SCA means any chest pain of anginal appearance occurring de novo, prolonged or recently worsening in a patient with or without coronary history, most often accompanied byECGabnormalitieswith type of st+ segment overshift for STEMI, a fortiori if the ECG was performed in per-critical [3]. Among the SCAs, we have the STEMI to which our patientissubjected, in circumferential, following an attack of the guilty artery posing a problem of complete interruption of the blood flow resulting in a necrosis of the   territory downstream. This will be followed by the ischemic cascade which will result in the clinical expression made of infarctoid chest pain (ITD) (which is only the immergée part of theiceberg):  infarctoid chest pain is the master symptom of Myocardial Ischemia (MI).

In particular, the absence of angina does not mean the absence of coronary artery disease. On the other hand, in proven coronary patients, the absence of angina does not necessarily imply a benign prognosis. Conversely, the severity of the symptomatology isnot correlated with the spread of coronary artery disease and even less with its severity. Asymptomatic or silent myocardial ischemia (IMS) is defined by the presence of a subshift of the ST segment without contemporary pain [4]. On the other hand, Dr COHN, one of the first researchers onmyocardial disease, deended the IMS as follows: Evidence (especially by various laboratory means) of myocardial   ischeddisease or its complications, myocardial infarction, heart failure, ristheusand sudden death, without chest pain or   other evalent anginal symptoms (e.g., dyspnea). I1 has developed an IMS classification, dividing patients into three types. Type 1 who is the patient totally asymptomatic, the one who has never had chest pain, nor dyspnee with documented coronary artery disease e. Next, we note type 2, which is the asymptomatic post-infarction patient. I1 is a patient who could have had angina before the infarction and at the time of his infarction but who subsequently became asymptomatic even with an electedro cardiographic evidence (or by other laboratory means) of myocardial ischemia. Finally, there is the patient with angina and pisodes of myocardial ischesilencieuse [5]. By its definition, we attach IMS to the context of our patient who, without having suffered from any form of clinical expression of ischemia, makes a STEMI revealed at the post-IDM stage by an event of thromboembolic complications.  In reference to his troponin level at admission with a decrease in kinetics, and an aspect of necrosis consumed at the ECG, let's classify our patient in the type 1, a STEMI in asymptomatic circumferential, passed unnoticed, despite the electrical changes during the same day of his admission. On this, Dr BEAUDRY, puts forward three possible causes of IMS: a) an adéquat insufflating stimulus; b) a defect in the peripheral perception of pain (by exemple:  diabetic neuropathy) and c) a defect in the central transmission in the painful sensation. The third possibility applies specially to type 1, to the patient who has never had angina or dyspnea as a symptom related to myocardial ischemia [6]. It was later shown that mental stress or cigarette consumption led to episodes of IMS. The circadian rhythm is also involved by a significant increase in heart rate and systolic blood pressure may precede the onset of IMS episodes of daily life. And the threshold of ischemia depends on the duration of the increase in heart rate [4]. Our patient is not diabetic, so he would not suffer from diabetic neuropathy, moreover, he is inveterate smoker.

As for the endocavitic thrombus, its formation is classically favored by the elements of the Virchow triad: blood stasis, endothelial lesion and hypercoagulability. These three elements are present during the acute phase of infarction. That is an estimated 12.2% of patients with previous STEMI have an endocavitic thrombus ⁷.

"On MRI, gadolinium does not penetrate the thrombus, late enhancement sequences show necrosis in hypersignal and thrombus in frank hyposignal" [7] (Figure 5).

These thrombi are mainly located next to the tip of the VG, concern anterior IDMs, with extensive infarction and only revascularization seems to limit the frequency of thrombi [7].