Gregory Doucende

Alteration in left ventricular normal and shear strains evaluated by 2D-strain echocardiography in the athlete's heart

The contraction of cardiomyocytes induces a systolic increase in left ventricular (LV) normal (radial, circumferential and longitudinal) and shear strains, whose functional consequences have not been evaluated, so far, in athletes. We used 2D ultrasound speckle tracking imaging (STI) to evaluate LV regional strain in high‐level cyclists compared to sedentary controls. Sixteen male elite cyclists and 23 sedentary controls underwent conventional, tissue Doppler, and STI echocardiography at rest. We assessed LV long and short axis normal strains and shear strains. We evaluated circumferential–longitudinal shear strain from LV torsion, and circumferential–radial shear strain from the difference between subendocardial and subepicardial torsion. Apical radial strain (42.7 ± 10.5%versus 52.2 ± 14.3%, P < 0.05) and LV torsion (6.0 ± 1.8 deg versus 9.2 ± 3.2 deg, P < 0.01) were lower in cyclists than in controls, respectively. Rotations and torsion were higher in the subendocardial than in the subepicardial region in sedentary controls, but not in cyclists. Haemodynamic and tissue Doppler based indexes of global LV diastolic and systolic functions were not different between cyclists and controls. Athletes heart is associated with specific LV adaptation including lower apical strain and lower myocardial shear strains, with no change in global LV diastolic and systolic function. These mechanical alterations could improve the cardiovascular adjustments to exercise by increasing the radial strain and torsional (and thus untwisting) response to exercise, a key element of diastolic filling and thus of cardiac performance in athletes.

Alteration in Left Ventricular Strains and Torsional Mechanics After Ultralong Duration Exercise in Athletes

Background—Numerous studies have reported evidence of cardiac injury associated with transient left ventricular (LV) systolic and diastolic dysfunction after prolonged and strenuous exercise. We used 2D ultrasound speckle tracking imaging to evaluate the effect of an ultralong-duration exercise on LV regional strains and torsion. We speculated that systolic dysfunction after exercise is associated with depressed LV strains and torsion, and diastolic dysfunction results from decreased and delayed untwisting, a key factor of LV suction and early filling. Methods and Results—Twenty-three triathletes underwent conventional and speckle tracking imaging echocardiography at rest before and immediately after an ultralong distance triathlon. Measurements included LV longitudinal, circumferential and radial strains, LV rotations, and LV torsion. After the race, LV systolic dysfunction was characterized by a decrease in LV longitudinal, radial, and circumferential strains, especially for apical radial strains (44.6±15.1% versus 31.1±13.8%, P<0.001). Peak torsion was slightly decreased (8.3±5.1° versus 6.4±3.9°, respectively, P=0.09) and significantly delayed (91±18% versus 128±31% of systolic duration, P<0.001) beside end-ejection. Peak untwisting was also depressed and delayed beside isovolumic relaxation. Conclusions—This study documented major alterations in cardiac strains and torsion after an ultralong distance triathlon. LV systolic strains were depressed but not delayed, whereas twisting was decreased and delayed. This altered pattern hampered the rapid untwisting during isovolumic relaxation phase, reducing LV diastolic suction and early filling.

Kinetics of left ventricular strains and torsion during incremental exercise in healthy subjects: the key role of torsional mechanics for systolic-diastolic coupling.

Background—The dynamics of systolic and diastolic strains and torsional mechanics of the left ventricle (LV) and their relation to diastolic filling never have been evaluated at various exercise intensities. Methods and Results—Speckle tracking echocardiography was performed in 20 healthy sedentary subjects at rest and during a progressive submaximal exercise test at 20%, 30%, and 40% of maximal aerobic power. LV twist increased progressively with exercise intensity (10.5±3.2 to 15.8±4.5°; P<0.001), whereas longitudinal strain remained unchanged after the first workload, underlining the key role of torsional reserve in systolic-diastolic coupling during exercise. The increase in diastolic untwisting (−88.7±34.2 to −182.9±53.5 deg · s−1; P<0.01) was correlated to enhanced systolic twist (R=0.61; P<0.001), and its magnitude of increase was significantly higher compared to diastolic longitudinal and circumferential strain rates (119±64% versus 65±44% and 57±24%, respectively), emphasizing its contribution to diastolic filling. The timing of peak untwisting and the chronology of diastolic mechanical events were unchanged during effort. Untwisting was driven mainly by apical rotation and determined mitral opening and isovolumic relaxation time (R=0.47 and 0.61, respectively; P<0.001), whereas basal rotation and longitudinal and circumferential diastolic strain rates were major determinants of increased early diastolic filling (R=0.64, 0.79, and 0.81, respectively; P<0.001). Conclusions—The use of speckle tracking echocardiography gives new insights into physiological adaptive LV mechanics during incremental exercise in healthy subjects, underlining the key role of torsional mechanics. It might be useful to better understand the mechanisms of diastolic dysfunction and exercise intolerance in various pathological conditions.Background— The dynamics of systolic and diastolic strains and torsional mechanics of the left ventricle (LV) and their relation to diastolic filling never have been evaluated at various exercise intensities. Methods and Results— Speckle tracking echocardiography was performed in 20 healthy sedentary subjects at rest and during a progressive submaximal exercise test at 20%, 30%, and 40% of maximal aerobic power. LV twist increased progressively with exercise intensity (10.5±3.2 to 15.8±4.5°; P <0.001), whereas longitudinal strain remained unchanged after the first workload, underlining the key role of torsional reserve in systolic-diastolic coupling during exercise. The increase in diastolic untwisting (−88.7±34.2 to −182.9±53.5 deg · s−1; P <0.01) was correlated to enhanced systolic twist ( R =0.61; P <0.001), and its magnitude of increase was significantly higher compared to diastolic longitudinal and circumferential strain rates (119±64% versus 65±44% and 57±24%, respectively), emphasizing its contribution to diastolic filling. The timing of peak untwisting and the chronology of diastolic mechanical events were unchanged during effort. Untwisting was driven mainly by apical rotation and determined mitral opening and isovolumic relaxation time ( R =0.47 and 0.61, respectively; P <0.001), whereas basal rotation and longitudinal and circumferential diastolic strain rates were major determinants of increased early diastolic filling ( R =0.64, 0.79, and 0.81, respectively; P <0.001). Conclusions— The use of speckle tracking echocardiography gives new insights into physiological adaptive LV mechanics during incremental exercise in healthy subjects, underlining the key role of torsional mechanics. It might be useful to better understand the mechanisms of diastolic dysfunction and exercise intolerance in various pathological conditions.

Exercise Response in Hypertrophic Cardiomyopathy: Blunted Left Ventricular Deformational and Twisting Reserve with Altered Systolic-Diastolic Coupling

Background— Abnormal left ventricular (LV) deformational mechanics have been demonstrated in patients with hypertrophic cardiomyopathy (HCM) at rest, but there is a lack of information on their adaptation to exercise. The aim of this study was to assess the adaptability of LV strains and torsional mechanics during exercise in HCM patients. Methods and Results— Twenty nonobstructive HCM patients (age, 48.3±12.3 years; 14 men) and 20 control subjects underwent speckle-tracking echocardiographic measurement of longitudinal, radial, and circumferential strains, systolic twist, and diastolic untwisting rate (UTR) at rest and submaximal exercise. HCM patients showed lower resting longitudinal (−15.7±5.0% versus −19.4±2.6%, P<0.001) and radial (38.1±11.3% versus 44.7±14.4%, P<0.05) strains but higher circumferential strain (−21.9±4.0% versus −18.8±2.3%, P<0.05) and twist (15.7±3.6° versus 9.3±2.6°, P<0.0001) than control subjects. Exercise induced an increase in all strains in control subjects but only a moderate increase in longitudinal strain (to −18.4±5.0%), without significant changes in radial and circumferential strains or twist in HCM patients. Exercise peak UTR was lower (−119.0±31.5°/s versus −137.3±41.1°/s) and occurred later (137±18% versus 125±11% systolic time, P<0.05) in HCM than in control subjects. A significant relationship between twist and UTR was obtained in control subjects (ß=−0.0807, P<0.001) but not in HCM patients (ß=−0.0051, P=0.68). Conclusions— HCM patients had severely limited strain adaptability and no LV twisting reserve at exercise. They had reduced and delayed UTR with reduced systolic-diastolic coupling efficiency by twist-untwist mechanics.Background— Abnormal left ventricular (LV) deformational mechanics have been demonstrated in patients with hypertrophic cardiomyopathy (HCM) at rest, but there is a lack of information on their adaptation to exercise. The aim of this study was to assess the adaptability of LV strains and torsional mechanics during exercise in HCM patients. Methods and Results— Twenty nonobstructive HCM patients (age, 48.3±12.3 years; 14 men) and 20 control subjects underwent speckle-tracking echocardiographic measurement of longitudinal, radial, and circumferential strains, systolic twist, and diastolic untwisting rate (UTR) at rest and submaximal exercise. HCM patients showed lower resting longitudinal (−15.7±5.0% versus −19.4±2.6%, P <0.001) and radial (38.1±11.3% versus 44.7±14.4%, P <0.05) strains but higher circumferential strain (−21.9±4.0% versus −18.8±2.3%, P <0.05) and twist (15.7±3.6° versus 9.3±2.6°, P <0.0001) than control subjects. Exercise induced an increase in all strains in control subjects but only a moderate increase in longitudinal strain (to −18.4±5.0%), without significant changes in radial and circumferential strains or twist in HCM patients. Exercise peak UTR was lower (−119.0±31.5°/s versus −137.3±41.1°/s) and occurred later (137±18% versus 125±11% systolic time, P <0.05) in HCM than in control subjects. A significant relationship between twist and UTR was obtained in control subjects (s=−0.0807, P <0.001) but not in HCM patients (s=−0.0051, P =0.68). Conclusions— HCM patients had severely limited strain adaptability and no LV twisting reserve at exercise. They had reduced and delayed UTR with reduced systolic-diastolic coupling efficiency by twist-untwist mechanics.

Phlebotomy eliminates the maximal cardiac output response to six weeks of exercise training

With this study we tested the hypothesis that 6 wk of endurance training increases maximal cardiac output (Qmax) relatively more by elevating blood volume (BV) than by inducing structural and functional changes within the heart. Nine healthy but untrained volunteers (Vo2max 47 ± 5 ml·min(-1)·kg(-1)) underwent supervised training (60 min; 4 times weekly at 65% Vo2max for 6 wk), and Qmax was determined by inert gas rebreathing during cycle ergometer exercise before and after the training period. After the training period, blood volume (determined in duplicates by CO rebreathing) was reestablished to pretraining values by phlebotomy and Qmax was quantified again. Resting echography revealed no structural heart adaptations as a consequence of the training intervention. After the training period, plasma volume (PV), red blood cell volume (RBCV), and BV increased (P < 0.05) by 147 ± 168 (5 ± 5%), 235 ± 64 (10 ± 3%), and 382 ± 204 ml (7 ± 4%), respectively. Vo2max was augmented (P < 0.05) by 10 ± 7% after the training period and decreased (P < 0.05) by 8 ± 7% with phlebotomy. Concomitantly, Qmax was increased (P < 0.05) from 18.9 ± 2.1 to 20.4 ± 2.3 l/min (9 ± 6%) as a consequence of the training intervention, and after normalization of BV by phlebotomy Qmax returned to pretraining values (18.1 ± 2.5 l/min; 12 ± 5% reversal). Thus the exercise training-induced increase in BV is the main mechanism increasing Qmax after 6 wk of endurance training in previously untrained subjects.

β-Adrenergic receptors desensitization is not involved in exercise-induced cardiac fatigue: NADPH oxidase-induced oxidative stress as a new trigger

Prolonged strenuous exercise (PSE) induces transient left ventricular (LV) dysfunction. Previous studies suggest that β-adrenergic pathway desensitization could be involved in this phenomenon, but it remains to be confirmed. Moreover, other underlying mechanisms involving oxidative stress have been recently proposed. The present study aimed to evaluate the involvement of both the β-adrenergic pathway and NADPH oxidase (Nox) enzyme-induced oxidative stress in myocardial dysfunction in rats following PSE. Rats were divided into 4 groups: controls (Ctrl), 4-h exercised on treadmill (PSE), and 2 groups in which Nox enzyme was inhibited with apocynin treatment (Ctrl APO and PSE APO, respectively). We evaluated cardiac function in vivo and ex vivo during basal conditions and isoproterenol stress. GSH/GSSG ratio, cardiac troponin I (cTnI) release, and lipid peroxidation (MDA) were evaluated. PSE induced a decrease in LV developed pressure, intrinsic myocardial contractility, and relaxation associated with an increase in plasma cTnI release. Our in vivo and ex vivo results demonstrated no differences in myocardial response to isoproterenol and of effective dose 50 between control and PSE rats. Interestingly, the LV dysfunction was reversed by apocynin treatment. Moreover, apocynin prevented cellular oxidation [GSH/GSSG ratio: PSE APO rats vs. PSE rats in arbitrary units (au): 1.98 ± 0.07 vs. 1.35 ± 0.10; P < 0.001]. However, no differences in MDA were observed between groups. These data suggest that myocardial dysfunction observed after PSE was not due to β-adrenergic receptor desensitization but could be due to a signaling oxidative stress from the Nox enzyme.

Time course of asymptomatic interstitial pulmonary oedema at high altitude.

The time course of asymptomatic pulmonary oedema during high-altitude exposure and its potential relationship with changes in cardiac function remain to clarify. Eleven volunteers were rapidly exposed to 4350m during a 4-day period. Each subject received clinical examination and thoracic ultrasonography to assess ultrasound lung comets (USLC) on day 1, 2 and 3 after arrival. Echocardiography was performed on day 2 and 4 at 4350m. All subjects had a significant increase in the number of USLC on day 1 (n=8±3), day 2 (n=7±4) and day 3 (n=3±2) compared to sea level (n=1±1) (P<0.01). Although left ventricle diastolic function and systolic tricuspid regurgitation gradient were significantly different at altitude compared to sea level, they did not correlate with the number of USLC (P>0.05). Asymptomatic pulmonary oedema seems to be transiently present in fast-ascending recreational climbers. The lack of correlation between the number of USLC and indices of cardiac changes suggest that non-cardiogenic mechanisms may underlie this transient increase in lung water.

Exercise Response in Hypertrophic CardiomyopathyClinical Perspective

Background— Abnormal left ventricular (LV) deformational mechanics have been demonstrated in patients with hypertrophic cardiomyopathy (HCM) at rest, but there is a lack of information on their adaptation to exercise. The aim of this study was to assess the adaptability of LV strains and torsional mechanics during exercise in HCM patients. Methods and Results— Twenty nonobstructive HCM patients (age, 48.3±12.3 years; 14 men) and 20 control subjects underwent speckle-tracking echocardiographic measurement of longitudinal, radial, and circumferential strains, systolic twist, and diastolic untwisting rate (UTR) at rest and submaximal exercise. HCM patients showed lower resting longitudinal (−15.7±5.0% versus −19.4±2.6%, P<0.001) and radial (38.1±11.3% versus 44.7±14.4%, P<0.05) strains but higher circumferential strain (−21.9±4.0% versus −18.8±2.3%, P<0.05) and twist (15.7±3.6° versus 9.3±2.6°, P<0.0001) than control subjects. Exercise induced an increase in all strains in control subjects but only a moderate increase in longitudinal strain (to −18.4±5.0%), without significant changes in radial and circumferential strains or twist in HCM patients. Exercise peak UTR was lower (−119.0±31.5°/s versus −137.3±41.1°/s) and occurred later (137±18% versus 125±11% systolic time, P<0.05) in HCM than in control subjects. A significant relationship between twist and UTR was obtained in control subjects (ß=−0.0807, P<0.001) but not in HCM patients (ß=−0.0051, P=0.68). Conclusions— HCM patients had severely limited strain adaptability and no LV twisting reserve at exercise. They had reduced and delayed UTR with reduced systolic-diastolic coupling efficiency by twist-untwist mechanics.Background— Abnormal left ventricular (LV) deformational mechanics have been demonstrated in patients with hypertrophic cardiomyopathy (HCM) at rest, but there is a lack of information on their adaptation to exercise. The aim of this study was to assess the adaptability of LV strains and torsional mechanics during exercise in HCM patients. Methods and Results— Twenty nonobstructive HCM patients (age, 48.3±12.3 years; 14 men) and 20 control subjects underwent speckle-tracking echocardiographic measurement of longitudinal, radial, and circumferential strains, systolic twist, and diastolic untwisting rate (UTR) at rest and submaximal exercise. HCM patients showed lower resting longitudinal (−15.7±5.0% versus −19.4±2.6%, P <0.001) and radial (38.1±11.3% versus 44.7±14.4%, P <0.05) strains but higher circumferential strain (−21.9±4.0% versus −18.8±2.3%, P <0.05) and twist (15.7±3.6° versus 9.3±2.6°, P <0.0001) than control subjects. Exercise induced an increase in all strains in control subjects but only a moderate increase in longitudinal strain (to −18.4±5.0%), without significant changes in radial and circumferential strains or twist in HCM patients. Exercise peak UTR was lower (−119.0±31.5°/s versus −137.3±41.1°/s) and occurred later (137±18% versus 125±11% systolic time, P <0.05) in HCM than in control subjects. A significant relationship between twist and UTR was obtained in control subjects (s=−0.0807, P <0.001) but not in HCM patients (s=−0.0051, P =0.68). Conclusions— HCM patients had severely limited strain adaptability and no LV twisting reserve at exercise. They had reduced and delayed UTR with reduced systolic-diastolic coupling efficiency by twist-untwist mechanics.

Exercise Response in Hypertrophic CardiomyopathyClinical Perspective: Blunted Left Ventricular Deformational and Twisting Reserve With Altered Systolic-Diastolic Coupling

Background— Abnormal left ventricular (LV) deformational mechanics have been demonstrated in patients with hypertrophic cardiomyopathy (HCM) at rest, but there is a lack of information on their adaptation to exercise. The aim of this study was to assess the adaptability of LV strains and torsional mechanics during exercise in HCM patients. Methods and Results— Twenty nonobstructive HCM patients (age, 48.3±12.3 years; 14 men) and 20 control subjects underwent speckle-tracking echocardiographic measurement of longitudinal, radial, and circumferential strains, systolic twist, and diastolic untwisting rate (UTR) at rest and submaximal exercise. HCM patients showed lower resting longitudinal (−15.7±5.0% versus −19.4±2.6%, P<0.001) and radial (38.1±11.3% versus 44.7±14.4%, P<0.05) strains but higher circumferential strain (−21.9±4.0% versus −18.8±2.3%, P<0.05) and twist (15.7±3.6° versus 9.3±2.6°, P<0.0001) than control subjects. Exercise induced an increase in all strains in control subjects but only a moderate increase in longitudinal strain (to −18.4±5.0%), without significant changes in radial and circumferential strains or twist in HCM patients. Exercise peak UTR was lower (−119.0±31.5°/s versus −137.3±41.1°/s) and occurred later (137±18% versus 125±11% systolic time, P<0.05) in HCM than in control subjects. A significant relationship between twist and UTR was obtained in control subjects (ß=−0.0807, P<0.001) but not in HCM patients (ß=−0.0051, P=0.68). Conclusions— HCM patients had severely limited strain adaptability and no LV twisting reserve at exercise. They had reduced and delayed UTR with reduced systolic-diastolic coupling efficiency by twist-untwist mechanics.Background— Abnormal left ventricular (LV) deformational mechanics have been demonstrated in patients with hypertrophic cardiomyopathy (HCM) at rest, but there is a lack of information on their adaptation to exercise. The aim of this study was to assess the adaptability of LV strains and torsional mechanics during exercise in HCM patients. Methods and Results— Twenty nonobstructive HCM patients (age, 48.3±12.3 years; 14 men) and 20 control subjects underwent speckle-tracking echocardiographic measurement of longitudinal, radial, and circumferential strains, systolic twist, and diastolic untwisting rate (UTR) at rest and submaximal exercise. HCM patients showed lower resting longitudinal (−15.7±5.0% versus −19.4±2.6%, P <0.001) and radial (38.1±11.3% versus 44.7±14.4%, P <0.05) strains but higher circumferential strain (−21.9±4.0% versus −18.8±2.3%, P <0.05) and twist (15.7±3.6° versus 9.3±2.6°, P <0.0001) than control subjects. Exercise induced an increase in all strains in control subjects but only a moderate increase in longitudinal strain (to −18.4±5.0%), without significant changes in radial and circumferential strains or twist in HCM patients. Exercise peak UTR was lower (−119.0±31.5°/s versus −137.3±41.1°/s) and occurred later (137±18% versus 125±11% systolic time, P <0.05) in HCM than in control subjects. A significant relationship between twist and UTR was obtained in control subjects (s=−0.0807, P <0.001) but not in HCM patients (s=−0.0051, P =0.68). Conclusions— HCM patients had severely limited strain adaptability and no LV twisting reserve at exercise. They had reduced and delayed UTR with reduced systolic-diastolic coupling efficiency by twist-untwist mechanics.

Kinetics of Left Ventricular Strains and Torsion During Incremental Exercise in Healthy SubjectsClinical Perspective: The Key Role of Torsional Mechanics for Systolic-Diastolic Coupling

Background—The dynamics of systolic and diastolic strains and torsional mechanics of the left ventricle (LV) and their relation to diastolic filling never have been evaluated at various exercise intensities. Methods and Results—Speckle tracking echocardiography was performed in 20 healthy sedentary subjects at rest and during a progressive submaximal exercise test at 20%, 30%, and 40% of maximal aerobic power. LV twist increased progressively with exercise intensity (10.5±3.2 to 15.8±4.5°; P<0.001), whereas longitudinal strain remained unchanged after the first workload, underlining the key role of torsional reserve in systolic-diastolic coupling during exercise. The increase in diastolic untwisting (−88.7±34.2 to −182.9±53.5 deg · s−1; P<0.01) was correlated to enhanced systolic twist (R=0.61; P<0.001), and its magnitude of increase was significantly higher compared to diastolic longitudinal and circumferential strain rates (119±64% versus 65±44% and 57±24%, respectively), emphasizing its contribution to diastolic filling. The timing of peak untwisting and the chronology of diastolic mechanical events were unchanged during effort. Untwisting was driven mainly by apical rotation and determined mitral opening and isovolumic relaxation time (R=0.47 and 0.61, respectively; P<0.001), whereas basal rotation and longitudinal and circumferential diastolic strain rates were major determinants of increased early diastolic filling (R=0.64, 0.79, and 0.81, respectively; P<0.001). Conclusions—The use of speckle tracking echocardiography gives new insights into physiological adaptive LV mechanics during incremental exercise in healthy subjects, underlining the key role of torsional mechanics. It might be useful to better understand the mechanisms of diastolic dysfunction and exercise intolerance in various pathological conditions.Background— The dynamics of systolic and diastolic strains and torsional mechanics of the left ventricle (LV) and their relation to diastolic filling never have been evaluated at various exercise intensities. Methods and Results— Speckle tracking echocardiography was performed in 20 healthy sedentary subjects at rest and during a progressive submaximal exercise test at 20%, 30%, and 40% of maximal aerobic power. LV twist increased progressively with exercise intensity (10.5±3.2 to 15.8±4.5°; P <0.001), whereas longitudinal strain remained unchanged after the first workload, underlining the key role of torsional reserve in systolic-diastolic coupling during exercise. The increase in diastolic untwisting (−88.7±34.2 to −182.9±53.5 deg · s−1; P <0.01) was correlated to enhanced systolic twist ( R =0.61; P <0.001), and its magnitude of increase was significantly higher compared to diastolic longitudinal and circumferential strain rates (119±64% versus 65±44% and 57±24%, respectively), emphasizing its contribution to diastolic filling. The timing of peak untwisting and the chronology of diastolic mechanical events were unchanged during effort. Untwisting was driven mainly by apical rotation and determined mitral opening and isovolumic relaxation time ( R =0.47 and 0.61, respectively; P <0.001), whereas basal rotation and longitudinal and circumferential diastolic strain rates were major determinants of increased early diastolic filling ( R =0.64, 0.79, and 0.81, respectively; P <0.001). Conclusions— The use of speckle tracking echocardiography gives new insights into physiological adaptive LV mechanics during incremental exercise in healthy subjects, underlining the key role of torsional mechanics. It might be useful to better understand the mechanisms of diastolic dysfunction and exercise intolerance in various pathological conditions.