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| + | ======= Coronary Heart Disease ======= | ||
| + | {{::coronary_heart_disease_.pptx|}} | ||
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| ====== Introduction ====== | ====== Introduction ====== | ||
| Coronary heart disease or ischemic heart disease is a disorder characterized by the buildup of plaques in the coronary arteries thus leading to the narrowing of the arteries (NIH, 2016). The buildup of plaques is known as atherosclerosis. The plaques tend to accumulate throughout the years blocking circulation in the arteries. Common symptoms include angina or better known as chest pain or discomfort, pressure in arms and shoulders, neck, jaw, or back, a weakened heart, and is also a contributing factor to a heart attack (NIH, 2016). Over time, CHD can contribute to weakened heart muscle and tissue which can lead to heart failure and arrhythmias. However, lifestyle changes such as changing diet, working out and reducing stress, along with medications can reduce the risk of developing coronary heart disease (NIH, 2016). CHD contributes to ⅓ of deaths in people over 35 years old (Sanchis-Gomar et. al., 2016). It is also a major cause of death in developed regions mostly due to poor lifestyle habits and diets. Causes of this disease are often attributed to physical inactivity, nicotine abuse, and bac nutrition practices (Sanchis-Gomar et. al., 2016). | Coronary heart disease or ischemic heart disease is a disorder characterized by the buildup of plaques in the coronary arteries thus leading to the narrowing of the arteries (NIH, 2016). The buildup of plaques is known as atherosclerosis. The plaques tend to accumulate throughout the years blocking circulation in the arteries. Common symptoms include angina or better known as chest pain or discomfort, pressure in arms and shoulders, neck, jaw, or back, a weakened heart, and is also a contributing factor to a heart attack (NIH, 2016). Over time, CHD can contribute to weakened heart muscle and tissue which can lead to heart failure and arrhythmias. However, lifestyle changes such as changing diet, working out and reducing stress, along with medications can reduce the risk of developing coronary heart disease (NIH, 2016). CHD contributes to ⅓ of deaths in people over 35 years old (Sanchis-Gomar et. al., 2016). It is also a major cause of death in developed regions mostly due to poor lifestyle habits and diets. Causes of this disease are often attributed to physical inactivity, nicotine abuse, and bac nutrition practices (Sanchis-Gomar et. al., 2016). | ||
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| CHD incidence is on the rise worldwide and is a major cause of death in developed countries. It results in approximately one-third of deaths in individuals over the age of 35 years (Sanchis-Gomar et al., 2016). In 2016, the Heart Disease and Stroke Statistics reports that 15.5 milllion people in the USA over the age of 20 have been diagnosed with a manifestation of CHD. In the USA, approximately one-half of middle-aged men and one-third of middle-aged women develop CHD (Sanchis-Gomar et al., 2016). Despite increasing prevalence, age-standardized death rates have decreased by 22% since 1990 due to a shift in age demographics. The lifetime risk of developing CHD in individuals with more than 2 risk factors is 37.5% for men and 18.3% for women (Sanchis-Gomar et al., 2016). Estimates show that men over the age of 40 and women over the age of 45 are at most risk of CHD. Prevalence of CHD increases with age for both men and women (Sanchis-Gomar et al., 2016). | CHD incidence is on the rise worldwide and is a major cause of death in developed countries. It results in approximately one-third of deaths in individuals over the age of 35 years (Sanchis-Gomar et al., 2016). In 2016, the Heart Disease and Stroke Statistics reports that 15.5 milllion people in the USA over the age of 20 have been diagnosed with a manifestation of CHD. In the USA, approximately one-half of middle-aged men and one-third of middle-aged women develop CHD (Sanchis-Gomar et al., 2016). Despite increasing prevalence, age-standardized death rates have decreased by 22% since 1990 due to a shift in age demographics. The lifetime risk of developing CHD in individuals with more than 2 risk factors is 37.5% for men and 18.3% for women (Sanchis-Gomar et al., 2016). Estimates show that men over the age of 40 and women over the age of 45 are at most risk of CHD. Prevalence of CHD increases with age for both men and women (Sanchis-Gomar et al., 2016). | ||
| {{ :fig_11.01.jpg?nolink |}} | {{ :fig_11.01.jpg?nolink |}} | ||
| - | **Figure 1:** Outlining the Coronary Heart Disease prevalence in males and females, in differing age groups along with varying ethnicities to compare epidemiological results. | + | **Figure 1: Outlining the Coronary Heart Disease prevalence in males and females, in differing age groups along with varying ethnicities to compare epidemiological results(Sanchis-Gomar et al., 2016).** |
| ====== Risk Factors ====== | ====== Risk Factors ====== | ||
| The exact etiology of CHD is unknown but several genetic and environmental risk factors have been associated with an increased risk of developing CHD (Torpy et al., 2009). | The exact etiology of CHD is unknown but several genetic and environmental risk factors have been associated with an increased risk of developing CHD (Torpy et al., 2009). | ||
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| {{ :screen_shot_2017-12-02_at_12.01.58_am.png |}} | {{ :screen_shot_2017-12-02_at_12.01.58_am.png |}} | ||
| - | **Figure 2:** Illustrates the observational pattern of the Electrocardiograph when the heart's electrical activity is modified. Top Left: Normal ECG Pattern, with baseline electrical levels. Top Right: Non-ST Elevation Myocardial Infarction, when there is partial blockage of the artery, the heart will show an ECG pattern with ST-depression. Bottom Right: ST-Elevation Myocardial Infarction, when there is a complete blockage of the artery, the heart will show an ECG pattern of ST-Elevation. Bottom Right: ST-Depression with T Inversion. | + | **Figure 2: Illustrates the observational pattern of the Electrocardiograph when the heart's electrical activity is modified. Top Left: Normal ECG Pattern, with baseline electrical levels. Top Right: Non-ST Elevation Myocardial Infarction, when there is partial blockage of the artery, the heart will show an ECG pattern with ST-depression. Bottom Right: ST-Elevation Myocardial Infarction, when there is a complete blockage of the artery, the heart will show an ECG pattern of ST-Elevation. Bottom Right: ST-Depression with T Inversion(Klabunde, 2016).** |
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| ==== Troponin Blood Test ==== | ==== Troponin Blood Test ==== | ||
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| {{ ::screen_shot_2017-12-02_at_12.06.15_am.png |}} | {{ ::screen_shot_2017-12-02_at_12.06.15_am.png |}} | ||
| - | **Figure 3:** Demonstrating Cardiac Troponin-T bound to actin filaments in cardiac muscle. | + | **Figure 3: Demonstrating Cardiac Troponin-T bound to actin filaments in cardiac muscle(Melanson et al., 2007).** |
| {{ ::screen_shot_2017-12-02_at_12.07.53_am.png |}} | {{ ::screen_shot_2017-12-02_at_12.07.53_am.png |}} | ||
| - | **Figure 4:** Acute myocardial infarction illustrated by soluble Troponin-T levels as high as 50 ug/L. B: Minor myocardial infarction as seen with drastically lower levels of Troponin-T in the blood, with only over 0.05 ug/L after 24-48 hours. | + | **Figure 4: Acute myocardial infarction illustrated by soluble Troponin-T levels as high as 50 ug/L. B: Minor myocardial infarction as seen with drastically lower levels of Troponin-T in the blood, with only over 0.05 ug/L after 24-48 hours(Melanson et al., 2007).** |
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| ==== Cardiac Catheterization ==== | ==== Cardiac Catheterization ==== | ||
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| {{ :diagnosis.jpg |}} | {{ :diagnosis.jpg |}} | ||
| - | **Figure 5:** Displaying cardiac catheterization beginning from a femoral artery entrance, making its way up the coronary artery to indicate the location of the plaque buildup, as well as take inter-arterial illustrations of the heart via a X-ray dye, thus conducting an angiogram. | + | **Figure 5: Displaying cardiac catheterization beginning from a femoral artery entrance, making its way up the coronary artery to indicate the location of the plaque buildup, as well as take inter-arterial illustrations of the heart via a X-ray dye, thus conducting an angiogram(Robinson, 2011).** |
| ====== Pathophysiology ====== | ====== Pathophysiology ====== | ||
| **Atherosclerosis:** | **Atherosclerosis:** | ||
| Atherosclerosis is the buildup of plaques in the arteries restricting the flow of oxygen-rich blood from moving inside the heart and body (Gibbons, 2013). The plaque is made up of fat, cholesterol, calcium, and other components and continues to grow larger in the arteries (Gibbons, 2013). As people age, the plaque narrows the arteries and hardens making it difficult for oxygenated blood to enter the heart and body (Gibbons, 2013). This can result in a heart attack or cardiac arrhythmia (Gibbons, 2013). Atherosclerosis can happen in any arteries in the body but can be attributed to CHD in the coronary arteries. This is what is responsible for angina or chest pain that is often contributed to CHD. | Atherosclerosis is the buildup of plaques in the arteries restricting the flow of oxygen-rich blood from moving inside the heart and body (Gibbons, 2013). The plaque is made up of fat, cholesterol, calcium, and other components and continues to grow larger in the arteries (Gibbons, 2013). As people age, the plaque narrows the arteries and hardens making it difficult for oxygenated blood to enter the heart and body (Gibbons, 2013). This can result in a heart attack or cardiac arrhythmia (Gibbons, 2013). Atherosclerosis can happen in any arteries in the body but can be attributed to CHD in the coronary arteries. This is what is responsible for angina or chest pain that is often contributed to CHD. | ||
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| **Lesion formation:** | **Lesion formation:** | ||
| Arterial inflammation has been considered a contributing factor to CHD and atherosclerosis (Libby and Theroux, 2011). Immune response and effector molecules contribute to the formation of lesions which arise from inflammation of the arterial walls. This inflammation results in atherosclerosis which is the main symptom of CHD (Hansson, 2005). Atherosclerotic lesions look like asymmetrical focal thickenings of the innermost layer of the artery and are made up of cells, connective tissue, and Lipids (Hansson, 2005). Inflammatory and immune cells along with vascular endothelial and smooth cells all contribute to the formation of fatty streaks, which is an accumulation of lipid-laden cells underneath the endothelium (Hansson, 2005). Fatty streaks are made up of macrophages and T cells (Hansson, 2005). These immune cells can signal a cytotoxic storm, recruiting inflammatory cytokines which are attributed to the inflammation that can occur (Hansson, 2005). The activation of plaques and inflammation contributes to cardiac ischemia and infarctions. Moreover, lesions can result in plaque rupturing and endothelial erosion (Hansson, 2005). If the plaque ruptures, many thrombotic materials can be exposed to the blood which can trigger acute coronary syndrome (Hansson, 2005). | Arterial inflammation has been considered a contributing factor to CHD and atherosclerosis (Libby and Theroux, 2011). Immune response and effector molecules contribute to the formation of lesions which arise from inflammation of the arterial walls. This inflammation results in atherosclerosis which is the main symptom of CHD (Hansson, 2005). Atherosclerotic lesions look like asymmetrical focal thickenings of the innermost layer of the artery and are made up of cells, connective tissue, and Lipids (Hansson, 2005). Inflammatory and immune cells along with vascular endothelial and smooth cells all contribute to the formation of fatty streaks, which is an accumulation of lipid-laden cells underneath the endothelium (Hansson, 2005). Fatty streaks are made up of macrophages and T cells (Hansson, 2005). These immune cells can signal a cytotoxic storm, recruiting inflammatory cytokines which are attributed to the inflammation that can occur (Hansson, 2005). The activation of plaques and inflammation contributes to cardiac ischemia and infarctions. Moreover, lesions can result in plaque rupturing and endothelial erosion (Hansson, 2005). If the plaque ruptures, many thrombotic materials can be exposed to the blood which can trigger acute coronary syndrome (Hansson, 2005). | ||
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| **Thrombosis:** | **Thrombosis:** | ||
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| {{ :screen_shot_2017-11-28_at_3.21.04_am.png?300 |}} | {{ :screen_shot_2017-11-28_at_3.21.04_am.png?300 |}} | ||
| - | **Figure 5:** Demonstrates the last stage of progression of atherosclerosis in which there is thrombus formation (Radar and Daugherty, 2008). | + | **Figure 6: Demonstrates the last stage of progression of atherosclerosis in which there is thrombus formation (Radar and Daugherty, 2008).** |
| ====== Treatment ====== | ====== Treatment ====== | ||
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| **Physical Activity:** | **Physical Activity:** | ||
| Physical activity can help to control coronary artery disease risk factors such as LDL cholesterol, high blood pressure, and help to maintain a healthy weight (National Heart, Lung, and Blood Institute, 2016). Physical activity lowers blood pressure, and triglycerides found in the blood, and raise HDL cholesterol levels. Physical activity is an effective way to overall improve and boost heart health, which can improve symptoms and reduce mortality in patients with coronary artery disease (Jolliffe et al., 2001). According to a study conducted in 2001, it was concluded that physical activity reduces total mortality of patients with coronary artery disease by 25 to 30 percent (Jolliffe et al., 2001). | Physical activity can help to control coronary artery disease risk factors such as LDL cholesterol, high blood pressure, and help to maintain a healthy weight (National Heart, Lung, and Blood Institute, 2016). Physical activity lowers blood pressure, and triglycerides found in the blood, and raise HDL cholesterol levels. Physical activity is an effective way to overall improve and boost heart health, which can improve symptoms and reduce mortality in patients with coronary artery disease (Jolliffe et al., 2001). According to a study conducted in 2001, it was concluded that physical activity reduces total mortality of patients with coronary artery disease by 25 to 30 percent (Jolliffe et al., 2001). | ||
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| ==== Aspirin ==== | ==== Aspirin ==== | ||
| Antiplatelet medicines prevent blood clots from forming in arteries, and can thereby prevent heart attack or stroke (Frishman et al., 2005). An example of an antiplatelet medication is aspirin. Aspirin prevents the conversion of arachidonic acid to proaggregatory molecule known as thromboxane (Frishman et al., 2005). Thromboxane is a vasoconstrictor, and a hypertensive agent, which facilitates platelet aggregation as it stimulates the activation of new platelets (Frishman et al., 2005). Aspirin inhibits cyclooxygenase (COX-1) in platelets and prevents platelet aggregation, and thus reduces clotting. Aspirin is an anti-prostaglandin which leads to reduced inflammation in blood vessels as well (Frishman et al., 2005). | Antiplatelet medicines prevent blood clots from forming in arteries, and can thereby prevent heart attack or stroke (Frishman et al., 2005). An example of an antiplatelet medication is aspirin. Aspirin prevents the conversion of arachidonic acid to proaggregatory molecule known as thromboxane (Frishman et al., 2005). Thromboxane is a vasoconstrictor, and a hypertensive agent, which facilitates platelet aggregation as it stimulates the activation of new platelets (Frishman et al., 2005). Aspirin inhibits cyclooxygenase (COX-1) in platelets and prevents platelet aggregation, and thus reduces clotting. Aspirin is an anti-prostaglandin which leads to reduced inflammation in blood vessels as well (Frishman et al., 2005). | ||
| - | **Figure 6:** {{ :screen_shot_2017-12-01_at_11.13.45_pm.png?200 |}} | + | {{ :screen_shot_2017-12-01_at_11.13.45_pm.png?200 |}} |
| + | **Figure 7: Shows the mechanism of action of aspirin as an anti-platelet drug (Frishman et al., 2005).** | ||
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| ==== Beta-Blockers ==== | ==== Beta-Blockers ==== | ||
| Beta-blockers is a medication that is used to control abnormal heart rhythms, and treat high blood pressure (Frishman et al., 2005). Beta-blockers are antagonists that block the beta-adrenergic receptors for epinephrine and norepinephrine that mediates a flight or fight response (Frishman et al., 2005). The beta receptors are found on cells of the heart muscles, smooth muscles, arteries, kidneys, and other tissues that are part of the sympathetic nervous system. The flight or fight response accelerates heart-rate and causes vasoconstriction increasing blood pressure as a result of stimulation of the beta-receptors by epinephrine and norepinephrine (Frishman et al., 2005). However, exogenously administered beta-blockers bind preferentially and reversibly to the beta-receptor and competitively inhibits the epinephrine and norepinephrine, and weakens the effect. This results in slowing the heart rate, decreasing cardiac output, lessens the force with which heart muscle contracts, and dilates blood vessels. Examples of beta blockers include atenolol, metoprolol, nebivolol, and bisoprolol (Frishman et al., 2005). | Beta-blockers is a medication that is used to control abnormal heart rhythms, and treat high blood pressure (Frishman et al., 2005). Beta-blockers are antagonists that block the beta-adrenergic receptors for epinephrine and norepinephrine that mediates a flight or fight response (Frishman et al., 2005). The beta receptors are found on cells of the heart muscles, smooth muscles, arteries, kidneys, and other tissues that are part of the sympathetic nervous system. The flight or fight response accelerates heart-rate and causes vasoconstriction increasing blood pressure as a result of stimulation of the beta-receptors by epinephrine and norepinephrine (Frishman et al., 2005). However, exogenously administered beta-blockers bind preferentially and reversibly to the beta-receptor and competitively inhibits the epinephrine and norepinephrine, and weakens the effect. This results in slowing the heart rate, decreasing cardiac output, lessens the force with which heart muscle contracts, and dilates blood vessels. Examples of beta blockers include atenolol, metoprolol, nebivolol, and bisoprolol (Frishman et al., 2005). | ||
| - | **Figure 7:** {{ :screen_shot_2017-11-27_at_12.06.14_am.png |}} | + | {{ :screen_shot_2017-11-27_at_12.06.14_am.png |}} |
| + | **Figure 8: Demonstrates beta-blockers as an antagonist, and its effects by lowering heart workload in a patient with coronary heart disease (Frishman et al., 2005).** | ||
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| ==== Nitroglycerin ==== | ==== Nitroglycerin ==== | ||
| Nitroglycerin is a medication used for high blood pressure. It is administered by mouth, under the tongue, applied to the skin, or by injection into a vein (Kukovetz et al., 1987). Nitroglycerin mode of action is not entirely clear, but it is an effective treatment that functions to dilate blood vessels as it is a precursor to nitric oxide, a potent vasodilator (Kukovetz et al., 1987). Nitroglycerin is converted to nitric oxide in the body my the enzyme mitochondrial aldehyde dehydrogenase. Once it is converted to nitric oxide in the blood, it activates guanylyl cyclase, which results in the formation of cyclic guanosine monophosphate (cGMP) from guanosine triphosphate (GTP) (Kukovetz et al., 1987). This activates protein kinase G, which stimulates dephosphorylation of myosin, and results in muscle relaxation and dilation of blood vessels (Kukovetz et al., 1987). | Nitroglycerin is a medication used for high blood pressure. It is administered by mouth, under the tongue, applied to the skin, or by injection into a vein (Kukovetz et al., 1987). Nitroglycerin mode of action is not entirely clear, but it is an effective treatment that functions to dilate blood vessels as it is a precursor to nitric oxide, a potent vasodilator (Kukovetz et al., 1987). Nitroglycerin is converted to nitric oxide in the body my the enzyme mitochondrial aldehyde dehydrogenase. Once it is converted to nitric oxide in the blood, it activates guanylyl cyclase, which results in the formation of cyclic guanosine monophosphate (cGMP) from guanosine triphosphate (GTP) (Kukovetz et al., 1987). This activates protein kinase G, which stimulates dephosphorylation of myosin, and results in muscle relaxation and dilation of blood vessels (Kukovetz et al., 1987). | ||
| - | **Figure 8:** {{ :screen_shot_2017-11-27_at_12.06.29_am.png?300 |}} | + | {{ :screen_shot_2017-11-27_at_12.06.29_am.png?300 |}} |
| + | **Figure 9: Illustrates nitroglycerin as a precursor for nitric oxide, and its direct activation of pathways to allow vasodilation(Kukovetz et al., 1987).** | ||
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| ==== Angioplasty ==== | ==== Angioplasty ==== | ||
| Coronary Angioplasty, also known as PCI is a nonsurgical procedure that improves the overall blood flow to the heart by cardiac catheterization. It requires the insertion of a catheter tube, and injection of contrast dye that is iodine based into coronary arteries (National Heart, Lung, and Blood Institute, 2016). This medicinal procedure is followed to open coronary arteries that are narrowed or blocked by the buildup of artherosclerotic plaque. The doctor will numb an area on the wrist or groin, and a small hole will be made to insert the catheter into the blood vessel (National Heart, Lung, and Blood Institute, 2016). The doctor uses live x-rays to guide the catheter to the heart to inject special contrast dye that will show the blockage. Another catheter is used over a guidewire, and a balloon is inflated at the tip of that catheter (National Heart, Lung, and Blood Institute, 2016). A small mest tube called a stent is placed in the artery to keep the artery open. After the procedure, the doctor will remove the catheter and close and bandage the opening on the wrist or groin (National Heart, Lung, and Blood Institute, 2016). If a stent is implanted, anticlotting medicines are prescribed for three to 12 months. Complications can arise from this procedure, which may include bleeding, blood vessel damage, and allergic reaction to the dye. The risk of complications is higher if the patient is older, and has extensive heart disease or multiple blockages in the coronary arteries (National Heart, Lung, and Blood Institute, 2016). | Coronary Angioplasty, also known as PCI is a nonsurgical procedure that improves the overall blood flow to the heart by cardiac catheterization. It requires the insertion of a catheter tube, and injection of contrast dye that is iodine based into coronary arteries (National Heart, Lung, and Blood Institute, 2016). This medicinal procedure is followed to open coronary arteries that are narrowed or blocked by the buildup of artherosclerotic plaque. The doctor will numb an area on the wrist or groin, and a small hole will be made to insert the catheter into the blood vessel (National Heart, Lung, and Blood Institute, 2016). The doctor uses live x-rays to guide the catheter to the heart to inject special contrast dye that will show the blockage. Another catheter is used over a guidewire, and a balloon is inflated at the tip of that catheter (National Heart, Lung, and Blood Institute, 2016). A small mest tube called a stent is placed in the artery to keep the artery open. After the procedure, the doctor will remove the catheter and close and bandage the opening on the wrist or groin (National Heart, Lung, and Blood Institute, 2016). If a stent is implanted, anticlotting medicines are prescribed for three to 12 months. Complications can arise from this procedure, which may include bleeding, blood vessel damage, and allergic reaction to the dye. The risk of complications is higher if the patient is older, and has extensive heart disease or multiple blockages in the coronary arteries (National Heart, Lung, and Blood Institute, 2016). | ||
| + | {{ :stents.jpeg |}} | ||
| + | **Figure 10: Illustrates a step-by-step procedure of angioplasty, which is a medicinal procedure for coronary artery disease (National Heart, Lung, and Blood Institute, 2016).** | ||
| ====== Future Therapeutics ====== | ====== Future Therapeutics ====== | ||
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| Eikelboom, J., & Hirsh, J. (2007). Combined antiplatelet and anticoagulant therapy: clinical benefits and risks. Journal of Thrombosis and Haemostasis, 5, 255–63. https://doi.org/10.1111/j.1538-7836.2007.02499.x | Eikelboom, J., & Hirsh, J. (2007). Combined antiplatelet and anticoagulant therapy: clinical benefits and risks. Journal of Thrombosis and Haemostasis, 5, 255–63. https://doi.org/10.1111/j.1538-7836.2007.02499.x | ||
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| + | Fitzmaurice, D. a, Blann, A. D., & Lip, G. Y. H. (2002). Bleeding risks of antithrombotic therapy. BMJ (Clinical Research Ed.), 325(7368), 828–31. https://doi.org/10.1136/bmj.325.7368.828 | ||
| Frank-Kamenetsky, M., Grefhorst, A., Anderson, N. N., Racie, T. S., Bramlage, B., Akinc, A., … Fitzgerald, K. (2008). Therapeutic RNAi targeting PCSK9 acutely lowers plasma cholesterol in rodents and LDL cholesterol in nonhuman primates. Proceedings of the National Academy of Sciences, 105(33), 11915–11920. https://doi.org/10.1073/pnas.0805434105 | Frank-Kamenetsky, M., Grefhorst, A., Anderson, N. N., Racie, T. S., Bramlage, B., Akinc, A., … Fitzgerald, K. (2008). Therapeutic RNAi targeting PCSK9 acutely lowers plasma cholesterol in rodents and LDL cholesterol in nonhuman primates. Proceedings of the National Academy of Sciences, 105(33), 11915–11920. https://doi.org/10.1073/pnas.0805434105 | ||
| - | Fitzmaurice, D. a, Blann, A. D., & Lip, G. Y. H. (2002). Bleeding risks of antithrombotic therapy. BMJ (Clinical Research Ed.), 325(7368), 828–31. https://doi.org/10.1136/bmj.325.7368.828 | + | Frishman, W. H., Cheng-Lai, A., & Nawarskas, J. (Eds.). (2005). Current cardiovascular drugs. Springer Science & Business Media. |
| Golomb, B. A., & Evans, M. A. (2008). Statin adverse effects : a review of the literature and evidence for a mitochondrial mechanism. American Journal of Cardiovascular Drugs : Drugs, Devices, and Other Interventions, 8(6), 373–418. https://doi.org/10.2165/0129784-200808060-00004 | Golomb, B. A., & Evans, M. A. (2008). Statin adverse effects : a review of the literature and evidence for a mitochondrial mechanism. American Journal of Cardiovascular Drugs : Drugs, Devices, and Other Interventions, 8(6), 373–418. https://doi.org/10.2165/0129784-200808060-00004 | ||
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| + | Jolliffe, J. A., Rees, K., Taylor, R. S., Thompson, D., Oldridge, N., & Ebrahim, S. (2001). Exercise-based rehabilitation for coronary heart disease. Cochrane Database Syst Rev, 1(1). | ||
| Klabunde, R. E. (2016). Electrophysiological changes during cardiac ischemia. Retrieved December 01, 2017 from http://www.cvphysiology.com/CAD/CAD012 | Klabunde, R. E. (2016). Electrophysiological changes during cardiac ischemia. Retrieved December 01, 2017 from http://www.cvphysiology.com/CAD/CAD012 | ||
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| + | Kukovetz, W. R., Holzmann, S., & Romanin, C. (1987). Mechanism of vasodilation by nitrates: role of cyclic GMP. Cardiology, 74(Suppl. 1), 12-19. | ||
| Libby, P., Ridker, P. M., & Maseri, A. (2002). Inflammation and atherosclerosis. Inflammation and Atherosclerosis, 105, 1135–1143. https://doi.org/10.1161/hc0902.104353 | Libby, P., Ridker, P. M., & Maseri, A. (2002). Inflammation and atherosclerosis. Inflammation and Atherosclerosis, 105, 1135–1143. https://doi.org/10.1161/hc0902.104353 | ||
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| + | Libby, P., & Theroux, P. (2005). Pathophysiology of coronary artery disease. Circulation, 111(25), 3481-3488 | ||
| Melanson, S. E. F, Tanasijevic, M. J., Jarolim, P. (2007). Cardiac troponin assays: a view from the clinical chemistry laboratory. Circulation, 116, 8. https://doi.org/10.1161/CIRCULATIONAHA.107.722975 | Melanson, S. E. F, Tanasijevic, M. J., Jarolim, P. (2007). Cardiac troponin assays: a view from the clinical chemistry laboratory. Circulation, 116, 8. https://doi.org/10.1161/CIRCULATIONAHA.107.722975 | ||
| Minihane, A. M., Vinoy, S., Russell, W. R., Baka, A., Roche, H. M., Tuohy, K. M., … Calder, P. C. (2015). Low-grade inflammation, diet composition and health: current research evidence and its translation. The British Journal of Nutrition, 114(7), 999–1012. https://doi.org/10.1017/S0007114515002093 | Minihane, A. M., Vinoy, S., Russell, W. R., Baka, A., Roche, H. M., Tuohy, K. M., … Calder, P. C. (2015). Low-grade inflammation, diet composition and health: current research evidence and its translation. The British Journal of Nutrition, 114(7), 999–1012. https://doi.org/10.1017/S0007114515002093 | ||
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| + | National Heart, Lung, and Blood Institute.(2016). How is Coronary Heart Disease Treated ?. Retrieved November 26, 2017, from https://www.nhlbi.nih.gov/health/health-topics/topics/cad | ||
| NHLBI. (2015a). How is a heart attack diagnosed? Retrieved December 01, 2017, from https://www.nhlbi.nih.gov/health/health-topics/topics/heartattack/diagnosis | NHLBI. (2015a). How is a heart attack diagnosed? Retrieved December 01, 2017, from https://www.nhlbi.nih.gov/health/health-topics/topics/heartattack/diagnosis | ||
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| R., H. (2004). Cardiovascular disease: Different strategies for primary and secondary prevention? Heart, 90(10), 1217–1223. https://doi.org/10.1136/hrt.2003.027680 | R., H. (2004). Cardiovascular disease: Different strategies for primary and secondary prevention? Heart, 90(10), 1217–1223. https://doi.org/10.1136/hrt.2003.027680 | ||
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| Ray KK Leiter LA Dufour R, Karakas M, Hall T, Troquay RP, Turner T, Visseren FL, Wijngaard P, Wright RS, Kastelein JJ, Landmesser U, K. D. (2017). Inclisiran in Patients at High Cardiovascular Risk with Elevated LDL Cholesterol. New England Journal of Medicine. Retrieved from http://ovidsp.ovid.com/ovidweb.cgi?T=JS&PAGE=reference&D=cctr&NEWS=N&AN=CN-01368245 | Ray KK Leiter LA Dufour R, Karakas M, Hall T, Troquay RP, Turner T, Visseren FL, Wijngaard P, Wright RS, Kastelein JJ, Landmesser U, K. D. (2017). Inclisiran in Patients at High Cardiovascular Risk with Elevated LDL Cholesterol. New England Journal of Medicine. Retrieved from http://ovidsp.ovid.com/ovidweb.cgi?T=JS&PAGE=reference&D=cctr&NEWS=N&AN=CN-01368245 | ||
