Change In EDV Research Articles

The Left ventricular ejection fraction and left ventricular volumes assessed from 99mTC single photon emission tomography technique during stress and rest in relation to age in normal volunteer students.

The heart is subject to structural and functional changes with advancing age. Left ventricular compliance appears to decline with age, which could explain why the elderly have such a high rate of heart failure. Changes in heart function with age are associated with an increased risk of cardiovascular death and morbidity. Various techniques have been used to measure the impact of age on heart structure and function. Subject and methods: The study included 221 healthy adult male and female volunteers (160 females and 61 males, 20–80 years of age). All healthy subjects volunteered to participate in this study. They were classified according to their age. All healthy subjects enrolled in the study underwent myocardial perfusion imaging following the 2-day rest–stress 99mTc sestamibi (GSPECT) protocol. At rest and during stress, end-diastolic volume, end-systolic volume, and ejection fraction using the GSPECT software were assessed both at rest and during stress for comparison. The following parameters were measured: left ventricular end-systolic volume (LVESV), left ventricular end-diastolic volume (LVEDV), and left ventricular ejection fraction (LVEF). The results show that the change in left ventricular ejection fraction (LVEF) decreased during rest and stress in all age groups. In contrast, the change in left ventricular end-systolic volume (LVESV) increased during stress and rest compared with the left ventricular end-diastolic volume (LVEDV) for all ages. Results show a significant change in EDV, ESV, and EF% (16.49%, 30.35%, -7.49%) with p-value < 0.05 for the groups (20- 49). Also a significant change in EDV, ESV, and EF% (12.13%, 24.86%,-1.62%), respectively, with p-value <0.05. for age range (50-80) years. In conclusion, in people with no cardiac functional or structural problems, the aging process is linked to considerable alterations in left and right ventricular EF, ESV, and EDV. When assessing SPECT with 99mTc investigations, our findings highlight the need to adopt age-adapted data as a reference standard. Keywords: SPECT with 99mTC, Age, Hemodynamics, Rest and Stress

Dosiahnennia kardiolohii u vyvchenni predyktoriv prohnozuvannia hostroi livoshlunochkovoi ta kryteriiv narostannia tiazhkosty khronichnoi sertsevoi nedostatnosty pid chas khvorob sertsia (ohliad literatury; rezultaty vlasnykh doslidzhen)

Introduction. Few works have been published in the literature on the prediction of predictors of acute and chronic heart failure. The aim of the study. Аnalyze the achievements of cardiology in the field of studying the predictors of predicting acute left ventricular failure and the criteria for the progression of CHF with various CVD. Materials and methods. Vikoristani 51 published an article and presented the results of public research in the field of predicting acute respiratory failure and progression of CHF in heart disease. Results. In most patients, the term after the transferred MI is associated with an increase in end-diastolic volume and end-systolic volume, which are prognostically unfavorable signs. In these cases, the development of LV remodeling is of great importance, as well as accepting the same name as MI, stroke, and HF. Predictors of unfavorable cardiovascular diseases dynamics: changes in EDV, ESV and left ventricular ejection fraction. It should be noted that GLS and diastolic dysfunction are important predictors of cardiovascular complications and SCD. The apparent mitral regurgitation increased the risk of death for 5 years of birth. On the basis of our research, we proved for the first time in 1991 that 4 pathogenetically related mechanisms play a leading role in the development of the initial stage of HF in SCD: central, regional pulmonary hemodynamics, microcirculation, and tissue exchange with the development of arteriolar hypoxemia, venous hyperoxia, reduction of ABB by O2 and utilization of oxygen by tissues, reduction of aerobic processes occurring in the H. A. Krebs cycle and replenishment of energy deficit due to increased glycolysis and pentose phosphate shunt (activities of succinate dehydrogenase and cytochrome oxidase). Conclusions. Based on the given data and own results of the study, predictors of predicting acute CHF and progression are: AMI, UA severe form, stable angina pectoris 3-4 FC, cardiac aneurysm, SBP more than 180 mm Hg. and is less than 100 mm Hg, age 70 years and older, AF, TP, VE of 3-5 gradations, “pirouette”-type VT, significant increase in EDV, ESV and decrease in LVEF. The study of predictors of acute progression and criteria for predicting CHF is of primary importance. Key words: predictor of acute left ventricular insufficiency, chronic heart failure

Continuous Estimation of Acute Changes in Preload Using Epicardially Attached Accelerometers.

A miniaturized accelerometer can be incorporated in temporary pacemaker leads which are routinely attached to the epicardium during cardiac surgery and provide continuous monitoring of cardiac motion during and following surgery. We tested if such a sensor could be used to assess volume status, which is essential in hemodynamically unstable patients. An accelerometer was attached to the epicardium of 9 pigs and recordings performed during baseline, fluid loading, and phlebotomy in a closed chest condition. Alterations in left ventricular (LV) preload alter myocardial tension which affects the frequency of myocardial acceleration associated with the first heart sound ( fS1). The accuracy of fS1 as an estimate of preload was evaluated using sonomicrometry measured end-diastolic volume (EDV[Formula: see text]). Standard clinical estimates of global end-diastolic volume using pulse index continuous cardiac output (PiCCO) measurements (GEDV[Formula: see text]) and pulmonary artery occlusion pressure (PAOP) were obtained for comparison. The diagnostic accuracy of identifying fluid responsiveness was analyzed for fS1, stroke volume variation (SVV[Formula: see text]), pulse pressure variation (PPV[Formula: see text]), GEDV[Formula: see text], and PAOP. Changes in fS1 correlated well to changes in EDV[Formula: see text] ( r2=0.81, 95%CI: [0.68, 0.89]), as did GEDV[Formula: see text] ( r2=0.59, 95%CI: [0.36, 0.76]) and PAOP ( r2=0.36, 95%CI: [0.01, 0.73]). The diagnostic accuracy [95%CI] in identifying fluid responsiveness was 0.79 [0.66, 0.94] for fS1, 0.72 [0.57, 0.86] for SVV[Formula: see text], and 0.63 (0.44, 0.82) for PAOP. An epicardially placed accelerometer can assess changes in preload in real-time. This novel method can facilitate continuous monitoring of the volemic status in open-heart surgery patients and help guiding fluid resuscitation.

Insight into Differing Exercise Stroke Volume Mechanics between Endurance Athletes and Non-Athletes

Background: In healthy subjects, stroke volume (SV) and heart rate (HR) combine to augment cardiac output. The degree to which SV can augment, compensating for abnormally low HR during exercise is unknown. Aim: To investigate differences in SV augmentation between endurance athletes (EA) and non-athletes (C) during exercise under pharmacological rate retardation. Methods: 25 participants (76% male) were divided into groups; EA (n = 9) bradycardic endurance athletes (BEA) (n = 6, resting HR <40 bpm), C (n = 9). All underwent cardiopulmonary exercise testing (CPET), determining maximal oxygen uptake (VO2max) and associated workload (W). Exercise echocardiogram followed, with images acquired at 3 incremental stages, final stage set equivalent to upright VO2max workload. On a second visit, tests were repeated following intravenous dual autonomic blockade (DAB) (0.04 mg/kg atropine, 0.2 mg/kg metoprolol). Left ventricle (LV) volumes (mL) calculated during rest and exercise using 2D bi-plane methods. Results: EA and BEA had higher LVSV compared to C at rest (80 ± 21 and 101 ± 19 vs 60 ± 12; p < 0.05) and peak exercise (94 ± 24 and 113 ± 30 vs 66 ± 16; p < 0.05). Exercise LVSV was not significantly affected by DAB in EA and BEA, however was reduced in C with DAB (66 ± 16 vs 57 ± 15; p < 0.05). Differences in SV were due to significantly lower exercise ESV in EA and BEA with DAB, C not significantly altered (interaction p = 0.004). No significant change in EDV with exercise or DAB across any groups (interaction p = 0.997). Conclusions: Athletes can better maintain SV during exercise under the challenge of DAB, predominantly via greater reductions in ESV. DAB seems an effective challenge to elucidate enhanced cardiac physiology.

Effects of oral lycopene supplementation on vascular function in patients with cardiovascular disease and healthy volunteers: a randomised controlled trial.

AimsThe mechanisms by which a ‘Mediterranean diet’ reduces cardiovascular disease (CVD) burden remain poorly understood. Lycopene is a potent antioxidant found in such diets with evidence suggesting beneficial effects. We wished to investigate the effects of lycopene on the vasculature in CVD patients and separately, in healthy volunteers (HV).Methods and ResultsWe randomised 36 statin treated CVD patients and 36 healthy volunteers in a 2∶1 treatment allocation ratio to either 7 mg lycopene or placebo daily for 2 months in a double-blind trial. Forearm responses to intra-arterial infusions of acetylcholine (endothelium-dependent vasodilatation; EDV), sodium nitroprusside (endothelium-independent vasodilatation; EIDV), and NG-monomethyl-L-arginine (basal nitric oxide (NO) synthase activity) were measured using venous plethysmography. A range of vascular and biochemical secondary endpoints were also explored. EDV in CVD patients post-lycopene improved by 53% (95% CI: +9% to +93%, P = 0.03 vs. placebo) without changes to EIDV, or basal NO responses. HVs did not show changes in EDV after lycopene treatment. Blood pressure, arterial stiffness, lipids and hsCRP levels were unchanged for lycopene vs. placebo treatment groups in the CVD arm as well as the HV arm. At baseline, CVD patients had impaired EDV compared with HV (30% lower; 95% CI: −45% to −10%, P = 0.008), despite lower LDL cholesterol (1.2 mmol/L lower, 95% CI: −1.6 to −0.9 mmol/L, P<0.001). Post-therapy EDV responses for lycopene-treated CVD patients were similar to HVs at baseline (2% lower, 95% CI: −30% to +30%, P = 0.85), also suggesting lycopene improved endothelial function.ConclusionsLycopene supplementation improves endothelial function in CVD patients on optimal secondary prevention, but not in HVs.Trial Registration ClinicalTrials.gov NCT01100385

Prediction of left ventricular remodelling after acute myocardial infarction by 3D strain echocardiography

Background: Left ventricular (LV) remodeling has been shown to be related mainly to myocardial infarction (MI) size. We aimed to analyze the respective predictive value of 3D strain parameters, including area strain and biomarkers for the development of early LV remodeling at 30 days after acute MI. Methods: 34 patients with a first MI underwent 3D echocardiography at 2 and 30 days after reperfusion. LV remodeling was defined as an increase in LV end-diastolic volume (EDV, ml) >15% from baseline values. LV volumes (ml), wall motion score index (WMSI), LV ejection fraction (LVEF, %), area strain (AS, %), global longitudinal (GLS, %), circumferential (GCS, %), and radial (GRS, %) strains were correlated with the relative change in EDV (%) at 30 days. Results: At 30 days, LV remodeling was present in 12 patients (35%). Peak values of Troponin (TN, mcg/L) (68 [43-146] vs. 34 [15-107], p=0.2) and creatine phosphokinase (CPK, U/L) (2312 [1717-4075] vs. 1452 [615-2848], p=0.08) were similar in the remodeling and in the non-remodeling groups. LVEF similarly increased in remodeling (47±10% to 56±8%) and in non remodeling (50±7% to 57±6%) groups (p<0.05). At baseline, both LVEF and WMSI were similar in remodeling vs non remodeling group. Among the 3D strain values, GLS was the only strain parameter to be significantly lower in remodeling group (p<0.03) (table). At one month, changes in LVEDV correlated with baseline values of WMSI (r=0.45, p=0.007), GLS (r=0.48, p<0.004), GCS (r=0.42, p<0.01), GRS (r=-0.39, p=0.02), and AS (r=0.47, p<0.006). At multivariate analysis, GLS was the only parameter predictive of remodeling with a cut-off value of -12% by ROC curve analysis (AUC=0.71[0.53-0.89], CI95%) with a sensitivity of 83% and specificity of 59%. View this table: Conclusions: Among all 3D strain parameters, global longitudinal strain appears to be the most accurate deformation parameter to predict early LV remodeling after acute myocardial infarction

Durable Scar Size Reduction Due to Allogeneic Mesenchymal Stem Cell Therapy Regulates Whole‐Chamber Remodeling

BackgroundIntramyocardial injection of mesenchymal stem cells (MSCs) in chronic ischemic cardiomyopathy is associated with reverse remodeling in experimental models and humans. Here, we tested the hypothesis that allogeneic MSC therapy drives ventricular remodeling by producing durable and progressive scar size reduction in ischemic cardiomyopathy.Methods and ResultsGottingen swine (n=12) underwent left anterior descending coronary artery myocardial infarction (MI), and 3 months post‐MI animals received either intramyocardial allogeneic MSC injection (200 mol/L cells; n=6) or left ventricle (LV) catheterization without injection (n=6). Swine were followed with serial cardiac magnetic resonance imaging for 9 months to assess structural and functional changes of the LV. Intramyocardial injection was performed using an integrated imaging platform combining electroanatomical mapping unipolar voltage and 3‐dimensional cardiac magnetic resonance imaging angiography–derived anatomy to accurately target infarct border zone injections. MSC‐treated animals had a 19.62±2.86% reduction in scar size at 3 months postinjection, which progressed to 28.09±2.31% from 3 to 6 months postinjection (P<0.0001). MSC‐treated animals had unchanged end‐diastolic volume (EDV; P=0.08) and end‐systolic volume (ESV; P=0.28) from preinjection to 6 months postinjection, whereas controls had progressive dilatation in both EDV (P=0.0002) and ESV (P=0.0002). In addition, MSC‐treated animals had improved LV sphericity index. Percentage change in infarct size correlated with percentage change in EDV (r=0.68; P=0.01) and ESV (r=0.77; P=0.001). Ejection fraction increased from 29.69±1.68% to 35.85±2.74% at 3 months post‐MSC injection and progressed to 39.02±2.42% 6 months postinjection (P=0.0001), whereas controls had a persistently depressed ejection fraction during follow‐up (P=0.33).ConclusionIntramyocardial injection of allogeneic MSCs leads to a sustained and progressive reduction in infarct size, which in turn drives reverse remodeling and increases in ejection fraction. These findings support ongoing biological activity of cell therapy for substantial periods and suggest optimal end points for future clinical trials.

Left Ventricular Remodeling After Anterior Wall Acute Myocardial Infarction in Modern Clinical Practice (from the REmodelage VEntriculaire [REVE] Study Group)

Left ventricular (LV) remodeling after acute myocardial infarction (AMI) has been well described in previous studies. However, there is a paucity of data on the incidence of and risk factors for LV remodeling in modern clinical practice that incorporates widespread use of acute reperfusion strategies and almost systematic use of "antiremodeling" medications, such as angiotensin-converting enzyme inhibitors and beta blockers. We enrolled 266 patients with anterior wall Q-wave AMI who had >or=3 segments of the infarct zone that were akinetic on echocardiography before discharge. Echocardiographic follow-up was performed 3 months and 1 year after AMI. LV volumes, ejection fraction, wall motion score index, and mitral flow velocities were determined in a blinded analysis at a core echocardiographic laboratory. Acute reperfusion was attempted in 220 patients (83%; primary angioplasty in 29% and thrombolysis in 54%). During hospitalization, 99% of patients underwent coronary angiography and 87% underwent coronary stenting of the infarct-related lesion. At 1 year, 95% of patients received an antiplatelet agent, 89% a beta blocker, 93% an angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker, and 93% a statin. Echocardiographic follow-up was obtained in 215 patients. There was recovery in LV systolic function as shown by a decrease in wall motion score index and an increase in ejection fraction. There was a significant increase in end-diastolic volume (EDV; 56.4 +/- 14.7 ml/m2 at baseline, 59.3 +/- 15.7 ml/m2 at 3 months, 62.8 +/- 18.7 ml/m2 at 1 year, p <0.0001). LV remodeling (>20% increase in EDV) was observed in 67 patients (31%). Peak creatine kinase level, systolic blood pressure, and wall motion score index were independently associated with changes in EDV. In conclusion, recent improvements in AMI management do not abolish LV remodeling, which remains a relatively frequent event after an initial anterior wall AMI.

Abnormal response to inotropic stimulation in young asymptomatic type I diabetic patients demonstrated by serial gated myocardial perfusion SPECT imaging

In subjects without underlying cardiac disease dobutamine is known to enhance systolic LV function and LV relaxation. As end-systolic (ES) and end-diastolic (ED) volumes (V) can be derived from gated SPECT we intent to study these volumes and their response to dobutamine in order to have a better understanding of the mechanism by which stroke volume (SV) increases during dobutamine infusion. We intent to do this in normal controls and in young diabetic subjects. After injection of sestamibi, serial gated SPECT were obtained at baseline, and during low doses of dobutamine infusion in 12 asymptomatic type I diabetic patients, and in 12 age matched controls. LV EDV, ESV, SV and EF were calculated with the QGS program. Gated SPECT showed comparable LV EF and SV in both groups at rest. There was a significant increase in LVEF and SV during dobutamine infusion but in the diabetic patients the increase in SV was due to a decrease in ESV from 25+/-5 to 20+/-6 ml/m2 (p=0.002) and no change in EDV. In normal controls, the increase in EF was due to an increase in EDV from 69+/-10 to 73+/-12 ml/m2 (p=0.002) with no significant change in ESV. These data confirm the presence of subclinical abnormalities of diastolic function in asymptomatic type I diabetic patients and show differences in adaptation to inotropic stimulation in order to preserve the increase in stroke volume and LV ejection fraction.

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 …