It takes time to heal a broken heart: Ventricular plasticity improves heart performance after myocardial infarction in rainbow trout, Oncorhynchus mykiss

Coronary arteriosclerosis is a common feature of both wild and farmed
salmonid fishes and may be linked to stress-induced cardiac pathologies.
Yet, the plasticity and capacity for long-term myocardial restructuring
and recovery following a restriction in coronary blood supply is unknown.
Here, we analyzed the consequences of acute (3 days) and chronic (from 33
to 62 days) coronary occlusion (i.e., coronary artery ligation) on cardiac
morphological characteristics and in vivo function in juvenile rainbow
trout, Oncorhynchus mykiss. Acute coronary occlusion resulted in elevated
resting heart rate and decreased inter-beat variability, which are both
markers of autonomic dysfunction following acute myocardial ischemia,
along with severely reduced heart rate scope (maximum – resting heart
rate) relative to sham-operated trout. We also observed a loss of
myocardial interstitial collagen and compact myocardium. Following
long-term coronary- ligation, resting heart rate and heart rate scope
normalized relative to sham-operated trout. Moreover, a distinct fibrous
collagen layer separating the compact myocardium into two layers had
formed. This may contribute to maintain ventricular integrity across the
cardiac cycle, or alternatively, demark a region of the compact myocardium
that continues to receive oxygen from the luminal venous blood. Taken
together, we demonstrate that rainbow trout may cope with the aversive
effects caused by coronary artery obstruction through plastic ventricular
remodeling, which, at least in part, restores cardiac performance and
myocardium oxygenation.