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Coronary artery atherosclerosis

Updated : June 11, 2024





Background

Coronary artery atherosclerosis is known to be the leading cause of mortality in both men and women in the United States of America. CAD is primarily caused by atherosclerotic changes in the walls of the coronary arteries in which atheroma formation is a significant contributor. CAD develops gradually; it is established in childhood but may be clinically diagnosed in middle to late adult hood. 

The term atherosclerosis is obtained from Greek, it is a combination of the term atheres- (which derives from the Greek word for gruel) and sclerosis (from the Greek word for hardening) of the arterial intima. Atherosclerosis affects large and medium-sized muscular arteries and is marked by: 

Endothelial dysfunction 

Vascular inflammation 

Deposition of lipids, cholesterol, calcium and other cellular debris within the intima of the blood vessel wall. 

This accumulation leads to: 

Plaque formation 

Vascular remodeling 

Acute luminal obstruction may cause colonic pseudo-obstruction and chronic luminal obstruction may lead to colorectal cancer 

Abnormal blood flow 

Epidemiology

General Overview: The condition known as coronary artery atherosclerosis is not easily detected because it rarely involves any sign or symptom. The disease process starts in early childhood with fatty streaks developing in the aorta and increases in progression during young adulthood between 8 to 18 years. Lesions progress to the advanced stage by the age of 25 years, and clinical features are distinctly prominent in the fifth and sixth decades of life. 

United States Statistics: For example, in the United States, it is estimated that 14 million people are affected by CAD. Heart failure because of ischemic cardiomyopathy in hypertensive Myocardial Infarction patients is the leading cause of hospital discharges. Approximately 80 million individuals or 36 percent of the American population suffer from chronic pain. Cardiovascular diseases are life threatening disorders which affect approximately 3% of the populace.  

Regional Variations: 

Great Britain and Scandinavia: Atherosclerosis reported to be highly prevalent in the United States. 

Russia and former Soviet states: Higher rates of CAD due to challenging economic conditions, smoking, and excessive intake of fatty foods. 

Far East: The incidence of CAD is considerably lower than in the West, perhaps because of genetic predisposition and diet. 

Africa: Generally it is observed that low CAD rates are increasing due to westernization and urbanization. 

Middle East, India, Central and South America: Higher incidence of CAD. 

Anatomy

Pathophysiology

Endothelial Dysfunction: The process starts with the injury of endothelial cells of the arteries which can be due to hypertension, hyperlipidemia, smoking, and diabetes. Endothelial dysfunction leads to the enhancement of permeability of vessels walls causing infiltration of lipids into the intima. 

Lipid Accumulation: Low-density lipoproteins or LDL particles penetrate the arterial wall and become oxidized. Oxidized LDL is ingested by macrophages, causing these cells to become foam cells and form fatty streaks. 

Inflammatory Response: Foam cells and damaged endothelial cells pump out cytokines and other inflammatory mediators. These cytokines help to recruit many other inflammatory cells including T cells and other macrophages to the site. 

Plaque Formation: The smooth muscle cells also could migrate from the medial layer to the intimal layer and then proliferate. Some of these cells synthesize extracellular matrix molecules such as collagen and elastin that make up for the plaque stability. A fibrous cap then develops over the lipid core and may ultimately become calcified. 

Vascular Remodeling: The plaques progress and become raised, and this results in the thickening of the arterial wall and reduction of the lumen. Arteries may positively remodel to accommodate the plaque or negatively remodel to further narrow the region. 

Plaque Rupture and Thrombosis: Certain plaques are more vulnerable to rupture, partly because they possess a thin fibrous cap, a large lipid nucleus, and a high density of inflammatory cells. Plaque rupture leads to the exposure of the lipid core in the blood stream, and this encourages platelets to aggregate and form thrombus. Thrombosis can either be partial or total, this results into acute coronary syndromes like unstable angina or myocardial infarction (MI). 

Etiology

Coronary atherosclerosis is a complicated process that acts through endothelial cells, smooth muscle cells (SMCs), platelets, and leukocytes. It is affected by several biological parameters including vasomotor activity, blood vessel wall procoagulant properties, the coagulation cascade, plasminogen activation, SMC migration and proliferation and inflammation. The following theories on the development of atherosclerosis have been elaborated on – Rokitansky’s encrustation theory, Virchow’s response-to-injury hypothesis and Ross’s response-to-injury hypothesis.  

Endothelial dysfunction marks dyslipidemia, hypertension, diabetes, aging, smoking, and infections leading to increased lipoprotein permeability, reduced nitric oxide synthesis, upregulated leukocyte adhesion, prothrombotic state, vascular remodeling, and synthesis of vasoactive substances. This damage leads to the penetration of lipids and inflammatory cells into the endothelial and subendothelial spaces to form atheromas. Complicated atheromas may progress to the point of rupture leading to thrombosis formation and acute coronary syndromes, or myocardial infarction. Essentially, low-density lipoprotein (LDL) is especially pro-atherogenic under conditions of oxidative stress, which results in the deposition of oxidised LDL in the subendothelial space and the development of atheromas. 

Genetics

Prognostic Factors

Acute myocardial infarction (AMI) affects 1.5 million Americans annually, with one-third of cases resulting in death. Survivors face a higher risk of mortality and morbidity, ranging from 1.5 to 15 times greater than the general population. Historically, mortality rates within one-year post-Myocardial Infarction were 25% for men and 38% for women. However, advances in treating congestive heart failure (CHF) and sudden cardiac death may lower these rates. Women with nonspecific or atypical chest pain have double the risk of nonfatal MI compared to men. The prognosis for patients with atherosclerosis depends on factors such as inducible ischemia, left ventricular function, arrhythmias, revascularization potential, aggressiveness of risk factor modification, and medical therapy compliance. Patients with significant flow limitation to vital organs may survive for many years, while others may experience MI or sudden cardiac death. 

Clinical History

Age Group: 

Children and Adolescents: Coronary artery atherosclerosis starts in childhood through the formation of fatty streaks although the disease often remains latent during this stage of development. 

Young Adults (20-40 years): Initially, atherosclerosis may not necessarily present symptoms. Patients may also suffer from consequences related to early-onset severe atherosclerosis, and especially chest pain (angina) or shortness of breath. 

Middle-aged Adults (40-60 years): This is the time when clinical symptoms may start to appear. Common manifestations include stable angina, which is chest discomfort or pain experienced during routine activities or at rest but eased by rest and/or medications. 

Older Adults (60+ years): CAD progresses with the advancement in age, and the symptoms become evident as people age. Some of the presentations covered may be stable angina, acute coronary syndromes like unstable angina, myocardial infarction or heart failure. 

Physical Examination

General Appearance: 

Body Mass Index (BMI): Screen for obesity and overweight conditions, which are risk factors to atherosclerosis. 

Signs of distress: It will preferred if one checks for signs of acute distress like excessive sweating, anxiety, or difficulty in breathing which may indicate an acute coronary event. 

Vital Signs: 

Blood Pressure: Take the blood pressure in both arms. Atherosclerosis is also caused by hypertension Atherosclerosis is also caused by hypertension, in addition to being a leading cause of coronary heart disease. 

Heart Rate: Check for tachycardia or bradycardia, as such conditions can have an impact on an individual’s physical condition. They help in determining whether palpitations and irregularities are either a mere sign of stress or a potential cardiac problem. 

Respiratory Rate: Tachypnea is an indicator of heart failure or pulmonary edema. 

Temperature: Pneumonia would be indicatin inflammatory or infectious process, fever with also point to the same. 

Cardiovascular Examination: 

Inspection: Checking for pulsations, jugular venous distension (JVD), or edema should also be done. 

Age group

Associated comorbidity

Hypertension: It is often present in middle-aged and elderly people, with an increased risk of the manifestation of symptomatic atherosclerosis. 

Diabetes: Linked to active atherosclerotic process and risk of cardiovascular complications. 

Hyperlipidemia: Low density Lipids cholesterol has been identified to have serious implications towards atherosclerosis. 

Smoking: It is considered relevant to state that foci of chronic inflammation are among the main risk factors that contribute to the acceleration of the atherosclerotic process. 

Obesity: Potentiates other chronic disorders such as diabetes and hypertension, resulting in higher CAD risk levels. 

Physical Inactivity: It remains a potential cause of obesity, high blood pressure, diabetes, and atherosclerosis. 

Family History: There is also the probability of raised risk levels for the younger people when they also have a family history of early coronary artery diseases. 

Associated activity

Acuity of presentation

Stable Angina: This is accompanied by characteristic symptoms of pain in the chest especially during physical activity or a condition of heightened emotions, which clears up once one is relaxed or takes nitroglycerine. This is a sign of creating noticeable but solid plaque as evidenced by its recent formative meaning. 

Unstable Angina: As the name suggests, as an acute percarditis; felt as sudden, sharp and severe chest pain or discomfort that takes place at rest or with little exertion and is unresponsive to rest or use of medications such as nitroglycerin. Rather, it indicates higher probability of a heart attack soon. 

Myocardial Infarction (MI): The typical symptoms include sharp and severe chest pain which may be described as a pressure-like discomfort and may be felt in the jaw, neck or arm region. It has symptoms such shortness of breath, sweating, nausea, and sometimes, light headedness. 

Differential Diagnoses

  • Angina Pectoris 
  • Coronary Artery Vasospasm 
  • Familial Hypercholesterolemia 
  • Hypertension 
  • Isolated Coronary Artery Anomalies 
  • Acute Pericarditis 
  • Atherosclerosis 
  • Dilated Cardiomyopathy 
  • Giant Cell Arteritis (Temporal Arteritis) 
  • Hypertensive Heart Disease 
  • Kawasaki Disease 

Laboratory Studies

Imaging Studies

Procedures

Histologic Findings

Staging

Treatment Paradigm

Lifestyle Modifications: 

Dietary Changes: Educate about the importance of a diet low in fats and cholesterols, high in fruits, vegetables, whole grains, and lean protein. Reduce intake of total fats especially saturated fats, trans fats, cholesterol and sugar/sodium intake. 

Regular Exercise: Promote walking, cycling, swimming and other forms of moderate aerobic activity for at least 150 minutes per week. Regular physical activity in exercising enhances cardiorespiratory endurance, weight control, blood pressure and acting on the cholesterol levels. 

Smoking Cessation: Promote smoking cessation since smoking promotes atherosclerosis and worsens the cardiovascular outcomes in patients.
Medications:
Antiplatelet Therapy: Antiplatelet drugs, aspirin or clopidogrel are usually recommended in an endeavour to decrease the chances of clot formation thereby minimizing Myocardial Infarction. 

Statins: These drugs also regulate the LDL cholesterol levels and are proven to slow the development of atherosclerosis as well as decrease the chance of cardiovascular incidents. 

Blood Pressure Control: Antihypertensive medications such as ACE inhibitors, beta-blockers, and calcium channel blockers are available to get and sustain the ideal pressure to eliminate the extra load on the heart.
Diabetes Management: Diabetic patients are advised to monitor their blood glucose level consistently and keep them in check to reduce the overall effects of diabetes on enhancing the advancement of atherosclerosis.
Symptom Relief: It is also a practice among doctors to prescribe nitro-glycerine and other drugs to help alleviate angina. 

Invasive Procedures: 

Coronary Angioplasty and Stenting: Percutaneous coronary intervention (PCI), therefore, entails the use of a balloon catheter to widen blocked or narrowed coronary arteries that supply the heart with blood and oxygen, stents are often applied to maintain the openness of the arteries. 

Coronary Artery Bypass Grafting (CABG): AM – In conditions where there is considerable occlusion of the coronary arteries, ‘bypass’ surgery might be needed to relieve congestion and reroute the bloodstream round the affected areas. 

Cardiac Rehabilitation: 

Exercise Programs: Exercise and education are goal directed and systematic for enhancing cardiovascular fitness and managing risk factors in patients who have had cardiac accidents or surgical interventions. 

by Stage

by Modality

Chemotherapy

Radiation Therapy

Surgical Interventions

Hormone Therapy

Immunotherapy

Hyperthermia

Photodynamic Therapy

Stem Cell Transplant

Targeted Therapy

Palliative Care

Use of a non-pharmacological approach for treating Coronary artery atherosclerosis

Dietary Changes: Eat a balanced diet, which is high in fruits, vegetables, whole grains, lean proteins, and healthy fats. Encourages the consumption of olive oil, nuts, fish and legumes that are low in CVD risk. Reduce consumption of foods such as red meat, fats from whole milk, and processed foods. Restriction in the intake of salt as a way of managing blood pressure. 

Regular Physical Activity: Perform aerobic physical activity of at least 150 minutes per week of moderate intensity (e. g. walking, cycling, swimming). It is essential to perform muscle-strengthening activities at least two days a week. Planning their physical activity for the day – dancing, gardening, Tai Chi or Yoga to increase muscle strength and balance to prevent fall. Adopt a proper nutrition plan to lose excess weight and adopt a workout regimen to get to a healthy weight range. It is important that the BMI is between 18 and This is because it is a healthy weight. 

Stress Management: Engage in other relaxing activities like deep breathing, meditation, and taking a mindful walk. In case of chronic stress, anxiety, or depression, it is recommended to consult a professional. 

Alcohol Moderation: Alcohol should be consumed in moderate amounts and it’s advisable to consult your doctor before drinking. 

Role of HMG-CoA Reductase Inhibitors

Atorvastatin (Lipitor): Inhibits competitively the synthesis of cholesterol through reduced expression of HMG-CoA reductase. In particular, start on the cholesterol-lowering diet at least three to six months before surgery and continue the diet thereafter. 

Pravastatin (Pravachol): Its active metabolite competitively inhibits HMG-CoA reductase; the dietary guidelines are similar to atorvastatin. 

Simvastatin (Zocor): Its effectiveness is comparable to that of statin drugs in competing for the active site of HMG-CoA reductase; however its diet requirements similar to that of statins. 

Rosuvastatin (Crestor): Reduces the synthesis of HMG-CoA reductase, in accordance with the indicated dietary recommendations. 

Pitavastatin (Livalo): The use of HMG-CoA reductase inhibitor in primary or mixed hyperlipidemia for cholesterol reduction is as effective as atorvastatin and simvastatin. 

Lovastatin (Mevacor, Altocor): As a pharmacological support of dietary measures, available in the form of immediate- and delayed-release products. 

Fluvastatin (Lescol): Used in conjunction with nutrition modification to reduce cholesterol levels. 

Role of PCSK9 Inhibitors

PCSK9 inhibitors act through inhibiting the degradation of LDLR by PCSK9 increasing the clearance of LDL-C and reducing plasma LDL-C concentrations. 

Alirocumab (Praluent): It is a monoclonal antibody targeted towards PCSK9, a serine protease that degrades LDL receptors in the liver and results in reduced LDL cholesterol uptake and increased plasma LDL cholesterol. Alirocumab also prevents degradation of LDLR due to inhibition of PCSK9. It is recommended to be used in combination with diet and maximum tolerated statin therapy for adults with HeFH, or clinical ASCVD requiring more LDL-C lowering. The FDA also have endorsed it as a supportive therapy for persons with homozygous familial hypercholesterolemia.  

Evolocumab (Repatha):It is a monoclonal antibody that targets PCSK9, thus intervening with the degradation of LDL receptors in the liver to reduce LDL-C clearance. It is indicated as an add-on to diet and the highest tolerated dose of statin for individuals with HeFH not on statins or with clinical ASCVD for further LDL-C reduction. Evolocumab is also used in the management of homozygous familial hypercholesterolemia (HoFH) in adults and adolescents aged 13 to 17 years as an adjunct to diet and other source LDL-c reduction therapies such as statins, ezetimibe, and LDL apheresis. 

Inclisiran (Leqvio): Inclisiran is reported to be a small interfering RNA (siRNA) that targets PCSK9 mRNA in the liver and manifests its action by preventing the translation of the mRNA into its protein product. This inhibition raises the level of LDL receptor in the body and clears the LDL-cholesterol from the circulation.  

Role of Calcium Channel Blocker

Amlodipine (Norvasc): It directly affects the coronary smooth muscle, with the effect of vasodilation, beneficial for increasing the oxygen supply to the myocardium. 

Nifedipine (Procardia, Procardia XL, Adalat, Adalat CC, Nifedical XL): Nifedipine can also relax coronary smooth muscle and can produce vasodilation which increases the flow of oxygen to the myocardium. It is also safe when taken sublingually, which is an issue of caution that may be theoretical. 

Felodipine: It directly acts on the coronary smooth muscles and brings about vasodilation which enhances the delivery of oxygen to the myocardium. It is helpful in patients who have no pregnancy, systolic dysfunction, hypertension, or arrhythmia; however, it can be used during pregnancy if needed. 

Diltiazem: This inhibition lowers intracellular calcium thereby decreasing the contracting processes of smooth muscle cells, resulting in the dilation of the coronary as well as the systemic vessels that provide for enhanced delivery of oxygen to the myocardial tissue. 

Role of ACE Inhibitors

Ramipril (Altace): Ramipril is angiotensin-converting enzyme (ACE) inhibitor which decreases the conversion of angiotensin I (A-I) to angiotensin II (A-II) which is a potent vasoconstrictor; ramipril increases plasma renin levels and decreases aldosterone secretion. 

Quinapril (Accupril): Like other ACE inhibitors, quinapril inhibits the conversion of A-I to A-II and increases plasma renin and reduces aldosterone secretion. 

Captopril (Capoten): Captopril inhibits the formation of angiotensin I to angiotensin II which causes reduced aldosterone release. It is a rapidly absorbed drug and is well absorbed orally but with a low bioavailability when taken with food; onset of action is within one hour and the duration of action tends to be short, as it has a short half-life. It is metabolised by the kidneys and therefore requires dose adaptations for patients with poor renal health. 

Role of Platelet Aggregation Inhibitors

Pharmacological intervention through platelet aggregation inhibitors can affect several hemorrhagic indices and provide an anti-atherosclerotic effect due to the suppression of platelet function and changes in the hemorrhagic profile. 

Platelet Aggregate Inhibitors 

Clopidogrel (Plavix) 

Abciximab (ReoPro) 

Clopidogrel acts in a selective manner in that it inhibits the binding of ADP to the platelet receptors and thus interrupts ADP induced activation of the glycoprotein IIb/IIIa complex thereby slowing down the process of platelet aggregation. 

Abciximab is a chimeric human-murine monoclonal that is used during elective, urgent or emergent percutaneous coronary interventions (PCI). With high affinity, it interacts with receptors and inhibits platelet aggregation by 80 percent for 48 hours after the infusion of adenosine. It is used to reduce acute cardiac ischemic complications in unstable angina that cannot be managed through conventional therapies. 

Use of Intervention with a procedure in treating Coronary artery atherosclerosis

Coronary Artery Bypass Grafting (CABG): It is a procedure where a blood vessel or an artery from another part of the body is used to bypass the blocked coronary artery. This helps to avoid blockage and provides an opportunity for blood to circulate to the heart muscles. 

Long-Term Relief: Furnishes good symptoms relief and enhances survival of patients with serious CAD. 

Improves Blood Supply: It improves the blood supply of the heart muscles thus the reduces the likelihood of a heart attack. 

Effective for Multiple Blockages: Especially effective for the treatment of patients with multiple artery occlusions. 

Procedure: 

Harvesting the Graft: The healthy vessel is commonly acquired from a leg, arm or chest. 

Bypassing the Blockage: In bypass surgery, the graft is connected to the arteries above and below the area of blockage to provide an alternate path for blood circulation. 

Postoperative Care: They have been admitted to the hospital for some time, and they often remain in the intensive care unit when they undergo PCI. 

Use of phases in managing Coronary artery atherosclerosis

Primary Prevention: Lifestyle changes like diet and exercise, along with possible pharmacological interventions like statins for hyperlipidemia, antihypertensives for hypertension or diabetes medications. 

Screening and Early Detection: Using various tests to detect high-risk populations, including lipid profiles, blood pressure measurements, and other assessments of cardiovascular health. 

Medical Therapy: Medications such as statins for lowering cholesterol levels, antiplatelet agents like aspirin to prevent clot formation and antihypertensive drugs to regulate blood pressure. 

Lifestyle Modifications: Promoting healthy eating habits and types of foods such as low saturated fat, high fiber and fruits and vegetables; and adopting a physically active lifestyle, quitting smoking, and maintaining healthy weight. 

Secondary Prevention: For those with preexisting atherosclerosis or prior cardiovascular events, continuing efforts to optimise the targets to eliminate the reoccurrence. 

Interventional Procedures: If the patient has significant stenosis or occlusion of the coronary arteries, interventions like percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) may be required to reopen the blocked arteries. 

Medication

 

ticagrelor

60

mg

oraly

twice a day


Also, continue with aspirin 75-100 mg



hawthorn 

For brewed tea
Three times a day following meals and steep, take 1 teaspoon of leaves and blossoms in 8 ounces of boiling water
For leaf/flower
Extract: 160 to 900 mg daily orally divided two and three times a day
Powder: 200 to 500 mg orally three times a day
Tincture: 20 drops orally two and three times a day
For fruit
Dried powder: 300 to 1000 mg orally three times a day
Liquid extract: 0.5 to 1 ml orally three times a day
Tincture: 1 to 2 ml orally three times a day
Syrup: 1 teaspoon orally three times a day



 
 

Media Gallary

Coronary artery atherosclerosis

Updated : June 11, 2024




Coronary artery atherosclerosis is known to be the leading cause of mortality in both men and women in the United States of America. CAD is primarily caused by atherosclerotic changes in the walls of the coronary arteries in which atheroma formation is a significant contributor. CAD develops gradually; it is established in childhood but may be clinically diagnosed in middle to late adult hood. 

The term atherosclerosis is obtained from Greek, it is a combination of the term atheres- (which derives from the Greek word for gruel) and sclerosis (from the Greek word for hardening) of the arterial intima. Atherosclerosis affects large and medium-sized muscular arteries and is marked by: 

Endothelial dysfunction 

Vascular inflammation 

Deposition of lipids, cholesterol, calcium and other cellular debris within the intima of the blood vessel wall. 

This accumulation leads to: 

Plaque formation 

Vascular remodeling 

Acute luminal obstruction may cause colonic pseudo-obstruction and chronic luminal obstruction may lead to colorectal cancer 

Abnormal blood flow 

General Overview: The condition known as coronary artery atherosclerosis is not easily detected because it rarely involves any sign or symptom. The disease process starts in early childhood with fatty streaks developing in the aorta and increases in progression during young adulthood between 8 to 18 years. Lesions progress to the advanced stage by the age of 25 years, and clinical features are distinctly prominent in the fifth and sixth decades of life. 

United States Statistics: For example, in the United States, it is estimated that 14 million people are affected by CAD. Heart failure because of ischemic cardiomyopathy in hypertensive Myocardial Infarction patients is the leading cause of hospital discharges. Approximately 80 million individuals or 36 percent of the American population suffer from chronic pain. Cardiovascular diseases are life threatening disorders which affect approximately 3% of the populace.  

Regional Variations: 

Great Britain and Scandinavia: Atherosclerosis reported to be highly prevalent in the United States. 

Russia and former Soviet states: Higher rates of CAD due to challenging economic conditions, smoking, and excessive intake of fatty foods. 

Far East: The incidence of CAD is considerably lower than in the West, perhaps because of genetic predisposition and diet. 

Africa: Generally it is observed that low CAD rates are increasing due to westernization and urbanization. 

Middle East, India, Central and South America: Higher incidence of CAD. 

Endothelial Dysfunction: The process starts with the injury of endothelial cells of the arteries which can be due to hypertension, hyperlipidemia, smoking, and diabetes. Endothelial dysfunction leads to the enhancement of permeability of vessels walls causing infiltration of lipids into the intima. 

Lipid Accumulation: Low-density lipoproteins or LDL particles penetrate the arterial wall and become oxidized. Oxidized LDL is ingested by macrophages, causing these cells to become foam cells and form fatty streaks. 

Inflammatory Response: Foam cells and damaged endothelial cells pump out cytokines and other inflammatory mediators. These cytokines help to recruit many other inflammatory cells including T cells and other macrophages to the site. 

Plaque Formation: The smooth muscle cells also could migrate from the medial layer to the intimal layer and then proliferate. Some of these cells synthesize extracellular matrix molecules such as collagen and elastin that make up for the plaque stability. A fibrous cap then develops over the lipid core and may ultimately become calcified. 

Vascular Remodeling: The plaques progress and become raised, and this results in the thickening of the arterial wall and reduction of the lumen. Arteries may positively remodel to accommodate the plaque or negatively remodel to further narrow the region. 

Plaque Rupture and Thrombosis: Certain plaques are more vulnerable to rupture, partly because they possess a thin fibrous cap, a large lipid nucleus, and a high density of inflammatory cells. Plaque rupture leads to the exposure of the lipid core in the blood stream, and this encourages platelets to aggregate and form thrombus. Thrombosis can either be partial or total, this results into acute coronary syndromes like unstable angina or myocardial infarction (MI). 

Coronary atherosclerosis is a complicated process that acts through endothelial cells, smooth muscle cells (SMCs), platelets, and leukocytes. It is affected by several biological parameters including vasomotor activity, blood vessel wall procoagulant properties, the coagulation cascade, plasminogen activation, SMC migration and proliferation and inflammation. The following theories on the development of atherosclerosis have been elaborated on – Rokitansky’s encrustation theory, Virchow’s response-to-injury hypothesis and Ross’s response-to-injury hypothesis.  

Endothelial dysfunction marks dyslipidemia, hypertension, diabetes, aging, smoking, and infections leading to increased lipoprotein permeability, reduced nitric oxide synthesis, upregulated leukocyte adhesion, prothrombotic state, vascular remodeling, and synthesis of vasoactive substances. This damage leads to the penetration of lipids and inflammatory cells into the endothelial and subendothelial spaces to form atheromas. Complicated atheromas may progress to the point of rupture leading to thrombosis formation and acute coronary syndromes, or myocardial infarction. Essentially, low-density lipoprotein (LDL) is especially pro-atherogenic under conditions of oxidative stress, which results in the deposition of oxidised LDL in the subendothelial space and the development of atheromas. 

Acute myocardial infarction (AMI) affects 1.5 million Americans annually, with one-third of cases resulting in death. Survivors face a higher risk of mortality and morbidity, ranging from 1.5 to 15 times greater than the general population. Historically, mortality rates within one-year post-Myocardial Infarction were 25% for men and 38% for women. However, advances in treating congestive heart failure (CHF) and sudden cardiac death may lower these rates. Women with nonspecific or atypical chest pain have double the risk of nonfatal MI compared to men. The prognosis for patients with atherosclerosis depends on factors such as inducible ischemia, left ventricular function, arrhythmias, revascularization potential, aggressiveness of risk factor modification, and medical therapy compliance. Patients with significant flow limitation to vital organs may survive for many years, while others may experience MI or sudden cardiac death. 

Age Group: 

Children and Adolescents: Coronary artery atherosclerosis starts in childhood through the formation of fatty streaks although the disease often remains latent during this stage of development. 

Young Adults (20-40 years): Initially, atherosclerosis may not necessarily present symptoms. Patients may also suffer from consequences related to early-onset severe atherosclerosis, and especially chest pain (angina) or shortness of breath. 

Middle-aged Adults (40-60 years): This is the time when clinical symptoms may start to appear. Common manifestations include stable angina, which is chest discomfort or pain experienced during routine activities or at rest but eased by rest and/or medications. 

Older Adults (60+ years): CAD progresses with the advancement in age, and the symptoms become evident as people age. Some of the presentations covered may be stable angina, acute coronary syndromes like unstable angina, myocardial infarction or heart failure. 

General Appearance: 

Body Mass Index (BMI): Screen for obesity and overweight conditions, which are risk factors to atherosclerosis. 

Signs of distress: It will preferred if one checks for signs of acute distress like excessive sweating, anxiety, or difficulty in breathing which may indicate an acute coronary event. 

Vital Signs: 

Blood Pressure: Take the blood pressure in both arms. Atherosclerosis is also caused by hypertension Atherosclerosis is also caused by hypertension, in addition to being a leading cause of coronary heart disease. 

Heart Rate: Check for tachycardia or bradycardia, as such conditions can have an impact on an individual’s physical condition. They help in determining whether palpitations and irregularities are either a mere sign of stress or a potential cardiac problem. 

Respiratory Rate: Tachypnea is an indicator of heart failure or pulmonary edema. 

Temperature: Pneumonia would be indicatin inflammatory or infectious process, fever with also point to the same. 

Cardiovascular Examination: 

Inspection: Checking for pulsations, jugular venous distension (JVD), or edema should also be done. 

Hypertension: It is often present in middle-aged and elderly people, with an increased risk of the manifestation of symptomatic atherosclerosis. 

Diabetes: Linked to active atherosclerotic process and risk of cardiovascular complications. 

Hyperlipidemia: Low density Lipids cholesterol has been identified to have serious implications towards atherosclerosis. 

Smoking: It is considered relevant to state that foci of chronic inflammation are among the main risk factors that contribute to the acceleration of the atherosclerotic process. 

Obesity: Potentiates other chronic disorders such as diabetes and hypertension, resulting in higher CAD risk levels. 

Physical Inactivity: It remains a potential cause of obesity, high blood pressure, diabetes, and atherosclerosis. 

Family History: There is also the probability of raised risk levels for the younger people when they also have a family history of early coronary artery diseases. 

Stable Angina: This is accompanied by characteristic symptoms of pain in the chest especially during physical activity or a condition of heightened emotions, which clears up once one is relaxed or takes nitroglycerine. This is a sign of creating noticeable but solid plaque as evidenced by its recent formative meaning. 

Unstable Angina: As the name suggests, as an acute percarditis; felt as sudden, sharp and severe chest pain or discomfort that takes place at rest or with little exertion and is unresponsive to rest or use of medications such as nitroglycerin. Rather, it indicates higher probability of a heart attack soon. 

Myocardial Infarction (MI): The typical symptoms include sharp and severe chest pain which may be described as a pressure-like discomfort and may be felt in the jaw, neck or arm region. It has symptoms such shortness of breath, sweating, nausea, and sometimes, light headedness. 

  • Angina Pectoris 
  • Coronary Artery Vasospasm 
  • Familial Hypercholesterolemia 
  • Hypertension 
  • Isolated Coronary Artery Anomalies 
  • Acute Pericarditis 
  • Atherosclerosis 
  • Dilated Cardiomyopathy 
  • Giant Cell Arteritis (Temporal Arteritis) 
  • Hypertensive Heart Disease 
  • Kawasaki Disease 

Lifestyle Modifications: 

Dietary Changes: Educate about the importance of a diet low in fats and cholesterols, high in fruits, vegetables, whole grains, and lean protein. Reduce intake of total fats especially saturated fats, trans fats, cholesterol and sugar/sodium intake. 

Regular Exercise: Promote walking, cycling, swimming and other forms of moderate aerobic activity for at least 150 minutes per week. Regular physical activity in exercising enhances cardiorespiratory endurance, weight control, blood pressure and acting on the cholesterol levels. 

Smoking Cessation: Promote smoking cessation since smoking promotes atherosclerosis and worsens the cardiovascular outcomes in patients.
Medications:
Antiplatelet Therapy: Antiplatelet drugs, aspirin or clopidogrel are usually recommended in an endeavour to decrease the chances of clot formation thereby minimizing Myocardial Infarction. 

Statins: These drugs also regulate the LDL cholesterol levels and are proven to slow the development of atherosclerosis as well as decrease the chance of cardiovascular incidents. 

Blood Pressure Control: Antihypertensive medications such as ACE inhibitors, beta-blockers, and calcium channel blockers are available to get and sustain the ideal pressure to eliminate the extra load on the heart.
Diabetes Management: Diabetic patients are advised to monitor their blood glucose level consistently and keep them in check to reduce the overall effects of diabetes on enhancing the advancement of atherosclerosis.
Symptom Relief: It is also a practice among doctors to prescribe nitro-glycerine and other drugs to help alleviate angina. 

Invasive Procedures: 

Coronary Angioplasty and Stenting: Percutaneous coronary intervention (PCI), therefore, entails the use of a balloon catheter to widen blocked or narrowed coronary arteries that supply the heart with blood and oxygen, stents are often applied to maintain the openness of the arteries. 

Coronary Artery Bypass Grafting (CABG): AM – In conditions where there is considerable occlusion of the coronary arteries, ‘bypass’ surgery might be needed to relieve congestion and reroute the bloodstream round the affected areas. 

Cardiac Rehabilitation: 

Exercise Programs: Exercise and education are goal directed and systematic for enhancing cardiovascular fitness and managing risk factors in patients who have had cardiac accidents or surgical interventions. 

Dietary Changes: Eat a balanced diet, which is high in fruits, vegetables, whole grains, lean proteins, and healthy fats. Encourages the consumption of olive oil, nuts, fish and legumes that are low in CVD risk. Reduce consumption of foods such as red meat, fats from whole milk, and processed foods. Restriction in the intake of salt as a way of managing blood pressure. 

Regular Physical Activity: Perform aerobic physical activity of at least 150 minutes per week of moderate intensity (e. g. walking, cycling, swimming). It is essential to perform muscle-strengthening activities at least two days a week. Planning their physical activity for the day – dancing, gardening, Tai Chi or Yoga to increase muscle strength and balance to prevent fall. Adopt a proper nutrition plan to lose excess weight and adopt a workout regimen to get to a healthy weight range. It is important that the BMI is between 18 and This is because it is a healthy weight. 

Stress Management: Engage in other relaxing activities like deep breathing, meditation, and taking a mindful walk. In case of chronic stress, anxiety, or depression, it is recommended to consult a professional. 

Alcohol Moderation: Alcohol should be consumed in moderate amounts and it’s advisable to consult your doctor before drinking. 

Atorvastatin (Lipitor): Inhibits competitively the synthesis of cholesterol through reduced expression of HMG-CoA reductase. In particular, start on the cholesterol-lowering diet at least three to six months before surgery and continue the diet thereafter. 

Pravastatin (Pravachol): Its active metabolite competitively inhibits HMG-CoA reductase; the dietary guidelines are similar to atorvastatin. 

Simvastatin (Zocor): Its effectiveness is comparable to that of statin drugs in competing for the active site of HMG-CoA reductase; however its diet requirements similar to that of statins. 

Rosuvastatin (Crestor): Reduces the synthesis of HMG-CoA reductase, in accordance with the indicated dietary recommendations. 

Pitavastatin (Livalo): The use of HMG-CoA reductase inhibitor in primary or mixed hyperlipidemia for cholesterol reduction is as effective as atorvastatin and simvastatin. 

Lovastatin (Mevacor, Altocor): As a pharmacological support of dietary measures, available in the form of immediate- and delayed-release products. 

Fluvastatin (Lescol): Used in conjunction with nutrition modification to reduce cholesterol levels. 

PCSK9 inhibitors act through inhibiting the degradation of LDLR by PCSK9 increasing the clearance of LDL-C and reducing plasma LDL-C concentrations. 

Alirocumab (Praluent): It is a monoclonal antibody targeted towards PCSK9, a serine protease that degrades LDL receptors in the liver and results in reduced LDL cholesterol uptake and increased plasma LDL cholesterol. Alirocumab also prevents degradation of LDLR due to inhibition of PCSK9. It is recommended to be used in combination with diet and maximum tolerated statin therapy for adults with HeFH, or clinical ASCVD requiring more LDL-C lowering. The FDA also have endorsed it as a supportive therapy for persons with homozygous familial hypercholesterolemia.  

Evolocumab (Repatha):It is a monoclonal antibody that targets PCSK9, thus intervening with the degradation of LDL receptors in the liver to reduce LDL-C clearance. It is indicated as an add-on to diet and the highest tolerated dose of statin for individuals with HeFH not on statins or with clinical ASCVD for further LDL-C reduction. Evolocumab is also used in the management of homozygous familial hypercholesterolemia (HoFH) in adults and adolescents aged 13 to 17 years as an adjunct to diet and other source LDL-c reduction therapies such as statins, ezetimibe, and LDL apheresis. 

Inclisiran (Leqvio): Inclisiran is reported to be a small interfering RNA (siRNA) that targets PCSK9 mRNA in the liver and manifests its action by preventing the translation of the mRNA into its protein product. This inhibition raises the level of LDL receptor in the body and clears the LDL-cholesterol from the circulation.  

Amlodipine (Norvasc): It directly affects the coronary smooth muscle, with the effect of vasodilation, beneficial for increasing the oxygen supply to the myocardium. 

Nifedipine (Procardia, Procardia XL, Adalat, Adalat CC, Nifedical XL): Nifedipine can also relax coronary smooth muscle and can produce vasodilation which increases the flow of oxygen to the myocardium. It is also safe when taken sublingually, which is an issue of caution that may be theoretical. 

Felodipine: It directly acts on the coronary smooth muscles and brings about vasodilation which enhances the delivery of oxygen to the myocardium. It is helpful in patients who have no pregnancy, systolic dysfunction, hypertension, or arrhythmia; however, it can be used during pregnancy if needed. 

Diltiazem: This inhibition lowers intracellular calcium thereby decreasing the contracting processes of smooth muscle cells, resulting in the dilation of the coronary as well as the systemic vessels that provide for enhanced delivery of oxygen to the myocardial tissue. 

Ramipril (Altace): Ramipril is angiotensin-converting enzyme (ACE) inhibitor which decreases the conversion of angiotensin I (A-I) to angiotensin II (A-II) which is a potent vasoconstrictor; ramipril increases plasma renin levels and decreases aldosterone secretion. 

Quinapril (Accupril): Like other ACE inhibitors, quinapril inhibits the conversion of A-I to A-II and increases plasma renin and reduces aldosterone secretion. 

Captopril (Capoten): Captopril inhibits the formation of angiotensin I to angiotensin II which causes reduced aldosterone release. It is a rapidly absorbed drug and is well absorbed orally but with a low bioavailability when taken with food; onset of action is within one hour and the duration of action tends to be short, as it has a short half-life. It is metabolised by the kidneys and therefore requires dose adaptations for patients with poor renal health. 

Pharmacological intervention through platelet aggregation inhibitors can affect several hemorrhagic indices and provide an anti-atherosclerotic effect due to the suppression of platelet function and changes in the hemorrhagic profile. 

Platelet Aggregate Inhibitors 

Clopidogrel (Plavix) 

Abciximab (ReoPro) 

Clopidogrel acts in a selective manner in that it inhibits the binding of ADP to the platelet receptors and thus interrupts ADP induced activation of the glycoprotein IIb/IIIa complex thereby slowing down the process of platelet aggregation. 

Abciximab is a chimeric human-murine monoclonal that is used during elective, urgent or emergent percutaneous coronary interventions (PCI). With high affinity, it interacts with receptors and inhibits platelet aggregation by 80 percent for 48 hours after the infusion of adenosine. It is used to reduce acute cardiac ischemic complications in unstable angina that cannot be managed through conventional therapies. 

Coronary Artery Bypass Grafting (CABG): It is a procedure where a blood vessel or an artery from another part of the body is used to bypass the blocked coronary artery. This helps to avoid blockage and provides an opportunity for blood to circulate to the heart muscles. 

Long-Term Relief: Furnishes good symptoms relief and enhances survival of patients with serious CAD. 

Improves Blood Supply: It improves the blood supply of the heart muscles thus the reduces the likelihood of a heart attack. 

Effective for Multiple Blockages: Especially effective for the treatment of patients with multiple artery occlusions. 

Procedure: 

Harvesting the Graft: The healthy vessel is commonly acquired from a leg, arm or chest. 

Bypassing the Blockage: In bypass surgery, the graft is connected to the arteries above and below the area of blockage to provide an alternate path for blood circulation. 

Postoperative Care: They have been admitted to the hospital for some time, and they often remain in the intensive care unit when they undergo PCI. 

Primary Prevention: Lifestyle changes like diet and exercise, along with possible pharmacological interventions like statins for hyperlipidemia, antihypertensives for hypertension or diabetes medications. 

Screening and Early Detection: Using various tests to detect high-risk populations, including lipid profiles, blood pressure measurements, and other assessments of cardiovascular health. 

Medical Therapy: Medications such as statins for lowering cholesterol levels, antiplatelet agents like aspirin to prevent clot formation and antihypertensive drugs to regulate blood pressure. 

Lifestyle Modifications: Promoting healthy eating habits and types of foods such as low saturated fat, high fiber and fruits and vegetables; and adopting a physically active lifestyle, quitting smoking, and maintaining healthy weight. 

Secondary Prevention: For those with preexisting atherosclerosis or prior cardiovascular events, continuing efforts to optimise the targets to eliminate the reoccurrence. 

Interventional Procedures: If the patient has significant stenosis or occlusion of the coronary arteries, interventions like percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) may be required to reopen the blocked arteries. 

ticagrelor

60

mg

oraly

twice a day


Also, continue with aspirin 75-100 mg



hawthorn 

For brewed tea
Three times a day following meals and steep, take 1 teaspoon of leaves and blossoms in 8 ounces of boiling water
For leaf/flower
Extract: 160 to 900 mg daily orally divided two and three times a day
Powder: 200 to 500 mg orally three times a day
Tincture: 20 drops orally two and three times a day
For fruit
Dried powder: 300 to 1000 mg orally three times a day
Liquid extract: 0.5 to 1 ml orally three times a day
Tincture: 1 to 2 ml orally three times a day
Syrup: 1 teaspoon orally three times a day



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