Abstract:The end-systolic pressure-volume relationship has been used as a load-independent measure of ventricular pump performance. Since ume ratio or the slope of the stress-volume relationship at end-systole to changes in contractile state. We therefore examined the effects of postextrasystolic potentiation (PESP) of inotropic state and of altered ventricular volume and load on the maximum stress-volume ratio (MSVR) and the slope of the end-systolic stress-volume relationship (fiber Emax) in open-chest dogs instrum… Show more
“…19 et al3 extended the earlier study by Gunther and Grossman,2 it was inferred that a myocardial factor might be operative in a small subset of patients with aortic stenosis and congestive heart failure, in whom the pressure gradient was small. However, the small control group comprising six normal subjects in the earlier study2 and the lack of controls in the subsequent study3 did not permit a statistical comparison of contractile function between normal subjects and patients with aortic stenosis.…”
To assess the relative contributions of afterload mismatch and impaired contractility to pump dysfunction in patients with chronic aortic valve disease, simultaneous left ventricular cineangiography and micromanometry were performed in 56 patients: 21 with severe aortic stenosis, 16 with severe aortic regurtitation, and 19 normal control subjects. Left ventricular mass was increased in patients with aortic stenosis and aortic regurgitation (172 + 52 and 224 ± 63 g/m2, respectively, vs 89 + 16 for control subjects; p < .05) as were end-diastolic volume (101 ± 39 and 167 ± 44 vs 77 + 16 ml/m2; p < .05) and end-systolic volume (50 + 40 and 84 ± 43 vs 24 7 ml/m2; p < .05). Although ejection fraction was depressed in both abnormal groups (0.56 ± 0.18 for patients with aortic stenosis and 0.53 + 0.13 for those with aortic regurgitation vs 0.69 0.05 for control subjects; p < .05), the decrease in ejection fraction was disproportionate to the mild degree of afterload mismatch (end ejection stress 129 + 17 in patients with aortic stenosis and 154 ± 58 in those with aortic regurgitation vs 117 46 kdyn/cm2 in control subjects; p = NS) with 10 of 21 patients with aortic stenosis and 12 of 16 patients with aortic regurgitation falling below the 95% prediction limit of the linear inverse relationship between ejection fraction and end-systolic stress for controls (EF = 0.78 -0.00074.ESS). The maximum stress:volume index ratio, which is an index of inotropic state that is independent of preload but sensitive to afterload, was also depressed in patients with aortic stenosis and aortic regurgitation (3.8 ± 1.4 and 2.5 ± 0.9 vs 5.0 1.3 kdyn/cm5/m2 for control subjects; p < .05), and first-order partial correlation demonstrated that this decrease was inversely related to left ventricular mass index. Thus, although afterload mismatch may adversely affect ventricular performance in patients with aortic valve disease, extensive hypertrophy and contractile dysfunction appear to be the major determinants of pump dysfunction. Circulation 73, No. 1, 47-53, 1986. AFTERLOAD MISMATCH has been recognized as a cause of impaired pump performance in patients with chronic aortic valve disease.'-5 However, separating the effect of myocardial contractile dysfunction from that of afterload mismatch on pump performance has been difficult because of the lack of a load-independent index of contractile function.Recently, the relationship between end-systolic stress and either ejection fraction or end-systolic volume has been used to estimate myocardial contractile
“…19 et al3 extended the earlier study by Gunther and Grossman,2 it was inferred that a myocardial factor might be operative in a small subset of patients with aortic stenosis and congestive heart failure, in whom the pressure gradient was small. However, the small control group comprising six normal subjects in the earlier study2 and the lack of controls in the subsequent study3 did not permit a statistical comparison of contractile function between normal subjects and patients with aortic stenosis.…”
To assess the relative contributions of afterload mismatch and impaired contractility to pump dysfunction in patients with chronic aortic valve disease, simultaneous left ventricular cineangiography and micromanometry were performed in 56 patients: 21 with severe aortic stenosis, 16 with severe aortic regurtitation, and 19 normal control subjects. Left ventricular mass was increased in patients with aortic stenosis and aortic regurgitation (172 + 52 and 224 ± 63 g/m2, respectively, vs 89 + 16 for control subjects; p < .05) as were end-diastolic volume (101 ± 39 and 167 ± 44 vs 77 + 16 ml/m2; p < .05) and end-systolic volume (50 + 40 and 84 ± 43 vs 24 7 ml/m2; p < .05). Although ejection fraction was depressed in both abnormal groups (0.56 ± 0.18 for patients with aortic stenosis and 0.53 + 0.13 for those with aortic regurgitation vs 0.69 0.05 for control subjects; p < .05), the decrease in ejection fraction was disproportionate to the mild degree of afterload mismatch (end ejection stress 129 + 17 in patients with aortic stenosis and 154 ± 58 in those with aortic regurgitation vs 117 46 kdyn/cm2 in control subjects; p = NS) with 10 of 21 patients with aortic stenosis and 12 of 16 patients with aortic regurgitation falling below the 95% prediction limit of the linear inverse relationship between ejection fraction and end-systolic stress for controls (EF = 0.78 -0.00074.ESS). The maximum stress:volume index ratio, which is an index of inotropic state that is independent of preload but sensitive to afterload, was also depressed in patients with aortic stenosis and aortic regurgitation (3.8 ± 1.4 and 2.5 ± 0.9 vs 5.0 1.3 kdyn/cm5/m2 for control subjects; p < .05), and first-order partial correlation demonstrated that this decrease was inversely related to left ventricular mass index. Thus, although afterload mismatch may adversely affect ventricular performance in patients with aortic valve disease, extensive hypertrophy and contractile dysfunction appear to be the major determinants of pump dysfunction. Circulation 73, No. 1, 47-53, 1986. AFTERLOAD MISMATCH has been recognized as a cause of impaired pump performance in patients with chronic aortic valve disease.'-5 However, separating the effect of myocardial contractile dysfunction from that of afterload mismatch on pump performance has been difficult because of the lack of a load-independent index of contractile function.Recently, the relationship between end-systolic stress and either ejection fraction or end-systolic volume has been used to estimate myocardial contractile
“…Other mechanisms responsible for the depressed left ventricular contractile state may relate to deformity of the ventricular cavity or hypertrophic ventricular septum. Wisenbaugh et al [23] noted that the MSVR in canine heart was afterload dependent when afterload was augmented by aortic constriction. In the present study, although end-systolic and mean systolic stress of the two groups in HCM were lower than those of the normal subjects, these two stresses were similar within the two HCM groups.…”
To evaluate the left ventricular contractile state in patients with nonobstructive hypertrophic cardiomyopathy (HCM), we analyzed the maximum stress-volume index ratio (MSVR) using catheter-tip cineangiography in 11 patients with HCM and 16 normal subjects. The value of the MSVR in normal subjects was 6.48 +/- 1.25 kdyn/cm5/m2 (mean +/- SD) and we defined the range of the mean +/- 2 SD as the normal MSVR range. Six patients with HCM placed inside the normal MSVR range (IN), but the other 5 patients placed outside and to the right of the normal range (RIGHT). This suggests that the contractile states of the patients of the RIGHT group were depressed. Compared with IN, the end-diastolic and end-systolic volume indices of RIGHT were larger (EDVI; 69.3 +/- 6.9 vs. 96.1 +/- 11.1 ml/m2, p less than 0.01, ESVI; 18.2 +/- 3.2 vs. 29.1 +/- 8.3 ml/m2, p less than 0.05), but the ejection fraction did not differ (IN 73.5 +/- 5.7 vs. RIGHT 69.6 +/- 8.3%, NS). End-diastolic pressure of IN and RIGHT was higher than that of normal subjects (IN 16.5 +/- 4.5, RIGHT 16.7 +/- 4.6 vs. 8.3 +/- 2.5 mm Hg, both p less than 0.05), but there was no difference between the two groups in HCM. End-systolic pressure did not differ among the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypothesis: The time from onset of contraction to dP/dtmax, td, is suggested as an index of contractility in the catheterization laboratory.
Methods: We studied 22 normal patients and 18 patients with myocardial failure in the catheterization laboratory. The two groups were completely separated on the td‐heart rate (HR) plane. In the normal patients, HR = 73 ± 19 beats/min, td= 73 ± 11 ms, and an inverse linear relation td = 109‐0.49 × HR (p<0.001) exist. In the patients with myocardial failure, despite significantly higher HR than in normal patients (HR = 93 ± 14 beats/min) (p <0.001), td paradoxically increased (td = 89 ±11 ms, p<0.0001).
Conclusions: These findings support a mathematical analysis of the left ventricular pressure (LVP) during isovolumic contraction in the time domain which shows that td and (dP/dt)/P reflect the time‐dependent aspects of contraction and, hence, decrease with increasing contractility. This study shows that td, at any given HR, is a reliable index of contractility. Thus, a ready‐to‐use td‐HR plot containing a well‐based separation line can provide a reliable and simple method for determining contractility in the catheterization laboratory by examining whether a patient's td value at any HR is below (normal) or above (impaired contractility) the separation line.
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