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SAMIKSHA HEART AND DIABETIC CARE IN YELAHANKA NEW TOWN Dyslipidemia Average total serum cholesterol and low-density lipoprotein (LDL) cholesterol levels increase in men until approximately age 70 and then level off. In women, total serum cholesterol and LDL-cholesterol levels rise sharply after menopause and average 15–20 mg/dL higher than in men after age 60. Highdensity lipoprotein (HDL) cholesterol levels average about 10 mg/dL higher in women than in men throughout adult life. Although the strength of association of cholesterol levels with cardiovascular disease declines with age, in part due to the confounding effects of comorbid conditions and nutritional factors, low HDL-cholesterol levels and high total cholesterol to HDL-cholesterol ratios remain independent predictors of coronary events in older persons, including those over 80 years of age. In addition, observational studies and clinical trials indicate that statin therapy is associated with a reduction in cardiovascular events in moderate to high risk patients up to age 85.3 In the PROSPER trial, for example, which randomized 5804 patients 70-82 years of age to pravastatin or placebo, those receiving pravastatin experienced a 15% reduction in the primary outcome of coronary death, nonfatal myocardial infarction, or nonfatal or fatal stroke during a mean follow-up period of 3.2 years. Conversely, limited data are available on statin therapy in lower risk patients and in patients over 85 years of age. Treatment of these subgroups must therefore be individualized based on an overall assessment of potential benefits and risks.
BEST DIABETOLOGISTS IN HEBBALA BANGALORE Diabetes Type 1 and type 2 diabetes and impaired glucose tolerance (IGT) are associated with an increased risk of coronary disease, peripheral vascular disease and cerebrovascular disease.21 Diabetics have a two- to threefold risk of coronary disease at all ages and those with IGT have a 1.5-fold risk. Diabetes is a stronger risk factor for women (3.3 times) than for men (1.9 times). The excess risk for type 1 patients is largely confined to those with diabetic renal disease. All type 2 patients are at increased risk.22 Diabetes is thought to increase coronary heart disease because: n increased insulin levels result in increased hepatic synthesis of LDL and triglycerides, causing a mixed dyslipidaemia n insulin resistance, which is characteristic of type 2 diabetes, is associated with numerous other cardiovascular risk factors: dyslipidaemia, hypertension, endothelial dysfunction and microalbuminuria n hyperglycaemia itself may cause endothelial damage n glycosylated LDL may be more atherogenic than non-glycosylated LDL. Table 1.12 Glucose tolerance, current WHO definitions (venous plasma glucose) Fasting glucose 2-hour post-glucose load (mmol/L) Normal glucose regulation < 6.0 < 7.8 Impaired fasting glucose 6.1–6.9 < 7.8 Impaired glucose tolerance < 7.0 7.8–11.0 Diabetes > 7.0 > 11.1 16 PRACTICAL CARDIOLOGY Glycaemic control The UKPDS Trial has shown a very significant reduction in the microvascular complications of diabetes with improved glycaemic control but the improvement in macrovascular complications did not quite reach significance. Nevertheless, the UKPDS trialists estimate that each 1% reduction in HbA1c leads to a 14% reduction in cardiovascular risk. Diabetics tend to have more diffuse coronary disease. shows a diffusely diseased right coronary artery from a type 2 diabetic patient before and after coronary stenting . Coronary artery surgery involves a higher risk for diabetics, and graft disease and progression of native disease occur earlier in these patients. Nevertheless, diabetics probably have a better prognosis after surgical revascularisation than after angioplasty because of their higher risk of restenosis following angioplastY
THE BEST CARDIOLOGISTS IN GANGAMMA CIRCLE BANGALORE Thrombogenic factors Thrombosis is an important pathological process in coronary artery disease. Factors increasing the tendency to thrombosis include: n smoking n hypertriglyceridaemia n elevated fibrinogen (possibly) n oestrogen-containing contraceptive pills n polycythaemia n increased von Willebrand factor (a marker of endothelial dysfunction). The following factors are associated with reduced thrombotic tendency: n low-dose aspirin n other anti-platelet drugs (e.g. clopidogrel) n fish oils and mono-unsaturated fatty acids. Alcohol intake Alcohol intake has a complex relationship with coronary heart disease, with moderate intake being associated with decreased risk, and nil or heavy intake being associated with increased risk. Moderate intake is defined as 10–30 g per day for men; the optimal level for women is uncertain and alcohol may not have the same protective effect for women. Moderate alcohol intake is thought to be protective by: n increasing HDL levels n having anti-platelet activity n having an anti-oxidant effect—some components of alcoholic drinks, especially red wine and possibly beer. The evidence for the protective effect of alcohol is not strong and non-drinkers should never be urged to take up drinking. Hypertension and cerebrovascular disease increase in a linear fashion with alcohol intake, as do triglyceride levels. Therefore the beneficial effects of alcohol intake on coronary disease occur only at moderate intakes, and for those patients with hypertension, hypertriglyceridaemia or cerebrovascular disease, alcohol intake probably does not confer benefit.
''SAMIKSHA HEART AND DIABETIC CARE'' Smoking The Framingham study found an 18% increase in coronary events for males and a 31% increase for females for every 10 cigarettes smoked per day. There is more of an association between smoking and myocardial infarction than between smoking and stable angina. Smoking increases the risk of stroke, coronary heart disease and peripheral vascular disease through a number of mechanisms (Table 1.11). Smoking is a major factor in the increased risk of coronary heart disease for women using oestrogen-containing contraceptive pills Some effects of smoking 1 Increased atherogenesis, probably by toxic injury to endothelial cells 2 Hypoxia, resulting in intimal proliferation 3 Thrombogenesis 4 Reduction in HDL 5 Oxidation of lipids 6 Increase in fibrinogen levels Smoking cessation is associated with a rapid decline in death rates from coronary disease, probably because of smoking’s thrombogenic effects. Smoking seems less important as a risk factor in populations with low LDL levels Smoking cessation Many strategies are available to help patients to give up smoking. These should all begin with an explanation of the reasons smoking cessation is worthwhile. Some explanation of the mechanism of its deleterious effects may be helpful. Patients who have recently presented with possible cardiac symptoms may be amenable to advice of this nature. It is also especially important to give strong advice about smoking to patients with multiple existing coronary risk factors. The rapidity at which benefits begin to occur, and the risks and difficulties involved in further cardiac treatment (e.g. coronary surgery) for smokers, should be emphasised. The postoperative risk is considerably higher for smokers, particularly for serious chest infections. This risk falls quickly (within four weeks) once smoking is stopped. Nicotine replacement patches may be helpful and appear safe even for patients with ischaemic heart disease. The drug bupropion, which is a non-tricyclic antidepressant, is now available for patients who wish to stop smoking. This drug seems safe for patients with cardiac disease, at least for those without unstable symptoms. It does not cause conduction abnormalities or increase the risk of ventricular arrhythmias. Patients should be advised to continue smoking when they first start the drug but plan to stop on a particular day after about a week of treatment. The drug is usually continued for at least seven weeks. The starting dose is 150 mg daily and then 150 mg twice a day. It is important to discuss strategies for smoking cessation with the patient and to try to establish a treatment plan that suits the individual. Passive smoking Evidence of an increased cardiovascular risk from environmental smoke has been available for some years.20 Legislation is gradually reducing the risk for people in occupations associated with smoking (e.g. serving in bars and restaurants) but patients with existing ischaemic heart disease should be advised to avoid exposure.
Cardiologist in Rajanukunte, Bangalore • Factors that increase triglyceride levels 1 Obesity 2 Alcohol 3 Diabetes 4 Oestrogen (including HRT in 20% of users) 5 Diuretics 6 Beta-blockers Secondary causes: • Cushing’s syndrome • acromegaly • uraemia • acute hepatitis
POPULAR CARDIOLOGISTS IN SAHAKARANAGAR Cardiomyopathies and valvular heart disease Regardless of the status of the coronary arterial tree, both primary and secondary heart muscle disease can produce anginal pain through the imbalance of the oxygen demand and supply. Hypertrophic cardiomyopathy is a relatively common cause of angina in the presence of normal coronary arteries. Aortic stenosis is the most common valvular cause of exertional chest tightness, which is probably due to myocardial ischaemia Exertional chest pain, which may be due to right ventricular angina, is a feature of pulmonary hypertension . Syndrome X There is some confusion regarding the ‘metabolic’ and ‘cardiac’ varieties. The former is a combination of insulin resistance, obesity, pro-inflammatory state and so on, leading to raised cardiovascular risk in the sufferers. The latter is, or should be, a form of stable effort angina that can be ascribed to coronary microvascular malfunction.23 The epicardial coronary tree is normal and the diagnosis is rather difficult to make except by exclusion. Acute coronary syndromes The terminology used to describe acute coronary syndromes (ACSs) continues to evolve as clinicians attempt to adjust to the accumulating evidence of the usefulness of modern cardiac markers and the treatment implications of different results. The most recent terminology is designed to help with treatment decisions based on the earliest clinical information from the patient. This comes from the history and the ECG. When the patient’s symptoms suggest an acute coronary syndrome, the first decisions about diagnosis and treatment are based on the ECG. If there is ST elevation present in a pattern to suggest myocardial infarction, the diagnosis is of ‘ST elevation myocardial infarction’ (STEMI). If there is no ST elevation, the initial diagnosis is of ‘non-ST elevation acute coronary syndrome’ (NSTEACS).24 This elegant phrase has replaced ‘non-ST elevation myocardial infarction’ (non- STEMI). The reason is that the diagnosis of infarction cannot be made in the absence of ST elevation until cardiac marker estimations are available. The decisions about treatment, however, need to be made immediately and are based on symptoms and ECG changes.
POPULAR CARDIOLOGIST IN AMRUTHA HALLI , BANGALORE Assessment of patients with hypertension A patient with definite or possible newly diagnosed hypertension needs at least a basic clinical assessment to look for possible aetiology, severity and signs of complications. The history Questioning should be directed towards the following areas. 1 Past history. Has hypertension been diagnosed before? What treatment was instituted? Why was it stopped? 2 Secondary causes. Important questions relate to: • a history of renal disease in the patient or his or her family, recurrent urinary tract infec-­ tions, heavy analgesic use or conditions leading to renal disease (e.g. systemic lupus erythematosus (SLE)) • symptoms suggesting phaeochromocytoma (flushing, sweats, palpitations) • symptoms suggesting sleep apnoea • muscle weakness suggesting the hypokalaemia of hyperaldosteronism • Cushing’s syndrome (weight gain, skin changes) • family history of hypertension. 3 Aggravating factors: • high salt intake • high alcohol intake • lack of exercise • use of medications: NSAIDs, appetite suppressants, nasal decongestants, monoamine oxidase inhibitors, ergotamine, cyclosporin, oestrogen-containing contraceptive pills • other: use of cocaine, liquorice, amphetamines. 4 Target organ damage: • stroke or transient ischaemic attack (TIA) • angina, dyspnoea • fatigue, oliguria • visual disturbance • claudication. 5 Coexisting risk factors: • smoking • diabetes • lipid levels, if known
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
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