Ratio of end-systolic stress to end-systolic volume: is it a useful clinical tool?

Carabello, Blasé A.

doi:10.1016/0735-1097(89)90207-6

Cited by 27 publications

(11 citation statements)

References 19 publications

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“…The finding of an inverse correlation between LV area or length in the two‐chamber view and age in our study agrees with the findings of previous transthoracic studies that demonstrated a decrease in both end‐systolic and end‐diastolic sizes of the LV with increasing age [14,27]. In contrast to others [14], we did not find an increase in LV wall thickness with increasing age, an observation that may be related to the careful exclusion of patients with increased arterial pressure from our study and the limited number of elderly patients.…”

Section: Discussionsupporting

confidence: 93%

“…The two‐dimensional data (diameters, lengths and areas) were normalized for body surface area (BSA) and are presented as indices (I). In addition, the following functional variables were calculated: fractional area change (FAC %)=(EDA − ESA/EDA) × 100, stroke area index (SAI)=EDAI − ESAI, fractional diameter shortening (FS %)=(EDD − ESD/EDD) × 100, wall thickening (WT %)=(ESWT − EDWT/ESWT) × 100, velocity of circumferential fibre shortening (Vcfc)=[(EDC − ESC)/(EDC × LVET)] ×√RR [8,9], end‐systolic (meridional) wall stress (ESWS)=1.33 × SAP × ESA/TESA − ESA [10,11], stroke‐work index (SWI)=MAP × (EDAI − ESAI) [12], LV mass index (LVMI)=1.055 × 0.833 [(TESA × TEDL) − (ESA × EDL)]/BSA [6], relative wall thickness (RWT)=2 × EDWT/EDD [6], arterial stiffness index (ASI)=SAP − DAP/SAI [13], end‐systolic pressure/area ratio=SAP/ESA and end‐systolic wall stress/area ratio=ESWS/ESA [14].…”

Section: Methodsmentioning

confidence: 99%

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Reference values for left ventricular function in subjects under general anaesthesia and controlled ventilation assessed by two-dimensional transoesophageal echocardiography

et al. 2001

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Section: Discussionsupporting

confidence: 93%

Section: Methodsmentioning

confidence: 99%

Reference values for left ventricular function in subjects under general anaesthesia and controlled ventilation assessed by two-dimensional transoesophageal echocardiography

et al. 2001

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“…We do not have information about either ventricular preload or the response of ventricular elastance to manipulation of loading conditions in our individuals and thus we can not make precise inferences about left ventricular contractility on the basis of this estimate of E es . However, considering the single point-determined E es as an index of the ability of the left ventricle to empty opposed to a given pressure [42] instead of an intrinsic property of the cardiac muscle, we used this index in the evaluation of ventricularvascular coupling, as suggested in a previous study [34]. Both in normotensive and hypertensive individuals the E a aE es ratio was on average close to 0.50, similar to previously reported normal values [10,11] which indicate optimal ventricular±vascular coupling in the whole hypertensive group.…”

Section: Ventricular±vascular Coupling and Left Ventricular Function mentioning

confidence: 99%

Impact of arterial elastance as a measure of vascular load on left ventricular geometry in hypertension

Saba

Ganau

Devereux

et al. 1999

Journal of Hypertension

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aObjective Effective arterial elastance (E a ), integrating the pulsatile component of left ventricular (LV) afterload, is an estimate of aortic input impedance. We evaluated relationships of E a with left ventricular anatomy and function in essential hypertension.Design A cross-sectional analysis in 81 normotensive and 174 untreated hypertensive individuals enrolled in a referral hypertension centre.Methods Using echocardiography we determined left ventricular mass index (LVMI), relative wall thickness (RWT), stroke volume (SV), endocardial (FS e ) and midwall (FS m ) fractional shortening and total peripheral resistance (TPR). Carotid pressure waveforms were obtained by arterial tonometry, and end-systolic pressure (P es ) was measured at the dicrotic notch. E a index (E a I) was calculated as P es /(SV index); LV elastance (E es ) was estimated as P es /LV end-systolic volume, and ventriculo± arterial coupling was evaluated by the E a /E es ratio.Results E a I was higher in hypertensives than in normotensives (3.02 6 0.63 versus 2.40 6 0.52 mmHg/l per m 2 ; P < 0.0001). Using the 95% upper con®dence limit in normotensives, hypertensives were divided in two groups with normal or elevated E a I. The 38 hypertensives with elevated E a I had higher RWT (0.41 6 0.06 versus 0.37 6 0.05), lower LVMI (87.5 6 18.5 versus 96.8 6 19.3 g/m 2 ), higher TPR (2247 6 408 versus 1658 6 371 dynes/cm s 25 ) and lower FS e and FS m (35 6 5 versus 39 6 5 and 16 6 2 versus 18 6 2%; all P < 0.05) than patients with normal E a I. E a /E es ratio was increased and cardiac output was reduced in hypertensives with elevated E a I.Conclusions High values of E a I identify a minority of hypertensive patients characterized by elevated TPR, left ventricular concentric remodelling, depressed left ventricular systolic function and impaired ventriculo± arterial coupling.

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“…Recent studies suggest that although this ratio appears to be relatively independent of changes in preload, it may be significantly influenced by changes in end-systolic volume and end-systolic pressure, that is, nonproportional changes in afterload. [16][17][18][19][20] Mild to moderate concentric left ventricular hypertrophy is commonly reported in weight lifters, rowers, and other athletes engaged in power-based sports. [33][34][35][36] Presumably, left ventricular hypertrophy develops due to repeated acute increases in left ventricular afterload and wall stress that occurs during the pressor response to isometric exercise.…”

Section: Submaximal Versus Maximal Deadliftmentioning

confidence: 99%

Continuous measurement of left ventricular performance during and after maximal isometric deadlift exercise.

et al. 1992

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BACKGROUND Isometric exercise produces a reflex increase in arterial blood pressure that is proportional to the intensity and mass of muscle used during contraction. Little is known about the transient effects of heavy weight lifting on left ventricular performance. In this study, we measured continuous changes in left ventricular performance during maximal large-muscle isometric exercise using the standing deadlift position. METHODS AND RESULTS Ten healthy young men performed serial deadlifts at 50% of maximal voluntary effort for 90 seconds and 100% of maximal effort for 30 seconds. Echocardiographic imaging (apical four-chamber view), arterial blood pressure (brachial artery catheter), and electrocardiographic monitoring were recorded throughout the deadlift and for 30 seconds of recovery. Aortic flow velocity was also monitored during a separate series of deadlifts. During 100% maximal deadlift, mean arterial pressure increased from 108 +/- 4 to 164 +/- 6 mm Hg. Left ventricular ejection fraction declined initially (from 57 +/- 2% to 49 +/- 3%) at 15 seconds into the lift and recovered (56 +/- 1%) due to significant increases in end-diastolic volume (104 +/- 11 ml to 132 +/- 16 ml) by the end of the lift. The peak systolic pressure/end-systolic volume ratio did not change during the deadlift. After cessation of the deadlift, mean arterial pressure declined precipitously (to 88 +/- 4 mm Hg) within 5 seconds and gradually returned to baseline after 30 seconds. Left ventricular performance indexes all increased significantly during the recovery phase (ejection fraction to 68 +/- 3%, peak systolic pressure/end-systolic volume ratio to 5.9 +/- 0.9). Findings were qualitatively similar for the 50% deadlift. CONCLUSIONS During an intense isometric deadlift, left ventricular performance declines initially but is restored by the Frank-Starling mechanism. Upon release of the deadlift, increased left ventricular performance develops in conjunction with a rapid decrease in arterial pressure. The combined effects of increased wall stress during the lift phase and enhanced contractility during the release phase probably contribute to left ventricular hypertrophy associated with repetitive weight training.

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Ratio of end-systolic stress to end-systolic volume: is it a useful clinical tool?

Cited by 27 publications

References 19 publications

Reference values for left ventricular function in subjects under general anaesthesia and controlled ventilation assessed by two-dimensional transoesophageal echocardiography

Reference values for left ventricular function in subjects under general anaesthesia and controlled ventilation assessed by two-dimensional transoesophageal echocardiography

Impact of arterial elastance as a measure of vascular load on left ventricular geometry in hypertension

Continuous measurement of left ventricular performance during and after maximal isometric deadlift exercise.

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