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» Home » CAD » Cardiology » Coronary artery disease » Coronary Heart Disease
Background
Coronary heart disease is a condition where the heart muscle does not receive enough blood and oxygen due to blocked or narrowed coronary arteries. This is caused by the build-up of plaques in the arteries, leading to an imbalance between the heart’s oxygen needs and the amount supplied.
It is the leading cause of death globally and has been on the rise since the early 20th century, peaking in the 1960s, and remains a significant cause of death today. Its risk factor includes smoking, high cholesterol, diabetes, sedentary lifestyle and a family history.
Epidemiology
Coronary heart disease is more common in developed countries, where lifestyle factors such as poor diet, lack of physical activity, and smoking are more prevalent. However, the incidence also increases in developing countries as these countries adopt westernized lifestyles. According to the World Health Organization, CHD is the leading cause of death globally, taking an estimated 17.9 million lives each year.
The prevalence is estimated to be around 10%, with the highest rates in high-income countries. The mortality rate varies depending on the disease stage, but it is generally high, with up to 20% of people passing away within a year of the diagnosis.
Anatomy
Pathophysiology
The pathophysiology of CHD is characterized by the build-up of atherosclerotic plaque in the coronary arteries. This plaque is made up of lipid-laden macrophages, also known as foam cells, which form a fatty streak in the subendothelial space of the intima layer. The fatty streak formation begins when monocytes migrate into the subendothelial space and take up oxidized low-density lipoprotein (LDL) particles.
T cells are activated and release cytokines, which aid in the formation of the subendothelial plaque. Additionally, growth factors activate smooth muscle cells, which take up oxidized LDL particles and collagen, and deposit them along with activated macrophages, increasing the amount of foam cells. As the plaque builds up, it narrows the vessel lumen and restricts blood flow, leading to chest pain or a heart attack.
Atherosclerotic plaque can grow in size over time or become stable if no further damage occurs to the endothelium. When the plaque becomes stable, a fibrous cap forms and the lesion calcifies. As the lesion becomes larger, it can restrict blood flow to the heart muscle, leading to chest pain during increased demand. However, the symptoms will subside during rest as the oxygen requirement decreases.
For a lesion to cause angina at rest, it must be at least 90% stenosed. The plaque can sometimes rupture, exposing tissue factors and leading to thrombosis. This can result in the complete or partial blockage of the lumen and the development of acute coronary syndrome (ACS), such as unstable angina, NSTEMI, or STEMI, depending on the level of damage.
Etiology
Coronary heart disease has various contributing factors that can be divided into non-modifiable and modifiable. Non-modifiable factors include characteristics such as gender, age, family history, and genetics which cannot be altered. Modifiable risk factors include behaviors and lifestyle choices such as smoking, obesity, lipid levels, and psychosocial variables, which can be changed.
The increased prevalence of ischemic heart diseases in the Western world can be attributed to a faster-paced lifestyle leading to unhealthy eating habits, such as fast-food consumption. In the US, better primary care in higher socioeconomic groups has led to a higher disease incidence in later stages of life.
Smoking remains the leading cause of cardiovascular diseases, with a prevalence of 15.5% among adults in the United States in 2016. Elevated levels of LDL cholesterol significantly contribute to the development of CHD, while high HDL cholesterol levels can lower the risk of the disease.
Genetics
Prognostic Factors
The prognosis of coronary heart disease can vary depending on the severity of the condition and the individual’s overall health. In general, early diagnosis and treatment can help improve the prognosis and reduce the risk of complications.
Lifestyle changes, such as smoking cessation, following a healthy diet, and regular exercise, can also help improve the prognosis. However, even with treatment, CHD can lead to serious complications such as heart attack or heart failure and can be fatal in some cases.
Clinical History
Physical Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
Medication
75
mg
Tablet
Orally
every day
CAD without a history of MI or stroke:
60
mg
Tablet
Orally
twice a day
provide together with a daily 75-100 mg aspirin maintenance dosage
Note:
Among individuals with coronary artery disease (CAD) who are at high risk for such events, to lower risk of first MI or stroke
The effectiveness was established in patients with type 2 diabetes mellitus, while use is not restricted to this situation (T2DM)
Use instead that precise dose for all Acute Coronary Syndrome patients.
10
mg
Tablet
Orally
every day
Note:
Indicated for Patients with CHD to lower their risk of MI, stroke, angina, and hospitalization for CHF
lowering the risk of stroke, heart attack, and revascularization procedures in those with several risk factors other than diabetes but no signs of coronary heart disease (CHD)
2.5
mg
Tablet
Orally
twice a day
Include 75-100 mg of aspirin in this dosage regimen once daily.
The therapy is started after the successful revascularization of the lower extremity. Before the therapy, maintain the hemostasis.
5 gm root extract twice daily for 60 days
4
mg
Orally
every day
2
weeks
; increase up to 8 mg/day orally divided into 2 times a day
Initiate treatment with an oral dose of 5-10 mg per day
Afterward, the maintenance dosage should be adjusted to 10 mg per day orally
Take a daily dose of 400 to 600 mg orally in divided doses
Future Trends
References
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» Home » CAD » Cardiology » Coronary artery disease » Coronary Heart Disease
Coronary heart disease is a condition where the heart muscle does not receive enough blood and oxygen due to blocked or narrowed coronary arteries. This is caused by the build-up of plaques in the arteries, leading to an imbalance between the heart’s oxygen needs and the amount supplied.
It is the leading cause of death globally and has been on the rise since the early 20th century, peaking in the 1960s, and remains a significant cause of death today. Its risk factor includes smoking, high cholesterol, diabetes, sedentary lifestyle and a family history.
Coronary heart disease is more common in developed countries, where lifestyle factors such as poor diet, lack of physical activity, and smoking are more prevalent. However, the incidence also increases in developing countries as these countries adopt westernized lifestyles. According to the World Health Organization, CHD is the leading cause of death globally, taking an estimated 17.9 million lives each year.
The prevalence is estimated to be around 10%, with the highest rates in high-income countries. The mortality rate varies depending on the disease stage, but it is generally high, with up to 20% of people passing away within a year of the diagnosis.
The pathophysiology of CHD is characterized by the build-up of atherosclerotic plaque in the coronary arteries. This plaque is made up of lipid-laden macrophages, also known as foam cells, which form a fatty streak in the subendothelial space of the intima layer. The fatty streak formation begins when monocytes migrate into the subendothelial space and take up oxidized low-density lipoprotein (LDL) particles.
T cells are activated and release cytokines, which aid in the formation of the subendothelial plaque. Additionally, growth factors activate smooth muscle cells, which take up oxidized LDL particles and collagen, and deposit them along with activated macrophages, increasing the amount of foam cells. As the plaque builds up, it narrows the vessel lumen and restricts blood flow, leading to chest pain or a heart attack.
Atherosclerotic plaque can grow in size over time or become stable if no further damage occurs to the endothelium. When the plaque becomes stable, a fibrous cap forms and the lesion calcifies. As the lesion becomes larger, it can restrict blood flow to the heart muscle, leading to chest pain during increased demand. However, the symptoms will subside during rest as the oxygen requirement decreases.
For a lesion to cause angina at rest, it must be at least 90% stenosed. The plaque can sometimes rupture, exposing tissue factors and leading to thrombosis. This can result in the complete or partial blockage of the lumen and the development of acute coronary syndrome (ACS), such as unstable angina, NSTEMI, or STEMI, depending on the level of damage.
Coronary heart disease has various contributing factors that can be divided into non-modifiable and modifiable. Non-modifiable factors include characteristics such as gender, age, family history, and genetics which cannot be altered. Modifiable risk factors include behaviors and lifestyle choices such as smoking, obesity, lipid levels, and psychosocial variables, which can be changed.
The increased prevalence of ischemic heart diseases in the Western world can be attributed to a faster-paced lifestyle leading to unhealthy eating habits, such as fast-food consumption. In the US, better primary care in higher socioeconomic groups has led to a higher disease incidence in later stages of life.
Smoking remains the leading cause of cardiovascular diseases, with a prevalence of 15.5% among adults in the United States in 2016. Elevated levels of LDL cholesterol significantly contribute to the development of CHD, while high HDL cholesterol levels can lower the risk of the disease.
The prognosis of coronary heart disease can vary depending on the severity of the condition and the individual’s overall health. In general, early diagnosis and treatment can help improve the prognosis and reduce the risk of complications.
Lifestyle changes, such as smoking cessation, following a healthy diet, and regular exercise, can also help improve the prognosis. However, even with treatment, CHD can lead to serious complications such as heart attack or heart failure and can be fatal in some cases.
75
mg
Tablet
Orally
every day
CAD without a history of MI or stroke:
60
mg
Tablet
Orally
twice a day
provide together with a daily 75-100 mg aspirin maintenance dosage
Note:
Among individuals with coronary artery disease (CAD) who are at high risk for such events, to lower risk of first MI or stroke
The effectiveness was established in patients with type 2 diabetes mellitus, while use is not restricted to this situation (T2DM)
Use instead that precise dose for all Acute Coronary Syndrome patients.
10
mg
Tablet
Orally
every day
Note:
Indicated for Patients with CHD to lower their risk of MI, stroke, angina, and hospitalization for CHF
lowering the risk of stroke, heart attack, and revascularization procedures in those with several risk factors other than diabetes but no signs of coronary heart disease (CHD)
2.5
mg
Tablet
Orally
twice a day
Include 75-100 mg of aspirin in this dosage regimen once daily.
The therapy is started after the successful revascularization of the lower extremity. Before the therapy, maintain the hemostasis.
5 gm root extract twice daily for 60 days
4
mg
Orally
every day
2
weeks
; increase up to 8 mg/day orally divided into 2 times a day
Initiate treatment with an oral dose of 5-10 mg per day
Afterward, the maintenance dosage should be adjusted to 10 mg per day orally
Take a daily dose of 400 to 600 mg orally in divided doses
Refer to the adult dosing
Coronary heart disease is a condition where the heart muscle does not receive enough blood and oxygen due to blocked or narrowed coronary arteries. This is caused by the build-up of plaques in the arteries, leading to an imbalance between the heart’s oxygen needs and the amount supplied.
It is the leading cause of death globally and has been on the rise since the early 20th century, peaking in the 1960s, and remains a significant cause of death today. Its risk factor includes smoking, high cholesterol, diabetes, sedentary lifestyle and a family history.
Coronary heart disease is more common in developed countries, where lifestyle factors such as poor diet, lack of physical activity, and smoking are more prevalent. However, the incidence also increases in developing countries as these countries adopt westernized lifestyles. According to the World Health Organization, CHD is the leading cause of death globally, taking an estimated 17.9 million lives each year.
The prevalence is estimated to be around 10%, with the highest rates in high-income countries. The mortality rate varies depending on the disease stage, but it is generally high, with up to 20% of people passing away within a year of the diagnosis.
The pathophysiology of CHD is characterized by the build-up of atherosclerotic plaque in the coronary arteries. This plaque is made up of lipid-laden macrophages, also known as foam cells, which form a fatty streak in the subendothelial space of the intima layer. The fatty streak formation begins when monocytes migrate into the subendothelial space and take up oxidized low-density lipoprotein (LDL) particles.
T cells are activated and release cytokines, which aid in the formation of the subendothelial plaque. Additionally, growth factors activate smooth muscle cells, which take up oxidized LDL particles and collagen, and deposit them along with activated macrophages, increasing the amount of foam cells. As the plaque builds up, it narrows the vessel lumen and restricts blood flow, leading to chest pain or a heart attack.
Atherosclerotic plaque can grow in size over time or become stable if no further damage occurs to the endothelium. When the plaque becomes stable, a fibrous cap forms and the lesion calcifies. As the lesion becomes larger, it can restrict blood flow to the heart muscle, leading to chest pain during increased demand. However, the symptoms will subside during rest as the oxygen requirement decreases.
For a lesion to cause angina at rest, it must be at least 90% stenosed. The plaque can sometimes rupture, exposing tissue factors and leading to thrombosis. This can result in the complete or partial blockage of the lumen and the development of acute coronary syndrome (ACS), such as unstable angina, NSTEMI, or STEMI, depending on the level of damage.
Coronary heart disease has various contributing factors that can be divided into non-modifiable and modifiable. Non-modifiable factors include characteristics such as gender, age, family history, and genetics which cannot be altered. Modifiable risk factors include behaviors and lifestyle choices such as smoking, obesity, lipid levels, and psychosocial variables, which can be changed.
The increased prevalence of ischemic heart diseases in the Western world can be attributed to a faster-paced lifestyle leading to unhealthy eating habits, such as fast-food consumption. In the US, better primary care in higher socioeconomic groups has led to a higher disease incidence in later stages of life.
Smoking remains the leading cause of cardiovascular diseases, with a prevalence of 15.5% among adults in the United States in 2016. Elevated levels of LDL cholesterol significantly contribute to the development of CHD, while high HDL cholesterol levels can lower the risk of the disease.
The prognosis of coronary heart disease can vary depending on the severity of the condition and the individual’s overall health. In general, early diagnosis and treatment can help improve the prognosis and reduce the risk of complications.
Lifestyle changes, such as smoking cessation, following a healthy diet, and regular exercise, can also help improve the prognosis. However, even with treatment, CHD can lead to serious complications such as heart attack or heart failure and can be fatal in some cases.
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North Adams, MA 01247
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Founded in 2014, medtigo is committed to providing high-quality, friendly physicians, transparent pricing, and a focus on building relationships and a lifestyle brand for medical professionals nationwide.
MASSACHUSETTS – USA
60 Roberts Drive, Suite 313,
North Adams, MA 01247
MAHARASHTRA – INDIA
7, Shree Krishna, 2nd Floor,
Opp Kiosk Koffee,
Shirole Lane, Off FC Road,
Pune 411004, Maharashtra
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