Mechanics of the left ventricular myocardial interstitium: effects of acute and chronic myocardial edema

Abstract

Myocardial interstitial edema forms as a result of several disease states and clinical interventions. Acute myocardial interstitial edema is associated with compromised systolic and diastolic cardiac function and increased stiffness of the left ventricular chamber. Formation of chronic myocardial interstitial edema results in deposition of interstitial collagen, which causes interstitial fibrosis. To assess the effect of myocardial interstitial edema on the mechanical properties of the left ventricle and the myocardial interstitium, we induced acute and chronic interstitial edema in dogs. Acute myocardial edema was generated by coronary sinus pressure elevation, while chronic myocardial edema was generated by chronic pulmonary artery banding. The pressure-volume relationships of the left ventricular myocardial interstitium and left ventricular chamber for control animals were compared with acutely and chronically edematous animals. Collagen content of nonedematous and chronically edematous animals was also compared. Generating acute myocardial interstitial edema resulted in decreased left ventricular chamber compliance compared with nonedematous animals. With chronic edema, the primary form of collagen changed from type I to III. Left ventricular chamber compliance in animals made chronically edematous was significantly higher than nonedematous animals. The change in primary collagen type secondary to chronic left ventricular myocardial interstitial edema provides direct evidence for structural remodeling. The resulting functional adaptation allows the chronically edematous heart to maintain left ventricular chamber compliance when challenged with acute edema, thus preserving cardiac function over a wide range of interstitial fluid pressures.

Functional and Morphological Parameters with Tissue Characterization of Cardiovascular Magnetic Imaging in Clinically Verified “Infarct-like Myocarditis”

“…The elevated LVMI in the AMC group (p = 0.034) results from acute inflammation with successive edema. Edema within the myocardium may result in capillary compression and reduced diastolic and systolic cardiac function [20,21]. We were able to identify wall motion abnormalities in 63 % of the AMC group, which can be broken down into regional distribution in 47 % and global distribution in 16 %.…”

The Role of Aquaporin 1 Activated by cGMP in Myocardial Edema Caused by Cardiopulmonary Bypass in Sheep

“…In addition, CPB has been associated with decreased myocardial systolic and diastolic function. The prevalence of generalized edema in neonates undergoing cardiovascular surgery with CPB has been reported to be 37% and 54% [4,5,41,42]. In our study, we found that the expression of cGMP and AQP1 were lowest at 6 h, and then began to increase, and reached peak levels at 48 h. Meanwhile, water content of myocardial tissue increased following the CPB surgery, and peaked at 48 h. These findings suggested that cGMP and AQP1 had important roles in water intake during CPB.…”

“…Conversely, the use of cardiopulmonary bypass (CPB) causes profound alterations in the homeostasis of physiological fluids, which often results in myocardial edema. CPB has been associated with decreased myocardial systolic and diastolic function [4,5]. However, none of these aspects of myocardial edema in CPB has been completely characterized.…”

Cardiorenal Syndrome Type 3: Pathophysiologic and Epidemiologic Considerations

“…The resulting alveolar congestion and edema is in part mediated by altered expression of epithelial sodium channel and aquiporin-5 expression. Similar mechanisms may also contribute to myocardial interstitial edema and dysfunction [44]. Transgenic sickle mice subjected to renal IRI exhibited significantly increased myocardial capillary congestion, serum amyloid-P (murine equivalent of C-reaction protein), and renal expression of caspase-3 compared with controls [45].…”

“…In addition, fluid removal in these patients, either through loop diuretics use [55] or ultrafiltration [56], was associated with higher survival. Fluid accumulation may adversely impact myocardial performance [44], predispose to ventricular arrhythmias [57] and may contribute to maladaptive ventricular remodelling and myocardial fibrosis [44,58].…”