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Dive into the research topics where Michael J. Brack is active.

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Featured researches published by Michael J. Brack.


The Lancet | 1995

Insertion/deletion polymorphism in the angiotensin-converting enzyme gene and risk of restenosis after coronary angioplasty.

Nilesh J. Samani; Michael J. Brack; James H. S. Cullen; D.P. de Bono; Anthony H. Gershlick; Daniel S. Martin; David Lodwick; J. D. Swales; Anoop Chauhan; Alex Harley

Early restenosis in over 30% of cases limits the benefits of percutaneous transluminal coronary angioplasty (PTCA). The mechanisms that underlie restenosis are uncertain, although experimental evidence suggests that the renin-angiotensin system is involved in the vascular response to angioplasty. An insertion(I)/deletion(D) polymorphism in the angiotensin-converting enzyme (ACE) gene, which influences plasma ACE level, has been associated with an increased risk of myocardial infarction in those with the DD genotype. To investigate whether this polymorphism influences the risk of restenosis after PTCA, 233 patients who underwent single-vessel angioplasty in the Subcutaneous Heparin and Angioplasty Restenosis Prevention (SHARP) study were genotyped for the I/D polymorphism and pre-PTCA, post-PTCA, and 4-month clinical and quantitative angiographic data were compared in the three genotype groups. The groups, (II 53, ID 117, and DD 63) were well matched for baseline clinical and both pre- and post-PTCA angiographic features. At 4-month follow-up there was no significant difference between the genotype groups with respect to any of the quantitative angiographic criteria of restenosis: minimal luminal diameter at the site of the angioplasty (DD 1.35 [SE 0.10] mm, ID/II 1.43 [0.05] mm, difference -0.08 [95% CI -0.30 to 0.14]), numbers of subjects with more than 50% diameter stenosis (DD 49%, ID/II 46%, relative risk 1.06 [0.79 to 1.43]), or the number of subjects with more than 50% loss of the acute diameter gain after PTCA (DD 54%, ID/II 43%, 1.26 [0.94 to 1.67]). Likewise, there was no difference in the number of subjects with angina or a positive exercise stress test. We conclude that, in patients undergoing elective PTCA, the I/D polymorphism in the ACE gene does not influence the extent of restenosis, and typing for the polymorphism will not be a useful predictor of risk before the procedure.


Atherosclerosis | 1996

Apolipoprotein E polymorphism does not predict risk of restenosis after coronary angioplasty

Nilesh J. Samani; Daniel S. Martin; Michael J. Brack; James H. S. Cullen; Robert Wallis; David Lodwick; Anoop Chauhan; Alex Harley; John R. Thompson; Anthony H. Gershlick; David de Bono

A recent report has suggested that the E4 allele of apolipoprotein (apo) E increases the risk of restenosis after percutaneous transluminal coronary angioplasty (PTCA) and also that it interacts synergistically with the deletion (D) allele of the angiotensin-converting enzyme (ACE) to increase the risk sixteen-fold. To investigate this further, we genotyped 231 subjects with successful PTCA who underwent planned repeat angiography at 4 months to assess the degree of restenosis. Subjects carrying the apo E4 allele (n = 71) were well matched with non-carriers (n = 160) for clinical and pre- and post-PTCA angiographic features. We found no increase in either apo E4 allele frequency (18.4% versus 15.6%, P = 0.42) or apo E4 homozygosity (2/106 versus 5/125, P = 0.30) in those with restenosis compared with those without. The relative risk of restenosis for apo E4 carriers was 1.11 (95% CI = 0.87-1.42). In apo E4 carriers, restenosis frequency was similar in those also carrying the ACE D allele and those without (28/55 (50.9%) versus 9/16 (56.2%), P = 0.71) and there was no significant increase in restenosis risk in carriers of both the apo E4 and ACE D alleles compared to the rest (odds ratio 1.30, 95% CI 0.68-2.50, P = 0.39). We conclude that in our cohort, the apo E4 allele does not either independently or acting synergistically with the ACE D allele increase the risk of restenosis after PTCA, and that apo E genotyping will not be a useful predictor of risk before the procedure.


American Heart Journal | 1994

ASSESSMENT OF MYOINTIMAL CELLULAR KINETICS IN A MODEL OF ANGIOPLASTY BY MEANS OF PROLIFERATING CELL NUCLEAR ANTIGEN EXPRESSION

Ranjit S. More; Guy N. Rutty; M J Underwood; Michael J. Brack; Anthony H. Gershlick

A detailed temporal assessment of cellular proliferation was carried out by means of immunostaining for proliferating cell nuclear antigen in a normolipemic rabbit model of balloon angioplasty to the iliac arteries. Assessment was made at 30 minutes, 2 hours, 1 day, 3 days, 7 days, 14 days, 1 month and 3 months after the procedure. Intimal hyperplasia was first noted at day 3; a prominent layer was formed by day 14. Cellular proliferation in the vessel media was observed as early as day 1 (percentage of positive-staining cells 0.5% +/- 0.2%), reaching a maximum by day 7 (16.9% +/- 5.1%) before returning to baseline levels by 1 month (0.2% +/- 0.02%); in the intima, cellular proliferation was first noted at day 7 (0.7% +/- 0.3%) and reached a maximum at day 14 (4.1% +/- 0.4%) before returning to baseline levels at 1 month (0.3% +/- 0.1%). Use of proliferating cell nuclear antigen expression in this model of angioplasty provided a simple and reproducible method of assessing cellular proliferation after vascular injury and may prove useful for monitoring the effects, in experimental models, of agents for reducing myointimal hyperplasia.


International Journal of Cardiology | 1994

Infected right atrial thrombi : a complication of central venous cannulation

I.R. Arnold; Michael J. Brack; P.K. Verma; A. McCance

Abstract We report three cases of infected right thrombi associated with central venous cannulae that required surgical removal to eradicate infection.


International Journal of Cardiology | 1993

Prothrombin fragment F1+2 concentrations for monitoring anticoagulation therapy with heparin

Michael J. Brack; Ranjit S. More; P.J.B. Hubner; Anthony H. Gershlick

We have compared the activated partial thromboplastin time with measurement of prothrombin fragment F1 + 2 concentrations (ELISA assay) during a 24-h period in a group of patients (n = 10) who had undergone elective coronary angioplasty and were anticoagulated post-procedure with heparin 1000 U/h. Four hours after the procedure all the patients were adequately anticoagulated according to activated partial thromboplastin time (median ratio 4.7:1) and the prothrombin fragment F1 + 2 concentration was significantly lower than pre-angioplasty values (0.5 vs 1.4 nmol/l, p = 0.04). At 24 h the median activated partial thromboplastin time ratio was still higher than the pre-procedure value (1.35 vs 0.9, p < 0.01), but the prothrombin fragment F1 + 2 concentration had risen to 2.1 nmol/l, with more variability in individual results within the patient group for the prothrombin fragment F1 + 2 concentration than for activated partial thromboplastin time (interquartile ranges (Q1, Q3) prothrombin fragment F1 + 2, 1.2-2.5; activated partial thromboplastin time, 1.2-1.5). The activated partial thromboplastin time is the standard method of monitoring the anticoagulant effect of heparin but may not fully reflect the functional coagulation status and accurately identify individual patients with less than adequate anticoagulation. Prothrombin fragment F1 + 2 concentrations may provide a more reliable indicator in individual patients of functional coagulation status in certain important situations where anticoagulation is critical such as following complicated coronary angioplasty.


International Journal of Cardiology | 1994

Monitoring anticoagulation following intracoronary procedures: which method?

Michael J. Brack; Ranjit S. More; L.N. Forbat; P.J.B. Hubner; Anthony H. Gershlick

We have assessed bedside kits for monitoring the activated partial thromboplastin time and the activated clotting time by comparing them with laboratory activated partial thromboplastin time values. To determine the accuracy of anticoagulation we have concurrently measured the plasma heparin concentrations, and plasma prothrombin fragment F1 + 2 concentrations. Serial samples were taken from patients undergoing elective percutaneous transluminal coronary angioplasty (n = 14). Readings were taken pre-procedure, 30 min after administration of a heparin bolus (10,000 U) and 1, 2 and 3 h after commencement of a constant heparin infusion (15 U/kg/h) postprocedure. Activated partial thromboplastin time results obtained with the bedside kit compared reliably with laboratory values (r = 0.8), were rapidly available and were reflected by appropriate changes in prothrombin fragment F1 + 2 and heparin concentrations. However, the relationship between activated partial thromboplastin time values and activated clotting time was less precise (r = 0.59). Therefore, for routine and frequent monitoring of anticoagulation with heparin, a bedside activated partial thromboplastin time kit provides adequate control of therapy but in instances were particularly tight control of anticoagulation is required, use of prothrombin fragment F1 + 2 concentrations may be more appropriate.


International Journal of Angiology | 1995

In vitro studies of a bispecific monoclonal antibody antithrombotic conjugate [ATC(3)]

Ranjit S. More; M J Underwood; Michael J. Brack; S. Pringle; David de Bono; Anthony H. Gershlick

We assessed whether chemical conjugation of a monoclonal antibody (M735) against platelet glycoprotein IIb/IIIa receptors to urokinase and to a monoclonal antibody which binds to damaged endothelium (P14G11) resulted in enhanced inhibition of platelet aggregation with maintenance of localizing features (to damaged endothelium). Conjugation of M735 (an IgM monoclonal antibody) to urokinase and P14G11 (an IgG2a monoclonal antibody) was carried out using SPDP [N-Succinimidyl-3-(2-pyridyldithio)-propionate] as the cross-linking reagent. The resulting triple conjugate [ATC(3)] had fibrinolytic activity and retained platelet and damaged endothelium localizing features. Enhanced inhibition of platelet aggregation (induced by either adenosine diphosphate (ADP), collagen, or thrombin) was observed compared with both an unconjugated mixture of the three individual components and to the M735-urokinase conjugate. We conclude that it is possible to produce a bimonoclonal antibody-urokinase agent which has both potent antiplatelet aggregatory effects and additional targeting or localizing features.


Thrombosis Research | 1993

Therapeutic levels of nitroglycerine do not affect the uptake and release of heparin by endothelial cells in vitro

Michael J. Brack; Ranjit S. More; E Spring; Anthony H. Gershlick

Intravenous heparin and nitroglycerin are frequently given in combination to patients with acute coronary syndromes such as unstable angina and post myocardial infarction angina. Heparin is prescribed since it has been shown that intracoronary thrombus formation is important in the pathophysiology of these acute conditions. However, it has been demonstrated that intravenous nitroglycerin can interfere with the anticoagulant effect of heparin. The exact mechanism of the interaction is unknown but it has been suggested that there is a direct effect on plasma heparin characterised by a reduction in circulating plasma heparin levels. Heparin binds to the surface of endothelial cells in a process that is time dependent, reversible and exhibits saturation kinetics. A possible mechanism of the observed effects on the plasma heparin levels produced by nitroglycerin may be the altered handling of heparin by endothelial cells. We have investigated this further by assessing the effects of therapeutic doses of nitroglycerin on heparin uptake and release by endothelial cells, using 35S labelled heparin and human umbilical vein endothelial cell cultures.


The Journal of Pathology | 1994

A time sequence of vessel wall changes in an experimental model of angioplasty

Ranjit S. More; Guy N. Rutty; M J Underwood; Michael J. Brack; Anthony H. Gershlick


International Journal of Cardiology | 1994

Plaque herniation through an intracoronary stent

Michael J. Brack; L.N. Forbat; J.D. Skehan; Anthony H. Gershlick

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S. Pringle

University of Leicester

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D.P. de Bono

University of Leicester

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Alex Harley

Blackpool Victoria Hospital

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