Changes in regional left ventricular (LV) performance induced by ventricular pacing were studied in two groups of open-chest anesthetized dogs. In the first group of five dogs, local function at the LV anterior base, anterior apex, and posterior apex was assessed by ultrasonic crystal pairs with atrial, right ventricular, LV apical, and LV base pacing. Ventricular pacing produced asynchrony of contraction and marked changes in the shortening pattern at each site, as well as an average 27% reduction in peak systolic pressure and peak dP/dt compared to atrial pacing. Moreover, the extent of shortening during LV ejection was reduced or unchanged at all sites measured during ventricular pacing. In the second group of five dogs, function of the septum and opposing LV lateral wall was studied with atrial and LV lateral wall pacing. Lateral function was assessed with a crystal pair and septal function by cineradiography of a lead bead implanted in the septum. Ventricular pacing produced reciprocal interaction between the two walls, with early lateral shortening inducing septal bulging and late septal shortening inducing lateral wall systolic lengthening. We conclude that ventricular pacing produces significant changes in regional myocardial function, likely induced by reciprocal interaction of opposing myocardial regions. Furthermore, such interaction appears deleterious to global ventricular function, presumably because volume is sequestered and pressure is dissipated into relatively inactive segments that are out of phase with the bulk of contracting myocardium.

SUMMARY. The relationship between left ventricular end-systolic pressure and volume has been proposed as a model of left ventricular contraction which may be useful for quantifying inotropic state independent of preload and afterload. Although the model has been well-validated in isolated hearts, systematic evaluation in conscious animals with an intact peripheral circulation has been limited. Accordingly, we derived end-systolic pressure-volume relationships in twelve conscious dogs, chronically instrumented to measure left ventricular pressure and dimensions from endocardial ultrasonic crystals in three orthogonal axes. We examined the linearity of the end-systolic pressure-volume relationship, its response to alterations of inotropic state and the peripheral circulation, and the influence of /?-adrenergic reflexes. End-systolic pressure-volume relationships were constructed by linear regression of end-systolic pressure-volume coordinates produced by transient inferior vena caval occlusions during atrial pacing. The relations were highly linear; of 127 inferior vena caval occlusions, the correlation coefficient was 0.96 ± 0.05 (mean ± SD). The slope of the end-systolic pressure-volume relationship was not significantly altered either by a moderate resistive afterload induced by angiotensin II infusion, or by a moderate increase in preload produced by dextran, but was increased from 4.7 ± 2.3 to 6.5 ± 2.2 mm Hg/ml (P < 0.05) in response to the positive inotropic stimulus of dobutamine. The volume intercept at zero end-systolic pressure was unaffected by dextran or dobutamine, but was decreased from 12 ± 8 to 5 ± 11 ml (P < 0.01) by angiotensin II infusion, indicating a leftward shift of the end-systolic pressure-volume relationship. Pretreatment with propranolol to block fimediated adrenergic reflexes did not affect the response to angiotensin or dextran. We conclude that linear end-systolic pressure-volume relationships can be derived in conscious dogs with intact sympathetic reflexes. The slope appears to reflect left ventricular contractile function and is indepednent of the level of afterload and preload. However, the relation is shifted leftward by high levels of arterial resistance, indicating that end-systolic pressure is a function, not only of end-systolic volume and inotropic state, but also of the peripheral circulation, in this intact animal model. (CircRes 54: 731-739, 1984) THE assessment of ventricular contractile function remains an important problem in clinical practice and in physiological investigation (Ross and Peterson, 1973;Sagawa et al., 1977;Sagawa, 1978;Weber et al., 1982). Because traditional isovolumic and ejection phase indices of ventricular performance are variably affected by preload and afterload, as well as by inotropic state (Mahler et al., 1975a), the search has continued for a load-independent measure of contractile function. In isolated hearts, Suga and Sagawa (1974) have demonstrated that the relation between end-systolic pressure and volume (P-V) is an index of contract...

We studied the effect of chronic right ventricular pressure overload on diastolic ventricular interdependence in dogs without pericardia, instrumented to measure left ventricular pressure, right ventricular pressure, and 3 left ventricular dimensions. We studied 12 dogs before (control) and nine dogs after 6 weeks of pulmonary artery constriction producing systolic right ventricular pressure greater than or equal to 70 mm Hg. Compared to control, following pulmonary artery band there was greater (P less than 0.01) interventricular septal mass (53 +/- 15 vs. 35 +/- 7 mg, mean +/- SD), thickness (15 +/- 2 vs. 10 +/- 1 mm), and ratio of the surface area of the interventricular septal to total left ventricular surface area (0.38 +/- 0.03 vs. 0.33 +/- 0.02), but unchanged left ventricular free wall mass (81 +/- 12 vs. 84 +/- 14 mg) and thickness (11 +/- 2 vs. 11 +/- 2 mm). End-diastolic right and left ventricular pressures and left ventricular volume were varied by vena cava and pulmonary artery occlusions and releases. Volume was calculated as an ellipsoid and the data in each dog fit to: left ventricular pressure = a0 + a1V + a2V2 + a3V3 + a4V4 + bPRV, r greater than or equal to 0.91 in each dog. During control, b was similar, whether calculated from both pulmonary artery and vena cava occlusions (0.47 +/- 0.09) or from vena cava occlusions alone (0.43 +/- 0.11), and was greater than the ratio of the interventricular septal surface area to left ventricular surface area (0.33 +/- 0.02, P less than 0.05). Following the pulmonary artery band, b decreased to 0.21 +/- 0.10 (P less than 0.05) and was less than the ratio of interventricular septal surface area to the left ventricular surface area which increased to 0.38 +/- 0.03 (P less than 0.05). We conclude that the effect of alterations in right ventricular pressure on the end-diastolic left ventricular pressure volume relationship, independent of the pericardium, is reduced following the pulmonary artery band that produces interventricular septal hypertrophy. These results are consistent with the hypothesis that the effect of alterations of right ventricular pressure on the diastolic left ventricular pressure-volume relationship depends on the relative elastance of the interventricular septum and left ventricular free wall, and not simply on the ratio of the interventricular septal surface area to the left ventricular surface area.

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