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HEART SPEACIALISTS IN BANGALORE Stress echocardiography Ischaemic areas of myocardium are known to have reduced contraction compared with normal areas. This can be demonstrated by high-quality echocardiograms. A number of standard views of the heart are obtained and the wall is divided into regions that are assessed for reduced motion. The echo equipment must be designed to store rest images and to present them next to stress images on a split screen so that direct comparison can be made. The stress can be provided by exercise or dobutamine infusion. Exercise echocardiography is difficult to perform because of movement problems and there is quite high inter-reporter variability, but both techniques can approach the accuracy of sestamibi testing in experienced hands. It is not possible to obtain images of adequate quality in all patients.
CARDIOLOGIST IN DODDABOMMASANDRA, BANGALORE Cardiac rehabilitation Although rehabilitation has been a part of the management of patients following a myocardial infarction since the beginning of the last century, ideas have changed radically about the form this should take. In the early 1900s Sir Thomas Lewis insisted his patients remain in bed and be ‘guarded by day and night nursing and helped in every way to avoid voluntary movement or effort’. These severe restrictions were continued for at least six to eight weeks. The thinking was that complete rest would reduce the risk of aneurysm formation and avoid hypoxia that might cause arrhythmias. Even after discharge mild exertion was discouraged for up to a year and return to work was most unusual. In the 1970s periods of bed rest of between one and four weeks were enforced and patients remained in hospital for up to four weeks. It is now clear that this de-conditioning has many adverse physical and psychological effects. Patients with uncomplicated infarcts are now mobilised in hospital within a day or so of admission and are often discharged on the third day if successful primary angioplasty has been performed. Many hospitals provide a supervised rehabilitation program for patients who have had an infarct or episode of unstable angina. The program begins in hospital as soon as possible after admission. It includes a graded exercise regimen and advice about risk factor control. Such programs have many benefits for patients to help them to return quickly to normal life, including work and sexual activity. The supervised exercise regimen helps restore the patient’s confidence. There is clear evidence of the benefits of exercise for patients with ischaemic heart disease.54 Rehabilitation programs have been shown to be cost-effective. Well-conducted programs are tailored to individual patients’ needs and are very popular with many patients.55 There are often long-term exercise groups available for people who have completed the formal classes. Non-cardiac causes of chest pain Pulmonary embolism
Average reductions in coronary events (benefits are greatest in patients with highest total risk) 1 Smoking cessation: 50% reduction in coronary events6 2 Low-dose aspirin in high-risk patients: 25% reduction in coronary events7 3 20% reduction in total cholesterol with statin treatment: 30% reduction in coronary events8 4 Treatment with pravastatin after acute coronary events: 22% reduction in mortality9 5 5–6 mmHg reduction in blood pressure: 15% reduction in coronary events (40% risk reduction for stroke)10 6 30 minutes of moderate exercise a day: 18% reduction in coronary events11 CARDIAC SPEACIALIST IN HEBBALA
CARDIOLOGIST IN YELAHANKA SECOND DEGREE AV BLICK There are two basic types of second-degree AV block: AV nodal Möbitz type I (Wenckebach) heart block, and the more distal and more sinister Möbitz type II heart block. Möbitz type I heart block is much more common. In Möbitz type I block the PR interval lengthens progressively with each cardiac cycle, until an atrial wave is not conducted. There is recovery of conduction and the next a wave is conducted with a shorter interval and the cycle begins again. The QRS complex is narrow (Fig 3.10) (unless associated with pre-existing BBB). The increment is largest between the first and second conducted P wave, and the PR interval continues to increase by less and less until a P wave is dropped. Möbitz type II heart block is almost always associated with a BBB (Fig 3.11), since its origin is intraventricular (below the AV node), and it tends to lapse suddenly into extreme bradycardia or asystole. It tends to be over-diagnosed, especially in the setting of 2:1 AV block (Fig 3.12). There is no lengthening of the PR interval before an atrial wave is not conducted. At times, atropine or exercise can demonstrate the site of the block, by increasing the block from 2:1 to a higher grade when the underlying mechanism is Möbitz II. Conversely, Wenckebach conduction may improve to 3:2 or better. For a distinction to be made between Möbitz type I and Möbitz type II, at least two consecutively conducted P waves have to be evaluated. This is impossible in 2:1 conduction (block) and can only be reported as 2:1 AV block (Fig 3.12). Yet this is very commonly reported as
POPULAR CARDIOLOGISTS IN SAHAKARANAGAR Left ventricular hypertrophy Although the ECG is reasonably specific, it is not as sensitive as echocardiography in detecting LVH. The LVH voltage alone may be a normal finding in younger subjects, but in adults over 35 years it usually connotes true LVH, especially if corroboratory findings are present Unfortunately, LVH with ST/T changes may be impossible to separate from LVH voltage complicated by ST/T changes of different, especially ischaemic, origin . Right ventricular hypertrophy The main criteria fSAor detecting RVH are RAD over +110° and a dominant R wave in V1 (in the absence of its other causes and in the presence of normal-duration QRS) In congenital heart disease conduction defects often come to obscure the hypertrophy patterns.
THE BEST CARDIOLOGISTS IN YELAHANKA Second-degree AV block There are two basic types of second-degree AV block: AV nodal Möbitz type I heart block, and the more distal and more sinister Möbitz type II heart block. Möbitz type I heart block is much more common. In Möbitz type I block the PR interval lengthens progressively with each cardiac cycle, until an atrial wave is not conducted. There is recovery of conduction and the next a wave is conducted with a shorter interval and the cycle begins again. The QRS complex is narrow (unless associated with pre-existing BBB). The increment is largest between the first and second conducted P wave, and the PR interval continues to increase by less and less until a P wave is dropped. Möbitz type II heart block is almost always associated with a BBB , since its origin is intraventricular (below the AV node), and it tends to lapse suddenly into extreme bradycardia or asystole. It tends to be over-diagnosed, especially in the setting of 2:1 AV block . There is no lengthening of the PR interval before an atrial wave is not conducted. At times, atropine or exercise can demonstrate the site of the block, by increasing the block from 2:1 to a higher grade when the underlying mechanism is Möbitz II. Conversely, Wenckebach conduction may improve to 3:2 or better. For a distinction to be made between Möbitz type I and Möbitz type II, at least two consecutively conducted P waves have to be evaluated. This is impossible in 2:1 conduction (block) and can only be reported as 2:1 AV block (Fig 3.12). Yet this is very commonly reported as Möbitz type
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
HEART DOCTORS IN CHIKKAJALA, BANGALORE; 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.
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.
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