Acute transient coronary sinus hypertension impairs left ventricular function and induces myocardial edema

Abstract

This study was performed to evaluate the direct and indirect effects of acute coronary sinus hypertension (CSH) on systolic and diastolic left ventricular (LV) function. Coronary sinus pressure was elevated to 25 mmHg for 3 h in eight pentobarbital-anesthetized dogs and then relieved. LV contractility was assessed by preload recruitable stroke work (PRSW) and end-systolic elastance (Ees). Diastolic function was assessed by the time constant of isovolumic relaxation (tau) and the end-diastolic pressure volume relationship (EDPVR). PRSW and Ees decreased progressively, and tau and the slope of the EDPVR increased progressively with CSH. These changes persisted after relief of CSH. beta-Adrenergic and cholinergic receptor blockade, performed in six dogs, did not alter the effects of CSH on systolic or diastolic function. The LV wet-to-dry weight ratios of the groups with CSH were significantly greater than those of a control group without CSH. We conclude that CSH results in changes in the left ventricle that depress contractility, prolong active relaxation, and increase diastolic stiffness. The dysfunction was not the direct effect of CSH or autonomic reflex activation, but may have been induced by fluid accumulation within the interstitium.

Effect of osmolarity on the zero-stress state and mechanical properties of aorta

“…Similar results were reported in a study of pig and rat myocardium in which crystalloid-induced myocardial edema was associated with an increase in stiffness and a decrease in the filling volume of the left ventricle (2). Pratt et al (27) also found that interstitial myocardial edema induced by acute transient coronary sinus hypertension depresses contractility and increases diastolic stiffness of the left ventricle in dogs. Contrary to these findings, a recent study of rat intestinal edema showed decreased stiffness and residual stress, which result in intestinal transit delay (28).…”

Pathophysiology and pathogenesis of post-resuscitation myocardial stunning

“…This impedes fluid removal from the cardiac interstitium via myocardial lymphatics, which results in fluid accumulation in the left ventricle and left ventricular dysfunction [74,80]. Moreover, the increased central venous pressure increases coronary sinus pressure and, thus, coronary microvascular pressure resulting in fluid filtration into the cardiac interstitium and additional fluid accumulation in the left ventricle [74,80,81]. Meanwhile, the sympathetic neural responsiveness is disrupted due to the effect of ischemia on neural cells, as well as due to the increased levels of exogenous epinephrine which downregulate the expression of a-and b-receptors leading to reduced inotropic and coronary vasoconstrictor responses.…”

Diagnostic usefulness of the oedema-infarct ratio to differentiate acute from chronic myocardial damage using magnetic resonance imaging

“…However, experimental studies have demonstrated that LV myocardial interstitial edema induces both systolic and diastolic LV dysfunction, increased coronary vascular resistance, and arrhythmias due to a decreased refractory period [26][27][28]. As mentioned above, mechanical alterations provide an increased myocardial stiffness as a consequence of an excessive interstitial water distribution and an alteration by the interaction of collagen fibres, leading to an increase in the diffusion distance needed to supply oxygen to the myocytes [29].…”