Anthropometric Measurements as Predictors of Low Birth Weight Among Tanzanian Neonates: A Hospital-Based Study
November 7, 2025
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Background
The most typical sign of ischemic cardiovascular disease, a leading global source of mortality and morbidity, is angina or chest discomfort. A comprehensive physical exam and history are essential for separating cardiac from non-cardiac causes of chest discomfort and identifying patients with acute coronary syndrome (ACS).
Angina, which can be further divided into unstable and stable angina, is one of the symptoms of ACS. The definition of stable angina is the presence of symptoms only with effort. Unstable angina or symptoms that appear when you’re at rest need more immediate assessment and treatment. Angina symptoms are present in almost 9 million individuals in the US, and identifying these symptoms is crucial to enhancing outcomes for patients.
Epidemiology
In western nations, 30 000 – 40 000 people per million suffer from chronic stable angina. Age-related prevalence rises in both men & women. Prevalence estimates range from 4 to 7 percent for men and 5 to 7 percent for women aged 45 to 64, respectively. The estimated prevalence is 14–15% for men & 10–12% for women aged 65–84, respectively.
Hypertension, hyperlipidemia, tobacco use in the past or present, diabetes mellitus, & obesity/metabolic syndrome are all modifiable factors for angina. An individual risk factor for CAD (coronary artery disease) is an elevated BMI. Aging, male sex, a family medical history of CAD, and ethnicity are examples of risk variables that cannot be changed.
Anatomy
Pathophysiology
The creation of energy necessary to promote contractility in the heart depends on an appropriate oxygen supply. Anaerobic glycolysis is increased by ischemia at the cellular level. This raises the concentrations of potassium, lactate, & hydrogen in the venous return of the myocardium’s ischemia or damaged region.
Competition between calcium ions and hydrogen ions results in hypokinesia and akinesia in the afflicted area. Stress, exercise, and low body temperature are the three triggers that would produce metabolic mismatch and unstable angina.
Etiology
Non-cardiac reasons, non-ischemic cardiac illness, and then ischemic cardiac disease can all produce chest pain. Other non-cardiac reasons include lung problems, musculoskeletal issues, panic/anxiety attacks, and gastric reflux disease. Pericardial illness is one of the non-ischemic heart causes. Most experts agree that coronary artery atherosclerosis & coronary vasospasm are the causes of chest pain brought on by myocardial ischemia.
A mismatch between myocardial oxygen demand and supply results from this situation. In unstable angina, the increased demand also arises while at rest, whereas in unstable angina, it only happens during effort. Exercise-induced increases in heart rate, blood pressure, & myocardial contractility are among the main causes of increased myocardial oxygen demand.
In healthy hearts, increased oxygen demand brought on by exercise is followed by coronary vasodilation. However, in those with coronary artery atherosclerosis, this function is impaired, leading to ischemia & chest discomfort. Similar to stable angina, vasospastic angina, commonly referred to as variant angina as well as Prinzmetal angina, also happens while at rest but is unconnected to coronary atherosclerosis.
Genetics
Prognostic Factors
The likelihood that chronic stable angina will result in cardiovascular events varies from patient to patient. Cardiac comorbidities, adherence to dietary and treatment regimen recommendations, and other factors all affect prognosis. Left ventricular systolic function, the amount of activity the patient can endure, and the degree of CAD present all have an impact on the long-term outcome.
Diabetes mellitus, prior MI, advancing age, hypertension, & male sex are risk factors for a worse prognosis. Additionally, it has been shown that the administration of nitrates is a poor predictor of mortality, most likely because it signals more severe disease.
Clinical History
Physical Examination
Physical examination
Physical examination results are typically normal for patients with stable angina. It’s crucial to identify possible causes of angina, including aortic stenosis. Angina pectoris is suggested by a positive Levine sign, which is defined by the patient clenching their hand over their sternum while discussing their discomfort.
Look for visible indications of widespread atherosclerosis or aberrant lipid metabolism, such as xanthelasma or xanthoma (e.g., diminished or absent peripheral pulses, arteriovenous nicking upon ophthalmic examination, or, raised light reflexes, carotid bruit). It may be more beneficial to examine individuals while they are having an angina episode.
Third and fourth cardiac sounds caused by LV systolic and diastolic disorder, as well as mitral regurgitation related to papillary muscle disorder, are useful physical observations. Pressure on the chest wall frequently causes pain that originates there.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Differential diagnosis
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
The goal of treating chronic stable angina is to control symptoms and prevent the development of cardiovascular events. Lifestyle changes, risk factor reduction, & medicinal treatment are crucial elements of management, which is complex in nature. Revascularization may be used when symptoms are resistant to medical treatment; however, while it may be effective in controlling problems, research has not demonstrated that it lowers the risk of significant cardiac events when compared to medical management. Regular exercise, maintaining a healthy weight, & quitting smoking are examples of lifestyle changes that should be supported.
Maintaining cholesterol, blood pressure, & blood sugar are examples of risk factor adjustment. Statins, aspirin, angiotensin receptor blockers, or angiotensin-converting enzyme inhibitors are examples of medications used to reduce risk factors and stop the progression of the disease. Medical treatment can be utilized to manage symptoms and lower the risk of atherosclerosis progression & cardiovascular events. Depending on how angina symptoms are alleviated, antianginal medicines can be divided into several classes. The general goal of symptom control is to reduce myocardial oxygen demand.
The majority of anginal episodes are brought on by a rise in the heart rate because it is the primary factor affecting oxygen uptake. Three kinds of angina medications—ivabradine, beta-blockers & non-dihydropyridine Ca channel blockers—reduce symptoms by lowering heart rate. In individuals with low ejection fraction and left ventricular failure, calcium channel inhibitors should be prevented. Relaxing the vascular smoothness is a different method of treating anginal complications.
As a result, the perfusion capacity is increased by widening the coronary arteries. Dihydropyridine Ca channel blockers, nicorandil, & nitrates are medicines that act in this manner. Ranolazine, another medication for chronic stable angina, blocks the late sodium influx in ventricular myocardial cells. The diastolic contractile disorder is lessened as a result. The treatment goals for unstable angina are minimizing myocardial damage, minimizing morbidity, & lowering mortality.
Nitrates – are used to relieve chest discomfort but have little mortality advantage. Vasodilation brought on by them lowers preload & left ventricular end-diastolic volume. This lowers the need for myocardium oxygen. They should not be used if you have hypotension or have recently taken phosphodiesterase blockers.
Morphine – No mortality advantage; used to treat pain when nitrates are unable to completely relieve it. Along with analgesia, it also results in mild vasodilation.
Beta-blockers – decrease mortality. They lower blood pressure, heart rate, and contractility, which lessens the need for myocardium oxygen.
Antiplatelet agents – In individuals with acute coronary syndromes, dual treatment with aspirin, so either ticagrelor, prasugrel, or clopidogrel lowers the risk of cardiac events – sudden cardiac death, stroke, and acute myocardial infarction.
Anticoagulants – reduce mortality in conjunction with antiplatelet medications by lowering re-infarction rates. given intravenously for immediate medical care.
Anatomic evaluation of the coronary arteries and revascularization consideration – Risk stratification techniques should be used to identify high-risk individuals and consider them for immediate revascularization.
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Instead of actual pain, the majority of angina pectoris patients experience retrosternal chest discomfort. A pressure, squeezing, heaviness, burning, or suffocating sensation best describes the former. Anginal pain is typically localized to the shoulders, back, epigastrium, and neck. Pain frequently radiates to the neck, arms, and shoulders.
Exercise, eating, exposure to colds, or mental trauma are common triggers of angina. It lasts for around 1 to 5 minutes and can be eased with nitroglycerin or rest. Angina pectoris is not frequently the cause of brief chest pain. With breathing, coughing, or shifting positions, angina does not fluctuate in intensity. Rarely is pain above and below the epigastrium anginal in character.
Inquire of patients regarding the frequency of angina, the degree of their discomfort, and the quantity of nitroglycerin they take when they experience angina.
Angina decubitus
Angina decubitus is a type of angina pectoris that strikes while the patient is lying down at night. According to others, it is brought on by an increase in myocardial demand for oxygen brought on by the expansion of blood volume brought on by an increase in venous return while reclining.
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
Medication
IR tablets
Initial dose:
50
mg
Orally
twice a day
Maintenance dose: 100-400 mg orally once a day
ER tablets:
Initial dose: 100 mg orally once a day
Maintenance dose: 100-400 mg orally once a day
50
mg
Orally
once a day
; after 1 week; can be increased up to 100 mg or 200 mg
15 - 45
mg
once a day
6 - 8
hrs
Initial:
40
mg
Orally
once a day
3 - 7
days
2.5 - 6.5
mg
Capsules
Oral
every 8 hrs
Dose Adjustments
Creatinine clearance:
10-50mg/min-administer every 24-72 hour
<10ml/min-administer every 72-96 hour
25 - 50
mg
Tablet
Orally 
twice a day
Immediate release
:
Initial dose: 30mg orally every 6 hours, increasing gradually every 1 to 2 days
Maintenance dose: 180-360mg orally divided every 6-8 hours. Do not exceed 360mg/day
Extended-release tablets
Initial dose: 180mg orally once a day, increasing gradually every 7 to 14 days
Maintenance dose: 360mg orally every day
Extended-release capsules
Initial dose: 120-180mg orally once a day, increasing gradually every 7 to 14 days
Maintenance dose: 540mg orally every day
Extended-release coated capsules
Initial dose: 120-180mg orally once a day, increasing gradually every 7 to 14 days
Maintenance dose: 480mg orally every day
400 - 1200
mg/day
capsule
Orally 
every 12 hours
Do not exceed 1200mg/day
10
mg
Tablet
Orally 
every 8 hrs
or 30-60 mg (extended-release) orally once a day
may increase every 7-14 days when required
Maintenance:
10-20 mg orally every 8hr up to 20-30 mg orally every 6-8hr
should not exceed more than 180 mg/day or 120 mg/day
If SL NTG is intolerable or unresponsive
5.0 mcg/min
May increase to 5 mcg/min every 3-5 minutes till 20 mcg/min, following
May increase to 10 mcg/min
May subsequently increase to 20 mcg/min
For PVC administration sets, higher dosages are necessary.
Tolerance is produced by continuous infusion for more than 24 hours.
Dose Adjustments
kidney failure
CrCl: 10–50 mg/min; give every 24–72 hours
CrCl below 10 mL/min: administer every 72 to 96 hours
1 to 2 spray(s) when required for angina, repeatable every 3–5 minutes, but no more than 3 sprays in a 15-minute period
Spray onto or beneath the tongue; should not inhale, rinse, or expectorate your mouth for five to ten minutes.
If pain continues after taking three dosages in 15 minutes, seek medical treatment.
Dose Adjustments
Prophylaxis Angina
1 to 2 sprays 5–10 minutes prior to any activity that may cause angina
kidney failure
CrCl: 10–50 mg/min; give every 24–72 hours
CrCl below 10 mL/min: administer every 72 to 96 hours
Indicated for acute relief of angina
0.3-0.6 mg (sublingually) every 5 minutes, up to a maximum of 3 times
This medication should be used as soon as the first sign of angina appears
Indicated for prophylaxis of angina
one tablet sublingual 5-10 minutes before engaging in activities that may provoke an angina attack
To prevent Angina Pectoris over an extended period, it is recommended to apply medication to the skin over the trunk area in the morning and then reapply after six hours
The dosage for each application should be 0.5-2 inches
Administer 2 to 6 nasal inhalations by waving the crushed ampule under the nose, and 0.3 ml by inhalation of crushed ampule repeat every 3 to 5 minutes if necessary.
Take a dose of 5 to 20 mg orally as immediate release every 8 to 12 hours initially and maintenance dose 10 to 40 mg orally every 8to 12 hours
Take a dose of 40 mg orally initially and maintenance dose 40 to 80 mg orally every 8to 12 hours
For sublingual prophylaxis: take a dose of 2.5 to 5 mg 15 minutes prior to performing activities to cause angina
For sublingual treatment: take a dose of 2.5 to 5 mg and it may repeat every 5 to 10 minutes
Not more than 3 doses in 15 to 30 minutes
Initially, 200 mg each day
After 10 days, increase the dose to 300 mg each day if required
The starting oral dose is 50 mg one time daily
If necessary and well-tolerated, the dose may be gradually increased to orally intake of 100 mg daily for maintenance dose
1 to 4 mg orally given every two to four times a day
Take a dose of 80 to 160 mg orally daily in 2 or 3 divided doses
Daily dose should not be more than 320 mg
Take a dose of 25 to 50 mg orally in each 6 to 12 hours
Daily dose should not be more than 200 mg
The usual therapeutic dose is 10 or 20 mg orally every 12 hours daily.
Maximum dose can go up to 40 mg for every twelve hours daily.
Indicated for treating & preventing angina pectoris
The suggested dosage is 10 mg to 20 mg by oral route every six hours a day
The dose may be raised to 40 mg every six hours a day
It is indicated for the management of Angina Pectoris
The usual recommended dose is 60 mg via oral administration three times per day
It was globally removed from the market in 1988 due to its association with QT prolongation and Torsades de pointes, resulting in sudden deaths
Dose Adjustments
Limited data is available
Keep 1 tablet under the tongue and allow it to dissolve slowly
Repeat after 5 minutes if symptoms are not relieved
For immediate-release tablets, the initial dosage is 5-10 mg orally two times daily, with 5 mg recommended for small patients
Each dose should be administered 7 hours apart
The recommended dose can be raised to 10 mg administered orally every 12 hours starting from the second or third day
The maintenance dosage is 20 mg orally every 12 hours
Initial dosage for extended-release tablets is 30-60 mg orally once a day in morning with increasing it to 120 mg orally once a day It is essential to wait for a minimum of 3 days before each dosage increase
In exceptional cases, if necessary, the dosage may be further increased to a maximum of 240 mg orally once a day
4 mg to 8 mg orally every day
Extract 160mg orally twice a day Tea 1 cup orally;1 g of dried leaves in 150 ml water Dried Ripe Berries 20 to 60g/day orally
The suggested dosage is 0.5 to 2 mg orally a day
Initial dose: 200-400mg/day divided orally
Do not exceed 800mg/day
10
mg
Tablets
Orally 
every 8 hrs
7 - 14
days
30-60 mg (extended release) orally once a day
Maintenance:
10-20 mg orally every 8hr up to 20-30 mg orally every 6-8hr
should not exceed more than 180 mg/day or 120 mg/day (extended-release)
1 to 2 spray(s) when required for angina, repeatable every 3–5 minutes, but no more than 3 sprays in a 15-minute period
Spray onto or beneath the tongue; should not inhale, rinse or expectorate your mouth for five to ten minutes.
If pain continues after taking three dosages in 15 minutes, seek medical treatment.
Prophylaxis Angina
1 to 2 sprays 5–10 minutes prior to any activity that may cause angina
Initiate with the minimal suggested dosage for adults
Future Trends
References
https://www.ncbi.nlm.nih.gov/books/NBK557672/
https://emedicine.medscape.com/article/150215-clinical#b2
The most typical sign of ischemic cardiovascular disease, a leading global source of mortality and morbidity, is angina or chest discomfort. A comprehensive physical exam and history are essential for separating cardiac from non-cardiac causes of chest discomfort and identifying patients with acute coronary syndrome (ACS).
Angina, which can be further divided into unstable and stable angina, is one of the symptoms of ACS. The definition of stable angina is the presence of symptoms only with effort. Unstable angina or symptoms that appear when you’re at rest need more immediate assessment and treatment. Angina symptoms are present in almost 9 million individuals in the US, and identifying these symptoms is crucial to enhancing outcomes for patients.
In western nations, 30 000 – 40 000 people per million suffer from chronic stable angina. Age-related prevalence rises in both men & women. Prevalence estimates range from 4 to 7 percent for men and 5 to 7 percent for women aged 45 to 64, respectively. The estimated prevalence is 14–15% for men & 10–12% for women aged 65–84, respectively.
Hypertension, hyperlipidemia, tobacco use in the past or present, diabetes mellitus, & obesity/metabolic syndrome are all modifiable factors for angina. An individual risk factor for CAD (coronary artery disease) is an elevated BMI. Aging, male sex, a family medical history of CAD, and ethnicity are examples of risk variables that cannot be changed.
The creation of energy necessary to promote contractility in the heart depends on an appropriate oxygen supply. Anaerobic glycolysis is increased by ischemia at the cellular level. This raises the concentrations of potassium, lactate, & hydrogen in the venous return of the myocardium’s ischemia or damaged region.
Competition between calcium ions and hydrogen ions results in hypokinesia and akinesia in the afflicted area. Stress, exercise, and low body temperature are the three triggers that would produce metabolic mismatch and unstable angina.
Non-cardiac reasons, non-ischemic cardiac illness, and then ischemic cardiac disease can all produce chest pain. Other non-cardiac reasons include lung problems, musculoskeletal issues, panic/anxiety attacks, and gastric reflux disease. Pericardial illness is one of the non-ischemic heart causes. Most experts agree that coronary artery atherosclerosis & coronary vasospasm are the causes of chest pain brought on by myocardial ischemia.
A mismatch between myocardial oxygen demand and supply results from this situation. In unstable angina, the increased demand also arises while at rest, whereas in unstable angina, it only happens during effort. Exercise-induced increases in heart rate, blood pressure, & myocardial contractility are among the main causes of increased myocardial oxygen demand.
In healthy hearts, increased oxygen demand brought on by exercise is followed by coronary vasodilation. However, in those with coronary artery atherosclerosis, this function is impaired, leading to ischemia & chest discomfort. Similar to stable angina, vasospastic angina, commonly referred to as variant angina as well as Prinzmetal angina, also happens while at rest but is unconnected to coronary atherosclerosis.
The likelihood that chronic stable angina will result in cardiovascular events varies from patient to patient. Cardiac comorbidities, adherence to dietary and treatment regimen recommendations, and other factors all affect prognosis. Left ventricular systolic function, the amount of activity the patient can endure, and the degree of CAD present all have an impact on the long-term outcome.
Diabetes mellitus, prior MI, advancing age, hypertension, & male sex are risk factors for a worse prognosis. Additionally, it has been shown that the administration of nitrates is a poor predictor of mortality, most likely because it signals more severe disease.
Physical examination
Physical examination results are typically normal for patients with stable angina. It’s crucial to identify possible causes of angina, including aortic stenosis. Angina pectoris is suggested by a positive Levine sign, which is defined by the patient clenching their hand over their sternum while discussing their discomfort.
Look for visible indications of widespread atherosclerosis or aberrant lipid metabolism, such as xanthelasma or xanthoma (e.g., diminished or absent peripheral pulses, arteriovenous nicking upon ophthalmic examination, or, raised light reflexes, carotid bruit). It may be more beneficial to examine individuals while they are having an angina episode.
Third and fourth cardiac sounds caused by LV systolic and diastolic disorder, as well as mitral regurgitation related to papillary muscle disorder, are useful physical observations. Pressure on the chest wall frequently causes pain that originates there.
Differential diagnosis
The goal of treating chronic stable angina is to control symptoms and prevent the development of cardiovascular events. Lifestyle changes, risk factor reduction, & medicinal treatment are crucial elements of management, which is complex in nature. Revascularization may be used when symptoms are resistant to medical treatment; however, while it may be effective in controlling problems, research has not demonstrated that it lowers the risk of significant cardiac events when compared to medical management. Regular exercise, maintaining a healthy weight, & quitting smoking are examples of lifestyle changes that should be supported.
Maintaining cholesterol, blood pressure, & blood sugar are examples of risk factor adjustment. Statins, aspirin, angiotensin receptor blockers, or angiotensin-converting enzyme inhibitors are examples of medications used to reduce risk factors and stop the progression of the disease. Medical treatment can be utilized to manage symptoms and lower the risk of atherosclerosis progression & cardiovascular events. Depending on how angina symptoms are alleviated, antianginal medicines can be divided into several classes. The general goal of symptom control is to reduce myocardial oxygen demand.
The majority of anginal episodes are brought on by a rise in the heart rate because it is the primary factor affecting oxygen uptake. Three kinds of angina medications—ivabradine, beta-blockers & non-dihydropyridine Ca channel blockers—reduce symptoms by lowering heart rate. In individuals with low ejection fraction and left ventricular failure, calcium channel inhibitors should be prevented. Relaxing the vascular smoothness is a different method of treating anginal complications.
As a result, the perfusion capacity is increased by widening the coronary arteries. Dihydropyridine Ca channel blockers, nicorandil, & nitrates are medicines that act in this manner. Ranolazine, another medication for chronic stable angina, blocks the late sodium influx in ventricular myocardial cells. The diastolic contractile disorder is lessened as a result. The treatment goals for unstable angina are minimizing myocardial damage, minimizing morbidity, & lowering mortality.
Nitrates – are used to relieve chest discomfort but have little mortality advantage. Vasodilation brought on by them lowers preload & left ventricular end-diastolic volume. This lowers the need for myocardium oxygen. They should not be used if you have hypotension or have recently taken phosphodiesterase blockers.
Morphine – No mortality advantage; used to treat pain when nitrates are unable to completely relieve it. Along with analgesia, it also results in mild vasodilation.
Beta-blockers – decrease mortality. They lower blood pressure, heart rate, and contractility, which lessens the need for myocardium oxygen.
Antiplatelet agents – In individuals with acute coronary syndromes, dual treatment with aspirin, so either ticagrelor, prasugrel, or clopidogrel lowers the risk of cardiac events – sudden cardiac death, stroke, and acute myocardial infarction.
Anticoagulants – reduce mortality in conjunction with antiplatelet medications by lowering re-infarction rates. given intravenously for immediate medical care.
Anatomic evaluation of the coronary arteries and revascularization consideration – Risk stratification techniques should be used to identify high-risk individuals and consider them for immediate revascularization.
Instead of actual pain, the majority of angina pectoris patients experience retrosternal chest discomfort. A pressure, squeezing, heaviness, burning, or suffocating sensation best describes the former. Anginal pain is typically localized to the shoulders, back, epigastrium, and neck. Pain frequently radiates to the neck, arms, and shoulders.
Exercise, eating, exposure to colds, or mental trauma are common triggers of angina. It lasts for around 1 to 5 minutes and can be eased with nitroglycerin or rest. Angina pectoris is not frequently the cause of brief chest pain. With breathing, coughing, or shifting positions, angina does not fluctuate in intensity. Rarely is pain above and below the epigastrium anginal in character.
Inquire of patients regarding the frequency of angina, the degree of their discomfort, and the quantity of nitroglycerin they take when they experience angina.
Angina decubitus
Angina decubitus is a type of angina pectoris that strikes while the patient is lying down at night. According to others, it is brought on by an increase in myocardial demand for oxygen brought on by the expansion of blood volume brought on by an increase in venous return while reclining.
https://www.ncbi.nlm.nih.gov/books/NBK557672/
https://emedicine.medscape.com/article/150215-clinical#b2
The most typical sign of ischemic cardiovascular disease, a leading global source of mortality and morbidity, is angina or chest discomfort. A comprehensive physical exam and history are essential for separating cardiac from non-cardiac causes of chest discomfort and identifying patients with acute coronary syndrome (ACS).
Angina, which can be further divided into unstable and stable angina, is one of the symptoms of ACS. The definition of stable angina is the presence of symptoms only with effort. Unstable angina or symptoms that appear when you’re at rest need more immediate assessment and treatment. Angina symptoms are present in almost 9 million individuals in the US, and identifying these symptoms is crucial to enhancing outcomes for patients.
In western nations, 30 000 – 40 000 people per million suffer from chronic stable angina. Age-related prevalence rises in both men & women. Prevalence estimates range from 4 to 7 percent for men and 5 to 7 percent for women aged 45 to 64, respectively. The estimated prevalence is 14–15% for men & 10–12% for women aged 65–84, respectively.
Hypertension, hyperlipidemia, tobacco use in the past or present, diabetes mellitus, & obesity/metabolic syndrome are all modifiable factors for angina. An individual risk factor for CAD (coronary artery disease) is an elevated BMI. Aging, male sex, a family medical history of CAD, and ethnicity are examples of risk variables that cannot be changed.
The creation of energy necessary to promote contractility in the heart depends on an appropriate oxygen supply. Anaerobic glycolysis is increased by ischemia at the cellular level. This raises the concentrations of potassium, lactate, & hydrogen in the venous return of the myocardium’s ischemia or damaged region.
Competition between calcium ions and hydrogen ions results in hypokinesia and akinesia in the afflicted area. Stress, exercise, and low body temperature are the three triggers that would produce metabolic mismatch and unstable angina.
Non-cardiac reasons, non-ischemic cardiac illness, and then ischemic cardiac disease can all produce chest pain. Other non-cardiac reasons include lung problems, musculoskeletal issues, panic/anxiety attacks, and gastric reflux disease. Pericardial illness is one of the non-ischemic heart causes. Most experts agree that coronary artery atherosclerosis & coronary vasospasm are the causes of chest pain brought on by myocardial ischemia.
A mismatch between myocardial oxygen demand and supply results from this situation. In unstable angina, the increased demand also arises while at rest, whereas in unstable angina, it only happens during effort. Exercise-induced increases in heart rate, blood pressure, & myocardial contractility are among the main causes of increased myocardial oxygen demand.
In healthy hearts, increased oxygen demand brought on by exercise is followed by coronary vasodilation. However, in those with coronary artery atherosclerosis, this function is impaired, leading to ischemia & chest discomfort. Similar to stable angina, vasospastic angina, commonly referred to as variant angina as well as Prinzmetal angina, also happens while at rest but is unconnected to coronary atherosclerosis.
The likelihood that chronic stable angina will result in cardiovascular events varies from patient to patient. Cardiac comorbidities, adherence to dietary and treatment regimen recommendations, and other factors all affect prognosis. Left ventricular systolic function, the amount of activity the patient can endure, and the degree of CAD present all have an impact on the long-term outcome.
Diabetes mellitus, prior MI, advancing age, hypertension, & male sex are risk factors for a worse prognosis. Additionally, it has been shown that the administration of nitrates is a poor predictor of mortality, most likely because it signals more severe disease.
Physical examination
Physical examination results are typically normal for patients with stable angina. It’s crucial to identify possible causes of angina, including aortic stenosis. Angina pectoris is suggested by a positive Levine sign, which is defined by the patient clenching their hand over their sternum while discussing their discomfort.
Look for visible indications of widespread atherosclerosis or aberrant lipid metabolism, such as xanthelasma or xanthoma (e.g., diminished or absent peripheral pulses, arteriovenous nicking upon ophthalmic examination, or, raised light reflexes, carotid bruit). It may be more beneficial to examine individuals while they are having an angina episode.
Third and fourth cardiac sounds caused by LV systolic and diastolic disorder, as well as mitral regurgitation related to papillary muscle disorder, are useful physical observations. Pressure on the chest wall frequently causes pain that originates there.
Differential diagnosis
The goal of treating chronic stable angina is to control symptoms and prevent the development of cardiovascular events. Lifestyle changes, risk factor reduction, & medicinal treatment are crucial elements of management, which is complex in nature. Revascularization may be used when symptoms are resistant to medical treatment; however, while it may be effective in controlling problems, research has not demonstrated that it lowers the risk of significant cardiac events when compared to medical management. Regular exercise, maintaining a healthy weight, & quitting smoking are examples of lifestyle changes that should be supported.
Maintaining cholesterol, blood pressure, & blood sugar are examples of risk factor adjustment. Statins, aspirin, angiotensin receptor blockers, or angiotensin-converting enzyme inhibitors are examples of medications used to reduce risk factors and stop the progression of the disease. Medical treatment can be utilized to manage symptoms and lower the risk of atherosclerosis progression & cardiovascular events. Depending on how angina symptoms are alleviated, antianginal medicines can be divided into several classes. The general goal of symptom control is to reduce myocardial oxygen demand.
The majority of anginal episodes are brought on by a rise in the heart rate because it is the primary factor affecting oxygen uptake. Three kinds of angina medications—ivabradine, beta-blockers & non-dihydropyridine Ca channel blockers—reduce symptoms by lowering heart rate. In individuals with low ejection fraction and left ventricular failure, calcium channel inhibitors should be prevented. Relaxing the vascular smoothness is a different method of treating anginal complications.
As a result, the perfusion capacity is increased by widening the coronary arteries. Dihydropyridine Ca channel blockers, nicorandil, & nitrates are medicines that act in this manner. Ranolazine, another medication for chronic stable angina, blocks the late sodium influx in ventricular myocardial cells. The diastolic contractile disorder is lessened as a result. The treatment goals for unstable angina are minimizing myocardial damage, minimizing morbidity, & lowering mortality.
Nitrates – are used to relieve chest discomfort but have little mortality advantage. Vasodilation brought on by them lowers preload & left ventricular end-diastolic volume. This lowers the need for myocardium oxygen. They should not be used if you have hypotension or have recently taken phosphodiesterase blockers.
Morphine – No mortality advantage; used to treat pain when nitrates are unable to completely relieve it. Along with analgesia, it also results in mild vasodilation.
Beta-blockers – decrease mortality. They lower blood pressure, heart rate, and contractility, which lessens the need for myocardium oxygen.
Antiplatelet agents – In individuals with acute coronary syndromes, dual treatment with aspirin, so either ticagrelor, prasugrel, or clopidogrel lowers the risk of cardiac events – sudden cardiac death, stroke, and acute myocardial infarction.
Anticoagulants – reduce mortality in conjunction with antiplatelet medications by lowering re-infarction rates. given intravenously for immediate medical care.
Anatomic evaluation of the coronary arteries and revascularization consideration – Risk stratification techniques should be used to identify high-risk individuals and consider them for immediate revascularization.
Instead of actual pain, the majority of angina pectoris patients experience retrosternal chest discomfort. A pressure, squeezing, heaviness, burning, or suffocating sensation best describes the former. Anginal pain is typically localized to the shoulders, back, epigastrium, and neck. Pain frequently radiates to the neck, arms, and shoulders.
Exercise, eating, exposure to colds, or mental trauma are common triggers of angina. It lasts for around 1 to 5 minutes and can be eased with nitroglycerin or rest. Angina pectoris is not frequently the cause of brief chest pain. With breathing, coughing, or shifting positions, angina does not fluctuate in intensity. Rarely is pain above and below the epigastrium anginal in character.
Inquire of patients regarding the frequency of angina, the degree of their discomfort, and the quantity of nitroglycerin they take when they experience angina.
Angina decubitus
Angina decubitus is a type of angina pectoris that strikes while the patient is lying down at night. According to others, it is brought on by an increase in myocardial demand for oxygen brought on by the expansion of blood volume brought on by an increase in venous return while reclining.
https://www.ncbi.nlm.nih.gov/books/NBK557672/
https://emedicine.medscape.com/article/150215-clinical#b2
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