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BEST CARDIOLOGY HOSPITALS IN BANGALORE Cardiac failure Cardiac failure is an increasingly common condition affecting about 1% of the population but much higher proportions of older people. It is responsible for an increasing number of hospital admissions. The various aetiologies have been discussed above, but the most common cause is now ischaemic heart disease rather than hypertensive heart disease. This reflects the improved modern management of hypertension in the population. The definition of heart failure has always included reference to the inability of the heart to meet the metabolic needs of the body. The earliest concepts of heart failure were of inadequate cardiac pump function and associated salt and water retention. Treatment was aimed at improving cardiac contractility and removing salt and water from the body. In the 1970s the concept of after-load reduction was introduced. This was based partly on the realisation that vasoconstriction was part of the problem. This has led to the modern neuro-hormonal concept of heart failure. It is clear that many of the features of cardiac failure are a result of stimulation of the renin-angiotensin-aldosterone system and sympathetic stimulation. These responses of the body to the fall in cardiac output temporarily increase cardiac performance and blood pressure by increasing vascular volumes, cardiac contractility and systemic resistance. In the medium and longer term these responses are maladaptive. They increase cardiac work and left ventricular volumes and lead to myocardial fibrosis with further loss of myocytes. Most recently it has become clear that heart failure is also an inflammatory condition, with evidence of cytokine activation. Work is underway to establish a role for treatment of this part of the condition. Current drug treatment has been successful in blocking many of the maladaptive aspects of neuro-hormonal stimulation. Many of these treatments have become established after benefits have been ascertained in large randomised controlled trials. These trials have also led to the abandoning of certain drugs (often those that increase cardiac performance) that were shown to have a detrimental effect on survival (e.g. Milrinone). The principles of treatment of heart failure are as follows: 1 Remove the exacerbating factors. 2 Relieve fluid retention. 3 Improve left ventricular function and reduce cardiac work; improve prognosis. 4 Protect against the adverse effects of drug treatment. 5 Assess for further management (e.g. revascularisation, transplant). 6 Manage complications (e.g. arrhythmias). 7 Protect high-risk patients from sudden death.
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.
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
Echocardiologist in Kattigenahalli, Bangalore • Pulmonary hypertension Treatment of pulmonary hypertension that is secondary to an underlying respiratory or cardiac condition begins with an attempt to optimise treatment or fix the underling condition. 1 COPD: bronchodilators, steroids, continuous oxygen. 2 Pulmonary fibrosis: oxygen. Aggressive treatment of an underlying connective tissue disease may halt or slow progression of the pulmonary pressures. 3 Pulmonary embolus: anticoagulation, vena caval filter and occasionally pulmonary embolectomy. 4 Mitral stenosis: valvotomy or replacement. 5 Mitral regurgitation: repair or replacement if left ventricular function remains reasonable. 6 Atrial septal defect: surgery or, if suitable, closure in the catheter laboratory, for example with an Amplatzer closure device. There must be evidence of reversibility of the pulmonary pressure if it is nearly as high as systemic pressure, otherwise closure will not improve the prognosis. 7 Eisenmenger’s syndrome: repair of the defect responsible for the shunt is not usually possible once reversal of shunting has occurred. Consider heart and lung transplant if conservative treatment (diuretics, digoxin and sometimes ACE inhibitors) has failed. General measures include continuous oxygen, diuretics, digoxin and aldactone for problems with right heart failure. Patients with pulmonary hypertension that is idiopathic or secondary to connective tissue disease can now be treated with bosentan. This drug is an endothelin receptor antagonist. Endothelin 1 is a potent vasoconstrictor whose levels have been shown to be elevated in patients with idiopathic pulmonary hypertension. Moderate or better improvements in functional capacity and pulmonary artery pressures have been demonstrated after treatment for these patients. The drug is available only for patients with class III symptoms and right atrial pressure greater than 8 mmHg. Patients must demonstrate stable or improved symptoms (usually via a six-minute walk test) for treatment to continue. The drug is very expensive. Its side effects include teratogenicity, an increase in liver enzymes and possibly male infertility. Prostacyclin analogues such as iloprost, which is taken by inhalation, can be effective. Similar restrictions apply to their prescription because of their cost. Continuous intravenous epoprostenol is available in some countries and has been shown to improve symptoms and prognosis in a number of small randomised trials for at least idiopathic pulmonary hypertension patients. Sildenafil (a phosphodiesterase inhibitor) is the most recent vasodilator to become fashionable for idiopathic pulmonary hypertension. A long-acting form has recently become available.
Echocardiologist in Kattigenahalli, Bangalore • Pulmonary hypertension Treatment of pulmonary hypertension that is secondary to an underlying respiratory or cardiac condition begins with an attempt to optimise treatment or fix the underling condition. 1 COPD: bronchodilators, steroids, continuous oxygen. 2 Pulmonary fibrosis: oxygen. Aggressive treatment of an underlying connective tissue disease may halt or slow progression of the pulmonary pressures. 3 Pulmonary embolus: anticoagulation, vena caval filter and occasionally pulmonary embolectomy. 4 Mitral stenosis: valvotomy or replacement. 5 Mitral regurgitation: repair or replacement if left ventricular function remains reasonable. 6 Atrial septal defect: surgery or, if suitable, closure in the catheter laboratory, for example with an Amplatzer closure device. There must be evidence of reversibility of the pulmonary pressure if it is nearly as high as systemic pressure, otherwise closure will not improve the prognosis. 7 Eisenmenger’s syndrome: repair of the defect responsible for the shunt is not usually possible once reversal of shunting has occurred. Consider heart and lung transplant if conservative treatment (diuretics, digoxin and sometimes ACE inhibitors) has failed. General measures include continuous oxygen, diuretics, digoxin and aldactone for problems with right heart failure. Patients with pulmonary hypertension that is idiopathic or secondary to connective tissue disease can now be treated with bosentan. This drug is an endothelin receptor antagonist. Endothelin 1 is a potent vasoconstrictor whose levels have been shown to be elevated in patients with idiopathic pulmonary hypertension. Moderate or better improvements in functional capacity and pulmonary artery pressures have been demonstrated after treatment for these patients. The drug is available only for patients with class III symptoms and right atrial pressure greater than 8 mmHg. Patients must demonstrate stable or improved symptoms (usually via a six-minute walk test) for treatment to continue. The drug is very expensive. Its side effects include teratogenicity, an increase in liver enzymes and possibly male infertility. Prostacyclin analogues such as iloprost, which is taken by inhalation, can be effective. Similar restrictions apply to their prescription because of their cost. Continuous intravenous epoprostenol is available in some countries and has been shown to improve symptoms and prognosis in a number of small randomised trials for at least idiopathic pulmonary hypertension patients. Sildenafil (a phosphodiesterase inhibitor) is the most recent vasodilator to become fashionable for idiopathic pulmonary hypertension. A long-acting form has recently become available.
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