The apical myocardial infarction is a subtype of the acute coronary syndrome, caused by myocardial ischemia. This particular type of infarction is subject to debate, given that its electrocardiography description does not always correlate with echocardiography findings. V1 to V4 abnormalities were considered to denote anteroseptal suffering, but other studies showed that the involvement of anteroapical and apical segments manifests with ECG changes in the same territory.
The presentation of an apical myocardial infarction patient depends on whether the disease is acute or chronic. Acute patients have the usual complaints of cardiac ischemia patients. A strictly apical location implies that the mass of the affected myocardial tissue is relatively small, therefore the patient is unlikely to present in cardiogenic shock, but rather be a Killip class I case, with no evidence of heart failure. Pulmonary edema presentation is also unlikely. In return, the patient complains of chest pain that often radiates to the epigastrium or malaise. The pain is severe and lasts for 30 to 60 minutes. The character of the disease is different in different individuals, being described as a squeezing, burning, pressure, aching or sharp sensation. In other cases, myocardial ischemia can go unrecognized, as the patient believes he or she is suffering from indigestion or has no complaints whatsoever. This latter situation is more frequently seen in diabetes, dementia or elderly patients. Symptoms are more frequent during the early morning hours [1].
Patients with a previous apical myocardial infarction may have heart failure signs if the acute event was not strictly apical, but involved significant parts of neighboring walls and was complicated by aneurysm formation that occupies a significant ventricular territory. The anterior wall is more frequently implicated than the inferior and posterior ones.
The first step in addressing a non-critical myocardial infarction patient should be obtaining the history of the disease and assessing risk factors [2] [3]. Clinical examination should assess the skin (color and presence of diaphoresis), blood pressure, pulse (frequency, rhythm and equality in similar territories), heart and breathing sounds, the presence of gastrointestinal symptoms such as nausea and vomiting, neck vein aspect, temperature (fever is present during the first two days of evolution [4]) and urinary output.
Once the suspicion of an acute myocardial infarction is raised, electrocardiography is usually the first investigation performed. As discussed above, the apical localization is rather difficult to define by this method, but modifications do appear in contiguous leads.
The electrocardiogram also detects newly installed branch blocks, also an indicator of ischemia, and potentially life-threatening arrhythmias [5] [6].
The protocol states that cardiac enzymes (troponin, myoglobin and creatine kinase) should be measured in a serial manner [7] [8]. Recent guidelines advise that high-sensitive troponin I or troponin T assays should be used [9] [2]. Brain natriuretic peptide or N-terminal pro-B-type natriuretic peptide is only useful in chronic myocardial infarction patients for risk stratification and heart failure prognosis [10] [11].
The exact localization of the infarction area is stated by imaging methods. Echocardiography is a useful, readily available and reliable method that helps to evaluate wall motion abnormalities. Multidetector computed tomography and single-photon emission CT (SPECT) or positron emission tomography (PET) scanning, although viable methods, are not routinely used in triage settings, but are useful in detecting ventricular aneurysms [12]. Classic coronary catheterization has the advantage of offering clear diagnosis and being a therapeutic procedure, as well.