A heart attack commonly does not have apparent symptoms; silent myocardial ischemia can occur in the absence of chest discomfort or other anginal equivalent symptoms, e.g., dyspnea, nausea, diaphoresis, etc., with ST-segment changes on EKG, reversible regional wall motion abnormalities, or perfusion defects on scintigraphy studies. MI occurs due to multiple factors resulting in an imbalance between consumption and production of adenosine triphosphate (ATP), causing ATP depletion leading to a cascade of biochemical events. Silent myocardial ischemia (SMI) obtained recognition at the beginning of the 20th century. About 70% to 80% of transient ischemic episodes do not present with anginal chest pain or any other symptoms (silent ischemia). Lack of pain in silent myocardial infarction (MI) increases morbidity and mortality since patients do not seek medical treatment in a timely fashion.[1][2]

Patient classification is as one of three types of silent ischemia:

• Type I: This is the least common form and occurs in completely asymptomatic patients with CAD (which may be severe) in the absence of anginal symptoms.

• Type II: This type occurs in patients with documented previous myocardial infarction.

• Type III: This is the most common form and occurs in patients with the usual forms of chronic stable angina, unstable angina, and vasospastic angina.

Diabetes mellitus (DM): Diabetes mellitus (DM) is a significant risk factor for coronary artery disease and correlates with a higher incidence of SMI. Cardiac autonomic dysfunction is the main culprit in diabetic patients which involves pain receptors, afferent neurons or higher areas of the brain.[3][4]

Studies have shown that atherogenic dyslipidemia strongly correlates with an increased risk of SMI and silent CAD in patients with DM and the management of atherogenic dyslipidemia might help to reduce the high residual burden of cardiovascular disease.[5]

In surgery: There is a relatively high incidence of perioperative MI in the geriatric population. Studies have shown that patients who underwent coronary artery bypass graft surgery had episodes of SMI detected by Holter monitoring. In the intensive care unit: Critically ill patients in the intensive care unit (ICU) admitted for noncardiac causes are also at risk of acute myocardial ischemia. Transient myocardial ischemia and advanced age are significant predictors of cardiac events.  Sleep apnea: Obstructive sleep apnea carries correlations with myocardial ischemia (silent or symptomatic), cardiac arrhythmias, pulmonary hypertension, heart failure, transient ischemic attack, and stroke.

Studies have shown that the incidence rate of SMI is higher in men than in women. There is an increased risk of coronary heart disease deaths and all-cause mortality among both men and women with SMI. But there is a potentially greater increased risk among women.[6]

A myocardial infarct is mainly caused by rupture of an atherosclerotic plaque in any of the blood vessels supplying oxygen to the heart. Pathophysiology involved in this process includes movement of inflammatory cells in the vessel wall, engulfment of cholesterol products causing these macrophages to become foam cells, releasing growth factors which causes fibrin and smooth muscles to become part of the plaque. Plaques may have a thin or thick fibrous cap, rupture of these plaques causes devastating injury.[7]

Histological findings in the setting of acute MI are as follows;

• Characteristic histological features within the first 24 hours of insult include; coagulation necrosis of cardiomyocyte, neutrophilic infiltration, accumulation of RBCs in the interstitial spaces and interstitial edema. Eosinophilic appearing ischemic cardiomyocytes with loss of the cross-striations and loss of the nuclei. Within the next 24 to 48 hours, coagulative necrosis establishes completely. After 3 to 5 days, there is a loss of myocyte nuclei and striations in the central portion of the infarct. By 5 to 7 days, macrophages and fibroblasts appear. At 1 week, the number of neutrophils starts to decline, and granulation tissue establishes with lymphocytic and plasma cell infiltration. 

• Healing continues and, may be complete as early as 4 weeks or may require 8 weeks or longer to complete depending on the extent of necrosis. Sometimes, borders of larger infarct heal leaving the central area unhealed with mummified myocyte for extended periods. 

• If reperfusion occurs early within 4 to 6 hours, there is a possibility that infarct would be sub-endocardial without transmural extension. Macrophages appear by day 2 to 3, and by day 3 to 5 fibroblast appears, with early signs of healing.  As compared with that of non-reperfused infarcts, subendocardial infarcts heal early. They may undergo full healing as few as in 2 to 3 weeks. While some larger infarcts and those who take longer to be reperfused, beyond 6 hours show extensive areas of hemorrhage.[8][9]