A mechanistic role for cardiac myocyte apoptosis in heart failure
J. Clin. Invest. Detlef Wencker, et al. 111:1497 doi:10.1172/JCI17664 [Go to this article.]

Figure 3
Very low levels of myocyte apoptosis are sufficient to cause a lethal, dilated cardiomyopathy. (a) Kaplan-Meier survival curve of WT mice, and transgenic line 7, 169, and C360A mice that have never been treated with FK1012H2. P < 0.0001 for line 7 vs. WT, line C360A, or line 169. (b) Representative two-dimensionally directed M-mode echocardiograms through the interventricular septum (IVS) and left ventricular posterior wall (PW) from 9-week-old WT and transgenic line 7 mice in the absence of FK1012H2. The electrocardiogram is shown at the bottom of each echocardiogram. (c) Quantitation of M-mode echocardiographic parameters in conscious WT and transgenic line 7, 169, and C360A mice in the absence of FK1012H2. EDD, left ventricular end-diastolic dimension; FS, fractional shortening. *P < 0.01, **P < 0.001. (d) Left ventricular hemodynamics by cardiac catheterization in 9-week-old WT and transgenic line 7 mice under basal conditions or in response to isoproterenol (500 pg i.v.), in the absence of FK1012H2. LVEDP, left ventricular end-diastolic pressure. *P < 0.02, **P < 0.002. (e) Histological analysis of 9-week-old WT and transgenic line 7 mouse hearts in the absence of FK1012H2. Coronal sections stained with H&E (bar, 1 mm), and sections from the indicated area of the left ventricular free wall stained with Masson’s trichrome (bar, 25 μm). (f) Apoptotic cardiac myocytes in WT and transgenic mice in the absence of FK1012H2. Left panels: Double staining for TUNEL (green) and desmin (red, to identify myocytes) in paraffin sections from the hearts of 9-week-old WT and line 7 transgenic mice in the absence of FK1012H2. Bar, 10 μm. Right panel: Number of TUNEL-positive cardiac myocytes per 10⁵ nuclei in 9-week-old WT and transgenic line 7 and C360A mice in the absence of FK1012H2. *P < 0.002, **P < 0.0003.