Clinical articles

Aldosterone is intimately linked to the pathophysiology of heart failure, and high levels of aldosterone are associated with worse prognosis. Many non-renal effects of aldosterone contribute to the congestive heart failure syndrome, including endothelial dysfunction, reactive myocardial fibrosis and cardiac remodelling. The precise mechanism by which aldosterone stimulates myocardial collagen accumulation and fibrosis is not yet fully understood. It may largely occur secondary to aldosterone-related endothelial dysfunction and inflammation, since endothelial dysfunction can lead to micro-thrombus formation and tissue micro-infarction, which repairs itself by fibrosis. Other contributory effects may include a direct impact of aldosterone on the collagen synthesis pathway.
In the RALES study, spironolactone in conjunction with an angiotensin-converting enzyme (ACE) inhibitor was found to reduce mortality in chronic moderate-to-severe heart failure; the EPHESUS study more recently reported significant reductions in death and hospitalisation when eplerenone was added to ACE inhibitor and beta blocker therapy in patients with clinical evidence of heart failure following acute myocardial infarction. Clinicians should now consider routinely adding an aldosterone receptor antagonist to standard therapy of patients with left ventricular dysfunction and heart failure in order to reduce cardiac morbidity and mortality.

Improvements in the management of acute myocardial infarction together with population ageing have contributed to a growing burden of heart failure. Around half of new cases of heart failure in patients aged less than 75 years are due to coronary artery disease; many of these patients develop heart failure in the context of acute myocardial infarction. Left ventricular systolic dysfunction is the single most common cause of heart failure after myocardial infarction. Of the estimated 65,000 new cases of heart failure in the UK each year, it is likely that around 15,000 occur in the context of acute myocardial infarction. Ventricular remodelling generally occurs in the early period after myocardial infarction, and early identification offers the potential to modify this process and reduce the risk of heart failure. Clear guidelines should be built into the myocardial infarction care pathway to ensure an integrated approach from hospital and community services.

Previous studies have identified a significant incidence of clinically unrecognised myocardial ischaemia in intensive care unit (ICU) patients, as determined by elevation of serum troponin. This pilot study demonstrates a similar high frequency of such a phenomenon in patients who are acutely ill, but without clinical evidence of myocardial ischaemia, on the general medical wards of a large city hospital. Elevation of serum troponin in these patients is associated with higher hospital mortality and increased lengths of hospital stay. Recognition that slight elevation of troponin levels may occur in the context of significant medical illness in acute general medical ward patients is important as it may avoid erroneous diagnosis of myocardial infarction and subsequent unnecessary investigations. A literature review of the various causes of an elevated troponin result is then presented.

Abstract Prior studies have suggested a gradation in clinical risk with increasing elevations of cardiac troponins in patients with non-ST elevation acute coronary syndromes (ACS). We hypothesised that patients with cardiac troponin-T (cTnT) between 0.01-0.1 μg/L might
be perceived as a low-risk group and consequently receive less active medical treatment.

The volume and complexity of patients undergoing percutaneous coronary intervention (PCI) is growing steadily. This, and the increasing tendency for these procedures to be unplanned, requires us to rethink the way we deliver care in this setting. This article addresses the processes involved, which include pooling of PCI lists, multidisciplinary team meetings and integrated care pathways for both elective and unplanned cases. The value of pre-assessment clinics, specific cardiac triage teams and “generic” catheter lab workers is also discussed. More traditional elements of the service such as on-call rotas are reappraised. Newer concepts, like dedicated PCI meetings to plan strategy and review previous problem cases for educational purposes, are also introduced.

Cardiac myxomas are the most common benign intracardiac tumour, and are more common in women. Since many patients suffer from cerebral or systemic embolism, early diagnosis is vital to plan for surgical intervention. Surgical excision is advocated as soon as possible, particularly in left atrial myxoma, because of the high risk of valvular obstruction and systemic embolisation. Patients with a family history of the disorder are at greater risk of tumour recurrence.

The new General Medical Services contract has introduced the term ‘maximally tolerated blood pressure treatment’, which it defines as a cut-off point at which a doctor might advise the patient to accept the current blood pressure level. Whilst this is a sensible idea, the contract does not give any guidance as to how the doctor should decide when that point has been reached. In this article the Primary Care Cardiovascular Society considers the issue, looking at available evidence, and publishes a consensus statement on the definition for maximally tolerated blood pressure treatment.

Aneurysms of the sinus of Valsalva associated
with infective endocarditis are rare. They can
present during an episode of acute endocarditis
or as late sequelae, with or without rupture. Their
management involves repair of the annulus and closure
of the aneurysm with a Dacron patch.

Interventions on individual risk factors are most effective when directed at those with highest absolute risk. Joint British Society Guidelines and National Service Frameworks (NSF) indicate that these individuals should be identified. There is a need to continuously categorise the population by risk to identify those for primary prevention. This article describes a project that was set up to use clinical information technology in an innovative way. It was introduced as an administrative routine for the whole population of a large district (Blyth Valley, Northumberland) through the general practices to which the patients belong.

Angiotensin-converting enzyme (ACE) is a key enzyme in the production of angiotensin II. The cloning of the ACE gene has made it possible to identify a deletion (D)-insertion (I) polymorphism that appears to affect the level of serum ACE activity. The aim of our study was to analyse the ACE gene I/D polymorphism in Turkish male athletes and to evaluate its relationship to left ventricular mass and function.
Forty male athletes (mean age 23.4+1.8 years) were included in this study, and they underwent both complete echocardiographic assessment and analysis of ACE I and D allele frequencies in peripheral blood by polymerase chain reaction. They were separated into three subgroups according to their ACE DD (n=13), DI (n=16) and II (n=11) genotypes. Thickness of the interventricular septum (IVS), the left ventricular posterior wall (LVPW) and left ventricular mass (LVM) and LVM index (LVMI) were measured by the M-mode. Left ventricular ejection fraction was calculated using Simpson’s method, and so was the myocardial performance index.
There was no statistically significant differences between the ACE DD, DI and II genotypes at the p>0.05 level by age, body mass index, heart rate, systolic and diastolic blood pressures. The thickness of the IVS (12 mm) and LVPW (10.7 mm), and LVM (302.8 g) and LVMI (157.3 g/m2) in ACE DD genotypes were higher than for both ACE DI (10.8 mm; 9.7 mm; 231.9 g; 125.3 g/m2) and II genotypes (9.0 mm; 8.6 mm; 185.0 g; 107.5 g/m2) in athletes. Left ventricular systolic and global functions among the three ACE genotypes were not different statistically.
Our findings suggest that left ventricular hypertrophy is partially determined by genetic disposition and DD genotype of ACE is a potential genetic marker associated with an elevated risk of left ventricular hypertrophy.