I was taken into coronary care unit following complaint of discomfort in the chest and reflected as a ST depression in my ECG. I was given oxygen tube through my nose - the oxygen was very cold and the flow rate irritated my nostrils and I said I was feeling unwell and lightheaded. I was then told that my heart rate fell to virtually zero but just three presses on my chest by the nurse brouht the rythym back. The troponin level in blood tests after ~12-13 hours was recorded as 0.1. However other blood tests revealed no raised levels of cardiac enzymes. Following medications (isosorbide mononitrate 2x 10mg, nicorandil 1 x 10mg , 75 mg clopidogrel) my ECG has returned to normal but I am now having an angiogram. What I would like to know is did I suffer a heart attack, if not what happened?
Troponin I and T are structural components of cardiac muscle. They are released into the bloodstream with myocardial injury. They are highly specific for myocardial injury--more so than CK-MB--and help to exclude elevations of CK with skeletal muscle trauma. Troponins will begin to increase following MI within 3 to 12 hours, about the same time frame as CK-MB. However, the rate of rise for early infarction may not be as dramatic as for CK-MB.
Creatine kinase can be further subdivided into three isoenzymes: MM, MB, and BB. The MM fraction is present in both cardiac and skeletal muscle, but the MB fraction is much more specific for cardiac muscle: about 15 to 40% of CK in cardiac muscle is MB, while less than 2% in skeletal muscle is MB. The BB fraction (found in brain, bowel, and bladder) is not routinely measured.
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. The CK-MB is also useful for diagnosis of reinfarction or extensive of an MI because it begins to fall after a day, dissipating in 1 to 3 days, so subsequent elevations are indicative of another event.
A "cardiac index" can provide a useful indicator for early MI. This is calculated as a ratio of total CK to CK-MB, and is a sensitive indicator of myocardial injury when the CK-MB is elevated.
Cardiac markers are substances released from heart muscle when it is damaged as a result of myocardial infarction. Depending on the marker, it can take between 2 to 24 hours for the level to increase in the blood. Additionally, determining the levels of cardiac markers in the laboratory - like many other lab measurements - takes substantial time. Cardiac markers are therefore not useful in diagnosing a myocardial infarction in the acute phase. The clinical presentation and results from an ECG are more appropriate in the acute situation.
Quick summary of Cardiac Enzymes Troponin is released during MI from the cytosolic pool of the myocytes. Its subsequent release is prolonged with degradation of actin and myosin filaments. Because it has increased specificity compared with CK-MB, troponin is a superior marker for myocardial injury. Differential diagnosis of troponin elevation includes acute infarction, severe pulmonary embolism causing acute right heart overload, heart failure, myocarditis. Troponins can also calculate infarct size but the peak must be measured in the 3rd day.
The causes of EKG ST depression include myocardial ischaemia, digoxin effect, ventricular hypertrophy, acute posterior MI (heart attack), etc., but usually the EKG tracing is an elevated ST for an MI..
Biochemically, Troponin 1 is positive for MI greater than 2.0 and tropinin T greater than 2.0. Troponins will remain elevated longer than CK (another biochemical marker)--up to 5 to 9 days for troponin I and up to 2 weeks for troponin T. 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. Slight possibility some cell damaged but the biochemical markers do not support event.
The angiogram will look for blocked vessels (ischemia) and estimate the left ventricle's pumping ability. If there are significant or some damaged heart cells the heart's pumping functionality will be impaired.
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