What do elevated cardiac enzyme levels mean?
Share on PinterestMedication is often prescribed following a cardiac enzyme test to prevent future heart attacks or treat heart damage.
A doctor will likely order other tests in addition to a cardiac enzyme test. This is because other factors besides heart attacks can cause high cardiac enzyme levels.
These tests may include the following:
- other blood tests
- chest X-ray
- stress test
- heart CT scan
If the reason for the elevated cardiac enzymes is not a heart attack, a doctor may treat whatever condition is causing the enzyme levels to be elevated. The doctor may also suggest that a person makes healthful lifestyle changes to keep the heart working as well as possible.
If a doctor determines that a heart attack caused the elevated cardiac enzymes levels, the person will require treatment in the hospital with medications or surgery to restore blood flow to the heart.
Doctors may also prescribe the following medications for a person who has had a heart attack:
- drugs that dissolve blood clots, known as thrombolytics
- blood thinners, such as heparin
- antiplatelet agents to keep blood clots from getting bigger
- ACE inhibitors
- pain medications
A doctor may recommend that a person who has just had a heart attack should have surgery in addition to treatment with medications. Doctors may suggest coronary stenting or coronary artery bypass surgery.
During this procedure, a doctor will guide a long thin tube through an artery to find blockages. When the doctor locates a blockage, they will use a tool on the end of the tube to open the blocked artery and insert a metal stent to keep the artery open.
The person who had the heart attack is normally awake or under light sedation. People require less recovery time after this procedure than after a coronary bypass.
A coronary artery bypass is major surgery that may occur immediately following a heart attack, or shortly after to give the heart a chance to recover.
During a coronary artery bypass, a doctor will remove a portion of the blocked artery and stitch the artery back together.
A 70 year old woman with history of diabetes type 2, hypertension, gout and polymyositis was admitted to our hospital. She presented to the ED with symptoms of light-headedness, dizziness and pre-syncopal episode earlier in the morning, along with a sudden onset of generalized body weakness. She denied any loss of consciousness or palpitations before presentation to the ED. She also complained of sharp pain in the upper right abdominal quadrant, verbally stated as 10/10 in pain, non-radiating, for 4 days duration, with associated nausea. Patient recently had right kidney surgery with a nephrostomy tube draining 5-10 ml of blood as well for the past 4 days. She had past history of nephrolithiasis one year ago, leading to severe right-sided hydronephrosis (Figure (Figure11).
Deltoid muscle biopsy from patient with frozen SDH/COX stain showing COX negative fibers with inflammatory myopathy-diagnosis: polymyositis/ cytochrome oxidase overlap syndrome.
Home medications were as follows: Cymbalta, 60 mg, oral, daily; Nexium 40 mg, oral, daily; Acetaminophen with Tramadol, 325 mg, oral, every 6 hours as needed; Glipizide 2.5 mg, oral, daily; Amlodipine 10 mg, oral, daily; Phenazopyridine 200 mg, oral, three times a day; Indomethacin 50 mg, oral, daily; Enablex 15 mg, PO, daily, and Methotrexate 10 mg, oral, weekly. The patient has a history of hypertension for 50 years, type II diabetes for 2 years and polymyositis for the past 5 years. Patient had no family history of cardiovascular disease, heart attack or stroke.
Admission vitals: Temperature 97.8°F, pulse rate of 80 beats-per-minute, blood pressure of 87/61 mmHg which improved to 130/83 mmHg after receiving intravenous fluids, oxygen saturation of 98% on room air. Physical exam: patient was awake and alert, with only pertinent findings of right upper quadrant tenderness. Neurological exam showed normal deep tendon reflexes, muscle strength was 3/5 bilaterally in the legs and 4/5 bilaterally in the arms, with a strong grip. The remainder of the physical exam was normal. Laboratory findings at admission: complete blood count, chemistry panel, magnesium, phosphorus, and lactate levels all within normal limits. Urine analysis showed moderate bacteria, significant proteinuria with nitrates and leukocytes present. Patient had glycosylated hemoglobin A1c of 6.4.
After admission to the internal medicine unit, the patient was examined to rule out causes of sepsis including any type of upper or lower urinary tract infection that could lead to the patient’s presentation. Blood and urine cultures were obtained which showed no growth at 3 days. Computer Tomography (CT) of the abdomen showed a small right kidney with reduced cortex thickness and with small amount of perinephric fluid accumulation with no signs of hydronephrosis. Patient was started on Imipenem to cover for pyelonephritis, and the right upper quadrant pain resolved in 4 days with stable vital signs.
To assess if the symptoms of lightheadedness, sudden generalized weakness and pre-syncopal episode were due to a cardiac cause (e.g. silent myocardial ischemia) or transient ischemic attack, cardiac evaluation, along with doppler ultrasound of the carotid arteries and CT of the brain, were performed. CT showed no signs of ischemia or hemorrhage, and an electrocardiogram (ECG) from the day of admission showed left axis deviation and signs of possible old anterior infarction with associated ST-T/ T wave abnormalities, unchanged compared to the ECG from a year ago. Carotid doppler was normal with no signs of stenosis. Cardiac enzymes results are shown in Table Table11.
Comparison of creatine kinase (CK), creatine kinase- cardiac muscle (CK-MB) and Troponin T showing no changes during hospital stay from baseline
Normal reference values (may change depending on provider): CK: 38-176 U/L; CK-MB: 0-3 ng/mL; Troponin T: <0.01 ng/mL; CK-BM/Total CK: <1%.
From patient’s admission one year ago, CK was 484 U/L, and CK-MB was 12.3 mg/mL, indicating elevated CK and CK-MB were due to polymyositis muscle breakdown. Further laboratory findings showed myoglobin 186.2 ng/mL (normal= 0-85 ng/mL), haptoglobin 337 mg/dL (normal= 41-165 mg/dL), with normal blood uria nitrogen (BUN), creatinine and thyroid function. Though there were no acute changes on ECG, the patient is at increased risk of coronary artery disease with a stress test pretest probability of 10%-90% risk due to her age and history of diabetes and hypertension. To further assess causes of the abnormal ECG, 2D echocardiogram of the heart was obtained which showed left ventricle ejection fraction of 65% to 70% with normal atria and ventricles. There was mild mitral regurgitation and mild tricuspid regurgitation with right ventricle systolic pressure of 43 mm, which was consistent with mild pulmonary hypertension. To ensure there were no signs of myocardial ischemia a nuclear stress test was performed instead of the traditional stress test due to the patient’s muscle weakness. The nuclear stress test measures blood flow to the myocardium at rest and during exercise, simulated with the use of medications. The study showed normal myocardial perfusion with normal left ventricular centrality at rest, and an ejection fraction of 54%, all within normal limits. Though all the tests performed indicated there were no signs of myocardial ischemia, we decided to obtain a Troponin I level, which was <0.05 ng/mL (normal 0.00-0.14 ng/mL). By performing all these tests we had concluded that there was no cardiac cause for the increased CK-MB and Troponin T, reflecting that patient’s Troponin T elevations must have been due to polymyositis.
Cardiac Enzyme Elevations After Stroke: The Importance of Specificity
strokeahaStrokeStrokeStroke0039-24991524-4628Lippincott Williams & Wilkins ResponseAy Hakan, MD, Arsava Ethem M., MD, and Saribaş Okay, MD01082002
We thank Drs Butcher and Parsons for their interest in our article. In the referred study,1 we serially determined cardiac enzyme levels including troponin T and CK-MB from day 1 to day 5 of stroke in 32 consecutive patients, 24 of whom had large middle cerebral artery territory infarctions, also including the insula. The study outlined a specific signature of cardiac enzyme changes, “normal troponin T along with elevated CK-MB.” Given that troponin T is a more sensitive and specific marker for minor myocardial injury, our results led us to two clinically important conclusions. First, CK-MB elevations after stroke are not cardiac in origin, and second, CK-MB falsely increases after stroke. The latter might be especially important for the diagnosis of acute coronary syndromes occurring within the acute phase of stroke. This is not a rare event and can occur in up to 9% of all stroke patients.2
Neurogenic influence on the heart is a well-known phenomenon with pathological proof of myocytolysis and electrophysiological proof of cardiac conduction abnormalities. The third proof, however, specific enzyme changes (subtle and gradual CK-MB elevations), is now in question. Indeed, the evidence linking human cerebral lesions to CK-MB elevations from a cardiac source is not concrete. Previous novel studies introducing CK-MB elevations after human cerebral injury fail to provide any direct proof of the heart as the cause of CK-MB elevations3–5; autonomic perturbations and elevated systemic catecholamine levels might have used sources other than the heart to cause the CK-MB elevations observed in these studies. The authors raise the issue that cardiac contribution to the CK-MB elevations observed in our patients (34% of all stroke patients) might still have occurred, especially in those with infarctions in the high-risk brain regions for myocardial injury. This assumption requires that underlying myocardial mechanisms that mediate troponin T release differ from those that mediate CK-MB release. Thus, neurogenic influences could increase CK-MB levels without altering troponin T. To our knowledge, there are no data compatible with this. In contrast, troponin T has been shown to be superior to CK-MB in both ischemic and nonischemic modes of myocardial injury.6,7 It seems more likely that if ever a cardiac contribution to the CK-MB elevations occurs, then troponin-T should also increase.
It is often problematic to identify the cause of cardiac perturbations and sudden deaths observed in patients with stroke. A concomitant coronary artery disease complicated by a coincidental plaque rupture triggered by stroke-related factors might be a cause. An accurate differentiation between the neurogenic and cardiogenic influences through the use of a serologic marker is the ultimate goal. Our study solves a piece of the puzzle by showing that CK-MB is not appropriate for this role. Drs Butcher and Parsons have delicately outlined the direction of future research in this field. While concurring with all, we should like to add that studies examining other cardiac-specific enzymes such as troponin I are also needed. Furthermore, these studies should be tailored with the capability to correlate cardiac enzyme levels with a more properly defined gold standard for neurogenic cardiac injury. Finally, they should not only enroll patients with isolated insular lesions, but also investigate unselected patients with various infarction patterns because the clinical importance of their results should have an impact in more general stroke populations.
Should I Worry About High Heart Enzymes?
What does it mean when your heart enzymes are high?
— Milly, South Carolina
High levels of cardiac enzymes can mean a number of things, but they often signal some type of damage to the heart. Enzymes are proteins that promote specific biochemical reactions within cells. Key enzymes that work within heart muscle cells include troponin (TnI, TnT), which helps control how the heart muscles contract, and creatine phosphokinase (CPK, CK), which is a critical player in the heart’s energy management process.
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Because cardiac enzymes generally operate within your heart, only low levels of these enzymes are normally found in your blood. But if your heart muscle is injured in some way — say, from a heart attack or even heart surgery — the enzymes then leak out of damaged heart-muscle cells, and their levels in the bloodstream rise. For this reason, if you’re having specific symptoms or have undergone certain procedures, doctors often test the level of your cardiac enzymes.
There are a number of reasons why cardiac enzyme tests might be ordered. If you’re having chest pain, shortness of breath, nausea, sweating, and abnormal electrocardiography (ECG) results, for instance, knowing your enzyme levels can help determine whether you are in the midst of a heart attack. Enzyme testing is also done to check for injury to the heart after some forms of cardiac surgery. During the recovery period following a heart attack or injury, such tests can also help determine whether a cardiac procedure or a medicine being used to dissolve a blockage (thrombolytic medicine) has successfully restored blood flow through a blocked coronary artery.
The results of these tests are not always completely clear-cut, however.
Because cardiac enzymes leak slowly into the bloodstream, high enzyme levels may not appear for six or more hours after the onset of a heart attack. For this reason, if someone is experiencing chest pain but their heart enzymes are normal, a heart attack cannot be completely ruled out. In such cases, repeated cardiac enzyme tests are normally conducted to confirm the diagnosis of a heart attack.
Additionally, because some heart enzymes are also found in other body tissues, such as the brain or skeletal muscle, their blood levels may rise when these other tissues are damaged.
Bottom line: You always need a doctor to analyze heart enzyme tests, and you may need more than one screening. To get a complete picture and determine the best treatment, your medical team will also take into consideration your symptoms, the findings from your physical examination, your electrocardiogram (EKG or ECG), and other tests. In most cases, high levels of cardiac enzymes are the result a heart attack — and measuring these enzymes is the gold standard for a heart attack diagnosis.
Learn more in the Everyday Health Heart Health Center.
What Are Elevated Heart Enzymes?
If your doctor told you that you have elevated heart enzymes, you might be wondering what that means. Heart enzymes are often measured if your doctor suspects heart damage, such as the kind that occurs after a heart attack.
When the heart becomes damaged, proteins become released in the blood known as cardiac enzymes. Measurable heart enzymes include kinase (CK) and a subtype of this enzyme called CK-MB.
CK is found in the heart, skeletal muscles, and brain. CK-MB is only found in the heart.
Measuring CK and CK-MB was the only way to measure a heart attack, but now doctors measure troponin as it reveals more about overall heart damage.
What Are the Causes Elevated Heart Enzymes?
There are several different causes for elevated heart enzymes, they include:
Heart diseases: Measuring heart enzymes is often done when a person complains of heart-related symptoms such as shortness of breath and chest pains. When the heart becomes damaged, enzymes from dying cells are leaked into the blood stream, which makes them measurable. Other heart diseases which can trigger elevated heart enzymes include heart failure, inflammation of the heart’s surrounding sac, inflammation of the heart muscle, and heart surgery.
Brain disorders: Lack of blood to the brain can trigger a stroke, which contributes to elevated heart enzymes. People who experience a stroke often may have an underlying heart condition which contributes to the stroke, causing the elevated enzymes.
Respiratory conditions: Certain lung disorders have been associated with elevated heart enzymes. The most common being pulmonary embolism – blood clot in the lung. When a blood clot travels to the lungs, the heart must overwork itself, which causes added stress and damage. This then results in the release of enzymes.
Kidney disease: High blood pressure and diabetes are contributing factors for kidney disease and having kidney disease increases the risk of heart disease. CK and CK-MB can be elevated in kidney disease patients even if they aren’t at risk for a heart attack. The kidneys are responsible for filtering the blood and removing excess enzymes, so if the kidneys are not working well, then there can be elevated enzymes in the body.
Severe infection: Sepsis – a severe blood infection – can trigger elevated heart enzymes because it affects all major organs including the heart and kidneys.
Muscle disorders: CK is present in skeletal muscle, so muscle disorders are associated with higher CK levels. Inflammatory muscle conditions can also trigger higher CK levels along with muscle injury, muscular dystrophy, and connective tissue disorders. Taking certain antidepressants and anti-fungal medications can also result in higher CK levels.
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