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Biomedical subjects

G Jackson

Publications and source records attributed to G Jackson.

At least 127 records · Page 7Linked to original sources
PubMed1999

The place of metabolic agents in the management of stable angina pectoris.

The treatment of stable angina should aim to relieve symptoms and in at-risk cases prolong life. Medical therapy, PTCA and CABG should be seen as complementary, not competitive, strategies. Optimal utilization of all three treatment modalities either alone or in combination can provide substantial and sustained symptomatic relief for angina patients. Metabolic agents such as Trimetazidine by acting at the cellular level and not influencing heart rate or blood pressure have a useful and unique role to play in addition to conventional haemodynamic agents such as the betablockers or calcium antagonists. This review looks at the role of trimetazidine as part of the overall management of the stable angina patient.

Angina Pectoris↗
PubMed1999

A systematic approach to erectile dysfunction in the cardiovascular patient: a consensus statement.

Sexual activity is no more stressful to the heart when compared with a number of other natural daily activities, e.g. walking one mile on the level in 20 minutes. The cardiac risk of sexual activity in patients diagnosed with cardiovascular disease is minimal in properly assessed and advised patients. Erectile dysfunction (ED) is common, affecting 10% of men aged 40-70 years and increases in frequency with age. ED and cardiovascular disease share many of the same risk factors and often coexist. ED in the diagnosed cardiovascular patient should be identified by routine questioning in general practice. Modern therapies can restore a sexual relationship in the majority of patients with ED and can lead to a substantial improvement in quality of life. The majority of patients assessed to be at low or intermediate cardiac risk, as defined later in this paper (Table 4), can be effectively managed in primary care. Primary care treatment for ED in patients defined as high risk can be initiated following a specialist opinion and/or confirmation that the patient's cardiovascular condition is stabilised. There is no evidence that currently licensed treatments for ED add to the overall cardiovascular risk in patients with or without diagnosed cardiovascular disease.

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↗
PubMed1998

Cytokine gene polymorphisms associating with severe acute graft-versus-host disease in HLA-identical sibling transplants.

It is now well known that the initial phase of graft-versus-host disease (GVHD) involves cytokine release during preconditioning of the recipient of an allogeneic bone marrow transplant (BMT). Tumor necrosis factor (TNF), in particular, has been implicated in pathological damage and is released pretransplant due to irradiation and cytotoxic preconditioning regimens. Interleukin-10 (IL-10), a natural immunosuppressant of TNF, may be involved in downregulation of these responses, which may be an individual patient-specific effect. In this study, we determined the genotype for polymorphisms associated with TNF and IL-10 in 80 potential allo-BMT recipients and correlated the genotype with the severity of GVHD in 49 patients for whom clinical data relating to GVHD was available. The widely studied TNF -308 polymorphism does not show any significant associations, but the d3 homozygous allele of the TNFd microsatellite is preferentially associated with grade III/IV GVHD (7 of 11 patients) compared with its occurrence in 8 of 38 patients with grade 0/II GVHD (P =.006). Alleles of the IL-10 (-)1064 promoter region microsatellite polymorphism that possess greater numbers of dinucleotide (CA) repeats also significantly associate with more severe GVHD. This region has been demonstrated to be important in the regulation of the IL-10 promoter. Eighteen of 38 patients with grade 0-II GVHD possessed alleles with greater numbers (12 or more) of dinucleotide repeats, compared with 9 of 11 cases with grade III-IV GVHD (P <.02). Of the 38 patients with grade 0-II GVHD, 3 of 38 had a both TNFd3/d3 and IL-10 (12-15) genotype, compared with 6 of 11 patients with grade III-IV GVHD (P <.001). There was no association of either the TNFd or IL-10 microsatellite polymorphisms with mortality (P =.43 and.51, respectively). Our results suggest that patient cytokine gene polymorphism genotypes may influence GVHD outcome by affecting cytokine activation during the pretransplant conditioning regimens, and these results are the first to suggest a genetic predisposition to this important transplant-related complication.

Acute Disease↗
PubMed1998

Predicting graft-versus-host disease in HLA-identical bone marrow transplant: a comparison of T-cell frequency analysis and a human skin explant model.

BACKGROUND: Graft-versus-host disease (GVHD) occurring after HLA-identical sibling bone marrow transplantation (BMT) is considered to be mainly caused by minor histocompatibility antigen (mHag) disparities between the recipient and donor. In our laboratory, a human skin explant model has been successfully used to predict acute GVHD in HLA-identical sibling BMT. More recently, the frequency analysis of host-reactive helper and cytotoxic T lymphocyte precursors (HTLp and CTLp, respectively) has been shown to have potential application for predicting GVHD. In the present study, HTLp and CTLp frequency analysis and the skin explant model were directly compared for their ability to predict acute GVHD in HLA-identical sibling BMT. METHODS: Host-reactive HTLp and CTLp frequencies were determined using a combined limiting dilution assay. A human skin explant model was used to detect graft-versus-host reactions in vitro. The results from the skin explant model (graft-versus-host reaction grades I-IV) and T cell frequency analysis (>/< 1:100,000) were correlated with posttransplant GVHD outcome, respectively. RESULTS: The skin explant model correctly predicted GVHD outcome in 77% of cases (P=0.03). HTLp frequencies were very low in all patient/donor pairs tested. None of them exceeded 1:100,000, although 9/18 recipients developed GVHD (> or =clinical grade II) after transplant. In all patients tested, the relationship between either high (>1:100,000) or low (<1:100,000) CTLp frequency and occurrence of GVHD appeared to be random (P=1.0). CONCLUSIONS: HTLp and CTLp frequency analysis did not predict the occurrence of acute GVHD after HLA-identical sibling BMT. The human skin explant model, however, remained an accurate indicator of acute GVHD and probably detects mHag disparities.

Acute Disease↗
PubMed1998

p53 induces angiogenesis-restricted dormancy in a mouse fibrosarcoma.

The p53 tumor-suppressor gene is inactivated in over 50% of all human cancers. In normal cells, p53 induces growth arrest and apoptosis in response to DNA damage. We show that p53 acts as potent tumor-suppressor gene independent of its well-documented effects on tumor-cell proliferation and apoptosis. p53 activates target genes in a murine fibrosarcoma cell-line but does not affect tumor cell-cycle progression or survival. Exogenous expression of wt-p53 does, however, block the angiogenic potential of the tumor cells resulting in formation of dormant tumors in vivo. These data provide evidence that: (1) p53 acts as a tumor suppressor gene independent of its anti-proliferative effects; (2) By inhibiting angiogenesis p53 can indirectly induce apoptosis in vivo but not in vitro; (3) p53-gene therapy which alters a tumors angiogenic potential, can revert tumors to a dormant phenotype.

Animals↗
PubMed1998

Bail-out stenting of the unprotected left main stem.

Two cases of life-threatening left main stem (LMS) complications during routine cardiac catheterization were successfully treated with intracoronary stenting prior to successful emergency bypass surgery. Intracoronary stenting is of value in stabilising patients before emergency bypass surgery and can save lives in LMS complications.

Aged↗
PubMed1998

A lipid hypothesis: prediction, observation and the triglyceride/HDL gap.

Lowering serum lipid levels prevents myocardial infarctions. But are we targeting the right lipoproteins in our preventive therapy? Are we getting the maximum benefit? Triglycerides certainly deserve more attention than they have yet received. Most of the trials of lipid-lowering therapy have ignored them and this omission may explain the divergence between the fall in morbidity predicted from the epidemiological evidence and the reductions observed in the clinical trials. The evidence that the statins reduce coronary morbidity and mortality, and that this reduction is associated with a fall in LDL cholesterol, is overwhelming. But the potential value of the statins may be limited by their relative inability to increase the concentration of cardioprotective HDL. The fibrates, either alone, or in combination with a statin, retain a central role in the management of patients with mixed hyperlipidaemia who are undoubtedly at high risk of premature coronary artery disease.

Anticholesteremic Agents↗
PubMed1997

Haemodynamic changes during dobutamine stress echocardiography in patients with and without ischaemia.

We studied haemodynamic changes during dobutamine stress echocardiography in 69 patients (mean age 58 years, 6 female, 63 male) referred for investigation of chest pain. We used a standard protocol of 3 min stages using infusion rates of 5, 10, 20, 30 and 40 micrograms/kg/min. Heart rate rose from 74 (13) to 123 (21) beats per min with the major increment occurring during the high dose phase of the study (> 20 micrograms/kg/min). Stroke volume was calculated as the product of left ventricular outflow tract cross-sectional area and the velocity integral of the continuous wave aortic signal. Mean stroke volume increased from 67.5 (22) ml pre-test to 82 (22) ml at 20 micrograms/kg/min dose (P < 0.0001) and 85 (21) ml at 40 micrograms/kg/min (P < 0.00001). Only 15 patients (26%) reached their maximal stroke volume by 10 micrograms/kg/min, 38 patients (65%) reached maximal stroke volume by 20 micrograms/kg/min. Patients with ischaemic responses tended to have a blunted rise in stroke volume from 67 (22) ml to 85 (22) ml at maximum compared with a rise from 69 (23) to 92 (19) ml in those without ischaemic (P = 0.09). In conclusion, the early rise in cardiac output during dobutamine stress was mainly due to a rise in stroke volume and the later due to an increase in heart rate. Individual increases in stroke volume did not adequately differentiate between ischaemic and non-ischaemic results.

Adult↗