April 2002 Br J Cardiol 2002;9:
There is an enormous gap between the publication of new evidence and its clinical implementations. Research on interventions that are designed to change professionals’ clinical behaviour is detailed here: specific generic interventions, interventions specific to cardiovascular medicine, and continuing medical education. Barriers to change include information problems, stress and inertia. Further research and evaluation are required.
April 2002 Br J Cardiol 2002;9:
The National Service Framework for Coronary Heart Disease emphasises the role of primary care in secondary prevention. More than 20% of men and 12% of women aged 65 years and over suffer from ischaemic heart disease. Lifestyle changes and drug treatment may effectively reduce risk but uptake of the evidence base is patchy. There are a number of possible approaches to enhance the uptake. Nurse-led clinics and health promotion clinics can lead to improvement in reported lifestyle and self-reported health status. Audit and feedback may lead to more use of appropriate drugs. Systematic recall will lead to better documentation that care conforms to standard practice, and nurses are at least as effective as doctors in achieving this. The first step is to set up accurate morbidity registers.
April 2002 Br J Cardiol 2002;9:
An integrated effort is needed to provide seamless care for patients between hospital and general practice. The use of protocols that are common to both sectors will lead to the best possible outcomes. It seems that secondary prevention may reduce sudden death and the 28-day mortality rate. The evidence base for the drugs used in secondary prevention is derived mostly from hospital trials. The relevant findings for aspirin, beta blockade, statins, ACE inhibitors and oral anticoagulants are discussed. After coronary revascularisation, special care is required if patients are to have a smooth path: both exercise and comprehensive cardiac rehabilitation are valuable.
April 2002 Br J Cardiol 2002;9:241-4
The role of cholesterol lowering in reducing cardiovascular risk is well established but a large proportion of qualifying patients at the highest risk are still not getting treatment with statins. Of those that do, most are not achieving recommended cholesterol targets. The cost of this, in terms of death and work days lost, is enormous. Patients should not be discharged after an acute event until secondary prevention has been initiated. Individual patient response to therapy should be subsequently monitored and adjusted as appropriate; patients should be reassured on statin safety.
April 2002 Br J Cardiol 2002;9:230-2
Mammen Ninan, Jonathan W Swan
Can left bundle branch block cause chest pain? Mammen Ninan, Jonathan W Swan Exercise-induced left bundle branch block usually indicates underlying coronary artery disease or myocardial disease. Association of left bundle branch block (LBBB) with chest pain in the absence of coronary artery disease is rare. We describe the case history of a patient with chest pain associated with left bundle branch block with normal coronary arteries and review the literature on left bundle branch block associated with chest pain.
April 2002 Br J Cardiol 2002;9:226-9
David J Bell, David A Sandler
This article describes the use of transthoracic echocardiography (TTE) in a series of 5,000 consecutive echocardiograms in a mid-sized UK district general hospital. The report highlights the basic demographics, reasons for the requests, yield of abnormal results and sources of the requests. The authors comment on the percentage of abnormal results for the different request categories and on how TTE can be best utilised as a cardiac investigation.
April 2002 Br J Cardiol 2002;9:223-5
Mark S Turner, Anthony P Salmon, Gareth Thomas, Andrew J Marshall
It has now become possible to close a patent foramen ovale (PFO) using a percutaneous device. In addition, it has become increasingly clear that right-to-left shunting through a PFO can cause both stroke and decompression illness, due to paradoxical embolism of blood clots or gas bubbles. For these reasons, diagnosis of large PFO with significant right-to-left shunts has become important. The diagnosis can be made by transthoracic echocardiography with injection of bubble contrast, combined with multiple sustained Valsalva manoeuvres. Whilst transoesophageal echocardiography provides detailed anatomical information, functional information (with regard to right-to-left shunting) is better provided by transthoracic studies where a Valsalva can be properly performed. Device closure can prevent right-to-left shunting and can be achieved using a number of different devices. However, device closure has yet to be proven beneficial in a randomised trial. In light of the clear evidence implicating PFO, we undertake closure procedures in selected patients.
April 2002 Br J Cardiol 2002;9:221-2
Archana Rao, Mandie Evans
We present three cases of patients who had chest pain with abnormal but non-diagnostic ECGs and negative troponin I, carried out in the appropriate time frame. All three went on to have extensive coronary artery disease demonstrated on coronary angiogram. These cases illustrate that use of troponin I alone as a marker for risk stratification of cardiac chest pain is not adequate: above all, a high index of clinical suspicion is of paramount importance.
April 2002 Br J Cardiol 2002;9:215-20
Philip MW Bath
Clinical research relating to stroke management is at something of a watershed. On the one hand, some therapies are well proven and established, and on the other some approaches have repeatedly failed. Examples of successes include antithrombotic (aspirin, dipyridamole, clopidogrel, warfarin) and antihypertensive therapies (diuretic, angiotensin-converting enzyme inhibitors), carotid endarterectomy for secondary prevention,1-4 and aspirin in acute ischaemic stroke.5 In contrast, several strategies have repeatedly failed, especially the use of anticoagulation and neuroprotection in acute ischaemic stroke. This review gazes into the crystal ball to see what we might be doing when managing patients with stroke in 10 years time.
April 2002 Br J Cardiol 2002;9:209-14
Yohan P Samarasinghe, Graham Ball, Michael D Feher
One of the potential side effects of the HMG CoA reductase inhibitors (statins) is a rise in creatinine kinase (CK) activity. This is sometimes accompanied by myalgia and rarely by rhabdomyolysis. Statins are increasingly being started earlier in the presentation of acute coronary syndromes but the rise in CK activity that they may cause could be a potential confounding factor in the diagnosis of myocardial infarction (MI) in this population. In this open-labelled, prospective study, 12 hypercholesterolaemic, Caucasian subjects, with a significant cardiovascular risk, were commenced on low-dose statin therapy. Blood samples were taken prior to commencing the statin then on day three and seven for lipid profile and CK activity. Patients maintained their normal lifestyles and usual medication. Interviews were conducted at each visit. A consistent fall in total and low density lipoprotein (LDL) cholesterol levels was shown over the study period of one week. Apart from one participant, who had a CK rise on day three with accompanying myalgia, there was no consistent change in CK activity within the group. High density lipoprotein (HDL) cholesterol levels also did not show any significant change over the week. We conclude that the rapid and consistent fall in both total and LDL cholesterol levels with low-dose statin was not paralleled by any consistent change in CK activity. The lack of change in CK activity over one week, following acute initiation of statin therapy, is unlikely to cause difficulty in the diagnosis of MI. If the beneficial effects of statin therapy are due to cholesterol reduction, then acute initiation in coronary syndromes would be favourable.