Relationship between transcardiac extraction of aldosterone and left ventricular remodeling in patients with first acute myocardial infarction: extracting aldosterone through the heart promotes ventricular remodeling after acute myocardial infarction.
OBJECTIVE
The purpose of this study was to evaluate whether plasma aldosterone (ALD) is extracted or produced through the heart in patients with acute myocardial infarction (AMI) and to determine the relationship between transcardiac extraction of plasma ALD and left ventricular (LV) remodeling.


BACKGROUND
Although we demonstrated that circulating ALD was extracted through the failing heart and that transcardiac extraction of ALD correlated with LV end-diastolic volume index (LVEDVI) in patients with congestive heart failure, the existence and increase of ALD synthase in the hearts of infarct rats were reported, suggesting cardiac production of ALD in patients with AMI.


METHODS
We measured plasma ALD in the aortic root (Ao) and coronary sinus (CS) in 57 consecutive patients who received successful revascularization and enalapril, with first AMI at acute phase and after one month. We also measured plasma procollagen type III aminoterminal peptide (PIIINP) in the CS.


RESULTS
Plasma ALD was significantly lower in the CS than it was in the Ao at the acute phase (84.7 +/- 6.3 pg/ml vs. 105.5 +/- 8.0 pg/ml, p < 0.0001). Significant positive correlations exist between the transcardiac gradient of ALD at the acute phase and the LVEDVI at one month. Moreover, the transcardiac gradient of plasma ALD at the acute phase has a significant correlation with plasma PIIINP, a biochemical marker of fibrosis, after one month. Stepwise multivariate analysis showed that transcardiac extraction of plasma ALD at the acute phase had an independent and significant positive relationship with a large LVEDVI after one month.


CONCLUSIONS
These results indicate that plasma ALD is extracted through the heart in patients with AMI at the acute phase and that the extracted ALD plays an important role in modulating post-infarct LV remodeling.
Hayashi
M
M
First Department of Internal Medicine, Shiga University of Medical Science, Seta-Tsukinowa, Otsu, Japan.
Tsutamoto
T
T
Wada
A
A
Maeda
K
K
Mabuchi
N
N
Tsutsui
T
T
Matsui
T
T
Fujii
M
M
Matsumoto
T
T
Yamamoto
T
T
Horie
H
H
Ohnishi
M
M
Kinoshita
M
M
D000208:Acute Disease; D000368:Aged; D000450:Aldosterone / Q000097:blood* / Q000502:physiology*; D015906:Angioplasty, Balloon, Coronary; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D001011:Aorta / Q000737:chemistry*; D015415:Biomarkers / Q000032:analysis / Q000097:blood; D003331:Coronary Vessels / Q000737:chemistry*; D019405:Cytochrome P-450 CYP11B2 / Q000032:analysis* / Q000502:physiology*; D018450:Disease Progression; D004656:Enalapril / Q000627:therapeutic use; D005260:Female; D005355:Fibrosis; D006333:Heart Failure / Q000209:etiology* / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D006801:Humans; D008297:Male; D008875:Middle Aged; D000451:Mineralocorticoid Receptor Antagonists; D015999:Multivariate Analysis; D009203:Myocardial Infarction / Q000150:complications* / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D010446:Peptide Fragments / Q000097:blood; D011347:Procollagen / Q000097:blood; D011446:Prospective Studies; D012720:Severity of Illness Index; D013318:Stroke Volume; D013997:Time Factors; D014680:Veins; D020257:Ventricular Remodeling / Q000502:physiology*
D000806:Angiotensin-Converting Enzyme Inhibitors; D015415:Biomarkers; D000451:Mineralocorticoid Receptor Antagonists; D010446:Peptide Fragments; D011347:Procollagen; C041876:procollagen Type III-N-terminal peptide; D000450:Aldosterone; D004656:Enalapril; D019405:Cytochrome P-450 CYP11B2