Mean Velocity Of Circumferential Shortening Research Articles

THE EFFECT OF ALBUMIN:CREATININE RATIO ON STANDARD ECHOCARDIOGRAPHIC PARAMETERS IN ADOLESCENT TYPE 1 DIABETES

Study Design Single center prospective cross-sectional study Patient Population The AdDIT study is a multi-centre, randomized, double-blind, placebo-controlled, 2x2 factorial design trial of angiotensinconverting enzyme inhibitor and statin therapy vs. placebo in 500 high-risk (>1.2 mg⁄mmol) T1D adolescents, defined on the basis of albumin excretion.1 It also includes a parallel observational study based on longitudinal follow-up of 400 low-risk (<0.8 mg⁄mmol) and medium-risk (0.8-1.2 mg⁄mmol) T1D adolescents who were screened but did not qualify for randomization. Subjects recruited in the current study were lowand mediumrisk from the parallel observational study and high-risk T1D adolescents that declined participation in the randomized controlled trial. All 199 T1D were compared with 178 adolescents recruited as healthy volunteers, who were not on any vasoactive medications, had no previous history of familial hyperlipidemia, diabetes, obesity, hypertension, or any other significant cardiac, renal or systemic disease and normal cardiac anatomy and function by screening echocardiogram. In subgroup analysis, 68 low-, 78 medium-and 53 high-risk were compared with 65 controls that underwent the same baseline clinical assessment. Anthropometric Assessment Height was measured by stadiometer to the nearest 0.1 cm and weight by electronic balance to the nearest 0.1 kg. Resting heart rate and right brachial blood pressure was measured using an age-appropriate cuff and averaging 3 readings with an automated DINAMAP® sphygmomanometer (Critikon, Tampa, Florida, USA). Echocardiographic Assessment Using a Vivid 7 ultrasound system (GE, General Electric Corp., Wisconsin, USA) with appropriate transducers ranging from frequencies 4-12 MHz depending on subject age and size, a standardized functional imaging protocol, including subcostal, parasternal, apical and suprasternal views, was performed according to published guidelines.2 Modalities employed in this study included M-mode, 2D and pulse Doppler blood flow measurements. Laboratory Assessment Glycemic control was measured by fasting blood glucose and haemoglobin A1c. Serum lipids including total, low-density lipoprotein and high-density lipoprotein cholesterol and triglycerides were measured. Serum creatinine was used to estimate glomerular filtration rate.3 Statistical Analysis Between groups comparisons were performed using Student’s ttests. Relationships were tested using Pearson’s correlations. Statistical significance was considered at p<0.05.

Measuring Stress Velocity Index Using Mean Blood Pressure: Simple yet Accurate?

The stress velocity index, or the relationship of the rate-corrected mean velocity of circumferential shortening (VCFc) to the end systolic wall stress (ESWS), is a sensitive, load-independent measure of left ventricular contractility. ESWS is technically difficult to obtain and requires simultaneous blood pressure measurement, carotid artery tracing, and phonocardiogram. We report our comparison of two simpler methods of measuring ESWS and, therefore, stress velocity index. Patients with normal cardiac anatomy who had completed anthracycline chemotherapy were evaluated. ESWS as measured by the standard method using a carotid artery tracing (ESWScar) was compared to ESWS obtained using mean arterial pressure (ESWSmap) or systolic blood pressure (ESWSsbp). The cohort included 63 patients, with 37 (59%) males and a median age of 13.1 years. The mean (+/-SD) ESWScar was 53.3+/-15.3 g/cm(2) (range, 26.3-94 g/cm(2)); ESWSmap, 53 +/-13.4 g/cm(2) (range, 27.1-86.1 g/cm(2)); and ESWSsbp, 72.9 +/- 18.2 g/cm(2) (range, 40.8-117.2 g/cm(2)). ESWSmap and ESWSsbp closely correlated with ESWScar (coefficient correlation r = 0.88 and r = 0.87, respectively). Using ESWSmap, all patients were correctly classified as having normal or abnormal contractility as defined by stress velocity index, whereas ESWSsbp detected only two of the six patients with impaired contractility. We conclude that ESWSmap is a simple, highly sensitive and specific method for assessing left ventricular contractility. ESWSmap correlates closely with ESWScar and can be incorporated into the monitoring of cardiac dysfunction in the anthracycline-treated population. Further studies are needed to determine if this simplified measure accurately assesses the ESWS in other cardiac disease states.

Early activation of cardiac and renal endothelin systems in experimental heart failure.

We investigated the time course of the expression of cardiac and renal endothelin systems in tachycardia-induced heart failure in dogs. Eleven beagles underwent rapid pacing at a progressively increased rate over a period of 5 wk, with a weekly clinical examination, echocardiography, measurement of circulating and urinary endothelin-1 (ET-1), and myocardial and renal tissue biopsies. Real-time quantitative PCR was used for determinations of tissue prepro-ET-1 (ppET-1), ET-1-converting enzyme (ECE-1), and ETA and ETB receptor mRNA. Cardiac and renal tissue ET-1 contents were evaluated by immunostaining and measured by radioimmunoassay at autopsy. Rapid pacing caused a progressive increase in end-systolic and end-diastolic ventricular volumes (P < 0.05) from week 2 together with a decrease in ejection fraction and in mean velocity of circumferential shortening (P < 0.05) from week 1. These changes were tightly correlated to myocardial ppET-1 and renal ETA receptor mRNA and less so to myocardial ECE-1 mRNA, and they occurred before any increase in plasma and urinary ET-1 (P < 0.05 from week 4) and clinical signs of heart failure. Renal ppET-1 did not change. Both cardiac and renal ET-1 peptide contents were increased at autopsy. We conclude that tachycardia-induced heart failure in dogs is characterized by an early activation of the cardiac and renal tissue endothelin systems, which occurs before any changes in circulating and urinary ET-1 and is closely related to altered ventricular function.

Left Ventricular Remodeling, Systolic Function, and Diastolic Function in Young Adults With β-Thalassemia Intermedia: A Doppler Echocardiography Study

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. 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. 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. 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.

Cardiac Performance in Turner’s Syndrome Patients on Growth Hormone Therapy

Objectives: To investigate possible cardiac morphofunctional alterations observed in 26 Turner’s syndrome (TS) patients on prolonged high-dose growth hormone (GH) therapy. Study Design: We examined 26 TS subjects treated with rhGH (1 U/kg/week) for a mean period of 4.9 years (range 1–7.8) and 37 age-, weight- and height-matched healthy girls. Left ventricular volume, mass, systolic function, cardiac index, systemic vascular resistance and diastolic function were evaluated by two-dimensional and Doppler echocardiography. Results: Heart rate and systolic blood pressure (BP) were higher in TS patients than in controls, while diastolic BP was lower. Left ventricular volumes, ejection fraction, mass index, M/V ratio and cardiac index did not differ significantly; systemic vascular resistance was slightly decreased. Left ventricular fractional shortening and mean velocity of circumferential shortening were slightly increased while end-systolic meridional stress was decreased in TS. Contractile state was normal in TS. Diastolic function assessment showed a shortening of isovolumetric relaxation and diastolic filling times with an increased atrial contribution and a normal pulmonary venous flow. Conclusion: Cardiac morphology in TS patients on GH therapy is similar to controls. The observed changes in left ventricular systolic and diastolic function should be interpreted as an adaptation to the higher heart rate and reduced peripheral vascular resistance induced by GH therapy.

Impairment of Cardiac Function and Bioenergetics in Adult Transgenic Mice Overexpressing the Bovine Growth Hormone Gene

Cardiovascular abnormalities represent the major cause of death in patients with acromegaly. We evaluated cardiac structure, function, and energy status in adult transgenic mice overexpressing bovine GH (bGH) gene. Female transgenic mice expressing bGH gene (n = 11) 8 months old and aged matched controls (n = 11) were used. They were studied with two-dimensional guided M-mode and Doppler echocardiography. The animals (n = 6) for each group were examined with 31P magnetic resonance spectroscopy to determine the cardiac energy status. Transgenic mice had a significantly higher body weight (BW), 53.2± 2.4 vs. 34.6 ± 3.7 g (P < 0.0001) and hypertrophy of left ventricle (LV) compared with normal controls: LV mass/BW 5.6 ± 1.6 vs. 2.7 ± 0.2 mg/g, P < 0.01. Several indexes of systolic function were depressed in transgenic animals compared with controls mice such as shortening fraction 25± 3.0% vs. 39.9 ± 3.1%; ejection fraction, 57 ± 9 vs. 77 ± 5; mean velocity of circumferential shortening, 4.5 ± 0.8 vs. 7.0± 1.1 circ/sec, p < 0.01. Creatine phosphate-to-ATP ratio was significantly lower in bGH overexpressing mice (1.3 ± 0.08 vs. 2.1 ± 0.23 in controls, P< 0.05). Ultrastructural examination of the hearts from transgenic mice revealed substantial changes of mitochondria. This study provides new insight into possible mechanisms behind the deteriorating effects of long exposure to high level of GH on heart function.

Impairment of cardiac function and bioenergetics in adult transgenic mice overexpressing the bovine growth hormone gene.

Cardiovascular abnormalities represent the major cause of death in patients with acromegaly. We evaluated cardiac structure, function, and energy status in adult transgenic mice overexpressing bovine GH (bGH) gene. Female transgenic mice expressing bGH gene (n = 11) 8 months old and aged matched controls (n = 11) were used. They were studied with two-dimensional guided M-mode and Doppler echocardiography. The animals (n = 6) for each group were examined with 31P magnetic resonance spectroscopy to determine the cardiac energy status. Transgenic mice had a significantly higher body weight (BW), 53.2+/-2.4 vs. 34.6+/-3.7 g (P < 0.0001) and hypertrophy of left ventricle (LV) compared with normal controls: LV mass/BW 5.6+/-1.6 vs. 2.7+/-0.2 mg/g, P < 0.01. Several indexes of systolic function were depressed in transgenic animals compared with controls mice such as shortening fraction 25+/-3.0% vs. 39.9+/-3.1%; ejection fraction, 57+/-9 vs. 77+/-5; mean velocity of circumferential shortening, 4.5+/-0.8 vs. 7.0+/-1.1 circ/sec, p < 0.01. Creatine phosphate-to-ATP ratio was significantly lower in bGH overexpressing mice (1.3+/-0.08 vs. 2.1+/-0.23 in controls, P < 0.05). Ultrastructural examination of the hearts from transgenic mice revealed substantial changes of mitochondria. This study provides new insight into possible mechanisms behind the deteriorating effects of long exposure to high level of GH on heart function.

Increased left ventricular systolic function in insulin dependent diabetic patients with normal albumin excretion.

Alterations in cardiovascular function may be an aetiological factor for the development of microalbuminuria in patients with insulin-dependent diabetes mellitus. We studied cardiac function with echocardiography in relation to the degree of albuminuria in 27 insulin-dependent diabetes mellitus patients and 13 healthy subjects. Patients were grouped according to urinary albumin excretion: <20 microg x min(-1) (normoalbuminuric), and 20 to 200 microg x min(-1) (microalbuminuric). None were or had been treated with cardiovascular drugs. The normoalbuminuric patients had a higher heart rate, mean velocity of circumferential shortening, stroke velocity index (a measure of contractility), and aortic peak velocity than controls. No difference in diastolic function was present. In the microalbuminuric group, the stroke velocity index was comparable to values observed in healthy subjects. The increased systolic performance (heart rate and contractility) may contribute to the renal hyperperfusion and glomerular hyperfiltration observed in insulin-dependent diabetes mellitus patients before the development of micro- and in turn macroalbuminuria. The possible cause effect mechanisms should be further studied, as preventive medical treatment of the hypercontractile heart is possible. In conclusion, cardiac contractility is increased in insulin-dependent diabetes mellitus patients with normoalbuminuria and returns to levels observed in healthy subjects when microalbuminuria develops.

Left ventricular performance following the arterial switch operation: use of noninvasive wall stress analysis in the postoperative period.

To determine postoperative left ventricular mechanics following the arterial switch operation (ASO). Prospective, cohort study. Pediatric cardiac recovery room. Nine neonates with transposition of the great arteries undergoing the ASO within the first week of life. Noninvasive ejection phase indices: shortening fraction (% SF), corrected mean velocity of circumferential shortening (VCFc), and wall stress analysis were used to calculate indices of specific left ventricular systolic mechanics. The % SF and VCFc were respectively adjusted for left ventricular afterload (end-systolic wall stress) to derive an index for left ventricular performance (stress-shortening relation) and contractility (stress-velocity relation). Left ventricular preload was assessed as the variance between the performance and contractility indices. All indexed data are reported as mean Zscore (i.e., number of standard deviations from the mean of a normal age- and body surface area-adjusted population). A mean Zscore of < -2 or > 2 was regarded as a significant variance from normal. Transmitral Doppler flow patterns were recorded at each postoperative interval and analyzed for isovolumic relaxation time (IVRT) as an index of left ventricular compliance. All nine patients did well clinically and completed the study. Noninvasive parameters were measured at mean intervals of 3 (early), 23 (intermediate), and 48 hrs (late postoperative) relative to the time of arrival in the cardiac recovery room. Postoperative left ventricular performance was decreased throughout the early (-4.0 +/- 1.5 SD), intermediate (-4.1 +/- 2.8), and late (-3.5 +/- 1.3) phases of recovery. In contrast, the overall left ventricular contractility remained normal throughout the three postoperative intervals (0.2 +/- 1.8, -1.2 +/- 1.9, and -1.0 +/- 1.6, respectively), although three of the nine patients had a diminished stress-velocity index during the study period. Left ventricular afterload was within normal range in the early (0.1 +/- 1.7) and intermediate (1.5 +/- 1.9) phases of recovery, but increased in the late postoperative period (2.5 +/- 2.9). Left ventricular preload was decreased significantly throughout the early (-4.2 +/- 1.3), intermediate (-2.8 +/- 2.0), and late (-2.5 +/- 1.0) postoperative phases. All nine patients demonstrated decreased preload during the recovery period. IVRT was decreased in the post-ASO patients at each phase of recovery compared with normal data (p < .001). Left ventricular performance is impaired in infants during the period immediately following the ASO. A persistent preload deficit closely matches the pattern of impaired ventricular performance. Decreased IVRT points to impaired ventricular compliance as the etiology of the altered preload. In contrast, left ventricular contractility remains normal in the majority of post-ASO patients. Decreased contractility may account for impaired ventricular performance in selected cases.

Breath-Hold Dobutamine Magnetic Resonance Myocardial Tagging: Normal Left Ventricular Response

Analysis of the changes in myocardial deformation produced by adrenergic stress has been limited by the imaging techniques used. We used rapid magnetic resonance imaging (MRI) myocardial tagging to map the dose-dependent response to incremental dobutamine in the normal human left ventricle. Thirteen volunteers underwent breath-hold tagged cine MRI during dobutamine infusion. Images were acquired throughout systole to a peak dose of 20 μg/kg/min. End-systolic percent circumferential shortening (%S) was measured at 3 transmural locations and 4 circumferential locations at 3 long-axis positions. Mean circumferential shortening velocity (CSV) was also calculated at each location and dose. Mean %S reached a maximum of 26 ± 3% at 10 μg/kg/min compared with 21 ± 4% at baseline (p <0.003). Peak %S was reached by 10 μg/kg/min before a significant increase in heart rate or blood pressure and was unchanged at higher doses. In contrast, CSV increased linearly with dobutamine dose from 4.4 ± 0.9 mm/s at baseline to 9.8 ± 1.4 mm/s at 20 μg/kg/min (p <0.0001). Breath-hold tagged dobutamine MRI is safe and effective in detecting regional and transmural changes in function during incremental dobutamine. CSV increased continuously across the dobutamine dose range. At low dose (≤10 μg/kg/min) %S increased without any change in blood pressure or heart rate. Maintenance of peak %S beyond 10 μg/kg/min in the presence of decreasing systolic intervals resulted from a continued increase in CSV. Thus, CSV may be the preferred measure of contractile function during dobutamine stimulation in human myocardium.

Left Ventricular Ejection Performance Before and Following Percutaneous Mitral Valvuloplasty in Mitral Stenosis

Background:In cases of pure mitral stenosis, it is known that the impairment of left ventricular (LV ejection performance is frequently accompanied, but long term follow up studies on the LV ejection performance after successful percutaneous mitral valvuloplasty are rare so far. Methods:An prospective investigation was performed on 32 cases of patients, 10 being male and 22 female, who have been maintained after successful percutaneous mitral valvuloplasty of pure mitral stenosis. The LV ejection performances have been measured with cardiomechanography and echocardiography before and following the procedure, and the follow-up periods were 24 months in average, in the range of 12 to 35 months. Results:The stroke volume, cardiac output, cardiac index, ejection fraction, mean velocity of circumferential shortening and fractional shortening(FS, which are indices of LV ejection performance, all increased in follow-up than before procedure. In addition, LV end-diastolic dimension and LV end-diastolic dimension index, which are indices of LV preload, increased, and the end-systolic LV wall stress which is an index of afterload, decreased. And the ratio of measured FS to expected FS, which is an index of myocardial contractility, increased in follow-up. Conclusion:The successful percutaneous mitral valvuloplasty of pure mitral stenosis is found to improve LV ejection performance in long term by increasing preload, decreasing afterload, and incr- easing myocardial contractility of left ventricle.

Cardiac-specific overexpression of phospholamban alters calcium kinetics and resultant cardiomyocyte mechanics in transgenic mice.

Phospholamban is the regulator of the cardiac sarcoplasmic reticulum (SR) Ca(2+)-ATPase activity and an important modulator of basal contractility in the heart. To determine whether all the SR Ca(2+)-ATPase enzymes are subject to regulation by phospholamban in vivo, transgenic mice were generated which overexpressed phospholamban in the heart, driven by the cardiac-specific alpha-myosin heavy chain promoter. Quantitative immunoblotting revealed a twofold increase in the phospholamban protein levels in transgenic hearts compared to wild type littermate hearts. The transgenic mice showed no phenotypic alterations and no changes in heart/body weight, heart/lung weight, and cardiomyocyte size. Isolated unloaded cardiac myocytes from transgenic mice exhibited diminished shortening fraction (63%) and decreased rates of shortening (64%) and relengthening (55%) compared to wild type (100%) cardiomyocytes. The decreases in contractile parameters of transgenic cardiomyocytes reflected decreases in the amplitude (83%) of the Ca2+ signal and prolongation (131%) in the time for decay of the Ca2+ signal, which was associated with a decrease in the apparent affinity of the SR Ca(2+)-ATPase for Ca2+ (56%), compared to wild type (100%) cardiomyocytes. In vivo analysis of left ventricular systolic function using M mode and pulsed-wave Doppler echocardiography revealed decreases in fractional shortening (79%) and the normalized mean velocity of circumferential shortening (67%) in transgenic mice compared to wild type (100%) mice. The differences in contractile parameters and Ca2+ kinetics in transgenic cardiomyocytes and the depressed left ventricular systolic function in transgenic mice were abolished upon isoproterenol stimulation. These findings indicate that a fraction of the Ca(2+)-ATPases in native SR is not under regulation by phospholamban. Expression of additional phospholamban molecules results in: (a) inhibition of SR Ca2+ transport; (b) decreases in systolic Ca2+ levels and contractile parameters in ventricular myocytes; and (c) depression of basal left ventricular systolic function in vivo.

In Vivo Echocardiographic Detection of Enhanced Left Ventricular Function in Gene-Targeted Mice With Phospholamban Deficiency

We evaluated the ability of M-mode and Doppler echocardiography to assess left ventricular (LV) function reliably and repeatedly in mice and tested whether these techniques could detect physiological alterations in phospholamban (PLB)-deficient mice. Anesthetized wild-type mice (n = 7) and mice deficient in PLB (n = 8) were studied with two-dimensional guided M-mode and Doppler echocardiography using a 9-MHz imaging and 5- to 7.5-MHz Doppler transducer. Data were acquired in the baseline state and after intraperitoneal isoproterenol administration (2.0 micrograms/g IP). Interobserver and intraobserver variability and reproducibility were excellent. PLB-deficient mice were associated with significant (P < .05) increases in several physiological parameters (mean +/- SD) compared with wild-type control mice: normalized mean velocity of circumferential shortening (7.7 +/- 2.1 versus 5.5 +/- 1.0 circ/sec), peak aortic velocity (105 +/- 13 versus 75 +/- 9.2 cm/s), mean aortic acceleration (57 +/- 16 versus 31 +/- 4 m/s2), and peak early-diastolic transmitral velocity (80.0 +/- 7.2 versus 66.9 +/- 7.7 cm/s). LV dimensions, shortening fractions, heart rates, late diastolic transmitral (A) velocities, and early to late (E/A) diastolic velocity ratios were similar in both groups. Isoproterenol administration resulted in significant increases in Doppler indices of ventricular function in control but not PLB-deficient mice. These findings indicate that assessment of LV function can be performed noninvasively in mice under varying physiological conditions and that PLB regulates basal LV function in vivo.

Cardiovascular effects of high-dose growth hormone treatment in growth hormone-deficient children.

Growth hormone (GH) hypersecretion is associated with an increased incidence of cardiac hypertrophy and subclinical abnormalities of left ventricular (LV) function. The unlimited availability of biosynthetic GH has led to progressively increased dosage when treating GH-deficient children, raising the question of its cardiovascular effects during long-term therapy. We compared 22 children (8 girls, 14 boys), mean age 12.1 years (range 3-17 years) with GH deficiency who were receiving chronic GH treatment (GH group) with 22 normal controls matched for sex and body size in order to evaluate: (1) LV volume, mass, and systolic function by two-dimensional guided M-mode echocardiography; (2) LV diastolic function by pulsed-wave Doppler sampling of the transmitral flow; and (3) cardiac output and systemic vascular resistance by Doppler echocardiography. All patients had been on chronic GH therapy for 13.8 +/- 7.6 months (range 5-30 months) with an average dose of 0.95 +/- 0.12 IU/kg per week (range 0.69-1.17 IU/kg per week). Blood pressure did not differ between the two groups. LV volume, mass, ejection fraction, and mean velocity of circumferential shortening did not differ significantly between the GH group and controls; nor did the peak- and end-systolic meridional stress. All patients had a normal contractile state as estimated by the relation between mean velocity of circumferential shortening and end-systolic meridional stress. The LV filling parameters did not differ between the two groups, and there was no difference in cardiac index and systemic vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Quantitated left ventricular systolic mechanics in children with septic shock utilizing noninvasive wall-stress analysis

Objective: To quantitate ventricular systolic mechanics in septic children. Design: Prospective wall-stress analysis was compared to standard ejection phase indices. Setting: University-based pediatric intensive care unit. Patients: Fifteen children with sepsis (hemodynamically stable, n = 5; in shock, n = 10). Measurements and Main Results: Left ventricular ejection phase indices: shortening fraction (shortening) and corrected mean velocity of circumferential shortening (velocity) were adjusted for end-systolic wall stress (stress). Ejection phase, performance (stress-shortening relation), contractility (stress-velocity relation), and afterload (stress) were indexed to age-corrected normal means, with variance of ≥2 sd regarded as significant. Preload index represented variance between performance and contractility indices. All hemodynamically stable septic patients had normal performance, contractility, and preload. Afterload was increased in three of five patients. Of the patients with septic shock, six often had decreased performance (decreased contractility and increased afterload, n = 4; decreased afterload, n = 1; and severe preload deficit, n = 1). Despite aggressive volume resuscitation, six of ten children in septic shock had evidence of diminished preload. Follow-up studies in the septic shock patients demonstrated reversal of depressed ventricular contractility within 3 to 6 days in all four patients initially affected (p < .05). One patient developed late decreased performance and contractility in association with multiple organ failure. Ventricular loading abnormalities persisted in a follow-up study of these patients including a preload deficit in five of ten patients in shock. Conclusions: The frequency rate (40%) of reversible impaired ventricular contractility in children with septic shock is significant. Afterload is normal or increased in the majority of septic subjects, possibly due to acute ventricular dilation. Decreased preload contributes to altered ventricular performance in the majority of children with septic shock, persisting days after the initiation of therapy. Wall-stress analysis provided detailed information regarding ventricular mechanics that was not otherwise obtainable by standard ejection phase indices. (Crit Care Med 1994; 22:1647–1658)

Quantitated left ventricular systolic mechanics in children with septic shock utilizing noninvasive wall-stress analysis

To quantitate ventricular systolic mechanics in septic children. Prospective wall-stress analysis was compared to standard ejection phase indices. University-based pediatric intensive care unit. Fifteen children with sepsis (hemodynamically stable, n = 5; in shock, n = 10). Left ventricular ejection phase indices: shortening fraction (shortening) and corrected mean velocity of circumferential shortening (velocity) were adjusted for end-systolic wall stress (stress). Ejection phase, performance (stress-shortening relation), contractility (stress-velocity relation), and afterload (stress) were indexed to age-corrected normal means, with variance of > or = 2 SD regarded as significant. Preload index represented variance between performance and contractility indices. All hemodynamically stable septic patients had normal performance, contractility, and preload. Afterload was increased in three of five patients. Of the patients with septic shock, six of ten had decreased performance (decreased contractility and increased afterload, n = 4; decreased afterload, n = 1; and severe preload deficit, n = 1). Despite aggressive volume resuscitation, six of ten children in septic shock had evidence of diminished preload. Follow-up studies in the septic shock patients demonstrated reversal of depressed ventricular contractility within 3 to 6 days in all four patients initially affected (p < .05). One patient developed late decreased performance and contractility in association with multiple organ failure. Ventricular loading abnormalities persisted in a follow-up study of these patients including a preload deficit in five of ten patients in shock. The frequency rate (40%) of reversible impaired ventricular contractility in children with septic shock is significant. Afterload is normal or increased in the majority of septic subjects, possibly due to acute ventricular dilation. Decreased preload contributes to altered ventricular performance in the majority of children with septic shock, persisting days after the initiation of therapy. Wall-stress analysis provided detailed information regarding ventricular mechanics that was not otherwise obtainable by standard ejection phase indices.

Left ventricular systolic performance is depressed in chronic pulmonary emphysema in dogs

The effect of chronic right ventricular (RV) pressure overload on left ventricular (LV) systolic function in chronic obstructive lung disease is unclear. To examine LV systolic performance in pulmonary emphysema, a chronic canine model was developed in which pulmonary artery pressure could be elevated to a level found in human disease. Severe emphysema was produced by the repeated instillations of the enzyme papain into the lung. Sonomicrometry was used to assess LV dimensions along the septal-lateral, apex-base, and anterior-posterior orthogonal axes of the LV. With the animal conscious, measurements of LV systolic function were obtained over a wide range of LV circumferential end-ejection stresses at baseline and after 1 yr of emphysema (post-1-yr study). In the emphysema group (n = 5), the results showed that at the post-1-yr study, measurements of LV ejection fraction, mean velocity of circumferential shortening, and rate of anterior-posterior dimensional shortening were reduced compared with those obtained at the baseline study. In the emphysema group, end-systolic volume was increased for a given end-systolic pressure or stress at the post-1-yr study compared with baseline values, while fractional shortening measured along the three axes was decreased. There were no similar changes in systolic parameters in control groups. We conclude that chronic RV pressure overload may cause an impairment in LV systolic performance in chronic emphysema.

Echocardiographic study of left ventricular function in type 1 diabetes mellitus: hypersensitivity of β-adrenergic stimulation

Systolic left ventricular function was investigated by echocardiography in 23 young, type 1 diabetics and 11 control subjects. A stimulation by isoproterenol was performed in order to study beta-adrenergic cardiac responsiveness. M-mode recordings were digitized and analyzed by computer. Systolic parameters such as left ventricular fractional shortening and mean velocity of circumferential shortening were not different, but maximal velocity of shortening was increased both at rest (P less than 0.01) and with isoproterenol (P less than 0.05) in the diabetics. An abnormal systolic anterior motion of the mitral valve was found during administration of isoproterenol in 65% of the diabetics and in only one control. These findings are suggestive of a hyperkinetic state, associated with a poor metabolic control (high value of HbA1), together with adrenergic hypersensitivity in type 1 diabetes mellitus.

Effects of chronic atenolol therapy on cardiovascular response to isometric exercise in essential hypertension.

Cardiovascular response to 2 min of isometric handgrip exercise at 50% of maximum voluntary contraction was studied echocardiographically in 10 essential hypertensives, before and during treatment with atenolol for a mean of 2 months. The patients responded with increases in heart rate, systolic and diastolic blood pressures, cardiac output and calculated triple product, no changes in stroke volume and total peripheral resistance, and decreases in ejection fraction, mean velocity of circumferential shortening and mean diastolic posterior wall velocity of the left ventricle before treatment. Chronic atenolol therapy attenuated the increases in heart rate, blood pressure and triple product, and the decreases in ejection fraction, mean velocity of circumferential shortening and mean diastolic posterior wall velocity of the left ventricle but resulted in a marked increase in total peripheral resistance. The pressure response and triple product rise in response to isometric handgrip exercise were also decreased. This suggests an obvious advantage to hypertensive patients who may, therefore, be protected from the risk of cardiovascular complications following isometric exercise.

Acute hemodynamic effects of MDL19205 on conscious dogs with mitral regurgitation.

To assess the effects of MDL19205, a combined inotropic-vasodilating agent, or an inodilator, on the left ventricle with subacute volume overload due to mitral regurgitation (MR), seven dogs were instrumented with a left ventricular (LV) micromanometer and a pair of ultrasonic crystals for the measurement of LV circumferential segment length. After examining the effects of this drug in the normal hearts, its effects were observed in the same dogs in which MR was produced by sectioning chordae tendineae. Mitral regurgitation caused increases in LV peak dP/dt (2,384 +/- 256 to 3,090 +/- 622 mmHg/sec; p less than 0.05), mean circumferential shortening velocity (Vcf; 1.41 +/- 0.25 to 1.85 +/- 0.20 sec-1; p less than 0.05), LV end-diastolic pressure (LVEDP; 8.2 +/- 1.6 to 15.8 +/- 3.7 mmHg; p less than 0.001), and LV end-diastolic length (LVEDL; 10 to 10.6 +/- 0.2mm; p less than 0.01). The dogs were intravenously administered MDL19205 7 to 14 days after they had completely recovered from the first and second operations. With 3 mg/kg of MDL19205, peak changes of hemodynamic indices occurred within 5 minutes in the hearts with MR LV dP/dt and mean Vcf significantly rose (from 3,090 +/- 622 to 5,356 +/- 811 mmHg/sec; p less than 0.001, 1.85 +/- 0.20 to 2.65 +/- 0.36 sec-1, p less than 0.001). LVEDP and LVEDL were returned to the control values obtained in the normal hearts (15.8 +/- 3.7 to 6.4 +/- 2.4 mmHg; p less than 0.001, 10.6 +/- 0.2 to 10 +/- 0.4; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)