Acute Coronary Syndrome Clinical Presentation

  • Author: David L Coven, MD, PhD; Chief Editor: Eric H Yang, MD   more...
 
Updated: Feb 21, 2012
 

History

The severity and duration of coronary artery obstruction, the volume of myocardium affected, the level of demand, and the ability of the rest of the heart to compensate are major determinants of a patient's clinical presentation and outcome. A patient may present to the ED because of a change in pattern or severity of symptoms.

Typically, angina is a symptom of myocardial ischemia that appears in circumstances of increased oxygen demand. It is usually described as a sensation of chest pressure or heaviness that is reproduced by activities or conditions that increase myocardial oxygen demand. A new case of angina is more difficult to diagnose because symptoms are often vague and similar to those caused by other conditions (eg, indigestion, anxiety).

However, not all patients experience chest pain. They may present with only neck, jaw, ear, arm, or epigastric discomfort. Some patients, including some who are elderly or who have diabetes, present with no pain, complaining only of episodic shortness of breath, severe weakness, light-headedness, diaphoresis, or nausea and vomiting. Elderly persons may also present only with altered mental status. Those with preexisting altered mental status or dementia may have no recollection of recent symptoms and may have no complaints.

In addition, evidence exists that women more often have coronary events without typical symptoms, which may explain the frequent failure of clinicians to initially diagnose ACS in women.

A summary of patient complaints is as follows:

  • Palpitations
  • Pain, which is usually described as pressure, squeezing, or a burning sensation across the precordium and may radiate to the neck, shoulder, jaw, back, upper abdomen, or either arm
  • Exertional dyspnea that resolves with pain or rest
  • Diaphoresis from sympathetic discharge
  • Nausea from vagal stimulation
  • Decreased exercise tolerance

Stable angina involves episodic pain lasting 5-15 minutes, is provoked by exertion, and is relieved by rest or nitroglycerin. In unstable angina, patients have increased risk for adverse cardiac events, such as myocardial infarction or death. New-onset exertional angina can occur at rest and is of increasing frequency or duration or is refractory to nitroglycerin. Variant angina (Prinzmetal angina) occurs primarily at rest, is triggered by smoking, and is thought to be due to coronary vasospasm.

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Physical Examination

Physical examination results are frequently normal. If chest pain is ongoing, the patient will usually lie quietly in bed and may appear anxious, diaphoretic, and pale. Physical findings can vary from normal to any of the following:

  • Hypotension - Indicates ventricular dysfunction due to myocardial ischemia, infarction, or acute valvular dysfunction
  • Hypertension - May precipitate angina or reflect elevated catecholamine levels due to anxiety or to exogenous sympathomimetic stimulation
  • Diaphoresis
  • Pulmonary edema and other signs of left heart failure
  • Extracardiac vascular disease
  • Jugular venous distention
  • Cool, clammy skin and diaphoresis in patients with cardiogenic shock

In addition, a third heart sound (S3) may be present, and frequently, a fourth heart sound (S4) exists. The latter is especially prevalent in patients with inferior-wall ischemia and may be heard in patients with ischemia or systolic murmur secondary to mitral regurgitation

A systolic murmur related to dynamic obstruction of the left ventricular (LV) outflow tract may also occur. It is caused by hyperdynamic motion of the basal left ventricular myocardium and may be heard in patients with an apical infarct.

A new murmur may reflect papillary muscle dysfunction. Rales on pulmonary examination may suggest LV dysfunction or mitral regurgitation.

Patients who present to the ED with chest pain who have a low short-term risk of a major adverse cardiac event must be identified to facilitate early discharge in order to avoid lengthy and costly hospital stays.[11] The ASPECT study tested a 2-hour, accelerated diagnostic protocol (ADP) that included the use of a structured pretest probability scoring method, electrocardiography, and a point-of-care biomarker panel that included troponin, creatine kinase MB, and myoglobin levels. The study suggests that ADP can identify patients at low risk for a short-term major adverse cardiac event who may be suitable for early discharge; such an approach could be used to decrease the overall observation periods and admissions for chest pain and has the potential to affect health-service delivery worldwide.

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Complications

Complications of ischemia include pulmonary edema, while those of myocardial infarction include rupture of the papillary muscle, left ventricular free wall, and ventricular septum.

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Contributor Information and Disclosures
Author

David L Coven, MD, PhD  Assistant Professor of Medicine, Columbia University College of Physicians and Surgeons; Attending Physician in Interventional Cardiology, St Luke's-Roosevelt Hospital Center

David L Coven, MD, PhD is a member of the following medical societies: American College of Physicians, American Medical Association, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Edward Bessman, MD  Chairman, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine

Edward Bessman, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Arun Kalyanasundaram, MD, MPH  Interventional Cardiology Fellow, Department of Cardiology, Cleveland Clinic

Arun Kalyanasundaram, MD, MPH is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, Society for Cardiac Angiography and Interventions, Society of General Internal Medicine, Society of Hospital Medicine, and Southern Medical Association

Disclosure: Nothing to disclose.

Gary Setnik, MD  Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other

Jamshid Shirani, MD  Director of Cardiology Fellowship Program, Director of Echocardiography Laboratory, St Luke's Hospital and Health Network

Jamshid Shirani, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American College of Physicians, American Federation for Medical Research, American Heart Association, American Society of Echocardiography, and Association of Subspecialty Professors

Disclosure: Nothing to disclose.

Specialty Editor Board

Craig T Basson, MD, PhD  Gladys and Roland Harriman Professor of Medicine, Director of the Center for Molecular Cardiology, Director of Cardiovascular Research, Division of Cardiology, Department of Medicine, Weill Cornell Medical College; Attending Physician, New York Presbyterian Hospital

Craig T Basson, MD, PhD is a member of the following medical societies: American College of Cardiology and American Heart Association

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

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.

David FM Brown, MD  Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Eric H Yang, MD  Associate Professor of Medicine, Director of Interventional Cardiology Fellowship Program, Henry Ford Hospital, University of North Carolina at Chapel Hill School of Medicine

Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

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A 50-year-old man with type 1 diabetes mellitus and hypertension presents after experiencing 1 hour of midsternal chest pain that began after eating a large meal. Pain is now present but is minimal. Aspirin is the single drug that will have the greatest potential impact on subsequent morbidity. In the setting of ongoing symptoms and electrocardiogram (ECG) changes, nitrates titrated to 10% reduction in blood pressure and symptoms, beta blockers, and heparin are all indicated. If the patient continues to have persistent signs and/or symptoms of ischemia, addition of a glycoprotein IIb/IIIa inhibitor should be considered.
A 62-year-old woman with a history of chronic stable angina and a "valve problem" presents with new chest pain. She is symptomatic on arrival, complaining of shortness of breath and precordial chest tightness. Her initial vital signs are blood pressure = 140/90 mm Hg and heart rate = 98. Her electrocardiogram (ECG) is as shown. She is given nitroglycerin sublingually, and her pressure decreases to 80/palpation. Right ventricular ischemia should be considered in this patient.
This plot shows changes in cardiac markers over time after the onset of symptoms. Peak A is the early release of myoglobin or creatine kinase isoenzyme MB (CK-MB) after acute myocardial infarction (AMI). Peak B is the cardiac troponin level after infarction. Peak C is the CK-MB level after infarction. Peak D is the cardiac troponin level after unstable angina. Data are plotted on a relative scale, where 1.0 is set at the myocardial-infarction cutoff concentration. Courtesy of Wu et al (1999). ROC = receiver operating characteristic.
Suggested algorithm for triaging patients with chest pain. ACS = ACS; ASA = aspirin; EKG = ECG; MI = myocardial infarction; Rx = treat; STEMI = ST-elevation myocardial infarction. Courtesy of Wu et al (1999).
Use of cardiac markers in the ED. Studies on troponins in ACS.
Use of cardiac markers in the ED. Troponin I levels and cardiac mortality in ACS.
Use of cardiac markers in the ED. Cardiac event rates in the platelet receptor inhibition for ischemic syndrome (PRISM) study based on troponin I results.
Use of cardiac markers in the ED. Effect of time to treatment in patients with acute coronary syndrome (ACS) who are treated with the GIIb/IIIa inhibitor eptifibatide.
Table. TIMI Risk Score for Unstable Angina and NSTEMI[43]
Characteristic Risk Score
History
Age ≥65 years1
At least 3 risk factors for coronary heart disease1
Previous coronary stenosis ≥50%1
Use of aspirin in previous 7 days1
Presentation
At least 2 anginal episodes in the previous 24 hours1
ST-segment elevation on admission ECG1
Elevated levels of serum biomarkers1
Total Score0-7
Note: Event rates significantly increased as the TIMI risk score increased in the test cohort in the TIMI IIB study. Rates were 4.7% for a score of 0/1, 8.3% for 2, 13.2% for 3, 19.9% for 4, 26.2% for 5, and 40.9% for 6/7 (P < .001, χ2 test for the trend). The pattern of increasing event rates with increasing TIMI risk score was confirmed in all 3 validation groups (P < .001).
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