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Cardiovascular system
Arterial disease
Angina pectoris
Stable angina
Unstable angina
Myocardial infarction
Prinzmetal angina
Coronary steal syndrome
Peripheral artery disease
Subclavian steal syndrome
Aneurysms
Aortic dissection
Vasculitis
Behcet's disease
Kawasaki disease
Hypertension
Hypertensive emergency
Renal artery stenosis
Coarctation of the aorta
Cushing syndrome
Conn syndrome
Pheochromocytoma
Polycystic kidney disease
Hypotension
Orthostatic hypotension
Abetalipoproteinemia
Familial hypercholesterolemia
Hypertriglyceridemia
Hyperlipidemia
Chronic venous insufficiency
Thrombophlebitis
Deep vein thrombosis
Lymphedema
Lymphangioma
Shock
Vascular tumors
Human herpesvirus 8 (Kaposi sarcoma)
Angiosarcomas
Truncus arteriosus
Transposition of the great vessels
Total anomalous pulmonary venous return
Tetralogy of Fallot
Hypoplastic left heart syndrome
Patent ductus arteriosus
Ventricular septal defect
Coarctation of the aorta
Atrial septal defect
Atrial flutter
Atrial fibrillation
Premature atrial contraction
Atrioventricular nodal reentrant tachycardia (AVNRT)
Wolff-Parkinson-White syndrome
Ventricular tachycardia
Brugada syndrome
Premature ventricular contraction
Long QT syndrome and Torsade de pointes
Ventricular fibrillation
Atrioventricular block
Bundle branch block
Pulseless electrical activity
Tricuspid valve disease
Pulmonary valve disease
Mitral valve disease
Aortic valve disease
Dilated cardiomyopathy
Restrictive cardiomyopathy
Hypertrophic cardiomyopathy
Heart failure
Cor pulmonale
Endocarditis
Myocarditis
Rheumatic heart disease
Pericarditis and pericardial effusion
Cardiac tamponade
Dressler syndrome
Cardiac tumors
Acyanotic congenital heart defects: Pathology review
Cyanotic congenital heart defects: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Coronary artery disease: Pathology review
Peripheral artery disease: Pathology review
Valvular heart disease: Pathology review
Cardiomyopathies: Pathology review
Heart failure: Pathology review
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart blocks: Pathology review
Aortic dissections and aneurysms: Pathology review
Pericardial disease: Pathology review
Endocarditis: Pathology review
Hypertension: Pathology review
Shock: Pathology review
Vasculitis: Pathology review
Cardiac and vascular tumors: Pathology review
Dyslipidemias: Pathology review
Angina pectoris
0 / 6 complete
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angina and p. 326
aortic stenosis p. 298
atherosclerosis p. 308
cilostazol/dipyridamole for p. 445
cocaine causing p. 594
contraindicated drugs p. 326, 329
drug therapy for p. 325, 326, 363
glycoprotein IIb/IIa inhibitors for p. 445
ischemic disease and p. 310
presentation p. 716
unstable/NSTEMI treatment p. 316
β -blockers for p. 247
stable angina with p. 310
angina p. 326
angina p. 325
angina treatment p. 326
angina p. 310
angina and p. 310
Angina comes from the latin angere, which means to strangle, and pectoris comes from pectus, meaning chest—so angina pectoris loosely translates to “strangling of the chest”, which actually makes a lot of sense, because angina pectoris is caused by reduced blood flow which causes ischemia to the heart muscle, or lack of oxygen to the heart, almost like the heart’s being strangled which causes terrible chest pain.
Stable angina or chronic angina is the most common type of angina and it usually happens when the patient has greater than or equal to 70% stenosis, meaning 70% of the artery is blocked by plaque buildup.
This small opening that blood flows through might be enough to supply the heart during rest, but if the body demands more blood and oxygen, like during exercise or stressful situations, the heart has to work harder, and therefore needs more blood and oxygen itself.
It’s during these time of exertion or emotional stress that people with stable angina have chest pain, since the blood flow isn’t meeting the metabolic demands of the heart muscle, or myocardium.
But the pain usually goes away with rest.
In the majority of cases, the underlying cause of stable angina is atherosclerosis of one or more the coronary arteries—arteries supplying blood to the heart muscles.
Other heart conditions that might lead to stable angina are ones that cause a thickened heart muscle wall, which would require more oxygen.
This increase in muscle size can be due to hypertrophic cardiomyopathy from a genetic cause, or as a result from the heart having to pump against higher pressures, as is the case in aortic stenosis, which is a narrowing of the aortic valve, or hypertension.
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