Acute transient coronary sinus hypertension impairs left ventricular function and induces myocardial edema
J W Pratt1, E R Schertel, S L Schaefer
1Department of Surgery, Ohio State University, Columbus 43210, USA.
Insights
Acute coronary sinus hypertension (CSH) impairs left ventricular (LV) systolic and diastolic function, leading to reduced contractility and increased stiffness. These effects persist even after pressure relief, likely due to interstitial fluid accumulation.
Area of Science:
- Cardiovascular Physiology
- Cardiac Mechanics
Background:
- Coronary sinus hypertension (CSH) is a condition that can affect cardiac function.
- Understanding the direct and indirect effects of CSH on the left ventricle (LV) is crucial for diagnosing and treating related heart conditions.
Purpose of the Study:
- To evaluate the direct and indirect effects of acute coronary sinus hypertension (CSH) on systolic and diastolic left ventricular (LV) function.
- To investigate the underlying mechanisms of LV dysfunction induced by CSH.
Main Methods:
- Acute coronary sinus hypertension (CSH) was induced in pentobarbital-anesthetized dogs by elevating coronary sinus pressure to 25 mmHg for 3 hours.
- Left ventricular (LV) systolic function was assessed using preload recruitable stroke work (PRSW) and end-systolic elastance (Ees).
- Diastolic function was evaluated by measuring the time constant of isovolumic relaxation (tau) and the end-diastolic pressure-volume relationship (EDPVR).
Main Results:
- CSH progressively decreased PRSW and Ees, indicating impaired systolic function.
- CSH progressively increased tau and the slope of the EDPVR, indicating prolonged relaxation and increased diastolic stiffness.
- These functional changes persisted after CSH relief and were not altered by beta-adrenergic and cholinergic receptor blockade.
- LV wet-to-dry weight ratios were significantly greater in dogs with CSH, suggesting interstitial fluid accumulation.
Conclusions:
- Acute coronary sinus hypertension (CSH) induces significant left ventricular (LV) dysfunction, characterized by depressed contractility, prolonged relaxation, and increased diastolic stiffness.
- The observed LV dysfunction is not a direct hemodynamic effect of CSH nor mediated by autonomic reflex activation.
- Interstitial fluid accumulation within the LV interstitium is the likely mechanism responsible for the observed cardiac dysfunction following CSH.
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.
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