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Diabetes clinics in Bettahalasur, Bangalore • The genetic dyslipidaemias Disorder Defect Lipoprotein elevation Clinical findings Pattern Drug treatment Familial chylomicronaemia Lipoprotein lipase defect Chylomicrons Eruptive xanthomata Pancreatitis I None Familial chylomicronaemia Apolipoprotein CII deficiency Chylomicrons, VLDL Pancreatitis I, V None Familial type III (dysbetalipoproteinaemia) Apolipoprotein BIE receptor deficiency Chylomicron remnants Eruptive xanthomata Atherosclerosis III IIa, IIb IV Fibrates Statins Nicotinic acid Familial hypercholestrolaemia (AUTO DOM 1:1500) Deficient LDL receptor LDL Xanthomata Atherosclerosis IIa Resin Statins Familial hypertriglyceridaemia Defect unknown VLDL Xanthomata IV Fibrates Nicotinic acid Multiple lipoprotein hyperlipidaemia Defect unknown LDL, VLDL Atherosclerosis IIa, IIb IV Fibrates Nicotinic acid Statins AUTO DOM = autosomal dominant inheritance; LDL = low-density lipoproteins; VLDL = very low-density lipoproteins.
Diabetes clinics in Bettahalasur, Bangalore • The genetic dyslipidaemias Disorder Defect Lipoprotein elevation Clinical findings Pattern Drug treatment Familial chylomicronaemia Lipoprotein lipase defect Chylomicrons Eruptive xanthomata Pancreatitis I None Familial chylomicronaemia Apolipoprotein CII deficiency Chylomicrons, VLDL Pancreatitis I, V None Familial type III (dysbetalipoproteinaemia) Apolipoprotein BIE receptor deficiency Chylomicron remnants Eruptive xanthomata Atherosclerosis III IIa, IIb IV Fibrates Statins Nicotinic acid Familial hypercholestrolaemia (AUTO DOM 1:1500) Deficient LDL receptor LDL Xanthomata Atherosclerosis IIa Resin Statins Familial hypertriglyceridaemia Defect unknown VLDL Xanthomata IV Fibrates Nicotinic acid Multiple lipoprotein hyperlipidaemia Defect unknown LDL, VLDL Atherosclerosis IIa, IIb IV Fibrates Nicotinic acid Statins AUTO DOM = autosomal dominant inheritance; LDL = low-density lipoproteins; VLDL = very low-density lipoproteins.
HEART SPECIALISTS IN YELAHANKA NEW TOWN BANGALORE The causes of coronary symptoms The symptoms of coronary artery disease are caused by the reduction of myocardial perfusion that results from narrowing of the lumen of one or more of the coronary arteries. This narrowing is most often the result of atherosclerosis. Other much less common causes include: 1 coronary artery spasm (often in an already diseased segment of artery but sometimes as a result of the use of cocaine) 2 thrombosis (usually on an already diseased, or occasionally aneurismal, segment) 3 embolism (e.g. from an infected aortic valve) 4 congenital coronary abnormality 5 vasculitis. Numerous other cardiac symptoms and problems can be the eventual result of atheromatous coronary disease. These include myocardial infarction , cardiac failure cardiac arrhythmias and some cardiac valve problems. Risk factor mechanisms of action Atherosclerosis is thought to result primarily from a disturbance of the vascular endothelium. The final common pathway for the effects of endothelial dysfunction is largely through abnormalities of nitric oxide (NO) production. This chemical, released by a healthy endothelium, is a potent vasodilator and has anti-inflammatory and other favourable actions on the arteries. Causes of this disturbance can be: n mechanical (hypertension) n chemical (oxidised lipids, components of cigarette smoke, hyperinsulinaemia) or n due to immunological injury. The damaged endothelium attracts inflammatory mediators, platelets and circulating lipids and promotes fibroblast and smooth muscle proliferation. This results in the formation of a plaque, which may narrow the arterial lumen. Plaques can remain stable (or sometimes regress), enlarge, rupture or erode (more common in diabetics). Most acute ischaemic events (acute coronary syndromes or acute myocardial infarctions) are thought to be the result of further luminal narrowing caused by the formation of partly or fully occlusive thrombus on a ruptured or eroded plaque. Coronary risk factors may therefore operate because they are atherogenic or thrombogenic. Plaque rupture Plaque rupture may be at least partly an inflammatory process involving inflammatory cells, cytokines and even bacteria. This may explain the association between inflammatory markers such as high-sensitivity C reactive protein (hsCRP) and a risk of acute coronary events. Although this association seems well established, there is still uncertainty about its role in overall risk assessment Plaques at risk of rupture are called vulnerable plaques. They typically have a thin fibrous cap. The shoulde of these caps are at risk of rupturing and allowing material from within the plaque to come
The causes of coronary symptoms The symptoms of coronary artery disease are caused by the reduction of myocardial perfusion that results from narrowing of the lumen of one or more of the coronary arteries. This narrowing is most often the result of atherosclerosis. Other much less common causes include: 1 coronary artery spasm (p. 146) (often in an already diseased segment of artery but sometimes as a result of the use of cocaine) 2 thrombosis (usually on an already diseased, or occasionally aneurismal, segment) 3 embolism (e.g. from an infected aortic valve) 4 congenital coronary abnormality
The causes of coronary symptoms The symptoms of coronary artery disease are caused by the reduction of myocardial perfusion that results from narrowing of the lumen of one or more of the coronary arteries. This narrowing is most often the result of atherosclerosis. Other much less common causes include: 1 coronary artery spasm (p. 146) (often in an already diseased segment of artery but sometimes as a result of the use of cocaine) 2 thrombosis (usually on an already diseased, or occasionally aneurismal, segment) 3 embolism (e.g. from an infected aortic valve) 4 congenital coronary abnormality HEART SPECIALIST IN YELAHANKA
CARDIOLOGIST IN SAHAKARANAGAR The causes of coronary symptoms The symptoms of coronary artery disease are caused by the reduction of myocardial perfusion that results from narrowing of the lumen of one or more of the coronary arteries. This narrowing is most often the result of atherosclerosis. Other much less common causes include: 1 coronary artery spasm (p. 146) (often in an already diseased segment of artery but sometimes as a result of the use of cocaine) 2 thrombosis (usually on an already diseased, or occasionally aneurismal, segment) 3 embolism (e.g. from an infected aortic valve) 4 congenital coronary abnormality 5 vasculitis.
CARDIOLOGIST IN YELAHANKA causes of coronary symptoms The symptoms of coronary artery disease are caused by the reduction of myocardial perfusion that results from narrowing of the lumen of one or more of the coronary arteries. This narrowing is most often the result of atherosclerosis. Other much less common causes include: 1 coronary artery spasm . (often in an already diseased segment of artery but sometimes as a result of the use of cocaine) 2 thrombosis (usually on an already diseased, or occasionally aneurismal, segment) 3 embolism (e.g. from an infected aortic valve) 4 congenital coronary abnormality 5 vasculitis.
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
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