Angina pectoris – commonly known as angina – is the sensation of chest pain, pressure, or squeezing, often due to ischemia of the heart muscle from obstruction or spasm of the coronary arteries.[1] While angina pectoris can derive from anemia, cardiac arrhythmias and heart failure, its main cause is coronary artery disease (CAD), an atherosclerotic process affecting the arteries feeding the heart.
Contents
- 1 Classification
- 2 Signs and symptoms
- 3 Cause
- 4 Pathophysiology
- 5 Diagnosis
- 6 Treatment
- 7 Epidemiology
- 8 History
- 9 References
- 10 Further reading
- 11 External links
Severe tachycardia (for example due to supraventricular tachycardia)
in an individual with normal coronary arteries can also lead to
increased troponins for example, it is presumed due to increased oxygen
demand and inadequate supply to the heart muscle.
Troponins are also increased in patients with heart failure, where they also predict mortality and ventricular rhythm abnormalities. They can rise in inflammatory conditions such as myocarditis and pericarditis with heart muscle involvement (which is then termed myopericarditis). Troponins can also indicate several forms of cardiomyopathy, such as dilated cardiomyopathy, hypertrophic cardiomyopathy or (left) ventricular hypertrophy, peripartum cardiomyopathy, Takotsubo cardiomyopathy, or infiltrative disorders such as cardiac amyloidosis.
Heart injury with increased troponins also occurs in cardiac contusion, defibrillation and internal or external cardioversion. Troponins are commonly increased in several procedures such as cardiac surgery and heart transplantation, closure of atrial septal defects, percutaneous coronary intervention, or radiofrequency ablation.
