]> 2026-07-31T07:52:15+00:00 WBR251 0 en Atheromatous plaque with 80% stenosis of the lumen without thrombus Coronary artery disease is defined as presence of a lesion that obstructs > 50% of at least one of the epicardial arteries. Symptoms of stable angina usually do not develop until the lesion obstrucs > 75% of the lumen. Diffuse coronary artery vasospasm causing flow limitation is incorrect Prinzmetal (variant) angina is caused by coronary vasospasm due to contraction of the vascular smooth muscle, rather than by atherosclerosis. It occurs more commonly among younger women and typically manifests as clustered angina that occurs nocturnally at rest rather than on exertion. Although approximately two-thirds of patients have concurrent atherosclerosis of a major coronary artery, this is often mild or not in proportion to the degree of symptoms. ECG changes may only be evident while the patient is experiencing an attack, where typically ECG of patients with Prinzmetal angina demonstrates ST-segment elevations (rather than depressions). Prinzmetal angina generally responds to calcium channel blockers. Ruptured atheroma with fully obstructive thrombus Ruptured atheroma with fully obstructive thrombus is the underlying pathophysiology of a myocardial infarction. The patient is likely to have acute transmural myocardial infarction of the lateral wall, as evidenced by the ECG changes. Calcification and thickening of the coronary intima Although fibrocalcific plaque with thickening of the coronary intima may be associated with nonocclusive thrombus, it does not typically cause symptoms of unstable angina. Dissection of the coronary wall with intraluminal flap Coronary artery dissection is most likely associated with percutaneous coronary interventions and is a rare cause of acute coronary syndrome and sudden death. The patient is likely having an acute transmural myocardial infarction of the lateral wall, as suggested by the clinical findings (persistent, substernal chest pain) and as evidenced by the ECG changes (ST-segment elevation in the lateral leads I, aVL, V5-V6). Clinically, stable/unstable angina are differentiated from a myocardial infarction (MI) by the persistence and radiation of symptoms, hemodynamic changes, and the absence of relief with rest or with pharmacological therapy (e.g. sublingual nitroglycerin). In MI, patients typically report substernal chest pain, often felt as chest pressure, that radiates to either the jaw, the left arm, or the epigastric region. Given that a MI and other life-threatening conditions should always be ruled out when patients present with chest pain, clinical differentiation between angina and myocardial infarction is not very relevant since all patients end up with a diagnostic work-up. The fatty streak is the the earliest evidence of atherosclerosis. It is characterized by non-obstructive, yellowish lesions in the arterial lumen. Although asymptomatic, fatty streaks often predispose to endothelial dysfunction, which subsequently results in a pro-inflammatory state that allows the aggregation of inflammatory mediators (leukocyte recruitment and foam cell formation from monocytes) and the entry and modification of lipids in the subendothelial intima. As lipids accumulate within the intima, they are trapped and oxidized, forming reactive oxygen species. The plaque progression is highly dependent on the smooth muscle cell migration into the intima following the formation of the fatty streak and the subendothelial changes that ensue. As the plaque grows, it can obstruct luminal blood flow, resulting in myocardial ischemia and clinical manifestations (e.g. stable angina). As the plaque grows further, its fibrous cap may rupture, and prothrombotic molecules (originally in the subendothelial within the lipid atheroma) are exposed. Once exposed, thrombosis occurs and an occlusive clot develops, resulting in a myocardial infarction.<br/> '''Educational Objective:''' As the atherogenic plaque grows, its fibrous cap may rupture, and prothrombotic molecules (originally in the subendothelial within the lipid atheroma) are exposed. Once exposed, thrombosis occurs and an occlusive clot develops, resulting in a myocardial infarction.<br/> '''References:''' Libby P. Inflammation in atherosclerosis. Nature. 2002;420(6917):868-74.<br> First Aid 2015 page 292. Pathology A 75-year-old woman presents to the emergency department (ED) with an acute-onset substernal chest pain for the past 30 minutes. She explains she was asymptomatic earlier today, but she felt a sudden, unusual chest pressure sensation while she was walking her dog in the afternoon. She recalls she has recently had a history of intermittent chest pains that are worsened by physical activity and relieved by rest, but her current chest pain has been constant and is markedly more severe than her usual symptoms. Upon further questioning, she reports her chest pain is associated with cold sweating, shortness of breath, and left upper extremity numbness. Her past medical history includes diabetes mellitus, hypertension, and dyslipidemia. In the ED, her temperature is 37.5 °C (99.5 °F), blood pressure is 90/65 mmHg, and heart rate is 115/min. Electrocardiogram demonstrates ST-segment elevation in leads I, aVL and V5-V6. Which of the following events is most likely to underlie her clinical presentation? C Cardiology 2020-10-28T02:53:43Z 2459150.6206366 WBR251