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THE BEST CARDIOLOGISTS IN YELAHANKAMedical treatment of stable angina Treatment of any disease must begin with a thorough explanation of the likely diagnosis, severity and prognosis. The possible investigations required and steps to be taken if symptoms persist despite treatment should be outlined. A warning (firm, but not alarming) should be given that a prolonged episode of chest pain (more than about 15 minutes) should prompt the patient to get to a hospital without delay. This may also be the first opportunity to speak to the patient about the control of risk factors (e.g. smoking, hyperlipidaemia) that will be important for the long-term prognosis. Risk factor assessment should form part of this initial consultation and include a request for measurement of the serum lipids . a b (a) An MDCT scan of a diseased right coronary artery and the corresponding coronary angiogram (b) An MDCT reconstructed image of the heart and great vessels 140 PRACTICAL CARDIOLOGY A patient with symptoms typical of angina but who seems stable enough not to need admission to hospital should be started on treatment while awaiting investigations to confirm the diagnosis (usually stress testing). Treatment should aim to improve symptoms and, if possible, improve the prognosis (i.e. reduce the risk of unstable angina, infarction or death). Some drugs that help control the symptoms of angina may also improve the prognosis; other treatment may help the longer-term outlook by improving risk factors. Anti-platelet
CARDIOLOGY DOCTORS IN HOSUR ROAD Pulmonary embolism This is not quite a cardiac condition and not quite a respiratory condition but it is often managed by cardiologists. Modern CT pulmonary angiography is very sensitive and specific for the diagnosis of PE. A negative scan that is of good quality effectively excludes the diagnosis. The scans are so sensitive that small distal emboli may be detected in patients who do not have convincing symptoms of embolism. This poses a therapeutic problem that may be avoided if scans are not ordered inappropriately. Some patients cannot have a CTPA, usually because of renal impairment that would make the injection of contrast risky. A V/Q nuclear scan is then a reasonable alternative to a CTPA. These scans are less accurate than CT pulmonary angiography but the clinical suspicion of PE and a lung scan reported as intermediate or high probability is an indication for treatment. Patients should be admitted to hospital and treatment begun with intravenous heparin or subcutaneous low molecular weight heparin. The latter has the advantage that the dose is determined by body weight and repeated measurements of clotting times are not required. In some cases it may be possible to treat patients with small pulmonary emboli at home with supervised low molecular weight heparin. Either way, soon after diagnosis patients should be started on oral anticoagulation treatment with warfarin. A stable INR may often be achieved within five days or so, the heparin ceased and the patient discharged. Most patients with dyspnoea as a result of PE begin to feel better within a few days of starting treatment. It is often difficult to know how long to continue treatment with warfarin. The usual recommendation for an uncomplicated first PE is three to six months. Recurrent PE may be an indication for lifelong treatment. It also suggests a need to investigate for clotting abnormalities (e.g. anti-thrombin III deficiency, protein S and protein C deficiency, abnormal Factor V and anti-nuclear antibody). A very large and life-threatening PE which is associated with the sudden onset of severe dyspnoea and hypotension may be an indication for thrombolytic treatment. An echocardiogram may show abnormal right ventricular function in these ill patients and help in the decision. Experience with this is limited and the optimum regimen is not really known. Tissue plasminogen activator (TPA) is now indicated for this purpose and current recommendations are for a 10 mg bolus over two minutes followed by 90 mg over two hours.
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.
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 YELAHANKA 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. 270 PRACTICAL CARDIOLOGY The examination may help in assessing the severity of the patient’s dyspnoea as he or she undresses. Try to work out the patient’s functional class from the history and examination (p. 256) (NYHA I–IIII, often called the NYHA–WHO class when related to pulmonary hypertension). There may be signs of chronic lung disease or congenital heart disease, or specific signs of pulmonary hypertension and right heart failure (p. 257). Investigations are directed at finding an underlying reason for pulmonary hypertension— idiopathic pulmonary hypertension is a diagnosis of exclusion—and at assessing its severity and potential reversibility. The chest X-ray is abnormal in 90% of IPH patients. It may show pulmonary fibrosis or an abnormal cardiac silhouette—RV dilatation. There may be large proximal pulmonary arteries that appear ‘pruned’ in the periphery, and the heart may appear enlarged because of right ventricle dilatation) Respiratory function tests may show a normal, restrictive or obstructive pattern. Moderate pulmonary hypertension itself is associated with a reduction in the diffusing capacity for the carbon monoxide test (DLCO) to about 50% of predicted. On the ECG look for signs of right heart strain or hypertrophy, which are present in up to 90% of patients The blood gas measurements may show hypercapnia—elevated pCO2 in hypoventilation syndromes—but hypocapnia is more common in IPH because of increased alveolar ventilation. Mild hypoxia (reduction in pO2) may be present in IPH, and is more severe when pulmonary hypertension is secondary to lung disease. On CT pulmonary angiogram (CTPA), ventilation/perfusion (V/Q) lung scan or Doppler venograms look for a deep venous thrombosis (DVT) and PE and assess the extent of involvement of the pulmonary bed. A high-resolution CT scan of the lungs is the best way of looking for interstitial lung disease. The six-minute walking test predicts survival and correlates with the NYHA–WHO class. Reduction in arterial oxygen concentration of more than 10% during this test predicts an almost threefold mortality risk over 29 months. Patients unable to manage 332 m in six minutes also have an adverse prognosis.
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