Widely known as a heart attack, myocardial infarction is a medical term used to describe an event in which either of blood supplies to the cardiac muscle was cut off causing cardiac muscle ischaemia and eventually, necrosis. This particular heart condition is a subclass of an acute coronary syndrome which comprises of unstable angina, non-ST elevated myocardial infarction and ST-elevated myocardial infarction. I'm going to focus on the ST-elevated myocardial infarction (STEMI) and probably later, compile both of the former heart condition into a single article.
Case in point:
A 65 years old gentleman presented to the emergency department of Hospital X complaining of central gripping chest pain which radiates to his left arm, started approximately an hour ago with a pain score of 7 out of 10. Further history taking revealed diaphoresis (excessive sweating), orthopnea (can't breathe while lying flat) and he had a strong family history of cardiac diseases. ECG shows an elevated ST-segment at the inferior lead (II, III and aVF) with reciprocal changes on the lateral lead (I and aVL). He was later diagnosed with ST-elevated myocardial infarction supported by his cardiac enzyme result which shows an elevated troponin I. Later, he was treated accordingly.
The above paragraph illustrates one of the most typical presentations of people who were diagnosed with STEMI but it is worth noting that some patients might present with features that suggest an atypical myocardial infarction; most of the time, thorough physical and laboratory investigation, can help you delineate between those conditions. According to Kumar and Clark's Clinical Medicine textbook, there are three types of myocardial infarction which was categorised based on its causes:
- Type 1 MI usually resulted from primary coronary events (rupture of atherosclerotic plaques, dissection etc. ) causing ischaemia, necrosis of the cardiac myocytes and eventually, MI.
- Type 2 can be caused by reduced oxygen supply to the cardiac muscle or increased oxygen demand due to stressful situations or secondary condition (anaemia, arrhythmias, hypertension).
- Type 3 (or 4, 5 depending on the cause of sudden MI) is usually diagnosed in people who experienced cardiac death either post coronary artery bypass graft (CABG) or post-percutaneous coronary intervention (PCI).
Even though we have 3 different types of MI, the pathophysiological route for all of them are quite similar. In people who have a higher risk of developing MI, especially those who have a certain degree of atherosclerotic plaque formation, they are at a higher risk of developing plaque rupture which in turn stimulate platelet adhesion and aggregation forming a thrombus that will eventually dislodge at the narrowest point of the coronary artery; it is usually worsened by the serotonin and thromboxane A2 which were released by the activated platelet leading to vasoconstriction eventually, reduction of flow to the cardiac myocytes. Ischaemic changes can usually be seen on the ECG in the form of an inverted T wave but this is highly non-specific.
Now, what are we going to do if someone presented to you with a chest pain resembling MI? In the past, treating MI with a cocktail of medications abbreviated as MONA (morphine, oxygen, nitroglycerin and aspirin) are considered a standard of practice to reduced mortality risk. Today, some articles indicate that giving them MONA without considering a few other related factors can do more harm than good. Moreover, it has been established by the latest study that the most important step to treat MI particularly an ST-elevated MI is reperfusion therapy, which I'm going to talk about soon.
Now, morphine is usually given to patients who complain of severe chest pain, well at least theoretically speaking. According to some of the most established textbooks on the market, morphine is only indicated when nitroglycerin can't provide pain relief but the Malaysian CPG recommended morphine as the initial pain killer being given to patients provided there is no contraindication. If their pain can't be suppressed by morphine, then, nitroglycerin can be instituted provided their systolic blood pressure (SBP) is more than 90 mmHg. Giving nitroglycerin to patients with low SBP can cause severe hypotension and bradycardia. If a patient presented with cardiogenic shock, none of those stated medications should be given as it can cause severe hypotensive symptoms and respiratory depression; in this case, an inotropic agent such as dopamine and dobutamine can be given along with fluid resuscitation if indicated.
What about oxygen? Yes, you can give oxygen to patients especially those with SpO2 of less than 95%, which is considered respiratory distress. Aspirin and clopidogrel are usually given if they weren't been provided with such medication already. This is to prevent the formation of thrombus especially when there is a rupture that would usually provoke platelet aggregation. Aspirin blocks the action of Thromboxane A2 and for those who are contraindicated for aspirin therapy, they can be treated solely with clopidogrel (monotherapy) as an early institution of either of those medications can improve patients rate of survival.
What about definitive treatment for this condition? Well, reperfusion therapy is quite a popular alternative and currently, there are two main methods which are fibrinolytic therapy and percutaneous coronary intervention (PCI). If we want to compare the effectiveness of both of the interventions then PCI can be described as the method which provides a superior physiological benefit to patients compared to fibrinolytic agents. However, in certain countries (in this case, Malaysia), only a few selected hospital can conduct PCI while most of them have fibrinolytic agents. Using the latter can be acceptable management especially if the time difference between the time of patients arrival to the time of patients receiving PCI (door to balloon time) is more than 90 minutes in a hospital with PCI facilities.
What if you want to transfer patients to another hospital with PCI capability? Sure, you can do that but only if the door to balloon time of fewer than 120 minutes. If it's longer than the recommended time, you are risking more harm than good compared to if the patient is being treated with fibrinolytic agents. There are others which institute a combination strategy to maximise outcome by utilising both PCI and fibrinolytic agents (called as pharmacoinvasive strategies) but that will be covered in another article. So how do you know which one is the best reperfusion strategy for patients? According to the Malaysian CPG, it comes down to the duration between the onset of symptoms and the time of patients arrival. It can either be early, late or very late.
Early (less than 3 hours from the onset of symptoms): Either of the reperfusion strategies can be used. Even though PCI can provide a much superior physiological benefit, there is no apparent/significant degree of effectiveness if patients presented to the health facility less than 3 hours after the onset of symptoms.
Late (between 3 to 12 hours from the onset of symptoms): The most effective treatment to reduce morbidity and mortality rate is PCI but the door to balloon time should follow as what has been discussed above. If it exceeded the time that has been recommended, then fibrinolytic agents can be given as an alternative or a pharmacoinvasive therapy can be instituted (giving patients fibrinolytic agents before transferring them to a PCI-capable centre).
Very late (more than 12 hours): If patients presented asymptomatic, then neither of those reperfusion therapies would be beneficial. However, if they presented with ischaemic symptoms, PCI would be the best alternative.
All patients who were suspected of having MI should be monitored closely in the CCU for any complications or deterioration. They should be referred to a cardiologist for long-term management. It seems easy but yet difficult. According to my supervisor, there is a lot of medical officers who missed the diagnosis of MI and it can be very dangerous. Patients can present with typical or atypical presentations; can you imagine if a patient presented to you with a chief complaint of indigestion but turns out he was having MI. I would hope later (hopefully August 2019) after I have successfully graduated from this medical school, I would good enough to explore and remember the fact that for every single chief complaint, think of the most common and fatal diagnosis first before excluding others.
References: [1], [2], [3], [4]
All images were taken from Pixabay
Images: [1], [2], [3], [4], [5], [6]
