Myocardial oedema: pathophysiological basis and implications for the failing heart

Abstract

Myocardial fluid homeostasis relies on a complex interplay between microvascular filtration, interstitial hydration, cardiomyocyte water uptake and lymphatic removal. Dysregulation of one or more of these mechanisms may result in myocardial oedema. Interstitial and intracellular fluid accumulation disrupts myocardial architecture, intercellular communication, and metabolic pathways, decreasing contractility and increasing myocardial stiffness. The widespread use of cardiac magnetic resonance enabled the identification of myocardial oedema as a clinically relevant imaging finding with prognostic implications in several types of heart failure. Furthermore, growing experimental evidence has contributed to a better understanding of the physical and molecular interactions in the microvascular barrier, myocardial interstitium and lymphatics and how they might be disrupted in heart failure. In this review, we summarize current knowledge on the factors controlling myocardial water balance in the healthy and failing heart and pinpoint the new potential therapeutic avenues.

Cardiac magnetic resonance imaging in detection of progressive graft dysfunction in pediatric heart transplantation

“…noted that not only was T2 elevated in patients with acute rejection, but also in patients with a history of acute rejection, which is similar to our finding of elevated T2 in patients with historical moderate/severe rejection 11 . The mechanism driving elevated global and peak T2 in these populations is likely multifactorial, such as inflammation from ongoing rejection or vascular inflammation related to CAV that is undetectable by EMB pathology and subclinical heart failure leading to disruption in myocardial fluid balance 34,35 . With recent advancements in graft surveillance utilizing cell‐free DNA and molecular technologies which are thought to be more specific than pathologist‐graded EMB, future exploration of the cause of inflammation using these tests in correlation with CMR is needed 36,37 …”

“…11 The mechanism driving elevated global and peak T2 in these populations is likely multifactorial, such as inflammation from ongoing rejection or vascular inflammation related to CAV that is undetectable by EMB pathology and subclinical heart failure leading to disruption in myocardial fluid balance. 34,35 With recent advancements in graft surveillance utilizing cell-free DNA and molecular technologies which are thought to be more specific than pathologist-graded EMB, future exploration of the cause of inflammation using these tests in correlation with CMR is needed. 36,37 With elevated T2 in both the population with historical moderate/severe rejection as well as CAV, there is potential for T2 as a surveillance marker that represents ongoing myocardial inflammation, which may contribute to progressive graft failure.…”

Myocardial Oedema as a Consequence of Viral Infection and Persistence – a Narrative Review with Focus on COVID-19 and Post COVID Sequelae

“…A key factor in myocardial fluid homeostasis and preventing interstitial fluid accumulation is the removal of filtered fluid via lymphatic fluid drainage [1,50]. Although myocardial fluid exchange is suspected to occur mainly on the venular side of the capillary bed [51], it is important to recognize that most tissues greatly rely on lymphatic fluid removal rather than venous capillary absorption for interstitial fluid removal and tissue fluid balance [32].…”

“…Myocardial fluid homeostasis is based on a complex interaction between microvascular filtration and absorption, interstitial hydration as well as water uptake by cardiomyocytes, and lymphatic removal [1]. Pathological conditions like ischaemia, ischaemia-reperfusion injury, inflammation, and hypertension disturb the subtle equilibrium and dysregulate myocardial fluid dynamics [2].…”

“…Myocardial oedema (MO) has been identified in various cardiac diseases including heart failure (HF) [1], ischaemia-reperfusion injury [7] , and myocarditis [8,9]. MO develops not only due to disturbances to the microvascular barrier leading to increased endothelial permeability through glycocalyx degradation and pericyte detachment, but also due to changes in the composition of the 2 myocardial extracellular matrix (mECM), the cardiac lymphatic system and cardiomyocyte homoeostasis [1]. Myocardial cells play a critical role in fluid homeostasis regulation through the control of ion pumps and membrane-bound proteins [10].…”