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.

CARDIOLOGISTS IN YELAHANKA NEWTOWN BANGALORE 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 shoulder regions of these caps are at risk of rupturing and allowing material from within the plaque to come in contact with the blood stream. This material is intensely thrombogenic. Stable fibrous plaques are much less likely to rupture in this way. Efforts are underway to develop tests that can identify vulnerable plaques. This is not yet possible, but multi-slice CT scanning and possibly MRI angiography may i

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

samiksha heart and diabetic care new town yelahanka banglore The Evaluation of the Cause of Heart Failure: The History History to include inquiry regarding: Hypertension Diabetes Dyslipidemia Valvular heart disease Coronary or peripheral vascular disease Myopathy Rheumatic fever Mediastinal irradiation History or symptoms of sleep-disordered breathing Exposure to cardiotoxic agents Current and past alcohol consumption Smoking Collagen vascular disease Exposure to sexually transmitted diseases Thyroid disorder Pheochromocytoma Obesity Family history to include inquiry regarding: Predisposition to atherosclerotic disease (Hx of MIs, strokes, PAD) Sudden cardiac death Myopathy Conduction system disease (need for pacemaker) Tachyarrhythmias Cardiomyopathy (unexplained HF) Skeletal myopathies

samiksha heart and diabetic care new town yelahanka banglore The Evaluation of the Cause of Heart Failure: The History History to include inquiry regarding: Hypertension Diabetes Dyslipidemia Valvular heart disease Coronary or peripheral vascular disease Myopathy Rheumatic fever Mediastinal irradiation History or symptoms of sleep-disordered breathing Exposure to cardiotoxic agents Current and past alcohol consumption Smoking Collagen vascular disease Exposure to sexually transmitted diseases Thyroid disorder Pheochromocytoma Obesity Family history to include inquiry regarding: Predisposition to atherosclerotic disease (Hx of MIs, strokes, PAD) Sudden cardiac death Myopathy Conduction system disease (need for pacemaker) Tachyarrhythmias Cardiomyopathy (unexplained HF) Skeletal myopathies

DCardiologist in Vidyaranyapura, Bangalore • etected 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 (p. 136), 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. hsCRP measurements and risk of vascular events (stroke, myocardial infarction, acute coronary syndrome) Low risk Intermediate High hsCRP level < 1 mg/L 1–3 mg/L > 3 mg/L Note: levels > 10 mg/L suggest acute inflammation and should be repeated after a few week In some studies erectile dysfunction has reliably preceded symptomatic coronary disease in twothirds of patients by an average of three years.30 A history of this problem in men indicates an increased risk of vascular events. It is strongly associated with other risk factors such as smoking and diabetes but remains significant after allowing for these. Infectious agents There is continuing mild interest in the role of infection in promoting atherosclerosis and especially unstable coronary syndromes. Chlamydia pneumoniae and Helicobacter pylori are commonly found in atheromatous plaques. It is possible one or more infectious agents could be the stimulus that sets off the inflammatory process that changes plaque structure, weakens the fibrous cap and unleashes the coagulation cascade that occludes the vessel. The ACADEMIC study was not associated with a reduction in early coronary events

DCardiologist in Vidyaranyapura, Bangalore • etected 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 (p. 136), 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. hsCRP measurements and risk of vascular events (stroke, myocardial infarction, acute coronary syndrome) Low risk Intermediate High hsCRP level < 1 mg/L 1–3 mg/L > 3 mg/L Note: levels > 10 mg/L suggest acute inflammation and should be repeated after a few week In some studies erectile dysfunction has reliably preceded symptomatic coronary disease in twothirds of patients by an average of three years.30 A history of this problem in men indicates an increased risk of vascular events. It is strongly associated with other risk factors such as smoking and diabetes but remains significant after allowing for these. Infectious agents There is continuing mild interest in the role of infection in promoting atherosclerosis and especially unstable coronary syndromes. Chlamydia pneumoniae and Helicobacter pylori are commonly found in atheromatous plaques. It is possible one or more infectious agents could be the stimulus that sets off the inflammatory process that changes plaque structure, weakens the fibrous cap and unleashes the coagulation cascade that occludes the vessel. The ACADEMIC study was not associated with a reduction in early coronary events

Cardiology doctors Mathikere – BELCardiologist in Doddaballapur Road, Bangalore • Intravascular ultrasound Intravascular ultrasound (IVUS) enables the production of cross-sectional ultrasound images of the coronary arteries . A fine ultrasound transducer is advanced into the coronary via a conventional cardiac catheter placed in the ostium. As the wire is withdrawn, images of the artery wall are recorded. This investigation has given much useful information about the nature of coronary plaques and how they differ in regard to their contents and structure. A more accurate measurement of the severity of lesions is possible. At conventional angiography the severity of a lesion is judged by comparing it with adjacent, apparently normal vessels. When these apparently normal areas are inspected with ultrasound, many are found to be quite abnormal. Areas that had been apparently successfully dilated by balloon angioplasty with a good angiographic result may appear quite severely narrowed when examined by IVUS. The struts of an implanted stent may be seen to be poorly opposed to the intima. This may explain some of the problems with restenosis and thrombosis after angioplasty. IVUS is unlikely to become a routine investigation because it remains expensive and time-consuming.

heart doctors Doctors in Vidyaranyapura Anti-platelet therapy Unless there is a contraindication (usually gastric intolerance but occasionally allergy) all patients with suspected angina should take aspirin.14 A daily dose of 75 mg is enough to cause irreversible cyclo-oxygenase inhibition of all the patient’s platelets. Recovery occurs only as platelets are replaced. This treatment causes significant reduction in platelet adhesiveness and reduces the risk of thrombosis within the coronary arteries following rupture of an atherosclerotic plaque. There is a definite improvement in mortality when aspirin is used after myocardial infarction and a probable improvement for patients with angina. The use of half an aspirin tablet (150 mg) is the cheapest approach to aspirin use, but 100 mg preparations in coated tablets and calendar packets are available. Patients unable to tolerate aspirin because of gastric side effects can often be treated with the combination of aspirin and a proton pump inhibitor. The relative risk of cerebral haemorrhage increases by 30% for patients taking aspirin but the absolute risk is less than 1 per 1000 patient years of treatment. For patients with aspirin allergy or intolerance, 75 mg of clopidogrel a day is usually a safer but expensive alternative. It is also associated with a small risk of gastrointestinal bleeding (1.99% versus 2.66% for aspirin over two years in the CAPRIE study). Combination (dual anti-platelet/aspirin and clopidogrel) treatment is not currently indicated for stable angina. Aspirin and clopidogrel resistance

heart doctors Doctors in Vidyaranyapura Anti-platelet therapy Unless there is a contraindication (usually gastric intolerance but occasionally allergy) all patients with suspected angina should take aspirin.14 A daily dose of 75 mg is enough to cause irreversible cyclo-oxygenase inhibition of all the patient’s platelets. Recovery occurs only as platelets are replaced. This treatment causes significant reduction in platelet adhesiveness and reduces the risk of thrombosis within the coronary arteries following rupture of an atherosclerotic plaque. There is a definite improvement in mortality when aspirin is used after myocardial infarction and a probable improvement for patients with angina. The use of half an aspirin tablet (150 mg) is the cheapest approach to aspirin use, but 100 mg preparations in coated tablets and calendar packets are available. Patients unable to tolerate aspirin because of gastric side effects can often be treated with the combination of aspirin and a proton pump inhibitor. The relative risk of cerebral haemorrhage increases by 30% for patients taking aspirin but the absolute risk is less than 1 per 1000 patient years of treatment. For patients with aspirin allergy or intolerance, 75 mg of clopidogrel a day is usually a safer but expensive alternative. It is also associated with a small risk of gastrointestinal bleeding (1.99% versus 2.66% for aspirin over two years in the CAPRIE study). Combination (dual anti-platelet/aspirin and clopidogrel) treatment is not currently indicated for stable angina. Aspirin and clopidogrel resistance