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HEART SPECIALISTS IN SILKBOARD BANGALORE Detected vascular abnormalities Calcium scoring High-resolution CT scanners can measure calcium within the coronary arteries in a single breath-hold scan. The measured calcium is given a number, the Agatston score. The presence of calcium within a coronary artery is a marker of coronary disease but not of obstructive disease. It does not give any information about the presence of soft plaque, which is more likely to be associated with an acute coronary event but a 0 score predicts a very low coronary risk. A high score has been shown to be an independent risk factor for future events.29 Prospective studies proving the value of calcium scoring have not been performed. Calcium scoring is likely to be superseded by multi-slice CT coronary angiography which can produce images of the coronary lumen and generate a calcium score. An elevated calcium score in an asymptomatic patient is probably best treated as an indication for aggressive risk factor management; for example, instituting statin treatment for a marginally elevated cholesterol level. Intima-media thickness High-frequency ultrasound transducers can measure accurately the thickness of the carotid intima up to its interface with the media. An intima-media thickness (IMT) of > 1.3 mm is associated with an increased cardiovascular risk, which remains significant after allowing for other risk factors. Ankle brachial index The ankle brachial index (ABI) is relatively easy to measure with a sphygmomanometer and a Doppler ultrasound device. The systolic blood pressure in the arm and in the posterior tibial and dorsalis pedis arteries is compared. An ABI of < 0.9 means a stenosis of at least 50% somewhere between the aorta and the foot. The test is a reliable sign of peripheral arterial disease and thus also coronary disease. Erectile dysfunction Erectile dysfunction is a marker of endothelial dysfunction. Because the penile arteries are smaller (1–2 mm) than the carotids (5–7 mm) and coronary arteries (3 mm), plaque burden and endothelial dysfunction may cause symptoms earlier here than in the other territories
THE BEST CARDIOLOGISTS IN YELAHANKA nvestigations of possible or probable stable angina Electrocardiography A standard 12-lead ECG should be obtained in all patients. This is likely to be normal in almost half of patients with subsequently proven coronary artery disease. Nevertheless, an abnormal trace lends weight to the symptoms and favours further investigation. Chest X-ray Routine radiology is not essential but may reveal important co-morbidities. It should always be performed in those with clinical evidence of hypertension, pericarditis (p. 174), heart failure or valvular disease, if only as a baseline. It is similarly indicated for patients with suspected or known pulmonary or systemic disease such as rheumatoid arthritis, COPD or alcoholism. Routine blood tests All patients with suspected angina should have the following routine investigations at presentation (NHF grade A recommendation): n fasting lipids, including total cholesterol, LDLs, HDLs and triglycerides—risk factors n fasting blood sugar—risk factor n full blood count—anaemia exacerbates angina n serum creatinine—impaired renal function is a risk factor and can be worsened by some cardiac investigations. If indicated clinically, thyroid function
THE BEST CARDIOLOGISTS IN YELAHANKAMedical treatment of stable angina Treatment of any disease must begin with a thorough explanation of the likely diagnosis, severity and prognosis. The possible investigations required and steps to be taken if symptoms persist despite treatment should be outlined. A warning (firm, but not alarming) should be given that a prolonged episode of chest pain (more than about 15 minutes) should prompt the patient to get to a hospital without delay. This may also be the first opportunity to speak to the patient about the control of risk factors (e.g. smoking, hyperlipidaemia) that will be important for the long-term prognosis. Risk factor assessment should form part of this initial consultation and include a request for measurement of the serum lipids . a b (a) An MDCT scan of a diseased right coronary artery and the corresponding coronary angiogram (b) An MDCT reconstructed image of the heart and great vessels 140 PRACTICAL CARDIOLOGY A patient with symptoms typical of angina but who seems stable enough not to need admission to hospital should be started on treatment while awaiting investigations to confirm the diagnosis (usually stress testing). Treatment should aim to improve symptoms and, if possible, improve the prognosis (i.e. reduce the risk of unstable angina, infarction or death). Some drugs that help control the symptoms of angina may also improve the prognosis; other treatment may help the longer-term outlook by improving risk factors. Anti-platelet
POPULAR CARDIOLOGIST IN KATTIGENAHALLI, BANGALORE Cyanotic congenital heart disease Some of the more common cyanotic lesions are discussed below. There are, however, a number of problems common to patients with cyanotic heart disease. 1 Erythrocytosis. Chronic cyanosis causes an increase in red cell numbers as a way of increasing oxygen carrying capacity. The platelet count is sometimes reduced and the white cell count normal. The increased blood viscosity associated with the high red cell mass causes a slight increase in the risk of stroke.37 Most patients have a stable elevated haemoglobin level, but venesection is recommended if this is greater than 20 g/dL and the haematocrit is greater than 65%. Levels as high as this can be associated with the hyperviscosity syndrome: headache, fatigue and difficulty concentrating. Recurrent venesection can cause iron depletion and the production of microcytic red cells, which are stiffer than normal cells and so increase viscosity further. 2 Bleeding. Reduced platelet numbers, abnormal platelet function and clotting factor deficiencies mean these patients have an increased risk of haemorrhage. The most dangerous problem is pulmonary haemorrhage but bleeding from the gums and menorrhagia are more common. The use of anticoagulation must be restricted to those with a strong indication for treatment. 3 Gallstones. Chronic cyanosis and increased haem turnover are associated with an increased incidence of pigment gallstones. 4 Renal dysfunction and gout. Congestion of the renal glomeruli is associated with a reduced glomerular filtration rate and proteinuria. This and the increased turnover of red cells lead to urate accumulation and gout. 5 Pulmonary hypertension. Lesions associated with increased flow through the pulmonary circulation (e.g. a large atrial septal defect) can lead to a reactive rise in pulmonary arterial resistance. This is more likely to occur if the left to right shunt is large. Eventually these pulmonary vascular changes become irreversible, pulmonary pressures equal or exceed systemic pressures, and central cyanosis occurs because the intra-cardiac shunt reverses (Eisenmenger’s syndrome). Flow is now from right to left. There is then no benefit in attempting to correct the underlying cardiac abnormality. Earlier and more successful treatment of children with congenital heart disease has reduced the number of patients with this inexorable disease. Careful management of these conditions can nevertheless improve patients’ symptoms and survival. Reasonable exercise tolerance is usually maintained into adult life for most patients but progressive deterioration then occurs. Haemorrhagic complications, especially haemoptysis, are common. Thrombotic stroke, cerebral abscess and pulmonary infarction can also occur.
THE BEST CARDIOLOGIST IN HEBBALA Hypertension as a risk factor Hypertension is a risk factor for coronary disease, but even more so for cerebrovascular disease and left ventricular failure.1 Control of blood pressure reduces this risk. Large randomised trials have shown that every 10–14 mmHg reduction in systolic and 5 mmHg reduction in diastolic blood pressure confers a 29% reduction in CHD risk and a 40% reduction in stroke risk. The risk of a coronary event in a man with blood pressure greater than 160/95 is five times the risk in a man with blood pressure of 140/90 or less. Hypertension can be diagnosed only by blood pressure measurements. There is little evidence that high blood pressure causes symptoms, except for malignant hypertension with cerebral oedema. The symptoms often ascribed to hypertension—epistaxis, dizziness, headache and fainting—are no more common in hypertensives than in normotensives. Anxiety (often about the blood pressure) and hyperventilation may explain some of these symptoms.2 The trials providing the above figures have been carried out using diuretics or beta-­blockers in the treatment of hypertension. Because these drugs may adversely affect lipid profiles and therefore coronary risk, it has been suggested that newer agents may produce a greater reduction in the risk of CHD events. However, this has not been proven. There is evidence from metaanalyses of blood pressure lowering trials that beta-blockers are less protective against stroke than other agents. They are more effective than placebo in providing protection against stroke. The reduction in blood pressure that is achieved is still more important than the choice of drug. The trials have shown that blood pressure reduction in the elderly, including those over the age of 80, is associated with reduced cardiovascular morbidity but not all-cause (overall) mortality. Treatment of isolated systolic hypertension, common in the elderly, has also shown benefit in terms of the reduced risk of stroke, cardiac failure and coronary disease.3 As in the case of other risk factors, the greatest absolute benefit in the treatment of hyper-­ tension is gained in those patients with existing heart disease, diabetes or multiple risk factors. Blood pressure is an important component of the total risk score . The effects of hypertension Cardiovascular Sustained hypertension results in increased left ventricular wall thickness (left ventricular hypertro-­ phy, LVH) and may ultimately lead to left ventricular dilatation and cardiac failure. LVH results in higher oxygen demands by the ventricle, making angina more likely. The mechanism by which hypertension is thought to increase CHD risk is mechanical damage to the endothelium, leading to increased permeability and therefore increased atherogenesis. Elevated blood pressure interacts with other hereditary and acquired risk factors, all of which are associated with endothelial dysfunction; some are probably implicated in the genesis of hypertension in the first place.4 Neurological Hypertension
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