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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.
POPULAR CARDIOLOGISTS IN H S R LAYOUT Ventricular tachycardia Ventricular tachycardia is defined as three or more ventricular ectopic beats at a rate over 100/minute. It is said to be sustained if it lasts more than 30 seconds. Most broad-complex tachycardias are ventricular (rather than supraventricular with aberrant conduction). The diagnosis of VT is greatly strengthened if there is a history of myocardial infarction or cardiac failure but, oddly enough, the patient’s haemodynamics are of no help. A number of criteria have evolved over the years to help ascertain the diagnosis of VT over aberrancy. These include: evidence of AV dissociation—P waves can be seen unrelated to the QRS complexes (they are usually visible only at relatively slow VT rates) the presence of supraventricular capture or fusion beats visible retrograde conduction with 2:1 block (P waves visible following every second complex) the presence of monophasic R, qR or QR patterns in V1, provided a septal infarction has not modified a RBBB a taller left rabbit ear in RR' or qRR' complexes in V1 n QS complexes in V1 with a slow S descent and sharp upstroke—the opposite of LBBB—or a broad small primary R wave in rS morphology (the Rosenbaum pattern) RAD in the frontal plane with LBBB-like QRS complexes
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
SAMIKSHA HEART AND DIABETIC CARE IN YELAHANKA Echocardiographic findings in certain cardiac abnormalities It is important to be aware that modern colour flow mapping is so sensitive that small amounts of regurgitation are often detected from quite normal valves. Deciding whether these jets are significant can be difficult and requires experience. Mitral stenosis Thickening and doming of the mitral valve leaflets is visible on M mode and 2D scanning , It may be possible to measure the valve area by planimetry . Secondary changes such as left atrial size and the presence of rheumatic disease of other valves can be seen. Doppler interrogation of the jet of blood entering the left ventricle through the mitral valve will enable estimation of the valve area by a formula called the pressure half-time equation This will usually give accurate and consistent estimates of the valve area and is especially useful for serial measurements over months or years. It will also be possible to detect associated mitral regurgitation with Doppler. Mitral regurgitation and mitral valve prolapse Here the mitral valve may appear normal and abnormal co-aptation of the leaflets is not usually visible . The left atrium will appear enlarged if significant chronic MR is present, and if this is severe left ventricular dilatation will be present. If the MR is due to mitral valve
DIABETIC SPECIALIST IN YALAHANKA Syncope and dizziness The history Syncope is a transient loss of consciousness resulting from cerebral anoxia, usually due to inadequate blood flow. Syncope may represent a simple faint or be a symptom of cardiac or neurological disease. Establish whether the patient actually loses consciousness and under what circumstances the syncope occurs—for example, on standing for prolonged periods or standing up suddenly (postural syncope), while passing urine (micturition syncope), on coughing (tussive syncope) or with sudden emotional stress (vasovagal syncope). Find out whether there is any warning such as dizziness or palpitations, and how long the episodes last. Recovery may be spontaneous or require attention from bystanders. Bystanders may also have noticed abnormal movements if the patient has epilepsy, but these can also occur in primary syncope. If the patient’s symptoms appear to be postural, enquire about the use of anti-hypertensive or anti-anginal drugs and other medications that may induce postural hypotension. If the episode is vasovagal, it may be precipitated by something unpleasant like the sight of blood, or it may occur in a hot crowded room; patients often feel nauseated and sweaty before fainting and may have had prior similar episodes, especially during adolescence and young adulthood. The diagnosis of this relatively benign and very common cause of syncope can usually be made from the history. Patients with very typical symptoms rarely require extensive investigations. If syncope is due to an arrhythmia there is often sudden loss of consciousness regardless of the patient’s posture. A history of rapid and irregular palpitations or a diagnosis of atrial fibrillation in the past suggests the possibility of sick sinus syndrome. These patients have intermittent tachycardia, usually due to atrial fibrillation, and episodes of profound bradycardia, often due to complete heart block. Chest pain may also occur if the patient has aortic stenosis or hypertrophic cardiomyopathy. Exertional syncope may occur in these patients because of obstruction to left ventricular outflow by aortic stenosis or septal hypertrophy . Dizziness that occurs even when the patient is lying down or that is made worse by movements of the head is more likely to be of neurological origin (vertigo), although recurrent tachyarrhythmias may occasionally cause dizziness in any position. Try to decide whether the dizziness is really vertiginous (there is a sensation of movement or spinning of the surroundings or the patient’s head), or whether it is a presyncopal feeling. A family history of syncope or sudden death raises the possibility of an ion channel abnormality (long QT syndrome, Brugada syndrome or hypertrophic cardiomyopathy). Attempts should be made to find out what the diagnosis was for the affected relatives. A past history of severe structural heart disease, especially heart failure,
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.
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
HEART SPECIALISTS IN GANGAMMA CIRCLE 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 • existing vascular disease • family history of ischaemic heart disease. 2• HYPERTENSION 6 Factors affecting choice of treatment: • diabetes (problems with thiazides and beta-blockers) • gout (problems with thiazides) • asthma (problems with beta-blockers) • heart failure (problems with verapamil, diltiazem, some beta-blockers, monoxidine) • severe peripheral arterial disease (problems with beta-blockers) • bradycardia or heart block (problems with beta-blockers, verapamil, diltiazem) • renovascular disease (problems with ACE inhibitors, angiotensin receptor antagonists (ARAs)) • problems with previous anti-hypertensive agents • allergies • likelihood of pregnancy (ACE inhibitors, diuretics and some calcium antagonists are contraindicated). The examination The physical examination should be undertaken with a view to establishing severity. 1 Measure the blood pressure. 2 Look for secondary causes. • Check the appearance for Cushing’s syndrome (central obesity, striae, muscle wasting), acromegaly, polycythaemia and uraemia. • Undertake abdominal palpation for renal masses (polycystic kidneys), occasionally adrenal mass, and auscultation for renal bruit (heard to the left or right of the mid-line above the umbilicus, often into the flanks). • Assess radiofemoral pulse delay and listen for mid
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
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