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.

Pre-hospital discharge testing after implantable cardioverter defibrillator implantation: a measure of safety or out of date? A retrospective analysis of 975 patients.

AIMS: The present study evaluates the relevance and additional safety value of pre-hospital discharge (PHD) testing in patients with implantable cardioverter defibrillator (ICD) therapy. METHODS: From June 1998 to May 2009, 975 patients (830 male, 145 female) with ICD were screened retrospectively for failed PHD and analysed for its consequences, risk factors, and patient characteristics after successful intra-operative testing in the implantation procedure. RESULTS: Pre-hospital discharge testing procedure was performed in 809 cases. No serious adverse events (e.g. death, persistant ventricular fibrillation or ventricular tachycardia, stroke) occurred. The overall incidence of failed PHD was 1.4% (n = 11). The underlying mechanisms were defibrillation threshold failure in 9/11 cases and sensing failure in 2/11 cases. CONCLUSIONS: In this study predictors for PHD-failure are: (i) cardiomyopathy other than ischaemic or dilative, (ii) young age, and (iii) small or very large left ventricular end-diastolic diameter ( < 40 or > 65 mm). Particularly, (i) manufacture of device or leads, (ii) lead design, (iii) medical treatment, or (iv) gender have no significant influence on PHD failure.

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.

Ventricular oversensing in 518 patients with implanted cardiac defibrillators: incidence, complications, and solutions.

The present study evaluates the incidence of various complications in implanted cardiac defibrillators (ICD) therapy due to ventricular oversensing (VO) and its complications. From June 1998 to May 2005, we retrospectively screened 518 patients (1085.6 patient years) for the occurrence of VO episodes (441 male, 77 female). The overall incidence was 7.3% (n = 38) with inappropriate shock deliveries accounting for 2.3% (n = 12). All VO episodes were caused by either T-wave oversensing (n = 10), myopotentials (n = 8), electrode failure (n = 5), interference with electromagnetic fields (n = 3), double-counting (n = 4), pacemaker interactions (n = 2), or others (n = 2). There were five life-threatening events due to inappropriate ICD reaction. In eight (22%) cases, ICD reprogramming was able to avoid further oversensing episodes (e.g. adaptation of sensitivity, T-wave suppression feature), 13 (35%) patients had to undergo invasive procedures (e.g. electrode replacing) to suppress VO, 16 (43%) were told to avoid the trigger situation, and one demanded to deactivate all ICD therapies because of inappropriate shock delivery. Our data demonstrate that VO is a rare complication, but might lead to life-threatening events. In most cases, VO episodes could be prevented by appropriate ICD reprogramming or avoidance of the initiating trigger.

Two distinct mechanisms mediate a differential regulation of protein kinase C isozymes in acute and prolonged myocardial ischemia.

An activation of protein kinase C (PKC) in acute myocardial ischemia has been shown previously using its translocation to the plasma membrane as an indirect parameter. However, whether PKC remains activated or whether other mechanisms such as altered gene expression may mediate an isozyme-specific regulation in prolonged ischemia have not been investigated. In isolated perfused rat hearts, PKC activity and the expression of PKC cardiac isozymes were determined on the protein level using enzyme activities and Western blot analyses and on the mRNA level using reverse transcriptase-polymerase chain reaction after various periods of global ischemia (1 to 60 minutes). As early as 1 minute after the onset of ischemia, PKC activity is translocated from the cytosol to the particulate fraction without change in total cardiac enzyme activity. This translocation involves all major cardiac isozymes of PKC (ie, PKCalpha, PKCdelta, PKCepsilon, and PKCzeta). This rapid, nonselective activation of PKCs is only transient. In contrast, prolonged ischemia (>/=15 minutes) leads to an increased cardiac PKC activity (119+/-7 versus 190+/-8 pmol/min per mg protein) residing in the cytosol. This is associated with an augmented, subtype-selective isozyme expression of PKCdelta and PKCvarepsilon (163% and 199%, respectively). The specific mRNAs for PKCdelta (948+/-83 versus 1501+/-138 ag/ng total RNA, 30 minutes of ischemia) and PKCepsilon (1597+/-166 versus 2611+/-252 ag/ng total RNA) are selectively increased. PKCalpha and PKCzeta remain unaltered. In conclusion, two distinct activation and regulation processes of PKC are characterized in acute myocardial ischemia. The early, but transient, translocation involves all constitutively expressed cardiac isozymes of PKC, whereas in prolonged ischemia an increased total PKC activity is associated with an isozyme-selective induction of PKCepsilon and PKCdelta. Whether these fundamentally different activation processes interact remains to be elucidated.

Microwave ablation of an ischemic sustained ventricular tachycardia during aortocoronary bypass, mitral valve and tricuspid valve surgery guided by a three-dimensional non-fluoroscopic mapping system (CARTO).

Postinfarct patients with malignant ventricular tachyarrhythmias (VTs) are prone to an increased risk for sudden cardiac death and implantation of an internal cardioverter-defibrillator (ICD) often is recommended. In cases where the VTs are incessant or refractory to medical treatment, disruption of the macro-reentry circuit, which represents the arrhythmogenic substrate for postinfarct VTs, is a major therapeutical goal for electro-physiologists. The precise identification of this underlying macro-reentrant circuit depends on conventional mapping techniques (i.e. diastolic potentials, entrainment) and more recently by a three-dimensional non-fluoroscopic electro-anatomical mapping system (CARTO), which integrates anatomical and electrophysiological information to reconstruct a three-dimensional activation and propagation map of the relevant VT. This reports describes on a patient with recurrent, drug-refractory, hemodynamically stable monomorphic VTs on the basis of a 2-vessel coronary artery disease, reduced left ventricular ejection fraction, who was scheduled for coronary artery bypass graft operation combined with mitral valve replacement and reconstruction of the tricuspid valve. Preoperatively, the underlying mechanism of the VT was identified by CARTO mapping with a slow conduction zone and a wide exit site at the inferoapico-basal portion of the left ventricle. In close cooperation between the cardiologists and the surgeons the decision for a simultaneous ablation approach during the subsequent operation was made. Successful ablation of the VT using microwave energy was confirmed by non-inducibility of the VT in the perioperative electrophysiologic study. This case report highlights the use of CARTO mapping to identify postinfarct VTs as well as the application of microwave energy as a useful tool to cure postinfarct ventricular arrhythmias.

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.

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.

Long term biventricular resynchronisation therapy in advanced heart failure: effect on neurohormones.

OBJECTIVE: To assess prospectively the effect of cardiac resynchronisation therapy (CRT) on New York Heart Association (NYHA) functional class, cardiac function, cardiopulmonary exercise performance, and neurohormonal activation during 24 months' follow up. DESIGN: Controlled study. PATIENTS AND RESULTS: 124 patients with severe congestive heart failure (ejection fraction < 35%, NYHA III-IV) and left bundle branch block (QRS duration > 150 ms) were enrolled (control group, n = 59; CRT group, n = 65) and followed up at 1, 3, 12, and 24 months. Compared with the control group, CRT led to significant short and long term improvements in functional NYHA functional class (mean (SEM) 2.1 (0.4) v 2.8 (0.4) at 24 months, p < 0.05), mean ejection fraction (25.7 (4)% v 21.1 (5)% at 24 months, p < 0.05), peak Vo(2) (16.8 (3.9) v 12.6 (3.5) ml/kg x min at 24 months, p < 0.01), and Vo(2) at anaerobic threshold (14.4 (3.7) v 10.8 (3.2) ml/kg x min at 24 months, p < 0.05). In addition, CRT for one and 12 months significantly decreased the plasma concentrations of noradrenaline (norepinephrine) and N-terminal fragment of pro-brain natriuretic peptide, whereas no changes were observed for other neurohormones such as antidiuretic hormone, aldosterone, and endothelin. CONCLUSION: Long term CRT (

[Occlusion by catheter intervention in patent foramen ovale via additional transseptal puncture]. / Katheterinterventioneller Verschluss eines ventiloffenen Foramen ovale über eine zusätzliche transseptale Punktion.

In patients with a cryptogenic cerebral ischemia, the percutaneous closure of a patent foramen ovale (PFO) has gained increasing acceptance as an alternative strategy to prevent paradoxical embolism. Promising data with low recurrence rates have been reported for several self-expanding double disk devices. The implantation of the device is usually performed by passing the PFO. However, in one patient with a TIA (m, 43 years) transesophageal echocardiography (TEE) revealed an atrial septum abnormality with a hypermobile septum and a very small distance (approximately 12 mm) between the PFO channel and the anterior mitral valve leaflet, which was too short to accommodate the regular implantation procedure of the device via the PFO-channel itself. In this particular case the device (PFO-Star TSD) was advanced to the left atrium via an additional transseptal puncture--performed under TEE guidance--to allow for complete closure of the PFO without impairment of the mitral valve function. No periinterventional complications were observed. During the follow-up period of 9 months the patient was completely asymptomatic with no functional impairment of the mitral valve and no residual intracardiac shunt.