Steffen P. Schoen

Continuity equation to evaluate aortic valve area (AVA(CE)) is critically dependent on accurate measurement of left ventricular outflow tract diameter and velocity. To circumvent these limitations, the present study aimed to generate nomograms for a facilitated estimation of aortic valve area using peak aortic valve pressure gradient (DeltapAv) and left ventricular ejection fraction (LVEF). Two hundred and fifty-five subjects with non-invasively and invasively defined aortic valve stenosis (AS) formed the basis of this study. Basis of the nomograms was the correlation analysis between DeltapAv and AVA as estimated by AVA(CE) within different LVEF groups. LVEF differed from 65.6 +/- 1.8% (Group I, LVEF > 60%) to 34.5 +/- 4.3% (Group IV, LVEF > or = 30%). DeltapAv and AVA varied from 85.6 +/- 19.5 mmHg and 0.69 +/- 0.16 cm2 in Group I to 58.5 +/- 15.9 mmHg and 0.73 +/- 0.23 cm2 in Group IV (DeltapAv: P < 0.001). Mean AVA(CE) showed no significant difference between the groups. Correlation between DeltapAv and AVA(CE) was statistically significant with P < 0.001 in all subgroups (R2 between 0.72 and 0.76). Furthermore, a prospective estimation of AVA using the developed nomograms correlated very well with invasively determined AS using the Gorlin formula (R2 = 0.76, SEE = 0.21 cm2, bias 0.04 cm2). The present study has established and confirmed a solid, easy to use nomogram-based method to accurately quantify severe AS.

A 73-year-old man presented to the emergency department with dyspnea of 2 days duration. Auscultation of the precordium was notable for a grade 2/6 systolic murmur. Echocardiography revealed a highly impaired left ventricular function and a calcified aortic valve stenosis with a mean pressure gradient of 25 mmHg and a valve area of 0.8 cm². Eye-catching was a thickened mid-ventricular and apical myocardium with a spongy appearance. On magnetic resonance imaging (MRI) multiple, prominent muscular trabeculations of the left ventricular myocardium (white arrows) with deep intertrabecular recesses were evident (Panel A, LV: left ventricle, LA: left atrium). These findings were consistent with non-compaction cardiomyopathy with accompanying low-gradient aortic valve stenosis. The patient underwent mechanical aortic valve replacement, during which the spongy left ventricular myocardium was visualized by video endoscopy (Panel B). The histological workup of an endomyocardial biopsy specimen showed irregular heart muscle fibres with vacuolar changes and large chromatin-dense nuclei as well as moderate interstitial fibrosis (Panel C, haematoxylin and eosin staining, magnification: original ×20). The patient made a full recovery and was discharged on heart failure medication and oral anticoagulation. Screening of first-degree relatives by MRI revealed left ventricular non-compaction with a preserved ejection fraction in the patient's asymptomatic son (Panel D, LV: left ventricle, LA: left atrium).

Background: In recent years percutaneous, transcatheter closure of atrial septal defects (ASD) or patent foramen ovale (PFO) was introduced into clinical practice. Objective: To investigate the functional effects on heart valves caused by an interatrial closure device. Methods and results: Between 2001 and 2006, 240 consecutive patients underwent percutaneous closure of an ASD or a PFO. Heart valve functions were defined by transoesophageal echocardiography before implantation and 3, 6 and 12 months after defect closure. A successful implantation procedure was performed in 98% of patients. Sufficient closure without residual shunt was achieved in 89% of patients with ASD and in 92% of patients with PFO. An overall major complication rate of 0.8% was apparent during the observation time (mean (SD) 27 (15) months). Long-term follow-up disclosed newly developed or worsened aortic valve regurgitation (AR) in 9% of patients with ASD and in 10% of patients with PFO. A potential cause for developing AR may be overgrowth of the device by tissue, leading to changes in interatrial septal geometry and traction on the root of the non-coronary aortic cusp. Conclusion: AR occurred in 9% of patients with closed ASD and in 10% of patients with closed PFO. Indication for closure should consider this potential complication despite an otherwise safe interventional procedure.

Background: To investigate the role of N-terminal pro-BNP (NT-proBNP) for the estimation of right heart failure and pulmonary pressure in patients with atrial septal defects (ASD) before and after percutaneous defect closure. Methods: We performed correlation analysis for NT-proBNP and right ventricular systolic pressure (RVSP) as well as right ventricular enddiastolic and endsystolic volume (RVEDV, RVESV) determined by cardiac magnetic resonance imaging (MRI) before and up to one year following ASD closure. Additionally NT-proBNP concentrations were correlated with right atrial (RA) and RV enddiastolic pressure (RVEDP), ASD size and interatrial left-to-right shunt. Results: Baseline RVSP was 33±8 mmHg, which decreased significantly during follow-up. Initially, NT-proBNP levels were 240±93 pg/ml. After closure, a reduction to 1167±62 pg/ml was obvious (p<0.01). Baseline MRI showed enlarged RV volumes in all individuals. At six and twelve months follow-up a significant reduction of RVEDV and RVESV was apparent. A positive correlation was noted between RV volumes and NT-proBNP (r=0.65, p<0.05). Furthermore RA pressure, RVEDP, RVSP and left-to-right shunt significantly correlated to peptide levels. No correlation was seen between ASD size and NT-proBNP. Conclusion: NT-proBNP correlates to right ventricular dilatation, pulmonary pressure and left-to-right shunt in volume load of the right heart caused by an underlying ASD.

Objective: To characterise prospectively by magnetic resonance imaging (MRI) changes in right ventricular (RV) volume, function, and mass after transcatheter closure of atrial septal defects (ASDs) and to evaluate the course of pulmonary pressure and functional class criteria. Methods: In 20 patients with secundum-type ASD and dilated RV diameter, MRI was performed to quantify RV end diastolic (RVEDV) and end systolic volumes (RVESV), RV mass, tricuspid annular diameter, and RV ejection fraction before and 6 and 12 months after transcatheter closure of the ASD. RV systolic pressure was measured during follow up by transthoracic echocardiography. Results: Functional class improved in the majority of patients after ASD closure. RVESV (from 81 (18) ml/m² to 53 (15) ml/m², p < 0.001), RVEDV (from 127 (17) ml/m² to 99 (18) ml/m², p < 0.001), and RV mass (from 79 (10) g to 63 (8) g, p < 0.01) decreased significantly during follow up, although tricuspid annular diameter did not. RV ejection fraction improved (by 9% compared with baseline, p < 0.05) and RV systolic pressure decreased significantly (from 33 (8) mm Hg to 24 (6) mm Hg, p < 0.001) after closure. Conclusion: MRI studies showed significant improvement of RV volumes, mass, and function after transcatheter closure of ASDs. Restoration of the RV leads to decreased pulmonary pressure resulting in a better functional class in the majority of patients.