Recovery of the Frank-Starling mechanism by coenzyme Q10 in patients with load-induced contractility depression

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Abstract
Summary Load-induced contractility depression, in which supernormal left ventricular ejection fraction and contractility at rest decrease by added afterload, is most often found in children with mitral valve prolapse who have symptoms. Patients have high ventricular end-diastolic pressure at rest, which is further increased by afterload challenge. The Frank-Starling mechanism may be maximally mobilized with high preload even at rest to compensate for the intrinsically depressed inotropic state. Therefore, preload reserve may be easily exhausted due to afterload addition. We aimed to determine left ventricular end-diastolic fiber length, stroke work, and contractility before and during handgrip by echocardiograms to obtain evidence for the Frank-Starling mechanism in patients and controls, including patients treated with coenzyme Q10. The subjects were divided into four groups, each consisting of 30 children aged 6–16 years group 1, normals; group 2, patients; group 3, the same patients as in group 2 after coenzyme Q10 therapy; and group 4, patients with asymptomatic mitral valve prolapse. Baseline values and percentage increases in systolic blood pressure, heart rate, and left ventricular wall stress showed no differences among the groups. Only in group 2 were the percentage increase in ejection fraction, fiber shortening velocity, contractility, and end-diastolic dimension strongly negative, despite supernormal baseline levels. In other groups, these were significantly positive, without intergroup differences. We conclude that in the heart with load-induced contractility depression, the Frank-Starling mechanism deviates from normal. The normal Frank-Starling mechanism was recovered due to coenzyme Q10 which may improve disturbed bioenergetic function at the molecular level.