Abstract
Myocardial edema is one of the most common complications of coronary artery bypass grafting (CABG) that is linearly related to many coronary artery diseases. Myocardial edema can cause several consequences including systolic dysfunction, diastolic dysfunction, arrhythmia, and cardiac tissue fibrosis that can increase mortality in CABG. Understanding myocardial fluid balance and tissue and systemic fluid regulation is crucial in order to ultimately link how coronary artery bypass grafting can cause myocardial edema in such a setting. The identification of susceptible patients by using imaging modalities is still challenging. Future studies about the technique of imaging modalities, examination protocols, prevention, and treatment of myocardial edema should be carried out, in order to limit myocardial edema occurrence and prevent complications.
Highlights
Myocardial edema is a medical condition that can be detected in many cardiac conditions [1, 2]
One of the causes of myocardial edema is myocardial injury as occurring in coronary artery bypass grafting (CABG). e increased number of patients undergoing CABG is linear with the increasing number of patients with coronary heart disease (CHD)
Myocardial edema is the earliest sign of cardiac dysfunction that later can contribute to post-CABG mortality [10, 11]
Summary
Myocardial edema is a medical condition that can be detected in many cardiac conditions [1, 2]. A small increase in the amount of myocardial fluid content can cause some significant systolic and diastolic disturbances [12]. Dysfunctions that are caused by myocardial edema include systolic dysfunction, diastolic dysfunction, cardiac arrhythmia, and tissue fibrosis. Cardiac arrhythmia and conduction disturbance increase myocardial stiffness and reduce compliance that can affect the systolic and diastolic function and alter the myocardial cellular fluid composition. The interstitial fluid pressure of myocardial tissue range between 15 and 120 mmHg (from end-diastolic to end-systolic phase). Capillaries and lymphatic vessels’ functions are disrupted during the systolic phase and in turn limit blood flow and transmicrovascular fluid flow from coronary vessels into interstitial space of myocardial tissue. Laine et al [13] mention that an increase in myocardial fluid content by 3.5% can reduce cardiac output by 30–50%. Body fluid regulation can be classified into cellular, tissue, and homeostasis of whole-body fluid that will be discussed later [10]
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