RT Journal Article
SR Electronic
T1 Post-ischaemic myocardial dysfunction (stunning) results from myofibrillar oedema
JF Heart
JO Heart
FD BMJ Publishing Group Ltd and British Cardiovascular Society
SP 166
OP 171
DO 10.1136/hrt.2006.102434
VO 94
IS 2
A1 T Bragadeesh
A1 A R Jayaweera
A1 M Pascotto
A1 A Micari
A1 D E Le
A1 C M Kramer
A1 F H Epstein
A1 S Kaul
YR 2008
UL http://heart.bmj.com/content/94/2/166.abstract
AB Objective: To test the hypothesis that myocardial stunning is due to myofibrillar oedema.Methods: Experiments were performed in anaesthetised closed-chest pigs. In 15 pigs (group 1), myocardial stunning was produced by repetitive ischaemia and reperfusion; 5 pigs each were studied at 2 hours, 2 days, and 5 days later. Circumferential left ventricular (LV) mid-wall myocardial strain (Ecc) was estimated in vivo using tagged magnetic resonance imaging. Myocardial water content (MWC) was measured post mortem, from which interfilament lattice distance (d) was calculated. In 6 pigs (group 2), myocardial dysfunction was produced by intracoronary administration of a mast cell degranulator. Animals were euthanised immediately upon induction of regional LV dysfunction to avoid development of inflammation. In 4 pigs (group 3), transmission electron microscopy (EM) was performed to quantify d in stunned versus normal myocardium.Results: In group 1 pigs, MWC was raised in the stunned compared with normal myocardium (p<0.02) and decreased over time. An inverse relation was found between Ecc and MWC in the stunned myocardium (r = −0.81) and between Ecc and d (r = −0.90). A similar relation was noted between wall thickening and increase in MWC in group 2 (r = −0.84) pigs. In group 3 pigs, d on EM was significantly lower (40 (3) nmol/l) in normal myocardium than in stunned myocardium (46.4 (4) nmol/l), p<0.001.Conclusions: Ischaemia–reperfusion results in myocardial oedema, with consequent myocyte swelling and myofibrillar oedema. The latter leads to an increase in d, causing myosin heads to either fail to latch, or to latch improperly, onto the actin filament with poor force generation, leading to myocardial dysfunction. As the myocardial oedema abates, myocyte function improves.