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Heart failure:
Alessandra Meris, Maria Amigoni, Hajime Uno, Jens Jakob Thune, Anil Verma, Lars Køber, Mikhail Bourgoun, John J. McMurray, Eric J. Velazquez, Aldo P. Maggioni, Jalal Ghali, J. Malcolm O. Arnold, Steven Zelenkofske, Marc A. Pfeffer, and Scott D. Solomon
Left atrial remodelling in patients with myocardial infarction complicated by heart failure, left ventricular dysfunction, or both: the VALIANT Echo Study
Eur Heart J 2009; 30: 56-65 [Abstract] [Full text] [PDF]
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[Read eLetter] Left atrium remodelling after acute myocardial infarction: different in different risk categories
Bogdan A. Popescu, Francesco Antonini-Canterin, Gian Luigi Nicolosi   (3 November 2009)

Left atrium remodelling after acute myocardial infarction: different in different risk categories 3 November 2009
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Bogdan A. Popescu,
Senior lecturer
“Carol Davila” University of Medicine, Institute of Cardiovascular Diseases, Bucharest, Romania,
Francesco Antonini-Canterin, Gian Luigi Nicolosi

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Re: Left atrium remodelling after acute myocardial infarction: different in different risk categories

We read with interest the article by Meris et al.[1] about the remodelling of the left atrium (LA) in patients with myocardial infarction complicated by heart failure (HF), left ventricular (LV) dysfunction, or both. The authors confirm previously demonstrated changes in LA size and the prognostic role of LA dilatation in the acute phase postinfarction in a cohort of high-risk patients from the VALIANT Echo Study (566 patients had an echocardiogram at baseline, and 379 patients were followed up to 20 months). Less than 30% of patients were in Killip class 1 at admission, mean LV ejection fraction was <40% at baseline, and mean indexed LV end -systolic volume was >68.2 ml/m2. All patients had HF, LV dysfunction, or both. Significant LA remodelling was found at 1 month, and remodelling of the LA continued up to 20 months. The baseline independent predictors of LA remodelling were hypertension, LV mass, and renal dysfunction. Changes in LA size were related to increasing in LV volume and worsening of mitral regurgitation. In this high-risk population, with a large extent of LA remodelling, LA dilatation represented not only a predictor of all- cause mortality, confirming previous studies,[2,3] but also of cardiovascular morbidity.

We have previously reported postinfarction LA remodelling in a large cohort of 514 low-risk patients from the GISSI-3 Echo Substudy followed with serial echocardiograms up to 6 months postinfarction.[4] It is of interest to compare the characteristics of postinfarction LA remodelling in two categories of patients at very different risk enrolled in these two large studies. The GISSI-3 Echo Substudy demonstrated the existence of LA remodelling (assessed as changes in indexed LA area) even in low risk postinfarction patients. There were 87% patients in Killip class 1 at admission, mean LV ejection fraction was 47±7%, and indexed LV end-systolic volume was 44±16 ml/m2 at baseline. There was no mortality at 6 months (by design), and the incidence of HF at 6 months was 21.8%. Left atrial remodelling was already significant before discharge (at 12±5 days postinfarction) and it continued throughout the 6 months of echo followup. The only independent predictor of LA remodeling in the GISSI-3 Echo Substudy was the extent of LV remodelling (changes in indexed LV end- diastolic volume), while hypertension, baseline severity of mitral regurgitation, and age were not significantly related to LA remodelling. The increase in LA size did not have a prognostic role in such a low-risk population, with few adverse events during follow-up.[4]

In summary, LA remodelling occurs early after myocardial infarction even in low-risk patients, but it only carries prognostic role in higher- risk patients, when the extent of remodelling is more pronounced (i.e. LA volume>32 ml/m2).[1-3] As LV remodelling was in both studies a major determinant of LA remodelling this may represent yet another argument for a more aggressive treatment of patients with acute myocardial infarction in order to limit the remodelling process of both the left ventricle and the left atrium, and to improve prognosis.[4]

References

1. Meris A, Amigoni M, Uno H, Thune JJ, Verma A, Køber L, Bourgoun M, McMurray JJ, Velazquez EJ, Maggioni AP, Ghali J, Arnold JMO, Zelenkofske S, Pfeffer MA, Solomon SD. Left atrial remodelling in patients with myocardial infarction complicated by heart failure, left ventricular dysfunction, or both: the VALIANT Echo Study. Eur Heart J 2009;30:56–65.

2. Møller JE, Hillis GS, Oh JK, Seward JB, Reeder GS, Wright RS, Park SW, Bailey KR, Pellikka PA. Left atrial volume. A powerful predictor of survival after acute myocardial infarction. Circulation 2003;107:2207–2212.

3. Beinart R, Boyko V, Schwammenthal E, Kuperstein R, Sagie A, Hod H, Matetzky S, Behar S, Eldar M, Feinberg MS. Long-term prognostic significance of left atrial volume in acute myocardial infarction. J Am Coll Cardiol 2004;44:327–334.

4. Popescu BA, Macor F, Antonini-Canterin F, Giannuzzi P, Temporelli PL, Bosimini E, Gentile F, Maggioni AP, Tavazzi L, Piazza R, Ascione L, Stoian I, Cervesato E, Nicolosi GL. Left atrium remodeling after acute myocardial infarction (results of the GISSI-3 Echo Substudy). Am J Cardiol 2004;93:1156-1159.

Conflict of Interest:

None declared