Can someone please help me understand my recent Stress test findings: Images show mild intensity small-sized defect, located in the distal anterior and apical wall. Rest images show no change of the defect compared to the stress images. This defect suggests infarction vs. artifact in the wall. Gated SPECT imaging demonstates abnormal septal motion of the distal anterior and apical wall. The left ventricular ejection fraction was calculated to be 56%.
I had a myocardial infarction 10 years ago and i had a an open heart surgery since then and now i am experiencing symptoms of stable angina and my angiogram is completely clear and the bypass is 100% success and all the tests are negative, can a thallium stress test be useful or it will not be conclusive because of the former heart attack
There is no clear scintigraphic or electrocardiographic evidence of prior myocardial infarction. The perfusion defect is in the distribution of the right coronary artery. There is no scintigraphic evidence of left ventricular dysfunction. Compared to the prior perfusion study of 09/29/09, the overall findings are similar.
It can also be used as a marker of myocardial infarction. Following a myocardial infarction, levels of LDH peak at 3-4 days and remain elevated for up to 10 days. In this way, elevated levels of LDH (where the level of LDH2 is higher than that of LDH1) can be useful for determining if a patient has had a myocardial infarction if they come to doctors several days after an episode of chest pain.
Check it with your Cartdiologist for the reason of increase in LDH.
This makes troponins a superior marker for diagnosing myocardial infarction in the recent past,. Troponin T lacks some specificity because elevations can appear with skeletal myopathies and with renal failure. For instance, troponin T will be high subsequent to heavy lifting
It is possible the heart cells were stunned from lack of oxygen for a short period of time, but when oxygenated blood is restored the cells usually begin to function normally.
I am a Vet so this Thallium stress test was performed at the VA. Test get posted quickly online but follow up by a doctor can take weeks. These results were just post and I'm trying to figure out if should be relieved or more worried. Any input would be appreciated.
The posted results are as follows:
"Exercise stress and rest myocardial perfusion SPECT
showed no areas of abnormal perfusion which indicate the presence
of myocardial ischemia, infarction, or hibernation.
PR INTERVAL SHORT and HIGH LATERAL MYOCARDIAL INFARCTION. What does all this mean? I'm I in trouble?
mother is 77 and recent stress tests and carotid doppler all fine. My recent EKGs (last 5 years) show different abnormalities, but cardiac specialist considers false positives due to echocardiogram and nuclear stress tests results (holter test and stress done 5 years ago - all ok then and the above tests were performed in May this year). I run on the treadmill 3-5 days per week (depending on my schedule) up to 5.5 mph with no problems.
a couple of weeks after I had a hard chest pain for 1-2 minutes, I went to cardiologist. He said EKG was normal and ordered a follow up stress test which he also said was normal. Going through paperwork today I see that my results say "SR, Poor Anterior Forces". It makes me wonder.I just called and they say it's just a normal thing. Would you be worried if you were me? My stress test and EKG in 2010 were normal also...no changes 2010 to 2013. I am a 66 yr old woman. Thanks.
IT can pick up abnormal rhythms of the heart, as well as evidence of an old myocardial infarction, an ongoing myocardial infarction, or active ischemia (restriction in blood supply to the heart). A stress test is a screening test for coronary artery disease. A stress test can show any abnormal blood flow to the heart muscle.
It is very possible for a stress test to be falsely normal in patients with coronary artery disease.
I have recently learned I have had a heart attack and would like an explanation of of the findings on the Persantine Stress test please. Is any of the damage considered to be reversible, would surgery be necessary at some point?
Observations:
There is severe perfusion defect involving the distal part of the anterior wall and extending to the apex.
Resting Myocardial Perfusion Study: same observation.
LV Function: The left ventricle is of normal size, there is apical hypokinesia.
Elevated troponins in the setting of chest pain may accurately predict a high likelihood of a myocardial infarction in the near future. New markers such as glycogen phosphorylase isoenzyme BB are under investigation.
The diagnosis of myocardial infarction requires two out of three components (history, ECG, and enzymes). When damage to the heart occurs, levels of cardiac markers rise over time, which is why blood tests for them are taken over a 24-hour period.
Modified Bruce protocol for treadmill testing is usually applied when poor condition of the subject is suspected clinically or while conducting a predischarge treadmill test after treatment for acute myocardial infarction. Pre discharge treadmill test is often a sign limited one unlike the symptom limited test done in other situations. Maximum heart rate aimed at is around 120 per minute, unlike the 220-age maximum predicted heart rate for the standard treadmill test.
The appearance of the ST segment changes dramatically in the presence of ischemia or during a myocardial infarction. During ischemia, the ST segment will become depressed and have a long duration and a large amplitude before it joins the T wave. The ST segment is elevated during an acute myocardial infarction. The ST segment is, therefore, a diagnostic segment of the EKG strip that is very important in the diagnoses of heart problems.
Was the CT scan able to rule out the myocardial bridging is not associated with myocardial infarction (heart attack) it is factor on rare occasions. The mechanism by which this occurs is unclear; vessel occlusion in this setting may be due to superimposed thrombosis (clots) or vasospasm. Endothelial (lining of vessel) injury as a result of myocardial bridging may predispose to thrombus formation.
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