[Noninvasive assessment of wall stress related velocity of circumferential fiber shortening as an index of left ventricular contractility in children].
Assessment of the myocardial contractility in terms of the velocity of circumferential fiber shortening appropriate to the actual left ventricular endsystolic wall stress requires endsystolic pressure measurement usually done invasively. But for noninvasive evaluation of this parameter, we elaborated an algorithm to derive the endsystolic pressure in the ascending aorta from oscillometric blood pressure measurements. In 99 infants, children, adolescents, and young adults (1 day-37 years, median 5.5 years) we performed direct pressure recordings in the ascending aorta while measuring the arterial blood pressure at the upper arm by the Dinamap 8100 Blood Pressure Monitor. If measured directly, endsystolic (ESP(direct)) and mean aortic pressure (MAP(direct)) correlated well: ESP(direct)) = 1, 04 * MAP(direct))-2.18; r(2) = 0.91; s(y.x.) = 5.1 mm Hg. Comparison between the endsystolic and the mean arterial pressure (MAP(Dinamap) resulted in: ESP(direct) = 1.19 * MAP(Dinamap)-4.8; r(2) = 0.74; s(y. x.) = 8.3 mm Hg. In 52 patients this equation was used to derive the endsystolic pressure from the mean arterial pressure. Then the endsystolic wall stress was determined using the calculated (ESSm(Dinamap)) as well as the directly measured endsystolic pressure (ESSm(direct)): mean difference (ESSm(Dinamap) - ESSm(direct)) = -2.1 kdyn/cm(2); 95% confidence limits: -16.2 to 12. 1 kdyn/cm(2); linear regression: ESSm(direct = 1.07 * ESSm(Dinamap) - 2.22; r(2) = 0.91; s(y.x.) = 7.1 kdyn/cm(2). In n = 12 infants with complex heart defects and severe congestive heart failure due to pulmonary hyperperfusion the contractility was monitored noninvasively to assess the effects of propranolol (1.5 to 2 mg/kg/day) given complementary to digoxin and diuretics. The advantage of noninvasive assessment of the contractility in clinical routine was confirmed by the result that long-term propranolol does not impair myocardial contractility in this setting.
Wessel
A
A
Klinik für Pädiatrische Kardiologie, Georg-August-Universität Göttingen, Robert-Koch-Str. 40, D-37075 Göttingen.
Buchhorn
R
R
Löber
M
M
Eigster
G
G
Hulpke-Wette
M
M
Bürsch
J
J
D000293:Adolescent; D000328:Adult; D000465:Algorithms; D001794:Blood Pressure / Q000502:physiology; D002648:Child; D002675:Child, Preschool; D005260:Female; D006330:Heart Defects, Congenital / Q000175:diagnosis* / Q000503:physiopathology; D006333:Heart Failure / Q000175:diagnosis* / Q000503:physiopathology; D006801:Humans; D006976:Hypertension, Pulmonary / Q000175:diagnosis / Q000503:physiopathology; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology*; D009991:Oscillometry; D012016:Reference Values; D013599:Systole / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis* / Q000503:physiopathology; D016277:Ventricular Function, Left / Q000502:physiology*