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heart doctors in Sahakara Nagar, Bangalore • A clinical approach to hypertension The aims of assessing the hypertensive patient are to: n assess the severity of hypertension n identify any secondary causes n identify aggravating factors n identify target organ damage n assess and manage coexisting CVD risk factors n identify factors affecting the choice of treatment n establish baseline clinical and laboratory data
PAPULAR CARDIOL0GISTS IN BANGALORE A clinical approach to hypertension The aims of assessing the hypertensive patient are to: assess the severity of hypertension identify any secondary causes identify aggravating factors identify target organ damage assess and manage coexisting CVD risk factors identify factors affecting the choice of treatment establish baseline clinical and laboratory data.
THE BEST CARDIOLOGIST IN YELAHANKA A clinical approach to hypertension The aims of assessing the hypertensive patient are to: assess the severity of hypertension identify any secondary causes identify aggravating factors identify target organ damage assess and manage coexisting CVD risk factors identify factors affecting the choice of treatment establish baseline clinical and laboratory data.
THE BEST HEART SPECIALISTS IN BANGALORE Angioplasty Balloon dilatation of coronary artery stenoses was first performed in the late 1970s by Andreas Grunzig. The technique has undergone many refinements and is now widely used for the treatment of angina not responding to medical treatment. Angioplasty has not been shown to improve the prognosis of patients with stable angina. Coronary artery bypass grafting (CABG) has similarly not been shown to prolong life for most stable angina patients. However, both treatments are very successful in relieving the symptoms of angina. The COURAGE Trial compared optimal medical treatment of angina with angioplasty but excluded patients with symptoms refractory to medical treatment.1 Not surprisingly, this group of stable mild angina patients had a similar outcome with angioplasty and medical treatment. The trial suggests that compared with optimal medical treatment, angioplasty is a safe and slightly more effective treatment for stable angina. Patients can make an informed choice between these two treatments. The majority of patients treated with angioplasty in Australia have acute coronary syndromes and here there is good evidence of prognostic benefit with angioplasty compared with medical treatment. In many centres one-, two- and complicated three-vessel disease are managed this way. It has been shown to be as effective as coronary surgery for these patients but at the price of a higher rate of re-intervention. This is because the greatest limitation of angioplasty is the rate of restenosis in vessels that have been dilated. Restenosis
CARDIOLOGY DOCTORS IN BANNERGHTTA ROAD ST elevation myocardial infarction Modern treatment of myocardial infarction has made a profound difference to the prognosis of this life-threatening condition. Before the introduction of CCUs, the expected in-hospital mortality of this condition was more than 20%. Monitoring and treatment of arrhythmias, and correction of biochemical and, where possible, haemodynamic complications in CCUs reduced this to about 12%. The ‘thrombolytic era’, which began with the publication of the results of the GISSI Trial, 31 has dramatically changed the approach to the management of infarction. The use of thrombolytic drugs (streptokinase in GISSI) reduced mortality to less than 10%, with greater benefit for those treated early.32 The addition of aspirin in later trials reduced mortality to about 7% and many CCUs now achieve mortality rates of 5 or 6%. There is no doubt that early treatment makes the greatest difference, but some benefit may be seen with treatment given up to 12 hours after the onset of symptoms of infarction. In centres where it can be performed primary angioplasty is the reperfusion treatment of choice for myocardial infarction. This is a grade A recommendation—level I evidence.33 Mortality rates below 5% can be achieved. The rationale for reperfusion treatment came with the realisation that infarction was caused by thrombosis within a coronary artery (a mechanism first proposed by Herrick in 191234) and that restoring blood flow before irreversible damage had occurred would be helpful. It has been known for a long time that the prognosis following myocardial infarction depends more than anything else on the amount of left ventricular damage that has occurred. For these reasons the early diagnosis of infarction has become very important. Patients with symptoms suggestive of infarction should have an ECG performed as soon as possible. If nondiagnostic changes are present, the tracing should be repeated frequently so that appropriate early decisions about treatment can be made if changes appear. The current ECG criteria for the use of reperfusion treatment (primary angioplasty
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
GOOD AND WELL CARDIOLOGISTS IN SILKBOARD BANGALORE 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
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
SAMIKSHA HEART AND DIABETIC CARE ''CONNECTIVE TISSUE DISORDERS'' ''Marfan Syndrome'' Marfan syndrome is a systemic connective tissue disorder with a frequency of 2 to 3 in 10, 000. The disorder is characterized by manifestations involving the cardiovascular, skeletal, and ocular systems. Current diagnostic criteria are based on involvement of above organ systems and family history. Cardiovascular manifestations include mitral valve prolapse, progressive aortic root enlargement, and ascending aortic aneurisms, possibly leading to aortic regurgitation, dissection, or rupture. Some characteristic skeletal manifestations of this syndrome include disproportional increase of linear bone growth resulting in malformations of the digits (arachnodactyly), craniofacial abnormalities, pectus excavatum/carinatum, and scoliosis. A common ocular involvement is severe myopia and lens dislocation in one or both eyes (ectopia lentis). Marfan syndrome is an autosomal dominant disorder caused by fibrillin-1 gene mutations encoding for the extracellular matrix protein fibrillin (Fbn-1). Fibrillin is an integral component of both elastic and nonelastic connective tissue. The mechanism of fibrillin mutation in Marfan syndrome remains unclear. However, animal models of Fbn-1 have demonstrated a role of TGF-beta signaling. In some patients with phenotypes similar to Marfan syndrome but without fibrillin- 1 gene mutations, TGF-beta receptor mutations have been identified, suggesting a significant role of TGF-beta pathway in the pathogenesis of Marfan syndrome features. Aortic root involvement remains the leading cause of death in patients with Marfan syndrome. Echocardiography is recommended to routinely screen and to follow aortic root dilation. In addition, all first-degree relatives of the family should have screening echocardiography. Patients should be advised against strenuous exercises. Medical therapy for Marfan syndrome includes beta-blockers to reduce myocardial contractility and pulse pressure. Animal models of Marfan syndrome have demonstrated a possible benefit of losartan in preventing progression of the disease by inhibiting the TGF-beta pathway, and this therapy is the subject of an active clinical trial. Elective aortic root replacement remains the therapy of choice once the aortic root becomes significantly enlarged. Marfan patients who become pregnant need to be counseled not only about the 50% chance of transmitting the disease but also the substantially increased risk of aortic rupture/dissection during and after pregnancy. Important components of Marfan syndrome counseling are consideration of contraception and pregnancy management. Loeys-Dietz Syndrome Recently, an aortic aneurysm syndrome has been identified with TGF-beta receptor mutations. Loeys-Dietz syndrome is an autosomal dominant condition with a characteristic triad of arterial tortuosity/aneurysm, hypertelorism, and bifid uvula or cleft palate. There is significant overlap with Marfan syndrome, and the management is similar in terms of cardiovascular manifestation. Early, elective, surgical intervention should be considered in patients with significant aneurysmal dilation of the aorta. Some clinicians have argued for much earlier surgical intervention for the dilated aorta in this condition, compared with Marfan syndrome, since there appears to be a much greater risk of rupture and dissection at earlier ages and smaller aortic sizes. Pregnancy counseling is also an integral part of therapy. Ehlers-Danlos Syndrome Ehlers-Danlos syndrome is a group of disorders that affect connective tissue development due to defects in collagen and connective tissue biosynthesis. Prevalence of the disease is about 1 in 400, 000 people in the United States. Cardiac manifestations include spontaneous rupture of medium to large sized arteries including the aorta. Frequently, extracardiac presentations include hyperextensible skin and hypermobile joints. To date, 11 types of the disorder have been recognized, but collagen defects have been described in only 6 types. Although all types of Ehlers-Danlos syndrome affect the joints and the skin, clinical features vary by type. Different features characterize each type of the syndrome. Type IV carries the poorest prognosis, especially due to spontaneous ruptures of arteries and organs. Extreme caution needs to be taken if surgical intervention is needed due to weakened connective tissue structures. Many genes, including ADAMTS2, COL1A1, COL1A2, COL3A1, COL5A1, COL5A2, PLOD1, and TNXB, have been implicated in the pathogenesis of Ehlers- Danlos syndrome, but the predominant cardiovascular concern exists in the Type IV vascular form of Ehlers-Danlos associated with mutations in the COL3A1 gene and aortic dilation/aneurysms. Other less commonly associated anomalies include ventricular septal defect, patent ductus arteriosus, bicuspid pulmonic valve, and Ebstein’s anomaly. Bicuspid aortic valve has been shown to demonstrate familial clustering. However, identifying culprit genes have been difficult due to variable penetrance and the common nature of the disorder.
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