Author + information
- Received June 25, 1992
- Revision received October 26, 1992
- Accepted November 3, 1992
- Published online May 1, 1993.
- Otto N. Krogmann, MD∗,a,
- Spyros Rammos, MDa,
- Markus Jakob, MDa,∗,
- William J. Corin, MDa,∗,
- Otto M. Hess, MDa,∗ and
- Maurice Bourgeois, MDa
- ↵∗Address for correspondence: Otto N. Krogmann, MD, Department of Pediatric Cardiology, Heinrich-Heine University. Moorenstrasse 5, D-4000 Düsseldorf 1, Germany.
Objectives. Left ventricular systolic and diastolic function were evaluated late after successful operation for aortic coarctation in childhood.
Background. Persistent arterial hypertension and left ventricular hypertrophy after coarctation repair might impair left ventricular function.
Methods. Biplane angiography and simultaneous high fidelity pressure measurements were performed in 12 patients 3 to 12 years postoperatively (residual pressure gradient 4 mm Hg), Eight patients were normotensive and four had borderline hypertension. Data at rest and after nitroprusside infusion (1.7 μg/kg per min) were evaluated and compared with data from 12 control subjects.
Results. Systolic left ventricular function (ejection fraction-end-systolic wall stress relation) was normal in all patients. However, left ventricular muscle mass (113 vs. 86 g/m2), right atrial pressure (5.2 vs. 1.9 mm Hg) and left ventricular end-diastolic pressure (16 vs. 11 mm Hg) were significantly higher in patients than in control subjects. There was a linear relation between muscle mass and left ventricular end-diastolic (r = 0.66, p < 0.001) or right atrial (r = 0.60, p < 0.01) pressure. Left ventricular relaxation and myocardial stiffness were normal. However, there was an upward shift of the diastolic pressure-volume curve when compared with control values, but this shift was reversed by the administration of nitroprusside.
Conclusions. Systolic function is normal late after coarctation repair. However, diastolic function can be abnormal with an upward shift of the diastolic pressure-volume curve that is reversed by nitroprusside administration and is probably due to residual left ventricular hypertrophy.
- Received June 25, 1992.
- Revision received October 26, 1992.
- Accepted November 3, 1992.