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HEART SPECIALISTS IN SILKBOARD Complex congenital heart disease: conduits Anatomy and physiology Babies with a very abnormal right ventricular outflow tract such as pulmonary atresia can have a conduit fashioned to direct blood from the systemic veins more directly to the pulmonary arterial circulation or from a systemic artery to the pulmonary circulation. These conduits are made from veins or occasionally from Gortex. 368 PRACTICAL CARDIOLOGY Complications Conduits of all types have a limited life and tend to deteriorate after 10 years. These patients are also at risk of ventricular arrhythmias and heart block. Follow-up Patients need regular expert echocardiography to assess the conduit function. The conduit may deteriorate significantly before symptoms occur. Further treatment Conduit deterioration is usually an indication for further surgery although it can occasionally be treated with balloon dilatation. Pregnancy and contraception Pregnancy is well tolerated in patients with good conduit function. There are no particular problems with contraception. Sports Patients should avoid competitive and contact sports.
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.
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
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
CARDIOLOGISTS IN DEVARABESANAHALLI BANGALORE Complex congenital heart disease: Fontan repair Anatomy and physiology Babies with a single ventricle or equivalent defect are often treated during childhood with a palliative operation to connect venous return directly to the pulmonary arteries—a Fontan repair. The prognosis is usually good: 75% of these patients survive at least 20 years. Complications Problems develop because of failure of the systemic ventricle, obstruction of the venous to pulmonary connection, atrial enlargement and AV valve regurgitation. Atrial arrhythmias become increasingly common. Sinus node dysfunction may necessitate pacing, which requires an epicardial electrode in most cases. Follow-up Echocardiography allows assessment of ventricular function and the AV valve. Obstruction in the Fontan connections can be examined with Doppler. MRI is increasingly useful for this assessment. Treatment Severe AV valve regurgitation, cyanosis and ventricular dysfunction are indications for intervention, including transplant or revision of the Fontan. Atrial arrhythmias can be treated with radiofrequency ablation. Pregnancy and contraception Pregnancy is possible in some patients with excellent Fontan function, good LV function and minimal AV valve regurgitation. Maternal risk is high if the Fontan is failing. There may be problems with the need to withdraw ACE inhibitors and with anticoagulation.
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.
CARDIOLOGISTS IN YELAHANKA 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.
''SAMIKSHA HEART AND DIABETIC CARE'' Smoking The Framingham study found an 18% increase in coronary events for males and a 31% increase for females for every 10 cigarettes smoked per day. There is more of an association between smoking and myocardial infarction than between smoking and stable angina. Smoking increases the risk of stroke, coronary heart disease and peripheral vascular disease through a number of mechanisms (Table 1.11). Smoking is a major factor in the increased risk of coronary heart disease for women using oestrogen-containing contraceptive pills Some effects of smoking 1 Increased atherogenesis, probably by toxic injury to endothelial cells 2 Hypoxia, resulting in intimal proliferation 3 Thrombogenesis 4 Reduction in HDL 5 Oxidation of lipids 6 Increase in fibrinogen levels Smoking cessation is associated with a rapid decline in death rates from coronary disease, probably because of smoking’s thrombogenic effects. Smoking seems less important as a risk factor in populations with low LDL levels Smoking cessation Many strategies are available to help patients to give up smoking. These should all begin with an explanation of the reasons smoking cessation is worthwhile. Some explanation of the mechanism of its deleterious effects may be helpful. Patients who have recently presented with possible cardiac symptoms may be amenable to advice of this nature. It is also especially important to give strong advice about smoking to patients with multiple existing coronary risk factors. The rapidity at which benefits begin to occur, and the risks and difficulties involved in further cardiac treatment (e.g. coronary surgery) for smokers, should be emphasised. The postoperative risk is considerably higher for smokers, particularly for serious chest infections. This risk falls quickly (within four weeks) once smoking is stopped. Nicotine replacement patches may be helpful and appear safe even for patients with ischaemic heart disease. The drug bupropion, which is a non-tricyclic antidepressant, is now available for patients who wish to stop smoking. This drug seems safe for patients with cardiac disease, at least for those without unstable symptoms. It does not cause conduction abnormalities or increase the risk of ventricular arrhythmias. Patients should be advised to continue smoking when they first start the drug but plan to stop on a particular day after about a week of treatment. The drug is usually continued for at least seven weeks. The starting dose is 150 mg daily and then 150 mg twice a day. It is important to discuss strategies for smoking cessation with the patient and to try to establish a treatment plan that suits the individual. Passive smoking Evidence of an increased cardiovascular risk from environmental smoke has been available for some years.20 Legislation is gradually reducing the risk for people in occupations associated with smoking (e.g. serving in bars and restaurants) but patients with existing ischaemic heart disease should be advised to avoid exposure.
THE BEST CARDIOLOGISTS IN YELAHANKA NEWTOWN BANGALORE Thrombogenic factors Thrombosis is an important pathological process in coronary artery disease. Factors increasing the tendency to thrombosis include: n 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 nother anti-platelet drugs (e.g. clopidogrel) fish oils and mono-unsaturated fatty acids.