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BEST DIABETOLOGISTS IN HEBBALA BANGALORE Diabetes Type 1 and type 2 diabetes and impaired glucose tolerance (IGT) are associated with an increased risk of coronary disease, peripheral vascular disease and cerebrovascular disease.21 Diabetics have a two- to threefold risk of coronary disease at all ages and those with IGT have a 1.5-fold risk. Diabetes is a stronger risk factor for women (3.3 times) than for men (1.9 times). The excess risk for type 1 patients is largely confined to those with diabetic renal disease. All type 2 patients are at increased risk.22 Diabetes is thought to increase coronary heart disease because: n increased insulin levels result in increased hepatic synthesis of LDL and triglycerides, causing a mixed dyslipidaemia n insulin resistance, which is characteristic of type 2 diabetes, is associated with numerous other cardiovascular risk factors: dyslipidaemia, hypertension, endothelial dysfunction and microalbuminuria n hyperglycaemia itself may cause endothelial damage n glycosylated LDL may be more atherogenic than non-glycosylated LDL. Table 1.12 Glucose tolerance, current WHO definitions (venous plasma glucose) Fasting glucose 2-hour post-glucose load (mmol/L) Normal glucose regulation < 6.0 < 7.8 Impaired fasting glucose 6.1–6.9 < 7.8 Impaired glucose tolerance < 7.0 7.8–11.0 Diabetes > 7.0 > 11.1 16 PRACTICAL CARDIOLOGY Glycaemic control The UKPDS Trial has shown a very significant reduction in the microvascular complications of diabetes with improved glycaemic control but the improvement in macrovascular complications did not quite reach significance. Nevertheless, the UKPDS trialists estimate that each 1% reduction in HbA1c leads to a 14% reduction in cardiovascular risk. Diabetics tend to have more diffuse coronary disease. shows a diffusely diseased right coronary artery from a type 2 diabetic patient before and after coronary stenting . Coronary artery surgery involves a higher risk for diabetics, and graft disease and progression of native disease occur earlier in these patients. Nevertheless, diabetics probably have a better prognosis after surgical revascularisation than after angioplasty because of their higher risk of restenosis following angioplastY
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,
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.
HEART SPECIALISTS IN GANGAMMA CIRCLE BANGALORE Cardiac drugs A detailed drug history is essential. Ask about anti-anginal and anti-failure drugs. It is important to attempt to ensure that the patient gets these drugs on the day of the operation. This applies most of all to beta-blockers. Withdrawal of beta-blockers used for angina can precipitate unstable angina or an infarct. There is also evidence that the use of beta-blockers in the peri-operative period reduces the risk of significant ischaemic events.36 This is probably not the case for nitrates and calcium antagonists. Aspirin used for any patient with ischaemic heart disease should be stopped for the shortest possible period before surgery (about three days) Warfarin, when used for protection against embolic events for atrial fibrillation, can usually be stopped four or five days pre-op and begun again soon afterwards. A possible exception is a patient with atrial fibrillation and a recent embolic event or a left atrial thrombus seen on echo. These patients may need to change to heparin, as detailed below. A history of infective endocarditis, known valvular heart disease (even if mild) or the presence of a prosthetic cardiac valve may be an indication for antibiotic prophylaxis. Patients with a prosthetic heart valve who are taking warfarin need careful management. If the valve is in the aortic position and it is a modern disc valve, it may be safe to allow the INR to fall moderately (to 1.8 or so) by the day of surgery and then to resume warfarin as soon as the patient can swallow. If the surgeon requires the INR to have fallen to normal or the patient has a valve in the mitral position, then cessation of warfarin and use of heparin is necessary. Normally the patient omits a warfarin dose and then is admitted to hospital three or four days before surgery. Intravenous heparin is begun and the APPT adjusted to 2 or 2.5 times normal. The heparin is stopped some hours before surgery and begun as soon afterwards as the surgeon allows. It is now possible, however, to use low molecular weight heparin instead. This can sometimes be given at home. Enoxaparin can be given daily in a dose of up to 2 mg/kg. Blood tests are not needed and subcutaneous injections are used, which means an intravenous infusion is not required. .
Left Ventricular Failure Single most important predictor of mortality following STEMI in patients with STEMI Systolic dysfunction alone or both systolic and diastolic dysfunction can occur. LVDD leads to pulmonary venous hypertension and pulmonary congestion. Systolic dysfunction - ↓ cardiac output and of the ejection fraction. Predictors of LVF infarct size, advanced age and diabetes.[190] Mortality increases in association with the severity of the hemodynamic deficit.
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