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Biomedical subjects

M Marber

Publications and source records attributed to M Marber.

11 recordsLinked to original sources
PubMed2005

Does a well developed collateral circulation predispose to restenosis after percutaneous coronary intervention? An intravascular ultrasound study.

OBJECTIVE: To evaluate whether a well developed collateral circulation predisposes to restenosis after percutaneous coronary intervention (PCI). DESIGN: Prospective observational study. PATIENTS AND SETTING: 58 patients undergoing elective single vessel PCI in a tertiary referral interventional cardiac unit in the UK. METHODS: Collateral flow index (CFI) was calculated as (Pw-Pv)/(Pa-Pv), where Pa, Pw, and Pv are aortic, coronary wedge, and right atrial pressures during maximum hyperaemia. Collateral supply was considered poor (CFI < 0.25) or good (CFI > or = 0.25). MAIN OUTCOME MEASURES: In-stent restenosis six months after PCI, classified as neointimal volume > or = 25% stent volume on intravascular ultrasound (IVUS), or minimum lumen area < or = 50% stent area on IVUS, or minimum lumen diameter < or = 50% reference vessel diameter on quantitative coronary angiography. RESULTS: Patients with good collaterals had more severe coronary stenoses at baseline (90 (11)% v 75 (16)%, p < 0.001). Restenosis rates were similar in poor and good collateral groups (35% v 43%, p = 0.76 for diameter restenosis, 27% v 45%, p = 0.34 for area restenosis, and 23% v 24%, p = 0.84 for volumetric restenosis). CFI was not correlated with diameter, area, or volumetric restenosis (r2 < 0.1 for each). By multivariate analysis, stent diameter, stent length, > 10% residual stenosis, and smoking history were predictive of restenosis. CONCLUSION: A well developed collateral circulation does not predict an increased risk of restenosis after PCI.

Angioplasty, Balloon, Coronary↗
PubMed2005

The immune responses to human and microbial heat shock proteins in periodontal disease with and without coronary heart disease.

The human 60 kDa and microbial 65 kDa heat shock proteins (HSP) have been implicated in the pathogenesis of chronic periodontitis (P) and coronary heart disease (CHD). We have studied four male non-smoking cohorts of 81 subjects, matched for age. Group (a) consisted of a healthy group with minimal gingivitis (n = 18), group (b) were patients with P (n = 23), group (c) patients with CHD and minimal gingivitis (n = 20) and group (d) patients with CHD and P (n = 20). T cells separated from peripheral blood were found to be primed to both microbial HSP65 and human HSP60 but significant CD4, human leucocyte antigen (HLA) class II-restricted proliferative responses were found only with the human HSP60 in patients with P (P < 0.001) and CHD without (P < 0.001) or with (P < 0.00001) periodontitis. Dose-dependent inhibition of T cell proliferative responses was carried out to determine the receptors involved in recognition of HSP60 and HSP65. Monoclonal antibodies to CD14 showed inhibition of T cell proliferation stimulated by both HSP60 and HSP65, consistent with the role of CD14 as a receptor for these HSPs in P and CHD. The toll-like receptor 2 (TLR-) and TLR-4 were then studied and these showed that TLR-4 was recognized by microbial HSP65, whereas TLR-2 was recognised by human HSP60 in both P and CHD. However, a dissociation was found in the HSP60 and TLR4 interaction, as TLR4 appeared to have been recognized by HSP60 in P but not in CHD. The results suggest an autoimmune or cross-reactive CD4(+) class II-restricted T cell response to the human HSP60 in P and CHD. Further studies are required to determine if there is a common epitope within HSP60 that stimulates T cell proliferation in P and CHD.

Adult↗
PubMed1999

Glycoprotein IIb/IIIa antagonists: do they have a role in the management of unstable angina?

Plaque rupture, platelet aggregation and thrombosis have central roles in the pathogenesis of acute coronary syndromes. Despite several trials showing the benefit of aspirin and heparin in patients presenting with unstable angina and acute myocardial infarction, these patients are still at risk. This has prompted the development and evaluation of several new therapeutic agents including low molecular weight heparin, new antiplatelet drugs (e.g. ticlopidine and clopidogrel), direct thrombin inhibitors, and intravenous and oral glycoprotein IIb/IIIa antagonists. The IIb/IIIa receptor is the final common pathway involved in platelet aggregation. Thus, whatever the stimulus for platelet activation, subsequent aggregation is mediated by the IIb/IIIa receptor binding fibrinogen. A variety of antibody, peptide and non-peptide compounds that block the IIb/IIIa receptor have been developed, and several studies have investigated the role of these agents in patients with acute coronary syndromes both within and outside the setting of percutaneous intervention. This article summarises the studies to date using IIb/IIIa antagonists, and discusses their role in patients with non-ST segment elevation acute coronary syndromes.

Angina, Unstable↗
PubMed1991

Delay to invasive investigation and revascularisation for coronary heart disease in south west Thames region: a two tier system?

OBJECTIVES: To assess the accessibility of invasive investigation and revascularisation procedures in the management of coronary heart disease in a defined population in the South West Thames region over 10 years, and to audit the performance of both the NHS and the private sector. DESIGN: Analysis of all patient referrals to the regional cardiothoracic centres for coronary heart disease during 1979-88. SETTING: North West Surrey District Health Authority, which had a mean catchment population of 205,000 during the study period. The health district is one of the 13 in the South West Thames region. PATIENTS: 823 patients aged 34-80 years with suspected coronary heart disease, 204 of whom were referred for private investigation and 619 were referred within the NHS. The NHS referrals were mainly to St Thomas's Hospital during 1979-83 and to St George's Hospital during 1984-8. MAIN OUTCOME MEASURES: Difference in time to investigation and intervention between the NHS and the private patients. RESULTS: After some variation in earlier years the mean (SD, range) waiting times from referral to cardiac catheterisation and then revascularisation increased progressively in NHS patients, to 115.8 (126.5, 22-482) days and 305.9 (164.4, 22-620) days respectively in 1988. There was no significant change over the 10 years in waiting times within the private sector, with a mean of 17.2 (18.2, 1-62) days to angiography and 22.8 (14.5, 2-152) days to surgery. Fifteen people on the NHS waiting list died of probable cardiac causes. No people on the private waiting list died. CONCLUSIONS: The performance of the NHS system in South West Thames region in response to emergency referral is adequate. The waiting time to routine investigation and revascularisation is prolonged and seems to be worsening despite increased investigative and surgical activity by the regional centre. The delays may subject NHS patients to unnecessary risk, which is not shared by private patients.

Adult↗