By Charles R. McKay, Shahbudin H. Rahimtoola (auth.), William H. Gaasch, Herbert J. Levine (eds.)
Sir Dominic Corrigan's vintage monograph "On everlasting Patency of the Mouth of the Aorta, or Inadequacy of the Aortic Valves" was once released in 1832. Descriptions of aortic regurgitation had formerly been released via others, yet Corrigan's contribution was once so finished that his identify remains to be heavily linked to this sickness. He defined the actual findings and the underlying gross pathologic anatomy of aortic regurgitation. He famous that surprising dying was once now not attribute of aortic regurgitation, because it was once in aortic stenosis, and his healing technique used to be in accordance with enterprise physiologic ideas. some time past one hundred fifty years we have now accelerated Corrigan's paintings, and we've got constructed an in depth appreciation of the common heritage, pathophysiology, diagnostic equipment, and remedy of power aortic regurgitation. Fifteen years in the past, cardiac catheterization and angiography had already completed frequent software within the review of aortic regurgitation, yet cardiac ultrasound, specially Doppler echocardiography, used to be in its infancy, and the application of radionuclide ventriculography used to be now not greatly appreciated.
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While increasing preload increases the strength of contraction and thus the amount of stroke work performed, shortening is halted at the same volume by the same end-systolic afterload if contractile state remains the same. End-systolic volume, while independent of preload, is dependent upon afterload and contractile state. As afterload increases at a given contractile state, the ventricle shortens less completely and end-systolic volume increases. As shown in Figure 3-2, the relationship between end-systolic afterload and end-systolic dimension (or volume) is linear [6,7, 10].
However, these studies of contractile function in aortic regurgitation must be interpreted with the previously noted limitation of the ESR in chronic eccentric hypertrophy in mind. The study by Schuler and coworkers  demonstrated a reduced slope of the end-systolic relationship of patients who had abnormal exercise ejection fractions. Since the end-diastolic volume index was similar in the group with the reduced slope, as well as in the group with normal slope, it is unlikely that it was eccentric hypertrophy and increased sarcomere number that caused the difference in slope.
The increased endsystolic volume could cause the slope of the ESR to be reduced, improperly suggesting reduced contractile function. Thus, it appears necessary to correct the ESR in situations where it is thought that eccentric hypertrophy has occurred. However, no unanimity currently exists on how to correct the relationship. Some investigators have suggested correction by multiplying the slope of the ESR by end-diastolic volume. This would account for the addition of series sarcomeres. However, end-diastolic volume could increase not just because of addition of sarcomeres in series but also due to increased fiber stretch (preload).