What Is STEMI Heart Attack?

Introduction

Myocardial infarction, commonly known as a heart attack, often occurs due to reduced or blocked blood flow to a section of the heart, resulting in the death of heart muscle tissue. Typically, this is caused by the presence of a blood clot in the coronary artery responsible for supplying that area of the heart muscle. Myocardial infarction can sometimes occur without noticeable symptoms, or it can become a severe event leading to a drop in heart function and sudden death. Patients may experience sensations of chest discomfort or pressure, which may extend to the neck, jaw, shoulder, or arm. In addition to a patient's medical history and physical examination, myocardial ischemia can be identified through changes in the electrocardiogram (ECG) and the elevation of cardiac troponins in biochemical markers. This condition is categorised into two groups: ST-elevation MI (STE-MI) and non-ST-elevation MI (NSTE-MI).¹

Pathophysiology

An ST-elevation myocardial infarction (STEMI) occurs when one or more coronary arteries supplying blood to the heart become blocked. This blockage is typically the result of the sudden disruption of blood flow due to factors like plaque rupture, erosion, fissuring, or dissection within the coronary arteries, leading to the formation of an obstructive blood clot. STEMI is most commonly instigated by the acute thrombotic occlusion of a coronary artery at the site of a previously ruptured atherosclerotic plaque. Plaque erosion and calcific nodules, although less frequent (around 30% and 5%, respectively), can also contribute to STEMI. Specifically, soft or lipid-rich plaques with thin fibrous caps are highly susceptible to rupture when subjected to repetitive shear stress, which exposes the lipid core. This exposure triggers local platelet aggregation, fibrin deposition, and the formation of a propagating blood clot that ultimately obstructs the artery. ^2,3

Risk factors

ST-elevation myocardial infarction (STEMI), commonly known as a heart attack, is influenced by a multitude of risk factors. Age, especially the age of 45 for men and 55 for women, along with being male, are prevalent contributors. A family history of heart disease, hypertension, smoking, elevated cholesterol levels, and diabetes all amplify the risk. Furthermore, factors such as obesity, physical inactivity, unhealthy dietary choices, alcohol misuse, and illicit drug use contribute to the potential for experiencing a STEMI. Additionally, chronic stress can exacerbate this risk. These risk factors frequently intersect, compounding the likelihood of a heart attack. Effectively managing these risks through lifestyle modifications and, when necessary, medications is pivotal in reducing the risk of STEMI.

Clinical presentation

The clinical presentation of ST-elevation myocardial infarction (STEMI) is characterised by distinct features. Foremost, patients commonly report severe chest discomfort, which is frequently described as intense, crushing, or pressure-like. This pain often extends to the neck, jaw, shoulder, and particularly the left arm, reflecting its classic radiation pattern. Alongside chest pain, individuals may also exhibit shortness of breath, indicating respiratory distress linked to the cardiac event. Nausea and vomiting are not uncommon, adding to the discomfort. Profuse sweating, often described as cold and clammy diaphoresis, is a telltale sign. Additionally, there can be heightened anxiety and a sense of impending doom, contributing to psychological distress. Patients may also report unusual fatigue or weakness. Importantly, not all individuals with STEMI manifest all these symptoms, and their severity can differ. Early recognition and medical intervention are paramount, as timely treatment profoundly impacts the prognosis. 

Diagnosis       

The diagnosis of ST-elevation myocardial infarction (STEMI) primarily relies on patient history and electrocardiogram (ECG) findings. While STEMI can sometimes be asymptomatic or lead to sudden cardiac death, the majority of patients typically present with classic ischemic-type chest discomfort accompanied by noticeable ST-segment elevation on a 12-lead ECG. This ECG pattern often includes reciprocal ST segment depression in other leads. However, it's worth noting that atypical clinical presentations are not uncommon, especially in diabetic and elderly patients. Furthermore, there are several less common ECG variants that can either indicate or strongly suggest STEMI.

In some cases, echocardiography can be a valuable tool for ruling out acute STEMI by demonstrating the absence of regional wall motion abnormalities. The confirmation of a STEMI diagnosis is typically achieved through elevated cardiac biomarkers. Troponin measurements are preferred over other biomarkers due to their superior sensitivity and specificity, making them a key component in STEMI diagnosis.⁴

Treatment

Following the diagnosis of acute ST-elevation myocardial infarction (STEMI), there are crucial steps to be taken. Firstly, it's essential to establish intravenous access and initiate cardiac monitoring. Patients who are hypoxemic or at risk of hypoxemia may benefit from oxygen therapy, although recent studies have raised concerns about its use in normoxic patients. 

The gold standard treatment for STEMI is percutaneous coronary intervention (PCI), which should be performed within 90 minutes of presentation at a PCI-capable hospital or within 120 minutes if transfer to such a facility is necessary. If PCI is not achievable within the initial 120 minutes of first medical contact, fibrinolytic therapy should be initiated within 30 minutes of the patient's arrival at the hospital.³

It's crucial to rule out conditions that may mimic acute coronary syndrome, such as acute aortic dissection or acute pulmonary embolism.

For all patients with acute myocardial infarction, a standard treatment regimen includes starting a beta blocker, high-intensity statin, aspirin, and a P2Y12 inhibitor as soon as possible, with certain exceptions. Nitroglycerin can be administered to alleviate anginal pain but should be avoided in patients who have used phosphodiesterase-inhibiting medication within the last 24 hours and in cases of right ventricular infarction. Additionally, anticoagulation therapy, including unfractionated heparin, low-molecular-weight heparin, bivalirudin, or fondaparinux, should be initiated. ³

Complications

ST- Elevated Myocardial infarction can lead to three critical mechanical complications that significantly threaten a patient's life. These complications include ventricular free wall rupture, interventricular septum rupture, and acute mitral regurgitation. 

Ventricular free wall rupture is particularly ominous, occurring within about 5 days in approximately half of the cases and within 2 weeks in a staggering 90% of instances. Unfortunately, it carries an alarming overall mortality rate exceeding 80%. 

Interventricular septum rupture, while slightly less common, is still a grave concern. It typically manifests 3 to 5 days after the initial myocardial infarction and is associated with an overall mortality rate greater than 70%.

In cases of ST-elevation myocardial infarction, acute mitral regurgitation is often severe and is connected with a 30-day survival rate of just 24%. These mechanical complications are of utmost concern and require immediate medical attention and intervention to enhance patient outcomes and reduce the risk of mortality.

Conclusion

In summary, myocardial infarction, commonly known as a heart attack, is a multifaceted and life-threatening condition characterised by a range of risk factors, clinical symptoms, and mechanical complications. Various factors, such as age, gender, family history, hypertension, and smoking, interact to influence the likelihood of a heart attack. Recognising the clinical presentation of ST-elevation myocardial infarction (STEMI), marked by symptoms like chest pain, breathlessness, and nausea, is pivotal for early intervention.

The diagnosis of STEMI hinges on patient history and changes observed in an electrocardiogram (ECG). Treatment mainly involves percutaneous coronary intervention (PCI) and medication to restore blood flow and prevent complications. However, mechanical complications, such as ventricular free wall rupture, interventricular septum rupture, and acute mitral regurgitation, present significant risks and require swift management.

The intricate nature of myocardial infarction underscores the significance of comprehensive strategies for risk reduction, timely diagnosis, and the imperative need for immediate medical attention to mitigate the potentially devastating outcomes of this condition.