Left Ventricular Meridional Wall Stress Research Articles

Beta-receptor desensitization after a multistage ultralong distance exercise in the desert?

Abstract Background Although cardiac function has been largely investigated during ultra-endurance exercise, few studies addressed to multi-stage endurance race. Methods Serial echocardiographic assessment of cardiac function was performed in male healthy subjects during the 2014 Marathon des Sables before the race (T1), at the second (T2) and fifth (T3) arrival (236 km) then after 48h recovery. Analysis were performed by 2 sonographers blind for the results of the other and the time of measure. Results Among the 20 athletes, 18 completed the study (mean age 42.4, median 42). RR intervals and (Left ventricular End Diastolic Volume (Simpson) (LVEDV) changed during the race and were correlated (r2 = 0.539, p<0.001); afterload approched by Left Ventricular Meridional Wall Stress (LVMWS) did not change. LV Global Longitudinal Peak Strain (PS) and subepicardial (Epi) PS did not vary. Subendocardial (Endo) LV.PS was lower at T2 /T1, concomitant to a (non-significant) drop in LVEDV; LV strain rate (SR) was lower at T4. RR and LVEDV were higher at T3 than at T2, and higher at T4 compared to T1 and T2. As preload conditions changed during the race, we studied the response of PS and SR to the change in preload (Starling mechanism). EndoPS/LVEDV, LVPS/LVEDV and SR/LVEDV did not change during the race but were lower after recovery. Conclusions 48h after a multistage ultralong duration exercise, we observed a drop in heart rate and contractility response to preload. The evolution of these parameters could be explained by a beta-receptors desensitization. These data need to be confirmed by other studies. Funding Acknowledgement Type of funding sources: Public hospital(s). Main funding source(s): CHU Dijon Bourgogne ARS Bourgogne Franche Comté Evolution of parameters

Performance indicators of left ventricular strain, wall stress and serum brain natriuretic peptide levels in chronic hemodialysis patients

Background: Left ventricular (LV) global longitudinal strain (GLS) is a reliable determinant of LV systolic function. The precise relationship between LV wall stress and serum brain natriuretic peptide (BNP) concentrations in hemodialysis (HD) patients require clariϐication. BNP levels are raised in patients with endstage renal disease (ESRD) and could reflect LV impairment amongst HD patients. Objective: This study sought to evaluate the clinical utility of LV–GLS, wall stress and serum BNP levels in chronic HD patients. The correlations between BNP levels with both LV wall stress and LV–GLS were assessed. Methodology: A total of 30 ESRD patients on regular HD – divided into 15 patients with LV ejection fraction (EF) <50% and 15 patients with LV EF > 50% – and 15 agematched healthy subjects were assessed. LV function and structure were measured using conventional echocardiography, including LV meridional wall stress (LVMWS), LV mass index (LVM I) and two-dimensional speckle tracking echocardiography for determination of LV–GLS. Serum BNP levels were evaluated after HD sessions. Results: There were significant increases in LVM SW (189.2 ± 81 vs. 72.2 ± 20.6 dynes/cm 2 2 1000, P < 0.0001), higher levels of BNP (1238 ± 1085.5 vs. 71 ± 23.4 pg/ml, P<0.0001), w hilst LV–GLS was signiϐicantly reduced (15.1 ± 3.1 vs. 20.8 ± 1.7%, P <0.0001) in HD patients, when compared to the controls. Higher values of LVMWS (246.9 ± 67.5 vs. 131.5 ± 43.6 dynes/cm 2 2 1000, P <0.0001) and BNP (1925.4 ± 1087 vs. 550.5 ± 496.5pg/ml, P < 0.0005) with further impairment of LV–GLS (13.8 ± 2.5 vs. 16.4 ± 5.4%, P < 0.05) were found in patients with LV EF 0 50% than those with LV EF > 50%. Serum levels of BNP were positively correlated with LVM I (r = 0.896, P < 0.0001) and LVMW S (r = 0.697, P < 0.0001), but negatively correlated with LV–GLS (r = 0 0.587, P < 0.0001). Conclusion: LV–GLS and LVMWS are useful imaging markers for detection of LV dysfunction in HD patients. Serum BNP level is influenced by LV structural abnormalities, being regarded as a crucial hemodynamic biomarker in those patients.

Beta-receptor desensitization evoked by a multistage ultralong distance exercise in the desert?

Few studies addressed to the evolution of cardiac function during a multistage ultra-long duration exercise (MULDE). Serial echocardiographic assessment of cardiac function was performed in male healthy subjects during the 2014 Marathon des Sables before the race (T1), at the second (T2) and fifth (T3) arrival (236 km) then after 48 h recovery. Analysis were performed by 2 sonographers blind for the results of the other and the time of measure. Statistical analysis was performed using ANOVA-RM to compare the evolution of the different parameters. Among the 20 athletes, 18 completed the study (mean age 42.4, median 42). RR intervals and (Left ventricular End Diastolic Volume (Simpson) (LVEDV) changed during the race and were correlated (r2 = 0.539, P < 0.001); afterload approached by Left Ventricular Meridional Wall Stress (LVMWS) did not change. LV Global Longitudinal Peak Strain (PS) and subepicardial (Epi) PS did not vary. Subendocardial (Endo) LV.PS was lower at T2/T1, concomitant to a (non-significant) drop in LVEDV; LV strain rate (SR) was lower at T4. RR and LVEDV were higher at T3 than at T2, and higher at T4 compared to T1 and T2. As preload conditions changed during the race, we studied the response of PS and SR to the change in preload (Starling mechanism). EndoPS/LVEDV, LVPS/LVEDV and SR/LVEDV did not change during the race but were lower after recovery ( Table 1 ). 48 h after a MULDE, we observed a drop in heart rate and contractility response to preload. The evolution of these parameters could be explained by a beta-receptors desensitization. These data need to be confirmed by other studies.

Clinical utility of left ventricular strain, wall stress and serum brain natriuretic peptide levels in chronic hemodialysis patients.

BackgroundLeft ventricular (LV) global longitudinal strain (GLS) reliably assesses LV systolic function. The precise relation between LV wall stress and serum Brain natriuretic peptide (BNP) concentrations in hemodialysis (HD) patients needs to be clarified. BNP levels are raised in patients with end-stage renal disease (ESRD) and could reflect LV impairment among HD patients.Aim of this workThis study sought to evaluate the clinical utility of LV-GLS, wall stress and serum BNP levels in chronic HD patients. The correlations between BNP levels with both LV wall stress and LV-GLS were assessed.Patients and methods30 ESRD patients on regular HD {categorized into 15 patients with LV ejection fraction (EF) ≤ 50% and 15 patients with LV EF > 50%} and 15-age matched healthy subjects were included. LV function and structure were assessed by conventional echocardiography including LV meridional wall stress (LVMWS), LV mass index (LVMI) and 2-dimensional speckle tracking echocardiography for determination of LV-GLS. Serum BNP levels were evaluated after HD session.ResultsThere were significant increase of LVMSW (189.2 ± 81 vs. 72.2 ± 20.6 dynes/cm2 × 1000, P < 0.0001), higher levels of BNP (1238 ± 1085.5 vs. 71 ± 23.4 pg/ml, P < 0.0001) while LV-GLS was significantly reduced (15.1 ± 3.1 vs. 20.8 ± 1.7%, P < 0.0001) in HD patients compared to controls. Higher values of LVMWS (246.9 ± 67.5 vs. 131.5 ± 43.6 dynes/cm2 × 1000, P < 0.0001) and BNP (1925.4 ± 1087 vs. 550.5 ± 496.5 pg/ml, P < 0.0005) with further impairment of LV-GLS (13.8 ± 2.5 vs. 16.4 ± 5.4%, P < 0.05) were found in patients with LV EF ≤ 50% than those with LV EF > 50%. Serum levels of BNP were positively correlated with LVMI (r = 0.896, P < 0.0001) and LVMWS (r = 0.697, P < 0.0001) but negatively correlated with LV-GLS (r = −0.587, P < 0.0001).ConclusionLV-GLS and LVMWS are useful imaging markers for detection of LV dysfunction in HD patients. Serum BNP level is influenced by LV structural abnormalities and suggested to be a crucial hemodynamic biomarker in those patients.

0136: Impact of a multi-stage ultra-long duration exercise on left ventricular contractility indexes: an echocardiographic study using multilayer speckle-tracking imaging

some controversy still exists about the reality and mechanics of exercise-induced cardiac fatigue. Little is known about the kinetics of the impact of ultra-long duration exercise (ULDE) on the left ventricular (LV) function. We studied evolution of LV contractility indexes by serial examinations during a multistage ULDE race. successive echocardiographic assessment was performed on 20 well-trained amateur male runners (42.8±3.5 year-old) participating in a 236 km 5-stage foot race in the Sahara desert. An echocardiograhic study was performed the day before the race (T1), following the completion of the second (41 km, T2) and the fifth (42.2 km, T3) stages, then within the second day of recovery (T4). Contractility indexes included biplan ejection fraction (EF), LV global longitudinal (GL) peak-strain (PS) and strain-rate (SR), subendocardial layer (ENDO) and sub-epicardial layer (EPI) longitudinal strain. LV preload was evaluated by LV End Diastolic Biplan Volume (LVEDV) and afterload by LV Meridional Wall Stress. no change of EF was observed during the study period. LV GLPS significantly decreased at T2 (from – 20.8±2 to –19±2.9%, p<0.05) while GLSR did not change (from –1.19±0.17 to –1.19±0.17). GLPS returned to initial values at T3 and T4; evolution of ENDO and EPI longitudinal PS strictly followed modifications of GLPS. Afterload did not change. There was a tendancy to a transient drop in preload at T2 (111±20 to 104±16mL); preload then increased in T3 (115±25mL, p<0.05 versus T2) and T4 (121±20mL, p<0.05 versus T1 and T2). transient drop in LV GLPS occured at early stage of the race but returned to pre-race value when exercise was repeated and remained stable 2 days after this race. Impact seemed to be of same magnitude in different layers of LV myocardium. Whether preload conditions influenced contractility indexes cannot be ruled out.

Prenatal nicotine exposure induces gender-associated left ventricular-arterial uncoupling in adult offspring.

Alterations in vascular or myocardial structure and function have been demonstrated in offspring subjected to prenatal nicotine exposure (PNE), however, limited data are available on how these changes interact. The present study assessed the hypothesis that prenatal nicotine exposure induced gender-specific alterations of left ventricular-arterial coupling indices in adult offspring. Female Sprague-Dawley rats were exposed to either nicotine (8 mg/kg/day) or saline via subcutaneous osmotic mini-pumps throughout gestation. Male and female offspring, aged 12 months, underwent non-invasive echocardiography and invasive left ventricular cannulation. Left ventricular-arterial coupling was analysed as the ratio of effective arterial elastance (Ea) to ventricular end-systolic elastance (Ees). The left ventricular myocardium and aorta were stained with hematoxylin and eosin and the myocardial cell cross-sectional area was calculated. Simultaneously, the ratio of medium thickness to internal diameter in the aorta and mesenteric artery was determined. The fibrosis component of left ventricle myocardium was analyzed by Sirius-red staining and further confirmed by hydroxyproline determination. The elastic properties of the aortic wall were analyzed by van Gieson staining. PNE caused significant increases in pulse pressure (56.36 ± 7.41 vs. 50.16 ± 4.94 mmHg; P<0.05) and left ventricular meridional wall stress (78.25 ± 9.12 vs. 69.64 ± 7.58 kdyne/cm(2); P<0.05) in male offspring compared with the control. Conversely, no similar effect was observed in female offspring. An elevated augmentation index was noted in male and female pups. Additionally, Ea/Ees was reduced in PNE males compared with control males, due to a disproportionate increase in Ees vs. Ea whereas in females, Ea/Ees did not differ significantly due to tandem increase in Ea and Ees. In addition, collagen cross-linking was markedly higher in male offspring, whereas it was unaltered in females compared with their respective controls. Fragmentation of the elastic network in the aorta and the increased ratio of medial thickness to internal diameter in the mesenteric artery were more evident in male offspring when compared with female offspring. PNE caused combined ventricular-arterial stiffening in male and female offspring, with lower Ea/Ees in males, while Ea/Ees was preserved in females. Enhanced collagen cross-linking in the myocardium, underdeveloped elastic fibers in the aorta and remodeled resistance vessels were associated with pathological ventricular arterial mismatching. The results of the present study indicated that male offspring were more susceptible to the development of ventricular and arterial dysfunction in response to PNE compared with female offspring.

Alterations in Left Ventricular Function are Repeated Consistently within the Same Cohort Following Two Separate Marathons

Cross-sectional investigation of the myocardium following prolonged exercise has revealed heterogeneous alterations in left ventricular (LV) function, and sporadic elevations in markers of cardiac damage. The repeatability of these phenomena within the same population has yet to be examined. PURPOSE: To investigate the incidence of alterations in markers of LV function and damage in a cohort of athletes following two identical marathons one year apart. METHODS: Seven male competitors in both the 2004 and 2005 London Marathons (mean completion time: 212 ± 36 min and 221 ± 48 min, respectively) underwent identical testing procedures pre- and post-race on each occasion. Left ventricular function was examined echocardiographically using 2-D, M-mode and flow propagation velocity (V). Parameters were analyzed via a two-way repeated measures ANOVA using pairwise comparisons with a Bonferroni correction. Serum was assayed for cardiac troponin T (cTnT). RESULTS: Loading did not differ between pre- and post-exercise on each occasion, as estimated by LV internal diameter in diastole and LV meridional wall stress. Systolic function, assessed by ejection fraction and systolic blood pressure/end systolic volume ratio, did not differ significantly pre- to post-exercise in either marathon. Similar significant reductions in the early to late diastolic filling ratio (E:A) were observed following both the 2004 and 2005 marathon (2.1 ± 0.6 to 1.2 ± 0.3 and 1.8 ± 0.5 to 1.1 ± 0.2, P ≥ 0.01), and delta E:A changes for each marathon were highly correlated (r = 0.849, P <0.05). A significant decrease in V following the 2005 marathon (67 ± 12 cm-sec1 vs. 61 ± 10 cm-sec1, P <0.05), and a downward trend in V following the 2004 marathon (P = 0.06), provided further evidence for a reduction in diastolic filling. An elevated heart rate following each race (54 ± 2 to 79 ± 9 beat.min−1 vs. 56 ± 4 to 83 ± 8 beat.min−1, P <0.05) was significantly related to the changes in E:A (r = −0.835 and r = −0.802, P <0.05). Elevated cTnT, indicative of cardiac damage, was detected in four athletes following the 2004 marathon, and in three athletes following the 2005 marathons (range: 0.017 – 0.29 ug/L). Only one individual exhibited elevated cTnT after both races. CONCLUSION: Consistent post-exercise reductions in LV diastolic filling within the same cohort is partially attributed to an elevated heart rate, however, an intrinsic impairment of LV relaxation may also be implicated. Elevations in cTnT were not consistent within the same cohort, and were unrelated to changes in LV function. Separate mechanisms are likely responsible for the cTnT release and altered LV function, although these remain to be elucidated.

Remodeling of the chronic severely failing ischemic sheep heart after coronary microembolization: functional, energetic, structural, and cellular responses.

The mandatory use of pharmacotherapy in human heart failure (HF) impedes further study of natural history and remodeling mechanisms. We created a sheep model of chronic, severe, ischemic HF [left ventricular (LV) ejection fraction (LVEF) <35% stable over 4 wk] by selective coronary microembolization under general anesthesia and followed hemodynamic, energetic, neurohumoral, structural, and cellular responses over 6 mo. Thirty-eight sheep were induced into HF (58% success), with 23 sheep followed for 6 mo (21 sheep with sufficient data for analysis) after the LVEF stabilized (median of 3 embolizations). Early doubling of LV end-diastolic pressure persisted, as did increases in LV end-diastolic volume, LV wall stress, and LV wall thinning. Contractile impairment (LV end-systolic elastance, LV preload recruitable stroke work, and dobutamine-responsive contractile reserve) and diastolic dysfunction also remained stable. Cardiac mechanical energy efficiency did not recover. Plasma atrial natriuretic peptide levels remained elevated, but rises in plasma aldosterone and renin activity were transient. Collagen content increased 170%, the type I-to-III phenotype ratio doubled in the LV, but right ventricular collagen remained unaltered. Fas ligand cytokine levels correlated with expression of both caspase-3 and -2, suggesting a link in the apoptotic "death cascade." Caspase-3 activity also bore a close relationship to LV meridional wall stress calculated from echocardiographic and intraventricular pressure measurements. We concluded that the stability of chronic untreated severe ischemic HF depends on the recruitment of myocardial remodeling mechanisms that involve an interaction among hemodynamic load, contractile efficiency/energetics, neurohumoral activation, response of the extracellular matrix, wall stress, and the myocyte apoptotic pathway.

Cardiac Function Following a Marathon in Recreational Runners

2284 PURPOSE: Cardiac dysfunction and minimal cardiac damage have been reported following prolonged exercise in trained individuals. Limited data exists examining the impact of prolonged exercise in recreational athletes. Accordingly, the purpose of the present study was to examine cardiac function following a Marathon in recreational runners. METHODS: 41 male and female subjects (age range 35 ± 10 yrs, range: 18-63 and marathon finish times 245.9 ± 45.6 min, range: 186–381min) volunteered to participate in this study. All were free of known heart disease and were not currently taking any medication. M-mode, 2-D and Doppler echocardiography was performed pre and immediately post-race (15-45min) to assess systolic function (stroke volume [SV], ejection fraction [EF]), diastolic function (E:A) as well as to indirectly quantify preload (LV internal dimension at end-diastole [LVIDd]). Afterload was represented by systolic blood pressure [sBP] and left ventricular meridional wall stress (LVMWS). Pre-post changes were analysed by students T-test and delta pre-post scores were correlated with age and finish time. RESULTS: SV was significantly reduced postrace (107.4 ± 22.5 vs. 98.4 ± 26.7%, P<0.05). EF remained unchanged pre to pos-race (75 ± 8 vs .75 ± 7 %, P>0.05) despite the reduction in preload and a maintained afterload (129 ± 13 vs. 122 ± 13 mmHg; P>0.05). The depression in preload could be partially explained by a moderate dehydration as body mass was significantly decreased postrace (75.3 ± 8.4 vs. 73.1 ± 8.5, P<0.05; r=-0.11, P>0.05). E:A ratio was significantly reduced post-exercise (1.74 ± 0.51 vs. 1.09 ± 0.30, P<0.05) in the absence of changes in after-load (sBP, LVMWS). The change in E:A was not related to the observed decrease in pre-load (LVIDd; 52.1 ± 3.7 vs. 50.4 ± 4.9mm, P<0.05), heart rate, age or finish time. CONCLUSIONS: Marathon running is not associated with depressed systolic function in recreational runners. In agreement with previous studies, global diastolic function is depressed following marathon running that is not associated with loading or HR and the etiology of this requires further research. Age and finish time did not correlate with any functional variable in this cohort.

Relation of mass/volume ratio to ECG abnormalities and symptoms in children with aortic stenosis/insufficiency.

In this study, to determine whether symptoms and ECG abnormalities relate to left ventricular (LV) mass, volume, and mass/volume (M/V) ratio in children with aortic stenosis (AS) and/or insufficiency (AI), the authors examined 23 patients with echocardiography. LV volumes and mass were calculated with echocardiography. Also, the peak and mean gradients across the aortic valve and left ventricular meridional wall stress (ESWS) were determined by use of echo Doppler techniques. Fourteen patients (mean age 5.84+/-3.49 years) had AS alone. Of these, 14 had symptoms and seven had abnormal-appearing ECGs. Nine patients (mean age 6.91+/-4.35 years) had AS/AI. Of these nine, four had symptoms and two had ECG abnormalities. The authors observed that the incidences of symptoms and ECG abnormalities were higher in the patients with AS than in those with AS/AI. There was no significant correlation between symptoms and ECG abnormalities with peak gradient, mean gradient, valve area, LV mass, volume, and mass/volume ratio in patients with AS/AI. However, significant correlation was found between symptoms and ECG abnormalities and ESWS in AS/AI patients. In conclusion, ECG abnormalities and symptoms do not always indicate the severity of AS and AS/AI.

Left ventricular mechanics in dilated cardiomyopathy

The influence of altered chamber shape on the evaluation of left ventricular (LV) mechanics in idiopathic dilated cardiomyopathy (IDC) is unknown. Nine patients with IDC and 7 subjects with normal LV function were studied with simultaneous LV pressure and M-mode echographic recordings in order to derive LV meridional wall stress. The major axis of the left ventricle, determined from the left ventriculogram at rest, allowed for derivation of circumferential wall stress. The IDC group was characterized by larger end-diastolic and end-systolic LV volumes, increased LV mass, depressed angiographic ejection fraction and more spherical LV chamber shape. Both end-systolic meridional (114 ± 30 kdyne/cm 2) and circumferential (251 ± 73 kdyne/cm 2) wall stresses were elevated in patients with IDC, although the ratio of these stresses was less than normal (2.2 ± 0.1 vs 2.7 ± 0.2, respectively). LV load alteration with phenylephrine or nitroglycerin allowed for construction of end-systolic stress-minor-axis dimension and end-systolic stress-minor-axis shortening relations. Similar mean slopes of the meridional end-systolic stress-dimension relation were noted in IDC and normal subjects, although the line was displaced to the right in IDC. The slope of the circumferential end-systolic stress-dimension relation was, however, decreased in patients with IDC. Moreover, the end-systolic stress-fractional minor-axis shortening relation in patients with IDC was displaced downward from the normal relation supporting depressed contractile function in these IDC patients. Thus, the altered LV shape in IDC is reflected in an altered distribution of substantially elevated orthogonal stresses. Multiplanar stress-length and stress-shortening relations were useful in identifying depressed contractile function in IDC. These results allude to important considerations in the assessment of contractile function in disease states that result in altered LV shape.

Combined hemodynamic-ultrasonic method for studying left ventricular wall stress: Comparison with angiography

Calculation of left ventricular wall stress in man has traditionally required angiographic and left ventricular pressure measurement, making study of interventions difficult. We have developed a combined hemodynamic-ultrasonic technique for measuring left ventricular meridional wall stress ( σ m ) throughout the cardiac cycle. Simultaneous measurements of left ventricular pressure, ultrasonically determined wall thickness (h[echo]), and minor axis (D[echo]) were made during cardiac catheterization in nine subjects, three with chronic left ventricular pressure overload, four with left ventricular volume overload and two with normal left ventricular function. Within 30 minutes, left ventricular cineangiography was performed in each subject and angiographic wall thickness (h[angio]) and minor axis (D[angio]) were measured. Comparison of values for each subject throughout the cardiac cycle (average 18 data points/cycle) yielded close correlation: For D(echo) versus D(angio), r values ranged from 0.82 to 0.98 whereas for h(echo) versus h(angio), r values ranged from 0.56 to 0.98 for the nine subjects. Meridional wall stress was calculated after the method of Sandler and Dodge as PR i 2 h(2 R i + h ) , where R i equals the inner wall radius, calculated as D/2 for both ultrasonic and angiographic methods. Agreement between ultrasonic and angiographic methods was excellent in each subject, with close superimposition of the stresstime plots constructed by the different techniques. In summary, a new method for measurement of left ventricular wall stress has been developed and validated by comparison with an angiographic reference standard. This method has potential advantages, including the ability to study meridional wall stress continuously and to assess its response to serial interventions.