Preservation of the end-systolic pressure/end-systolic dimension relation following pindolol in congestive heart failure

Binkley, Philip F.; Lewe, Robert F.; Unverferth, Donald V.; Leier, Carl V.

doi:10.1016/0002-8703(88)90016-6

Cited by 6 publications

(1 citation statement)

References 31 publications

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“…In a 7th patient, both end-systolic volume and end-systolic di mension changed inappropriately with increasing endsystolic pressure. In 2 other series of patients using the end-systolic pressure-dimension relationship in dilated cardiomyopathy, both of which contained small num bers of patients, the slope of the relationship has been appropriate and remained appropriate after an interven tion [29,30].…”

Section: At Atmentioning

confidence: 99%

Limitations of the End-Systolic Pressure-Diameter Relationship in Patients with Severe Congestive Heart Failure

Rahko¹,

Orie²,

Miller³

et al. 1990

Am J Noninvas Cardiol

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The purpose of this study was to evaluate the usefulness of the end-systolic pressure-volume relationship, the end-systolic pressure-dimension relationship and the end-systolic wall stress-mean rate corrected velocity of circumferential fiber shortening relationship in patients with severe congestive heart failure due to a dilated cardiomyopathy. In the 18 patients evaluated, ejection fraction was significantly reduced at 26 ± 11% (mean ± SD). Left ventricular volume was measured by radionuclide ventriculography and dimension by echocardiography. Systolic pressure was increased with phenylephrine to obtain three levels of end-systolic pressure. In 17/18 patients end-systolic volume increased with increasing end-systolic pressure but there was a poor correlation of the slope of the end-systolic pressure-volume relationship with all other indices of left ventricular function. For a similar increase in end-systolic pressure, end-systolic dimension increased in only 11/18 patients. In the remainder, end-systolic dimension either failed to change or decreased. The change in end-systolic volume correlated poorly with the change in end-systolic dimension (r = 0.11). For the end-systolic wall stress-velocity relationship, 13/18 appropriately decreased their ratecorrected mean velocity of circumferential fiber shortening with increasing end-systolic wall stress. In the other 5 patients, the shortening velocity changed inappropriately. All of these patients also had an inappropriate change in end-systolic dimension with increasing end-systolic pressure. Comparing the 7 patients with an inappropriate change in end-systolic dimension slope to the other 11, the group with an inappropriate response had a greater end-diastolic volume index (115 ± 21 vs. 79 ± 24 ml/m^2, p = 0.006), a greater end-systolic volume index (90 ± 25 vs. 58 ± 23 ml/m^2, p = 0.02), greater end-systolic wall stress (121 ± 33 vs. 88 ± 21 g/cm^2, p = 0.02) and greater end-systolic dimension (65 ± 14 vs. 54 ± 8 mm, p = 0.05). We conclude that the end-systolic pressure-dimension and stress-velocity relationships derived using a short-axis dimension are not reliable in patients with severe congestive heart failure due to a dilated cardiomyopathy. This is particularly true in very dilated left ventricles. The end-systolic pressure-volume relationship derived by radionuclide angiography is superior to the pressure-dimension and stress-velocity relationships in that it changes appropriately in most patients with severe congestive heart failure. However, the slope of this relationship has no easily defined correlation with ejection phase measurements of left ventricular function.

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Section: At Atmentioning

confidence: 99%