Left ventricular distensibility and passive elastic stiffness in atrial septal defect

Abstract

Diminished left ventricular distensibility has been postulated as a cause of left ventricular failure in atrial septal defect. To evaluate this hypothesis the indexes of left ventricular compliance and stiffness were estimated in 15 patients with atrial septal defect and the results compared with those in 10 normal subjects. Age, peak left ventricular systolic pressure, end-diastolic pressure, ejection fraction and cardiac index did not differ significantly between groups. Left ventricular end-diastolic volume for the atrial septal defect group was significantly less than that for the control group (mean +/- SD, 61 +/- 9 ml/m2 versus 73 +/- 13, p less than 0.05) in keeping with previous studies. The slope of the log pressure-volume relation was significantly greater in the group with atrial septal defect than in the normal group (0.056 +/- 0.010 versus 0.044 +/- 0.008, p less than 0.01), consistent with increased chamber stiffness. For a group of six patients with atrial septal defect and elevated left ventricular end-diastolic pressure, normalized compliance was significantly less than that in the control group (0.017 +/- 0.001 versus 0.036 +/- 0.007, p less than 0.02). The slope k of the elastic stiffness-stress relation for the total group with atrial septal defect was significantly greater than that of the normal group (21.0 +/- 2.3 versus 18.1 +/- 2.3, p less than 0.01). An index of muscle fiber stretch (dV/VdP x end-diastolic stress x 100) was significantly less in the atrial septal defect group than in the control group (74 +/- 24 versus 106 +/- 22, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Abnormal cardiac inflow patterns during postnatal development in a mouse model of Holt-Oram syndrome

“…This finding is consistent with that in humans with ASD (3,6). This result also explains the fact that the long-term growth of Tbx5 mutants is not affected, probably because the normal systemic cardiac output is maintained.…”

“…In humans with ASD, right ventricular dilatation significantly alters left ventricular geometry (e.g., a flattened inter- ventricular septum toward the left ventricle at end systole and early diastole and decreased left ventricular chamber dimension), increases left ventricular chamber stiffness and reduces its compliance, and consequently impairs left ventricular filling (3,6,17). However, all these abnormalities are not associated with significant changes in the mitral flow pattern in patients with normal pulmonary pressure (21,30,34).…”

“…As seen in humans with right ventricular volume and/or pressure overload caused by ASD, left ventricular diastolic filling is impaired because of right heart dilatation and abnormal interaction of both ventricles (3,6,19,30). Because ASD and resultant right heart dilatation are the major structural anomalies in Tbx5 del/ϩ mice, it is of interest to explore the consequent functional abnormalities of this model compared with those in humans.…”

Pathophysiology of Congenital Heart Disease in the Adult

“…10 With similarly sized ASDs, therefore, adults tend to have larger shunts as they age. It is part of the reason why children are rarely symptomatic but patients in their fourth or fifth decade may begin to develop the symptoms frequently associated with ASD.…”

Fenestration of a Gore Helex Septal Occluder device in a patient with diastolic dysfunction of the left ventricle

“…Diastolic dysfunction of the left ventricle in the setting of atrial septal defect has been previously reported [5] and may be a consequence of diastolic ventricular interaction with constraint of left ventricular filling caused by right ventricular dilation [6]. This phenomenon is usually not clinically relevant in younger patients undergoing ASD closure as elasticity of the left ventricle can accommodate the extra preload following closure.…”