LEFT-VENTRICULAR MAXIMAL SYSTOLIC ELASTANCE CALCULATED BY A COMBINATION OF M-MODE ECHOCARDIOGRAPHY AND STANDARD MANOMETRY

1. A method for obtaining the end-systolic left ventricular (LV) pressure-diameter and stress-diameter relationships in man was critically analyzed.2. Pressure-diameter and stress-diameter relationships were determined throughout the cardiac cycle by combining standard LV manometry with M-mode echocardiography. Nine adult patients with heart disease and without heart failure were studied during intracardiac catheterization under three different conditions of arterial pressure, i.e., basal (B) condition (mean +/- SD systolic pressure, 102 +/- 10 mmHg) and two stable states of arterial hypertension (H(I), 121 +/- 12 mmHg; H(II), 147 +/- 17 mmHg) induced by venous infusion of phenylephrine after parasympathetic autonomic blockade with 0.04 mg/kg atropine.3. Significant reflex heart rate variation with arterial hypertension was observed (B, 115 +/- 20 bpm; H(I), 103 +/- 14 bpm; H(II), 101 +/- 13 bpm) in spite of the parasympathetic blockade with atropine. The linear end-systolic pressure-diameter and stress-diameter relationships ranged from 53.0 to 160.0 mmHg/cm and from 97.0 to 195.0 g/cm3, respectively.4. The end-systolic LV pressure-diameter and stress-diameter relationship lines presented high and variable slopes. The slopes, which are indicators of myocardial contractility, are susceptible to modifications by small deviations in the measurement of the ventricular diameter or by delay in the pressure curve recording.

LEFT-VENTRICULAR MASS ESTIMATED BY M-MODE ECHOCARDIOGRAM IS NOT ALTERED BY CHANGES IN CARDIAC SHAPE AND DIMENSIONS DUE TO ACUTE ARTERIAL-HYPERTENSION

The effect of changes in left ventricular (LV) shape and dimensions due to acute arterial hypertension induced by mechanical obstruction of the aorta for 10 min on LV mass values estimated by M-mode echocardiogram was studied in 14 anesthetized dogs. Although the systolic pressure increased from 117.5 +/- 19.9 to 175.4 +/- 22.9 mmHg altered ventricular diameter from 2.77 +/- 0.49 cm to 3.17 +/- 0.67 cm (P<0.05) and wall thickness from 0.83 +/- 0.09 to 0.75 +/- 0.09 cm (P<0.05), LV mass estimated before (73.5 +/- 19.1 g) and after (78.3 +/- 26.4 g) hypertension was not significantly different. We demonstrate here for the first time that changes in LV dimensions induced by acute arterial hypertension do not modify LV mass values estimated by the M-mode electrocardiogram method.

Improved systolic ventricular function with normal myocardial mechanics in compensated cardiac hypertrophy

There is still controversy about the relation between changes in myocardial contractile function and global left ventricular (LV) performance during stable concentric hypertrophy. To clarify this, we analyzed LV function in vivo and myocardial mechanics in vitro in rats with pressure overload-induced cardiac hypertrophy. Male Wistar rats (70 g) Underwent ascending aortic stenosis for 8 weeks (group AAS, n = 9). LV performance wits assessed by transthoracic echocardiography Under anesthesia. Myocardial function Was studied in isolated papillary muscle preparations during isometric contraction. The data were compared with age- and sex-matched sham-operated rats (group C, 11 = 9). LV weight-to-body weight ratio (C: 2.13 +/- 0.14 mg/g; AAS: 3.24 +/- 0.44) LV relative wall thickness (C: 0.18 +/- 0.02; AAS: 0.33 +/- 0.09), and LV fractional shortening (C: 54 +/- 5%; AAS: 70 +/- 8%) were increased in group AAS (P<0.05). Echocardio-graphic analysis also indicated a significant association (r = 0.74 P<0.001) between the percent fractional shortening index and LV relative wall thickness. The performance of AAS isolated In muscle revealed that active tension (C: 6.6 +/- 1.7 g/mm(2); AAS: 6.5 +/- 1.5 g/mm(2)) and maximum rate of tension development (C: 69 +/- 21 g/mm(2)/s AAS: 69 +/- 18 g/mm(2)/s) were not significantly different Front group C (P>0.05). In conclusion, compensated pressure-overload myocardial hypertrophy is associated with preserved myocardial function and increased ventricular performance. The improved LV function might be due to the ventricular remodeling, characterized by an increased relative wall thickness.

Association between hypervolemia and ventricular hypertrophy in hemodialysis patients

Background: Left ventricular hypertrophy (LVH) is a well-known predictor of cardiovascular mortality in patients who have end-stage renal disease and are maintained on hemodialysis (HD), and LVH is not always correlated with the severity of hypertension in these patients. The purpose of this study was to investigate the role of other factors contributing to LVH.Methods: A total of 50 patients with HD were classified in three groups according to whether their LV mass index (LVMI) was higher than (n = 15), equal to (n = 20), or lower than (n = 15) that predicted by a formula based on their ambulatory blood pressure monitoring (ABPM).Results: Subjects with higher LVMI than predicted had significantly greater inter-HD weight gain (3.4 +/- 0.8 v 2.7 +/- 0.8 and 2.6 +/- 05 kg, respectively, in the other two groups, P < .05), and subjects with lower LVMI than predicted had a tendency toward a more pronounced nocturnal dipping pattern of BP (P = .07 v the other two groups), although daytime and night-time average BP levels did not differ between groups. All other clinical and laboratory parameters were similar among the three groups except higher cardiac output and various indices of LVH, which were more pronounced in the group with higher LVMI by ABPM. This group had also the lowest survival rate over the 2 to 3 years of follow-up, with five deaths versus two in each of the other two groups.Conclusions: the data suggest that correct management of inter-HD weight gain by nutritional counseling and shorter inter-HD intervals may prevent LVH and improve survival independently of BP control. (C) 2004 American Journal of Hypertension, Ltd.