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Volume 9, Number 4, April 2002


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EDITORIALStatins: myalgia and myositis
Anthony S Wierzbicki

Br J Cardiol 2002;9:193-194.

EDITORIALThe quest for diagnostic certainty: an unreal expectation in a real world
Paul Collinson, Peter Stubbs

Br J Cardiol 2002;9:195-197.

PRIMARY CAREWhat’s new in hypertension
Is it time to forget about diastolic blood pressure? Should we abandon the mercury sphygmomanometer? Is non-pharmacological intervention a waste of time? These were some of the questions discussed at the first Primary Care Cardiovascular Society (PCCS) meeting of 2002 which was carried out jointly with the British Hypertension Society (BHS) on 26th February. The meeting – chaired by Professors Bryan Williams (Leicester Royal Infirmary) and Richard Hobbs (University of Birmingham) – focused on practical advice and trial evidence. Ola Soyinka reports.

Br J Cardiol 2002;9:233-240.

REVIEWAcute effects of low-dose statins on serum cholesterol and creatinine kinase activity
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.

Br J Cardiol 2002;9:209-214.

REVIEWFuture perspectives in stroke management
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.

Br J Cardiol 2002;9:215-220.

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REVIEWCardiac troponins and the risk stratification of chest pain
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.

Br J Cardiol 2002;9:221-222.

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REVIEWPatent foramen ovale, a normal variant or a congenital abnormality requiring treatment?
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.

Br J Cardiol 2002;9:223-225.

REVIEWFive thousand echocardiograms: what have we done?
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.

Br J Cardiol 2002;9:226-229.

REVIEWCan we do more to get patients to cholesterol targets?
Richard Hobbs

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.

Br J Cardiol 2002;9:241-244.

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CASE REPORTCan left bundle branch block cause chest pain?
Mammen Ninan, Jonathan W Swan

Br J Cardiol 2002;9:230-232.