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Dive into the research topics where Bradley Marchant is active.

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Featured researches published by Bradley Marchant.


Heart | 1993

Circadian and seasonal factors in the pathogenesis of acute myocardial infarction: the influence of environmental temperature.

Bradley Marchant; Kulasegaram Ranjadayalan; Robert Stevenson; Paul Wilkinson; A. D. Timmis

OBJECTIVE--To determine the circadian and seasonal variations in the incidence of acute myocardial infarction and the influence of environmental temperature. PATIENTS--633 consecutive patients with acute myocardial infarction admitted to a coronary care unit over four years. SETTING--Coronary care unit in a district general hospital. DESIGN--An observational study. RESULTS--The onset of acute myocardial infarction had a circadian rhythm with a peak in the second quarter of the day. A seasonal variation was also found with a significant winter peak. There was, however, an excess of infarctions on colder days in both winter and summer indicating that the effect of environmental temperature on the onset of acute myocardial infarction is independent of the time of year. CONCLUSION--Acute myocardial infarction is more common in winter and more common on colder days, independent of season. Environmental temperature may play an important part in the pathogenesis of acute myocardial infarction.


American Journal of Cardiology | 1994

Relation between heart rate variability early after acute myocardial infarction and long-term mortality

Sudhir Vaishnav; Robert Stevenson; Bradley Marchant; K. Lagi; Kulasegaram Ranjadayalan; Adam Timmis

The relation between both time and frequency domain analyses of RR variability and mortality was examined in a series of 226 consecutive patients with acute myocardial infarction admitted to 3 district hospitals in London. All patients underwent 24-hour Holter monitoring early after infarction (mean 83 hours, range 48 to 180), and time and frequency domain analyses of RR variability were performed using commercially available software. During an 8-month follow-up period (range 3 to 12 months), there were 19 cardiac deaths (8.4%). Time domain analysis confirmed reduced RR variability (SDRR, SDANN, SD) among nonsurvivors compared with survivors. However, there was no difference between the groups when the percentage of absolute differences between successive RR intervals > 50 ms (pNN50) and the root-mean-square of successive differences (RMSSD)--vagal measures of RR variability--were analyzed. Frequency domain analysis demonstrated a significant difference between those who died and the survivors when the low-frequency component--modulated by both vagal and sympathetic mechanisms--was analyzed; however, this was less marked when the high-frequency component--modulated by vagal activity--was analyzed. None of these measures of RR variability was related to infarct site or left ventricular ejection fraction. In conclusion, the data confirm the association between low RR variability and mortality after acute myocardial infarction. However, the mechanism does not appear to relate exclusively to decreased parasympathetic tone. The data suggest that the increased risk of early mortality associated with reduced RR variability reflects an imbalance in sympathovagal function that is unrelated to left ventricular function.


Journal of the American College of Cardiology | 1993

Silent myocardial ischemia: role of subclinical neuropathy in patients with and without diabetes.

Bradley Marchant; Velaithan Umachandran; Robert Stevenson; Peter G. Kopelman; Adam Timmis

OBJECTIVES Silent myocardial ischemia is common in patients with diabetes. This study was designed to assess the role of subclinical autonomic impairment in diabetic patients with silent ischemia. BACKGROUND Studies have suggested that silent ischemia is more common in diabetic patients with microvascular complications, but this has not been a consistent finding. METHODS Twenty-two diabetic and 30 nondiabetic patients with proved coronary artery disease and a history of angina and ischemia on treadmill stress testing underwent clinical tests of autonomic function and measurement of 24-h heart rate variability. Diabetic patients with a history of microvascular complications were excluded. RESULTS Although all 52 patients manifested ischemia during treadmill testing, only 36 patients experienced angina (angina group), whereas 16 did not (silent ischemia group). Diabetic and nondiabetic patients were similar in age (59 +/- 1 vs. 61 +/- 2 years, p = 0.56) and extent of coronary artery disease. However, clinical tests showed reduced parasympathetic function in the diabetic patients (Valsalva ratio 1.38 +/- 0.07 vs. 1.60 +/- 0.06; p = 0.007). Patients in the silent ischemia group were more often diabetic (33% vs. 63%, p = 0.05) and had prolonged time to ischemia on treadmill testing (200 +/- 20 vs. 271 +/- 20 s, p = 0.03). In addition, autonomic function was impaired in the silent group (supine/standing heart rate ratio 1.15 +/- 0.02 vs. 1.05 +/- 0.02, p = 0.002). Subgroup analysis showed that abnormalities of autonomic function were confined to the diabetic patients in the silent group. CONCLUSIONS Despite the absence of overt microvascular complications, diabetic patients with silent exertional ischemia have evidence of significant autonomic impairment compared with findings in symptomatic patients. This difference is not seen in nondiabetic patients and indicates that subclinical neuropathy is an important cause of silent ischemia in patients with diabetes.


BMJ | 1996

Comparison of case fatality in south Asian and white patients after acute myocardial infarction: observational study

Paul Wilkinson; Jeremy Sayer; Koorithottumkal Laji; Christopher Grundy; Bradley Marchant; Peter Kopelman; Adam Timmis

Abstract Objective: To compare mortality in south Asian (Indian, Pakistani, and Bangladeshi) and white patients in the six months after hospital admission for acute myocardial infarction. Design: Observational study. Setting: District general hospital in east London. Patients: 149 south Asian and 313 white patients aged <65 years admitted to the coronary care unit with acute myocardial infarction from 1 December 1988 to 31 December 1992. Main outcome measure: All cause mortality in the first six months after myocardial infarction. Results: The admission rate in the south Asians was estimated to be 2.04 times that in the white patients. Most aspects of treatment were similar in the two groups, except that a higher proportion of the south Asians received thrombolytic drugs (81.2% v 73.8%). After adjustment for age, sex, previous myocardial infarction, and treatment with thrombolysis or aspirin, or both, the south Asians had a poorer survival over the six months from myocardial infarction (hazard ratio 2.02 (95% confidence interval 1.14 to 3.56), P=0.018), but a substantially higher proportion were diabetic (38% v 11%, P<0.001), and additional adjustment for diabetes removed much of their excess risk (adjusted hazard ratio 1.26 (0.68 to 2.33), P=0.47). Conclusion: South Asian patients had a higher risk of admission with myocardial infarction and a higher risk of death over the ensuing six months than the white patients. The higher case fatality among the south Asians, largely attributable to diabetes, may contribute to the increased risk of death from coronary heart disease in south Asians living in Britain. Key messages This study shows that south Asians have high mortality in the first six months after a heart attack This may contribute to the high standardised mortality ratios for coronary disease in south Asians living in the Britain Diabetes may be an important contributor to this excess risk The high prevalence of diabetes and relatively poor prognosis after myocardial infarction in south Asian patients are important to consider in clinical management


Heart | 1997

Attenuation or absence of circadian and seasonal rhythms of acute myocardial infarction.

Jeremy Sayer; Paul Wilkinson; K Ranjadayalan; S. Ray; Bradley Marchant; A. D. Timmis

OBJECTIVES: To 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 SETTING: Prospective, observational study in a general hospital. PATIENTS AND METHODS: 1225 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. RESULTS: A 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 beta 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 beta blockers or aspirin on admission. CONCLUSIONS: The absence of circadian and seasonal rhythms of acute myocardial infarction in almost identical subgroups suggests that common mechanisms are involved in driving these rhythms. The autonomic nervous system is a likely candidate because the rhythms were absent in patients taking beta blockers as well as in patients in whom derangement of autonomic function commonly occurs.


Heart | 1993

Reassessment of treadmill stress testing for risk stratification in patients with acute myocardial infarction treated by thrombolysis.

Robert Stevenson; Velaitham Umachandran; Kulasegaram Ranjadayalan; Paul Wilkinson; Bradley Marchant; A. D. Timmis

OBJECTIVES--To evaluate the role of a treadmill stress test for identifying patients at risk of recurrent ischaemic events after acute myocardial infarction treated by thrombolysis. BACKGROUND--The natural history of myocardial infarction has changed with the introduction of thrombolytic treatment; there is a lower mortality but a higher incidence of recurrent thrombotic events (reinfarction, unstable angina). The treadmill stress continues to be recommended for risk stratification after acute myocardial infarction even though its value has never been formally reassessed in the thrombolytic era. METHODS--Prospective observational study in which 256 consecutive patients who presented with acute myocardial infarction treated by thrombolysis underwent an early treadmill stress test and were followed up for 10 (range 6-12) months. RESULTS--Recurrent ischaemic events occurred in 41 patients (unstable angina 15, reinfarction 21, death five) and a further 21 required revascularisation. Both ST depression at a low workload and low exercise tolerance (< 7 metabolic equivalents of the task (METS) were predictive of recurrent events, with respective hazard ratios of 1.93 (95% confidence interval (95% CI) 1.17-3.20; p < 0.01)) and 1.67 (95% CI 1.0-2.78; p < 0.05). These variables identified 50% and 70% of patients who subsequently sustained a recurrent ischaemic event, but the corresponding values for positive predictive accuracy were only 26% and 21%. Thus they are of limited value as a screening measure for identifying patients likely to benefit from invasive investigation and revascularisation. None of the other variables (ST elevation, haemodynamic responses, ventricular extrasystoles, angina) was significantly associated with recurrent ischaemic events. CONCLUSIONS--The treadmill stress test is of limited value for identifying patients at risk of recurrent ischaemic events after acute myocardial infarction treated by thrombolysis.


Journal of the American College of Cardiology | 1991

Irregular coronary lesion morphology after thrombolysis predicts early clinical instability

Simon W. Davies; Bradley Marchant; John P. Lyons; Adam Timmis; Martin T. Rothman; C Layton; R Balcon

After successful thrombolytic treatment for acute myocardial infarction, recurrent ischemia and infarction may occur with little warning. Coronary lesion morphology was analyzed from angiograms performed in 72 consecutive patients at 1 to 8 days after streptokinase treatment for acute myocardial infarction and the data were evaluated in relation to the subsequent clinical course. All patients were clinically stable at the time of angiography and continued to receive heparin infusion for greater than or equal to 4 days after thrombolysis. The infarct-related artery was patent in 55 patients (76%). In the 10 days after angiography, 15 patients developed prolonged episodes of angina at rest; the condition of 4 stabilized with medical treatment, but 11 required urgent medical intervention (coronary angioplasty in 8 and bypass surgery in 3). There were no differences in age, gender, left ventricular function or extent of coronary artery disease between those patients who developed unstable angina and those who had a stable in-hospital course. However, the median plaque ulceration index of the infarct-related lesion was 6.7 (95% confidence limits 6.3, 10) in the 15 patients with an unstable course versus 3.3 (2, 4.4) in those with a stable course (p less than 0.001). There were no differences between the two patient groups in the severity of stenosis, length of diseased segment, symmetry/eccentricity, presence of a shoulder, location at branch point or bend, presence of globular or linear filling defects, contrast staining or collateral supply. These data show that after thrombolysis, the degree of irregularity of the infarct-related artery is a critical determinant of early clinical instability.(ABSTRACT TRUNCATED AT 250 WORDS)


Journal of the American College of Cardiology | 1990

Coronary lesion morphology in acute myocardial infarction: Demonstration of early remodeling after streptokinase treatment

Simon W. Davies; Bradley Marchant; John P. Lyons; Adam Timmis; Martin T. Rothman; C Layton; R Balcon

Coronary lesion morphology was analyzed in 72 patients 1 to 8 days after streptokinase treatment for acute myocardial infarction and compared with lesion morphology in a control group of 24 patients with stable angina. In the streptokinase group the infarct-related artery was patent in 55 patients (76%). Compared with stenoses in the stable angina group, there were no differences in the stenosis length, severity, calcification or in the proportion located at an acute bend or at a branch point. However, lesions in the streptokinase group were more often irregular (p less than 0.005) and eccentric (p less than 0.01), had a shoulder (p less than 0.0001), globular filling defects (p less than 0.01), linear filling defects (p less than 0.00005) and contrast staining (p less than 0.05). Plaque ulceration index was higher in the streptokinase than in the stable angina group (6.2 +/- 7.9 versus 3.5 +/- 3.4, p less than 0.001). Of the 72 streptokinase-treated patients, 35 were maintained on heparin infusion until angioplasty 2 to 10 days later. At repeat angiography before angioplasty, globular lesion filling defects seen in eight patients had disappeared, whereas linear filling defects persisted in 7 of 14 cases. Fewer lesions were irregular (p less than 0.0001) and the ulceration index decreased from 7.4 +/- 10.4 to 3.0 +/- 1.6 (p less than 0.001). These data show that the lesion in the infarct-related artery after streptokinase treatment is irregular and often associated with filling defects, perhaps corresponding to plaque fissuring and intraluminal thrombosis.(ABSTRACT TRUNCATED AT 250 WORDS)


Journal of the American College of Cardiology | 1994

Mechanisms of cold intolerances in patients with angina

Bradley Marchant; Gavin C. Donaldson; Khurshid Mridha; Matthew Scarborough; Adam Timmis

Abstract Objectives. Patients with angina often report that symptoms are worse in cold weather, This study was designed to determine differences between cold-tolerant and cold-intolerant patients in the hemodynamic and ichemic response to exercise at cold temperature and to assess the role of catechlomines and baroreceptor function. Background. Studies have suggested that the heart rate response may differ at cold temperatures, but the mechanism and role of this variation have not been examined. Methods. Seven cold-intolerant and seven cold-tolerant patients with angina underwent exercise treadmill testing at 6 and 25 °C wtth measurement of catecholamines. Baroreceptor function was assessed by the decrease in systolic blood pressure after patients stood up from the supine position. Results. Norepinephrine levels increased by 139% in the cold environment, but there were no differences between cold-intolerant and cold-tolerant patients. Consequently, blood pressure was higher in the cold environment in all patients, but the heart rate was similar. However, cold-intolerant patients had a steeper heart rate response in the cold and developed ischemia (mean [±SEM] 201 ± 58 vs. 242 ± 50 s, p = 0.05) and (348 ± 87 vs. 449 ± 60 s, p = 0.04) earlier in the cold environment, a difference not seen in the cold-tolerant patients Baroreceptor function was impaired in cold-intolerant patients. (decrease in systolic blood presure after patients stood up from the supine position 19 ± 7 vs. 0 ± 4 mm Hg, p = 0.04). Conclusions. Exposure to cold causes an increase in blood pressure with an associated increase in myocardial oxygen demand in all patients. In cold-tolerant patients, this increase may be offset by a reduction in heart rate if baroreceptor function is normal. If baroceptor function is abnormal, heart rate may not decrease in response to a cold-induced increased in pressure. This mechanisms may account for some of the variability in tolerance to cold exposure that affects patients with exertional angina.


American Heart Journal | 1991

The perception of angina in diabetes : relation to somatic pain threshold and autonomic function

Velaitham Umachandran; Kulasegaram Ranjadayalan; Gamini Ambepityia; Bradley Marchant; Peter G. Kopelman; Adam Timmis

Silent ischemia is common in diabetic patients with coronary heart disease. These patients may also have more subtle alteration in the perception of angina as reflected by prolongation of anginal perceptual threshold--the time from onset of 0.1 mV ST segment depression to the onset of chest pain during treadmill exercise. Silent ischemia may be associated with a generalized hyposensitivity to pain, although the pathophysiologic mechanism is obscure. The purpose of the present study was to determine whether diabetic patients with prolonged anginal perceptual thresholds are also hyposensitive to painful stimuli and to investigate whether this is associated with autonomic neuropathy. Nineteen diabetic and 25 nondiabetic patients with exertional angina were exercised on a treadmill to measure anginal perceptual threshold. Somatic pain threshold was measured by calf sphygmomanometry. The cuff was inflated rapidly until pain occurred, and six repeat inflations were done to test reproducibility. Because there was no significant difference between measurements (coefficient of variation = 0.156) the mean value for each patient provided a measure of somatic pain threshold. The diabetic group had a longer anginal perceptual threshold (138 +/- 64 seconds vs 34 +/- 51 seconds, p less than 0.001), which correlated positively with the somatic pain threshold (r = 0.5, p = 0.03); patients with more prolonged anginal perceptual thresholds tended to have higher somatic pain thresholds. In the diabetic group anginal perceptual (r = -0.3, p = NS) and somatic pain (r = -0.4, p = 0.05) thresholds tended to increase as the ratio of peak to minimal heart rate during the Valsalva maneuver fell below 1.21, but these variables were unrelated in the nondiabetic group.(ABSTRACT TRUNCATED AT 250 WORDS)

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Adam Timmis

Queen Mary University of London

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Marek Malik

Imperial College London

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Lars Køber

Copenhagen University Hospital

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