Volume 9, Number 8, September 2002
EDITORIALBiotechnology and cardiovascular medicine – a hazy past and bright future?
Melinda Swann, Adam Raman, Michael Kirchengast Br J Cardiol 2002;9:431-433. HOT
TOPICPRIMARY CAREGP use of beta blockers in heart failure
General practitioner Mike Mead gives a step-by-step guide on how to treat heart failure in primary care, including how to start patients on beta blockers. This article explains how general practitioners can diagnose and treat heart failure in primary care. Diagnosis is difficult and four diagnostic tests – the electrocardiogram, chest x-ray, blood test for natriuretic peptides and echocardiography – are recommended as being of particular value in confirming the diagnosis in primary care.
A six-step treatment strategy is then given advising i) confirming the diagnosis, ii) excluding other treatable causes of heart failure, iii) giving general advice to the patient, iv) starting treatment with a diuretic, v) then adding an angiotensin-converting enzyme inhibitor, and, vi) finally adding a beta blocker. A 10-point plan explaining in detail how to start beta blockers in primary care concludes the article. Br J Cardiol 2002;9:481-487. PRIMARY CAREWaiting for a bypass: a comment from primary care
Peter Stott
Br J Cardiol 2002;9:491-492. HOT
TOPICPRIMARY CARESecondary prevention in patients awaiting CABG in the North West of England
This study looks at how well cardiovascular risk factors were being controlled in a high-risk group of patients awaiting coronary artery bypass surgery. It shows significant short falls in the implementation of currently advocated strategies. Recent guidelines emphasise the importance of cholesterol, blood pressure and diabetes control in the progression of coronary artery disease. In this study, the implementation of therapies to control such cardiovascular risk factors was assessed in patients with established coronary artery disease awaiting coronary artery bypass surgery. Some 15% of patients continued to smoke and a significant proportion of patients did not achieve target levels for total cholesterol, low density lipoprotein and blood pressure control. Amongst the diabetic patients, 88% demonstrated a HbA1C above 7%. Br J Cardiol 2002;9:488-490. HOT
TOPICREVIEWHypertrophic cardiomyopathy: from gene to bedside
Sami Firoozi, Julia Rahman, William J McKenna Hypertrophic cardiomyopathy (HCM) is the commonest inherited cardiovascular disorder with a prevalence of one in 500 in the general population. It is believed to be a disease of the cardiac sarcomere and is caused by a variety of mutations in genes responsible for sarcomeric contractile proteins. It is characterised macroscopically by myocardial hypertrophy and microscopically by myocyte fibrosis and disarray.
Most patients tend to present with functional limitation and symptoms such as palpitation, chest pain or syncope. The underlying mechanisms involved are complex, multiple and not yet fully understood. Further clarification of these mechanisms may enable improvements in current symptom control or the development of new avenues of therapy.
A small but significant proportion of patients suffer sudden cardiac death and this can be the initial presentation of the condition. In fact, HCM is the commonest cause of sudden death among individuals below the age of 30 years. The identification of this high-risk cohort remains the most important aspect of HCM management, particularly in light of growing evidence of the effectiveness of prophylactic strategies. Br J Cardiol 2002;9:449-459. HOT
TOPICREVIEWThe role of orlistat in the treatment of obese patients with mild to moderate hypercholesterolaemia: consequences for coronary risk
Iain Broom, Elixabeth Hughes, Paul Dodson, John Reckless, on behalf of the Orlistat UK Study Group This study investigated the effect of orlistat on weight loss and serum lipid parameters in obese patients with hypercholesterolaemia. A total of 215 adult obese patients (body mass index ≥30 kg/m2) with hypercholesterolaemia (total plasma cholesterol ≥6.5 mmol/L or plasma low density lipoprotein cholesterol ≥4.2 mmol/L) were recruited for screening at 12 out-patient clinics in the UK. Of these, 142 patients were randomised to receive double-blind treatment for 24 weeks with orlistat 120 mg (n=71) or placebo (n=71) three times daily in combination with a mildly hypocaloric diet. Patients completing the double-blind phase (orlistat n=42, placebo n=55) were eligible to enter a further 28-week open-label phase and received orlistat 120 mg three times daily in combination with the hypocaloric diet.
Mean weight loss after 24 weeks was 4.4 kg (4.4%) in the orlistat group vs. 2.6 kg (2.5%) with placebo (p<0.01). At the end of the double-blind phase, 44.0% of orlistat-treated patients vs. 18.0% of placebo recipients had lost ≥5% of their initial body weight (p<0.001), and 7.6% vs. 4.2% had lost ≥10% (p=NS). Patients who continued on orlistat during the open-label phase had a mean weight loss of 4.97 kg (4.86%) after 52 weeks. Patients who switched to orlistat had a mean weight loss of 4.28 kg (4.23%). Orlistat was associated with significantly greater reductions than placebo in plasma total cholesterol (-10.88 + 1.36% vs. -3.25 + 1.33%; p<0.001) and LDL-cholesterol (-14.14 + 2.68% vs. -3.68 + 3.61%; p<0.05) during the double-blind phase. Despite similar weight loss at the end of the 52-week period, patients who remained on orlistat throughout the study had greater improvements in plasma lipid concentrations than patients who switched to orlistat after 24 weeks.
Orlistat, in combination with a mildly hypocaloric diet, promotes clinically meaningful weight loss and improvements in lipid concentrations in obese patients with hypercholesterolaemia. Br J Cardiol 2002;9:460-468. REVIEWExtended-release fluvastatin 80 mg shows greater efficacy, with comparable tolerability, versus immediate-release fluvastatin 40 mg for once daily treatment of primary hypercholesterolaemia
Donald B Hunninghake, Michael Davidson, Howard R Knapp, Helmut G Schrott, Sheryl Manfreda, and the Fluvastatin Study Group A new extended-release (XL) formulation of fluvastatin has been developed for once daily treatment of primary hypercholesterolaemia. This study was designed to determine the safety and effect of fluvastatin XL 80 mg on a range of lipid parameters compared with the immediate-release (IR) formulation of fluvastatin 40 mg.
In a multicentre, double-blind study, 555 patients with primary hypercholesterolaemia (Fredrickson types IIa or IIb) were randomised to 24 weeks treatment with fluvastatin XL 80 mg or IR 40 mg, each given once daily at bedtime. The study found the least square mean reduction in LDL-C after 24 weeks treatment was 32.6% in the fluvastatin XL 80 mg group (n=312) and 23.9% in the fluvastatin IR 40 mg group (n=165), an 8.7% between-treatment difference (95% confidence interval: 6.5%, 10.9%) in favour of the XL formulation (p<0.001). A higher proportion of patients in the fluvastatin XL 80 mg group achieved ≥ 35% reductions in low-density lipoprotein cholesterol (42.3% vs. 13.3%). High-density lipoprotein cholesterol levels were increased by 9.1% and 7.0%, respectively in the XL and IR groups; median triglyceride levels fell by 19% and 13%, respectively. Tolerability was comparable in the two groups, and there were no laboratory safety concerns.
The study concluded that fluvastatin XL 80 mg once daily is safe as a starting dose and effectively lowers low-density lipoprotein cholesterol and triglyceride levels in patients with primary hypercholesterolaemia. Br J Cardiol 2002;9:469-475. REVIEWRapid appraisal of clinicians’ reactions to guidance from the National Institute of Clinical Excellence on use of glycoprotein IIb/IIIa antagonists for acute coronary syndromes
Khaled Alfakih, Alistair Hall, Mike Robinson Br J Cardiol 2002;9:476-477. HOT
TOPICCASE REPORTPleuritic chest pain and hypoxia – a diagnostic dilemma
Sanjiv Mahadeva, Pulak Sahay, Richard V Lewis Br J Cardiol 2002;9:478-480. AICLeague tables, risk assessment and an opportunity to improve standards
Stephen Westaby The implications of the Secretary of State’s approval of the introduction of league tables for cardiac surgeons are discussed. Surgeons are to be ranked according to mortality rates for first-time coronary artery bypass graft operations. It is questionable whether anybody will gain from this information: the focus of surgeons’ attention is transferred from patient care to self-preservation. The introduction of league tables in New York State has resulted in surgeons being reluctant to operate on higher risk patients and in secondary referrals of patients out of the State. League tables also encourage the manipulation of risk factor status.
Many factors other than the individual surgeon’s skill influence the quality of care and patient outcomes. These factors include the patient’s status, the timing of surgery, the surgical team, equipment in the operating room and post-operative care.
An alternative to the punitive process of public reporting is the application of continuous quality improvement to healthcare. This starts from the position that most negative outcomes are due not to individual failures but to failures of process and systems. Br J Cardiol 2002;9:AIC5-AIC10. AICWill league tables have an adverse effect on the practice of coronary revascularisation in the UK?
Nick Curzen Br J Cardiol 2002;9:AIC11. AICAre waiting times for coronary artery bypass graft surgery longer than they should be? Implications of the NICE guidelines for coronary artery stents
Marios Tryfonidis, Brian Prendergast, Nicholas Curzen The objective of this study was to test the hypothesis that some patients on the routine waiting list for coronary artery bypass (CABG) surgery are suitable for percutaneous coronary intervention (PCI), as suggested in the NICE appraisal of coronary artery stents. A retrospective analysis was performed of 100 consecutive patients who had recently undergone CABG surgery from the routine waiting list in a tertiary cardiothoracic centre. The coronary angiograms of these patients were reviewed by an interventional cardiologist and a cardiac surgeon to assess patients’ potential suitability for PCI.
The mean total waiting time from being listed for angiography to having CABG surgery was 18.7 months. The mean delay from angiography to CABG surgery was 13.5 months. Of the 100-patient cohort, 70 were referred by a non-interventional cardiologist and 30 by an interventionalist (ratio 2.3:1). Fifteen patients were deemed potentially suitable for PCI after angiographic review. Of these, 13 (87%) were referred by a non-interventional cardiologist without angiographic review by an interventional specialist. The majority (86%) of the 15 patients deemed potentially suitable for PCI had single or double vessel coronary artery disease, in contrast to the population as a whole (38%).
These data suggest (a) that current CABG waiting lists could be reduced by up to 15% if coronary angiograms were reviewed by an interventional cardiologist in addition to a consultant cardiothoracic surgeon and (b) that referral arrangements should be adopted to facilitate such a review. The clinical implications of these data could be fully assessed by rolling out prospectively to other groups in the Coronary Heart Disease Collaborative. Br J Cardiol 2002;9:AIC13-AIC17. AICAre waiting times for coronary artery bypass graft surgery longer than they should be? Implications of the NICE guidelines for coronary artery stents
Stephen Large Br J Cardiol 2002;9:AIC19. HOT
TOPICAICVolumetric haemodynamic monitoring and continuous pulse contour analysis – an untapped resource for coronary and high dependency care units?
Tushar V Saluhke, Duncan LA Wyncoll Critically ill patients in the coronary care or high dependency units (CCU, HDU) need accurate assessment of their haemodynamic status to guide fluid or vasoactive drug therapy. Both central venous pressure and pulmonary artery occlusion pressure are poor guides to cardiac filling and pulmonary oedema, and using a pulmonary artery catheter often fails to improve clinical outcome.
The PiCCO system is a relatively new and less invasive approach to cardiac monitoring. It has been used extensively in intensive care and is reviewed in this article. This approach uses thermo-dilution techniques to reliably calculate volumetric measurements of cardiac preload and cardiac output, and can provide continuous real-time cardiac output and stroke volume variation measurements through pulse contour analysis. The reliability and accuracy of this method has drastically refined fluid and vasopressor management of the hypotensive patient and the management and prevention of pulmonary oedema. This method of measuring cardiac output correlates well with gold standard methods of cardiac output calculation and has been validated in adults and children.
The PiCCO system can be an invaluable tool in the optimisation of the circulation in cardiac, medical and surgical patients commonly seen in the CCU and HDU. Br J Cardiol 2002;9:AIC20-AIC25. AICThe evolving role of the cardiac inotrope, enoximone, in heart failure
Liam J Cormican, A Craig Davidson Chronic heart failure is a progressive syndrome which continues to have high rates of morbidity and mortality. Heart failure rates are increasing in parallel with the ageing population, as are rates of hospitalisation for acute episodes of decompensated failure. Little progress has been made in the medical management of such episodes. Positive inotropes, including selective phosphodiesterase III inhibitors, are associated with increased mortality when administered over the long term. Now newer approaches, using selective agents such as enoximone orally at lower doses alone or in combination with carefully titrated beta1-selective adrenergic blockade, may provide a more favourable outcome in terms of symptom management, functional status and improved survival. Trials are underway to determine whether this is the case. Published trials with enoximone and protocols for forthcoming trials are reviewed. Br J Cardiol 2002;9:AIC26-AIC31. AICPergolide and coronary artery dissection
Annalise Geldenhuys, Tony Mourant, Trevor Johnston, John Glynn Br J Cardiol 2002;9:AIC32.
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