Change In End-systolic Volume Index Research Articles

Left ventricular volume change and long-term outcomes in ischaemic cardiomyopathy with or without surgical revascularisation: A post-hoc analysis of a randomised controlled trial.

SummaryBackgroundWhether the association between post-therapeutic left ventricular volume change and long-term outcomes in ischaemic cardiomyopathy is influenced by the performance of coronary artery bypass grafting (CABG) remains unclear. We sought to perform a post-hoc analysis of the Surgical Treatment of Ischaemic Heart Failure (STICH) trial to investigate this association in patients treated with medical therapy (MED) with or without CABG.MethodsFrom July 24, 2002, to May 5, 2007, 1212 patients with ischaemic cardiomyopathy were enrolled in the STICH trial (NCT00023595) from 99 sites in 22 countries, and were randomly assigned to undergo CABG plus MED or MED alone. We completed a post-hoc analysis of this trial. Patients with paired left ventricular end-systolic volume index (ESVI) measured at baseline and 4-months were included in our analysis. The association between change in ESVI from baseline to 4-months and cardiovascular mortality or all-cause mortality was assessed in MED arm and CABG plus MED arm.Findings523 patients were included, with 291 (55.6%) assigned to MED arm and 232 (44.4%) to CABG plus MED arm. At a 4-month follow-up, ESVI reduction was more likely to occur among patients undergoing CABG plus MED. After a median follow-up of 10.3 years, for each 26% (1- standard deviation) decrement in ESVI, it was associated with a 22% lower risk of cardiovascular mortality (HR 0.78; 95% CI, 0.65-0.94) and 19% lower risk of all-cause mortality (HR 0.81; 95% CI, 0.69-0.95) in MED arm, whereas this association was not shown in CABG plus MED arm (cardiovascular mortality: HR 0.90; 95%CI, 0.74-1.10; all-cause mortality: HR 0.93; 95%CI, 0.79-1.09). A 16% reduction in ESVI was determined to be the most appropriate threshold of change in ESVI in the MED arm.InterpretationIn patients with ischaemic cardiomyopathy, left ventricular volume change was associated with long-term prognosis after medical therapy alone, whereas was likely not an optimal benchmark for evaluating the survival benefits associated with CABG. A more than 16% reduction in ESVI might assist in therapeutic efficacy assessment and prognostic evaluation in medically treated patients.FundingNational Natural Science Foundation of China; Natural Science Funds of Guangdong Province.

Two-dimensional knowledge-based volumetric reconstruction of the right ventricle documents short-term improvement in pulmonary hypertension.

Data are scarce about short-term right ventricular changes in pulmonary hypertension. Two-dimensional knowledge-based reconstruction of the right ventricle with 2D echocardiography (2DKBR) has been shown to be a valid alternative to Cardiac MRI. In this longitudinal study 25 pulmonary hypertension patients underwent 2DKBR of the right ventricle, assessment of NT-proBNP levels and functional class at baseline and after a mean follow-up of 6.1months. Patients were followed up clinically for a further mean of 8.2months. The majority of patients had connective tissue disease (CTD) associated pulmonary arterial hypertension (n=15) or chronic thromboembolic pulmonary hypertension (CTEPH; n=6). A total of 15 patients underwent an intervention, either new targeted therapy, escalation of targeted therapy or pulmonary endarterectomy. A total of 10 clinically stable patients were routinely followed up without any change in therapy. There were significant improvements in the right ventricular end-diastolic volume index (111±29mL/m² vs 100±36mL/m²; P=.038), end-systolic volume index (72±23mL/m² vs 61±25mL/m²; P=.001), and ejection fraction (35±10% vs 40±9%; P=.030). Changes in NT-proBNP levels correlated strongest with changes in end-systolic volume index (r=-.77; P=<.0001). Four patients experienced clinical worsening during extended follow-up, dilatation of the right ventricle was associated with clinical worsening. In a CTD and CTEPH dominated patient population significant reverse remodeling and improvement of ejection fraction occurred despite a short follow-up and was paralleled by significant changes in NT-proBNP levels. Further right ventricular dilatation was associated with worse clinical outcome. 2DKBR is a feasible substitute for Cardiac MRI to follow-up right ventricular indices in pulmonary hypertension.

Effects of Interleukin-1 Blockade With Anakinra on Adverse Cardiac Remodeling and Heart Failure After Acute Myocardial Infarction [from the Virginia Commonwealth University-Anakinra Remodeling Trial (2) (VCU-ART2) Pilot Study

A first pilot study of interleukin-1 blockade in ST-segment elevation acute myocardial infarction showed improved remodeling. In the present second pilot study, we enrolled 30 patients with clinically stable ST-segment elevation acute myocardial infarction randomized to anakinra, recombinant interleukin-1 receptor antagonist, 100 mg/day for 14 days or placebo in a double-blind fashion. The primary end point was the difference in the interval change in left ventricular (LV) end-systolic volume index between the 2 groups within 10 to 14 weeks. The secondary end points included changes in the LV end-diastolic volume index, LV ejection fraction, and C-reactive protein levels. No significant changes in end-systolic volume index, LV end-diastolic volume index, or LV ejection fraction were seen in the placebo group. Compared to placebo, treatment with anakinra led to no measurable differences in these parameters. Anakinra significantly blunted the increase in C-reactive protein between admission and 72 hours (+0.8 mg/dl, interquartile range-6.4 to+4.2, vs+21.1 mg/dl, interquartile range+8.7 to+36.6, p= 0.002), which correlated with the changes in LV end-diastolic volume index and LV end-systolic volume index at 10 to 14weeks (R=+0.83, p= 0.002, and R=+0.55, p= 0.077, respectively). One patient in the placebo group (7%) died. One patient (7%) in the anakinra group developed recurrent acute myocardial infarction. More patients were diagnosed with new-onset heartfailure in the placebo group (4, 27%) than in the anakinra group (1, 7%; p= 0.13). When the data were pooled with those from the first Virginia Commonwealth University-Anakinra Remodeling Trial (n= 40), this difference reached statistical significance (30% vs 5%, p= 0.035). In conclusion, interleukin-1 blockade with anakinra blunted the acute inflammatory response associated with ST-segment elevation acute myocardial infarction. Although it failed to show a statistically significant effect on LV end-systolic volume index, LV end-diastolic volume index, or LV ejection fraction in this cohort of clinically stable patients with near-normal LV dimensions and function, anakinra led to a numerically lower incidence of heart failure.

Correlation of autologous skeletal myoblast survival with changes in left ventricular remodeling in dilated ischemic heart failure

The effect of autologous skeletal myoblast transplantation has not been rigorously studied in the setting of end-stage ischemic heart failure free of concomitant coronary revascularization. The aims of the present study were to determine autologous skeletal myoblast survival and its effects on left ventricular function and remodeling in sheep with dilated ischemic heart failure. Ischemic heart failure (left ventricular ejection fraction, 30% +/- 2%; left ventricular end-systolic volume index, 82 +/- 9 mL/m2) was created in sheep (n = 11) with serial left circumflex coronary artery microembolizations. Instruments were inserted for the long-term determination of left ventricular global and regional dimensions, hemodynamics, and pressure-volume analysis after autologous skeletal myoblast transplantation (approximately 3.0 x 10(8) myoblasts; heart failure plus autologous skeletal myoblast group, n = 5) or without (heart failure-control group, n = 6). Measurements were performed in conscious animals. Autologous skeletal myoblast-derived skeletal muscle was found in all injected animals at 6 weeks. In ischemic heart failure, autologous skeletal myoblast cardiomyoplasty failed to improve systolic (left ventricular ejection fraction, 29% +/- 4%; dP/dT(max), 2863 +/- 152 mm Hg/s; end-systolic elastance, 1.6 +/- 0.22) or diastolic (left ventricular end-diastolic pressure, 21 +/- 2 mm Hg; time constant of relaxation (Tau), 34 +/- 4 ms; dP/dT(min), -1880 +/- 68 mm Hg/s) function. There was, however, attenuation in the left ventricular dilatation after autologous skeletal myoblast transplantation (change in end-systolic volume index, 14% +/- 4% vs 32% +/- 6%; P < .05). The effects of autologous skeletal myoblast-derived skeletal muscle were exclusive to the left ventricular short-axis dimension and dependent on autologous skeletal myoblast survival (R2 = 0.59, P = .006, n = 11). Autologous skeletal cardiomyoplasty was able to attenuate left ventricular remodeling in sheep with end-stage ischemic heart failure.

Left Ventricular Remodeling after Myocardial Infarction in Antecedent Hypertensive Patients

Antecedent hypertension adversely affects mortality and heart failure after myocardial infarction (MI). In addition, accelerated ventricular remodeling is a contributor to the increased mortality observed after MI. The purpose of this study was to assess the relationship of antecedent hypertension to ventricular remodeling after MI. Ninety-four patients presenting with a first acute MI who were treated with reperfusion therapy within 12 h of their symptom onset were enrolled in this study. All of them underwent left ventriculography immediately after reperfusion therapy and again at 6 months after the occurrence of MI. Patients were divided into two groups: a hypertensive group and a normotensive group. End-diastolic volume index (EDVI), end-systolic volume index (ESVI), and ejection fraction (EF) values in the acute phase were compared to those at 6 months after acute MI in either group. The hypertensive group showed a significant increase in both EDVI and ESVI after 6 months, whereas the normotensive group did not. In addition, there was no change in EF in the hypertensive group, whereas EF increased significantly after 6 months in the normotensive group. As a result, the percent changes in ESVI and EF were significantly different between the hypertensive group and normotensive group. The results demonstrated that antecedent hypertension interacts with ventricular cavity dilatation after MI.

Arterial and cardiac aging: major shareholders in cardiovascular disease enterprises: Part II: the aging heart in health: links to heart disease.

The preceding article in this series1 reviewed evidence as to why age-associated changes in the central arterial system are risky with respect to vascular disease. In a similar vane, the focus of this article is on the potential link between age-associated changes in the heart and clinical cardiac disease outcomes. Left ventricular hypertrophy, heart failure, and atrial fibrillation increase dramatically with age (Figure 1). The prevalence of left ventricular hypertrophy (LVH) also increases with rising blood pressure and body mass index, a measure of obesity.2–4 Whether identified by electrocardiography or echocardiography, left ventricular hypertrophy has been shown to be associated with increased risk for coronary heart disease, sudden death, stroke, and overall cardiovascular disease.4,5 Figure 1. A, Prevalence of echocardiographic left ventricular hypertrophy (LVH) in women according to baseline age and systolic blood pressure. B, Prevalence of echocardiographic LVH in men according to baseline age and systolic blood pressure. Both A and B are reprinted from Levy D, Anderson KM, Savage DD, et al. Echocardiographically detected left ventricular hypertrophy: prevalence and risk factors: the Framingham Heart Study. Ann Intern Med . 1988;108:7–13. C, Prevalence of heart failure by age in Framingham Heart Study men (light bars) and women (dark bars). Reprinted from Ho KK, Pinsky JL, Kannel WB, et al. The epidemiology of heart failure: the Framingham Study. J Am Coll Cardiol 1993;22:6A–13A. D, Prevalence of AF by age in subjects from the Framingham Heart Study. Reprinted from Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for stroke: the Framingham Study. Stroke . 1991;22:983–988. It has been increasingly appreciated that the development of heart failure with apparently preserved systolic function, as evidenced by a “normal” ejection fraction, occurs in about one-third to one-half of older patients with heart failure.6–9 In a …

Exercise MR imaging in the assessment of pulmonary regurgitation and biventricular function in patients after tetralogy of fallot repair.

To assess the responses of pulmonary regurgitation (PR) and biventricular function to submaximal exercise by using a magnetic resonance (MR) imaging exercise protocol with young adult patients who underwent tetralogy of Fallot repair at a young age. Fifteen patients with corrected tetralogy of Fallot (mean age, 17.5 years +/- 2.5 [SD]) underwent MR imaging at rest and during exercise for the evaluation of PR and biventricular function. Results were compared with findings from 16 control subjects (mean age, 17.5 years +/- 2.3). Mean age at tetralogy of Fallot repair was 2.1 years +/- 1.6, and mean follow-up time after repair was 15.4 years +/- 2.6. Exercise level at MR imaging was calculated individually and corresponded to 60% of peak oxygen uptake. The parameters of cardiac function obtained at rest and during exercise were compared by using a paired t test. An unpaired t test was used to compare parameters of cardiac function between patients and control subjects. PR decreased during exercise (from 27 mL/m(2) +/- 17 to 23 mL/m(2) +/- 15; P =.012). At rest, right ventricular (RV) ejection fraction was normal (>47%) in 80% of patients. RV response to exercise in the patient group was abnormal compared with response in the control group, as demonstrated by an increase in RV end-diastolic volume index (132 mL/m(2) +/- 36 to 137 mL/m(2) +/- 38; P =.041) and no significant change in end-systolic volume index or ejection fraction. In only one patient, RV ejection fraction increased by more than 5%. Left ventricular response was not different between patients and control subjects. MR imaging is well suited to assess cardiac response to exercise, and findings revealed a decrease in PR and an abnormal RV response to exercise in patients with corrected tetralogy of Fallot.

Low-dose dobutamine responsiveness in idiopathic dilated cardiomyopathy: relation to exercise capacity and clinical outcome.

To evaluate myocardial contractile reserve using low-dose dobutamine echocardiography in patients with chronic heart failure secondary to idiopathic dilated cardiomyopathy stratified by peak exercise oxygen consumption (VO(2)). Sixty clinically stable patients (56+/-11 years; 45 males) with idiopathic cardiomyopathy and NYHA class I to III symptoms of heart failure were studied and followed-up for 13+/-3 months. All patients underwent cardiopulmonary exercise testing and low-dose dobutamine. The dobutamine infusion protocol consisted of an initial dose of 2.5 micro. kg(-1)per 3 min, increasing by 2.5 micro. kg(-1)per min every 3 min; the maximal dose was 10 micro. kg(-1)per min. The end-systolic volume index, left ventricular ejection fraction and cardiac output were measured at baseline and peak dobutamine dose and their change calculated as ((peak dose value-baseline value)/baseline value]x100. Ten normal subjects with normal left ventricular function and no coronary artery lesions served as a control group to compare low-dose dobutamine results. All analysed echocardiographic variables either at baseline or following dobutamine infusion were significantly lower in patients with chronic heart failure as a whole compared to the control group. When the patients were grouped according to Weber's classification, a statistically significant decrease in percentange changes in end-systolic volume index (rho=-0.77;P<0.0001), left ventricular ejection fraction (rho=-0.72;P<0.0001) and cardiac output (rho=-0. 82;P<0.0001) from class A to class C was observed. The mean percentage decrease in end-systolic volume index following the dobutamine infusion was 28.7+/-9% in class A (peak VO(2)>20 ml. kg(-1). min(-1)), 18.6+/-8% in class B (peak VO(2)between 16 and 20 ml. kg. min(-1)), and only 6.4+/-6% in class C (peak VO(2)between 10 and 16 ml. kg(-1). min(-1)) patient groups. At multivariate analysis, only the percentage change in end-systolic volume index was significantly associated with a peak VO(2)<15 ml. kg(-1). min(-1)(P=0.006). During the follow-up, 17 patients had events (15 readmissions for worsening heart failure and two deaths). At multivariate analysis, only the percentage change in end-systolic volume index was significantly associated with the occurrence of events (P=0.003). The area under the receiver operating characteristic curve for percentage change in end-systolic volume index was not significantly different from that for peak VO(2)(0. 86+/-0.04 vs 0.80+/-0.06;P:ns). This study indicates that in patients with chronic heart failure secondary to idiopathic cardiomyopathy, the cardiac response to low-dose dobutamine, as assessed by echocardiography, is correlated with peak VO(2), an objective and accurate measure of the severity of the disease and clinical outcome.

Stress echocardiography in hyperthyroidism.

Exertion symptoms occur frequently in subjects with hyperthyroidism. Using stress echocardiography, exercise capacity and global left ventricular function can be assessed noninvasively. To evaluate stress-induced changes in cardiovascular function, 42 patients with untreated thyrotoxicosis were examined using exercise echocardiography. Studies were performed during hyperthyroidism, after treatment with propranolol, and after restoration of euthyroidism. Twenty-two healthy subjects served as controls. Ergometry was performed with patients in a semisupine position using a continuous ramp protocol starting at 20 watts/min. In contrast to control and euthyroidism, the change in end-systolic volume index from rest to maximal exercise was lower in hyperthyroidism. At rest, the stroke volume index, ejection fraction, and cardiac index were significantly increased in hyperthyroidism, but exhibited a blunted response to exercise, which normalized after restoration of euthyroidism. Propranolol treatment also led to a significant increase of delta (delta) stroke volume index. Maximal work load and delta heart rate were markedly lower in hyper- vs. euthyroidism. Compared to the control value, systemic vascular resistance was lowered by 36% in hyperthyroidism at rest, but no further decline was noted at maximal exercise. The delta stroke volume index, delta ejection fraction, delta heart rate, and maximal work load were significantly reduced in severe hyperthyroidism. Negative correlations between free T3 and diastolic blood pressure, maximal work load, delta heart rate, and delta ejection fraction were noted. Thus, in hyperthyroidism, stress echocardiography revealed impaired chronotropic, contractile, and vasodilatatory cardiovascular reserves, which were reversible when euthyroidism was restored.

Relation of left ventricular volume and function over one year after acute myocardial infarction to infarct size determined by technetium-99m sestamibi

Twenty patients with a first acute myocardial infarction (AMI) (15 anterior, 5 inferior) who received successful reperfusion therapy underwent tomographic imaging with technetium-99m (Tc-99m) sestamibi and radionuclide ventriculography at discharge, 6 weeks, and 1 year after AMI. Patency of the infarct-related artery after reperfusion (thrombolysis, 8 patients; coronary angioplasty, 12 patients) was confirmed by angiography in all patients. Tc-99m sestamibi perfusion defect at discharge (a measure of infarct size) was quantitated using previous methods and expressed as a percentage of the left ventricle (28 ± 19%, range 0 to 59%). This perfusion defect size correlated closely with ejection fraction at discharge (r = −0.87), 6 weeks (r = −0.81) and at 1 year (r = −0.78, all p < 0.0001). Perfusion defect size at discharge also correlated closely with end-systolic volume index at discharge (r = 0.71, p < 0.0005), 6 weeks (r = 0.63, p < 0.005) and at 1 year (r = 0.76, p < 0.0001). Perfusion defect size at discharge did not correlate significantly with end-diastolic volume index at discharge or at 6 weeks, but did correlate at 1 year (r = 0.66, p < 0.005). There was no significant group change in end-systolic or end-diastolic volume indexes from discharge to 1 year later, although 7 patients had definite individual changes in end-diastolic volume index (3 increased and 4 decreased). There was no relation between defect size and late changes in end-systolic volume index, but there was a weak correlation between defect size and late changes in end-diastolic volume index (r = 0.42, p = 0.07). Tc-99m sestamibi perfusion defect at discharge correlates with ejection fraction, and end-diastolic and endsystolic volume indexes 1 year after AMI. In most patients with patent infarct-related arteries after AMI, there does not appear to be a significant overall increase in ventricular volume during the first year after infarction.

Regulation of stroke volume during submaximal and maximal upright exercise in normal man.

To characterize the hemodynamic factors that regulate stroke volume during upright exercise in normal man, 24 asymptomatic male volunteers were evaluated by simultaneous right heart catheterization, radionuclide angiography, and expired gas analysis during staged upright bicycle exercise to exhaustion. From rest to peak exercise, oxygen consumption increased from 0.33 to 2.55 liters/min (7.7-fold), cardiac index increased from 3.0 to 9.7 liters/min per m2 (3.2-fold), and arteriovenous oxygen difference increased from 5.8 to 14.1 vol% (2.5-fold). The increase in cardiac index resulted from an increase in heart rate from 73 to 167 beats/min (2.5-fold), and an increase in left ventricular stroke volume index from 41 to 58 ml/m2 (1.4-fold). During low levels of exercise, there was a linear increase in cardiac index due to an increase in both heart rate and stroke volume index; stroke volume index increased as a result of an increase in left ventricular filling pressure and end-diastolic volume index and, to a much smaller extent, a decrease in end-systolic volume index. During high levels of exercise, further increases in cardiac index resulted entirely from an increase in heart rate, since stroke volume index increased no further. Left ventricular end-diastolic volume index decreased despite a linear increase in pulmonary artery wedge pressure; stroke volume index was maintained by a further decrease in end-systolic volume index. The degree to which stroke volume index increased during exercise in individuals correlated with the change in end-diastolic volume index (r = 0.66) but not with the change in end-systolic volume index (r = 0.07). Thus, the mechanism by which left ventricular stroke volume increases during upright exercise in man is dependent upon the changing relationship between heart rate, left ventricular filling, and left ventricular contractility. At low levels of exertion, an increase in left ventricular filling pressure and end-diastolic volume are important determinants of the stroke volume response through the Starling mechanism. At high levels of exertion, the exercise tachycardia is accompanied by a decrease in end-diastolic volume despite a progressive increase in filling pressure, so that stroke volume must be maintained by a decrease in end-systolic volume.

Noninvasive measurement of the rest and exercise peak systolic pressure/end-systolic volume ratio: A sensitive two-dimensional echocardiographic indicator of left ventricular function

Thirty-five patients with previous myocardial infarction and 25 normal subjects underwent subcostal view two-dimensional echocardiography at rest and at peak up-right bicycle exercise. The purpose was to assess changes in left ventricular volume with maximal upright bicycle exercise and to compare the utility of the peak systolic pressure/end-systolic volume index ratio and ejection fraction as indicators of left ventricular function. With exercise, normal subjects had a decrease in end-systolic volume index (22 +/- 8 to 11 +/- 3 ml/m2) (p less than 0.001); the normal ejection fraction (59 +/- 9 to 72 +/- 8%, p less than 0.001) and the pressure/volume ratio (6 +/- 3 to 18 +/- 6, p less than 0.001) increased. In patients with prior myocardial infarction there was no change in end-systolic volume index, ejection fraction or pressure/volume ratio with exercise. Although at peak exercise significant differences between normal subjects and patients with prior infarction were demonstrated in end-systolic volume index (p less than 0.001), ejection fraction (p less than 0.001) and pressure/volume ratio (p less than 0.001), the pressure/volume ratio provided sharper delineation between the two groups than did ejection fraction. The exponential relation of the pressure/volume ratio and ejection fraction at peak exercise demonstrates that the pressure/volume ratio is more sensitive as an indicator of normal or borderline left ventricular function and that ejection fraction is more sensitive in quantifying the degree of left ventricular dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)