Coronary artery disease
Inflammation is important in the pathogenesis of atherosclerosis. Endothelial cell dysfunction leads to macrophage and low-density lipoprotein (LDL) accumulations, causing foam cell formation and fatty streaks. This results in smooth muscle cell migration, proliferation, and extracellular matrix deposition, defined as a fibrous plaque. As the disease progresses, the fibrous plaque worsens and will eventually form a complex atheroma.
The hallmark symptom of ischemia is retrosternal chest pain / discomfort that may radiate to the neck, jaw, or left arm. Often, patients with this condition rest to ease the discomfort. The pain also generally improves with use of nitroglycerin. The pain is short-lived and starts gradually, rising to a maximum intensity within minutes, often described as "crescendo angina." Chest pain that reaches a peak within seconds should raise the possibility of an alternative diagnosis, notably . Other common symptoms include palpitations, nausea or heartburn-like symptoms, and hypotension. Atypical symptoms, such as dyspnea or syncope, are seen more often in women, elderly patients, and diabetic patients. Women tend to develop heart disease at a later age compared with men, with diabetes / insulin resistance, hypertension, obesity, and smoking being the strongest risk factors for early-onset CAD in women. There also appears to be an independent association between both hypertensive disorders during pregnancy and low birth weight with development of atherosclerotic cardiovascular disease.
Modifiable risk factors for development of CAD include smoking, hypertension, hyperlipidemia, type 2 diabetes mellitus, high glycemic index and glycemic load, obesity, and a sedentary lifestyle. Increased urinary sodium is associated with increased risk. Nonmodifiable risk factors include increasing age, male sex, postmenopausal status in women, and family history of CAD. Multiple forms of predominantly air pollution are risk factors for CAD.
I25.10 – Atherosclerotic heart disease of native coronary artery without angina pectoris
53741008 – Coronary arteriosclerosis
- Acute coronary syndrome – New onset chest pain, pain of a new character, or pain of prolonged duration not relieved by rest; ECG is usually abnormal:
- Unstable angina
- Myocardial infarction
- NSTEMI – no ST elevation on ECG but with acute elevations of cardiac markers
- STEMI – ST or T wave changes across a vascular region with acute elevations of cardiac markers
- Microvascular angina
- Pericarditis – Sharp pain, positional (improved with leaning forward), recent illness or myocardial infarction (or other risk factors), pericardial friction rub, diffuse ST elevations on ECG.
- Aortic dissection – Tearing chest pain that radiates to the back, hypotension, tachycardia, visible on CT.
- Coronary vasospasm
- Coronary artery dissection
- Stress-induced cardiomyopathy
- Heart failure
- Mitral valve disease (eg, prolapse, regurgitation, or stenosis)
- Substance related (eg, cocaine-related cardiomyopathy)
- Expanding aortic aneurysm – Positive risk factors (many are the same), visible on ultrasound or CT.
- Pulmonary embolism – Pleuritic chest pain, tachycardia, shortness of breath, syncope, evidence of right heart strain on ECG, CT angiogram.
- Pneumonia – Pleuritic chest pain, cough, fever.
- Acute chest syndrome
- Pulmonary hypertension
- Gastroesophageal reflux disease (GERD) – Burning pain, pain after eating large or spicy meals, pain on abdominal examination.
- Peptic ulcer disease – Look for positive risk factors.
- Esophageal spasm
- Eosinophilic esophagitis
- Hiatal hernia
- Esophageal rupture / perforation
- Referred pain from abdominal viscera (eg, acute cholecystitis, acute pancreatitis) – Look for positive risk factors, liver function tests, pancreatic enzyme levels.
- Sickle cell crisis
- Costochondritis – Sharp, localized, reproducible pain; history of traumatic injury.
- Rheumatic diseases (eg, rheumatoid arthritis, fibromyalgia)
- Herpes zoster (shingles) – Look for rash.