Relation Of Wall Stress Research Articles

Relation between right ventricular wall stress, fibrosis, and function in right ventricular pressure loading.

Right ventricle (RV) pressure loading can lead to RV fibrosis and dysfunction. We previously found increased RV, septal hinge-point and left ventricle (LV) fibrosis in experimental RV pressure loading. However, the relation of RV wall stress to biventricular fibrosis and dysfunction is incompletely defined. Rabbits underwent progressive pulmonary artery banding (PAB) over 3 wk with hemodynamics, echocardiography, and myocardial samples obtained at a terminal experiment at 6 wk. An additional group received PAB and treatment with an endothelin receptor antagonist. The endocardial and epicardial borders of short-axis echo images were traced and analyzed with invasive pressures to yield regional end-diastolic (ED) and end-systolic (ES) wall stress. To increase clinical translation, computer model-derived wall stress was compared with Laplace wall stress. The relation of wall stress with fibrosis (picrosirius red staining) and ventricular function was analyzed. ED wall stress in all regions and RV and LV free-wall ES wall stress were increased in PAB rabbits versus sham animals. Laplace wall stress correlated well with computational models. In PAB, fibrosis was highest in the RV free wall, then septal hinge regions, and lowest in the septum and LV free wall. Fibrosis was moderately related to ED (r = 0.47, P = 0.0011), but not ES wall stress. RV ED wall stress was strongly related to echo indexes of function (strain rate: r = 0.71, P = 0.048; E', r = -0.75, P = 0.0077; tricuspid annular plane systolic excursion: r = 0.85, P = 0.0038) and RV fractional area change (r = 0.77, P = 0.027). ED, more than ES, wall stress is related moderately to fibrosis and strongly to function in experimental RV pressure loading, especially at the septal hinge-point regions, where fibrosis is prominent. This suggests that wall stress partially links RV pressure loading, fibrosis, and dysfunction and may be useful to follow clinically.NEW & NOTEWORTHY Biventricular fibrosis and dysfunction impact outcomes in RV pressure loading, but their relation to wall stress is poorly defined. Using a pulmonary artery band rabbit model, we entered echocardiography and catheter data into a computer model to yield regional end-diastolic (EDWS) and end-systolic (ESWS) wall stress. EDWS, more than ESWS, correlated with fibrosis and dysfunction, especially at the fibrosis-intense septal hinge-point regions. Thus, wall stress may be clinically useful in linking RV pressure loading to regional fibrosis and dysfunction.

Serial echocardiographic and Doppler evaluation of left ventricular systolic performance and diastolic filling in premature infants.

To examine the effects of somatic growth on left ventricular systolic and diastolic functions in premature infants, we performed serial two-dimensional, M-mode and Doppler echocardiograms of 18 premature infants in the early neonatal period (mean of 14 days) and on the day when they were discharged from the hospital (mean of 94 days). The relation between rate-corrected mean velocity of fiber shortening and end-systolic wall stress relation was used as a load-independent estimate of contractility. Diastolic function was assessed by transmitral Doppler filling velocity patterns. The end-systolic wall stress was significantly lower in the first examination than in the second examination (38+/-8 vs. 46+/-10 g/cm2, P < 0.005). However, there was no significant difference in the rate-corrected velocity of fiber shortening between the two examinations. An inverse linear relation between the end-systolic wall stress and the rate-corrected mean velocity of fiber shortening was found in each examination. The slopes of these two regression lines showed no significant difference, suggesting that the left ventricular contractility is on the same level during this study period. The transmitral Doppler flow velocity patterns markedly altered between the two observations. The peak E wave, peak A wave, peak E/A ratio, flow velocity time integral of E/A wave, the first third filling fraction, and the normalized peak filling rate to stroke volume increased significantly during the study period (78+/-14 vs. 31+/-9 cm/s, 61+/-12 vs. 33+/-7 cm/s, 1.29+/-0.18 vs. 0.93+/-0.19, 1.75+/-0.58 vs. 1.17+/-0.24, 0.42+/-0.07 vs. 0.37+/-0.05, and 9.48+/-1.71 vs. 7.30+/-0.96/s, respectively, P < 0.001), suggesting a relative shift of Doppler filling into the early diastole. We demonstrated that the age- and growth-related alterations in the transmitral Doppler filling patterns occurred dramatically without changes in contractility during the first 3 months after birth. This diastolic filling change may be related to the age-related maturation in the left ventricular diastolic properties.

Assessment of left ventricular function by meridional and circumferential endsystolic stress/minor-axis shortening relations in dilated cardiomyopathy

Echocardiographic meridional wall stress-endocardial shortening relations provide estimates of left ventricular (LV) contractility that do not uniformly detect myocardial dysfunction despite severe symptoms in dilated cardiomyopathy. To improve detection of myocardial dysfunction in patients with congestive heart failure (CHF) due to dilated cardiomyopathy, echocardiographic meridional and circumferential end-systolic stress were related to endocardial and midwall shortening in 42 patients (95% dead within a mean of 22 months) with dilated cardiomyopathy and 140 normal subjects. A method to estimate LV long-axis dimension from M-mode minoraxis epicardial measurements was developed in a separate series of 115 subjects. Endocardial shortening to meridional wall stress relation identified 31 of 42 CHF patients falling below the 95% normal confidence interval of the reference population; use of midwall shortening decreased this number to 26 (p = NS). The use of circumferential wall stress identified 39 of 42 patients with subnormal endocardial LV shortening and 41 of 42 patients with depressed midwall performance (p < 0.01 vs use of meridional stress). The circumferential/meridional wall stress ratio was 2.6 ± 0.5 in normal subjects and 1.3 ± 0.2 in CHF patients (p < 0.0001). Thus, use of circumferential end-systolic stress as the measure of afterload improves the detection of myocardial dysfunction by stress/shortening relations in patients with CHF. The ratio between the 2 stresses decreases with more spherical LV shape. Midwall and endocardial shortening measurements are equivalent in the setting of thin LV walls as occurs in dilated cardiomyopathy.

Cardiac dysfunction late after cardiotoxic therapy for childhood cancer

Despite a wealth of data documenting acute cardiac injury from anthracycline therapy and/or mediastinal radiotherapy used for childhood cancer, little information is available on the long-term consequence of these insults. Twenty-nine patients (mean age 15 ± 4.3 years) from The Late Effects Follow-Up Clinic For Childhood Cancer study, who had been in continuous, complete remission and off chemotherapy for a minimum of 2 years (mean follow-up 7.2 ± 3.2) were studied. All patients had normal ejection fractions before and during cancer therapy and all were in New York Heart Association class I at the time of study. Systolic and diastolic functions were assessed by 2-dimensional echocardiography, Doppler flow velocity, and radionuclide angiography, and results were compared with normal control subjects. Left ventricular mass and mass index were significantly reduced in the patient population. Fractional shortening was decreased overall and end-systolic wall stress was much higher in patients than in controls. However, contractility, as assessed by the relation of wall stress to rate-corrected velocity of shortening, was decreased by ≥2 SDs in only 6 of 28 patients, and the force-mass relation was actually increased in the patient group as a whole. Mitral valve inflow velocities were significantly increased but the pattern was abnormal. These results suggest a pattern consistent with a thin-walled, compliant left ventricle with reduced muscle mass performing under above-normal levels of wall stress. Contractility measurements were normal or increased in the group, but some patients clearly demonstrated development of reduced contractile function. Close follow-up of survivors of aggressive cancer therapy will be necessary as the natural history of these cardiac function abnormalities becomes known.

Left ventricular remodelling and disparate changes in contractility and relaxation during the development of and recovery from experimental heart failure.

Canine pacing induced heart failure is characterised by impaired left ventricular contractility and relaxation, and clinical recovery after cessation of pacing. It is unclear whether the impairment is responsive to adrenergic stimulation. The aim of this study was to assess left ventricular contractility and relaxation and their response to beta adrenergic stimulation during heart failure and after recovery. Eight dogs were paced (250 beats.min-1) for 3 weeks to severe heart failure and recovered for 4 weeks after cessation of pacing. During these periods, haemodynamic and echocardiographic measurements were made with and without beta adrenergic stimulation. At heart failure, impaired left ventricular contractility was evidenced by reduced dP/dt [1412(SD 156) mm Hg.s-1 from 2437(382) mm Hg.s-1 at control, p < 0.01] and a downward displacement of the velocity of circumferential fibre shortening-end systolic wall stress relation. Impaired left ventricular relaxation was evidenced by raised end diastolic pressure [35(6) mm Hg from 7(4) mm Hg at control, p < 0.01] and prolonged relaxation time constant tau [28(4) ms from 17(6) ms, p < 0.01]. The ability of beta adrenergic stimulation to augment contractility was reduced: there was blunted dP/dt response to dobutamine. The ability of beta adrenergic stimulation to shorten relaxation was maintained: there was a similar degree of shortening of tau by dobutamine. At recovery, dP/dt returned to control and the shortening-stress relation moved upward, suggesting return of contractility. The response of dP/dt to dobutamine was restored. However, tau remained prolonged indicating persistent abnormal relaxation. In pacing induced heart failure, there is a dissociation between the normal ability of beta adrenergic stimulation to augment contractility and shorten relaxation, and a differential capacity for recovery of contractility and relaxation.

Left ventricular diastolic dysfunction late after coarctation repair in childhood: Influence of left ventricular hypertrophy

Objectives. Left ventricular systolic and diastolic function were evaluated late after successful operation for aortic coarctation in childhood.Background. Persistent arterial hypertension and left ventricular hypertrophy after coarctation repair might impair left ventricular function.Methods. Biplane angiography and simultaneous high fidelity pressure measurements were performed in 12 patients 3 to 12 years postoperatively (residual pressure gradient 4 mm Hg), Eight patients were normotensive and four had borderline hypertension. Data at rest and after nitroprusside infusion (1.7 μg/kg per min) were evaluated and compared with data from 12 control subjects.Results. Systolic left ventricular function (ejection fraction-end-systolic wall stress relation) was normal in all patients. However, left ventricular muscle mass (113 vs. 86 g/m2), right atrial pressure (5.2 vs. 1.9 mm Hg) and left ventricular end-diastolic pressure (16 vs. 11 mm Hg) were significantly higher in patients than in control subjects. There was a linear relation between muscle mass and left ventricular end-diastolic (r = 0.66, p < 0.001) or right atrial (r = 0.60, p < 0.01) pressure. Left ventricular relaxation and myocardial stiffness were normal. However, there was an upward shift of the diastolic pressure-volume curve when compared with control values, but this shift was reversed by the administration of nitroprusside.Conclusions. Systolic function is normal late after coarctation repair. However, diastolic function can be abnormal with an upward shift of the diastolic pressure-volume curve that is reversed by nitroprusside administration and is probably due to residual left ventricular hypertrophy.

Ambulatory blood pressure monitoring and left ventricular mass and function after successful surgical repair of coarctation of the aorta

Late cardiovascular morbidity and mortality remain significant despite apparently successful surgical repair of aortic coarctation. Alterations in cardiac function have been reported in normotensive patients who have had successful repair, the reasons for which remain unclear. This study addresses the relation between ambulatory blood pressure measurements and alterations in left ventricular performance in 20 patients with normotension at rest after successful repair of aortic coarctation. Exercise testing, ambulatory blood pressure monitoring and two-dimensional echocardiographic studies in 13 boys and 7 girls (mean age 14.2 ± 2.31 and 14.7 ± 3 years, respectively) who had no evidence of recoarctation were compared with the findings in 20 matched control subjects.No difference was found in systolic blood pressure at rest or peak exercise between patients and control subjects. Male patients developed a significant arm/leg gradient at peak exercise. Systolic ambulatory blood pressure was higher throughout the day in the male group. In the female group, systolic blood pressure was higher only during sleep. No difference was found in diastolic blood pressure or heart rate. The transverse aortic arch was smaller and the left ventricular mass greater in all patients. The relation of wall stress to rate-corrected velocity of shortening was 2 SD above normal in 8 of the 20 patients, suggesting that some have enhanced contractility. The E/A ratio on the atrial echocardiogram was significantly reduced in the patient group.Successfully treated patients who are normotensive at rest after operation are still at risk for developing end organ damage, which is probably explained by incipient mild hypertension documented by ambulatory blood pressure monitoring.

Late potentials and their relation to ventricular function in human immunodeficiency virus infection

Signal-averaged electrocardiograms were performed in 225 patients with serologic evidence of human immunodeficiency virus infection as part of a prospective longitudinal study of patients with HIV-associated heart disease and 12 seronegative control subjects. The duration of signal-averaged QRS vector, root-mean-square voltage of the terminal 40 ms of the vector magnitude and the duration of the low-amplitude (< 40 μV) signal were determined during serial visits at 4-month intervals. One or more of these variables was abnormal on initial visit in 59 of patients (26%); QRS duration was >114 ms in 9 patients (4%), root-mean-square voltage < 20 μV in 55 patients (24%) and low-amplitude signal duration >39 ms in 43 (19%). In contrast, none of the seronegative control subjects had any abnormal variables (p < 0.03). During follow-up (mean 10 ± 8 months), 26 patients with initially normal studies developed abnormal variables and 24 with abnormal signal-averaged electrocardiograms reverted to normal. Left ventricular contractility was assessed by echocardiography using the rate-corrected velocity of fiber shortening-end-diastolic wall stress relation. Late potentials were not related to contractile abnormalities. Clinical arrhythmias were rare and did not appear more frequent among patients with late potentials. Thus, late potentials were both common and evanescent in patients infected with human immunodeficiency virus.