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Increased myocardial apoptosis in patients with unfavorable left ventricular remodeling and early symptomatic post-infarction heart failure

Antonio Abbate, MD^*,*, Giuseppe G. L. Biondi-Zoccai, MD^*, Rossana Bussani, MD, Aldo Dobrina, MD, Debora Camilot, MD, Florinda Feroce, MD, Raffaele Rossiello, MD, Feliciano Baldi, MD, Furio Silvestri, MD, Luigi M. Biasucci, MD, FACC^* and Alfonso Baldi, MD

^* Institute of Cardiology, Catholic University of the Sacred Heart, Rome, Italy
Department of Pathologic Anatomy, University of Trieste, Trieste, Italy
Department of Physiology and Pathology, University of Trieste, Trieste, Italy
Department of Biochemistry and Biophysics "F. Cedrangolo", Section of Pathologic Anatomy, Second University of Naples, Naples, Italy

View larger version (156K): [in a new window]   Figure 1 Characterization of apoptotic myocardiocytes. (A) Hematoxylin/van Gieson stain. Site of recent infarction: reparative fibrosis, newly sprouted vessels, and granulation tissue (original magnification x500). (B) In situ end labeling of deoxyribonucleic acid (TUNEL) staining. Region of the left ventricle at the site of infarction: TUNEL-positive nuclei (brown) are evident (original magnification x500; 3-amino-9-ethylcarbazide [AEC], lightly counterstained with hematoxylin). (C) Double staining: nuclear staining for TUNEL and cytoplasmic staining for muscle actin. TUNEL-positive cells (brown nuclear staining) co-express cytoplasmic muscle actin (original magnification x600; AEC, lightly counterstained with hematoxylin). (D) Double staining: nuclear staining for TUNEL and cytoplasmic staining for caspase-3 (original magnification x600; AEC, lightly counterstained with hematoxylin).

View larger version (17K): [in a new window]   Figure 2 Myocardial apoptosis in subjects with early symptomatic post-infarction heart failure. Apoptotic rate at the site of the infarction was increased nearly fourfold in subjects with symptomatic heart failure at the time of initial hospitalization for acute myocardial infarction or subsequently before death versus the remaining subjects (26.2% [24.5% to 28.8%] vs. 6.4% [1.9% to 13.3%], p = 0.001). Column height = median value; vertical bar = interquartile range.

View larger version (22K): [in a new window]   Figure 3 Correlations between macroscopic signs of post-infarction left ventricular (LV) remodeling and apoptotic rate (AR) at the site of acute myocardial infarction and in remote unaffected LV regions. Correlation between AR at the site of infarction and LV longitudinal (A) and transverse (B) diameter, free wall thickness (C), transverse diameter-to-free wall thickness (D), and cardiac weight (E). Correlation between AR in remote regions and the same LV macroscopic parameters (F to L), respectively. Black and white dots represent subjects with (filled squares) and without (empty squares) early symptomatic post-infarction heart failure, respectively.

View larger version (23K): [in a new window]   Figure 4 Myocardial apoptosis in progressive left ventricular (LV) remodeling. Increasing apoptotic rate (AR) in infarct (A) and remote sites (B) in progressive unfavorable LV remodeling. Column height = median value; vertical bar = interquartile range. p = 0.050 at Kruskal-Wallis three-way test for A, and p = 0.11 for B. No statistically significant differences were found comparing the three groups separately at Mann-Whitney, Bonferroni adjusted, two-way U test. *p = 0.014 for cases with compensatory hypertrophy (AR of 3.2% [0.5 to 12.0]) versus the other two groups characterized by LV dilation combined (AR of 26.0% [22.6 to 28.7]) (at Mann-Whitney U test). **p = 0.050 for cases with end-stage dilation (AR of 0.9% [0.7 to 1.1]) versus the other two groups with LV hypertrophy combined (AR of 0.4% [0.3 to 0.7]) (at Mann-Whitney U test).