Ten weeks of rapid ventricular pacing creates a long-term model of left ventricular dysfunction.

OBJECTIVE: Rapid ventricular pacing produces a reliable model of heart failure. Cessation after 4 weeks of rapid ventricular pacing results in rapid normalization of left ventricular function, but the left ventricle remains persistently dilated. We present novel data that show that prolonged rapid ventricular pacing (10 weeks) creates a model of chronic left ventricular dysfunction. METHODS: In 9 dogs undergoing 10 weeks of rapid ventricular pacing, left ventricular function and volumes were serially assessed by using 2-dimensional echocardiography and pressure-volume analysis for 12 weeks after cessation of pacing. RESULTS: Increased end-diastolic volume and decreased systolic and diastolic function were seen at the end of pacing. By 2 weeks of recovery from rapid ventricular pacing, end-diastolic volume and ejection fraction were partially recovered but did not improve further thereafter. Load-independent and load-sensitive indices of function obtained by pressure-volume analysis at 8 and 12 weeks of recovery confirmed a persistence of both systolic and diastolic dysfunction. In addition, left ventricular mass increased with pacing and remained elevated at 8 and 12 weeks of recovery. Four of these dogs studied at 6 months of recovery showed similar left ventricular abnormalities. CONCLUSION: Ten weeks of rapid ventricular pacing creates a long-term model of left ventricular dysfunction.

Modified rapid ventricular pacing: a chronic model of heart failure for evaluation of new surgical therapies.

Rapid ventricular pacing (RVP) in dogs creates a well characterized model of dilated cardiomyopathy. Standard pacing protocols use RVP at 240-260 beats/min for 2-4 weeks, and result in high mortality rates if continued longer. The authors describe a modification of RVP that results in significant heart failure by 4 weeks, but can be continued for up to 10 weeks with low mortality. Nineteen mongrels underwent RVP at 215 beats/min for 10 weeks. Serial pressure-volume analysis and echocardiography were performed in this model to assess longitudinally changes in left ventricular (LV) function and volumes. The mortality rate was 10%. Significant progressive LV dysfunction with concomitant LV enlargement was observed throughout the pacing period. Finally, norepinephrine levels were elevated at the end of pacing, consistent with an activated sympathetic system. This modified RVP protocol permits long-term pacing with a low mortality rate and results in progressive heart failure throughout the pacing period. This model would be useful in the long-term evaluation of newer surgical and medical therapies of the failing heart.

Assessment of left ventricular mechanics in patients with asymptomatic aortic regurgitation: a two-dimensional echocardiographic study.

We describe a noninvasive method for determining end-systolic meridional and circumferential wall stress and left ventricular architecture as the ratio of muscle to cavity area. With this technique, which uses two-dimensional echocardiography and cuff-determined values for systolic blood pressure, we assessed wall stress and left ventricular architecture in 15 normal subjects and 15 asymptomatic patients with severe chronic aortic regurgitation at rest and after load manipulations with sublingual nitroglycerin. Resting end-systolic meridional and circumferential stress were increased in patients with aortic regurgitation (113.9 +/- 29 and 260 +/- 50.7 X 10(3) dynes/cm2) compared with those in normal subjects (85.6 +/- 15.4 and 214.1 +/- 28.4 X 10(3) dynes/cm2) (both p less than .01) and remained significantly greater after nitroglycerin. Meridional stress values obtained from two-dimensional echocardiographic studies correlated closely (r = .89) with values calculated from simultaneously recorded M mode echocardiograms. Ejection fraction in patients with aortic regurgitation and normal subjects were similar at rest (55 +/- 10% vs 59 +/- 6%) and were unchanged by nitroglycerin. In spite of the increased left ventricular mass in patients with aortic regurgitation (227 +/- 60 g vs 130 +/- 22 g in normal subjects), the mass-to-volume ratio and the ratio of muscle to cavity area in diastole in patients with aortic regurgitation were significantly lower than normal (0.90 +/- 0.23 vs 1.30 +/- 0.21 and 0.91 +/- 0.23 vs 1.11 +/- 0.18 [p less than .005 and p less than .02]). These differences were exaggerated after nitroglycerin, while concomitant changes in relative wall thickness were virtually undetected by M mode echocardiography. Thus this technique can be used for early recognition of afterload excess and changes in left ventricular architecture in patients with aortic regurgitation. Furthermore, the mean slopes of the circumferential stress-diameter and meridional stress-length lines, which represent load-independent indexes of myocardial contractile state, could be assessed and were similar in the group of patients with asymptomatic aortic regurgitation and normal subjects, indicating that overall myocardial contractility was still normal. We conclude that circumferential and meridional wall stress, myocardial contractility, and left ventricular architecture can be determined noninvasively. These measurements may prove to be useful in assessing patients with primary myocardial or valvular heart disease and determining their long-term management.