Category Archives: Cardiovascular disease

TREATMENT

A significant ASD (i.e. a pulmonary flow that is more than 50% increased when compared with systemic flow) should be repaired before the age of 10 years or as soon as possible if first diagnosed in adulthood. There is a good result from surgery unless pulmonary hypertension has developed. Persistent ductus arteriosus (PDA) The ductus arteriosus connects the pulmonary artery at its bifurcation to the descendin

Congenital heart disease

A congenital cardiac malformation occurs in about 1% of live births. There is an overall male predominance, although some individual lesions (e.g. atrial septal defect and persistent ductus arteriosus) occur more commonlyin females. The aetiology of congenital cardiac disease is often unknown but involves: MATERNAL RUBELLA INFECTION (persistent ductus arteriosus, and pulmonary valvular and arterial stenosis)

Infective endocarditis

Infective endocarditis is an infection of the endocardium or vascular endothelium. The disease may occasionally occur as a fulminating or acute infection, but more commonly runs an insidious course and is known as subacute  (bacterial) endocarditis (SBE). The incidence is 6-7 per 100000 per year in the UK, but is much more common in developing countries. Endocarditis occurs most commonly on rheumatic or cong

TRICUSPID REGURGITATION

Functional tricuspid regurgitation may occur whenever the right ventricle dilates, e.g. in cor pulmonale, myocardial infarction or pulmonary hypertension. Organic tricuspid regurgitation may occur with rheumatic heart disease, infective endocarditis, carcinoid syndrome, Ebstein’s anomaly (a congenitally malpositioned tricuspid valve) and other congenital abnormalities of the atrioventricular valves. SYM

INVESTIGATION

Chest X-ray The chest X-ray usually reveals a relatively small heart with a prominent, dilated, ascending aorta. This occurs because turbulent blood flow above the stenosed aortic valve produces so-called ‘poststenotic dilatation’. The aortic valve may be calcified. When heart failure occurs, the CTR increases. ECG The ECG shows left ventricular hypertrophy and left atrial delay. A left ventricula

AORTIC STENOSIS

There are three causes of aortic valve stenosis: 1 Congenital aortic valve stenosis develops progressively because of turbulent blood flow through a congenitally abnormal (usually bicuspid) aortic valve. Most congenitally abnormal aortic valves occur in men. 2 Rheumatic fever results in progressive fusion, thickening and calcification of a previously normal threecusped aortic valve. In rheumatic heart disease

MITRAL REGURGITATION

Of the many causes of mitral valve regurgitation, rheumatic heart disease (50%) and the prolapsing mitral valve are the most common. Any disease that causes dilatation of the left ventricle may cause mild mitral regurgitation, e.g.: • Aortic valve disease • Acute rheumatic fever • Myocarditis • Cardiomyopathy • Hypertensive heart disease • Ischaemic heart disease Other causes IN HYPERTROPHIC CARDIOM

INVESTIGATION

Chest X-ray The chest X-ray usually shows a generally small heart with an enlarged left atrium. Pulmonary venous hypertension is usually also present. Late in the course of the disease a calcified mitral valve may be seen on a penetrated or lateral view. The signs of pulmonary oedema or pulmonary hypertension may also be apparent when the disease is severe. ECG In sinus rhythm the ECG shows a bifid P wave due

Valvular heart disease

MITRAL STENOSIS Almost all mitral stenosis is due to rheumatic heart disease: • At least 50% of sufferers have a history of rheumatic fever or chorea. • The single most common valve lesion due to rheumatic fever is pure mitral stenosis (50%). • The mitral valve is affected in over 90% of those with rheumatic valvular heart disease. • Rheumatic mitral stenosis is much more common in women. • The patho

Rheumatic fever

between 5 and 15 years of age) as a result of infection with group A streptococci. It affects the heart, skin, joints and central nervous system. It is common in the Middle and Far East, eastern Europe and South America, but it is now rare in the UK, western Europe and North America. This decline in the incidence of rheumatic fever (from 10% of children in the 1920s to 0.01% today) parallels the reduction in