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PubMed2001

Relationship between left ventricular diastolic relaxation and systolic function in hypertension: The Hypertension Genetic Epidemiology Network (HyperGEN) Study.

The relation of impaired left ventricular relaxation, as measured by prolonged isovolumic relaxation time, to ventricular systolic function in hypertension remains uncertain in population-based samples. In the Hypertension Genetic Epidemiology Network (HyperGEN) Study, echocardiograms were analyzed in 1457 hypertensive participants without diabetes, >/=2+ valvular regurgitation, or coronary disease. Impaired relaxation (isovolumic relaxation time >100 ms) was present in 219 (15%) of the participants; they were older and had higher arterial pressure than did those with normal relaxation. Ventricular chamber size, wall thicknesses, mass, and relative wall thickness were greater, and stress-corrected midwall shortening and end-systolic stress/end-systolic volume index were lower with impaired relaxation than with normal relaxation time. Fractional shortening and ejection fraction did not differ between the groups. In logistic regression, the likelihood of prolonged isovolumic relaxation time decreased with higher stress-corrected midwall shortening (odds ratio, 0.97%; 95% confidence interval, 0.96 to 0.99), independently of age, heart rate, and ventricular mass. Neither ejection fraction nor the end-systolic stress/end-systolic volume index was independently related to isovolumic relaxation time. In hypertension, impaired left ventricular relaxation parallels ventricular midwall dysfunction but not systolic chamber function. Whether combined diastolic and systolic dysfunction identifies hypertensive patients at especially high risk of cardiovascular events requires further study.

Adult↗
PubMed1981

Effect of atrial systole on canine and porcine coronary blood flow.

A feature of phasic coronary flow patterns recorded in conscious chronically instrumented dogs is the atrial cove--a transient depression of arterial flow that occurs during atrial systole. The association between the hemodynamic effects of atrial systole and the atrial cove was studied in anesthetized dogs and pigs with complete heart block. Many atrial coves are available for study in these preparations because atrial activity continues unabated during the diastolic ventricular arrest that follows cessation of electrical pacing. The effect of atrial systole is to translate the pressure-flow relation found during diastole to a higher intercept pressure without change in slope. The increase in the intercept pressure equals the increase in intramyocardial pressure measured with microtransducers embedded in the left ventricular wall. The decrement in flow during the atrial cove is a direct function of the change in intramyocardial pressure and an inverse function of coronary vascular resistance. Each atrial systole is associated with a forward flow transient in the coronary veins, the peak of which occurs at the same instant as does the nadir of atrial flow. These data suggest that the coronary vessels are acting as collapsible tubes and that the waterfall model of the coronary circulation is applicable. The following sequence is proposed to account for the atrial cove. Atrial systole ejects a bolus of blood into the left ventricle increasing both ventricular cavity and intramyocardial pressures. The increase in intramyocardial pressure raises the back pressure opposing coronary flow, reducing the arterial perfusion pressure gradient and causing flow to fall.

Animals↗
PubMed1981

Equal oxygen consumption rates of isovolumic and ejecting contractions with equal systolic pressure-volume areas in canine left ventricle.

Left ventricle systolic pressure-volume area (PVA) has been found to be highly linearly correlated with cardiac oxygen consumption rate per beat (VO2) in a given canine heart with a stable inotropic background. PVA is a specific area in the pressure-volume (P-V) diagram that is bounded by the end-systolic and end-diastolic P-V relationship lines and the systolic segment of the P-V loop, consisting of the sum of external mechanical work and what is considered the end-systolic elastic potential energy in the ventricular wall. In this study, we compared VO2's of steady state entirely isovolumic and variously ejecting contractions that were made to have equal PVA's in the canine left ventricle. We found that VO2's of these isovolumic and ejecting contractions with equal PVA's (isovolumic vs. ejecting = 1008 +/- 64 (SE) vs. 1022 +/- 62 mm Hg ml/beat, n = 32 pairs in 10 hearts) were equal to each other (0.0375 +/- 0.0021 vs. 0.0368 +/- 0.0021 ml O2/beat) regardless of the marked differences in stroke volume (0 vs. 9.8 +/- 0.6 ml), end-diastolic volume (20.3 +/- 0.8 vs. 23.7 +/- 0.9 ml), end-systolic volume (20.3 +/- 0.8 vs. 13.9 +/- 0.7 ml), peak pressure (123 +/- 5 vs. 88 +/- 5 mm Hg), stroke work (0 vs. 636 +/- 36 mm Hg ml/beat), and calculated peak total wall force (1588 +/- 77 vs. 1077 +/- 72 g). Therefore, we conclude that PVA can serve as a reliable predictor of VO2 in a given canine left ventricle with a stable inotropic background whether the contraction mode is isovolumic or ejecting.

Animals↗
PubMed1984

Effect of arterial impedance changes on the end-systolic pressure-volume relation.

To study the end-systolic pressure-volume relationship of left ventricle ejection against physiological afterload, we imposed seven simulated arterial impedances on excised canine left ventricles connected to a newly developed servo-pump system. We set each of the impedance parameters (resistance, capacitance, and characteristic impedance) to 50, 100, and 200% of normal value (resistance: 3 mm Hg sec/ml; capacitance: 0.4 ml/mm Hg; characteristic impedance: 0.2 mm Hg sec/ml), while leaving the other parameters normal. Under a given impedance, the end-systolic pressure-volume relationship was determined by preloading the ventricle at four different end-diastolic volumes. There was no significant change in the slope of the end-systolic pressure-volume relationship with changes in any of the afterloading impedance parameters. However, the volume intercept of the end-systolic pressure-volume relationship decreased significantly with resistance from 5.5 +/- 1.0 (SE) ml at resistance equal to 1.5 mm Hg sec/ml to 0.6 +/- 1.8 ml at resistance equal to 6 mm Hg sec/ml (P less than 0.01). The volume axis intercept also decreased with characteristic impedance, from 5.9 +/- 2.0 ml at a characteristic impedance of 0.1 mm Hg sec/ml to 5.4 +/- 2.1 ml at a characteristic impedance of 0.4 mm Hg sec/ml, (P less than 0.05). We conclude that the slope of the end-systolic pressure-volume relationship is insensitive to a wide range of changes in afterload impedance, but its volume intercept is dependent on resistance and characteristic impedance.

Animals↗
PubMed1989

Effect of acutely increased right ventricular afterload on work output from the left ventricle in conscious dogs. Systolic ventricular interaction.

In seven conscious, chronically instrumented dogs, left ventricular volume was calculated with an ellipsoidal model from the anteroposterior, septal-free wall, and base-to-apex left ventricular dimensions, measured by implanted ultrasonic transducers. Matched micromanometers measured left and right ventricular transmural and transseptal pressures. Ventricular pressures and volumes were varied by inflation of implanted vena caval and pulmonary arterial occluders. When compared with vena caval occlusion at matched left ventricular end-diastolic volumes, graded pulmonary arterial occlusions were associated with higher right ventricular systolic pressures, reduced left-to-right transseptal systolic pressure gradients, and leftward systolic septal displacement, with increased septal-free wall segment shortening (all p less than 0.05). Graded pulmonary arterial occlusions, like vena caval occlusions, reduced left ventricular end-diastolic volume, but left ventricular stroke work at a given end-diastolic volume was greater during pulmonary arterial occlusions (2,674 +/- 380 10(-3) erg) than during vena caval occlusion (1,886 +/- 450 10(-3) erg, p less than 0.05). These data indicate that, while transient pulmonary arterial occlusion reduces left ventricular preload, the concomitant increase in right ventricular systolic pressure, which is the pressure external to the interventricular septal segment of the left ventricle, augments septal shortening and assists left ventricular pump function at a given preload through direct systolic ventricular interaction.

Animals↗
PubMed1992

In-plane myocardial wall stress is not the primary determinant of coronary systolic flow impediment. A study in the isolated, perfused dog septum.

The hypothesis that ventricular in-plane tensile wall stresses are the major determinant of systolic coronary flow was investigated in this study. We measured coronary artery inflow in the maximally vasodilated bed of the isolated beating septum (n = 10) during two modes of contraction characterized by markedly different levels of developed in-plane stress. An increase in contractility was induced by changing from the control steady-state pacing state to a postextrasystolic potentiated state induced by a modified rapid pacing protocol. Over a range of increments of passive stretch, the systolic flow impediment versus the diastolic wall strain was described by an inverse linear relation. Despite the differences in developed in-plane wall stresses between the two modes of contraction (p less than 0.001), the slope and intercept of these relations in both the control and potentiated states were not different for the low versus high developed stress modes. The systolic flow impediment versus diastolic wall strain relation for the potentiated beats, compared with the control beats, was characterized by an increase in the intercept in both the low developed stress beats (p less than 0.05) and the high developed stress beats (p less than 0.05). These data indicate that the impediment to coronary flow during systole is not primarily determined by systolic myocardial in-plane tensile wall stresses but rather by the contractile state of the muscle.

Animals↗
PubMed1989

Morbidity and mortality in the Systolic Hypertension in the Elderly Program (SHEP) pilot study.

The pilot study of the Systolic Hypertension in the Elderly Program was a randomized, double-blind, placebo-controlled trial of drug therapy for isolated systolic hypertension. It followed 551 elderly participants with untreated blood pressures of greater than 160/less than 90 mm Hg for an average of 34 months. Mean age of the participants was 72 years; 63% were women, and 82% were white. Pretreatment blood pressures averaged 172/75 mm Hg. Participants were randomly assigned to treatment with chlorthalidone or placebo as Step I medication. Blood pressures at annual visits averaged 141/68 and 157/73 mm Hg for the drug-treated and placebo-treated groups, respectively, with 60% and 33% of the survivors on blinded medication having systolic blood pressures of less than 160 mm Hg at their last annual visit. All-cause mortality rates for the drug-treated and placebo-treated groups were 25.4 and 22.7 deaths per 1,000 participant-years of risk, and rates for definite "first stroke" were 8.3 and 12.8 per 1,000 years of risk. Differences between groups were significant for systolic and diastolic blood pressure but not for death or stroke rates. A full-scale study has begun to determine the effects of drug therapy for isolated systolic hypertension on stroke and mortality rates.

Antihypertensive Agents↗
PubMed1993

Predictors of carotid stenosis in older adults with and without isolated systolic hypertension.

BACKGROUND AND PURPOSE: This study was designed to determine the prevalence of carotid stenosis and atherosclerosis in older adults with and without isolated systolic hypertension and to determine risk factors for carotid artery disease in these two groups. METHODS: Duplex scans were performed on 187 participants of the Systolic Hypertension in the Elderly Program and on 187 normotensive control subjects. Doppler measures of blood flow velocity were used to determine the prevalence of internal carotid artery stenosis. RESULTS: Carotid stenosis was found in 25% of hypertensive participants but in only 7% of normotensive participants (p < 0.001). Among hypertensive participants, carotid stenosis was correlated with lower diastolic blood pressure (p = 0.022). In multivariate analysis, systolic blood pressure of > or = 160 mm Hg was the strongest predictor of carotid stenosis. Other variables independently related to stenosis were diastolic blood pressure of < 75 mm Hg (p = 0.001), alcohol use (p = 0.005), heart rate of > or = 80 beats per minute (p = 0.013), smoking (p = 0.034), high concentration of apoprotein B (p = 0.001), and low concentration of high density lipoprotein cholesterol (borderline significant, p = 0.069). Among hypertensive participants, the strongest predictor of carotid stenosis was low diastolic blood pressure. This relation persisted even after taking into account differences in pulse pressure. CONCLUSIONS: Isolated systolic hypertension is strongly correlated with carotid stenosis, and among those with isolated systolic hypertension low diastolic blood pressure is a marker for carotid stenosis.

Aged↗
PubMed2001

One-year study of felodipine or placebo for stage 1 isolated systolic hypertension.

Asubstantial number of older hypertensive patients have stage 1 isolated systolic hypertension (systolic blood pressure between 140 and 159 mm Hg and diastolic blood pressure <90 mm Hg), but there are currently no data showing that drug treatment is effective, safe, and/or beneficial. To compare the effects of active treatment compared with placebo on blood pressure, left ventricular hypertrophy, and quality of life among older stage 1 isolated systolic hypertensive patients, a randomized, double-blind, parallel-group, multicenter clinical trial comparing felodipine (2.5, 5, or 10 mg once daily) and matching placebo was performed in 171 patients (49% male, average age 66+/-7 years, with 49% white and 30% Hispanic) with a baseline blood pressure of 149+/-7/83+/-6 mm Hg. During 52 weeks of treatment, patients randomized to active treatment achieved significantly lower blood pressures (137.0+/-11.7/80.2+/-7.6 mm Hg for extended-release felodipine versus 147.5+/-16.0/83.5+/-9.7 mm Hg for placebo, P<0.01 for each), a reduced incidence of left ventricular hypertrophy (7% for extended release felodipine versus 24% for placebo, P<0.04), and improved quality of life (change in Psychological General Well-Being index, 3.0+/-6.8 for extended-release felodipine versus -0.8+/-10.3 for placebo, P<0.01) versus baseline. There were no clinically significant differences between treatments in tolerability or adverse effects. Stage 1 isolated systolic hypertension can be effectively and safely treated pharmacologically. Treatment reduced progression to the higher stages of hypertension, reduced the incidence of left ventricular hypertrophy, and improved an overall measure of the quality of life. Larger and longer studies will be needed to document any long-term reduction in cardiovascular event rates associated with treating stage 1 systolic hypertension.

Aged↗
PubMed1991

Importance of mitral subvalvular apparatus in terms of cardiac energetics and systolic mechanics in the ejecting canine heart.

To assess the importance of the intact mitral subvalvular apparatus for left ventricular (LV) energetics, data from nine open-chest ejecting canine hearts were analyzed using piezoelectric crystals to measure LV volume. After mitral valve replacement with preservation of all chordae tendineae, baseline LV function was assessed during transient caval occlusion: A quadratic fit of the LV end-systolic pressure-volume data was used to determine the curvilinear end-systolic pressure-volume relationship (ESPVR). All chordae were then divided with exteriorized snares. Reassessment revealed deterioration of global LV pump function: (a) the coefficient of nonlinearity, decreased (less negative) by 90% (P = 0.06); (b) slope of the curvilinear ESPVR at the volume axis intercept, decreased by 75% (P = 0.01); and V100, end-systolic volume at 100 mmHg end-systolic pressure, increased by 42% (P less than 0.02). Similarly, preload recruitable stroke work fell significantly (-14%) and Vw1,000 (end-diastolic volume [EDV] at stroke work [SW] of 1,000 mmHg.ml) rose by 17% (P less than 0.04). With respect to LV energetics, the total mechanical energy generated by the ventricle decreased, as indicated by a decline in the slope of the pressure volume area (PVA)-EDV relationship (120 +/- 13 [mean +/- SD] vs. 105 +/- 13 mmHg, P less than 0.001). Additionally, comparison of LV SW and PVA from single beats with matched EDV showed that the efficiency of converting mechanical energy to external work (SW/PVA) declined by 14% (0.65 +/- 0.13 vs. 0.56 +/- 0.08, P less than 0.03) after chordal division. While effective systemic arterial elastance, Ea, also fell significantly (P = 0.03) after the chordae were severed, the Ea/Ees ratio (Ees = slope of the linear ESPVR) increased by 124% (0.91 +/- 0.53 vs. 2.04 +/- 0.87, P = 0.001) due to a proportionally greater decline in Ees. This indicates a mismatch in ventriculo-arterial interaction, deviating from that required for maximal external output (viz., Ea/Ees = 1). These adverse effects of chordal division may be related to the observed changes in LV geometry (i.e., eccentricity). We conclude that the intact mitral subvalvular apparatus is important in optimizing LV energetics and ventriculo-vascular coupling in addition to the enhancement of LV systolic performance.

Animals↗
PubMed1993

The effects of hypoxic acidemia on left ventricular end-systolic elastance in fetal sheep.

Using the conductance catheter technique, we measured the effects of hypoxic acidemia on left ventricular end-systolic elastance in anesthetized, 133-d gestation, in utero fetal sheep (n = 7). Conductance and Millar catheters were introduced into the left ventricle through a carotid artery cutdown. Fetuses were rendered progressively hypoxic and acidemic by placental embolization with repeated injections of 5 x 10(5) 50-microns plastic spheres every 15 min via a catheter placed in the fetal abdominal aorta. We recorded pressure-volume data and arterial blood gases at 15-min intervals. End-systolic elastance was computed using a single-beat method of extrapolating maximum isovolumic pressure. A mean of five boluses was required to cause fetal death. Placental embolization caused progressive fetal acidemia. Mean baseline fetal arterial pH was 7.32 +/- 0.06 (mean +/- SD) and gradually decreased with embolization (p < 0.0001). A linear relationship was found to exist between elastance and pH with a mean decrease of 0.46 kPa/mL per 0.1-unit drop in pH (r = 0.96; p < 0.0001). Despite the decrease in end-systolic elastance, stroke volume and left-ventricular output were maintained due to a parallel decrease in afterload. The decrease in end-systolic elastance was gradual and extended over the entire clinically important range of pH, rather than being a terminal event. This study, which, to our knowledge, is the first to use the conductance catheter to measure fetal left ventricular function demonstrates that hypoxic acidemia adversely affects myocardial contractility assessed by end-systolic elastance.

Acidosis↗
PubMed1984

Normalization of end-systolic pressure-volume relation and Emax of different sized hearts.

A shift of the ventricular end-systolic pressure-volume (P-V) relation and a change in its slope Emax reasonably reflect a change in contractility in a given ventricle. However, comparison of Emax's of different sized hearts may be difficult without an appropriate normalization. We attempted to normalize Emax of different sized hearts to the force-length (F-L) relation of unit mass of myocardium in the ventricular wall. We formulated the end-systolic P-V relation as (end-systolic pressure) = Emax (end-systolic volume Vi - Vd), where Vd = volume axis intercept of the end-systolic P-V relation line. As a first step, both thick wall sphere and cylinder models of the ventricle with a wall volume of Vm were used. Circumferential F-L relation of unit myocardium in different ventricular wall layers were formulated as functions of Emax, Vd, and Vm. We found that as long as the product of Emax and Vd remains constant, the F-L relation in the midwall layer and the average F-L relation in the wall remain relatively unchanged regardless of wide changes in Vm and Vi. The elevation of the F-L relation curve, which represents myocardial contractility, was found to change in proportion to Emax Vd, largely independent of Vm and Vi, or the size of the ventricle.

Cardiac Volume↗
PubMed1989

Left ventricular systolic and diastolic time intervals in familial amyloid polyneuropathy.

To determine left ventricular (LV) systolic and diastolic properties in patients with familial amyloid polyneuropathy (FAP), we analyzed simultaneous recordings of the electrocardiogram, phonocardiogram, carotid arterial pulse, and apex cardiogram in 14 patients and 21 normal subjects. LV systolic and diastolic time intervals were measured. Correlations between the intervals and neurologic disabilities, duration of illness, and age were examined. We found that in patients with FAP, 1) LV relaxation was impaired, especially in early diastole, whereas systolic function was generally preserved, 2) abnormal LV relaxation could be seen before the development of both clinically identifiable heart disease and the abnormalities in systolic function, 3) indexes of LV systolic function and relaxation decreased in parallel with the progress of the disease, duration of illness, and age, and 4) electromechanical delay was markedly increased.

Adult↗
PubMed1990

Increased dependence on slow filling for left ventricular diastolic filling in patients with coronary artery disease and a depressed systolic function--assessment with radionuclide ventriculography.

Contributions of rapid filling, slow filling and atrial systole to the left ventricular (LV) filling volume were analyzed with the use of radionuclide ventriculography at rest, both globally and regionally, in 34 patients with isolated disease of the left anterior descending coronary artery. The patients included 17 with a normal ejection fraction (EF greater than or equal to 50%; group 1) and 17 with a depressed EF (less than 50%; group 2), and the data were compared with those obtained from 13 normal subjects. A computer program subdivided the LV image into 4 regions, and time-activity curves were constructed globally and regionally by reverse-gating from the R wave. In both groups the contribution of rapid filling to the LV filling volume was decreased significantly in the affected septal and apical regions, and in the global left ventricle compared with that in normal subjects. In group 1, the contribution of atrial systole showed an increase in these affected regions and in the global left ventricle. In contrast, in group 2, the atrial contribution was not increased globally or regionally as much as was expected. However, the contribution of slow filling was either increased significantly or tended to increase in the affected regions and in the global left ventricle. There were negative correlations between the contribution of rapid filling and that of slow filling in the global left ventricle (r = -0.73, p less than 0.001) and in each of the septal, apical and lateral regions (r greater than or equal to -0.60, p less than 0.001), which suggested that the contribution of slow filling as well as of atrial systole undergoes an increase as rapid filling is impaired. Thus, in patients with coronary artery disease, the left ventricle relies on slow filling as well as atrial systole to affect diastolic LV filling in the affected regions and in the global left ventricle in the presence of LV systolic dysfunction.

Adult↗
PubMed1991

Theoretical validity of predicting right ventricular systolic pressure by a quantitative index of interventricular septal displacement in acute right ventricular pressure overload.

A leftward shift of the interventricular septum (IVS) of the heart is observed in patients with right ventricular pressure overload (RVPO). We simulated the leftward displacement of IVS in a modified ellipsoidal model on the assumption that the IVS generates the same tension as the left ventricular (LV) free-wall in acute RVPO, and derived the relational equations between ventricular pressures (RVP, LVP) and eccentricity index (EI = LVAPD/LVSLD, LVAPD: left ventricular anterior-posterior diameter, LVSLD: left ventricular septal-lateral diameter). The equations indicate that RVP/LVP correlates with simultaneous EI, independent of the absolute LV wall tensions and the LV size. To confirm this result, we undertook recurrent pulmonary embolizations in anesthetized open-chest dogs, and analyzed the relationship between RVP/LVP and EI at four phases in systole through the course of RVPO and shock. The advance of RVPO shifted the peak of RVP toward late-systole and made the values of RVP/LVP and EI significantly greater at late-systole than at early-systole. There were significant linear relationships between instantaneous EI and RVP/LVP at each phase, expect for the early systole in the shock stage, and the regression lines on all phases were similar to one another. These results are consistent with our theoretical ones. Therefore we conclude that it is reasonable to predict RVP by using EI, theoretically and experimentally.

Algorithms↗
PubMed1996

Right ventricular systolic performance before and after surgery for tricuspid regurgitation associated with mitral stenosis.

The reversibility of right ventricular function in patients with mitral stenosis associated with secondary tricuspid regurgitation (TR) is as yet undetermined. We assessed the right ventricular systolic performance by cardiac catheterization before and 19 months after surgery in 18 patients who underwent DeVega's tricuspid annuloplasty plus mitral valve replacement (MS plus TR group) and in 9 with mitral valve replacement for isolated mitral stenosis (MS group). After surgery, the right ventricular systolic pressure decreased significantly in both groups (both p < 0.01). In the MS plus TR group, the postoperative right ventricular end-diastolic and end-systolic volume indices (RVEDVI and RVESVI, respectively) were significantly decreased compared with the respective preoperative values (both p < 0.001). No significant difference was noted between the groups with regard to the right ventricular peak-systolic pressure/end-systolic volume index ratio (RVPSP/ESVI) either before or after surgery. Various left ventricular indices were comparable between the groups both before and after surgery. Linear regression analysis revealed significant correlations between RVEDVI and the RVPSP/ESVI, and between RVPSP and the RVPSP/ESVI both before and after surgery. These results indicate that right ventricular systolic performance in patients with MS plus secondary TR became comparable to those that in patients with isolated MS after surgery, and that this was probably due to nearly equivalent right ventricular contractility before surgery.

Adult↗
PubMed1994

Thoracocardiographic-derived left ventricular systolic time intervals.

Thoracocardiography noninvasively estimates left ventricular performance by recording ventricular volume curves with inductive plethysmography. We studied timing of these curves to evaluate their potential to accurately track systolic time intervals in comparison with standard methods. Thoracocardiographic left ventricular volume curves, carotid pressure pulses determined by applanation tonometry, the phonocardiogram and ECG were recorded simultaneously in ten normal subjects at various body positions achieved with a tilt table. An equation was derived to predict preejection period from onset of ejection in thoracocardiographic curves. Ventricular ejection time was calculated as total electromechanical systole obtained by phonocardiography minus preejection period. The equation was validated prospectively in 31 measurements in critically ill patients. In normal subjects, the interval ECG Q wave to ejection onset in thoracocardiographic curves correlated well with preejection period from applanation tonometry and phonocardiography (r = 0.92; standard error of estimate (SEE), 8 ms; p < 0.001). Thoracocardiographic curves showed a delay that varied with body position according to the regression equation: delay = 40 ms + 10 x sine (tilt angle) (where r = 0.62; SEE, 7 ms; p < 0.001). Application of this equation in the prospective study in patients revealed close agreement in systolic time intervals from thoracocardiography and simultaneous applanation tonometry plus phonocardiography, respectively. The mean difference +/- SD between methods in preejection periods was 3 +/- 7 ms and in the ratios of preejection period to left ventricular ejection time, 0.02 +/- 0.05. Trends of changes in systolic time intervals were identical for the two methods. We conclude that thoracocardiography combined with phonocardiography provides accurate systolic time intervals when corrected for a position-dependent delay of its waveforms.

Adult↗
PubMed2002

Left ventricular remodeling, systolic function, and diastolic function in young adults with beta-thalassemia intermedia: a Doppler echocardiography study.

BACKGROUND: The aim of this study was to investigate the left ventricular (LV) remodeling and function in 24 asymptomatic young adults affected by beta-thalassemia intermedia (TI), in order to compare the obtained data with that of 80 patients affected by beta-thalassemia major (TM) and 65 healthy subjects. METHODS: LV volumes and shapes, mass index, mass/volume ratio, systolic and diastolic function, stroke volume, and cardiac index were determined by two-dimensional and M-mode echocardiography. RESULTS: In the TM and TI groups, LV volumes, diastolic and systolic shapes were significantly different from the control subjects, but the ejection fraction was slightly reduced only in the TM group. The TI group had larger LV volumes than did the TM group (mean [+/- SD] end-diastolic volume index, 99.4 +/- 21.9 vs 82.7 +/- 21.5 mL/m(2), respectively [p < 0.005]; mean end-systolic volume index, 42.8 +/- 12.2 vs 36.1 +/- 12.9 mL/m(2), respectively [p < 0.05]). Both groups showed an increase of the LV mass index, but the mass/volume ratio did not differ from the control subjects. The systolic volume index and the cardiac index were increased in both groups, but the increase was more pronounced in the TI group. Fractional shortening (FS) and the mean velocity of circumferential shortening (mVCFc) were decreased in the TM group (FS, 33.6 +/- 5.5% vs 36.9 +/- 4.1, respectively [p < 0.001]; mVCFc, 1.06 +/- 0.18 vs 1.17 +/- 0.12 circumference per second, respectively [p < 0.0001]). The LV contractile state was depressed only in the TM group, and the preload index was normal in both. LV filling showed an increase in the total flow velocity integral due to increases in the peak E wave (E) and peak A wave (A) velocities and integrals, with an increase of the E/A ratio in the TM group and a slight decrease in the TI group. The isovolumic relaxation time was prolonged in both groups. There was no major derangement in the pulmonary venous flow. CONCLUSIONS: Asymptomatic young adults with TI show significant increases in LV volumes, LV mass, and cardiac index that are more pronounced than those in TM patients. LV systolic function is preserved in the TI group but is slightly depressed in the TM group due to the increase of afterload and to reduced contractility. The hemodynamic and hematologic factors involved in the etiopathogenesis of these findings are discussed, such as the treatment strategy.

Adult↗