Most people usually link the phrase “heart attack” with “massive”; something you are indisputedly aware of.
Some are massive and, in these instances, it’s relatively easy to know if it is indeed a heart attack. Typically, there will have been crushing chest pain lasting more than a few minutes. One would hope this has led to an immediate call to 000 and a trip in an ambulance to hospital.
Often ambulance officers will have performed an electrocardiogram (ECG) and transmitted the results to the hospital, which will have selected and be ready with the appropriate treatment. In this case, the chest pain and the characteristic ECG changes are enough – those wiggly lines mean a lot to an experienced reader.
However, most heart attacks are not “massive”. In these instances, further tests are necessary and the diagnosis can become quite challenging. The pain may not be typical and the ECG may be normal or difficult to interpret.
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Different types of heart attacks.
“Heart attack” is not just one thing: there are five internationally-recognised types.
The one we think of first is when a plaque in a large coronary artery – consisting of cholesterol, cells and cellular debris that has built up over the years – suddenly cracks or erodes. This exposes the inside of the plaque to the blood flowing down the artery. The blood clots at this point, causing a thrombosis that narrows or blocks the artery.
If the artery is completely blocked, this is likely to cause death of heart muscle cells downstream and myocardial infarction, colloquially called a heart attack.
Two different kinds of heart attack are distinguished by the ECG changes – STEMI (ST segment elevation myocardial infarction) and NSTEMI (non-STEMI) – which may require different treatments. STEMI generally means the artery has blocked completely. If the artery is only partly narrowed and the downstream muscle causes pain but survives the syndrome, it is known as unstable angina.
Cardiologists prefer the term acute coronary syndrome (ACS) to describe the spectrum of consequences of short-term lack of blood and oxygen to the heart muscle. As this is a spectrum, it is perhaps not surprising that it has been difficult to come up with a dichotomous separation of “heart attack” or “no heart attack”.
Heart attack or no heart attack.
Medical advances over the decades have provided some clarity. But this has also caused a rethink among those trying to define the various levels of heart attack, both for management decisions and for practical purposes such as insurance.
For many years, diagnosis has depended on measurements of the changes in levels of enzymes released by dying heart muscle cells. These rise in the blood some hours after the initial event peaks and then gradually fall, with different enzymes following a different time course.
Until the 1990s, the enzymes that were used for this purpose included a panel of up to three. Each followed a vastly different time course. However, they are not specific to heart muscle cells and a rise could be due to many other conditions.
Testing was refined with the development of a muscle-specific enzyme test for creatinine kinase (CK). But the search was on for a test that would both identify loss of heart muscle by levels rising earlier and be more specific to the heart.
Measurement of troponin was the next big advance in the mid-1990s and revolutionised the classification of heart attacks. Troponin is released from muscle one to three hours after an artery is blocked and may stay high for up to 14 days. It is more specific to heart muscle than previous enzyme tests.
Over the past decade, the test has been refined to be more and more sensitive. But each test needs its own threshold level for an abnormal result, so an absolute result of a test in one laboratory may not be comparable to that of another. (Post continues after gallery.)
Nevertheless, the availability and refinement of the troponin test used properly has introduced a level of certainty in the diagnosis of acute heart syndromes that was not previously available. Myocardial infarction can be ruled out earlier. Small infarcts can be identified that would previously have been missed.
The problem with measuring troponin.
Troponin measurements introduced their own problems too. During the late 1990s, it seemed that a sizable proportion of people presenting to emergency departments had rising troponin levels but no other signs of heart attack. The tests were picking up smaller and smaller amounts of heart muscle damage.
So somebody presenting in the 1990s would get a different diagnosis to another person with the same problem presenting this decade in the high-sensitivity troponin era.
Clinicians are becoming aware of a number of situations where false positives can occur. This may result from damage to the heart from trauma, frequent defibrillator shocks, heart failure, disease of the aorta, pulmonary embolism, kidney failure, stroke, various drugs and critical illnesses such as burns and sepsis.
Troponin can also miss heart attacks if used alone, or the blood is taken outside the window when levels are elevated, or the laboratory uses an insensitive troponin test.
The Australian national guidelines for diagnosing myocardial infarction are due for release in the next few months by the National Heart Foundation and the Cardiac Society of Australia and New Zealand and will consider these problems.
In the meantime, the third universal definition of myocardial infarction is the internationally recognised and accepted guideline.