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Coronary Artery Atherosclerosis Clinical Presentation

  • Author: F Brian Boudi, MD, FACP; Chief Editor: Yasmine Subhi Ali, MD, FACC, FACP, MSCI  more...
Updated: Apr 25, 2016


The symptoms of atherosclerosis vary widely. Patients with mild atherosclerosis may present with clinically important symptoms and signs of disease and MI, or sudden cardiac death may be the first symptom of coronary heart disease. However, many patients with anatomically advanced disease may have no symptoms and experience no functional impairment.

The spectrum of presentation includes symptoms and signs consistent with the following conditions:

  • Asymptomatic state (subclinical phase)
  • Stable angina pectoris
  • Unstable angina (ie, ACS)
  • AMI
  • Chronic ischemic cardiomyopathy
  • Congestive heart failure
  • Sudden cardiac arrest

History may include the following:

  • Chest pain
  • Shortness of breath
  • Weakness, tiredness, reduced exertional capacity
  • Dizziness, palpitations
  • Leg swelling
  • Weight gain
  • Symptoms related to risk factors

Progressive luminal narrowing of an artery due to expansion of a fibrous plaque results in impairment of flow once at least 50-70% of the lumen diameter is obstructed. This impairment in flow results in symptoms of inadequate blood supply to the target organ in the event of increased metabolic activity and oxygen demand. Stable angina pectoris, intermittent claudication, and mesenteric angina are examples of the clinical consequences of this mismatch.

Rupture of a plaque or denudation of the endothelium overlying a fibrous plaque may result in exposure of the highly thrombogenic subendothelium and lipid core. This exposure may result in thrombus formation, which may partially or completely occlude flow in the involved artery. Unstable angina pectoris, MI, transient ischemic attack, and stroke are examples of the clinical sequelae of partial or complete acute occlusion of an artery. Atheroembolism is a distinct clinical entity that may occur spontaneously or as a complication of aortic surgery, angiography, or thrombolytic therapy in patients with advanced and diffuse atherosclerosis.

Angina pectoris is characterized by retrosternal chest discomfort that typically radiates to the left arm and may be associated with dyspnea. Angina pectoris is exacerbated by exertion and relieved by rest or nitrate therapy. Unstable angina pectoris describes a pattern of increasing frequency or intensity of episodes of angina pectoris and includes pain at rest. A prolonged episode of angina pectoris that may be associated with diaphoresis is suggestive of MI.


Physical Examination

Tachycardia is common in persons with ACS and AMI. Heart rate irregularity may signal the presence of atrial fibrillation or frequent supraventricular or ventricular ectopic beats. Ventricular tachycardia is the most common cause of death in persons with AMI.

High or low blood pressure may be noted. Hypotension often reflects hemodynamic compromise and is a predictor of poor outcome in the setting of AMI. Diaphoresis is a common finding. Patients often have rapid breathing (ie, tachypnea). Signs and symptoms of congestive heart failure (CHF) may indicate cardiogenic shock or a mechanical complication of AMI, such as ischemic mitral valve regurgitation.

An S4 gallop is a common early finding. The presence of an S3 is an indication of reduced left ventricular function. Heart murmurs, particularly those of mitral regurgitation and ventricular septal defect, may be found after the initial presentation; their presence indicates a grave prognosis. The murmur of aortic insufficiency may signal the presence of aortic dissection as a primary etiology, with or without the complication of AMI. Central obesity is often seen. Patients may develop xanthelasmas, livedo reticularis, or both. Patients may have scarring from CABG or similar surgeries.

The following may also be noted:

  • Shock
  • Syncope
  • Leg edema
  • Pulmonary congestion
  • Rales
  • Diagonal ear crease
  • Short stature
  • Baldness
  • Thoracic hairiness
Contributor Information and Disclosures

F Brian Boudi, MD, FACP Clinical Associate Professor, University of Arizona College of Medicine (Phoenix Campus); Fellow, Sarver Heart Center, University of Arizona College of Medicine; Regional Faculty, American Heart Association; Adjunct Assistant Professor of Medicine, Mid-Western University; Staff Physician, Site Director for Clinical Rotations Emergency Medicine, Phoenix Veterans Administration Health Care System

F Brian Boudi, MD, FACP is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American College of Physicians, American Society of Echocardiography, Arizona Medical Association, Association of Program Directors in Internal Medicine, American College of Healthcare Executives, American Society of Nuclear Cardiology

Disclosure: Nothing to disclose.


Chowdhury H Ahsan, MD, PhD, MRCP, FSCAI Clinical Professor of Medicine, Director of Cardiac Catheterization and Intervention, Marlon Cardiac Catheterization Laboratory, Director of Cardiovascular Research, University Medical Center, University of Nevada School of Medicine

Chowdhury H Ahsan, MD, PhD, MRCP, FSCAI is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, Society for Cardiovascular Angiography and Interventions, American Stroke Association

Disclosure: Received consulting fee from sanofi for consulting; Received honoraria from astra zeneca for speaking and teaching; Received honoraria from BI for speaking and teaching.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief Editor

Yasmine Subhi Ali, MD, FACC, FACP, MSCI President, Nashville Preventive Cardiology, PLLC; Assistant Clinical Professor of Medicine, Vanderbilt University School of Medicine

Yasmine Subhi Ali, MD, FACC, FACP, MSCI is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, Tennessee Medical Association, National Lipid Association

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: MCG Health, LLC; MedStudy<br/>Serve(d) as a speaker or a member of a speakers bureau for: MedStudy<br/>Received honoraria from MedStudy for independent contractor; Received salary from MCG Health, LLC for employment; Received fees from for independent contractor.


Steven J Compton, MD, FACC, FACP Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society

Disclosure: Nothing to disclose.

John A McPherson, MD, FACC, FAHA, FSCAI Associate Professor of Medicine, Division of Cardiovascular Medicine, Director of Cardiovascular Intensive Care Unit, Vanderbilt Heart and Vascular Institute

John A McPherson, MD, FACC, FAHA, FSCAI is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Society for Cardiac Angiography and Interventions, Society of Critical Care Medicine, and Tennessee Medical Association

Disclosure: CardioDx Consulting fee Consulting; Gilead Consulting fee Consulting; Abbott Vascular Corp. Consulting fee Consulting

James L Orford, MBChB

Disclosure: Nothing to disclose.

Andrew P Selwyn, MD, MA, FACC, FRCP

Disclosure: Nothing to disclose.

George A Stouffer III, MD Henry A Foscue Distinguished Professor of Medicine and Cardiology, Director of Interventional Cardiology, Cardiac Catheterization Laboratory, Chief of Clinical Cardiology, Division of Cardiology, University of North Carolina Medical Center

George A Stouffer III, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Stress test, part 1. Resting ECG showing normal baseline ST segments. (See the image below for part 2.)
Stress test, part 2. Stress ECG showing significant ST-segment depression. (See the image above for part 1.)
Stress nuclear imaging showing anterior, apical, and septal wall perfusion defect during stress, which is reversible as observed on the rest images. This defect strongly suggests the presence of significant stenosis in the left anterior descending coronary artery.
Cardiac catheterization and coronary angiography in the left panel shows severe left anterior descending coronary artery stenosis. This lesion was treated with stent placement in the left anterior descending coronary artery, as observed in the right panel.
A vulnerable plaque and the mechanism of plaque rupture.
Positive and negative arterial remodeling.
H and E, low power, of an atheromatous plaque of the coronary artery. The wall is thickened and no internal or external elastic lamina is seen. There is a thick fibrous cap containing some neovascularization in the lower left.
H and E, low power, of an atheromatous plaque of the coronary artery. There is marked luminal narrowing. The fibrous cap on the left contains a central lipid core containing macrophages and cholesterol clefts (lower center). Calcification (dark purple) is seen on the right.
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