Left ventricular aneurysm repair in rats: structural, functional, and molecular consequences.
OBJECTIVE
This study examined the effects of aneurysm repair in a rat model of myocardial infarction on functional indices and on the spatiotemporal distribution of cardiac contractile protein and natriuretic peptide messenger RNA.


METHODS
In a rat infarct model, expanded left ventricular aneurysms were plicated 4 weeks after infarction. At 30 weeks, transverse heart sections were taken at 4 levels (apex [level 1] through base [level 4]) and assessed by in situ hybridization histochemistry to determine regional messenger RNA levels of pre-pro-atrial natriuretic peptide, cardiac alpha-actin, skeletal alpha-actin, myosin light chain-2v, and beta-myosin heavy chain.


RESULTS
Rats with plicated left ventricular aneurysms had reduced left ventricular endocardial circumference (19%, P <.005), lower heart weight ratio (31%, P <.05), left ventricular end-diastolic pressures (51%, P <.05), and increased +/-dP/dt (34%-38%, P <.05). Cardiac messenger RNA levels of pre-pro-atrial natriuretic peptide were reduced in the septum (levels 2 and 3), and skeletal alpha-actin levels were reduced in the septum and left ventricular free wall of plicated rats (level 3). beta-Myosin heavy chain levels were markedly reduced in peri-infarct regions of the left ventricular free wall, septum, and right ventricle in plicated rats at level 4, whereas myosin light chain-2v levels were reduced at levels 2 and 4 in the left ventricular free wall and at level 4 in the right ventricle.


CONCLUSIONS
Plication of left ventricular aneurysm after infarction in the rat significantly reduced cardiac hypertrophy, improved cardiac function, and reduced the upregulation of pre-pro-atrial natriuretic peptide and both fetal and adult contractile protein isoforms associated with cardiac hypertrophy.
Sakaguchi
G
G
Departments of Clinical Pharmacology and Therapeutics and Cardiac Surgery, Austin and Repatriation Medical Centre, Heidelberg, Victoria 3084, Australia.
Young
R L
RL
Komeda
M
M
Yamanaka
K
K
Buxton
B F
BF
Louis
W J
WJ
D000199:Actins / Q000235:genetics / Q000378:metabolism; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000235:genetics / Q000378:metabolism; D015415:Biomarkers; D024722:Cardiac Myosins; D015342:DNA Probes / Q000737:chemistry; D005260:Female; D006322:Heart Aneurysm / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000601:surgery*; D006346:Heart Septum / Q000378:metabolism / Q000473:pathology; D006352:Heart Ventricles / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology / Q000601:surgery; D017403:In Situ Hybridization; D009206:Myocardium / Q000378:metabolism*; D018995:Myosin Heavy Chains / Q000235:genetics / Q000378:metabolism; D018994:Myosin Light Chains / Q000235:genetics / Q000378:metabolism; D009929:Organ Size; D011498:Protein Precursors / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D016277:Ventricular Function, Left / Q000502:physiology
D000199:Actins; D015415:Biomarkers; D015342:DNA Probes; D018994:Myosin Light Chains; D011498:Protein Precursors; D012333:RNA, Messenger; C107184:myosin light chain 2; D009320:Atrial Natriuretic Factor; D024722:Cardiac Myosins; D018995:Myosin Heavy Chains