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THE BEST CARDIOLOGISTS IN YELAHANKA nvestigations of possible or probable stable angina Electrocardiography A standard 12-lead ECG should be obtained in all patients. This is likely to be normal in almost half of patients with subsequently proven coronary artery disease. Nevertheless, an abnormal trace lends weight to the symptoms and favours further investigation. Chest X-ray Routine radiology is not essential but may reveal important co-morbidities. It should always be performed in those with clinical evidence of hypertension, pericarditis (p. 174), heart failure or valvular disease, if only as a baseline. It is similarly indicated for patients with suspected or known pulmonary or systemic disease such as rheumatoid arthritis, COPD or alcoholism. Routine blood tests All patients with suspected angina should have the following routine investigations at presentation (NHF grade A recommendation): n fasting lipids, including total cholesterol, LDLs, HDLs and triglycerides—risk factors n fasting blood sugar—risk factor n full blood count—anaemia exacerbates angina n serum creatinine—impaired renal function is a risk factor and can be worsened by some cardiac investigations. If indicated clinically, thyroid function
THE BEST CARDIOLOGISTS NEAR HSR LAYOUT Coronary angiography (cardiac catheterisation) This procedure enables the cardiologist to visualise the coronary arteries . It is the standard against which other less-invasive investigations are assessed. Selective catheterisation of the right and left coronary ostia is performed. Contrast is then injected into the vessels and digital tape or disc storage of the images obtained. In most hospitals the patient is admitted on the morning of the test and allowed to go home that afternoon. The procedure is most often performed through the femoral artery (Judkins technique) . This artery can be punctured through the skin under local anaesthetic. A fine softtipped guide wire is then advanced into the artery and the needle withdrawn (Seldinger method). A short guiding sheath can then be placed over the wire and long cardiac catheters advanced through this sheath along a long guide wire into the femoral artery and up via the aorta to the aortic arch. The catheter and wire are advanced under X-ray control. Usually one catheter with a curved tip (pig-tail catheter; is advanced across the aortic valve into the left ventricle where left ventricular pressures are measured via a pressure transducer connected to the other end of the catheter. Measurement of the left ventricular end-diastolic pressure gives an indication of left ventricular function. Raised end-diastolic pressure (over 15 mmHg) suggests left ventricular dysfunction . The catheter is then connected to a pressure injector. This enables injection of a large volume of contrast over a few seconds; for example, 35 mL at 15 mL/second. X-ray recording during injection produces a left ventriculogram , Here left ventricular contraction can be assessed and the ejection fraction (percentage of end-diastolic volume ejected with each systole) estimated. The normal is 60% or more. The figure obtained by this method tends to be higher than that produced by the nuclear imaging method—gated blood pool scanning. The guide wire is reintroduced and the catheter withdrawn to be replaced by one shaped to fit into the right or left coronary orifice...
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
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 HEBBALABANGALORE Case-based learning: cardiovascular risk assessment Mr RF is 60 years old and presents for a check-up because he is concerned he may be at risk of heart disease. Objectives for the group to understand How should this type of request be managed What can be done to assess an individual’s future cardiac risk, and what can be done to improve the prognosis for those at increased risk Epidemiology and population health The presenter should ask the group to consider the concept of risk factors for cardiovascular disease and the differences between population risk factors and those for an individual. How did the concept of risk factors arise Presenting symptoms and clinical examination What questions should be asked of Mr RF to begin the risk factor assessment 1 Is there a history of ischaemic heart disease or symptoms of heart disease 2 Has his cholesterol level been checked in the past What was itHas it been treated with diet or drugs, or both Has the level improved 3 Is he a diabetic, or has he had an abnormal blood sugar measurement 4 Is there a history of high blood pressure Has this been treated If so, how 5 Is there a history of heart disease in the familIf so, who has been affected and at what age 6 Does he smoke? How many cigarettes a day If he has ceased smoking, when did he stop 7 Does he exercise regularly 8 Have any cardiac investigations been performed before What were the results 9 Is there a history of peripheral arterial disease (claudication) or erectile dysfunction The group should appreciate that considerable information about risk can be obtained by asking simple questions. What physical examination should be performed
GOOD CARDIOLOGY CLINICS IN YELAHANKA NWE TOWN BANGALORE Summary of recommendations for CHD risk factor reduction Assess the severity and presence of all risk factors: family history blood pressure non-fasting serum cholesterol (if greater than 5.5 mmol/L, or other risk factors are present, proceed to fasting HDL, LDL, trig.) diabetesn smoking dietary history. 1• CORONARY RISK FACTORS 23 Manage risk factors by: encouraging smoking cessation undertaking dietary modification: • ensure dietary fat is less than 30% of total kJ intake and less than 30% of total saturated fat • increase intake of fish and plant oils • restrict kJ intake if patient is overweight • reduce salt and alcohol intake in hypertensive patients controlling blood pressure with lifestyle and medication maintaining diabetic control encouraging regular physical activity using prophylactic drugs in high-risk patients • aspirin • statins • beta-blockers or ACE inhibitors after AMI • ACE inhibitors in left ventricular (LV) dysfunction screening relatives of high-risk patie
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.
DIABETIC CLINICS IN DODDABALLAPUR ROAD BAMNGALORE Low-density lipoproteins Sixty to seventy per cent of total cholesterol is transported as LDL, and total cholesterol measurements usually reflect LDL levels. In both males and females, coronary heart disease risk is proportional to LDL and total cholesterol. As seen above, LDL supplies cholesterol to peripheral tissues. High concentrations of LDL in the serum accelerate atheroma by interacting with damaged endothelium. Oxidation of LDL accelerates this process. A total cholesterol of 5.5 mmol/L, or LDL of 3.5 mmol/L, is usually considered the upper limit of normal but even these levels seem to be responsible for an increased population risk of atheroma. Populations with lower average levels than these have less coronary disease. Lower levels are beneficial for patients with established coronary disease or multiple risk factors. It is not yet clear whether the lowering of total cholesterol to less than 4.0 (LDL 2.0) provides further benefit or whether a target level is indeed the correct approach. Trials of more aggressive cholesterol lowering are underway.14 Although a reduced HDL level (< 1) is associated with increased risk, there is no evidence as yet that raising HDL has beneficial effects. An elevation of triglyceride levels (> 1.7) is also considered a marker of increased risk, but there is no evidence to what level they should be reduced. Exogenous
CARDIAC CLINICS IN YELAHANKA NEWTOWN BANGALORE Thrombogenic factors Thrombosis is an important pathological process in coronary artery disease. Factors increasing the tendency to thrombosis include: smoking hypertriglyceridaemia elevated fibrinogen (possibly) oestrogen-containing contraceptive pills polycythaemia increased von Willebrand factor (a marker of endothelial dysfunction). The following factors are associated with reduced thrombotic tendency: low-dose aspirin other anti-platelet drugs (e.g. clopidogrel) fish oils and mono-unsaturated fatty acids. Alcohol intake
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