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Angina, also known as angina pectoris.
Vascular reactivity and arterial function are important markers of vascular reactivity and arterial function that may be the initial steps of atherosclerotic process.
Refers to chest pain or pressure, usually due to not enough blood flow to the heart muscle.
Angina due to ischemic heart disease affects approximately 1.6% of the population, being slightly more common in men than women (1.7% to 1.5%).
In the United States, 10.2 million are estimated to experience angina with approximately 500,000 new cases occurring each year.
The prevalence of angina rises with increasing age, with a mean age of onset of 62.3 years.
After five years post-onset, 4.8% of individuals with angina subsequently died from coronary heart disease.
Men with angina have an increased risk of subsequent acute myocardial infarction and coronary heart disease related death than women.
A typical presentation is chest discomfort and associated symptoms precipitated by some activity with minimal or non-existent symptoms at rest or after administration of sublingual nitroglycerin.
Angina is more often the presenting symptom of coronary artery disease in women than in men.
Manifests as pressure, fullness, squeezing or pain in the center of the chest, and there can also be discomfort in the neck, jaw, shoulders, back or arms.
Anginal pain is not usually sharp or stabbing or influenced by respiration.
Some people present with atypical symptoms, including breathlessness, nausea, or epigastric discomfort or burning.
These atypical symptoms are particularly likely in older people, women, and those with diabetes.k
It is usually due to obstruction or spasm of the arteries that supply blood to the heart muscle.
Other causes of angina include: anemia, abnormal heart rhythms and heart failure.
The main mechanism of coronary artery obstruction is atherosclerosis.
There is only a weak relationship between the severity of anginal pain and degree of oxygen deprivation in the heart muscle.
There can be severe pain with little or no risk of a myocardial infarction and a heart attack can occur without pain.
Patients with an average age of 62 years, who have moderate to severe degrees of angina,that is, grading by classes II, III, and IV have a 5-year survival rate of approximately 92%.
Unstable angina refers to sudden-onset angina at rest, and angina lasting more than 15 minutes.
Unstable angina is grouped with similar conditions as the acute coronary syndrome.
Unstable angina is defined as angina pectoris that changes or worsens.
It has at least one of these three features:
it occurs at rest or with minimal exertion.
Unstable angina usually lasts more than 10 minutes.
Unstable angina is severe and of new onset, within the prior 4–6 weeks.
Unstable angina occurs with a crescendo pattern, meaning it is distinctly more severe, prolonged, or frequent than before.
Unstable angina may occur at rest, which may be a serious indicator of an impending heart attack.
Unstable angina pathogenesis is due to the reduction of coronary flow due to transient platelet aggregation on apparently normal endothelium, coronary artery spasms, or coronary thrombosis.
Unstable angina starts with atherosclerosis, progresses through inflammation to yield an active unstable plaque, which undergoes thrombosis and results in acute myocardial ischemia, which, if not reversed, results in cell necrosis.
64% of all unstable angina events occur between 22:00 and 08:00 when patients are at rest.
In stable angina, the developing atheroma is protected with a fibrous cap.
This cap may rupture in unstable angina, allowing blood clots to precipitate and further decrease the area of the coronary vessel’s lumen.
The anove explains why, in many cases, unstable angina develops independently of activity.
Effort angina to the classic type of angina related to myocardial ischemia.
Anginal symptoms typically abate several minutes after activity and recur when activity resumes.
Other precipitants of stable angina include cold weather, heavy meals, and emotional stress.
Cardiac syndrome X, sometimes known as microvascular angina is characterized by angina-like chest pain, in the context of normal epicardial coronary arteries.
Cardiac X syndrome cause
involves endothelial dysfunction and reduced flow in the tiny resistance blood vessels of the heart.
As microvascular angina is not characterized by major arterial blockage, it is more difficult to recognize and to be diagnosed.
The Women’s Ischemia Syndrome Evaluation (WISE), suggest that microvascular angina is part of the pathophysiology of ischemic heart disease.
This may explain the higher rates of angina in women than in men, as well as their predilection towards ischemia and acute coronary syndromes in the absence of obstructive coronary artery disease.
Angina may manifest as chest discomfort rather than actual pain: the discomfort is usually described as a pressure, heaviness, tightness, squeezing, burning, or choking sensation.
Anginal pains may also be experienced in the epigastrium, back, neck area, jaw, or shoulders.
Anginal pain can be ref2241ed pain, and is due to the fact that the spinal level that receives visceral sensation from the heart simultaneously receives cutaneous sensation from parts of the skin specified by that spinal nerve’s dermatome, without an ability to discriminate the two.
Typical locations for ref2241ed pain: arms, often inner left arm, shoulders, and neck into the jaw.
Anginal symptoms are typically precipitated by exertion or emotional stress.
Angina is exacerbated by having a full stomach and by exposure to cold temperatures.
Anginal discomfort may be accompanied by shortness of breath, sweating, nausea, increased pulse rate and the blood pressure increases.
Angina results when there is an imbalance between the heart’s oxygen demand and supply.
Chest pain that lasts only a few seconds is normally not angina.
Myocardial ischemia is a result of the myocardium receiving insufficient blood and oxygen to function normally either because of increased oxygen demand by the myocardium or because of decreased supply to the myocardium.
The impaired perfusion of blood and reduced delivery of oxygen and nutrients are directly correlated to blocked or narrowed blood vessels.
Autonomic symptoms such as nausea, vomiting, and pallor may be present.
Risk factors for angina include: cigarette smoking, diabetes, high cholesterol, high blood pressure, sedentary lifestyle, and family history of premature heart disease.
Chronic stable angina management involves minimizing symptoms with antianginal medications or coronary artery revascularization and secondary prevention of cardiovascular events via risk reduction with antiplatelet agents and statins.
The Coronary Artery Disease in General Practice (CADENCE) study indicated that 29% of stable angina patients experienced weekly angina associated with physical limitations and worse quality of life compared to individuals with minimal angina (less than once a week angina over the preceding 4 weeks).
The Coronary Artery Disease in General Practice (CADENCE) study revealed that inpatients with stable angina weekly angina associated with female sex, history of heart failure and peripheral artery disease.
Current treatments such as nitrates, calcium channel blockers, and beta blockers have not reduced the risk of cardiovascular events such as death or myocardial infarction in chronic stable angina
Coital angina occurs minutes to hours after sexual activity.
Treatments for chronic stable angina such as nitrates, calcium channel blockers, and beta blockers have not reduced major cardiovascular events such as death or myocardial infarction.
PCI treatment for patients with angina, does not reduce the risk of death from any cause, death from cardiac causes, or myocardial infarction.
Coital angina represents less than 5% of anginal attacks.
Coital angina prevalence higher in men than women.
In a randomized, double blind, placebo controlled trial, PCI was shown as an effective antianginal treatment in patients with stable angina, who had objective evidence of ischemia (ORBITA-2).