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
Thus, CK-MB is a very good marker for acute myocardial injury, because of its excellent specificity, and it rises in serum within 2 to 8 hours of onset of acute myocardial infarction. Serial measurements every 2 to 4 hours for a period of 9 to 12 hours after the patient is first seen will provide a pattern to determine whether the CK-MB is rising, indicative of myocardial injury.
I (38, Male, non-smoking, 5'9" 69 k.g.) was diagnosed with a myocardial bridge late last year. As part of health check up for insurance, I underwent a treadmill test, and was told that it was "positive for ischemic heart disease". I had no symptoms whatsoever.
I went for CT coronary angiography, and the following was reported:
1. calcium score zero
2. RCA, AM normal. no stenosis.occlusion
3. PDA, PLVB, normal. Filling from RCA. no stenosis.
4.
Segmented LV wall motion abnormalities (hypokinesis) are characteristics of myocardial infarction. The damaged myocyte heart cells inhibit the contractilty of the heart chamber thereby reducing EF (ejection fraction...amount of blood pumped into circulation with each heartbeat...normal is 55 to 75%).
The Cardiac Arrhythmia Suppression Trial (CAST) revealed significantly higher mortality associated with flecainide in patients with a recent history (more than six days but less than two years prior to study) of myocardial infarction (MI) and non-life-threatening ventricular ectopy relative to placebo (5.1% versus 2.3%). The risk of death relative to placebo in patients with a recent history of Q-wave MI and non-Q-wave MI is 8.7 and 1.7, respectively.
the extent of myocardial injury, the age of the infarct, its location, the presence of conduction defects, the presence of previous infarcts or acute pericarditis, changes in electrolyte concentrations, and the administration of cardioactive drugs. Nevertheless, serial standard 12-lead EKGs remain a clinically useful method for the detection and localization of MI.
With an infarction changes in the QRS-complex are seen. These are manifestations of myocardial necrosis.
Your value of 49% is below the normal range, which could be due to causes like myocardial infarction or valvular disorders or sometimes hypertension. So, further evaluation can help to detect the cause and therapy is based on the results.
Ejection fraction can be improved by lifestyle changes, medications and procedures, such as the insertion of an implantable defibrillator (ICD) if indicated.
Abnormal nuclear myocardial perfusion imaging study with evidence of LAD distribution ischemia and RCA distribution infarction. Normal LV size. Normal systolic function. EF normal, 59%.
However, most atherosclerotic plaques will remain harmless and only vulnerable plaques (a minority) have the potential of causing myocardial infarction. Disruption of the vulnerable plaque or plaque erosion and subsequent thrombosis (clots) is the most common pathophysiological mechanism leading to an acute coronary syndrome.
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.
Thank you for the response, my coronary arteries were found to be clear of atheroma on angiogram. What is the likelihood of experiencing two STMI within five years due to Prinzmetals? I obviously wonder if I may experience another in the future. I am only46yrs old. My first MI was aged 39yrs and my second aged 45yrs. I am on Diltiazem 420mgs daily, Losartan 100mgs and a statin. I experience angina almost on a daily basis so also use GTN as required.
People with a history of heart attack (myocardial infarction) and even those with coronary artery bypass grafts or angioplasty but with no angina, can trek up to high altitude provided they are fit and able to walk rigorously at low altitude. The high altitude does not seem to add any extra burden to the heart
If blood pressure is controlled and there is no chest (pain), no problem. It is the elevated blood pressure and its consequences that are the issue.
Why there can be mixed EKG signals during an acute myocardial infarction, because the central area of dead cells is generally surrounded by an area of injury, which in turn is surrounded by an area of heart cells with insufficient oxygen so various stages of myocardial damage can coexist. The distinction between cells that lack good blood flow and dead cells is a determination whether the conditions are reversible.
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