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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.
CARDIOLOGISTS IN H S R LAYOUT 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. 364 PRACTICAL CARDIOLOGY In a recent European survey, survival for patients with simple defects and Eisenmenger’s was to 32.5 years, but only 25.8 years for those with Eisenmenger’s resulting from complex abnormalities.38 There is a 50% maternal mortality risk with pregnancy. Quite minor surgical procedures are associated with high risk. Trials with endothelin antagonists are being conducted and continuous oxygen treatment can provide symptomatic relief. Lung and heart lung transplant should be considered for some of these patients. 6 Endocarditis. Most patients with congenital heart disease have a lifelong risk of infective endocarditis. Constant reminders of this risk should be given to the patients and their usual doctors. As well as appropriate antibiotic prophylaxis . before procedures, a high index of suspicion is very important. A febrile illness should not be treated with antibiotics until at least two sets of blood cultures have been taken. Early referral
Cardiologist in Chikkajala, 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.
CARDIOLOGISTS IN DEVARABESANAHALLI BANGALORE Complex congenital heart disease: Fontan repair Anatomy and physiology Babies with a single ventricle or equivalent defect are often treated during childhood with a palliative operation to connect venous return directly to the pulmonary arteries—a Fontan repair. The prognosis is usually good: 75% of these patients survive at least 20 years. Complications Problems develop because of failure of the systemic ventricle, obstruction of the venous to pulmonary connection, atrial enlargement and AV valve regurgitation. Atrial arrhythmias become increasingly common. Sinus node dysfunction may necessitate pacing, which requires an epicardial electrode in most cases. Follow-up Echocardiography allows assessment of ventricular function and the AV valve. Obstruction in the Fontan connections can be examined with Doppler. MRI is increasingly useful for this assessment. Treatment Severe AV valve regurgitation, cyanosis and ventricular dysfunction are indications for intervention, including transplant or revision of the Fontan. Atrial arrhythmias can be treated with radiofrequency ablation. Pregnancy and contraception Pregnancy is possible in some patients with excellent Fontan function, good LV function and minimal AV valve regurgitation. Maternal risk is high if the Fontan is failing. There may be problems with the need to withdraw ACE inhibitors and with anticoagulation.
HEART SPECIALISTS IN YELAHANKA NEW TOWN BANGALORE The causes of coronary symptoms The symptoms of coronary artery disease are caused by the reduction of myocardial perfusion that results from narrowing of the lumen of one or more of the coronary arteries. This narrowing is most often the result of atherosclerosis. Other much less common causes include: 1 coronary artery spasm (often in an already diseased segment of artery but sometimes as a result of the use of cocaine) 2 thrombosis (usually on an already diseased, or occasionally aneurismal, segment) 3 embolism (e.g. from an infected aortic valve) 4 congenital coronary abnormality 5 vasculitis. Numerous other cardiac symptoms and problems can be the eventual result of atheromatous coronary disease. These include myocardial infarction , cardiac failure cardiac arrhythmias and some cardiac valve problems. Risk factor mechanisms of action Atherosclerosis is thought to result primarily from a disturbance of the vascular endothelium. The final common pathway for the effects of endothelial dysfunction is largely through abnormalities of nitric oxide (NO) production. This chemical, released by a healthy endothelium, is a potent vasodilator and has anti-inflammatory and other favourable actions on the arteries. Causes of this disturbance can be: n mechanical (hypertension) n chemical (oxidised lipids, components of cigarette smoke, hyperinsulinaemia) or n due to immunological injury. The damaged endothelium attracts inflammatory mediators, platelets and circulating lipids and promotes fibroblast and smooth muscle proliferation. This results in the formation of a plaque, which may narrow the arterial lumen. Plaques can remain stable (or sometimes regress), enlarge, rupture or erode (more common in diabetics). Most acute ischaemic events (acute coronary syndromes or acute myocardial infarctions) are thought to be the result of further luminal narrowing caused by the formation of partly or fully occlusive thrombus on a ruptured or eroded plaque. Coronary risk factors may therefore operate because they are atherogenic or thrombogenic. Plaque rupture Plaque rupture may be at least partly an inflammatory process involving inflammatory cells, cytokines and even bacteria. This may explain the association between inflammatory markers such as high-sensitivity C reactive protein (hsCRP) and a risk of acute coronary events. Although this association seems well established, there is still uncertainty about its role in overall risk assessment Plaques at risk of rupture are called vulnerable plaques. They typically have a thin fibrous cap. The shoulde of these caps are at risk of rupturing and allowing material from within the plaque to come
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