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Background The purpose of the current study was to create a model of myocardial infarction (MI) that is homogeneous in size with a low immediate (24 hours) mortality. Methods and Results Male and female rats (n = 256) underwent left ventricle (LV) ablation (Ab) by a radiofrequency current (1000 kHz; 12 watts for 12 seconds) to promote a MI. A transmural MI occurred in all rats. Post-Ab complex arrhythmias were frequent (atrioventricular block, ventricular tachycardia, and fibrillation), which rapidly and spontaneously reverted to sinus rhythm. Among 66 male rats, immediate mortality occurred in 7.5%. Small MI size dispersion was characterized by smaller variability following Ab (x ± SD: 45 ± 8%) when compared with coronary occlusion (Oc; 40 ± 19%). The histopathologic evaluations identified lesions similar to those which occurred following Oc, with scarring complete at 4 weeks. The hemodynamic and Doppler echocardiograms showed comparable increases in LV dimension, end-diastolic pressure, and pulmonary water content 1 and 4 weeks post-MI. Papillary muscle mechanics 6 weeks post-MI had matched inotropic and lusitropic dysfunction. Conclusions LV Ab gave rise to a MI within a narrow size limit and with a low immediate mortality. LV Ab resulted in histopathologic evolution, ventricular dilation, and dysfunction, impairment in myocardial mechanics, and congestive outcome that reproduced a MI from Oc.

We analyzed whether digitoxin affects the survival of rats with congestive heart failure.The influence of digitoxin (0.1 mg.100 g.day, orally) on the survival of infarcted female rats (n=170) randomized as Control Infarcted (CI, n=85) or Digitoxin (D, n=85) was evaluated for 280 days. Mean survival was 235+/-7 days for CI and 255+/-5 days for D (log-rank test: P=.0602). Digitoxin did not affect survival in rats with congestive heart failure from myocardial infarction40% of the left ventricle, but did prolong survival in rats with infarctionor=40%. The log-rank test defined higher mortality (P=.0161) in CI40% (56%) than in D40% (34%), with a hazard ratio of 2.03. Pulmonary water content and papillary muscle mechanics were analyzed in CI (n=7) and D (n=14) survivors. Significant differences were observed regarding pulmonary water content (CI: 82+/-0.3; D: 80+/-0.3%; P=.0014), developed tension (CI: 2.7+/-0.3; D: 3.8+/-0.3g/mm(2); P=.0286) and +dT/dt (CI: 24+/-3; D: 39+/-4 mg mm(2).s; P=.0109).In conclusion, long-term digitoxin administration reduced cardiac impairment after myocardium infarction, attenuated myocardial dysfunction, reduced pulmonary congestion, and provided the first evidence regarding the efficiency of digitoxin in prolonging survival in experimental cardiac failure.

Doppler echocardiogram is useful for the evaluation of anatomical and functional changes in late myocardial infarction (MI) in rats. However, no studies have evaluated the prognostic value of echocardiographic parameters 1 week after MI.Doppler echocardiogram was performed in 84 female Wistar rats 1 week after MI to determine infarction size, left chambers dimensions, fractional area change (FAC) of the left ventricle (LV), mitral inflow and tissue Doppler, myocardial performance index (MPI), and signs of pulmonary hypertension. The 365-day follow-up showed 53.6% mortality rate. Nonsurvivors showed larger (P.05) MI size and cavity dimensions, poorer diastolic and systolic function, and higher frequency of pulmonary hypertension. Parameters at early stage of MI associated with higher mortality risk by Cox multivariate regression model were FACor=37% (relative risk [RR] 3.78, 95% CI, 1.50-9.53), MPIor=0.60 (RR 3.49, 95% CI, 1.80-6.76), LV systolic areaor=0.26 cm(2) (RR 4.38, 95% CI, 1.88-10.21), E/E' ratioor=20.3 (RR 2.12, 95% CI, 1.15-4.34), and E/A ratio associated with FAC (RR 2.99, 95% CI, 1.44-6.18).Some diastolic and systolic Doppler echocardiographic parameters in rats may be able to predict late mortality risk after MI.

Background Immediate functional effects of left ventricle reduction (LVR) are not yet fully defined. Those effects have been studied in the experimental model of myocardial infarction scar plication (MISP) in the rat. Methods and Results A Doppler echocardiogram was performed immediately before and after MISP in 20 rats with infarction of the left ventricle (LV) larger than 40%. LV diastolic volume reduction (475 ± 114 versus 185 ± 65 μL) was accompanied by heart rate decrease (230 ± 25 versus 166 ± 27 beats/min) and increase of ejection fraction (37 ± 7 versus 67 ± 12%), fractional shortening (18 ± 3 versus 46 ± 8%) and posterior wall shortening velocity (1.50 ± 0.62 versus 2.01 ± 0.46 cm/s). LV diastolic volume/stroke volume slope was steeper after LVR, suggesting enhancement of the Frank-Starling mechanism. Restrictive pattern of left atrial emptying was alleviated after LVR (E wave: 101 ± 15 versus 66 ± 14 cm/s; E/A ratio: 6.8 ± 2.9 versus 5.0 ± 2.2; E wave deceleration time: 36 ± 6 versus 51 ± 10 msec) even though left atrial diameter (0.69 ± 0.07 versus 0.66 ± 0.06 cm) and A wave (18.0 ± 9.4 versus 15.8 ± 7.8 cm/s) did not vary. Additionally, a pulmonary flow profile suggesting pulmonary hypertension was observed in 12 of 17 animals before, and in only 3 after, LVR. Conclusion LVR favors cardiac function not only by reducing afterload. The present data are in consonance with previous suggestions that the Frank-Starling mechanism is enhanced after MISP and, in addition to LV ejection function improvement, the unprecedented facilitation of left atrial emptying after LVR was particularly noteworthy. Even though LVR restricts ventricular distensibility, atrial emptying can be facilitated, probably on account of LV ejection improvement.