Heart function including ejection fraction (EF) is important in clinical practice because it is related to prognosis. Whether the patient suffers from valvular heart disease or ischemic heart disease, a measure of heart function including ejection fraction (EF) can predict future clinical outcome and assist in risk stratification. Several approaches to detect patients at risk for cardiac events have proven to be of value. These include exercise testing, assessment of exercise capacity, and determination of left ventricular function.
Heart function including ejection fraction (EF):
Ejection fraction (EF) is a percent measurement of how much blood the left ventricle (LV) pumps with each contraction. The left ventricle (LV) does not empty out with each contraction. Normally the left ventricle (LV) ejects between 50% and 70% of the blood it contains. Below is an echocardiogram of a patient with a normal ejection fraction (EF= 55-60%).
The stroke volume (SV) is calculated by taking the amount of blood estimated when the left ventricle is completely filled (end diastole= LVEDV = 131 ml) and subtracting the amount of blood remaining within the left ventricle when it is finished contracting (end-systole = LVESV = 55 ml). The derived stroke volume (SV = 76 ml) is then divided by the amount of blood contained when the left ventricle is completely filled (LVEDV = 131 ml) to obtain the ejection fraction (EF = 58%) (diagram below).
Patients with normal heart function and ejection fraction (EF) usually feel comfortable with exercise activity unless the patient is deconditioned and suffers from being sedentary. Another condition where patients can be suffering from shortness of breath but have a normal ejection fraction is called diastolic heart failure. The patients with this condition usually have a left ventricle with thicker and stiffer walls. The heart holds a smaller amount of blood and cannot meet the body’s needs. This is also called “heart failure with preserved ejection fraction” (HFPEF). Several elderly patients with hypertension and diabetes can be affected by this condition. Below is an MRI study followed by an echocardiogram of a patient with severe left ventricular hypertrophy and normal heart function and ejection fraction. You can see how such a thickened myocardial wall can lead to increased in stiffness and reduced compliance and elevated pressure within the left ventricle during diastole or when it is trying to fill.
A borderline heart function and ejection fraction (EF) (41-49%) can result from a cardiomyopathy, valvular heart disease or ischemic heart disease (pts with coronary artery blockages). This usually leads to shortness of breath during activity. Below is a patient with coronary disease and critical stenosis of the proximal LAD. There is hypokinesis or reduced contraction in the distal anterior wall and apex. This also contributes to a mildly reduced heart function and ejection fraction at 49%. This patient experienced shortness of breath running up a hill.
The MRI below was performed at Brookwood Baptist Medical Center at Princeton. The patient suffered an anterior myocardial infarction few months prior. Dr Bracer obtained the images using a 1.5T GE MRI system. We can see some hypokinesis of the anterior wall and overall mildly reduced heart function and ejection fraction.
A reduced heart function and ejection fraction (EF) (<40%) usually manifests as fatigue and shortness of breath, sometimes even at rest. It is usually a manifestation of a cardiomyopathy and it can be ischemic or non-ischemic. Below is an example of a patient with severe non-ischemic cardiomyopathy and ejection fraction of less than 20%. The echocardiogram depicts an enlarged and weakened left ventricle.
Below is an MRI of a patient who suffered an extensive myocardial infarction. The patient presented as an anterior STEMI with total occlusion of the LAD. Despite early intervention and PCI with coronary stenting of the LAD, the patient suffered extensive damage with a large scar involving the distal antero-septum, apex and distal antero-lateral walls (yellow arrow). Notice the thinning and absence of contraction of these walls. The global function is severely reduced and there is evidence of clinical heart failure with bilateral pleural effusions (blue arrow). In addition, there is a small pericardial effusion surrounding the right ventricle and in part the right atrium (red arrow).
Heart function assessed by measuring left ventricular volumes.
In patients with valvular insufficiency or ischemic heart disease, the enlargement of the left ventricular volume (particularly end-systolic LVESV) can be related to a poor prognosis. For this reason, serial measurements of left ventricular size and function are used to follow these patients so that surgical intervention can be performed prior to irreversible damage to the heart is done. Similarly, patients recovering from a large myocardial infarction can develop adverse left ventricular remodeling leading to irreversible damage and the development of clinical heart failure. Below is an MRI study of a patient who sustained a large anterior myocardial infarction. At baseline (upper image), the left ventricular end-diastolic volume (LVEDV) measured 250 ml, the end systolic volume (LVESV) 173 ml with reduced heart function and ejection fraction (EF) 30%. One year later, another MRI study (lower image) was performed on the same patient and revealed an enlargement of left ventricular size with LVEDV of 314 ml, LVESV of 241 ml and a weakening of the heart function and ejection fraction EF of 23%. This is called adverse remodeling and has a poorer prognosis in patients after a myocardial infarction.
Heart function assessed by analyzing regional left ventricular function.
Assessing regional function or wall motion of the left ventricle allows for the detection of ischemic heart disease (patients with coronary artery blockages). It can also detect areas of myocardial fibrosis or scarring. Regional wall motion abnormality has been linked to prognosis. In the Strong Heart study for example, men older than 60 years of age with segmental wall motion were found to have a 2.5 fold increase in coronary vascular events.
The normal wall motion of the heart is represented by a normal wall thickening during the contraction of the left ventricle. Regional heart function abnormality can be described as a weakening of the contraction of some parts of the heart muscle. This does not always lead to weakening of the global heart function. It usually depends on the degree and the extent of the heart walls involved. Below are two MRI studies depicting extensive antero-apical scars (yellow arrows). These patients suffered anterior STEMIs caused by occlusion of the proximal LAD or widow maker. This results in a large area of myocardial damage with thinning and absence of contraction (akinesis) of the walls. The area of damage is large and affects the global function of the heart. The left ventricle is enlarged and the heart function and ejection fraction EF is severely reduced (<20%).
Experimental studies have shown that a reduction of coronary blood flow resulting from transient occlusion or progressive constriction of a coronary artery results in the segmental wall motion abnormality. Studies by Gould have shown that such a reduction of coronary blood flow at rest is not present until the severity of the stenosis or narrowing exceeds 85%. Restoration of normal flow is associated with an eventual return to normal wall motion. In patients with coronary artery disease and without a previous myocardial infarction, segmental wall motion abnormality increases with decreased coronary blood flow. Myocardial perfusion using nuclear imaging technique correlates well with segmental wall motion analysis. In patients without a prior myocardial infarction, resting or stress-induced wall motion abnormalities, occur almost exclusively in regions with jeopardized perfusion. These regional abnormalities are potentially reversible when treated with myocardial revascularization (PCI or CABG). Recovery of segmental wall motion is seen also in patients treated after a myocardial infarction. Below is a patient treated with a non STEMI myocardial infarction. The wall motion abnormality (akinesis or absence of thickening) (yellow arrow, upper image) was restored toward normal (hypokinesis, yellow arrow, lower image) by reopening his artery using percutaneous coronary intervention and potentially by the stem-cell therapy that he may have received as part of the Athersys trial.
If you like the information in this article, make sure you read: Can heart attack damage be reversed? Stem cells in the treatment of a heart attack: a non-STEMI. Surviving a heart attack; the Big one and Stem cells in the treatment of Heart Failure.
We would like to acknowledge the expertise of Jay Roberson at VitalEngine and Dr Ricardo Bracer for the MRI imaging.
Comments are purely for informational purposes and are not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Disclaimer
Dear Alain
Many thanks for the great article.
I recently had an heart echocardiogram and the only parameter that bothers me is LVIDD in 59 mm other parameters completely fine (EF 70 % ,no problems with any of the valves and normal wall function).Am very physically active (basketball, running and weightlifting )
My question is should I be really concern with this LVIDD 59 mm ?
am 178 cm tall and weigh in 84 kilograms
Your answer would be greatly appreciated
Thank you for your comments. You are referring to internal dimension of the left ventricle when it is completely filled (LVIDD). At 59 mm, it can be considered at upper limit of normal to slightly increased. With the function being completely normal (EF = 70%) it is likely a healthy and physiological adaptation to the mostly endurance-type of exercise you are doing. Morganroth has described an increased in LV internal dimension and mass in endurance athletes. This cardiac adaptation to exercise training encompasses morphological and functional changes referred to as “athlete’s heart”.
Hello Alain,
Thank you for the article.
There is something that I didn’t understand very well. Is it possible for someone to have an EF of 20% with a stenosis of 70% in the LMCA? Or can we say that an EF of 20% can’t be caused with a stenosis that is less than 85%?
I would be very happy to get your opinion on that.
Best regards
Thank you for your help. The doctor also said he has acemetric out flow tract w/o dynamic gradiant. What does that mean. Thank you in advance.
It means there is some thickening of the heart muscle however it is not leading to any significant obstruction and will likely need monitoring only.
you can follow our twitter at @MustafaAhmedMD
Excellent article.
I have a long standing stable moderate 2-3/4 aortic regurgitation. I I am a 58 year old male, My last echo showed my LVEDD was 155mls and my ejection fraction in the range of 50-55. I have mild LV and atrial enlargement. My cardiologist said my result was satisfactory and to have another echo in a year.
Generally speaking is a LVEDD of 155 mls and a EJ of 50-55 still in the normal range.
Reference to LVEDD should be LVEDV- apologies
Hello Doctors – I recently had a stress test performed and below are the results. The week before, I had an electrocardiogram done for the first time in 5 years. I am a 60 yr old male, and had a heart attack in Nov 2011, and a CABG in March 2012. Since that time, I have never had issues of any kind, and visit the doctor regularly. Evidently, this echo is very similar to the last one years ago.
The doctor is recommending an ICD; which he also recommended 5 years ago.
If time ever permits, a review and short reply in the future would be greatly appreciated.Thanking you in advance for taking time to read this information,
Miles G. Arena
NM MYOCARDIUM PERFUSION STRESS AND REST – DetailsPrinter friendly page–New window will open
About This Test
Details
Study Result
Impression
1. No evidence of myocardial ischemia.
2. Large sized, severe fixed defect involving the inferior/inferolateral
left ventricular wall in the RCA and LCX vascular territory. Additionally,
a small sized and mild severity cardiac apical defect in the LAD vascular
territory. These findings suggest sequelae from a prior MI.
3. LVEF 27-28% with diffuse hypokinesis and severe hypokinesis of inferior
and inferolateral walls.
I, Samuel Bezold, MD., have reviewed this study and agree with the above
report.
Narrative
* * * * * * * * ORIGINAL REPORT * * * * * * * *
EXAM: NM MYOCARDIUM PERFUSION STRESS AND REST
HISTORY: 60-year-old male with drop in LVEF Prior revascularization (either
PTCA or CABG)
COMPARISON: None.
Procedure: Myocardial perfusion exam was gathered with a one-day protocol.
At rest patient received 16.48 mCi of technetium 99m Myoview and a gated
SPECT was obtained.
Then, patient received a 0.4 mg Lexiscan infusion followed by intravenous
injection of 41.6 mCi of technetium 99m Myoview, a gated SPECT scan was
obtained.
COMPARISON: None.
FINDINGS:
Pre Stress Test vitals are: BP 135/84?HR 53?Resp 16?O2 sat 99
?
Injection vitals are: BP 126/91?HR 67?Resp 17?O2 sat 99
?
Recovery vitals are: BP 123/78?HR 61?Resp 16?O2 sat 99
There is a large size and severe fixed defect involving the
inferior/inferolateral cardiac wall in the inferior and inferolateral walls
from apex to base.
In addition, there is a small size and mild severity fixed defect involving
the true apex.
The end-diastolic volume is at rest 148 mL and stress 133 mL.
The LVEF at rest is 27 % and stress 28 %.
Global hypokinesis noted with severe hypokinesis of inferior and
inferolateral walls.
Component Results
There is no component information for this result.
General Information
Collected:
12/05/2018 1:14 PM
Resulted:
12/05/2018 5:02 PM
Ordered By:
Syed A Gilani, MD
Result Status:
Final result
This test result has been released by an automatic process.
Hello. My 69 yr old mother was in the process of getting lung and heart clearance for a hip replacement in her near future. Long story short, ECG showed problem with left bundle branch. Sent to cardiologist and stress test performed. Results showed NORMAL ischemia, but 14% ejection fraction. No symptoms. No high BP. No swelling in the legs, feet or ankles. No significant shortness of breath, at least nothing that we thought unusual for her age and being about 40 pounds overweight. Mild asthma. Managed high cholesterol. Fatigue, yes. No known heart palpitations or discomfort. She is scheduled for ECHO in two days. I’ve spoken to two of my nurse friends who’ve both worked years of cardiac and they both find it strange that she doesn’t really symptoms and that she was told her ischemia was normal. How is this? I know 14% EF is horrible. I’m scared to death from what I’m reading about all of this. Any advice? Is this too advanced to be treated? Or is it basically going to end up being a diagnosis of cardiomyopathy? Can stress tests (she didn’t have the treadmill one because of her hip) possibly give inaccurate readings of EF? Otherwise why did they tell her that her ischemia was normal. Thank you so much. I’d appreciate any information on this. J
I AM AN HEART PATIENT WITH EF WELL BELOW 10%.
TELL ME OR GUIDE ME TO WHAT SHOULD I DO
You need to be on an optimal medical treatment regimen for heart failure
You need ideally to be under the care of a dedicated advanced HF specialist
You can follow our twitter at @MustafaAhmedMD
Disclaimer: The comment response is opinion and in no way affiliated with my employer. It is a vague response that is not to be used as direct medical advice and in no way should replace the opinion of a medical provider.
I am 31 years old, 30lbs overweight, have years of eating bad/junk food, and suffer from obstructive sleep apnea (undiagnosed for 20+ years until now). I recently went for a “myocardial perfusion” (nuclear rest and stress test), and it said “Normal.” However it also says that my LVEF was 53% at rest, and 47% with stress (running 10mins at 94% of max predicted heart rate). Why is it so much lower under stress? Is it just because I don’t do a lot of cardio, or is that a problem? I see that a percentage or two in difference is normal, but this is 6%! Is this normal? It also says that “gated images demonstrate mild distal septal hypokinesis (non-specific).” What does that mean? It also says “further assessment with echocardiography is suggested.” Does that mean the echo have the final word? The cardiologist I was seeing told me that I am fine and healthy as I could be, and to just lose the excess weight and start exercising. But I get the idea that because I’m “young” that he just assumes everything is okay. Can someone tell me what this all means? Can I improve my EF?
Its a good question and you should certainly ask it. It would not be unreasonable to perform a stress echo in this circumstance to correlate.Ask why does your heart function go down instead of up when under stress. I suspect its reporting error if they aren’t worried, nevertheless it will be nice for you to have reassurance.
You can follow our twitter at @MustafaAhmedMD
Disclaimer: The comment response is opinion and in no way affiliated with my employer. It is a vague response that is not to be used as direct medical advice and in no way should replace the opinion of a medical provider.
Brief summary..I have mild to moderate mitral regurgitation due to leaflet thickening. I have routine echos and my EF% has went down the last 2 years. It used to always be 60-65%. Then in 2018 it was 55-60% and now my echo this year says 50-55% and that is in the normal low. It also mentions mild valvular arotic stenosis, which is new. Should I be concerned about this decrease in EF%? My cardiologists is out of town and I can’t see her for 2 weeks so I was hoping for some advice.
Have you found out your issue as I have similar? any info would be great.
I learned much from your article. I have mitral valve insufficiency and have been experiencing shortness of breath and fatigue for a while. Saw a pulmonary doctor, she did Chest CT and Pulmonary Function testing-nothing wrong there. Said possibly I had pulmonary hypertension? At any rate, saw my cardiologist for regular annual check up. Had a PET scan done, and am wondering about the EF. They seem high at resting and stress. Here are the results and any insight on the EF numbers would be appreciated. Scheduled for echocardiogram on 02/26/2020. Reason for Appointment
1. PET – SP
Vital Signs
Wt 150 lbs, Ht 61 in, BMI 28.34 Index, BP 106/66 mm Hg, HR 70 /min, Oxygen sat % 99 %.
Examination
Stress Test:
Nurse: Bill Farmer, RN.
Technologist: Robin Jones, CNMT.
Ordering Physician: Dr. Pasupuleti.
Interpreting Physician: Dr. Pasupuleti.
Study Quaility: Good .
Procedure: Cardiac Positron Emission Tomography: The patient underwent a stress test utilizing 0.4mg of IV Lexiscan infusion over 10-15 seconds. The patient experienced stomach pressure during the procedure and received no medications. The patient had a myocardial perfusion imaging performed using same day imaging protocol, with the injection of 30.0 mCi of Rubidium-82 at 30 seconds into Lexiscan infusion, and the injection of 30.0 mCi of Rubidium-82 at rest. Imaging was performed by gated resting and gated stress technique ,.
Data Summary:
TID: 1.06
Resting EDV: 47
Resting ESV:5
Resting EF:88%
Stress EDV: 47
Stress ESV:4
Stress EF: 92%
Baseline BP:103/66
Baseline HR:70
Peak Stress BP:76/46
Maximum HR Achieved:94 .
Exercise Level: N/A .
*Pre-Stress EKG: Normal Sinus Rhythm .
*Stress EKG: Normal Sinus Rhythm , No ST changes.
*Arrhythmias observed None .
*Resting Left Ventricle size Normal .
*Peak Stress Left Ventricle Size Normal .
*Right Ventricle appears Normal .
*Post stress global LVEF is Normal .
*FINDINGS:
1. small reversible myocardial perfusion defect noted in the basal anterior wall (area of reversible ischemia 3%).
2. Normal wall thickening.
3. Normal LV systolic function..
*CONCLUSIONS:
1. small reversible myocardial perfusion defect noted in the basal anterior wall (area of reversible ischemia 3%). Low risk stress test.
2. EF 88%
3. Normal LV systolic function..
Assessments
1. Anginal equivalent – I20.8
Treatment
1. Anginal equivalent