2004, Volume 11, Issue 01, pages 1-80

The management of advanced heart failure when medical treatment alone is no longer sufficient was the focus of the 2003 British Society for Heart Failure (BSH) annual autumn meeting, held in Oxford on 28 November.

A joint British Journal of Cardiology and H.E.A.R.T UK round table meeting held at the National Heart and Lung Institute, 18th November 2003.

It seems ironic that, at a time of ultra-specialisation, when the public is demanding higher standards from doctors, academic medicine is being downgraded. Cardiac pathology represents a perfect case in point.

Echocardiography remains the ‘gold standard’ for the objective assessment of left ventricular systolic function. Even with the high prevalence of left ventricular systolic dysfunction, echocardiography is not universally available within UK primary care, despite the fact that the condition is predominantly managed within this arena. We describe a service within one Primary Care Trust, where general practitioners and nurses refer patients who are suspected of having, or who are at high risk of developing heart failure, for a clinical assessment and an echocardiogram. Following this, a treatment plan is formulated and those with systolic dysfunction are followed up by a heart failure nurse. She ensures that the treatment regimen is adhered to and that the correct physiological and biochemical monitoring takes place. In our study we found that of those referred, only 33% had evidence of left ventricular systolic dysfunction, with 62% showing normal function. Of those patients with left ventricular systolic dysfunction, 86% required a significant change in their medication. Three months after the assessment, using the ‘Minnesota Living with Heart Failure Questionnaire’, considerable improvement was noted in the quality of life of patients with left ventricular systolic dysfunction. This paper suggests that there is considerable scope for improvement in the management of chronic heart failure.

The secondary prevention of coronary heart disease (CHD) is a recognised priority for primary care and is a fundamental part of the published National Service Framework (NSF). The majority of patients receive statins to reduce their total cholesterol (TC) and low-density lipoprotein chol-esterol (LDL-C) levels. The NSF set out targets for both TC and LDL-C. This study was designed to investigate the applicability of these targets in a real-life setting. One hundred and ten patients aged under 75 with established CHD were screened and their lipids measured. Eighty (73%) were on a statin. Mean TC was 6.3 mmol/L before treatment and 4.8 mmol/L after. Of these 80 patients, 46 (58%) had a TC below 5.0 mmol/L. Only 39% of patients met the stricter criterion of less than 5.0 mmol/L and a 25% fall in TC. No patient whose pre-treatment TC was below 5.0 mmol/L had reached a 25% reduction as well. The use of a threshold and a percentage may be potentially confusing to GPs and reduce the implementation of these targets.

In patients presenting with persistent hoarseness due to left recurrent laryngeal nerve (LRLN) palsy and an abnormal left hilum on chest radiographs, a major cause is bronchogenic carcinoma. We describe two cases presenting with such a combination of symptoms and signs in whom a diagnosis of bronchogenic carcinoma was suspected. In each case, the LRLN palsy was in fact due to direct compression of the nerve by an aortic aneurysm.

The ACTION (A Coronary disease Trial Investigating Outcome with Nifedipine GITS) study is the largest ever performed randomised trial of an anti-anginal drug in patients with chronic stable angina. Its aim is to assess the effect of nifedipine GITS 60 mg versus placebo on standard therapy for coronary artery disease on event-free survival; its composite end point includes death from any cause, acute myocardial infarction, hospitalisation for overt heart failure, emergency coronary angiography, disabling stroke and procedures for peripheral revascularisation. ACTION is one in a series of trials assessing drug effects in chronic stable coronary artery disease. The IONA (Impact Of Nicorandil in Angina) and EUROPA (EURopean trial On reduction of cardiac events with Perindopril in stable coronary artery disease) studies demonstrated that the K-ATP channel activator nicorandil and the angiotensin-converting enzyme inhibitor perindopril reduced the primary composite end point for cardiac events by 17% and 20%, respectively. Nifedipine GITS is an effective antihypertensive and anti-anginal drug. In the INSIGHT trial, nifedipine GITS 30/60 mg demonstrated comparable outcomes to a diuretic combination therapy with significant effects on intermediate end points. ENCORE I (Evaluation of Nifedipine and Cerivastatin on Recovery of coronary Endothelial function) demonstrated that nifedipine GITS 30/60 mg positively affected the pathophysiology of coronary artery disease. We therefore anticipate that nifedipine will affect blood pressure, anginal symptoms and resulting complications, and the coronary atherosclerotic process in those patients randomised to receive this agent in the ACTION study.

Arrhythmias are more common in the elderly and in many situations are of prognostic importance. The incidence of arrhythmias in the elderly is increasing, most likely due to enhanced longevity. Alterations in heart rate and rhythm may occur because of age-related change within the heart. Elderly people are more likely to experience co-morbid health problems, intercurrent illness and adverse drug reactions, all of which may result in arrhythmias. Falls are a common problem in elderly people; an arrhythmic cause should always be considered.

Angiotensin-converting enzyme (ACE) inhibitor therapy only partially suppresses aldosterone production and ‘aldosterone escape’ occurs in up to 40% of patients with congestive heart failure (CHF). The RALES and EPHESUS studies show clearly that even in the presence of ACE inhibitor therapy, aldosterone contributes to mortality in CHF. There are many mechanisms for this. Firstly, aldosterone contributes to endothelial dysfunction and attenuates endothelium-dependent vasodilatation, at least partly by reducing nitric oxide bioavailability. Aldosterone also promotes myocardial fibrosis and cardiac remodelling by enhancing collagen synthesis, resulting in increased myocardial stiffness and increased left ventricular mass. These mechanisms mediated by aldosterone contribute to increased risk of ventricular arrhythmias and sudden cardiac death. Inhibition of aldosterone’s effect on mineralocorticoid receptors should now be considered standard therapy in populations of CHF patients. Aldosterone blockers also reduce the blood pressure in all types of hypertensive patients and may have an additional role as add-on therapy in hypertension, especially to lessen target organ damage.

Some patients with initial normal levels of high-density lipoprotein cholesterol (HDL-C) have lower HDL-C levels during lipid-lowering treatment. The aim of this study was to estimate the prevalence of low HDL-C (< 1.0 mmol/L; < 40 mg/dL) before and during lipid-lowering treatment. Additionally, the prevalence of low HDL-C during fibrate and statin treatment was compared. All patients attending two Health Insurance Associations during February and March 2002 for continuing reimbursement of their lipid-lowering drug were included in this study. Date of birth, sex and the actual lipid-lowering drug were recorded. The most recent lipoprotein levels and those after a three-month diet before the start of the treatment were recorded. In total, 2,259 patients (56% women) were included; 69% were treated with statins and 31% with fibrates. Low HDL-C levels were found before the initiation of the treatment in 7% of the statin patients and in 11% of the fibrate patients. During treatment, 10% of the statin patients and 13% of the fibrate patients had low HDL-C levels. The proportion of patients whose HDL-C decreased below 1.0 mmol/L (40 mg/dL) during treatment was 6% for statins and 4% for fibrates. Although lipid-lowering drugs are known to increase HDL-C levels slightly, not all patients benefit from this effect.

We summarise the natural history and pathophysiology of mitral valve stenosis and regurgitation. The indications for surgery, and the various surgical options including mitral valvotomy, mitral valve repair and mitral valve replacement with bioprosthetic and mechanical valves are discussed. The results of surgery for mitral valve disease in the UK are summarised.

In 2000, the European Society of Cardiology and American College of Cardiology issued a consensus document concerning the redefinition of myocardial infarction (MI). They proposed that the diagnosis of acute MI should be based on the rise and fall of specific markers combined with at least one of the following: ischaemic symptoms, ECG changes consistent with ischaemia or infarction, or coronary intervention. The implications of this redefinition are widespread, and it has been met with mixed opinions from physicians. Here we present the results of a survey, sent to 1,000 consultants in cardiology and general medicine, concerning the availability and their use of cardiac markers and their current working diagnosis of MI. Four case studies were included in the survey. Some 361 responses were analysed. Creatine kinase (CK) remains the most frequently used marker for the diagnosis of MI, but 23% of consultants had moved to a definition based on troponins. Fourteen per cent of consultants no longer used CK in their practice. Ninety-two per cent of consultants had access to troponin assays. Definitions varied widely between consultants, even within individual hospitals, as did the responses to the case studies.

We summarise the natural history and pathophysiology of mitral valve stenosis and regurgitation. The indications for surgery, and the various surgical options including mitral valvotomy, mitral valve repair and mitral valve replacement with bioprosthetic and mechanical valves are discussed. The results of surgery for mitral valve disease in the UK are summarised.