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Popular Cardiologist in Amrutha Halli, Bangalore Non-steroidal anti-inflammatory drugs Non-steroidal anti-inflammatory drugs (NSAIDs) are in common use for arthritic and muscular pain. The traditional NSAIDs (and aspirin) inhibit both cyclo-oxygenase (COX) 1 and 2 iso-forms. The specific COX-2 inhibitors that are associated with a lower risk of gastrointestinal bleeding than the non-selective inhibitors have been widely used since their introduction. Reports of increased cardiovascular risk emerged first with rofecoxib, then with other COX-2 inhibitors, and then with the non-selective older drugs (but not aspirin). A large Finnish casecontrolled study of admissions with first myocardial infarction showed an average increased risk of 40% for users of these drugs.28 The study was complicated by its inability to track over-thecounter NSAIDs. Further work is underway, but patients with known ischaemic heart disease or at high risk should be discouraged from using these drugs.
Popular Cardiologist in Amrutha Halli, Bangalore Non-steroidal anti-inflammatory drugs Non-steroidal anti-inflammatory drugs (NSAIDs) are in common use for arthritic and muscular pain. The traditional NSAIDs (and aspirin) inhibit both cyclo-oxygenase (COX) 1 and 2 iso-forms. The specific COX-2 inhibitors that are associated with a lower risk of gastrointestinal bleeding than the non-selective inhibitors have been widely used since their introduction. Reports of increased cardiovascular risk emerged first with rofecoxib, then with other COX-2 inhibitors, and then with the non-selective older drugs (but not aspirin). A large Finnish casecontrolled study of admissions with first myocardial infarction showed an average increased risk of 40% for users of these drugs.28 The study was complicated by its inability to track over-thecounter NSAIDs. Further work is underway, but patients with known ischaemic heart disease or at high risk should be discouraged from using these drugs.
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,
''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.
SAMIKSHA HEART AND DIABETIC CARE '' CHEST PAIN'' Indications for Echocardiography in Patients with Chest Pain Class I: Evidence or general agreement or both exists that the procedure is useful or beneficial 1. Diagnosis of underlying cardiac disease in patients with chest pain and clinical evidence of valvular, pericardial, or primary myocardial disease 2. Evaluation of chest pain in patients with suspected acute myocardial ischemia, when baseline ECG is nondiagnostic and when study can be obtained during pain or soon after its abatement 3. Evaluation of chest pain in patients with suspected aortic dissection 4. Chest pain in patients with severe hemodynamic instability Class III: Conditions for which evidence and/or general agreement exist that the procedure is not useful/effective 1. Evaluation of chest pain for which a noncardiac etiology is apparent Figure 48–22 2. Diagnosis of chest pain in a patient with electrocardiographic changes diagnostic of myocardial ischemia/infarction Chetlin et al. ACC/AHA Guidelines for the Clinical Application of Echocardiography. Circulation. 1997;95.
DCardiologist in Vidyaranyapura, Bangalore • etected vascular abnormalities Calcium scoring High-resolution CT scanners can measure calcium within the coronary arteries in a single breath-hold scan. The measured calcium is given a number, the Agatston score. The presence of calcium within a coronary artery is a marker of coronary disease but not of obstructive disease. It does not give any information about the presence of soft plaque, which is more likely to be associated with an acute coronary event but a 0 score predicts a very low coronary risk. A high score has been shown to be an independent risk factor for future events.29 Prospective studies proving the value of calcium scoring have not been performed. Calcium scoring is likely to be superseded by multi-slice CT coronary angiography (p. 136), which can produce images of the coronary lumen and generate a calcium score. An elevated calcium score in an asymptomatic patient is probably best treated as an indication for aggressive risk factor management; for example, instituting statin treatment for a marginally elevated cholesterol level. Intima-media thickness High-frequency ultrasound transducers can measure accurately the thickness of the carotid intima up to its interface with the media. An intima-media thickness (IMT) of > 1.3 mm is associated with an increased cardiovascular risk, which remains significant after allowing for other risk factors. Ankle brachial index The ankle brachial index (ABI) is relatively easy to measure with a sphygmomanometer and a Doppler ultrasound device. The systolic blood pressure in the arm and in the posterior tibial and dorsalis pedis arteries is compared. An ABI of < 0.9 means a stenosis of at least 50% somewhere between the aorta and the foot. The test is a reliable sign of peripheral arterial disease and thus also coronary disease. Erectile dysfunction Erectile dysfunction is a marker of endothelial dysfunction. Because the penile arteries are smaller (1–2 mm) than the carotids (5–7 mm) and coronary arteries (3 mm), plaque burden and endothelial dysfunction may cause symptoms earlier here than in the other territories. hsCRP measurements and risk of vascular events (stroke, myocardial infarction, acute coronary syndrome) Low risk Intermediate High hsCRP level < 1 mg/L 1–3 mg/L > 3 mg/L Note: levels > 10 mg/L suggest acute inflammation and should be repeated after a few week In some studies erectile dysfunction has reliably preceded symptomatic coronary disease in twothirds of patients by an average of three years.30 A history of this problem in men indicates an increased risk of vascular events. It is strongly associated with other risk factors such as smoking and diabetes but remains significant after allowing for these. Infectious agents There is continuing mild interest in the role of infection in promoting atherosclerosis and especially unstable coronary syndromes. Chlamydia pneumoniae and Helicobacter pylori are commonly found in atheromatous plaques. It is possible one or more infectious agents could be the stimulus that sets off the inflammatory process that changes plaque structure, weakens the fibrous cap and unleashes the coagulation cascade that occludes the vessel. The ACADEMIC study was not associated with a reduction in early coronary events
DCardiologist in Vidyaranyapura, Bangalore • etected vascular abnormalities Calcium scoring High-resolution CT scanners can measure calcium within the coronary arteries in a single breath-hold scan. The measured calcium is given a number, the Agatston score. The presence of calcium within a coronary artery is a marker of coronary disease but not of obstructive disease. It does not give any information about the presence of soft plaque, which is more likely to be associated with an acute coronary event but a 0 score predicts a very low coronary risk. A high score has been shown to be an independent risk factor for future events.29 Prospective studies proving the value of calcium scoring have not been performed. Calcium scoring is likely to be superseded by multi-slice CT coronary angiography (p. 136), which can produce images of the coronary lumen and generate a calcium score. An elevated calcium score in an asymptomatic patient is probably best treated as an indication for aggressive risk factor management; for example, instituting statin treatment for a marginally elevated cholesterol level. Intima-media thickness High-frequency ultrasound transducers can measure accurately the thickness of the carotid intima up to its interface with the media. An intima-media thickness (IMT) of > 1.3 mm is associated with an increased cardiovascular risk, which remains significant after allowing for other risk factors. Ankle brachial index The ankle brachial index (ABI) is relatively easy to measure with a sphygmomanometer and a Doppler ultrasound device. The systolic blood pressure in the arm and in the posterior tibial and dorsalis pedis arteries is compared. An ABI of < 0.9 means a stenosis of at least 50% somewhere between the aorta and the foot. The test is a reliable sign of peripheral arterial disease and thus also coronary disease. Erectile dysfunction Erectile dysfunction is a marker of endothelial dysfunction. Because the penile arteries are smaller (1–2 mm) than the carotids (5–7 mm) and coronary arteries (3 mm), plaque burden and endothelial dysfunction may cause symptoms earlier here than in the other territories. hsCRP measurements and risk of vascular events (stroke, myocardial infarction, acute coronary syndrome) Low risk Intermediate High hsCRP level < 1 mg/L 1–3 mg/L > 3 mg/L Note: levels > 10 mg/L suggest acute inflammation and should be repeated after a few week In some studies erectile dysfunction has reliably preceded symptomatic coronary disease in twothirds of patients by an average of three years.30 A history of this problem in men indicates an increased risk of vascular events. It is strongly associated with other risk factors such as smoking and diabetes but remains significant after allowing for these. Infectious agents There is continuing mild interest in the role of infection in promoting atherosclerosis and especially unstable coronary syndromes. Chlamydia pneumoniae and Helicobacter pylori are commonly found in atheromatous plaques. It is possible one or more infectious agents could be the stimulus that sets off the inflammatory process that changes plaque structure, weakens the fibrous cap and unleashes the coagulation cascade that occludes the vessel. The ACADEMIC study was not associated with a reduction in early coronary events
heart doctors Doctors in Vidyaranyapura Anti-platelet therapy Unless there is a contraindication (usually gastric intolerance but occasionally allergy) all patients with suspected angina should take aspirin.14 A daily dose of 75 mg is enough to cause irreversible cyclo-oxygenase inhibition of all the patient’s platelets. Recovery occurs only as platelets are replaced. This treatment causes significant reduction in platelet adhesiveness and reduces the risk of thrombosis within the coronary arteries following rupture of an atherosclerotic plaque. There is a definite improvement in mortality when aspirin is used after myocardial infarction and a probable improvement for patients with angina. The use of half an aspirin tablet (150 mg) is the cheapest approach to aspirin use, but 100 mg preparations in coated tablets and calendar packets are available. Patients unable to tolerate aspirin because of gastric side effects can often be treated with the combination of aspirin and a proton pump inhibitor. The relative risk of cerebral haemorrhage increases by 30% for patients taking aspirin but the absolute risk is less than 1 per 1000 patient years of treatment. For patients with aspirin allergy or intolerance, 75 mg of clopidogrel a day is usually a safer but expensive alternative. It is also associated with a small risk of gastrointestinal bleeding (1.99% versus 2.66% for aspirin over two years in the CAPRIE study). Combination (dual anti-platelet/aspirin and clopidogrel) treatment is not currently indicated for stable angina. Aspirin and clopidogrel resistance
heart doctors Doctors in Vidyaranyapura Anti-platelet therapy Unless there is a contraindication (usually gastric intolerance but occasionally allergy) all patients with suspected angina should take aspirin.14 A daily dose of 75 mg is enough to cause irreversible cyclo-oxygenase inhibition of all the patient’s platelets. Recovery occurs only as platelets are replaced. This treatment causes significant reduction in platelet adhesiveness and reduces the risk of thrombosis within the coronary arteries following rupture of an atherosclerotic plaque. There is a definite improvement in mortality when aspirin is used after myocardial infarction and a probable improvement for patients with angina. The use of half an aspirin tablet (150 mg) is the cheapest approach to aspirin use, but 100 mg preparations in coated tablets and calendar packets are available. Patients unable to tolerate aspirin because of gastric side effects can often be treated with the combination of aspirin and a proton pump inhibitor. The relative risk of cerebral haemorrhage increases by 30% for patients taking aspirin but the absolute risk is less than 1 per 1000 patient years of treatment. For patients with aspirin allergy or intolerance, 75 mg of clopidogrel a day is usually a safer but expensive alternative. It is also associated with a small risk of gastrointestinal bleeding (1.99% versus 2.66% for aspirin over two years in the CAPRIE study). Combination (dual anti-platelet/aspirin and clopidogrel) treatment is not currently indicated for stable angina. Aspirin and clopidogrel resistance
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