Left ventricular performance during exercise in long-term type 1 diabetic men: an echocardiography study

Summary. M-mode echocardiograms were recorded and digitized during semisupine bicycle exercise in 10 young (<40 years) long-term (≥12 years) type 1 diabetic men, without heart symptoms, and 10 controls. Recordings were done at rest, during workloads of 50 and 100 W and 1, 3 and 5 min post-exercise. The groups were comparable at rest. Exercise intervention caused a higher heart rate and systolic blood pressure response in the diabetics. Overall, diabetics had a smaller left ventricular (LV) end-diastolic dimension, but it did not change during exercise within either group; LV end-systolic dimensions (ESD), however, decreased in both. The fractional shortening, normalized peak shortening rate and systolic blood pressure/ESD ratio increased in both groups. However, fractional shortening was lower in the diabetics during peak exercise, while the two latter variables of LV systolic function were similar to the controls. Furthermore, fractional shortening during peak exercise remained lower in the diabetics even when adjusted for systolic blood pressure by covariance analysis. Therefore, the decreased LV performance during exercise in the diabetic subjects is most likely secondary to reduced LV diastolic filling, as indicated by their smaller end-diastolic dimension, rather than due to decreased contractility or a higher afterload.     

Cardiovascular hemodynamics of bicycle and handgrip exercise in normal subjects before and after administration of propranolol

Radionuclide angiography was used to study the effects of supine and upright bicycle exercise and handgrip exercise in 17 (12 well-trained) normal subjects before (control) and immediately after the administration of propranolol (160 mg/day for 4 days). Cardiac hemodynamic values were related to position in that control left ventricular volumes and the cardiac index were greater in the supine position than in the upright at rest but resting left ventricular ejection fraction was similar in both positions. The pressure volume index was greater in the upright position than in the supine. At maximal exercise before treatment, however, similar cardiovascular hemodynamic measurements were recorded in both positions. Propranolol increased left ventricular end-diastolic volume at rest and at maximal exercise. Left ventricular end-systolic volume, however, was substantially greater only in the upright position both at rest and at maximal exercise when compared with control values. Heart rate, systolic arterial pressure, cardiac index, and pressure volume index were decreased at rest and maximal exercise after treatment with propranolol. Ejection fraction was decreased in the upright position after propranolol administration but was unchanged in the supine position. Handgrip exercise primarily increased heart rate and arterial pressure and did not affect cardiac volume, and this response was unaffected by propranolol.     

Angiotensin-converting enzyme inhibition facilitates alveolar-capillary gas transfer and improves ventilation-perfusion coupling in patients with left ventricular dysfunction

OBJECTIVE: The backward effects of left ventricular dysfunction include alterations in alveolar-capillary gas transfer and ventilation-perfusion coupling. Because the angiotensin-converting enzyme (ACE) is highly concentrated in the vascular endothelium of the lungs, we examined whether ACE inhibitors may influence the pulmonary function in patients with congestive heart failure. METHODS: In 20 patients with idiopathic cardiomyopathy, pulmonary function and exercise capacity were evaluated at baseline and 6 and 12 months after treatment with enalapril (10 mg twice a day) was started. The study also included 19 age- and sex-matched control subjects with mild primary hypertension and normal left ventricular function who were given enalapril as a standard treatment of high blood pressure. RESULTS: In congestive heart failure, forced expiratory volume in 1 second, vital capacity, and total lung capacity did not vary significantly with enalapril; alveolar-capillary diffusion of carbon monoxide (DL(CO)) increased toward normal; exercise tolerance time, peak exercise oxygen uptake (peak VO2), minute ventilation and tidal volume (peak VT) also increased; and the ratio of volume of dead space (VD) to VT (peak VD/VT) at peak exercise reduced. Changes in peak VO2 showed a direct correlation with those in DL(CO) and an inverse correlation with those in peak VD/VT. Results at 6 and 12 months were comparable. Enalapril did not affect these variables in the control population. CONCLUSIONS: In patients with idiopathic cardiomyopathy heart failure, but not in control subjects, gas transfer and ventilation-perfusion improved with ACE inhibition. These pulmonary changes may contribute to the associated increase in exercise tolerance.     

Left ventricular response to dynamic and static exercise: evaluation by radiocardiography in healthy men

The effects of dynamic and static exercise on left ventricular haemodynamics were compared in 13 healthy male volunteers using single detector radiocardiography. Static hand grip effort was performed for four minutes at 30% of the maximum contraction. During dynamic exercise the subjects bicycled on an ergometer to 85% of the predicted heart rate for their age. Static exercise increased the heart rate, systolic and diastolic blood pressure and cardiac output (p less than 0.001 for all), but there were no significant changes in the stroke volume, left ventricular end-diastolic volume or ejection fraction from the resting values. Dynamic exercise in a supine position clearly increased the heart rate, systolic blood pressure and cardiac output (p less than 0.001 for all) to a greater extent than the hand grip, together with a significant augmentation of the stroke volume (p less than 0.001) and the ejection fraction (p less than 0.01). The dynamic exercise produced only an insignificant increase in left ventricular end-diastolic volume. Thus, the normal left ventricular volume response to the increase in preload during dynamic exercise was a significant augmentation of stroke volume and ejection fraction. On the other hand, the static exercise in the same subjects mainly increased the left ventricular afterload while the left ventricular volume changes remained minimal.     

Exercise capacity and cardiac function in type 1 diabetic patients treated with continuous subcutaneous insulin infusion. A controlled study

In order to investigate the effect of improved glycaemic control on exercise capacity and cardiac function, bicycle exercise and echocardiography at rest and after exercise was performed in 24 short-term type 1 diabetic patients, randomized to conventional insulin therapy (CIT) or to continuous subcutaneous insulin infusion (CSII). After 6 months significant improvement in glycaemic control was seen in the CSII group showing a decrease in mean blood glucose and haemoglobin A1c (HbA1c), while no change was observed in the CIT group. Exercise capacity increased by 24% (p less than 0.01) in the CSII group and decreased by 16% (NS) in the CIT group. In the CSII group fractional shortening of the left ventricle during rest decreased by 14% (p less than 0.02), while an increase of 2% (NS) was seen in the CIT group. Further, changes of left ventricular fractional shortening during rest were inversely correlated to changes in exercise capacity. After exercise, fractional shortening of the left ventricle and rate-pressure product was unchanged in the two groups. In conclusion this study shows a beneficial effect of improved glycaemic control induced by CSII on exercise capacity possibly by reducing resting state demands to the cardiovascular system.     

Left ventricular performance during prolonged exercise: absence of systolic dysfunction

We assessed left ventricular systolic and diastolic performance during and after prolonged exercise under controlled conditions in a group of healthy, trained men. Previous studies have examined the effects of prolonged effort on left ventricular function, yet it remains unclear whether or not left ventricular dysfunction (e.g. cardiac fatigue) can be produced under such conditions. We studied 15 healthy men, aged 27+/-1 years (mean+/-S.E.M.). Subjects exercised on bicycles at a constant work rate (60% of maximum oxygen uptake per min) for 150 min. Measurements of gas exchange, blood pressure and haematocrit were obtained, concurrent with the assessment of left ventricular function using equilibrium radionuclide angiography, at rest, during exercise (every 30 min) and after 30 min of recovery. Fluid replacement was provided and monitored during the exercise period. The baseline resting and exercise ejection fractions were 66+/-2% and 78+/-2% respectively. During exercise, subjects consumed 1816+/-136 ml of fluid, and the haematocrit had increased at 120 min of exercise (from 47.2%+/-0.6 to 49.9+/-0.8%; P<0.05). There was no change in either systolic or diastolic blood pressure throughout the exercise period, but heart rate drifted upwards from 141+/-2 beats/min after 30 min to 154+/-3 beats/min after 150 min (P<0.05). There was a small decline (8%; P<0.05) in end-diastolic volume at 150 min. No changes were observed in left ventricular ejection fraction, the pressure/volume ratio or end-systolic volume. After 30 min of sitting in recovery, heart rate was still higher than the pre-exercise value (84+/-3 compared with 69+/-2 beats/min; P<0.05), as were measures of peak filling rate and time to peak filling (P<0.05). The ejection fraction in the post-exercise recovery period was similar to the pre-exercise value. The results indicate that prolonged exercise of moderate duration may not induce abnormal left ventricular systolic function or cardiac fatigue during exercise.     

Diastolic function is reduced in adolescents with type 1 diabetes in response to exercise

OBJECTIVE To determine whether adolescents with type 1 diabetes have left ventricular functional changes at rest and during acute exercise and whether these changes are affected by metabolic control and diabetes duration. RESEARCH DESIGN AND METHODS The study evaluated 53 adolescents with type 1 diabetes and 22 control adolescents. Baseline data included peak exercise capacity and body composition by dual-energy X-ray absorptiometry. Left ventricular functional parameters were obtained at rest and during acute exercise using magnetic resonance imaging. RESULTS Compared with nondiabetic control subjects, adolescents with type 1 diabetes had lower exercise capacity (44.7 ± 09 vs. 48.5 ± 1.4 mL/kg fat-free mass [FFM]/min; P < 0.05). Stroke volume was reduced in the diabetes group at rest (1.86 ± 0.04 vs. 2.05 ± 0.07 mL/kg FFM; P = 0.02) and during acute exercise (1.89 ± 0.04 vs. 2.17 ± 0.06 mL/kg FFM; P = 0.01). Diabetic adolescents also had reduced end-diastolic volume at rest (2.94 ± 0.06 vs. 3.26 ± 0.09 mL/kg FFM; P = 0.01) and during acute exercise (2.78 ± 0.05 vs. 3.09 ± 0.08 mL/kg FFM; P = 0.01). End-systolic volume was lower in the diabetic group at rest (1.08 ± 0.03 vs. 1.21 ± 0.04 mL/kg FFM; P = 0.01) but not during acute exercise. Exercise capacity and resting and exercise stroke volumes were correlated with glycemic control but not with diabetes duration. CONCLUSIONS Adolescents with type 1 diabetes have reduced exercise capacity and display alterations in cardiac function compared with nondiabetic control subjects, associated with reduced stroke volume during exercise.     

Left ventricular function at rest and during exercise in coronary insufficiency — A simultaneous evaluation by means of radionuclide angiocardiography and catheterization

Summary. Left ventricular function was assessed simultaneously with heart catheterization and equilibrium radionuclide angiocardiography at rest and during supine exercise in ten patients with effort angina. At rest all had normal haemodynamics. During exercise all developed angina with signs of left ventricular dysfunction in the form of high left ventricular filling pressure, 31±2 mm Hg (mean±SEM) and pathological decreases in left ventricular ejection fraction (11 ± 1 % units). Left ventricular end-systolic volume increased significantly (43 ± 7%), but the increase in left ventricular end-diastolic volume (13 ± 7%) was not significant. The discordance between the changes in left ventricular filling pressure and the changes in left ventricular end-diastolic volume is discussed. Radionuclide angiocardiography revealed left ventricular dysfunction as frequently as did heart catheterization.     

Divergent cardiac response to exercise in essential hypertension vs. normotension and the effect of enalapril

The aims of this study were to examine (1) the cardiac response to exercise in essential hypertension and (2) the effect of long-term enalapril treatment on cardiac reserve. Ten normotensive control subjects and 15 patients with moderate, essential hypertension underwent radionuclide ventriculography during graded, supine exercise (0 W–50 W–100 W). The hypertensive patients were studied during monotherapy using hydrochlorothiazide and 3 and 12 months after supplementation with enalapril 10–40 mg o.d. During exercise, the control subjects demonstrated a 17% increase in left ventricular ejection fraction (LVEF) mediated by a 30% decrease in end-systolic volume, a small increase in stroke volume and a minor biphasic (increase–decrease) change in end-diastolic volume. In the hypertensive patients, both the end-diastolic and the end-systolic volume increased substantially with no increase in LVEF, although stroke volume increased by 33%. Long-term therapy with enalapril induced only a minor change towards a more normal pattern of cardiac response to exercise. The hypertensive patients increased their stroke volume during exercise by recruiting preload reserve instead of increasing contractility. Long-term treatment with enalapril had little, if any, effect on this abnormal cardiac response.     

An index of the contractile state of the myocardium in man

There is a profound need, on both clinical and physiologic grounds, for a measure of the contractile state of the intact ventricle. Such a measure can be obtained by evaluating the force-velocity relationship with a correction for myocardial fiber length. The force-velocity relation can be expressed as the ratio of maximum rate of pressure rise to maximum isovolumetric pressure, a quantity which was described by Hill as the maximum rate of proportional rise of pressure and which is similar to the velocity constant of a chemical reaction. Division of this ratio by an estimate of ventricular circumference corrects for variations due to differences in initial fiber length.This index was evaluated in 11 normal subjects and 46 patients with cardiac disease during left heart catheterization. Maximum rate of pressure rise was obtained by electronic differentiation of the ventricular pressure pulse, and ventricular circumference, assuming a spherical ventricle, was calculated from volumes measured by indicator washout.The contractility index of normal subjects did not differ from that of patients with mitral stenosis, atrial septal defect, or chronic pulmonary disease (patients without left ventricular overloading). In contrast, in patients with left ventricular failure, the indices were more than two standard deviations below the mean value for normal subjects. Such a reduction was not noted in patients with pressure or volume overloading of the left ventricle before the onset of myocardial failure. During exercise, the index rose uniformly in patients without left ventricular disease, responded variably in compensated patients with volume or pressure overloading, and was virtually unchanged in patients with left ventricular decompensation. The administration of isoproterenol or digitalis resulted in increased contractility regardless of the patient's status. It is concluded that the use of this index in physiologic studies of the ventricle and in diagnostic and therapeutic decisions is justified.     

Cardiac performance during exercise in hypertensive patients without ventricular hypertrophy

Background  Reduced systolic reserve on effort may be present in subjects with hypertension but no evidence of hypertensive cardiomyopathy. We assessed the determinants of abnormal cardiac performance during exercise in hypertensive patients without left ventricular hypertrophy.
Materials and methods  Thirty-five newly diagnosed, never-treated-earlier hypertensive patients without definite indication for left ventricular hypertrophy at echocardiography underwent radionuclide ambulatory monitoring of left ventricular function at rest and during upright bicycle exercise testing.
Results  The patients were classified into two groups according to their ejection fraction response to exercise. In 21 patients (group 1), the ejection fraction increased ≥ 5% with exercise and in 14 patients (group 2), the ejection fraction either increased < 5% or decreased with exercise. Patients of group 1 had lower peak filling rate at rest and less augmentation in end-diastolic volume during exercise (both P  <   0·01) when compared with patients of group 2. A significant relationship between the magnitude of change in ejection fraction with exercise and both peak filling rate at rest ( r  = 0·58, P  <   0·01) and exercise-induced change in end-diastolic volume ( r  = 0·45, P  <   0·01) was found.
Conclusions  In newly diagnosed, never-treated-earlier hypertensive subjects with no evidence of hypertensive cardiomyopathy, the cardiac response to exercise is dependent on adequate diastolic filling volume to maintain systolic performance.     

Hypertensive left ventricular hypertrophy is linked to an enhanced catecholamine response to submaximal exercise.

BACKGROUND: The serial plasma catecholamine response to exercise has not been studied fully in relation to left ventricular hypertrophy (LVH) in patients with hypertension (HT). This study determined whether plasma catecholamine responses to exercise are altered in essential HT in the presence or absence of LVH. MATERIALS AND METHODS: Plasma noradrenaline (NA) and plasma adrenaline (A) were measured at rest, during and after treadmill exercise in 59 hypertensive subjects and 22 age-matched control subjects. Patients were divided into LVH(-) (n = 20) and LVH(+) (n = 39) stratified by left ventricular mass index [LVMI: control subjects, LVH(-), LVH(+): 114 +/- 4, 105 +/- 3, 151 +/- 3 g m-2]. RESULTS: Exercise time (9.9 +/- 0.6, 7.6 +/- 0.7, 7.3 +/- 0.6 min) was shorter in patients with HT. Both systolic and diastolic blood pressures were higher in patients with HT, and no difference was observed between LVH(-) and LVH(+) patients. Resting plasma NA was not different (157 +/- 16, 173 +/- 17, 167 +/- 14 pg mL-1), but plasma NA at stage I (300 +/- 30, 342 +/- 40, 469 +/- 40 pg mL-1) was higher in LVH(+) patients than in LVH(-) patients or control subjects. Plasma A response to exercise was similar among the three groups. There was a positive correlation (r = 0.38, P < 0.001) between LVMI and Deltaplasma NA at stage I in all subjects. CONCLUSIONS: Patients with essential HT with LVH had augmented plasma NA response during submaximal exercise, whereas patients without LVH did not exhibit this augmentation. The positive correlation between LVMI and Deltaplasma NA suggested a possible association between the degree of cardiac hypertrophy and sympathetic activation during exercise.     

Short-Term and Long-Term Changes of Left Ventricular Volumes During Rate-Adaptive and Single-Rate Pacing

To evaluate the adaptation of the heart to exercise during pacing, 15 patients with permanent endocardial pacemakers were studied; nine patients had atrioventricular universal (DDD) pacemakers (Symbios 7005) and six patients had activity detecting rate-responsive ventricular (VVIR) pacemakers (Activitrax 8403). Left ventricular function in each patient during rate variable pacing was compared to ventricular function during VVI single-rate pacing. End-systolic and end-diastolic volume changes during exercise were measured by radionuclide angiography and the amount of volume change was used to assess left ventricular function. Both short-term (within 4 hours) and long-term measurements (after at least 4 weeks) were made at rest and at 50% of the maximal exercise capacity in DDD or VVIR mode and were compared with VVI single-rate pacing. All patients, when changed from DDD or VVIR mode to VVI single-rate pacing showed a significant increase of the end-diastolic volume during exercise, which increased even more after long-term VVI pacing. During long-term rate variable pacing, there was no increase of the end-diastolic volume during exercise. DDD or VVIR pacing initially showed a substantial increase of the end-systolic volume during exercise combined with a decrease of left ventricular ejection fraction, suggesting a decrease of the left ventricular contractility. After 4 weeks, contractility improved both with DDD and VVIR pacing. We conclude that short-term DDD and VVIR pacing induces a temporary impairment of left ventricular function that improves after 4 weeks, whereas long-term VVI pacing is associated with left ventricular dilatation even at moderate levels of exercise.     

Effects of Metformin on Collagen Glycation and Diastolic Dysfunction in Diabetic Myocardium

BACKGROUND: Collagen accumulation in the myocardial interstitium of diabetic animals is considered to promote diastolic stiffness through advanced glycosylation. Because in vitro data suggest that metformin can modify glycosylation, this study was undertaken in a canine diabetic model 4 months in duration. METHODS AND RESULTS: Untreated diabetics (group II) and diabetics treated with metformin alone (group III) or with insulin (group IV) were compared in the basal state and during volume infusion. Basal hemoglobin A(1c), heart rate, aortic pressure, and ejection fraction were comparable. Left ventricular end-diastolic pressure was significantly increased in the untreated diabetics of group II, associated with a reduced end-diastolic volume. By contrast these parameters in the metformin-treated diabetics of group III were comparable with those in the normals of group I. Similarly in group IV end-diastolic volume was higher than that in group II, but filling pressure, although lower, was not significantly so. Calculation of left ventricular chamber stiffness in the basal state indicated a higher level for group II compared with controls and the treatment groups. During the systemic infusion of dextran, the untreated diabetics of group II had the largest end-diastolic pressure increase and the smallest rise of end-diastolic volume of the treatment groups, consistent with a significantly greater chamber stiffness. Myocardial collagen concentration was increased in group II with an interstitial distribution on morphological exam. Levels of collagen-linked advanced glycosylation end products isolated from the left ventricular were significantly greater in group II than in group I. Treatment with metformin prevented the increment observed in the untreated diabetic but had no effect on the elevated collagen concentration. CONCLUSIONS: Untreated diabetics exhibited increased diastolic chamber stiffness associated with collagen-linked glycation in myocardium compared with control animals. Chronic metformin use prevented the abnormalities of function and composition.     

Left ventricular response to graded isometric exercise in patients with coronary heart disease

Summary. The effects of graded isometric exercise on left ventricular performance were characterized in 11 male patients (53 ± 2 years) with coronary artery disease (CAD) and in 12 normal subjects (11 male and one female, 36 ± 5 years). The echocardiographic indices of left ventricular function at rest were similar in both groups. Heart rate and blood pressure increased significantly in both groups in response to 40 and 60% of handgrip maximal voluntary contraction (MVC). Left ventricular end-diastolic dimension increased significantly (from 50 ± 1 to 56 ± 1 mm; P < 0·01) with 60% of MVC in CAD group but not in the healthy subjects. The patients with CAD also exhibited significant (P < 0·01) increases in end-systolic dimension (from 34 ± 1 to 40 ± 2 with 40% and to 44 ± 1 mm with 60% MVC). End-diastolic and end-systolic dimensions did not change during isometric exercise in the healthy subjects. Mean velocity of circumferential shortening (mV_CF) increased with 60% MVC in normal subjects. In the CAD group mV_CF decreased significantly (from 1.08 ± 0·06 to 0·86 ± 0·06 with 40% and to 0·74 ± 0·04 d·s^-1 with 60% MVC; P < 0·01). At comparable mean blood pressures, mV_CF was significantly lower in the CAD group than in normal subjects. These results demonstrate that progressive deterioration of left ventricular function during increasing levels of isometric exercise in patients with CAD can be detected with echocardiography.     

Systolic time intervals and the QT-QS2 interval in young female diabetics

To detect subclinical cardiomyopathy in diabetic patients without evidence of coronary artery disease, systolic time intervals were measured in 51 insulin-treated young female diabetics (mean age 27 years and mean duration of diabetes 12 years) and in 15 healthy women of the same age. The ratio of the pre-ejection period to the left ventricular ejection time (PEP/LVET) was used as an index of left ventricular performance. The PEP/LVET ratio was normal in all diabetics and did not differ statistically from that in the control group. The electrical (QT) and electromechanical (QS2) systole were measured from the same high velocity recordings. The QT-QS2 interval (mean +/- SD) was shorter in the diabetic group (-16 +/- 22 ms vs. -33 +/- 9 ms, p less than 0.01). Ten diabetics but none of the healthy women, had the QT interval longer than the QS2. This was a result of both shortening of the QS2 and prolongation of the QT. In conclusion, our results suggest normal myocardial contractility in these young female diabetics. The significance and mechanism of the shortened QT-QS2 interval in the diabetics need further investigation.     

Abnormal Vascular Responses to Exercise in Patients with Aortic Stenosis

We tested the hypothesis that the normal forearm vasoconstrictor response to leg exercise is inhibited or reversed in patients with aortic stenosis, possibly because of activation of left ventricular baroreceptors. Forearm vascular responses to supine leg exercise were measured in 10 patients with aortic stenosis and in 2 control groups of 6 patients with mitral stenosis and 5 patients without valvular heart disease.Forearm vasoconstriction occurred during exercise in the control groups. In contrast, forearm blood flow increased and forearm vascular resistance did not change in patients with aortic stenosis. In six patients with aortic stenosis and a history of exertional syncope, forearm vasodilatation occurred during the second minute of leg exercise. Inhibition or reversal of forearm vasoconstrictor responses in aortic stenosis was asscociated with significant increases in left ventricular pressure.In three patients with aortic stenosis and exertional syncope, forearm vasodilator responses to exercise changed to vasoconstrictor responses after aortic valve replacement.The results indicate that forearm vasoconstrictor responses to leg exercise are inhibited or reversed in patients with aortic stenosis, possibly because of activation of left ventricular baroreceptors. The observations suggest that reflex vasodilatation resulting from activation of left ventricular baroreceptors may contribute to exertional syncope in patients with aortic stenosis.     

Perhexiline during exercise training in coronary heart disease

The effects of low-dose perhexiline on the exercise training response of 22 male patients, 14 after myocardial infarction and 8 after coronary artery bypass who underwent exercise training, were examined. All subjects underwent treadmill exercise testing and resting left ventricular function evaluation by radionuclide ventriculography before and after an 8-wk course of three-times-weekly exercise training. Blood levels of perhexiline confirmed that there was a steady state sufficient for antianginal therapy. There were no side effects. There were improvements in exercise tolerance in treated and placebo groups. There were no significant intergroup differences. Resting left ventricular ejection fraction and end-systolic and diastolic dimensions were not altered. Resting blood pressures were not affected by treatment. There was no evidence of a beta-adrenoceptor-blocking effect. Perhexiline during exercise training did not impair the training response.     

单心动周期全容积成像对右心室流出道起源室性期前收缩患者左心室容积及收缩同步性的研究

目的 探讨正常人及频发右室流出道(right ventricular outflow tract,RVOT)起源室性期前收缩患者左室容积改变模式.方法 应用单心动周期全容积成像(instantaneous full-volume imaging,IFI)技术分析29例RVOT起源室性期前收缩患者在室性期前收缩、窦性心搏时以及30例正常人左室容积参数[收缩末容积(ESV)、舒张末容积(EDV)、每搏量(SV)、射血分数(EF)]和左室收缩期节段容积变化同步性参数[收缩失同步性指数(SDI)、收缩末离散度(DISPES)、平均收缩末时间(MES)、收缩前时间容积(PreContr)、收缩后时间容积(PostContr)].进行左室容积收缩波序标测.结果 与正常对照组比较,RVOT起源室性期前收缩患者在室性期前收缩时左室容积参数EDV、SV、EF均显著降低(P＜0.01);左室收缩期节段容积变化同步性参数均显著增高(P＜0.01).室性期前收缩患者在窦性心搏时各项容积参数与正常对照组比较差异无统计学意义,而同步性参数中MES、PreContr与正常对照组比较差异有统计学意义(P＜0.01).结论 室性期前收缩时左室收缩期整体容积及节段容积的改变存在失同步状态,而在窦性心搏时也可能存在心肌收缩模式的改变.IFI技术可用于定量分析室性期前收缩患者左室容积的变化.

Abstract：

Objective To assess alternations in left ventricular volume and systolic synchrony in patients with frequent premature ventricular complexes(PVCs) from the right ventricular outflow tract(RVOT).Methods Twenty-nine patients with frequent isolated PVCs from RVOT were included and 30 healthy subjects as control.Instantaneous full-volume imaging(IFI) was performed to evaluate left ventricle volumetric parameters,including end-systolic volume (ESV),end-diastolic volume (EDV),stroke volume (SV),ejection fraction (EF),and systolic synchrony parameters,including systolic dyssynchrony index (SDI),dispersion end-systole (DISPES),mean end-systolic time (MES),pre-contraction time volume (PreContr) and post-contraction time volume (PostContr).Contraction front mapping was performed to visualize volumetric contraction sequence.All values of patients with PVCs were recorded during sinus beats (PVC-S) and premature ventricular beats (PVC-V) respectively.Results Significant differences were observed in left ventricular systolic volumetric and synchrony parameters between PVC-V and control subjects (P＜0.01),as well as in MES and PreContr between PVC-S and control subjects (P＜0.01).Conclusions Left ventricular systolic dysynchrony was demonstrated in patients with PVCs from RVOT.IFI was a novel tool to analyze left ventricular global and regional volumetric alternations.     

Pulmonary artery occlusion pressure and central venous pressure fail to predict ventricular filling volume, cardiac performance, or the response to volume infusion in normal subjects

OBJECTIVE: Pulmonary artery occlusion pressure and central venous pressure have been considered to be reliable measures of left and right ventricular preload in patients requiring invasive hemodynamic monitoring. Studies in recent years have questioned the correlation between these estimates of ventricular filling pressures and ventricular end-diastolic volumes/cardiac performance variables in specific patient groups, but clinicians have continued to consider the relationship valid in the broader context. The objective of this study was to assess the relationship between pressure estimates of ventricular preload (pulmonary artery occlusion pressure, central venous pressure) and end-diastolic ventricular volumes/cardiac performance in healthy volunteers. DESIGN: Prospective, nonrandomized, nonblinded interventional study. SETTING: Cardiac catheterization and echocardiography laboratories. SUBJECTS: Normal healthy volunteers (n = 12 group 1, n = 32 group 2). INTERVENTIONS: Pulmonary catheterization and radionuclide cineangiography (group 1) and volumetric echocardiography (group 2) during 3 L of normal saline infusion over 3 hrs. MEASUREMENTS AND MAIN RESULTS: In group 1, the initial pulmonary artery occlusion pressure and central venous pressure did not correlate significantly with initial end-diastolic ventricular volume indexes or cardiac performance (cardiac index and stroke volume index). Changes in pulmonary artery occlusion pressure and central venous pressure following saline infusion also did not correlate with changes in end-diastolic ventricular volume indexes or cardiac performance. In contrast, initial end-diastolic ventricular volume indexes and changes in these ventricular volume indexes in response to 3 L of normal saline loading correlated well with initial stroke volume index and changes in stroke volume index, respectively. The relationship between left ventricular end-diastolic volume index and stroke volume index was confirmed in group 2 subjects using mathematically independent techniques to measure these variables. In addition, initial central venous pressure, right ventricular end-diastolic volume index, pulmonary artery occlusion pressure, and left ventricular end-diastolic volume index failed to correlate significantly with changes in cardiac performance in response to saline infusion in group 1 subjects. CONCLUSIONS: Normal healthy volunteers demonstrate a lack of correlation between initial central venous pressure/pulmonary artery occlusion pressure and both end-diastolic ventricular volume indexes and stroke volume index. Similar results are found with respect to changes in these variables following volume infusion. In contrast, initial end-diastolic ventricular volume indexes and changes in end-diastolic ventricular volume indexes in response to saline loading correlate strongly with initial and postsaline loading changes in cardiac performance as measured by stroke volume index. These data suggest that the lack of correlation of these variables in specific patient groups described in other studies represents a more universal phenomenon that includes normal subjects. Neither central venous pressure nor pulmonary artery occlusion pressure appears to be a useful predictor of ventricular preload with respect to optimizing cardiac performance.