PubMed Health⌕ Search

Biomedical subjects

K Barakat

Publications and source records attributed to K Barakat.

At least 19 recordsLinked to original sources
PubMed2006

Phase transitions of methane using molecular dynamics simulations.

Using a short ranged Lennard-Jones interaction and a long ranged electrostatic potential, CH4 under high pressure was modeled. Molecular dynamics simulations on small clusters (108 and 256 molecules) were used to explore the phase diagram. Regarding phase transitions at different temperatures, our numerical findings are consistent with experimental results to a great degree. In addition, the hysteresis effect is displayed in our results.

Journal Article↗
PubMed2003

Bangladeshi patients present with non-classic features of acute myocardial infarction and are treated less aggressively in east London, UK.

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. PARTICIPANTS: 263 white and 108 Bangladeshi patients admitted with Q wave AMI. MAIN OUTCOME MEASURE: Character of presenting symptoms, their interpretation by the patient, and the provision of emergency treatment. RESULTS: There were no significant differences between Bangladeshi and white patients in the time from pain onset to hospital arrival (arrival time 64.5 (117.5) minutes v 63.0 (140.3) minutes, p = 0.63), but once in hospital it took almost twice as long for Bangladeshi as for white patients to receive thrombolysis (median (interquartile range) door to needle time 42.5 (78.0) minutes v 26.0 (47.7) minutes, p = 0.012). Bangladeshis were significantly less likely than whites to complain of central chest pain (odds ratio (OR) 0.11, 95% confidence interval (CI) 0.03 to 0.38; p = 0.0006) or to offer classic descriptions of the character of the pain (OR 0.25, 95% CI 0.09 to 0.74; p = 0.0118). These differences persisted after adjustment for age, sex, and risk factor profile differences including diabetes. Proportions of Bangladeshi and whites interpreting their symptoms as "heart attack" were similar (45.2% v 46.9%; p = 0.99). CONCLUSIONS: Bangladeshi patients with AMI often present with atypical symptoms, which may lead to slower triage in the casualty department and delay in essential treatment. This needs recognition by emergency staff if mortality rates in this high risk group are to be reduced.

Age Distribution↗
PubMed2001

Interaction between smoking and the glycoprotein IIIa P1(A2) polymorphism in non-ST-elevation acute coronary syndromes.

OBJECTIVES: The goal of this study was to determine the interaction between smoking and the glycoprotein IIIa P1(A2) polymorphism in patients admitted with non-ST-elevation acute coronary syndromes (ACS). BACKGROUND: An increased incidence of the P1(A2) polymorphism in smokers presenting with ST-elevation acute myocardial infarction (AMI) has recently been reported. We, therefore, postulated that, as a consequence of this interaction, fewer smokers with the P1(A2) polymorphism would present with non-ST-elevation ACS. METHODS: We performed a prospective cohort analysis of 220 white Caucasoid patients admitted with non-ST-elevation ACS fulfilling Braunwald class IIIb criteria for unstable angina who were stratified by smoking status. RESULTS: There were twice as many nonsmokers as smokers. Nonsmokers compared with smokers were older (mean [SD]; 63.9 [11.2] vs. 57.6 [10.3]; p < 0.0001), more likely to have had a previous admission with unstable angina (24.3% vs. 13.2%; p = 0.051) and AMI (45.8% vs. 30.3%; p < 0.026), more likely to have undergone revascularization (24.3% vs. 1.8%; p = 0.028) and were more likely to be on aspirin on admission (60.4% vs. 44.7%; p = 0.026). The proportion of nonsmokers positive for the P1(A2) polymorphism was equivalent to that expected for this population but was significantly reduced in smokers (28.7% vs. 10%; Pearson chi-square = 9.09, p = 0.0026). In a logistic regression model, the odds ratio (OR) for being positive for the P1(A2) polymorphism was significantly reduced by smoking (OR [interquartile range]: 0.26 [0.11 to 0.62]; p = 0.0026). CONCLUSIONS: There is a significant reduction in the P1(A2) polymorphism in smokers admitted with non-ST-elevation ACS compared with nonsmokers, which suggests an interaction between smoking and this polymorphism.

Acute Disease↗
PubMed2001

Screening for carotid artery disease before cardiac surgery: is current clinical practice evidence based?

BACKGROUND: There is no clear consensus as to the correct screening procedure to identify patients undergoing cardiac surgery and who are at greatest risk of stroke because of the presence of significant carotid artery stenosis. Such screening is important because some patients benefit from combined carotid and cardiac surgery and, regardless of this, the information gained puts the cardiac surgeon in a position to provide an accurate assessment of surgical risk. Our objective was to examine current clinical practice of carotid artery investigation prior to urgent cardiac surgery and to review this illustrative practice in the context of the world literature. HYPOTHESIS: The study aimed to establish that current typical practice for screening cardiac surgical patients for carotid artery disease is illogical according to the evidence in the world literature. METHODS: The study consisted of a retrospective assessment of all patients undergoing urgent cardiac surgery and a Medline-derived literature review, and included all patients undergoing urgent cardiac surgery at a tertiary cardiothoracic center between January 1 and December 31, 1997. RESULTS: Of 529 patients undergoing urgent cardiac surgery, 44 (8%) were screened preoperatively by duplex Doppler ultrasonography for carotid disease. The indications for screening were asymptomatic carotid bruit in 24 patients, history of stroke or transient ischemic attack (TIA) in 12 patients, and neither stroke, TIA, or bruit in 7 patients. The tests were requested either by the attending cardiologists or by the cardiac surgeon to whom they were referred. One patient had already been diagnosed as having carotid artery disease in the past. Thirteen patients underwent additional carotid investigations. Eleven patients were demonstrated to have internal carotid artery stenosis > or = 60% and 3 patients underwent combined cardiac and carotid surgery. Review of the literature revealed the following groups to be at increased risk of future stroke unrelated to surgery, and of postoperative stroke: those with a history of stroke or TIA, those with carotid bruits, and, of importance, all patients with significant carotid stenosis. Recent data suggest that symptomatic patients and the elderly are at greatest risk. CONCLUSIONS: Only 8% of patients undergoing urgent cardiac surgery in a 1-year period were screened for carotid artery disease. We suggest that screening should definitely be performed in all patients with a history of stroke or TIA, all patients with a bruit, and all patients aged > 65 years. The literature suggests, however, that significant reductions in stroke rate could be achieved by screening the whole cardiac surgical population, although there is a paucity of data that are specifically pertinent to this patient subgroup. Further data are therefore required for the construction of a scientifically valid and medicolegally sound policy.

Cardiac Surgical Procedures↗
PubMed2001

Angiotensin-converting enzyme inhibition is associated with reduced troponin release in non-ST-elevation acute coronary syndromes.

OBJECTIVES: This study was done to determine the effects of angiotensin-converting enzyme (ACE) inhibition and other clinical factors on troponin release in non-ST-elevation acute coronary syndrome (ACS). BACKGROUND: Troponin is now widely used as a marker of risk in ACS, but determinants of its release have not been defined. METHODS: This was a prospective cohort study of 301 consecutive patients admitted with non-ST-elevation ACS. Baseline clinical data were recorded, ACE gene polymorphism was determined and serial blood samples were obtained for troponin-I assay. RESULTS: Significant troponin-I release (>0.1 microg/l) was detected in 93 (31%) patients. Pretreatment with ACE inhibitors, recorded in 53 patients (17.6%), independently reduced the odds of troponin-I release (odds ratio 0.25; 95% confidence intervals 0.10 to 0.64) and was associated with lower maximum troponin-I concentrations (median [interquartile range]) compared with patients not pretreated with ACE inhibitors (0.44 microg/l [0.19 to 2.65 microg/l] vs. 4.18 microg/l [0.91 to 12.41 microg/l], p = 0.01). Pretreatment with aspirin, recorded in 173 patients (57.5%), did not significantly reduce the odds of troponin-I release after adjustment but was associated with lower maximum troponin-I concentrations compared with patients not pretreated with aspirin (2.31 microg/l [0.72 to 8.02 microg/l] vs. 5.85 microg/l [1.19 to 12.79 microg/l], p = 0.05). The ACE genotyping (n = 268) showed 81 patients (30%) DD homozygous and 77 (29%) II homozygous. There was no association between ACE genotype and troponin release. CONCLUSIONS: We conclude that ACE inhibition reduces troponin release in non-ST-elevation ACS. This is likely to be mediated by the beneficial effects of treatment on vascular reactivity and the coagulation system.

Aged↗
PubMed2001

Genetic susceptibility to macrovascular complications of type 2 diabetes mellitus.

Patients with type 2 diabetes mellitus have a threefold increased risk of developing macrovascular disease such that 75% of such patients will die of cardiovascular complications. This increased risk is, however, not completely explained by traditional risk factors such as smoking, hypercholesterolaemia, hypertension and glycaemic control. Moreover, the fact that not all patients with type 2 diabetes develop these complications, together with evidence of family clustering (a heritability of 50%), suggests that a proportion of the susceptibility to ischaemic heart disease in type 2 diabetes may be genetic. Unravelling the polygenic susceptibility factors for the complications of a disease that itself has multifactorial inheritance has proved difficult and has focused largely on the candidate gene approach. A review of some of the studies testing candidate genes specifically in patients with both type 2 diabetes and ischaemic heart disease is presented. These studies focus largely on four main areas: lipoprotein metabolism, glycation and oxidation pathways, haemostatic cascade, and other candidate genes.

Diabetes Mellitus, Type 2↗
PubMed2001

Socioeconomic differentials in recurrent ischaemia and mortality after acute myocardial infarction.

OBJECTIVE: To examine the influence of socioeconomic deprivation on case fatality following acute myocardial infarction. DESIGN: Prospective cohort observational study. SETTING: General hospital. PATIENTS: 1417 white and south Asian patients admitted with acute myocardial infarction between January 1988 and December 1996, and classified by the Carstairs socioeconomic deprivation score of the enumeration district of residence. MAIN OUTCOME MEASURES: 30 day and one year survival. RESULTS: There was little variation across deprivation groups in age, sex, or smoking status, though a higher proportion of patients from more deprived enumeration districts were diabetic and of south Asian origin, and a higher proportion of them developed Q wave infarction and left ventricular failure. There was no appreciable variation in clinical treatment with deprivation. Patients from more deprived enumeration districts had a higher risk of recurrent ischaemic events (death, recurrent myocardial infarction, or unstable angina) over the first 30 days: event free survival (95% confidence interval (CI)) of the most deprived quartile was 0.79 (95% CI 0.74 to 0.83) compared with 0.85 (95% CI 0.80 to 0.88) in the least deprived quartile. The unadjusted hazard ratio corresponding to an increase from the 5th to 95th centile of the deprivation distribution was 1.54 (95% CI 1.02 to 2.32), and 1.59 (95% CI 1.03 to 2.44) after adjustment for age, sex, racial group, diabetes, acute treatment with thrombolysis and aspirin, and left ventricular failure. Survival from 30 days to one year, however, did not show a socioeconomic gradient (hazard ratio adjusted for the same variables was 1.07 (95% CI 0.68 to 1.70)). CONCLUSIONS: In patients hospitalised with acute myocardial infarction, there is a strong association between early recurrent ischaemic events and socioeconomic deprivation that is not accounted for by clinical presentation or treatment. This association appears to be attenuated over time.

Adult↗
PubMed2001

Changing face of acute myocardial infarction in east London: a prospective cohort study of trends in management and outcome in the reperfusion era.

AIMS: To define the trends in management and outcome of acute myocardial infarction over the first decade since the widespread adoption of thrombolytic therapy. METHODS: Prospective cohort study of 1737 consecutive patients with acute myocardial infarction admitted for coronary care between January 1988 and December 1997. RESULTS: Trend analysis with comparison of early (1988-1992) and late (1993-1997) cohorts showed significant increments in median age (interquartile range) from 62 (54-70) to 64 (55-72) years (P < 0.01) but the proportion of smokers fell from 72.7% to 65.8% (P < 0.01). The proportion of patients receiving thrombolytic therapy increased from 70% to 78.1% (P < 0.01) as median door-to-needle times fell significantly from 92 (60-145) to 68 (45-123) minutes (P < 0.01). The proportion of patients discharged on aspirin increased from 88.2% to 95.9% (P < 0.01), -blockers increased from 37.4% to 45.8% (P < 0.01), and angiotensin converting enzyme inhibitors increased from 12.4% to 35.7% (P < 0.01). Median hospital stay fell from 9 (7-11) to 6 (5-9) days (P < 0.0001). Although the severity of infarction declined, judged by reductions in the frequency of Q-wave development from 78.1% to 73.9% (P = 0.01) and peak CK from 1250 (569-2085) to 1004 (511-1722) IU/l, survival (95% confidence intervals) for the early and late cohorts did not change significantly either at 30 days [0.86 (0.83-0.88) vs. 0.85 (0.83-0.88)] or at 1 year [0.79 (0.76-0.81) vs 0.78 (0.76-0.81)]. CONCLUSION: The decade from 1988-1997 saw significant changes in the demographic characteristics and risk factor profiles of patients with acute myocardial infarction admitted for coronary care. We observed trends towards increasingly aggressive antithrombotic treatment and early discharge policies, with more patients being prescribed drugs for secondary prevention. The combined effects of these complex changes on the outcome of infarction defy simple analysis and there was no palpable change in short- and longer-term.

Aged↗
PubMed2000

Determination of brain and plasma drug concentrations by liquid chromatography/tandem mass spectrometry.

A method is described for the evaluation of drug concentrations in plasma and brain from treated rats. The analyte is recovered from plasma or brain homogenate by liquid-liquid extraction and subsequently analyzed by liquid chromatography/tandem mass spectrometry (LC/MS/MS). A simple experimental protocol renders the procedure valuable for obtaining information rapidly on brain penetration and plasma exposure of specific classes of compounds. This methodology has been applied to evaluate brain penetration with 30 different compounds from the same discovery program. In an attempt to increase throughput in our screening efforts, mixture dosing was evaluated. Results from single compound administration were compared with results following administration of a mixture of four compounds. Preliminary results, with specific classes of compounds, show no major differences (ranking order) in brain or plasma concentrations between mixture dosing and single compound administration, suggesting that mixture dosing could be applicable to brain penetration studies in the drug discovery phase.

Animals↗
PubMed2000

Acute myocardial infarction in women: contribution of treatment variables to adverse outcome.

BACKGROUND: Women have excessive mortality rates after acute myocardial infarction compared with men. The extent to which this increased risk can be attributed to differences in treatment is not well-understood. METHODS: This was an observational follow-up study of 1737 patients admitted with acute myocardial infarction for coronary care between January 1, 1988, and December 31, 1997. RESULTS: Compared with men, women took longer to arrive at the hospital (132.5 minutes [range 76 to 291 minutes] vs 120 minutes [range 60 to 240 minutes]; P =.006), were less likely to receive aspirin acutely (87.8% vs 91.3%; P =.03), had longer door-to-needle times (90 minutes [range 60 to 143.5 minutes] vs 78 minutes [range 50 to 131 minutes]; P =.004), and were less likely to be given beta-blockers at hospital discharge (31.6% vs 44.9%; P <.0001). Estimated survival (95% confidence interval [CI]) at 30 days was only 78.4% (range 74.4% to 81.9%) for women compared with 88.0% (range 86.1% to 89.7%) for men. Women were older and more often white, but their excess risk (hazard ratio 2.09; 95% CI, 1.59-2.75) persisted after adjustment for age, racial group, and diabetes (hazard ratio 1.52; 95% CI, 1.15-2.01). Additional adjustment for emergency thrombolytic and aspirin therapy caused a further small reduction in the excess risk for women (hazard ratio 1.46; 95% CI, 1. 09-1.98), but with adjustment for aspirin and beta-blockers prescribed at discharge, the excess risk attributable to being female disappeared as the hazard ratio fell to 0.75 (95% CI, 0.31-1. 84). Estimated 30-day survival free of reinfarction and unstable angina was also lower for women than for men (75% [range 71% to 79%] vs 86% [range 84% to 88%]); again, the excess risk for women persisted despite adjustment for age and racial group before disappearing as treatment variables were introduced into the model. The influence of treatment variables on the differential risks for women and men disappeared at 12 months. CONCLUSIONS: This study has shown that women with acute myocardial infarction arrived later at the hospital, were less likely to be given aspirin therapy acutely, had longer door-to-needle times, and, on discharge from the hospital, were less likely to be prescribed beta-blockers for secondary prevention. The data suggest that the failure to treat women as vigorously as men made a significant contribution to their worse outcome.

Adrenergic beta-Antagonists↗
PubMed2000

Permanent transfemoral pacemaker implantation is the technique of choice for patients in whom the superior vena cava is inaccessible.

We describe transfemoral pacemaker implantation in three patients in whom pacing via the superior vena cava was not possible or suboptimal. The first was an 88-year-old man with superior vena cava obstruction presenting with fractured epicardial pacing leads. Recent pneumonia increased the risks of a general anesthetic. The second patient was a 57-year-old man who was intolerant of a pectorally sited pacemaker because of the thinness of his anterior chest wall. The third patient was a 69-year-old woman who presented with an infected eroding pectorally sited pacemaker. Scarring secondary to a previous pacemaker infection rendered the contralateral pectoral site inaccessible. Since the subclavian route was inaccessible (case 1) or suboptimal (case 2 and 3), we implanted transvenous pacemakers via the femoral route, which was safe, and effective, during a 6-month follow-up period.

Aged↗
PubMed2000

Influence of previous aspirin treatment and smoking on the electrocardiographic manifestations of injury in acute myocardial infarction.

OBJECTIVE: To examine demographic and clinical characteristics of patients with acute myocardial infarction in order to identify factors affecting the electrocardiographic evolution of injury. METHODS: Prospective 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. RESULTS: Smoking 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. CONCLUSIONS: The 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.

Aged↗
PubMed2000

Transvenous pacing lead-induced thrombosis: a series of cases with a review of the literature.

Although transvenous pacing is a safe treatment modality for bradyarrhythmias, serious thrombotic and embolic complications are reported to occur in 0.6-3.5% of cases. We describe 5 cases of pacemaker-associated thrombosis, 3 with a superior vena cava syndrome (SVC), 1 with an axillary vein thrombosis and 1 with a thrombus attached to the pacing lead in the right atrium. All of the patients were initially treated with intravenous heparin which proved successful as the sole treatment in only the least severe case (axillary vein thrombosis). One of the patients with SVC obstruction was successfully treated with intravenous heparin followed by thrombolytic therapy. The remaining 3 cases (2 SVC syndromes and 1 right atrial thrombus) required surgical removal of thrombus and pacing leads. Both of the patients with evidence of infection were in the group for whom failure of medical therapy necessitated surgery.

Adult↗
PubMed1999

How should age affect management of acute myocardial infarction? A prospective cohort study.

BACKGROUND: About 75% of patients with acute myocardial infarction are older than 70 years, but patients in this age group are commonly treated less vigorously than younger patients. This differential treatment may partly reflect clinicians' misconceptions about the outlook of such patients, and the importance of age in clinical decisions. We examined how age does and should affect the management of patients and risk stratification in acute myocardial infarction. METHODS: In this prospective cohort study, we recruited 1225 consecutive patients admitted with acute myocardial infarction to a district general hospital in east London. The primary endpoint was death. We used tabulation and regression methods to analyse the association between age group and clinical variables. FINDINGS: Patients aged 70 years or older took a longer time to arrive in hospital and were less likely to receive thrombolysis or discharge beta-blockers than patients younger than 60 years: odds ratio 0.63 (95% CI 9.45-0.88) for thrombolysis and 0.25 (0.16-0.37) for beta-blockade, adjusted for sex, diabetes, previous acute myocardial infarction, Q wave infarction, and left-ventricular failure. Left-ventricular failure was the strongest independent predictor of death within 1 year of infarction with a hazard ratio of 4.76 (3.53-6.43), adjusted for age, sex, diabetes, and Q wave infarction. Patients aged 70 years or older without left-ventricular failure had significantly better survival at 1 year after acute myocardial infarction than patients under 60 years with left-ventricular failure. 70.8% (62.2-78.2) of the older patients who survived to hospital discharge were still alive 3 years later. INTERPRETATION: Elderly patients with acute myocardial infarction were treated less vigorously than younger patients. The prognosis of acute myocardial infarction, however, was substantially affected by the development of left-ventricular failure and other clinical indices, such that many older patients had a better outlook than younger patients with adverse clinical factors. In planning risk-based management, consideration of age independently of clinical status is inappropriate.

Adrenergic beta-Antagonists↗
PubMed1999

Platelet IIb/IIIa antagonists followed by delayed stent implantation. A new treatment for vein graft lesions containing massive thrombus.

The percutaneous treatment of saphenous vein graft lesions containing angiographically massive thrombus is associated with a high risk of distal embolisation and no-reflow. The optimal management for these lesions remains unclear and a challenge to the interventional cardiologist. Five cases are described in whom the risks of percutaneous angioplasty were felt to be excessive owing to a high thrombus load. Each case was treated with a bolus and infusion of abciximab (ReoPro; Eli Lilly-a platelet glycoprotein IIb/IIIa receptor antagonist) at least 24 hours before further angiography. Repeat angiography of the culprit vein graft, following treatment with abciximab alone, demonstrated a major reduction in the thrombus score and the presence of TIMI 3 flow in each case. Immediately following repeat angiography, angioplasty with stent insertion was performed successfully with no distal embolisation or no-reflow phenomenon. This staged approach, with abciximab used alone to reduce thrombus load, is a new treatment for vein graft lesions containing massive thrombus.

Abciximab↗
PubMed1998

Tripeptide growth hormone secretagogues.

A series of C-terminus capped dipeptides and tripeptides was synthesized as growth hormone (GH) secretagogues. Among them, tripeptide Aib-D-Trp-D-homoPhe-OEt showed low nanomolar activity in the rat pituitary assay. Thus, we have demonstrated that the GH secretagogue activity of the hexa-hepta-GH releasing peptides can be mimicked at the tripeptide level.

Amino Acid Sequence↗