LV end-systolic elastance (ELV in mm Hg/mL) is an indexof contractility that is load independent.29 It is determinedinvasively as follows: ELVLV end-systolic pressure/(endsystolic volumeV0), where V0 represents the volume (x axis)intercept of the end-systolic pressure-volume relationship.The noninvasive calculation is possible by 2 methods. In 1method, V0 is ignored (VO is less than end-systolic volume),ie, LV end-systolic pressure/end systolic volume. In the other,systolic and diastolic blood pressures, EF, stroke volume,preejection, and ejection periods are needed. Its normalresting value is 2.31 mm Hg/mL. Therefore, the EA/ELVratio is normally 1.00.36. EA and ELV increase proportionatelywith age in normal men, and their ratio remainsunchanged.30 Normal women show a higher increase in ELVwith age, so the ratio decreases slightly.31In hypertensive men, EA and ELV are greater than in normalcontrol subject, but their ratio remains normal. Hypertensivewomen develop a disproportionately greater increase in ELV,so their ratio is significantly lower than normal subjects.32 Inpatients with systolic heart failure, EA increases as a result ofincreased peripheral vascular resistance, whereas ELV is decreased.Thus, the EA/ELV ratio increases with reduced myocardialefficiency.33 In DHF, both EA and ELV increase, and in3 studies,34–36 the EA/ELV ratio was similar in DHF patientscompared with those with hypertension but not heart failure.Therefore, the consensus from the published literature supportsthe notion that abnormal ventricular-arterial coupling atrest is not the culprit for developing DHF. However, 1 studynoted a reduced vasodilator reserve with exercise37; additionaldata are needed during exercise for reliableconclusions.