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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 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
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.
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.
HEART DOCTORS IN YELAHANKA NEWTOWN, BANGALORE Management of ACS (NSTEACS) Patients with this diagnosis represent a rather heterogeneous group. Some have had the recent onset of angina at the extremes of exercise, others have angina at rest associated with ECG changes. This variation has made attempts to study the effects of different treatment rather difficult. Although the majority of patients with myocardial infarction have a preceding period of unstable angina, only about 5% of all patients admitted to hospital with a diagnosis of an ACS go on to infarct during that admission. The in-hospital mortality for these patients is low. Mortality rates of less than 2% are usual. Nevertheless, there is a real short-term and longerterm risk of infarction, recurrent admission with unstable symptoms and death which is higher than that of patients with stable angina. The diagnosis should therefore lead to admission to a CCU. The cardiac enzymes are, by definition, not elevated in these patients but the newer, more sensitive tests for troponin T and troponin I may be abnormal and indicate a worse prognosis . In the CCU, bed rest, oxygen and ECG monitoring are routinely enforced and any mobile phones taken away (allegedly to protect the monitoring equipment). Recurrence of chest pain can be assessed quickly and ECGs performed to look for changes suggesting infarction. The cardiac biomarkers can be checked regularly. All patients should receive aspirin (300 mg) unless there is a contraindication. Patients with an intermediate or a higher risk should also be given clopidogrel (usually a 300–600 mg loading dose). The use of intravenous heparin has become standard treatment. A typical starting dose is 5000 units as a bolus followed by 24, 000 units over 24 hours. The activated partial thromboplastin time (APPT) should be measured after about six hours of treatment and the infusion rate of heparin adjusted to maintain this at about twice normal. Heparin is generally safe when used in this way. Bleeding problems may sometimes occur and the platelet count should be checked every few days so that heparin-induced thrombocytopenia (HITS), a rare but serious complication, can be detected early. Low molecular weight heparins are at least as effective as unfractionated heparin. These drugs have some advantages over heparin. Their dose response effect is more predictable and they cause less thrombocytopenia. They are effective given subcutaneously without APPT monitoring and are now cheaper than IV heparin when savings on APPT monitoring and the use of infusion sets are considered. A standard twice-daily dose is given according to the patient’s weight—1 mg/kg for enoxaparin (Clexane). The dose is reduced by half for those with moderate or severe renal impairment and for those over the age of 75. Additional treatment should include beta-blockers unless these are contraindicated. These drugs reduce the number of ischaemic episodes and probably the risk of myocardial infarction. Nitrates can be a useful adjunctive treatment. They may be given orally, topically or intravenously. The IV dose can be titrated up or down depending on the amount of pain the patient is experiencing and the severity of side effects such as hypotension and headache. The problem of tachyphylaxis with nitrates can be overcome by steady increases in the IV dose if necessary. Calcium antagonists are appropriate treatment for patients intolerant of beta-blockers and may sometimes be added to beta-blockers. Nifedipine, especially in its short-acting form, should not be used for patients with acute coronary syndromes unless they are already taking beta-blockers. Thrombolytic drugs have been disappointing when used for NSTEACS. In trials where they have been used for patients with ischaemic chest pain but without ST elevation there has been a trend towards an adverse outcome. This may be related to the rebound hypercoagulable state that can occur after their use. In general they should not be used for the treatment of NSTEACS. Glycoprotein IIb/IIIa inhibitors (p. 198) should be given for high-risk patients,
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
''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.
Popular Cardiologists in Yelahanka cardiac patient having a non-cardiac operation: points to remember 1 A careful cardiac history and examination will identify patients at high risk. 2 The preoperative assessment for a major operation should not be left until the night before the operation. 3 Patients on warfarin present special problems. 4 Cardiac drugs should be continued if possible right up to the time of surgery. Anti-platelet drugs should be stopped only if really necessary.
Popular Cardiologists in Yelahanka cardiac patient having a non-cardiac operation: points to remember 1 A careful cardiac history and examination will identify patients at high risk. 2 The preoperative assessment for a major operation should not be left until the night before the operation. 3 Patients on warfarin present special problems. 4 Cardiac drugs should be continued if possible right up to the time of surgery. Anti-platelet drugs should be stopped only if really necessary.
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