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The systolic arterial pressure/end-systolic volume relationship in patients with severe left ventricular dysfunction

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Abstract

Performance of the intact left ventricle is well-defined by the end-systolic pressure/end-systolic volume relationship that appears independent of preload and afterload. To determine whether noninvasive measurements of this relationship could distinguish normal from abnormal subjects, we evaluated the relationship between arterial systolic pressure (determined by cuff sphygnonanometry) and radionuclide estimates of end-systolic volume in 12 normal subjects and 24 patients with severe left ventricular dysfunction. Data were acquired at rest, after atropine injection, and then during at least three increments of arterial pressure (average total increase approximately 45 mm Hg) using phenylephrine.

The relationship between peak-systolic pressure (SP) and end-systolic volume (ESV) was found to be linear in all subjects (r≧0.91). The slope of this line was steeper in normal subjects than in myopathic patients (73±21.7 vs 20.8±8.7 mm Hg/volume unit/m2,P<0.001) and the zero pressure intercept also was greater (49.8±30 mm Hg vs 27.1±44.2 mm Hg,P<0.01). Similarly, resting ejection fraction (EF) was greater in the normals (0.71±0.88 vs 0.21±0.07%P<0.001) and end-diastolic volume (EDV) was smaller (4.14±0.88 vs 6.58±0.65 volume units,P<0.01).

Systolic pressure/end-systolic volume relationship determined by these noninvasive methods was linear in both patients with severely reduced cardiac function and normal control subjects, clearly distinguishing normal from severely impaired left ventricles. This noninvasively determined pressure-volume relationship may be a useful index to identify patients who may benefit from inotropic agents—to regulate their long-term inotropic therapy-and possibly to distinguish inotropic vs vasodilator effects on the heart.

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Slutsky, R.A., Watkins, J. & Engler, R. The systolic arterial pressure/end-systolic volume relationship in patients with severe left ventricular dysfunction. Cardiovasc Intervent Radiol 7, 59–64 (1984). https://doi.org/10.1007/BF02552680

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