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Popular Cardiologist in Rajanukunte, Bangalore • Coexisting disease and patient risk profile LVH: Choose ACE inhibitors, ARAs, alpha-blockers, beta-blockers, calcium antagonists. Previous acute myocardial infarction (AMI): Choose beta-blockers, ACE inhibitors in left ventricular dysfunction (LVD). Angina: Choose beta-blockers, verapamil, diltiazem. Cardiac failure or LVD: ACE inhibitors (and ARAs) and beta-blockers (carvedilol, bisoprolol and slow-release metoprolol) reduce symptoms and mortality. Monoxi-­ dine is contraindicated. Diuretics reduce symptoms, but loop diuretics (frusemide) are too short-acting to be useful for hypertension. Diabetes: ACE inhibitors and ARAs protect renal function in patients with pro-­ teinuria.16 Aortic stenosis: Vasodilators should be used with caution. Renovascular disease: ACE inhibitors and ARAs are effective but can lead to deterioration of renal function. Potassium and creatinine levels should be monitored. ACE inhibitors and ARAs are contraindicated in bilateral renal artery stenosis, or where there is a single functioning kidney. PVD: Beta-blockers are relatively contraindicated. Stroke: ARAs and low-dose thiazides are more effective for prevention than beta-blockers. Diabetes: Diuretics have an adverse effect on glucose metabolism. ACE inhibitors and ARAs are of value in reducing the development of diabetic nephropathy. Dyslipidaemia: Alpha-blockers have a mild beneficial effect on serum lipids. ACE inhibi-­ tors and calcium antagonists have a neutral effect. Gout: Diuretics inhibit uric acid excretion and are relatively contraindicated. Asthma and chronic obstructive pulmonary disease (COPD): Beta-blockers are usually contraindicated. Depression: Methyldopa, calcium antagonists and clonidine may aggravate.
Popular Cardiologist in Rajanukunte, Bangalore • Coexisting disease and patient risk profile LVH: Choose ACE inhibitors, ARAs, alpha-blockers, beta-blockers, calcium antagonists. Previous acute myocardial infarction (AMI): Choose beta-blockers, ACE inhibitors in left ventricular dysfunction (LVD). Angina: Choose beta-blockers, verapamil, diltiazem. Cardiac failure or LVD: ACE inhibitors (and ARAs) and beta-blockers (carvedilol, bisoprolol and slow-release metoprolol) reduce symptoms and mortality. Monoxi-­ dine is contraindicated. Diuretics reduce symptoms, but loop diuretics (frusemide) are too short-acting to be useful for hypertension. Diabetes: ACE inhibitors and ARAs protect renal function in patients with pro-­ teinuria.16 Aortic stenosis: Vasodilators should be used with caution. Renovascular disease: ACE inhibitors and ARAs are effective but can lead to deterioration of renal function. Potassium and creatinine levels should be monitored. ACE inhibitors and ARAs are contraindicated in bilateral renal artery stenosis, or where there is a single functioning kidney. PVD: Beta-blockers are relatively contraindicated. Stroke: ARAs and low-dose thiazides are more effective for prevention than beta-blockers. Diabetes: Diuretics have an adverse effect on glucose metabolism. ACE inhibitors and ARAs are of value in reducing the development of diabetic nephropathy. Dyslipidaemia: Alpha-blockers have a mild beneficial effect on serum lipids. ACE inhibi-­ tors and calcium antagonists have a neutral effect. Gout: Diuretics inhibit uric acid excretion and are relatively contraindicated. Asthma and chronic obstructive pulmonary disease (COPD): Beta-blockers are usually contraindicated. Depression: Methyldopa, calcium antagonists and clonidine may aggravate.
It may also improve arterial oxygenation by reducing pulmonary vascular congestion DIURETICS. Mild heart failure responds well to diuretics such as furosemide, Dose - 10 to 40 mg, repeated at 3- to 4-hour intervals if necessary. It reduces pulmonary capillary pressure reduces dyspnea. Decreased LVDV↓ LV wall tension - ↓ myocardial oxygen requirements and may lead to improvement of contractility and augmentation of the ejection fraction, stroke volume, and cardiac output. The reduction of elevated left ventricular filling pressure may also enhance myocardial oxygen delivery by diminishing the impedance to coronary perfusion attributable to elevated ventricular wall tension. .
Cardiologist in Rajanukunte, Bangalore • Factors that increase triglyceride levels 1 Obesity 2 Alcohol 3 Diabetes 4 Oestrogen (including HRT in 20% of users) 5 Diuretics 6 Beta-blockers Secondary causes: • Cushing’s syndrome • acromegaly • uraemia • acute hepatitis
THE BEST CARDIOLOGIST IN HEBBALA Hypertension as a risk factor Hypertension is a risk factor for coronary disease, but even more so for cerebrovascular disease and left ventricular failure.1 Control of blood pressure reduces this risk. Large randomised trials have shown that every 10–14 mmHg reduction in systolic and 5 mmHg reduction in diastolic blood pressure confers a 29% reduction in CHD risk and a 40% reduction in stroke risk. The risk of a coronary event in a man with blood pressure greater than 160/95 is five times the risk in a man with blood pressure of 140/90 or less. Hypertension can be diagnosed only by blood pressure measurements. There is little evidence that high blood pressure causes symptoms, except for malignant hypertension with cerebral oedema. The symptoms often ascribed to hypertension—epistaxis, dizziness, headache and fainting—are no more common in hypertensives than in normotensives. Anxiety (often about the blood pressure) and hyperventilation may explain some of these symptoms.2 The trials providing the above figures have been carried out using diuretics or beta-­blockers in the treatment of hypertension. Because these drugs may adversely affect lipid profiles and therefore coronary risk, it has been suggested that newer agents may produce a greater reduction in the risk of CHD events. However, this has not been proven. There is evidence from metaanalyses of blood pressure lowering trials that beta-blockers are less protective against stroke than other agents. They are more effective than placebo in providing protection against stroke. The reduction in blood pressure that is achieved is still more important than the choice of drug. The trials have shown that blood pressure reduction in the elderly, including those over the age of 80, is associated with reduced cardiovascular morbidity but not all-cause (overall) mortality. Treatment of isolated systolic hypertension, common in the elderly, has also shown benefit in terms of the reduced risk of stroke, cardiac failure and coronary disease.3 As in the case of other risk factors, the greatest absolute benefit in the treatment of hyper-­ tension is gained in those patients with existing heart disease, diabetes or multiple risk factors. Blood pressure is an important component of the total risk score . The effects of hypertension Cardiovascular Sustained hypertension results in increased left ventricular wall thickness (left ventricular hypertro-­ phy, LVH) and may ultimately lead to left ventricular dilatation and cardiac failure. LVH results in higher oxygen demands by the ventricle, making angina more likely. The mechanism by which hypertension is thought to increase CHD risk is mechanical damage to the endothelium, leading to increased permeability and therefore increased atherogenesis. Elevated blood pressure interacts with other hereditary and acquired risk factors, all of which are associated with endothelial dysfunction; some are probably implicated in the genesis of hypertension in the first place.4 Neurological Hypertension
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