Acute myocardial infarction, as part of the Acute Coronary Syndrome spectrum, is a common problem and in patients who are alert, the diagnosis can often be considered based on the symptoms alone which include:
- Severe central 'crushing' chest pain
- Radiation of pain to the neck, jaw or arms
- Nausea and vomiting
- Cold sweating
However, in the patient who is unconscious lying on a bed in the ICU, how is it possible to even know if they have developed an AMI?
Most patients are usually linked up to a bedside monitor and that can often provide a clear picture of the situation by seeing a rhythm change and abnormal ECG features as described above. The other additional method is to check for cardiac enzymes.
Remember that there are several enzymes released during muscle damage which include:
- Creatinine Kinase and the MB fraction (positive for up to 48 hours)
- Aspartate Transaminase
- Lactate Dehydrogenase
- Troponin T and Troponin-I (positive for up to 10 days)
By failing to check the Troponin, it is possible to miss an AMI. Sometimes, the CK and AST can be normal (especially after several days; the AST may not rise at all !!) and the physician is fooled into a false sense of confidence that an AMI has not occurred. However, the AST and CK can soon fall after an AMI whereas the Troponin can stay elevated for over a week.
For example, in the UK, I experienced one such case in a patients who presented with typical chest pain but who's ECGs were completely normal in addition to the CK and AST. He was treated with aspirin and LMW heparin as was the protocol for 'atypical' chest pain. His Troponin T was positive at 12 hours. The patient had no evidence of renal failure. This patient was transferred for percutaneous intervention (PCI) treatment. In this case, the history was all important and the usual ECG and CK /AST were unrevealing. Only the Troponin-T being positive confirmed our worst thoughts.
Renal failure has been cited as a reason not to do a Troponin test in some institutions because it can be falsely raised. One should not be fooled into thinking that a Troponin should not be measured just because the patient has renal failure - quite the contrary. Remember that patients with renal failure are at high risk of coronary disease and hence, these two problems go hand in hand. It is better to over investigate such patients by performing a troponin test to include or exclude an AMI rather than assuming it is just because of renal failure.
In respect of a patient on an ICU, a rise in the CK, a change in the ECG, blood pressure instability, dysrhythmias etc should alert the physician to the possibility of an undiagnosed acute coronary event. In such cases, a 12 lead ECG is mandatory as is a Troponin test. If the latter test is negative initially, it does not exclude an AMI !
It can take a minimum of 6 hours for the Troponin to become positive and most authorities state that 12 hours post-event is when Troponin can be truly said to be positive or negative [>9 hours after onset of symptoms and negative Troponins indicates low probability of myocardial damage / infarction]. Hence, the Troponin should be rechecked at least 6-9 hours after onset of symptoms with an initial negative test.
One group [Hamm, CW. Cardiac biomarkers for rapid evaluation of chest pain. Circulation 2001; 104:1454], investigated if AMI diagnosis could be made rapidly within 90 minutes by measuring serum CK-MB, troponin I, and myoglobin in the event that an ECG was non-diagnostic. Their results were interesting with sensitivity and specificity over 95% for diagnosing AMI. However, the test needs to be validated and therefore, this triple cardiac enzyme test is not currently advocated. The problem in using myoglobin is that it is a non-specific marker.
Currently, recommendations for investigation of acute coronary syndrome state that if ACS is suspected, the Troponin T or I should be performed and only in centres where it is not available should the CK-MB be performed. The measurement of total CK is again, non-specific, and should not be used to make the diagnosis of an AMI.
However, the total CK being raised can certainly provide a clue that an ACS might have occurred especially in the unconscious patient, and hence, performing a Troponin-T or I would be the Gold Standard for diagnosis taking into account ECG +/- Echo findings.
A cardiac echo is also important. An echo may reveal regional wall motion abnormalities which may become evident even before then onset of pain in AMI patients. Such abnormalities were seen in patients undergoing PCI treatment when their coronary arteries were reversibly occluded by the angioplasty balloon. It is said that having no obvious echocardiographic abnormalities excludes an AMI although the reverse is not true i.e. a hypokinetic echo result does not always equal AMI. Hence, it can be difficult to sometimes know if an abnormality is truly due to an AMI. Hence, performing a 12-lead ECG and comparing it to a previous ECG (if available) plus cardiac biomarkers are necessary to absolutely identify if an AMI has taken place.
Currently, the European Guidelines from the European Resuscitation Council 2005 do not mention about the use of echocardiography to sustain a diagnosis of AMI. However, the 2003 task force of the American College of Cardiology recommend using echocardiography to aid in the diagnosis of AMI unless it has been proven by other means [history / ECG / Cardiac markers].
Remember that cardiac markers can also be raised in other conditions. For example, myocarditis, PE, cardiac intervention etc, can cause positive Troponins. A diagnosis that is common in Japan is 'Octopus Trap Heart' - also termed Takotsubo, a form of localised myocardial stunning with the absence of significant coronary artery disease whereby the heart chamber changes shape and takes on the form of an octopus trap. Please visit the following website for an excellent review of the topic. Note that takotsubo can only truly be diagnosed once ACS has been ruled out by coronary angiography. Treatment for takotsubo is considered supportive although UpToDate 16.2 suggests use of aspirin, ACE-I / ARB and beta-blockers as for heart failure, whereas ACS requires the addition of:
- Low Molecular Weight Heparin
- Coronary stenting / Revascularisation surgery
In order to differentiate non-ACS causes from ACS, percutaneous intervention e.g. coronary angiography, is helpful. PE workup would involve D-Dimer testing, use of a PE scoring system e.g. Modified Well's Score / Modified Geneva Score, leg dopplers, echocardiography and ultimately, spiral CT.
Hence, in summary, when dealing with an unconscious patient on an ICU with the concern about an AMI, it is important to rely on the combination of tests as described above, and not one test alone. Remember that common things are common, such as AMI, and to thoroughly investigate is the correct management in addition to starting cardiac medications [as outlined above] before a final diagnosis of AMI is determined or excluded, as delaying treatment can result in muscle damage and hence I quote the famous words of 'Time is Muscle'. If the final diagnosis turns out to be the rare takotsubo then so be it, but if not and it is the common ACS, then at least the patient would have been treated rather than waiting to make a perfect diagnosis at the expense of the patient's heart muscle.