October 2002 Br J Cardiol 2002;9:501-3
The first reported combined heart and kidney transplant occurred in 1978.1 The patient died of gram negative sepsis 15 days after transplantation. It was not until 1986 that a case was reported with long-term (> 18-month) survival.2 Since that time, there have been more than 40 publications examining the pros and cons of simultaneous heart and kidney transplantation. Initial reports consisted mainly of small case series demonstrating proof of concept and adequate 1–3 year survival, mostly in line with that of heart transplantation alone.3-5 Later it was noted that simultaneous transplantation seemed to protect against rejection of the heart transplant (although different immunosuppressive protocols were frequently employed) and that rejection of one organ often occurred independently of immunological damage to the other.
September 2002 Br J Cardiol 2002;9:431-3
Melinda Swann, Adam Raman, Michael Kirchengast
Biotechnology and cardiovascular medicine – a hazy past and bright future? Melinda Swann, Adam Raman, Michael KirchengastFrom such successful beginnings, the biotechnology sector has since gone on to have a rather hazy past, for which there are many plausible explanations. In March 2000, the sector was grossly overvalued and, since then, investors’ aversion to the area has flourished due to the perceived risk they felt they were taking. This has led to the growth of many biotechnology companies being stunted since access to capital has become more difficult – studies, especially long-term survival trials in cardiovascular medicine.
September 2002 Br J Cardiol (Acute Interv Cardiol) 2002;9(1):AIC 11
Within the last year we have witnessed the advent of public scrutiny of the results of surgical coronary revascularisation. The methodology em-ployed in order to achieve this scrutiny was flawed, as was the way the inadequate and incomplete results were presented to the general public. Data were presented without careful critical appraisal of what the figures actually meant. Little or no account was taken of context, risk assessment or case mix. This was either because of ignorance upon the part of those involved in publication or because of an inadequate level of concern for accuracy. In either case it was irresponsible. Inevitably, to make matters worse, any attempt to explain the fallibility of the presented figures and the flaws in their interpretation has lead to the charge of having something to hide.
September 2002 Br J Cardiol (Acute Interv Cardiol) 2002;9(1):AIC 19
Tryfonidis, Prendergast and Curzen present their findings of work designed to answer the very pertinent question “Are waiting times for coronary artery bypass grafting (CABG) longer than they should be?”. This question requires some reflection before we review the authors’ work and comments.
September 2002 Br J Cardiol (Acute Interv Cardiol) 2002;9(1):AIC 32
Annalise Geldenhuys, Tony Mourant, Trevor Johnston, John Glynn
This report describes a 48-year-old woman with Parkinson”s disease who developed coronary artery dissection. We believe that dissection in this patient was probably caused by treatment with the anti-Parkinsonian drug pergolide.
August 2002 Br J Cardiol 2002;9:
BJCardio editorial team
The Impact of Nicorandil in Angina (IONA) study A report from a British Cardiac Society Satellite Symposium, 2002 Angina pectoris is not a benign disease: it is associated with significant morbidity and mortality and it affects more than 10% of men over the age of 60 years.
July 2002 Br J Cardiol 2002;9:377
I am delighted that The British Journal of Cardiology is to become an official journal of the British Hypertension Society (BHS) information service. The BHS information service was developed to provide doctors and other health care professionals with information about hypertension. This includes details of current clinical management guidelines, recommended blood pressure monitoring devices and succinct summaries of management issues pertaining to specific clinical scenarios.
July 2002 Br J Cardiol 2002;9:373-6
Gareth J Morgan-Hughes, Carl A Roobottom, Andrew J Marshall
Concerning atherosclerosis imaging and coronary calcium concentrates predominantly on electron beam computed tomography (EBCT).1 Non-invasive coronary artery imaging can take the form of coronary artery calcium assessment or coronary angiography. Imaging can be performed with EBCT, or since 2001, with the latest generation of helical (‘spiral’) CT scanners (known as ‘multislice’ CT scanners in view of simultaneous acquisition of four image ‘slices’). There are major differences between EBCT and multi-slice helical CT. Whereas with helical CT the patient is continually advanced through a rapid mechanically rotating gantry (X-ray source and detector array), EBCT relies on X-rays produced with an electronically steered electron beam.
June 2002 Br J Cardiol 2002;9:
BJCardio editorial team
Taking vascular disease beyond convention Using the full lipid profile to identify and reduce the risk of coronary heart disease Lipid levels: risks and targets Prioritisation of high-risk coronary heart disease patients for statin intervention Key guideline cholesterol targets and full lipid profiling Scientific summary Introduction S1 Lipid levels: risks and targets S2 Prioritisation of high-risk coronary heart disease patients for statin intervention S3 Section 1: Key guideline cholesterol targets and full lipid profiling S4 Section 2: Scientific summary S5 Section 3: Patient identification S7 Section 4: Management strategies S9 Section 5: Practical use of clinical laboratories S10 Section 6: Tools for full lipid profiling and risk status calculation S11 Conclusion S11 Acknowledgements S12 Appendix 1: HDL, the metabolic syndrome and CHD risk S12 Appendix 2: Joint British societies coronary risk prediction charts S14 References S15 Patient identification Management strategies Practical use of clinical laboratories Tools for full lipid profiling and risk status calculation HDL, the metabolic syndrome and CHD risk.
June 2002 Br J Cardiol 2002;9:313-6
Jamil Mayet, Rebecca Lane
Left ventricular hypertrophy (LVH) is more than just an adaptive response to the increase in left ventricular wall stress caused by hypertension. It has long been known that it is an indicator of a poor prognosis: the increased risk associated with LVH is independent of the blood pressure level.