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.
Departments of Clinical Pharmacology and Therapeutics and Cardiac Surgery, Austin and Repatriation Medical Centre, Heidelberg, Victoria 3084, Australia.
G
G
Sakaguchi
R L
RL
Young
M
M
Komeda
K
K
Yamanaka
B F
BF
Buxton
W J
WJ
Louis
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