I have written an article regarding treatment modalities that can be given to patients with ST-elevated myocardial infarction 10 days ago, but today, I have realised that some of the details being pointed out in the Malaysian CPG can be quite rigid when compared to what's happening in a clinical situation.
For example, if patients with chest pain presented to the health facilities less than 3 hours after the onset of symptoms, according to Malaysian CPG, neither PCI nor thrombolytic agents are superior to one another and yet, as I went along with my daily academic routine of case presentation and discussion, PCI is still considered superior to thrombolytic therapies. Regardless, I hope all of you were able to get some knowledge from that article; today we are going to talk about one of the most feared atypical presentations of myocardial infarction, also known as the silent myocardial infarction (SMI).
Pretty much everything that has been described by the name itself, when you were experiencing a silent myocardial infarction, you can be asymptomatic. No chest pain, no shortness of breath, no excessive sweating, nothing whatsoever. So, how do we diagnose such conditions? Well, silent myocardial infarction can usually be diagnosed among people who are diabetics or it can simply be an incidental finding while you were doing your annual checkup.
According to the World Health Organisation (WHO), myocardial infarction (ischaemic heart disease) is the leading cause of death, globally, accounting for more than 15 million death in 2016. Considering the problem with SMI in terms of its pathophysiology and presentation, it can be justifiable to do a much more aggressive screening for people who were suspected to have diabetes which, in theory, they are at risk of cardiac autonomic dysfunction (or sometimes called as autonomic neuropathy).
According to an article which was written by Draman et al in 2013, even though annual medical screening can be one of the ways to diagnose or rule out SMI, it remains contentious.
First, no screening test demonstrates sufficient specificity to avoid the need for invasive tests if the initial screening test is positive. Secondly, the benefit of detecting underlying asymptomatic coronary artery disease in patients who have not had an infarct remains unclear.
The American Diabetes Association (ADA) recommends that diabetes should be considered as a coronary artery disease equivalent and the risk factors for coronary artery disease should be treated aggressively in a patient with diabetes whether or not he or she is known to have coronary artery disease. Therefore, while detection of SMI in a patient with diabetes may lead to further measures such as attempted revascularization or institution of β-blockers, direct evidence that these measures improve prognosis in patients with diabetes who have not had a myocardial infarction and who are asymptomatic is lacking.
There has been some difference in opinion regarding treatment for people who were diagnosed with SMI. As discussed in the previous article, usually, people who were diagnosed with MI would be subjected to an intensive pharmacological approach. There are symptomatic treatments and a few other treatments which are supposed to be given to patients in order to protect the remaining cardiac muscle from ischaemia but if their condition deteriorates despite intensive treatment, surgical modalities can be a lifesaver.
Well, in theory, it can always be compared to other condition which can be deemed as similar; since people who were experiencing SMI has ST-elevated segment as one of their ECG changes, then it can be thought to respond pretty much like people who were experiencing ST-elevated myocardial infarction. This will prompt, treatment protocol pertaining to STEMI such as early revascularisation and prescribing beta blockers which currently doesn't seem to have enough evidence to suggest they could be therapeutic for people who experience SMI. In 2009:
The Bypass Angioplasty Revascularization Investigation (BARI) 2 Diabetes Trial did not show any difference in cardiovascular outcome in patients treated with coronary revascularization compared with intensive medical therapy alone.
Earlier in 2009, The Detection of Ischemia in Asymptomatic Diabetics (DIAD) has published a study which shows that despite conducting a screening program to identify people at risk of getting cardiovascular events for the next 5 years (among people with diabetes type II), those screening tests can't really affect the likelihood of them (patients) being diagnosed with any related cardiac pathology. If we tried to put both of these conclusions into perspective, we can't really say that screening people with diabetes for any risk of future cardiovascular events for early revascularisation can provide some sort of advantage in terms of their morbidity or mortality rate related to cardiovascular events.
The paper (I've mentioned earlier) which was written by Draman et al has illustrated a clinical scenario of which the patient with SMI is treated by giving clopidogrel and aspirin (both 75 mg in tablet form) along with tablet bisoprolol 5 mg (beta blockers). The patient was admitted into a cardiac rehabilitation program, unfortunately, he died 1 year later.
SMI is not something new. It (probably) has been identified during the first large-scaled Framingham study which found that among 5127 patients who are diagnosed with myocardial infarction, only 708 of them are detected through incidental ECG finding that would have suggested a cardiovascular event (ST-segment changes). Half of them presented with atypical symptoms such as indigestion etc. but the other half were asymptomatic (SMI). This is such a significant finding as, without proper interventions, they could end up with heart failure, stroke and ultimately death.
Subsequent studies proved that this condition is relatively common among people with diabetes mellitus as compared to the general population. In 2004, DIAD has found that the prevalence of SMI among 1,123 diabetic patients without any known history or suspected case of coronary arterial diseases is 22%. It can't simply be ruled out by a negative cardiac stress test but can be predicted by assessing patients' cardiac autonomic function.
So how does this happen? It's not clear to me regarding the exact pathophysiological route that can lead to SMI, but according to an article written in 1977 by Faerman et al:
Several explanations are possible (including a different threshold of pain sensitivity or psychological denial) but cardiac autonomic neuropathy almost certainly plays an important role, potentially involving dysfunction at varying levels – from the pain receptors, afferent neurons or gating mechanisms to the supratentorial translation of ischaemia into pain. Many years ago, an autopsy study in a diabetic patient who had silent infarction found pathologic changes in cardiac afferent neurons consistent with a neuropathy, and the prolonged anginal threshold reported in patients with DM has been found to occur in association with reduced heart rate variability, an early sign of cardiac autonomic nerve dysfunction (CAN).
This can bring a harmful effect to the patient as they weren't aware of their own myocardial infarction which is usually notified by chest pain and other associated symptoms. They will create a false perception of their own exercise tolerant which motivates them to continue, worsening their ischaemic symptoms.
References: [1], [2], [3], [4], [5], [6].
All images were taken from Pixabay
Images: [1], [2], [3], [4], [5]
