Troponin can remain elevated for around 2 weeks . This means if a patient is stented due to high troponin, for 2 weeks it would be very difficult to establish if another attack is occurring using this testing method.
I can't see how you can determine 'when' an attack occurred by the troponin level. The higher the level the worse the attack, but there is no time tag. What if, for example, a mild attack occurred on day one and the symptoms were ignored. Then three days later the symptoms worsened and the patient visited ER. The attack was initially three days ago, but how could this be deducted by the troponin?
Some insight, people who have a heart attack can have normal troponin concentrations, and some people with increased troponin concentrations have no apparent heart injury. My experience there was no elevation of the marker because I had had a silent heart attack and my first symptoms where congested heart failure and I was in ICU for several days.
An explanation can be heart cell damage can occur without necrosis of heart cells. The heart cells can be in a low oxygen level due to ischemia and be viable although non functional causing hypokinesis (impaired wall movement). With heart attack aside, troponin levels may also be elevated with acute or chronic conditions such as myocarditis (heart inflammation), congestive heart failure, severe infections, kidney disease, etc. So a health history would help evaluate, consequently your father could have had had a heart attack and troponin level for a heart attack marker not represented with first visit.
Ruling out hypokinesis from a lack of oxygen due ischemia, and or other causes for hypoxia, with a heart attack troponin usually remains elevated but it the half-life is about 2 hours. Initially troponin in the blood initially rises in about 4 to 6 hours and peak concentrations appear at about 18 to 24 hours. There is a numerical window available for an assessement for time of current heart attack
Unstable angina does not increase troponin level. There are scenarios that can be considered There was a heart attack on first visit and some of the residual marker remained...a doctor should be able to distinguish whether that would enter the numerical equation if prior heart attack occurred and extrapolate into the calculation.
Or there wasn't a heart attack prior to the troponin test and the calculation can be based on half-life and peak levels within 18 to 24 hours, etc. I believe the "when" can be determine with some acceptable degree of confidence....my opinion and I am differentially and integrally challenged with the calculus.:)
Thanks for your question, and if you have any other questions or comments you are welcome to respond. Take care,
"Unstable angina does not increase troponin level"
Really? I was always led to believe that stable angina will always produce lower levels of troponin than unstable angina. Surely with stable angina, the heart is fine at rest, but once pain is felt at rest, this is classed as unstable and troponin will increase?
I personally still don't believe you can say 'when' the attack started, you would have to rely on a historical pain description from the patient.
After my father's first heart attack, which was an UNSTEMI, his troponin level went down to .515 ng/mL and CKMB to 3.0 ng/mL. Troponins peaked at 1.240 on first heart attack and hospital didn't check troponin levels for 3 days even though he had unstable angina. From what I have read, symptoms of unstable angina and NSTEMI heart attacks are identical. Only a troponin test can truely indicate whether a person has unstable angina or NSTEMI since EKGs may not pick up electrical changes in heart. After an incident happened in hosptial in which nurse did not give my father nitroglycerin under the tongue for several hours when he needed it because she didn't notify doctor of my fathr's low blood pressure, my father had a second NSTEMI heart. It was during his second heart attack that his troponin went to 3.560 and CK MB to 30.8. From what I have read CK MB because it rises much slower than troponin does, is a better indicator of the "whens" of a heart attack. In my father's case, CK MB went from 3.0 to 30.8, this is a big increase in only 3 days. Thus, while the nurses actions which provoked my father's second heart attack, I believe hospital is neglect in not montoring his troponin and CKMB levels for the 3 days my father had unstable angina. I believe my father could have had the beginnings of his second NSTEMI in those 3 days. Is this possible?
That's true, that's why it's called a non-stemi, the EKG is normal. The markers in the blood rise and peak around 4-6 hours after an attack begins, but you don't know how long they have been peaked before detection and they can remain peaked for at least a week. I personally agree that because the markers increased over those three days, they should have been much more alert because the heart muscle was under more stress.
When I was admitted in March this year, I was having MI non-stemi and my troponin was around 0.78. I felt very nauseous when I laid down, so it was not possible to do angioplasty at that time. They agreed to wait until the Monday (it was currently friday) but if things got worse I would be rushed in. I had no chest pains thanks to GTN and keeping my BP low, but they did take a troponin test EVERY 12 hours over the weekend to keep an eye on things. It didn't elevate any further. If it had, they would have insisted on angioplasty at that time.
You say "Thus, while the nurses actions which provoked my father's second heart attack" and I'm intrigued as to what they did?
As I mentioned before, my father had angina. It was relieved by nitroglycerin under the tongue. Because my father's blood pressue was low, nurse did not give nitro to my father and she didn't call doctor so that he would give her orders to stablize his blood pressure so that he could take the nitro. I have had the State Dept. of Health investigate the case. They state that the nurse should have taken blood pressure readings so that when blood pressure readings go back to normal, she should have administred nitro to my father. State Dept of Health found violations by hospital caused by nurse. However, I don't understand why they also did not cite the doctor as being in violation also. Nurse did call up hospital on call doctor, they called "chief of residency doctor" because my father had chest pain that extended to shoulders. That sure sounds like a heart attack to me! Chief resident doctor comes, gives my father nitro and Tylenol for the pain. I think a high school student would have enough brains to give my father aspirin in case my father was having a heart attack! My father's angina pain goes from 8/10 to 3/10; however, he still had pain. When a person takes 3 nitro pills, pain should go away completely. Doctor orders EKG and walks away.
About 6 hours later they test for troponin, that is when it showed 3,560! Doctor says in his report, that the pain my father was experiencing he believed was not from the heart since EKG, he ordered did not show any changes and that troponin levels were coming down! What a lie since troponin levels weren't taken for 3 days and an NSTEMI many times wouldn't show up on EKG! My father who was 93 was taken to Critical Care after almost 4 hours after troponin level of 3.560 was discovered. I was later told he had a big heart attack. Troponin levels work backwards. So the 3.560 shows that the heart attack occurred 4-6 hours before. Blood troponins level was taken at 10:30, and my father's chest pain which intensified and spread to shoulders was at 4:30 AM. Therefore,the heart attack can be proven to have broke out around 4:30 AM.
The Department of Health came down on the nurse and for correction measures the hospital was told to start educating nursing staff on prompt communication with doctors. However, nobody mentions the doctor! Doctor was negligent in treating my father as a medical emergency,that is against Medicare ruling and the patients bill of rights! Since the hospital wanted to take a "conservative" approach to my father's heart problems because of his age, they should have given him drugs to break up the clot. They did nothing! Unbelievable!!!
2 days after the heart attack, they did a catherization and found his heart was too badly damaged to do anything! He died a few weeks afterwards. After, the big heart attack the hospital caused, all doctors saw his case as hopeless!
What do you all think of this!
Q by ed34: "That's true, that's why it's called a non-stemi, the EKG is normal."
Doctors use the term STEMI, or ST elevation MI to describe this type of heart attack.
...That is not exactly true. It is my understanding that “ST elevation” in STEMI refers to a specific pattern on the ECG that is sometimes seen in patients with completely blocked arteries and having an MI as well with NSTEM segment that indicate an MI but not as severe and less occlusion...both are abnormal EKG tracings.
Suscousin, you are correct. Only a troponin test can truely indicate whether a person has unstable angina or MI. ..."NSTEMI since EKGs may not pick up electrical changes in heart". (Also, the EKG can have an abnormal tracing but is not able to distinquish between MI and/or blocked cornary vessels).
...."Troponin T (cTnT) and troponin I (cTnI) are released only following cardiac damage CK and CK-MB are found in skeletal muscle as well as cardiac muscle - therefore if there is damage to skeletal muscle, elevations of CK and CK-MB will occur and can make the diagnosis of myocardial infarction difficult. In such a situation levels of cTnT and/or cTnI WILL NOT unless myocardial infarction has occurred". Unstable angina does not cause heart muscle damage unless there is an infract.
"Elevation of cTnT or TnI is absolutely indicative of cardiac damage, but this can occur as a result of causes other than MI (infract) e.g. myocarditis, coronary artery spasm from cocaine, severe cardiac failure,cardiac trauma from surgery or road traffic accident, and pulmonary embolus can cause cardiac damage with an accompanying elevation of cardiac troponin." Other clinical evidence and health history to differentiate.
"Subtypes I and T of troponin are sensitive indicators of damage to the heart muscle. Troponin levels are normally not measurable on blood tests, but become elevated with damage or inflammation of the heart muscle (cardiac muscle). Troponin levels are measured in cases of suspected heart damage, especially in trying to determine if a person has had a heart attack. Troponin levels may help distinguish between a diagnosis of angina, chest wall pain or other chest discomfort from a heart attack that causes troponin levels to rise".
However, to be consistent with my position on the matter for the last 7 years I am of the opinion there is heart muscle damage with ischemic unstable or stable angina. When there is angina pectoris the reduction of oxygenated blood can cause necrosis of some heart cells as not all cells have equal vulnerability of the millions of heart cells. Also, reduction of oxygenated blood to the brain causes necrosis of brain cells and there is no question about and that is an example.
I stay with my opinion that the time of a heart attack can be determined by the metrics availabile.
If you believe "the time of heart attack can determined by the metrics available" when do you think my father's second NSTEMI began? Do you think it could have begun during the 3 days he had unstable angina and then with the incident with the nurse as I mentioned above, his heart attack really came out or did the heart attack start with the nursing incident in which a lack of administrating his nitro when he did have chest pain, caused him to have the NSTEMI heart attack? I have a lot of literature which states that if with 3 nitro pills, angina does not go away, then call 911. My father was given the nitro almost 5 hours after his angina began, it began in the stomach, then worked into the chest. Pain was continuous.
What I also don't understand is how is this emergency resident doctor thinks my father's pain was not due to the heart. I see all of this as negligence on the part of the doctor. My father should have been treated immediately as having a heart attack. My father's troponin levels were taken about 5 1/2 hours after administration of nitro.
As stated in my first post there is a half life of the enzymes, there is a record of the peek, there are documented times of visits, there may be subjective times of symptoms, etc,. There can be a continuim etablished for expectations based on all possible variables. To determine variables, etc. and do a differential and intregral calculus can be done with acceptable probability and high degree of confidence with the technology available. That would require a professional with a medical degree and a statistical analysis.
From a practical standpoint, it seems if someone had the same symptoms on the last visit as the first within 36 hours it is very likely the two events are related. If related proper treatment on the first visit may have prevented the second visit whether it was a heart attack at the time or angina pectoris with the first visit. Why would it be necessary to establish a finding of having a prior heart attack untreated when negligence can be due to not appropriately testing and treating the symptoms on the first visit?
"When a person takes 3 nitro pills, pain should go away completely"
Not true and a common misconception. If you have for example a 99% blockage high up in a vessel, then this is likely going to cause chest pain at rest and GTN will usually relieve the symptoms. If the blockage is a 100% clot, then GTN will not relieve the symptoms.
I'm not an expert on drug busting drugs, and I'm not certain if the medication would dissolve a clot quickly enough to save heart muscle ?
I agree with you that my father's second heart attack was due to the fact that the doctors did not properly assess nor treat his first heart attack. They assessed he had the first NSTEMI by means of a troponin test , however, because of his age most all of the doctors at the hospital wanted him to be treated "conservatively" with heparin, nitro and beta blockers. Because my father had had a bad reaction to plavix in the past, shown by his vomiting up blood clots and nose bleeds, he stopped taking plavix. However, it now has occurred to me that if the doctors had been more vigilant of his blood count when he was taking Plavix, that maybe he would not have had the nose bleeds and coughing up of blood.
While my father was having unstable angina, there was one heart doctor who completely disagreed with all the other hospital doctors. This doctor believed my father would be a good candidate for catherization and a procedure to unblock arteries. All the other hospital doctors believed he would not be a good candidate. Then when my father and I told this doctor who wanted to possible do a procedure to unblock his arteries that my father had had a bad reaction to Plavix in the past and we didn't like the idea of his going on Plavix, he stomped out of the room and said that if my father did not want to take Plavix, he couldn't do angioplasty on my father. However, 2 days after my father had the 2nd NSTEMI, this same doctor put my father on Plavix and did a catherization. However, with the 2 NSTEMI, my father's heart was too badly damaged.
When my father arrived at the hospital with NSTEMI that was very small, doctors could have done a CT heart scan which is an uninvasive way to look at the arteries. It appears that doctors at hospital were afraid to even give my father a catherization given the fact that he was 93 yrs.old. However, my father's last catherization was done 16 years prior and his last stress test was 12 years prior. How could the hospital doctors even have a chance of properly treating my father if they did not know his heart condition. I definitely see negligence in not giving my father a diagnostic test to see how his artery status was. Do you agree, Ken?
The fact that my father's angina did not go completely away, indicates that something was very wrong and that his condition should have been treated as medical emergency which it wasn't by the on-call emergency physician. THis doctor gave him 3 nitro pills, 5 minutes apart, medication for pain, no aspirin and walked away. As I wrote above, this doctor did not believe my father's pain was related to the heart. The doctor is far from being a brilliant doctor, since 6 hours later his troponin levels rose to 3.560 indicating that his pain was from the heart. NSTEMI heart attacks are generally treated with clot busting drugs or angioplasty or both. In my father's case, these procedures were not followed. Hospital just followed treatment plan after my father's first NSTEMI at hospital, heparin, betablockers and later in the day, nitro drip. Truely, I believe an intelligent high school student would have more sense. At least they know, that aspirin is given to a person when they think person is having a heart attack.