Latent pulmonary hypertension in atrial septal defect: Dynamic stress echocardiography reveals unapparent pulmonary hypertension and confirms rapid normalisation after ASD closure.

OBJECTIVE: Closure of atrial septal defects (ASD) prevents pulmonary hypertension, right heart failure and thromboembolic stroke. The exact timing for ASD closure is controversial. METHODS: In a prospective study to address the question whether unapparent pulmonary hypertension can be revealed prior to right ventricular (RV) remodelling, patients were investigated before and 6, 12, and 24 months after ASD closure using exercise stress echocardiography (ESE) and ergospirometry (n = 24). RESULTS: At rest, RV systolic pressure (RVSP) was normal in 58.8 %, slightly elevated in 26.5 %, and moderately elevated in 11.8 %. One patient showed severe pulmonary hypertension. During ESE, all patients with normal RVSP at rest exhibited an increase (25.7 ± 1.2 mmHg vs. 45.3 ± 2.3 mmHg, p < 0.001). After closure the RVSP was lower, both at rest and ESE. RV diameters decreased too. Tricuspid annulus plane systolic excursion (TAPSE) at rest remained lower after closure (24.0 ± 0.9 vs. 22.0 ± 0.9 mm, p < 0.05). TAPSE in ESE was elevated, and stayed stable after closure (30.1 ± 1.8 mm vs. 29.3 ± 1.6 mm). Before closure, RV systolic tissue velocities (s(a)) at rest were normal and decreased after closure (14.0 ± 1.0 cm/s vs. 11.5 ± 0.7 (6 month) vs. 10.6 ± 0.5 cm/s (12 month), p < 0.05). During ESE, s(a) velocity was similar before and after closure (23.0 ± 1.3 cm/s vs. 23.3 ± 1.9 cm/s). Maximal oxygen uptake (VO2/kg) did not differ between baseline and follow-ups. CONCLUSION: Latent pulmonary hypertension may become apparent in ESE. ASD closure leads to a significant reduction in this stress-induced pulmonary hypertension and to a decrease in the right heart diameters indicating reverse RV remodelling. RV functional parameters at rest did not improve. The VO2/kg did not change after ASD closure.

Elevation of left-sided diaphragm leading to myocardial infarction by compression of the left circumflex artery.

A previously healthy 46-year-old male presented to our emergency department with severe thoracic pain, dyspnea and vomiting, which had suddenly started 2 hours before. He had no history of unusual features and no cardiovascular risk factors. The 12-lead electrocardiogram indicated a posterolateral myocardial infarction. Immediate coronary catheterization revealed occlusion of the proximal left circumflex artery (LCX). Recanalization and coronary stent implantation were successful. No other coronary lesions were detectable that could have indicated coronary artery disease. During catheterization, superposed intestinal loops in the left thorax were striking. The chest X-ray revealed crass cranial displacement of the left-sided diaphragm with intestinal loops beneath, leading to compression of the ipsilateral lung and to a mediastinal shift to the right. Thoracic computed tomography showed compression by the elevated diaphragm of the posterior atrioventricular groove and the left circumflex (LCX) artery embedded in this. Clinical workup revealed no muscular disorder or central dysfunction responsible for diaphragm elevation; no reason for a phrenic nerve lesion was found. The patient subsequently developed ventilatory failure, necessitating intermittent noninvasive bilevel positive airway pressure. After 5 days of intermittent ventilation, the elevation of the diaphragm reduced noticeably and respiratory assistance could be stopped. The cause of this reversible unilateral diaphragm elevation remained unknown.

Receptor-independent sensitization of the adenylyl cylase after chronic treatment with cyclosporine A.

Chronic treatment with cyclosporine A (CyA) is often complicated by severe hypertension. If activation of the beta-adrenergic-receptor-linked adenylyl cyclase (AC) system contributes to hypertension is unresolved. Rats were treated with CyA (20 mg kg(-1) day(-1)) for 7 days. beta-adrenergic, muscarinic, and alpha-adrenergic receptors, G-proteins, and the activity of AC were determined in cardiac and pulmonary plasma membranes. The density of cardiac beta-adrenergic receptors, muscarinic receptors, alpha-adrenergic receptors, G(alphas) and, G(alphai) remained unchanged after treatment with CyA. However, CyA increased the responsiveness of AC to different stimulators. The responsiveness of AC was even more pronounced after solubilization and partial purification, suggesting a direct modulation of the enzyme. These data suggest that CyA modulates the activity of the sympathoadrenergic system by a direct, receptor-independent sensitization of AC, suggesting that this pathway contributes to hypertension in patients treated with CyA.

Incidence of aortic valve regurgitation and outcome after percutaneous closure of atrial septal defects and patent foramen ovale.

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.

NT-proBNP correlates with right heart haemodynamic parameters and volumes in patients with atrial septal defects.

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 116+/-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.

Transcatheter closure of atrial septal defects improves right ventricular volume, mass, function, pulmonary pressure, and functional class: a magnetic resonance imaging study.

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.

[Bacterial pericarditis]. / Bakterielle Perikarditis.

HISTORY AND CLINICAL FINDINGS: A 65-year-old previously healthy man was referred because of high fever, progressive dyspnea and retrosternal pain for 2 days. On admission, the patient was already in a reduced general condition, blood pressure was 120/70 mmHg, heart rate irregular at 75/min and temperature at 39.7 degrees C. Auscultation of the heart revealed distant heart sounds, murmurs were not present, but mild rales were heard over both lung bases. Jugular veins were congested. INVESTIGATIONS: ECG showed a generalized ST-segment elevation with preserved R-waves, slightly depressed PR-segment and atrial bigemini. Chest X-ray revealed an enlarged cardiac silhouette with signs of a pneumopericardium. Transthoracic echocardiography showed a circular pericardial effusion and haemodynamic impairment. Percutaneous pericardiocentesis revealed a purulent effusion with microbiological proof of pneumococci. The primary infectious focus was a maxillary sinusitis caused by pneumococci. DIAGNOSIS: Bacterial pericarditis due to by haematogenous spread of pneumococci. TREATMENT AND COURSE: Antibiotic therapy consisted of intravenous ceftriaxon and gentamicin. To rinse the pericardial space and drain the thick, purulent effusion subxiphoidal, pericardiocentesis and insertion of a drainage tube were done. Physiological saline was put into the pericardial space several times a day, drained and analysed microbiologically. In the meantime rinsing of the infected maxillary sinus was performed. Transthoracic echocardiography was done repeatedly to rule out complications of bacterial pericarditis, especially constrictive pericarditis. The pericardial tube was removed after proof of a sterile drainage 9 days after insertion. The patient was discharged after 4 weeks of hospitalization without clinical or echocardiographic signs of diastolic dysfunction. CONCLUSION: Suspected bacterial pericarditis must be treated as an emergency and confirmed or ruled out by percutaneous pericardiocentesis.

Clinical evaluation data from a comparative dental implant investigation in dogs.

This report presents one-year clinical evaluation data from 120 ceramic and titanium cylindrical and titanium blade-type implants placed in the mandibles of 30 adult dogs. Ninety-six of the implants supported fixed bridges. The bone and gingival health was evaluated by the following indices: crevicular fluid volume index; gingival bleeding index; plaque accumulation index; clinical mobility index; and a quantitative mobility index utilizing the Periotest instrument. Results from this investigation suggest that, overall, the ceramic implants exhibited more fractures and had more mobile implants than did the titanium implant systems. Overall, complete one-year clinical evaluation data demonstrate healthy tissue responses to 112 of the 120 implants. Further, the Periotest instrument appears to offer a more quantitative assessment of clinical mobility. Also, it appears that the clinical evaluation protocol utilized in this study is a valid procedure to use for the assessment of clinical serviceability.