V Leiden mutation was found in 9 of 109 (8%) MI patients and 5 of 112 (4%) control subjects (P = .42). In conclusion, this study shows no evidence of an association between factor V Leiden and acute MI.     

Transferring patients for primary angioplasty: a retrospective analysis of 104 selected high risk patients with acute myocardial infarction

Objective—To investigate the feasibility of primary coronary angioplasty as a treatment option in patients with acute myocardial infarction after initial diagnosis in a local community hospital.
Setting—Referral centre for interventional treatment of coronary artery disease.
Methods—During a five year period, 520 candidates for primary coronary angioplasty were treated in our institution, 104 after transfer from a community hospital. The transferred patients and the non-transferred patients (n = 416) were compared with regard to baseline clinical characteristics, time interval from symptom onset to treatment, and clinical outcome at six months.
Results—In this setting, the influence of transportation on total ischaemic time was limited, and there was no difference in clinical outcome between the transferred and the non-transferred patients. Clinical outcome was mainly dependent on the indication for transfer.
Conclusions—Safe and expedient transportation may facilitate the more widespread use of primary angioplasty in patients with acute myocardial infarction. A large randomised multicentre trial is needed to compare the relative merits of intravenous thrombolytic treatment in a local hospital with primary angioplasty after transfer in selected high risk patients with acute myocardial infarction.

Keywords: myocardial infarction;  coronary angioplasty;  reperfusion     

von Willebrand factor, tissue plasminogen activator, and dehydroepiandrosterone sulphate predict cardiovascular death in a 10 year follow up of survivors of acute myocardial infarction

Background—Haemostasis plays a major part in the process initiating a myocardial infarction. The impact of haemostatic variables on long term prognosis is unknown.
Objective—To evaluate von Willebrand factor (vWF), tissue plasminogen activator antigen (t-PA) and its activity before and after venous occlusion, plasminogen activator inhibitor (PAI-1), dehydroepiandrosterone sulphate (DHEAS), and established clinical risk factors as long term predictors for reinfarction and mortality.
Patients—123 consecutive survivors of myocardial infarction followed up for 10 years.
Design—Study entry took place between 1982 and 1983. Fifty seven patients died (54 of cardiovascular disease) during the mean observation time of 10 years.
Results—Cox's univariate regression analysis showed that cardiovascular mortality was significantly associated with age, hypertension, previous history of angina pectoris, DHEAS, mass concentration of t-PA, and vWF. These associations were significant for vWF and mass concentration of t-PA after adjusting for age and hypertension.
Conclusions—A low concentration of DHEAS and high levels of the endothelially derived haemostatic variables vWF and mass concentration of t-PA are predictors of cardiovascular mortality in survivors of myocardial infarction. This association is independent of established clinical risk factors for mass concentration of t-PA and vWF.

Keywords: myocardial infarction;  risk factors;  fibrinolysis;  tissue plasminogen activator;  plasminogen activator inhibitor;  von Willebrand factor;  dehydroepiandrosterone sulphate     

Dispersion of ventricular repolarisation: a marker of ventricular arrhythmias in patients with previous myocardial infarction

Objective—To examine whether, in coronary patients after myocardial infarction, the dispersion of ventricular repolarisation measured through QT and JT intervals from a surface electrocardiogram could allow separation of those with ventricular tachyarrhythmias (VT) complicating their myocardial infarct from those without.
Design—A retrospective comparative study.
Setting—University hospital.
Patients—39 patients with myocardial infarction complicated by VT, 300 patients after myocardial infarction without arrhythmic events, and 1000 normal subjects. The myocardial infarction groups were divided into anterior, inferior, and mixed locations.
Interventions—A computer algorithm examined an averaged cycle from a 10 second record of 15 simultaneous leads (12 lead ECG + Frank XYZ leads). After interactive editing, four intervals were computed: QTapex, JTapex, QTend, and JTend. For each interval, the dispersion was defined as the difference between the maximum and minimum values across the 15 leads.
Results—The mean values of all four dispersion indices were higher in patients with myocardial infarction than in normal subjects (p < 0.01). In the infarct groups, patients with VT had significantly greater mean and centile dispersion values than those without VT. For instance, the 97.5th centile value of QTend was 65 ms in normal individuals, 90 ms in infarct patients without arrhythmia, and 128 ms in those with VT; 70% of the infarct patients who developed serious ventricular arrhythmias had values exceeding the 97.5th centile of the normal group, while only 18% of the infarct patients without arrhythmia had dispersion values above this normal upper limit. Among the infarct patients, nearly half of those (18 of 39) with tachyarrhythmias had dispersion values that exceeded the 97.5th centile of those without arrhythmia.
Conclusions—Dispersion of ventricular repolarisation may be a good non-invasive tool for discriminating coronary patients susceptible to VT from those who are at low risk.

Keywords: QT dispersion;  myocardial infarction;  computer analysis;  arrhythmias     

Role of orthotopic heart transplantation in the management of patients with recurrent ventricular tachyarrhythmias following myocardial infarction

Objective—To report the outcome of an intention to treat by heart transplantation strategy in two groups of patients after infarction, one with both left ventricular failure (LVF) and ventricular tachyarrhythmias (VTA) (group A) and the other with progressive LVF following antiarrhythmic surgery for VTA (group B).
Patients and methods—Group A comprised 17 consecutive patients for whom transplantation was considered the best primary non-pharmacological treatment; group B comprised five consecutive patients assessed and planned for transplantation after antiarrhythmic surgery.
Results—In group A, eight patients underwent transplantation and all survived the first 30 day period. At median follow up of 55 months (range 11 to 109) seven of this subgroup were still alive. Five patients died of recurrent VTA before transplantation, despite circulatory support. In the face of uncontrollable VTA, four of these underwent "high risk" antiarrhythmic surgery while awaiting transplantation: three died of LVF within 30 days and one was saved by heart transplantation two days after arrhythmia surgery. Mortality for the transplantation strategy in group A patients was 47% by intention to treat analysis. Quality of life in the eight actually transplanted, however, was good and only one died during median follow up of 56 months. The five patients in group B were accepted for transplantation for progressive LVF at a median of 21 months (range 12 to 28) after antiarrhythmic surgery. One died of LVF before transplantation, 22 months after initial surgery; another died of high output LVF three days after transplantation. Thus mortality of the intended strategy was 40%. The three transplanted patients are alive and well at 8-86 months.
Conclusions—Although the short and medium term outcome in category A or B patients who undergo transplantation is good, the overall success of the transplantation strategy in category A patients is limited by lack of donors in the short time frame in which they are required.

Keywords: heart transplantation;  ventricular arrhythmias;  myocardial infarction     

Effect of time from onset to coming under care on fatality of patients with acute myocardial infarction: effect of resuscitation and thrombolytic treatment

Objective—To examine the relation between time from onset of symptoms and coming under ambulance and hospital care on fatality in patients with evolving acute myocardial infarction, and on the proportions who survive because of resuscitation and thrombolytic treatment.
Design—Prospective community and hospital study over two years. Delay was measured from the onset of symptoms to arrival at hospital, and from the onset to coming under care from ambulance personnel.
Setting—Four general hospitals serving three United Kingdom health districts.
Patients—2213 patients under 75 years of age, 111 of whom had been successfully resuscitated from out of hospital cardiac arrest.
Interventions—Resuscitation from cardiac arrest; thrombolytic treatment.
Main outcome measures—30 day fatality and lives saved by the two forms of treatment.
Results—Times from symptom onset to coming under hospital care and to starting thrombolytic treatment (given to 53% of patients) were  1 hour in 15% and 2% of patients respectively,  2 hours in 54% and 25%, and  4 hours in 67% and 55%. Overall, 30 day fatality was 138/1000 patients treated; 64/1000 (95% confidence interval 54 to 74) survived because of treatment, and 80% of this salvage was attributable to resuscitation. Delay was an important factor: 107/1000 (60 to 144) lives were saved for those coming under care within 1 hour compared with 21/1000 (5 to 37) for those who delayed for more than 12 hours. Further analysis including the 111 patients with out of hospital arrest showed that 34% of those coming to hospital by ambulance came under ambulance care within 1 hour; for this subset, 30 day fatality was 173/1000, and 136 (109 to 163) lives were saved by treatment.
Conclusions—Results of treatment are strongly related to delay in coming under care. Reduction in delay can reduce mortality from acute myocardial infarction.

Keywords: acute myocardial infarction;  fatality;  resuscitation;  thrombolytic treatment     

Interleukin 8 released after acute myocardial infarction is mainly bound to erythrocytes

Objective—To determine whether rapid clearance of interleukin 8 (IL-8) from plasma through binding to the erythrocyte chemokine receptor may be responsible for failure to detect IL-8 consistently after acute myocardial infarction.
Design—Plasma concentrations of IL-8 were measured at frequent intervals in 43 consecutive patients. In 21 of these, erythrocyte bound IL-8 concentrations were also measured. The influence of infarct size, type of treatment, and the presence of early successful reperfusion on IL-8 release was assessed.
Results—Peak IL-8 concentrations in plasma were raised in 31 of the 43 patients (68%). Median plasma IL-8 concentrations were 16.0 pg/ml (range 2.4 to 225.0 pg/ml) six hours after the onset of chest pain. Twelve hours after the onset of symptoms, plasma IL-8 concentrations had already returned to normal in 27 patients. In contrast, in 18 of 21 patients (86%), erythrocyte bound IL-8 concentrations were raised at between 6 and 30 hours, with a median peak value of 59.8 pg/ml (range 19 to 148 pg/ml). No correlation between peak creatine kinase MB and peak IL-8 (plasma or erythrocyte bound) was observed. There was a significant difference in peak plasma IL-8 concentrations between patients who underwent direct PTCA (19.4 pg/ml) and those who received conservative treatment (9.9 pg/ml; p = 0.0206), but no correlation with the presence of early successful reperfusion.
Conclusions—IL-8 is released in plasma after acute myocardial infarction and subsequently binds to red blood cells, resulting in only a transient rise of plasma IL-8 and a more prolonged increase of erythrocyte bound IL-8.

Keywords: acute myocardial infarction;  interleukin 8     

Granulocyte colony stimulating factor in neutropenic patients with infective endocarditis

A well known complication in the treatment of infectious endocarditis is development of neutropenia caused by treatment with antibiotics in high concentrations over long periods. Neutropenia often necessitates discontinuation of antibiotic treatment. Three patients with infectious endocarditis who developed neutropenia are reported. The patients were treated with granulocyte colony stimulating factor (G-CSF), a haematopoietic growth factor that stimulates neutrophils. G-CSF induced an immediate increase in white blood cell count, primarily neutrophils. G-CSF may be effective in ameliorating neutropenia in patients who receive antibiotics for treatment of infectious endocarditis.

Keywords: granulocyte colony stimulating factor;  neutropenia;  endocarditis     

Dipyridamole thallium-201 scintigraphy for early risk stratification of patients after uncomplicated myocardial infarction

Objective—To determine the safety and prognostic value of dipyridamole thallium-201 scintigraphy performed in patients within three to five days of acute myocardial infarction, including those receiving thrombolytic treatment.
Design—A prospective study of dipyridamole thallium-201 scintigraphy in patients early after acute myocardial infarction.
Setting—University hospital.
Patients—200 patients who were clinically uncomplicated at day 3 after infarction, 92 (46%) of whom had received thrombolysis.
Main outcome measures—Incidence of cardiac death, non-fatal reinfarction, readmission to hospital for unstable angina, or non-elective revascularisation procedure within six months' follow up.
Results—No patient had a serious complication from the dipyridamole study. At six month follow up, 55 patients (28%) had suffered a defined cardiac event. Patients who received thrombolysis had the same extent of thallium-201 redistribution and the same occurrence of subsequent cardiac events as those not receiving thrombolysis. Patients who subsequently had an event had more myocardial segments showing thallium-201 redistribution than event free patients: 2.7 (SD 1.9) v 1.2 (1.4), respectively (p < 0.001). Among all clinical and scintigraphic variables, multivariate analysis identified the extent of thallium-201 redistribution as the only independent predictor of outcome (p < 0.001). Among 63 patients (32%) of the study cohort who showed more than two myocardial segments with thallium-201 redistribution, the adjusted risk ratio for a cardiac event was 7.5 (95% confidence interval 2.9 to 19.1) compared with patients without any redistribution.
Conclusions—Dipyridamole thallium-201 scintigraphy can be performed safely within a few days of the event in patients with uncomplicated myocardial infarction, including those who received thrombolysis, and can identify a subgroup of patients at high risk of future ischaemic events.

Keywords: dipyridamole; thallium; myocardial infarction; prognosis     

Acute assessment of microvascular perfusion patterns by myocardial contrast echocardiography during myocardial infarction: relation to timing and extent of functional recovery

OBJECTIVE: To examine the relation between the initial microvascular perfusion pattern, as assessed by intracoronary myocardial contrast echocardiography (MCE), immediately after restoration of TIMI (thrombolysis in myocardial infarction) (TIMI) grade 3 flow during acute myocardial infarction, and the extent and timing of functional recovery in the area at risk. SETTING: Referral centre for interventional cardiology. METHODS: Intracoronary MCE was performed 15 minutes after TIMI grade 3 recanalisation of the infarct artery in 25 patients. Segmental myocardial contrast patterns were graded semiquantitatively (0, none; 0.5, heterogeneous; 1, homogeneous). Functional recovery was assessed by echocardiography on days 9 and 42. RESULTS: Among 174 myocardial segments in the area at risk, wall motion recovery on day 9 was observed in 40% of MCE grade 1 segments but there was no significant recovery in grade 0 or 0.5 segments. On day 42, recovery had occurred in 56% of MCE grade 1 segments (p < 0. 0001 v MCE grade 0 and 0.5; p = 0.0001 v MCE grade 1 on day 9), and 22% of MCE grade 0.5 segments (p = 0.02 v MCE grade 0; p = 0.0005 v MCE grade 0.5 on day 9); MCE grade 0 segments did not recover. Negative predictive value in predicting recovery by contrast enhancement was 95% and 89% by days 9 and 42, respectively. CONCLUSIONS: Contractile recovery occurs earliest in well reperfused segments. Up to one quarter of segments with heterogeneous contrast enhancement show wall motion recovery within the first six weeks. Myocardial perfusion after recanalisation in acute myocardial infarction, even if heterogeneous, is a prerequisite for postischaemic functional recovery. Thus preservation of acute myocardial perfusion is associated with more complete and early functional recovery.     

Relation between the kinetics of thallium-201 in myocardial scintigraphy and myocardial metabolism in patients with acute myocardial infarction

Objective—To investigate the relations between myocardial metabolism and the kinetics of thallium-201 in myocardial scintigraphy.
Methods—46 patients within six weeks after the onset of acute myocardial infarction underwent resting myocardial dual isotope, single acquisition, single photon emission computed tomography (SPECT) using radioiodinated 15-iodophenyl 3-methyl pentadecaenoic acid (BMIPP) and thallium-201, exercise thallium-201 SPECT, and positron emission tomography (PET) using nitrogen-13 ammonia (NH₃) and [F18]fluorodeoxyglucose (FDG) under fasting conditions. The left ventricle was divided into nine segments, and the severity of defects was assessed visually.
Results—In the resting SPECT, less BMIPP uptake than thallium-201 uptake was observed in all of 40 segments with reverse redistribution of thallium-201, and in 21 of 88 segments with a fixed defect of thallium-201 (p < 0.0001); and more FDG uptake than NH₃ uptake (NH₃-FDG mismatch) was observed in 35 of 40 segments with reverse redistribution and in 38 of 88 segments with fixed defect (p < 0.0001). Less BMIPP uptake in the resting SPECT was observed in 49 of 54 segments with slow stress redistribution in exercise SPECT, and in nine of 17 segments with rapid stress redistribution (p < 0.0005); NH₃-FDG mismatch was observed in 42 of 54 segments with slow stress redistribution and in five of 17 segments with rapid stress redistribution (p < 0.0005).
Conclusions—Thallium-201 myocardial scintigraphy provides information about not only myocardial perfusion and viability but also about myocardial metabolism in patients with acute myocardial infarction.

Keywords: thallium-201 SPECT;  BMIPP SPECT;  FDG PET;  myocardial infarction;  redistribution     

Atrial fibrillation is associated with a lower exercise capacity in male chronic heart failure patients

Objective—To study the influence of atrial fibrillation on peak oxygen uptake (peak O₂) in chronic heart failure. An unfavourable effect of atrial fibrillation has been shown in several patient populations, but the results have not been consistent in chronic heart failure.
Methods—Data were analysed from male heart transplant candidates who were able to perform graded bicycle ergometry until exhaustion with respiratory gas analysis and measurement of heart rate. Patients in atrial fibrillation (n = 18) were compared with patients in sinus rhythm (n = 93).
Results—Age, weight, height, and aetiology of chronic heart failure did not differ significantly between the two groups. Cardiac catheterisation at supine rest showed that heart rate was comparable, but that stroke volume and cardiac output were lower (p < 0.05) in atrial fibrillation. Systolic and diastolic left ventricular function, assessed by radionuclide angiography at rest, were not significantly different. Peak O₂ (mean (SD): 13.8 (3.6) v 17.1 (5.6) ml/kg/min; p < 0.01) and peak work load (78 (27) v 98 (36) W; p < 0.05) were lower in the patients with atrial fibrillation, though respiratory gas exchange ratio and Borg score were similar in the two groups. Patients with atrial fibrillation had a higher heart rate sitting at rest before exercise (93 (16) v 84 (16) beats/min) and at peak effort (156 (23) v 140 (25) beats/min) (p < 0.05).
Conclusions—Atrial fibrillation is associated with a 20% lower peak O₂ in patients with chronic heart failure, suggesting that preserved atrial contraction or a regular rhythm, or both, are critical to maintain cardiac output and exercise performance.

Keywords: peak oxygen uptake;  exercise capacity;  chronic heart failure;  atrial fibrillation     

High factor VIII antigen levels increase the risk of venous thrombosis but are not associated with polymorphisms in the von Willebrand factor and factor VIII gene

High factor VIII levels increase the risk of venous thromboembolism, but the mechanisms that cause high factor VIII levels are unclear. In 301 thrombosis patients and 301 matched healthy controls, factor VIII antigen (VIII:Ag) levels > or = 150 IU/dl increased the thrombosis risk more than fivefold. We investigated whether high factor VIII:Ag levels result from a genetic variation in the factor VIII or von Willebrand factor (VWF) genes. Six polymorphisms in the VWF gene and two CA-repeats in the factor VIII gene were not associated with plasma VWF levels, factor VIII:Ag levels, or thrombosis risk. Our data do not support the hypothesis that a single functional sequence variation in the factor VIII or VWF gene explains the majority of high factor VIII levels and thrombotic risk.     

Heartstart Scotland: the use of paramedic skills in out of hospital resuscitation

Objective—To assess the frequency with which paramedic skills were used in out of hospital cardiac arrest and the effect of tracheal intubation on outcome.
Design—Retrospective analysis of ambulance service reports and hospital records.
Setting—Scottish Ambulance Service and hospitals admitting acute patients throughout Scotland.
Results—A total of 8651 out of hospital resuscitation attempts were recorded and tracheal intubation was attempted in 3427 (39.6%) arrests. One hundred and thirty six patients (3.7%) were intubated and 476 (9.1%) of the patients who were not intubated survived to hospital discharge (p < 0.001). Among the patients who were defibrillated the proportion intubated was highest in the patients who received the greatest number of shocks (p < 0.01). Among subjects receiving similar numbers of shocks survival rates were lower for intubated patients (p < 0.01). Patients with unwitnessed arrests were most frequently intubated and survival rates were lowest in this group.
Conclusions—Patients who are intubated seem to have lower survival rates. This may however reflect the difficulty of the resuscitation attempt rather than the effects of intubation. The use of basic life support skills rapidly after cardiac arrest is associated with the best survival rates.

Keywords: paramedics;  resuscitation;  myocardial infarction;  tracheal intubation;  prehospital care     

Change in ST segment elevation 60 minutes after thrombolytic initiation predicts clinical outcome as accurately as later electrocardiographic changes

Objective—To compare prospectively the prognostic accuracy of a 50% decrease in ST segment elevation on standard 12-lead electrocardiograms (ECGs) recorded at 60, 90, and 180 minutes after thrombolysis initiation in acute myocardial infarction.
Design—Consecutive sample prospective cohort study.
Setting—A single coronary care unit in the north of England.
Patients—190 consecutive patients receiving thrombolysis for first acute myocardial infarction.
Interventions—Thrombolysis at baseline.
Main outcome measures—Cardiac mortality and left ventricular size and function assessed 36 days later.
Results—Failure of ST segment elevation to resolve by 50% in the single lead of maximum ST elevation or the sum ST elevation of all infarct related ECG leads at each of the times studied was associated with a significantly higher mortality, larger left ventricular volume, and lower ejection fraction. There was some variation according to infarct site with only the 60 minute ECG predicting mortality after inferior myocardial infarction and only in anterior myocardial infarction was persistent ST elevation associated with worse left ventricular function. The analysis of the lead of maximum ST elevation at 60 minutes from thrombolysis performed as well as later ECGs in receiver operating characteristic curves for predicting clinical outcome.
Conclusion—The standard 12-lead ECG at 60 minutes predicts clinical outcome as accurately as later ECGs after thrombolysis for first acute myocardial infarction.

Keywords: myocardial infarction;  thrombolysis;  ST segment elevation     

Coronary event and case fatality rates in an English population: results of the Oxford myocardial infarction incidence study

Objectives—To determine coronary event and case fatality rates in an English population aged less than 80 years in Oxfordshire, and to compare these rates with those reported by the UK monitoring trends and determinants of cardiovascular disease (MONICA) centres in Scotland and Northern Ireland and those ascertained in Oxfordshire in 1966-67.
Design—A population wide surveillance study conducted in 1994-95 using prospective and retrospective case ascertainment.
Setting—A resident population in Oxfordshire of 568 800.
Subjects—Patients with suspected myocardial infarction or coronary death.
Outcome measures—A diagnosis of definite or possible myocardial infarction or coronary death using WHO MONICA diagnostic criteria based on symptoms, electrocardiograms, cardiac enzymes, necropsy findings, and past medical history.
Results—The annual rate for a first or recurrent coronary event per 100 000 population aged less than 65 years in 1994-95 was 273 for men and 66 for women after age adjustment to a standard world population. Rates in the age group 65-79 years were 1350 for men and 677 for women. Between 1966-67 and 1994-95, the age standardised event rate in the age group 30-69 years decreased significantly by 33% (95% confidence interval (CI) 44 to 21) in men, and there was a non-significant reduction of 8% (95% CI −33 to 17) in women. The age standardised 28 day case fatality rates also decreased significantly by 28% (95% CI 41 to 15) in men and by 32% (95% CI 55 to 9) in women.
Conclusions—The coronary event rate in Oxfordshire was much lower than rates reported by MONICA centres in Glasgow and Belfast, and similar to rates reported by MONICA centres in France and northern Italy. The substantially lower event rate accounts for lower coronary heart disease mortality in Oxfordshire than in Scotland and Northern Ireland. The reduced coronary mortality in this region is attributable to declines in coronary event and case fatality rates.

Keywords: myocardial infarction;  coronary heart disease;  incidence;  case fatality