paper Heart Disease
The state of cardiac heart diseases that can not perform normal functions , called the uncompensated state , abnormal blood circulation causing shortness of breath ( dyspnea ) , fatigue , pain in the heart area . Renal function abnormalities , liver toak , as well as blood pressure and sodium resorption occurs , SHG occurs edema . Coronary disease is a disease whose incidence is increasing in modern society with changes in diet and daily activities . This disease occurs when plaque containing lipoproteins , cholesterol , calcium and tissue debris formed in the interior surface of the coronary arteries causing hardening and narrowing of the coronary vessels of the heart muscle memperdarahi tersebut.plak may be equated with the bumps in the road to slow the flow of vehicles .
Exposed to risk factors that cause heart disease as where noted cardiologist in One Congress in Munich Germany , namely : a. Smoking smooking or b . High blood pressure c . Diabetes or Diabetes d . The scheme of distribution of fat = > e waist to hip ratio . Eating the wrong f . Excessive physical activity g . Consuming Alcohol h . The amount of fat in the blood i . psychosocial factors
Clinical symptoms of Heart Disease : Palpitations are complaints that nearly 100 % was found in patients with hyperthyroidism . Mechanism may explain the fact that this has not been clear , but it is associated with a direct effect of thyroid hormones on the SA node and the presence of excessive vulnerability hyperthyroid patients to stimulation of the sympathetic system . Palpitations is perceived both at rest and during sleep and will grow quickly if the person worked , after a meal or in an emotional state . Patients with hyperthyroidism often experience shortness of breath . This can be explained because in patients with hyperthyroidism there is an increase in cardiac output and oxygen consumption during and after activity . Additionally vital capacity in patients with hyperthyroidism would decrease accompanied by impaired circulation and pulmonary ventilation . If not found signs of heart failure , shortness of breath may be caused by weakness of the respiratory muscles . Precordial pain ( angina ) pain resembling angina pectoris often found in patients with hyperthyroidism . This is presumably due to an increase in oxygen consumption by the heart muscle (due to the direct effect of T3 on the heart muscle and an increase in peripheral oxygen demand ) . Some patients experienced angina during the first hyperthyroidism . Symptoms of angina and electrocardiographic abnormalities associated picture of angina can occur without the presence of coronary artery disease , it is likely due to the relative ischemia ( imbalance between supply and demand ) or coronary artery vasospasm .
Heart Disease Physical Examination : The frequency of the pulse is usually increased ( 90-125 beats / min ) and will grow rapidly if there is a long and emotional changes . Due to the high cardiac output and low peripheral resistance is not uncommon in patients with hyperthyroidism found a picture similar to the pulse of aortic insufficiency and a seller pulsus magnus . Pulse is more than 80 beats / min at rest should be suspected the existence of a hyperthyroid . In patients with pulmonary hypertension hyperthyroidism may be present and functional valvular regurgitation . Several cases of hyperthyroid patients showed abnormalities are reversible pumonal hypertension , moderate to severe tricuspid regurgitation and right heart failure . In hyperthyroid disease " acropachy " , can be found clubbing fingertips on clinical examination . This is due to impaired pulmonary hemodynamics
Prognosis and Diagnosis of Heart Disease Pathogenesis and treatment as early as possible is important to prevent the occurrence of cardiac complications in patients with hyperthyroidism . Osman (2007 ) reported a mortality rate of 6.6 % in the period of 5-6 years after treatment of hyperthyroidism . The cause of death was heart failure and cardiac ischemia . The cause of the pathogenesis of atherosclerosis - up has not been determined with certainty , but the most likely theory is the theory of endothelial damage . Possibility of endothelial damage caused by oxidized LDL cholesterol , infectious agents , smoking , hyperglycemia , and hiperhomocystenemia . As a result of the oxidation of LDL , monocytes will enter into the tunica intima and transformed into macrophages . This process will release 02 reactive radicals , particularly superoxide anion 02 - ( also assisted by homocysteine ) that damage cells and lead to endothelial NO formed by endothelial lose its activity to inhibit the adhesion of platelets and monocytes in anti- proliferative effects of endothelial and muscle and vasodilatation of blood vessels . Inhibition of vasodilation will encourage spasm . Even at an early stage , LDL stimulates the expression of adhesion molecules that allow blood vessels berploriferasi . Oxidation of LDL also led to changes in the bond . No longer recognized by the LDL receptor Apo B 100 but recognized by scavenger receptors are mostly found in macrophages . As a result, LDL and macrophages phagocytosing many will turn into foam cells that persist . Lipoprotein ( a) can be oxidized and difagosit in the same way . Simultaneously, monocyte chemotactic factors and platelets will trigger the migration of smooth muscle cells from the media to the intima . In the intima , these cells will be stimulated by PDGF berploriferasi and various other growth factors triggers . Muscle cells will also be transformed into foam cells by taking oxidized LDL . Cell foam will form the extracellular matrix also plays a role in the formation of atheroma .
- Plaque rupture
Rupture of atherosclerotic plaques is considered the most important cause of unstable angina pectoris , so suddenly subtotal or total occlusion of the coronary arteries that previously had minimal narrowing . Unstable plaque consists of a core that contains a lot of fat and macrophage cell infiltration . Sometimes cracks occur at the weakest wall plaque because of the protease enzyme produced by macrophages and enzymatically weaken the wall plaque ( fibrous cap ) . Rupture leads to the activation , adhesion , and platelet aggregation and thrombus formation leading to activation . When the blood vessels shut thrombus 100 % going to happen infarction with ST segment elevation , whereas when the thrombus does not clog 100 % , and only cause severe stenosis will occur unstable angina .
- Thrombosis and platelet aggregation
The occurrence of thrombosis after plaque disrupted due to the interaction between fat , smooth muscle cells , macrophages , and collagen . As a reaction to the disruption of endothelial function , platelet aggregation and platelet occurs unload granulation triggering a broader aggregation , vasoconstriction and thrombus formation . Systemic and inflammatory factors play a role in the occurrence of a change hemostase and coagulation and thrombosis instrumental in starting the intermittent , in unstable angina .
- vasospasm
It is estimated that the presence of endothelial dysfunction and vasoactive substance produced by platelets play a role in changes in vascular tone and cause spasm . Spasm often occurs in the presence of unstable plaque and have a role in thrombus formation .
- Erosion of the plaque without rupture
Any deformities and lesions due to increased smooth muscle cells can lead to narrowing of the vessels quickly and complaints ischemia .
Heart Disease Investigation
v Exercise test : Patients who showed a higher risk need examination by a treadmill exercise test . If the result is negative then the prognosis is good . Meanwhile, if the result is positive , especially if obtained in the ST segment depression , it is recommended for coronary angiography examination , to assess the state of the coronary artery revascularization does require action .
v Echocardiography : This test actually does not provide data for diagnosis of unstable angina directly . But when it seemed the disruption of left ventricular function , the presence of mitral insufficiency and cardiac regional wall motion abnormalities , indicating a poor prognosis .
v An ECG ECG at rest and not during an attack of angina is often still normal . EKG can indicate that the patient had received in the past myocardial infarction . Sometimes showed enlargement of the left ventricle . Can also showed ST segment changes and T-wave which is not typical . At the time of the attack , the ECG will show ST segment depression and negative T wave can be .
LABORATORY STUDIES
Examination of troponin T or I, and CK - MB examination is the most important marker .
management
Ø Common actions : patients need hospital care , rested ( bed rest ) , was given a sedative and oxygen . Administration of morphine or pethidine necessary in patients who still feel chest pain despite already received nitroglycerin .
Ø pharmacological therapy
Ø Anti ischemia
causes vasodilation of peripheral veins and arterioles , AA . nitrate with preload and afterload reducing effects so as to reduce wall stress and oxygen demand . Nitrates also increase the oxygen supply to the coronary artery vasodilatation and improve collateral blood flow . Collateral vessels provide an alternative route when the myocardial perfusion major epicardial coronary artery stenosis or occlusion . These channels are dormant under normal circumstances but within a few hours of existing collateral dilated and develop characteristics of mature blood vessels .
lowering the oxygen demand miokatdium melaluiàb . effects of beta blockers decrease the heart rate and myocardial contraction force . Example : propranolol , metoprolol , atenolol . coronary vasodilation and lower blood pressure c . calcium antagonists
Ø Drug antiagregasi platelets
reduce cardiac death and fatal and non-fatal infarction reduces to a. aspirin patients with angina stabil.merupakan second-line drugs if the patient can not bear aspirin , the effect sama.b. ticlopidine inhibit platelet aggregation , reduce stroke , infarction , and cardiovascular death c . clopidogrel denganàd fibrinogen binding . glycoprotein IIb / IIIa receptor inhibitors GP IIb / IIIa receptor on platelets is the last bond in the process of platelet aggregation . Because GP IIb / IIIa receptor inhibitor was then occupied by the platelet fibrinogen binding and platelet aggregation can be prevented not happen .
Ø Drugs are antikoagulanàa antithrombin . Unfractionated heparin .
Preventing Heart Disease and Stroke with Plant Medicine
Prevention efforts to prevent heart disease and stroke begins to improve the lifestyle and controlling risk factors , thereby reducing the chances of developing the disease . For the prevention of heart disease and stroke to avoid obesity / overweight and high cholesterol . Start by eating more vegetables , fruits , grains , canola and fish . Reduce meat , snacks ( snacks ) , and high-calorie foods that contain saturated fats and many others . Foods that contain lots of cholesterol accumulate in blood vessel walls and cause atherosclerosis that trigger heart disease and stroke .
Quitting smoking is a target that should be achieved , also avoid cigarette smoke from the environment . Smoking causes reduced elasticity of blood vessels , thus increasing the hardening of the arteries , and increases the blood clotting factors that trigger heart disease and stroke . Smokers have the chance of stroke and coronary heart disease approximately two -fold higher compared with non-smokers .
Reduce drinking alcohol . The more alcohol then it is likely the type of hemorrhagic stroke , especially higher . Alcohol can raise blood pressure , weakens the heart , blood thicken and cause arterial spasms . Perform sports / physical activity . Exercise can help reduce body weight , controlling cholesterol levels , lower blood pressure and other risk factors that are affected by heart disease and stroke
Control of high blood pressure and blood sugar levels . Hypertension is a major factor of stroke and coronary heart disease . Diabetes also increases the risk of stroke 1.5-4 fold , especially if the blood sugar is not controlled . Avoid the use of illegal drugs such as heroin , cocaine , amphetamines , because drugs such drugs can increase the risk of stroke 7 -fold compared with non- drug users .
Some types of herbs that can be used to prevent heart disease and stroke has the effect of blood circulation and as an anticoagulant that prevents blood clots , heart disease and stroke are the main causes of vascular disorders .
The state of cardiac heart diseases that can not perform normal functions , called the uncompensated state , abnormal blood circulation causing shortness of breath ( dyspnea ) , fatigue , pain in the heart area . Renal function abnormalities , liver toak , as well as blood pressure and sodium resorption occurs , SHG occurs edema . Coronary disease is a disease whose incidence is increasing in modern society with changes in diet and daily activities . This disease occurs when plaque containing lipoproteins , cholesterol , calcium and tissue debris formed in the interior surface of the coronary arteries causing hardening and narrowing of the coronary vessels of the heart muscle memperdarahi tersebut.plak may be equated with the bumps in the road to slow the flow of vehicles .
Exposed to risk factors that cause heart disease as where noted cardiologist in One Congress in Munich Germany , namely : a. Smoking smooking or b . High blood pressure c . Diabetes or Diabetes d . The scheme of distribution of fat = > e waist to hip ratio . Eating the wrong f . Excessive physical activity g . Consuming Alcohol h . The amount of fat in the blood i . psychosocial factors
Clinical symptoms of Heart Disease : Palpitations are complaints that nearly 100 % was found in patients with hyperthyroidism . Mechanism may explain the fact that this has not been clear , but it is associated with a direct effect of thyroid hormones on the SA node and the presence of excessive vulnerability hyperthyroid patients to stimulation of the sympathetic system . Palpitations is perceived both at rest and during sleep and will grow quickly if the person worked , after a meal or in an emotional state . Patients with hyperthyroidism often experience shortness of breath . This can be explained because in patients with hyperthyroidism there is an increase in cardiac output and oxygen consumption during and after activity . Additionally vital capacity in patients with hyperthyroidism would decrease accompanied by impaired circulation and pulmonary ventilation . If not found signs of heart failure , shortness of breath may be caused by weakness of the respiratory muscles . Precordial pain ( angina ) pain resembling angina pectoris often found in patients with hyperthyroidism . This is presumably due to an increase in oxygen consumption by the heart muscle (due to the direct effect of T3 on the heart muscle and an increase in peripheral oxygen demand ) . Some patients experienced angina during the first hyperthyroidism . Symptoms of angina and electrocardiographic abnormalities associated picture of angina can occur without the presence of coronary artery disease , it is likely due to the relative ischemia ( imbalance between supply and demand ) or coronary artery vasospasm .
Heart Disease Physical Examination : The frequency of the pulse is usually increased ( 90-125 beats / min ) and will grow rapidly if there is a long and emotional changes . Due to the high cardiac output and low peripheral resistance is not uncommon in patients with hyperthyroidism found a picture similar to the pulse of aortic insufficiency and a seller pulsus magnus . Pulse is more than 80 beats / min at rest should be suspected the existence of a hyperthyroid . In patients with pulmonary hypertension hyperthyroidism may be present and functional valvular regurgitation . Several cases of hyperthyroid patients showed abnormalities are reversible pumonal hypertension , moderate to severe tricuspid regurgitation and right heart failure . In hyperthyroid disease " acropachy " , can be found clubbing fingertips on clinical examination . This is due to impaired pulmonary hemodynamics
Prognosis and Diagnosis of Heart Disease Pathogenesis and treatment as early as possible is important to prevent the occurrence of cardiac complications in patients with hyperthyroidism . Osman (2007 ) reported a mortality rate of 6.6 % in the period of 5-6 years after treatment of hyperthyroidism . The cause of death was heart failure and cardiac ischemia . The cause of the pathogenesis of atherosclerosis - up has not been determined with certainty , but the most likely theory is the theory of endothelial damage . Possibility of endothelial damage caused by oxidized LDL cholesterol , infectious agents , smoking , hyperglycemia , and hiperhomocystenemia . As a result of the oxidation of LDL , monocytes will enter into the tunica intima and transformed into macrophages . This process will release 02 reactive radicals , particularly superoxide anion 02 - ( also assisted by homocysteine ) that damage cells and lead to endothelial NO formed by endothelial lose its activity to inhibit the adhesion of platelets and monocytes in anti- proliferative effects of endothelial and muscle and vasodilatation of blood vessels . Inhibition of vasodilation will encourage spasm . Even at an early stage , LDL stimulates the expression of adhesion molecules that allow blood vessels berploriferasi . Oxidation of LDL also led to changes in the bond . No longer recognized by the LDL receptor Apo B 100 but recognized by scavenger receptors are mostly found in macrophages . As a result, LDL and macrophages phagocytosing many will turn into foam cells that persist . Lipoprotein ( a) can be oxidized and difagosit in the same way . Simultaneously, monocyte chemotactic factors and platelets will trigger the migration of smooth muscle cells from the media to the intima . In the intima , these cells will be stimulated by PDGF berploriferasi and various other growth factors triggers . Muscle cells will also be transformed into foam cells by taking oxidized LDL . Cell foam will form the extracellular matrix also plays a role in the formation of atheroma .
- Plaque rupture
Rupture of atherosclerotic plaques is considered the most important cause of unstable angina pectoris , so suddenly subtotal or total occlusion of the coronary arteries that previously had minimal narrowing . Unstable plaque consists of a core that contains a lot of fat and macrophage cell infiltration . Sometimes cracks occur at the weakest wall plaque because of the protease enzyme produced by macrophages and enzymatically weaken the wall plaque ( fibrous cap ) . Rupture leads to the activation , adhesion , and platelet aggregation and thrombus formation leading to activation . When the blood vessels shut thrombus 100 % going to happen infarction with ST segment elevation , whereas when the thrombus does not clog 100 % , and only cause severe stenosis will occur unstable angina .
- Thrombosis and platelet aggregation
The occurrence of thrombosis after plaque disrupted due to the interaction between fat , smooth muscle cells , macrophages , and collagen . As a reaction to the disruption of endothelial function , platelet aggregation and platelet occurs unload granulation triggering a broader aggregation , vasoconstriction and thrombus formation . Systemic and inflammatory factors play a role in the occurrence of a change hemostase and coagulation and thrombosis instrumental in starting the intermittent , in unstable angina .
- vasospasm
It is estimated that the presence of endothelial dysfunction and vasoactive substance produced by platelets play a role in changes in vascular tone and cause spasm . Spasm often occurs in the presence of unstable plaque and have a role in thrombus formation .
- Erosion of the plaque without rupture
Any deformities and lesions due to increased smooth muscle cells can lead to narrowing of the vessels quickly and complaints ischemia .
Heart Disease Investigation
v Exercise test : Patients who showed a higher risk need examination by a treadmill exercise test . If the result is negative then the prognosis is good . Meanwhile, if the result is positive , especially if obtained in the ST segment depression , it is recommended for coronary angiography examination , to assess the state of the coronary artery revascularization does require action .
v Echocardiography : This test actually does not provide data for diagnosis of unstable angina directly . But when it seemed the disruption of left ventricular function , the presence of mitral insufficiency and cardiac regional wall motion abnormalities , indicating a poor prognosis .
v An ECG ECG at rest and not during an attack of angina is often still normal . EKG can indicate that the patient had received in the past myocardial infarction . Sometimes showed enlargement of the left ventricle . Can also showed ST segment changes and T-wave which is not typical . At the time of the attack , the ECG will show ST segment depression and negative T wave can be .
LABORATORY STUDIES
Examination of troponin T or I, and CK - MB examination is the most important marker .
management
Ø Common actions : patients need hospital care , rested ( bed rest ) , was given a sedative and oxygen . Administration of morphine or pethidine necessary in patients who still feel chest pain despite already received nitroglycerin .
Ø pharmacological therapy
Ø Anti ischemia
causes vasodilation of peripheral veins and arterioles , AA . nitrate with preload and afterload reducing effects so as to reduce wall stress and oxygen demand . Nitrates also increase the oxygen supply to the coronary artery vasodilatation and improve collateral blood flow . Collateral vessels provide an alternative route when the myocardial perfusion major epicardial coronary artery stenosis or occlusion . These channels are dormant under normal circumstances but within a few hours of existing collateral dilated and develop characteristics of mature blood vessels .
lowering the oxygen demand miokatdium melaluiàb . effects of beta blockers decrease the heart rate and myocardial contraction force . Example : propranolol , metoprolol , atenolol . coronary vasodilation and lower blood pressure c . calcium antagonists
Ø Drug antiagregasi platelets
reduce cardiac death and fatal and non-fatal infarction reduces to a. aspirin patients with angina stabil.merupakan second-line drugs if the patient can not bear aspirin , the effect sama.b. ticlopidine inhibit platelet aggregation , reduce stroke , infarction , and cardiovascular death c . clopidogrel denganàd fibrinogen binding . glycoprotein IIb / IIIa receptor inhibitors GP IIb / IIIa receptor on platelets is the last bond in the process of platelet aggregation . Because GP IIb / IIIa receptor inhibitor was then occupied by the platelet fibrinogen binding and platelet aggregation can be prevented not happen .
Ø Drugs are antikoagulanàa antithrombin . Unfractionated heparin .
Preventing Heart Disease and Stroke with Plant Medicine
Prevention efforts to prevent heart disease and stroke begins to improve the lifestyle and controlling risk factors , thereby reducing the chances of developing the disease . For the prevention of heart disease and stroke to avoid obesity / overweight and high cholesterol . Start by eating more vegetables , fruits , grains , canola and fish . Reduce meat , snacks ( snacks ) , and high-calorie foods that contain saturated fats and many others . Foods that contain lots of cholesterol accumulate in blood vessel walls and cause atherosclerosis that trigger heart disease and stroke .
Quitting smoking is a target that should be achieved , also avoid cigarette smoke from the environment . Smoking causes reduced elasticity of blood vessels , thus increasing the hardening of the arteries , and increases the blood clotting factors that trigger heart disease and stroke . Smokers have the chance of stroke and coronary heart disease approximately two -fold higher compared with non-smokers .
Reduce drinking alcohol . The more alcohol then it is likely the type of hemorrhagic stroke , especially higher . Alcohol can raise blood pressure , weakens the heart , blood thicken and cause arterial spasms . Perform sports / physical activity . Exercise can help reduce body weight , controlling cholesterol levels , lower blood pressure and other risk factors that are affected by heart disease and stroke
Control of high blood pressure and blood sugar levels . Hypertension is a major factor of stroke and coronary heart disease . Diabetes also increases the risk of stroke 1.5-4 fold , especially if the blood sugar is not controlled . Avoid the use of illegal drugs such as heroin , cocaine , amphetamines , because drugs such drugs can increase the risk of stroke 7 -fold compared with non- drug users .
Some types of herbs that can be used to prevent heart disease and stroke has the effect of blood circulation and as an anticoagulant that prevents blood clots , heart disease and stroke are the main causes of vascular disorders .
