SAMIKSHA HEART AND DIABETIC CARE Welcome to samiksha heart and diabetic care. Our institution was initially started in yelahanka , north bangalore in may 2013. The reason why our centre was started to make available the basic and advanced Cardiac and diabetic services and treatment accessible early. Samiksha heart and diabetic care offers a vast array of outpatient cardiac services. Our centre is fully equipped to provide patients with all of the usual cardiodiagnostic services (ECGs, echocardiography, stress tests, holter monitors, ambulatory BP monitering etc.) needed to effectively manage your cardiovascular health. We diagnose and treat any cardiac disorder – simple or complex from diagnosis to intervention and comprehensive treatment. we share the common dream of giving you the compassionate healthcare that you deserve. Our specialized services have been designed to deliver the care that is best suited to your needs. Despite all the latest advances we feel that the old fashioned physician-patient relationship can be maintained here . We just don’t treat diseases, we care for you as a person. Accessibility, cost and care are optimal in our centre. We believe in making your concerns ours. Our services ensure your constant comfort and quick recovery. However, unlike the same services provided through the hospital our practice helps our patients reduce the cost of their health care. We look forward to seeing you in our practice, where we put our patients first. Success for us is the smile on our patients’ faces as they leave our hospital.

It may also improve arterial oxygenation by reducing pulmonary vascular congestion DIURETICS. Mild heart failure responds well to diuretics such as furosemide, Dose - 10 to 40 mg, repeated at 3- to 4-hour intervals if necessary. It reduces pulmonary capillary pressure reduces dyspnea. Decreased LVDV↓ LV wall tension - ↓ myocardial oxygen requirements and may lead to improvement of contractility and augmentation of the ejection fraction, stroke volume, and cardiac output. The reduction of elevated left ventricular filling pressure may also enhance myocardial oxygen delivery by diminishing the impedance to coronary perfusion attributable to elevated ventricular wall tension. .

Important coronary risk factors 1 Existing vascular disease (coronary, cerebral or peripheral) 2 Age 3 Dyslipidaemia 4 Smoking 5 Family history 6 Hypertension 7 Male sex/hormonal factors 8 Diabetes 9 Renal impairment 10 Obesity 11 Inactivity 12 Thrombogenic factors 13 Other dietary factors 14 Homocystinaemia 15 Psychological factors 16 Elevated hsCRP 17 Abnormal CT calcium score/coronary angiogram 18 Left ventricular hypertrophy (hypertensive patients) 19 Abnormal

THE CARDIOLOGY CLINICS IN BANGALORE Important coronary risk factors 1 Existing vascular disease (coronary, cerebral or peripheral) 2 Age 3 Dyslipidaemia 4 Smoking 5 Family history 6 Hypertension 7 Male sex/hormonal factors 8 Diabetes 9 Renal impairment 10 Obesity 11 Inactivity 12 Thrombogenic factors 13 Other dietary factors 14 Homocystinaemia 15 Psychological factors 16 Elevated hsCRP 17 Abnormal CT calcium score/coronary angiogram 18 Left ventricular hypertrophy (hypertensive patients) 19 Abnormal

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 CARDIOLOGISTS IN YELAHANKA Pulmonary hypertension Pulmonary hypertension is an uncommon but important cause of dyspnoea. Many patients with this chronic and often severe illness will have raised pulmonary artery pressures as a result of a cardiac or respiratory illness. Other patients may present with increasing dyspnoea without an obvious cardiac or respiratory problem. Idiopathic (primary) pulmonary hypertension (IPH) is diagnosed only when other causes of pulmonary hypertension have been excluded. By definition, pulmonary hypertension is present when the mean pulmonary artery pressure (PAP) exceeds 25 mmHg at rest or 30 mmHg during exercise. The classification of pulmonary hypertension has been revised. The Venice classification was released in 2003. The term ‘primary pulmonary hypertension’ has been replaced with ‘idiopathic pulmonary hypertension’ Patients may have used fenfluramine or phenermine (appetite-suppressing drugs), or both. Use of these drugs for long periods has been associated with the greatest risk of developing pulmonary hypertension. In cases of IPH there may be a family history (6%; autosomal dominant condition with incomplete penetrance, 20–80%). The majority of familial cases are associates with a mutation on the BMPR2 gene. There may be associated symptoms including fatigue, chest pain, syncope and oedema. Cough and haemoptysis can be present. 270 PRACTICAL CARDIOLOGY The examination may help in assessing the severity of the patient’s dyspnoea as he or she undresses. Try to work out the patient’s functional class from the history and examination (p. 256) (NYHA I–IIII, often called the NYHA–WHO class when related to pulmonary hypertension). There may be signs of chronic lung disease or congenital heart disease, or specific signs of pulmonary hypertension and right heart failure (p. 257). Investigations are directed at finding an underlying reason for pulmonary hypertension— idiopathic pulmonary hypertension is a diagnosis of exclusion—and at assessing its severity and potential reversibility. The chest X-ray is abnormal in 90% of IPH patients. It may show pulmonary fibrosis or an abnormal cardiac silhouette—RV dilatation. There may be large proximal pulmonary arteries that appear ‘pruned’ in the periphery, and the heart may appear enlarged because of right ventricle dilatation) Respiratory function tests may show a normal, restrictive or obstructive pattern. Moderate pulmonary hypertension itself is associated with a reduction in the diffusing capacity for the carbon monoxide test (DLCO) to about 50% of predicted. On the ECG look for signs of right heart strain or hypertrophy, which are present in up to 90% of patients The blood gas measurements may show hypercapnia—elevated pCO2 in hypoventilation syndromes—but hypocapnia is more common in IPH because of increased alveolar ventilation. Mild hypoxia (reduction in pO2) may be present in IPH, and is more severe when pulmonary hypertension is secondary to lung disease. On CT pulmonary angiogram (CTPA), ventilation/perfusion (V/Q) lung scan or Doppler venograms look for a deep venous thrombosis (DVT) and PE and assess the extent of involvement of the pulmonary bed. A high-resolution CT scan of the lungs is the best way of looking for interstitial lung disease. The six-minute walking test predicts survival and correlates with the NYHA–WHO class. Reduction in arterial oxygen concentration of more than 10% during this test predicts an almost threefold mortality risk over 29 months. Patients unable to manage 332 m in six minutes also have an adverse prognosis.

HEART DOCTORS IN YELAHANKA NEWTOWN, BANGALORE Management of ACS (NSTEACS) Patients with this diagnosis represent a rather heterogeneous group. Some have had the recent onset of angina at the extremes of exercise, others have angina at rest associated with ECG changes. This variation has made attempts to study the effects of different treatment rather difficult. Although the majority of patients with myocardial infarction have a preceding period of unstable angina, only about 5% of all patients admitted to hospital with a diagnosis of an ACS go on to infarct during that admission. The in-hospital mortality for these patients is low. Mortality rates of less than 2% are usual. Nevertheless, there is a real short-term and longerterm risk of infarction, recurrent admission with unstable symptoms and death which is higher than that of patients with stable angina. The diagnosis should therefore lead to admission to a CCU. The cardiac enzymes are, by definition, not elevated in these patients but the newer, more sensitive tests for troponin T and troponin I may be abnormal and indicate a worse prognosis . In the CCU, bed rest, oxygen and ECG monitoring are routinely enforced and any mobile phones taken away (allegedly to protect the monitoring equipment). Recurrence of chest pain can be assessed quickly and ECGs performed to look for changes suggesting infarction. The cardiac biomarkers can be checked regularly. All patients should receive aspirin (300 mg) unless there is a contraindication. Patients with an intermediate or a higher risk should also be given clopidogrel (usually a 300–600 mg loading dose). The use of intravenous heparin has become standard treatment. A typical starting dose is 5000 units as a bolus followed by 24, 000 units over 24 hours. The activated partial thromboplastin time (APPT) should be measured after about six hours of treatment and the infusion rate of heparin adjusted to maintain this at about twice normal. Heparin is generally safe when used in this way. Bleeding problems may sometimes occur and the platelet count should be checked every few days so that heparin-induced thrombocytopenia (HITS), a rare but serious complication, can be detected early. Low molecular weight heparins are at least as effective as unfractionated heparin. These drugs have some advantages over heparin. Their dose response effect is more predictable and they cause less thrombocytopenia. They are effective given subcutaneously without APPT monitoring and are now cheaper than IV heparin when savings on APPT monitoring and the use of infusion sets are considered. A standard twice-daily dose is given according to the patient’s weight—1 mg/kg for enoxaparin (Clexane). The dose is reduced by half for those with moderate or severe renal impairment and for those over the age of 75. Additional treatment should include beta-blockers unless these are contraindicated. These drugs reduce the number of ischaemic episodes and probably the risk of myocardial infarction. Nitrates can be a useful adjunctive treatment. They may be given orally, topically or intravenously. The IV dose can be titrated up or down depending on the amount of pain the patient is experiencing and the severity of side effects such as hypotension and headache. The problem of tachyphylaxis with nitrates can be overcome by steady increases in the IV dose if necessary. Calcium antagonists are appropriate treatment for patients intolerant of beta-blockers and may sometimes be added to beta-blockers. Nifedipine, especially in its short-acting form, should not be used for patients with acute coronary syndromes unless they are already taking beta-blockers. Thrombolytic drugs have been disappointing when used for NSTEACS. In trials where they have been used for patients with ischaemic chest pain but without ST elevation there has been a trend towards an adverse outcome. This may be related to the rebound hypercoagulable state that can occur after their use. In general they should not be used for the treatment of NSTEACS. Glycoprotein IIb/IIIa inhibitors (p. 198) should be given for high-risk patients,

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

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

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.