Left Ventricular End-systolic Wall Research Articles

Isometric exercise testing and echocardiography at rest in aortic valve incompetence

Thirty patients with aortic valve incompetence and 21 control subjects were examined by M-mode echocardiography at rest and radionuclide ventriculography during submaximal handgrip exercise. The patients had greater left ventricular dimensions and end-systolic wall stress values but peak systolic wall stress values did not differ. During exercise the controls' ejection fraction increased by 3 +/- 4%, 95% confidence interval (CI) from +1% to +5%, while the aortic incompetence patients showed no change -1% +/- 5%, CI from -3 to +1%. The 15 symptomatic aortic incompetence patients had a different ejection fraction response from the controls (-2 +/- 4%, p less than 0.01), CI from 4% to +1%, but the 15 asymptomatic patients had not (0 +/- 6%, not significant, CI from -3% to +3%). Three symptomatic and two asymptomatic patients with a decrease in ejection fraction below 5% during handgrip were not identified by left ventricular size and function of systolic loading conditions at rest. Neither echocardiographic or radionuclide parameters of left ventricular size and function at rest correlated with the individual ejection fraction changes during handgrip. Thus, in aortic valve incompetence, the radionuclide angiography assessed functional response to handgrip cannot be predicted by left ventricular size and function or systolic loading conditions at rest.

Cardiac determinants of regression of left ventricular hypertrophy in essential hypertension with antihypertensive treatment

To study the cardiac determinants of regression of left ventricular hypertrophy in hypertension, left ventricular mass, fractional shortening and end-systolic wall stress were measured echocardiographically in 36 patients with essential hypertension and left ventricular hypertrophy. The patients were classified into two groups. Group I consisted of 15 patients with subnormal end-systolic wall stress, and Group II consisted of 21 patients with normal end-systolic wall stress. There were no significant differences between groups in systolic or diastolic blood pressure. After treatment for 4.4±1.7 years, echocardiographic studies were repeated. There were no significant differences between groups in the duration of the follow-up period and the kinds of antihypertensive drugs.After treatment, blood pressure decreased significantly in both groups (p < 0.001 for both), with no significant difference between groups. Left ventricular mass increased significantly in Group I (from 331 ± 7 to 363 ± 24 g, mean ± SEM, p < 0.05), whereas it decreased significantly in Group II (from 318 ± 16 to 268 ± 17 g, p < 0.001). Myocardial contractility (the relation between end-systolic wall stress and fractional shortening) remained almost the same as before treatment.In conclusion, in patients with hypertensive ventricular hypertrophy with subnormal end-systolic wall stress (inappropriate hypertrophy, probably induced by a neurohumoral factor), a decrease in blood pressure with antihypertensive treatment does not lead to regression of left ventricular hypertrophy, but rather to an increase in left ventricular mass. In patients with normal end-systolic wall stress (appropriate hypertrophy, probably induced by high arterial pressure) antihypertensive treatment decreases left ventricular mass if it has the potency to cause regression of hypertrophy.

Influence of UDCG-115 on hemodynamics and myocardial energetics in patients with idiopathic dilated cardiomyopathy

The influence of the new inotropic and vasodllating agent UDCG-115 on hemodynamics and myocardial oxygen metabolism was investigated in 11 patients with idiopathic dilated cardiomyopathy (New York Heart Association class II to III). After intravenous administration of UDCG-115, cardiac index increased from 3.03 ± 0.68 to 3.76 ± 1.07 L/min/m 2 ( p < 0.01), left ventricular ejection fraction increased from 31 ± 13 to 39 ± 16% ( p < 0.01), and maximum rate of left ventricular pressure rise increased from 935 ± 248 to 1056 ± 284 mm Hg/sec ( p < 0.05). Left ventricular end-diastolic wall stress (index of preload) and left ventricular end-systolic wall stress (index of afterload) decreased by 41% ( p < 0.01) and 34% ( p < 0.001), respectively. Heart rate did not change significantly. With UDCG-115 myocardial oxygen consumption decreased from 14.3 ± 5.1 to 10.6 ± 3.8 ml/min/100 gm ( p < 0.05), and the ratio of myocardial oxygen supply to myocardial oxygen demand increased from 1.40 ± 0.08 to 1.53 ± 0.17 ( p < 0.05). Thus intravenous UDCG-115 improves left ventricular function by increasing inotropism and reducing preload and afterload in patients with idiopathic dilated cardiomyopathy and moderate congestive heart failure. The systemic hemodynamic actions are associated with favorable effects on myocardial energetics.

Long-term function of human cardiac allografts assessed by two-dimensional echocardiography

Previous studies from our laboratory demonstrated increasing left ventricular mass in cyclosporine-treated cardiac allograft recipients over 30 days after transplantation, but the long-term evolution of this process and possible effects on allograft function are unknown. Accordingly, quantitative two-dimensional echocardiography was performed 2 and 23 days and 15 months postoperatively in 14 recipients treated with cyclosporine and prednisone. Changes in left ventricular ejection fraction, end-diastolic volume, mass, and end-systolic wall stress were analyzed. Comparison of studies at 2 and 23 days revealed significant (p less than 0.01) increases in ejection fraction (54% +/- 8% [standard deviation] to 62% +/- 4%), end-diastolic volume (84% +/- 32 ml to 96 +/- 31 ml), and left ventricular mass (118 +/- 45 gm to 136 +/- 41 gm). Comparison of studies at 23 days and 15 months revealed no significant change in end-diastolic volume or left ventricular mass, whereas ejection fraction decreased slightly (62% +/- 4% to 57% +/- 4%, p less than 0.01). End-systolic wall stress decreased when data at 2 days and 15 months were compared (83 +/- 24 gm/cm2 versus 66 +/- 18 gm/cm2, p less than 0.05), but no change in contractility was apparent from the ejection fraction/end-systolic stress relation. We conclude that left ventricular mass and end-diastolic volume increase early after transplantation in cyclosporine-treated cardiac allograft recipients, but these changes are not predictive of long-term results, which are characterized by no significant late variation in left ventricular mass, end-diastolic volume, or contractility.

Effects of dopamine on left ventricular afterload and contractile state in heart failure: Relation to the activation of beta1-adrenoceptors and dopamine receptors

Although long-term therapy with oral beta-adrenoceptor agonists in patients with heart failure is generally associated with the development of diminished pharmacologic efficacy, the ingestion of levodopa, which is decarboxylated endogenously to dopamine, is associated with a sustained improvement in cardiac function. The beneficial hemodynamic actions of dopanine in patients with heart failure have been attributed to a positive inotropic effect that is mediated through activation of beta1-adrenoceptors. However, a reduction in left ventricular afterload resulting from the activation of dopamine receptors may also lead to an improvement in the performance of the failing heart.To ascertain the relative importance of the positive inotropic and afterload-reducing effects of dopamine in patients with heart failure, dopamine (2, 4, 6 μg/kg per min), dobutamine (2, 6, 10 μg/kg per min) and nitroprusside (0.125 to 2.0 μg/kg per min) were administered to 13 patients with dilated cardiontyopathy while monitoring left ventricular wall thickness and dimensions by echocardiography and left ventricular and aortic pressures with a micromanometer-tipped catheter. Altering left ventricular afterload, quantified as end-systolic circumferential wall stress, with nitroprusside allowed generation of the left ventricular end-systolic circumferential wall stress-velocity of fiber shortening relation that represented the baseline contractile state of the myocardium.Left ventricular velocity of fiber shortening was elevated during the administration of dobutamine and dopamine when compared with measurements obtained with nitroprusside at the same left ventricular end-systolic circumferential wall stress. Furthermore, left ventricular end-systolic wall stress decreased with dopamine but not with dobutamine. Thus, the beta1-adrenoceptor activity of dopamine and dobutamine augmented the contractile state of the myocardium. The reduction in left ventricular afterload induced by dopamine but not dobutamine may reflect activation of peripheral vascular dopamine receptors by the former.

Classification of hypertrophied hearts in essential hypertension: evaluation by left ventricular wall stress and adrenergic responses.

Left ventricular mass, fractional shortening, and end systolic wall stress (mechanical indices) measured by echocardiography and the response of fractional shortening and end systolic wall stress to the infusion of isoproterenol (0.02 microgram/kg/min for 5 min) (a non-mechanical index) were studied in 57 patients (mean (SD) age 49(8)) with essential hypertension. Nineteen patients had subnormal end systolic wall stress (group 1), 25 patients had normal end systolic wall stress and slightly increased left ventricular mass (group 2A), and 13 patients had normal end systolic wall stress and considerably increased left ventricular mass (group 2B). Plasma noradrenaline concentration was higher in group 2B than in the other groups. When end systolic wall stress was greater than 12 g/cm2 this variable showed a significant inverse linear relation with fractional shortening before isoproterenol infusion. The inotropic response to isoproterenol was measured as the increase of fractional shortening corrected for the decrease of end systolic wall stress (delta fractional shortening/--delta end systolic wall stress). The mean (SD) change in delta fractional shortening/--delta end systolic wall stress was significantly larger in group 1 (1.40 (0.60) cm2/g) than in group 2A (0.85 (0.39) cm2/g), and was significantly larger in group 2A than in group 2B (0.56 (0.15) cm2/g). In patients with hypertensive hypertrophy with subnormal end systolic wall stress (inappropriate hypertrophy) the beta adrenergic response is increased; in hypertensive hypertrophy with normal end systolic wall stress (appropriate hypertrophy), however, it is normal, or becomes reduced as plasma noradrenaline increases.

Left ventricular end-systolic wall stress--dimension relationship in unanesthetized dogs with perinephritic hypertension.

To study myocardial contractility in hypertensive hearts with normal wall motion, we examined left ventricular end-systolic wall stress-dimension relationships (ESWDR) during a baseline period (CS: control stage) and in the eighth week after induction of systemic hypertension by Page's method (HS: hypertensive stage) in unanesthetized dogs. The mean aortic blood pressure increased from 94 +/- 11 to 142 +/- 26 mmHg (p less than 0.01). The end-diastolic left ventricular posterior wall thickness increased significantly during the HS (9.4 +/- 1.3 vs 7.3 +/- 1.3 mm; HS vs CS), and its dimension was significantly (p less than 0.05) smaller than it was during the CS (37.0 +/- 4.2 vs 39.9 +/- 4.6 mm; HS vs CS). There were no significant differences between the 2 stages in left ventricular fractional shortening (31.9 +/- 5.0 vs 32.6 +/- 2.8; HS vs CS), in end-systolic meridional left ventricular wall stress (75.3 +/- 10.8 vs 68.3 +/- 15.6 10(3) dynes/cm2; HS vs CS), or in the ESWDR slopes (98.6 +/- 17.7 vs 94.0 +/- 19.7; HS vs CS). The ESWDR dimension intercepts significantly decreased from 2.0 +/- 0.3 to 1.8 +/- 0.3 cm during the HS; that is, the relationship shifted to the left with no significant change in the slope. At autopsy, the ratio of left ventricular weight to body weight of the hypertensive dogs was significantly (p less than 0.01) greater than that of sham-operated control dogs (6.0 +/- 0.9 vs 4.3 +/- 0.5 g/kg).(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular end-systolic wall stress to volume relationship before and after surgical closure of ventricular septal defect.

Left ventricular function was examined angiographically in 64 patients with ventricular septal defect and 13 postoperative patients with a preoperatively large shunt (postoperative group). The unoperated 64 patients were divided into three groups; small (left-to-right shunt ratio less than 35%), moderate (35%-50%), and large (greater than 50%). The control group consisted of 27 patients with Kawasaki disease. For assessing left ventricular function, left ventricular shape and the end-systolic wall stress to end-systolic volume index ratio, as well as left ventricular ejection fraction were examined. Left ventricular ejection fraction was higher in the small-shunt group (p less than 0.05) than in the control group, but normal in the other groups. Left ventricular end-diastolic shape was normal only in the small-shunt group and more spherical in the other groups. The large-shunt group alone manifested more spherical left ventricular end-systolic shape and lower end-systolic wall stress to end-systolic volume index (p less than 0.001). These findings suggest that the left ventricular dysfunction is present in patients with a left-to-right shunt larger than 50%, but this change was reversible in patients who underwent early repair of ventricular septal defect.

Systemic vascular resistance: an unreliable index of left ventricular afterload: Lang RM, Borow KM, Neumann A, et al: Circulation 74:1114–1123, 1986

Systemic vascular resistance (SVR) is a frequently used clinical index of left ventricular afterload. However, SVR may not adequately assess left ventricular afterload (i.e., ventricular internal fiber load during systole) since it reflects only peripheral vasomotor tone. In contrast, left ventricular end-systolic wall stress (sigma es) reflects the combined effects of peripheral loading conditions and left ventricular chamber pressure, dimension, and wall thickness. To determine the relationship between SVR and sigma es, left ventricular afterload and contractility were pharmacologically altered in eight dogs instrumented with central aortic microtip and Swan-Ganz thermodilution catheters. Left ventricular wall thicknesses and dimensions were measured from two-dimensionally targeted M mode echocardiograms. Aortic, right atrial, and left ventricular end-systolic pressures as well as cardiac output were recorded. SVR and sigma es were determined under control conditions as well as during infusions of nitro...

Echocardiographic contrast agents: Effect of microbubbles and carrier solutions on left ventricular contractility

Recently, there has been a resurgence of interest in the use of contrast-enhanced echocardiography as a means of noninvasively assessing myocardial perfusion. However, if injections of echocardiographic contrast agents are to be used for this purpose it is essential that they are not intrinsically toxic to the heart. In this study, the left ventricular end-systolic wall stress-rate-corrected velocity of fiber shortening relation, a load independent index of contractility, was studied in nine dogs. Two-dimensional and targeted M-mode echocardiographic as well as central aortic pressure tracings were made during echocardiographically gated, pressure- and volume-controlled aortic root injections of nonsonicated and sonicated Renografin-76, saline and dextrose 70% (n = 6), and sonicated and hand-agitated Renografin-76/saline mixture (n = 5). Two of nine dogs received all agents. Off-line computer videodensitometric analysis documented myocardial perfusion. In all cases, data were obtained at control and 5 and 15 seconds after injection. Additional data were collected at 25 seconds after injection for the Renografin-76/saline mixture. Alterations in contractility were measured relative to control as changes in rate-corrected velocity of fiber shortening after afterload (measured as end-systolic wall stress) was eliminated as a confounding variable. Under no condition did saline or Renografin-76 cause alterations in left ventricular contractility. Nonsonicated and sonicated dextrose 70% increased left ventricular contractility at 15 seconds but not at 5 seconds after injection. Hand-agitated Renografin-76/saline mixture induced a negative inotropic effect at 5 and 15 seconds after injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Association between the exercise ejection fraction response and systolic wall stress in patients with chronic aortic insufficiency.

We studied the exercise ejection fraction response in 56 patients with chronic aortic insufficiency. All had left ventricular dilatation but preserved resting ejection fraction and minimal or no symptoms. The exercise ejection fraction increased by 0.05 units or greater in 18 (32%) patients (group I), remained within 0.05 units of the resting value in 18 (32%) patients (group II), and fell by 0.05 units or greater in 20 (36%) patients (group III). There were no significant differences among the groups in left ventricular end-diastolic dimension, end-systolic dimension, or fractional shortening by echocardiography or in resting left ventricular volumes and ejection fraction by radionuclide angiography. Left ventricular end-systolic wall stress was significantly higher in group III than in either group I or group II (89 +/- 20 vs 70 +/- 18 and 69 +/- 17 X 10(3) dyne/cm2; p less than .005). At peak exercise there were no differences among groups in systolic blood pressure. However, end-systolic volume increased from 65 +/- 28 to 77 +/- 36 ml/m2 in group III and fell from 50 +/- 21 to 28 +/- 18 ml/m2 in group I during exercise. Thus, at peak exercise end-systolic volume was nearly three times greater in group III than in group I. Although stress could not be determined directly during exercise, the directional changes in its determinants suggest that it also would have been higher in group III patients. A highly significant inverse correlation was present between the ejection fraction response and the change in end-systolic volume (r = -.87, p less than .0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular performance in patients with coexistent mitral stenosis and aortic insufficiency

Isolated mitral stenosis and isolated aortic insufficiency impose unique and opposite loading conditions on the left ventricle. To assess these combined effects, hemodynamic and angiographic factors were compared among normal subjects and patients with isolated mitral stenosis, isolated aortic insufficiency or combined mitral stenosis and aortic insufficiency. Left ventricular end-diastolic volume index was lower in patients with combined lesions and severe or moderate aortic insufficiency than in patients with isolated severe or moderate aortic insufficiency (138 +/- 19 versus 206 +/- 20 cc/m2 and 87 +/- 5 versus 145 +/- 22 cc/m2, respectively) (p less than 0.05 for both). Left ventricular end-diastolic and end-systolic volume indexes were normal in two-thirds of patients with combined lesions and moderate or severe aortic insufficiency, whereas these indexes were high in all but one patient with isolated moderate or severe aortic insufficiency. Among patients with moderate or severe aortic insufficiency, 8 of 14 with isolated insufficiency had a reduced ejection fraction or circumferential fiber shortening rate compared with 5 of the 9 patients with combined lesions. Among patients with isolated aortic insufficiency, left ventricular end-systolic wall stress and end-diastolic and end-systolic volume indexes were higher (p less than 0.05) in those with reduced ejection performance than in those with normal ejection performance. These variables did not differ between patients with reduced or normal ejection performance in the group with combined lesions. The contractile index (ratio of end-systolic wall stress to end-systolic volume index) was significantly depressed in patients with severe aortic insufficiency in the groups with isolated aortic insufficiency or combined lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Assessment of left ventricular contractility in patients receiving doxorubicin.

The usual indices of left ventricular systolic performance have been incapable of accurately recognizing early myocardial impairment in many patients treated with doxorubicin. Recently, several new load-independent, highly sensitive indices of left ventricular contractility have been developed including the slope value of the endsystolic pressure (Pes)-dimension (Des) relation and the position of the left ventricular end-systolic wall stress (sigma es)-percent fractional shortening (% delta D) relation. We used these indices to study 46 patients receiving either low dose or high dose doxorubicin. Results were compared with data from 30 healthy subjects. Resting % delta D failed to accurately recognize left ventricular dysfunction in 9 of 17 patients with low normal values. These patients had reduced afterload, as measured by sigma es, permitting normal extent of left ventricular fiber shortening despite impaired contractility as quantified by diminished Pes-Des slope values. There was 98% concordance between the relative position of the sigma es-% delta D relation and the slope value of the Pes-Des, relation. These indices offer an improved means of recognizing and quantitating impaired contractility in patients treated with doxorubicin.

Reversal of left ventricular hypertrophy by antihypertensive therapy.

The effect of antihypertensive therapy on left ventricular hypertrophy due to essential hypertension was determined echocardiographicallv in 27 previously untreated subjects with essential hypertension. Fifteen were treated with hydrochlorothiazide alone, while 12 received additional therapy with methyldopa to control blood pressure. After a mean treatment interval of 11 months, mean blood pressure had fallen from 167/109 to 138/94 mm Hg ( P < 0.001). Simultaneously, echocardiographic left ventricular posterior wall thickness fell from 11 to 10 cm ( P < 0.07) and septal thickness fell from 1.3 to 1.2 cm ( P < 0.05). End-diastolic relative wall thickness, an index of concentric hypertrophy, fell from 0.50 to 0.45 ( P < 0.01, normal mean value = 0.33 ± 0.06). Estimated endsystolic left ventricular wall stress was normal both before and after treatment. No significant differences were demonstrable between the two treatment subgroups. We conclude that, in asymptomatic essential hypertension, treatment with diuretic or diuretic plus methyldopa can result in nearly complete reversal of left ventricular hypertrophy, provided that good blood pressure control is obtained.

Cardiocirculatory adjustments during pregnancy -- an echocardiographic study.

Adaptation of the circulation to pregnancy occurs via a complicated series of changes not yet completely understood. To define pertinent alterations, echocardiographic measurements of left ventricular function were performed every 4 weeks in 13 normal pregnant women. Six weeks postpartum each women was reexamined; thus each woman served as her own nonpregnant control. Left ventricular dimensions, left venticular wall thickness, shortening fraction, and rate of change of these measurements were recorded. As expected, cardiac output was increased throughout pregnancy. Up to 20 weeks gestation this occurred via an increased heart rate. After 20 weeks gestation stroke volume increased significantly, with 20% at 20--26 weeks up to 30% at term (p < 0.01). With the end-diastolic wall thickness remaining equal, myocardial hypertrophy occurred. This was corroborated by an increase in end-systolic left ventricular wall thickness towards term: from 13.8 mm (S.D. +/- 1.73) in early pregnancy to 16.6 mm (S.D. +/- 1.62) at term, with end-systolic left ventricular dimension unchanged. It was concluded that during pregnancy the mechanism to produce a higher cardiac output shifts from an increase in cardiac frequency to elevation of stroke volume with concomitant myocardial hypertrophy. Due to changes in heart rate and afterload, no conclusions could be drawn regarding myocardial contractility.

Echocardiographic assessment of the severity of aortic stenosis in children and adolescents

The magnitude of ventricular hypertrophy in response to afterloading is determined by wall stress, with wall thickness increasing in proportion to ventricular load until systolic wall stress is normalized. With use of echocardiographic measurements of left ventricular end-systolic wall thickness (Ws) and cavity transverse dimension (Ds), the pressure constant k was calculated in 16 patients without left heart obstruction according to the formula k = P-Ds/Ws. The mean value for k was 225 +/- 6.7 (standard deviation) mm Hg. From this value, left ventricular pressure was estimated in 13 patients with aortic stenosis aged 4 to 17 years using the formula P = k-Ws/Ds. No subject had evidence of cardiac failure. Peak systolic aortic pressure difference (delta P) was calculated by subtracting cuff-measured brachial arterial peak systolic pressure from the estimated left ventricular pressure. Excellent correlation was obtained between the estimated delta P and that found at cardiac catheterization (r = 0.89). In two patients, echocardiographic data predicted significant obstruction in the presence of normal electrocardiographic, vectorcardiographic and vector lead tracings. Echocardiography offers a noninvasive method for estimating the severity of aortic stenosis, in the absence of myocardial failure; it appears to be more sensitive than other currently employed techniques.

Relations between afterload, stroke volume, and descending limb of Starling's curve.

Relations between afterload, stroke volume, and descending limb of Starling's curve.