What blood tests are done for chest pain

For a suspected heart attack, paramedics can often perform initial testing in the ambulance while the patient is en route to the hospital. Image: Thinkstock

Every 43 seconds, someone in the United States has a heart attack. If one day that someone is you or a loved one, it may be helpful to know what's likely to happen, both en route to the hospital and after you arrive.

For starters, always call 911 to be transported via ambulance rather than going by car. Contrary to what you might assume, speed isn't the only rationale. "If you're having a heart attack, there are two reasons why you want to be in an ambulance," says Dr. Joshua Kosowsky, assistant professor of emergency medicine at Harvard Medical School. One is that in the unlikely event of cardiac arrest, the ambulance has the equipment and trained personnel to restart your heart. Cardiac arrest, which results from an electrical malfunction that stops the heart's pumping ability, is fatal without prompt treatment. However, most heart attacks do not cause cardiac arrest, Dr. Kosowsky stresses. "It's rare, but it's certainly not a risk you want to take while you're driving or riding in a car."

ECG in the ambulance

The other reason to travel via ambulance is that in many places in the United States, if a person calls 911 complaining of chest pain, the dispatcher will send paramedics who are trained to perform an electrocardiogram (ECG). This simple, painless test records your heart's electrical activity through 12 small electrodes placed on your chest, arms, and legs. A six-second recording can then be transmitted to the receiving emergency department, which can help speed up the process of getting you the care you need.

Some people don't experience the typical symptom of crushing chest pain during a heart attack, however, so they may hesitate to call 911. People with pain that waxes and wanes or who have subtler symptoms (such as jaw pain or shortness of breath) may show up at the emergency room on their own. Even if you do this, you're still likely to get rapid care. The person who greets you might be a receptionist rather than a doctor or nurse, but most emergency departments follow a specific protocol for a suspected heart attack. "If you mention any symptom that sounds like it might be a heart attack, the first thing they'll do is to get you an ECG, ideally within 10 minutes of your arrival," says Dr. Kosowsky.

A doctor then interprets the ECG, which will reveal if you're having a major heart attack, in which an artery feeding your heart is blocked, choking off the blood supply to part of your heart muscle. This usually creates a distinct signature on the ECG and means you'll quickly receive treatment to open the blocked artery.

Blood tests and beyond

But not all heart attacks show up on the first ECG. So even if it looks normal, you're still not out of the woods, says Dr. Kosowsky. The next step is an evaluation by a doctor or other clinician, who will ask about your medical history and details about the location, duration, and intensity of your symptoms. You'll also have a blood test to measure troponin, a protein that rises in response to heart muscle damage. This blood test is very sensitive. But keep in mind that elevated levels don't always show up right away. That's why doctors sometimes have people stay for several hours to get a follow-up troponin measurement.

Other possible tests include a chest x-ray to look for alternative causes of chest discomfort, such as pneumonia or heart failure. A doctor also might give you a trial of medication to see whether it relieves your symptoms, and additional ECGs may be performed over time.

Often, if several troponin tests come back normal, the doctor may want to check your risk of a future heart attack with an exercise stress test. This test can reveal how your heart responds to the demands of increased blood flow needed during exercise. During a standard exercise test, you walk on a treadmill at progressively faster speeds, while trained staff monitors your heart's electrical activity, your heart rate, and your blood pressure.

An imaging test may also be performed to quantify the degree of blood flow to the heart. One option is an echocardiogram, a noninvasive test that involves placing an ultrasound probe on your chest to create a moving image of your beating heart. Restricted blood flow in the heart's arteries changes the movement of the heart, which an experienced echocardiographer can detect.

Another option is a nuclear perfusion test, which entails injecting a radioactive substance called a tracer into a vein. The tracer then travels through your blood to your heart. A special camera that records the radioactive particles emitted from the tracer circles around the heart, taking images from multiple angles. A computer then combines these images to create a detailed picture of the blood flow to the heart.

In certain situations, if the source of your symptoms remains unclear, a physician might order a computed tomography angiography (CTA) scan. For this test, you receive an injection of a contrast dye into your arm or hand. The dye "lights up" in an image to reveal a three-dimensional view of your heart's arteries, courtesy of multiple rapid-fire x-rays taken during the scan.

Sometimes, even after all the testing, doctors don't know for certain what's causing your chest pain. "If that's the case, it's still worth asking the doctor what his or her best guess is, because that will help you determine what next steps to take," says Dr. Kosowsky.

Tightness, pressure, squeezing, stabbing, or dull pain, most often in the center of the chest Pain that spreads to the shoulders, neck, or arms Irregular or rapid heartbeat Cold sweat or clammy skin Lightheadedness, weakness, or dizziness Shortness of breath Nausea, indigestion, and sometimes vomiting

Heart disease is the primary cause of illness and death in the United States.

• 50 000 000 patients have hypertension

• 7 600 000 patients suffer a myocardial infarction each year

• 4 900 000 patients have been diagnosed with congestive heart failure1

Because improved detection of heart disease can save lives, blood tests have been used for approximately 50 years to detect substances that are present in the blood that indicate either disease or a future risk of the development of a disease (Table). Blood tests detect substances that normally are not present or measure substances that, when elevated above normal levels, indicate disease.

Available Blood-Based Tests for Heart Disease

Substance Detected by Blood TestPatient SymptomsIndications of Elevations

BNP indicates B-type natriuretic peptide; pro-BNP, N-terminal pro–B-type natriuretic peptide; HDL, high-density lipoprotein; and LDL, low-density lipoprotein.
Cardiac troponins (I and T)	Chest pain or potential heart attack	Injury to the heart
Ischemia modified albumin	Chest pain or potential heart attack	Possible diminished blood flow to the heart
Natriuretic peptides (BNP and pro-BNP)	Shortness of breath; possible heart failure	Probable congestive heart failure
Lipids (cholesterol, HDL, LDL)	Current or future risk of atherosclerosis	Increased risk of atherosclerosis
C-reactive protein	Current or future risk of atherosclerosis	Increased risk of cardiac events
Lipoprotein phospholipase A2	Current or future risk of atherosclerosis	Increased risk of cardiac events

Tests to Detect Heart Attacks

Patients presenting to the emergency department with chest discomfort will have an initial assessment for a possible heart attack (myocardial infarction). Electrocardiograms (ECGs or EKGs) are used in the evaluation of patients with chest discomfort but can be normal or not diagnostic in patients with a myocardial infarction. Thus, blood will be obtained to check for any heart damage that can be indicated by abnormal protein levels in the blood. The specific proteins that are the subjects of these blood tests include:

• Creatine kinase (CK)

• Creatine kinase-MB (CKMB)

• Myoglobin

• Cardiac troponin I or cardiac troponin T

These proteins are normally present within the heart cells and are released into the blood after a heart attack. Their presence in the blood can indicate heart damage. However, some of these proteins (CK, CKMB, and myoglobin) are also found in other muscles. Thus, these proteins are not specific to the heart, and elevated levels within the blood can be caused by problems with other muscles in the body.

A newer blood test (designed to detect cardiac troponin) is both more sensitive and more specific for heart damage. Cardiac troponins are found only in the heart. Depending on the hospital, either troponin I or troponin T is measured; in general, both work equally well. Current guidelines recommend that several measurements be obtained over a period of 8 to 12 hours after admission. Because there is a lag from the onset of heart damage to appearance of troponin in the blood, serial monitoring is important to avoid missing a heart attack. Patients with elevated cardiac troponin blood levels have likely suffered heart damage and are at increased cardiac risk. A lack of troponin (or any of the other proteins mentioned above) does not demonstrate an absence of heart disease, only the absence of heart damage. Further testing is necessary after the blood testing to determine if the chest discomfort is a warning sign of a heart attack (see also the Cardiology Patient Page by Ornato and Hand. Warning signs of a heart attack. Circulation. 2001;103:e124–125). This testing may occur in the hospital or in your doctor’s office.

Another test has been recently released for use in patients who present to the emergency department with chest pain. Ischemia modified albumin (IMA) is indicated for use in patients who are felt by their doctors to possibly be experiencing warning signs of a heart attack (ischemia). This test measures changes that may occur to albumin when ischemia has occurred. The Food and Drug Adminstration has cleared this test for excluding ischemia in patients with negative troponins and normal ECGs. However, patients without evidence of ischemia can also have high levels of IMA. Thus, patients with elevated levels of IMA require further testing to determine whether a problem exists.

Tests for Heart Failure

Heart failure is one of the leading causes of illness in the United States and the primary reason for hospital admission for patients over 65 years of age. Heart failure is an inability of the heart to pump a sufficient amount of blood to the body. The most common cause is a weakened heart muscle (usually caused by repeated heart attacks). The diagnosis of heart failure is made on the basis of the patient’s presentation and confirmatory tests.

New blood tests also assist physicians in the diagnosis of heart failure. These tests measure substances called natriuretic peptides, which are produced in increased amounts by the heart in response to congestive heart failure. These natriuretic peptides assist in the body’s response to heart failure by lowering the pressure in the lungs and increasing the flow of urine. Tests for 2 kinds of natriuretic peptides are currently available for the diagnosis of heart failure: BNP (B-type natriuretic peptide) and pro-BNP (N-terminal pro–B-type natriuretic peptide). Blood levels of both of these substances become elevated in patients with congestive heart failure. Physicians most often use these tests to differentiate patients with congestive heart failure from those with lung (pulmonary) problems. Patients without elevations are very unlikely to have a cardiac cause of their shortness of breath. These levels rise and fall rapidly in response to changes in the degree of congestive heart failure. It is hoped that serial measurements of natriuretic peptides over several days will allow physicians to adjust medical therapy for congestive heart failure so that it is more accurate.

Detection of Future Cardiac Risk

Heart attacks and heart failure are usually the end result of blockages forming in the arteries of the heart caused by atherosclerosis. It has been recognized for over 4 decades that elevations in lipids, especially cholesterol, form a potent risk for future heart disease. Measurement of levels of total cholesterol as well as low-density lipoprotein (LDL, also known as “bad cholesterol”), high-density lipoprotein (HDL, also known as “good cholesterol”), and triglycerides are critical for cardiac risk factor management. Attention to diet, exercise, and drug therapy has been shown to improve lipid levels and lower risk. However, approximately one-third of patients who present with heart attacks have normal cholesterol levels. Clearly, in such patients, other factors are responsible.

Attention has been focused on a blood test that measures the level of C-reactive protein (CRP). CRP is a marker for inflammation, and atherosclerosis has an inflammatory component. Patients with elevated levels of CRP have an increased risk for heart attack, stroke, sudden death, and vascular disease. Physicians are beginning to add the measurement of blood CRP levels to other measures of risk to recommend potential options to reduce risk.

The level of CRP has been shown to correlate with future risk as follows:

• CRP level less than 1: lowest risk

• CRP levels of 1 to 3: intermediate risk

• CRP greater than 3: highest risk

There are several non-drug therapy ways to lower CRP, and all patients with elevated levels of CRP should try to incorporate these modifications. These include weight loss, diet, exercise, and smoking cessation. Diabetes can also increase levels of CRP, and patients with elevations of CRP should be tested for diabetes. Some drugs, particularly aspirin and cholesterol-lowering drugs (especially statins), have been shown to decrease CRP levels. Patients with other risk factors and elevations of CRP may have their therapy adjusted to compensate for the CRP elevations. At present, it is not recommended that patients with CRP elevations but no other risk factors be placed on drug therapy; it is not yet known if drug therapy to lower CRP lowers future risk of heart disease (see also the Cardiology Patient Page by Ridker. C-reactive protein: a simple test to help predict risk of heart attack and stroke. Circulation. 2003;108:81–85).

Finally, another test (the PLAQ test) has just been released that measures the level of lipoprotein phospholipase A2 (Lp-PLA2). Lp-PLA2 generates oxidized molecules within the blood vessel wall that are more prone to lead to both atherosclerosis and irritability of the atherosclerotic plaque. Elevations in the levels of Lp-PLA2 have been shown to indicate greater risk of plaque formation and rupture independent of the levels of either lipids or CRP. Patients with elevated levels of Lp-PLA2 seem to be at a greater risk of cardiac events. Many of the therapies listed above for the treatment of elevations of CRP are thought likely to also help with elevations of Lp-PLA2.

Footnotes

References

• 1 American Heart Association. Heart disease and stroke statistics – 2003 update. Available at: //www.americanheart.org/downloadable/heart/10590179711482003HDSStatsBookREV7-03.pdf. Accessed December 19, 2003.Google Scholar
• 1. American Heart Association. Circulation: a journal of the American Heart Association. Available at: //www.circulationaha.org. Accessed December 19, 2003.Google Scholar
• 2. American Heart Association web site. Available at: //www.americanheart.org. Accessed December 19, 2003.Google Scholar
• 3. Mayo Clinic web site. Available at: //www.mayoclinic.com. Accessed December 19, 2003.Google Scholar
• 4. Cleveland Clinic web site. Available at: //www.clevelandclinic.org. Accessed December 19, 2003.Google Scholar
• 5. Brigham and Women’s Hospital web site. Available at: //www.brighamandwomens.org. Accessed December 19, 2003.Google Scholar
• 6. WebMD. Available at: //www.WebMD.com. Accessed December 19, 2003.Google Scholar

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Two patients, aged 3 days (weight 2 kg) and 40 years (weight 80 kg) underwent gadolinium-enhanced magnetic resonance angiography (MRA) because of diagnostic uncertainty. The newborn infant was antenatally diagnosed with truncus arteriosis. Postnatal echocardiography confirmed the diagnosis. It was thought that the branch pulmonary arteries were confluent (type II); however, an MRA was requested to clarify this. The MR angiograms (Figure 1) showed the right pulmonary artery arising from the left side of the ascending aorta. The left pulmonary artery, which was disconnected from the right pulmonary artery, was supplied by the patent ductus arteriosis arising from the underside of the aortic arch. The MRA findings were confirmed at surgery.

Figure 1. Three-dimensional reconstructed MRA of the new-born patient. Blue shows the superior vena cava, pulmonary veins, right and left atria, and right ventricle. Red shows the aorta and main branches, right pulmonary artery (RPA), and left ventricle. Orange shows the patent ductus arteriosis and left pulmonary artery. A, Posterior view. B, Posterior view without the descending aorta showing the disconnected left and right pulmonary arteries. C (anterior view) and D (left lateral view) show the RPA arising from the left side of the ascending aorta. Reconstruction was performed off-line. Heart and major vessels were segmented in a semi-automated manner (seeding, threshholding, and eventual manual editing) using Analyze (Mayo Clinic). The segmented data sets were then rendered and vizualised using vtk (Schroeder W, Martin K, Lorensen B. The Visualization Toolkit. 2nd ed. New Jersey: Prentice Hall, 1998).

The adult patient had been diagnosed with pulmonary atresia and ventricular septal defect in childhood and had been managed conservatively. Nevertheless, he began to experience reduced exercise tolerance and became cyanotic. An MRA was requested to outline the source of his pulmonary blood supply. The MR angiograms (Figure 2) showed a large left pulmonary artery arising from the left side of the ascending aorta, with pruning of its distal branches. On the right side, the patient had a number of small pulmonary arteries that were not supplied by the aorta or its main branches. A double aortic arch was also discovered. The patient is being assessed for heart-lung transplantation.

Figure 2. Maximum intensity projections of the adult patient MRA. A, Anterior view. B, Left anterior oblique view. A large left pulmonary artery arises just above the aortic valve with pruning of its distal vessels. There is a double aortic arch with both arches being widely patent into the descending aorta. Few small pulmonary vessels are present on the right side.

The editor of Images in Cardiovascular Medicine is Hugh A. McAllister, Jr, MD, Chief, Department of Pathology, St Luke’s Episcopal Hospital and Texas Heart Institute, and Clinical Professor of Pathology, University of Texas Medical School and Baylor College of Medicine.

Circulation encourages readers to submit cardiovascular images to the Circulation Editorial Office, St Luke’s Episcopal Hospital/Texas Heart Institute, 6720 Bertner Ave, MC1-267, Houston, TX 77030.

Footnotes

January 27, 2004
Vol 109, Issue 3