Biomedical subjects

Thomas Meinertz

Publications and source records attributed to Thomas Meinertz.

At least 37 records · Page 2Linked to original sources

PubMed2005

13-year follow-up of the German angioplasty bypass surgery investigation.

AIMS: The German Angioplasty Bypass Surgery Investigation was designed to compare symptomatic efficacy and safety of percutaneous coronary balloon angioplasty (PTCA) with coronary artery bypass surgery (CABG) in patients with symptomatic multi-vessel disease. This follow-up study was performed to determine the long-term outcome of patients following these interventions. METHODS AND RESULTS: From 1986 to 1991, 359 patients with angina CCS class II-IV, age below 75 years, and coronary multi-vessel disease requiring revascularization of at least two major coronary vessels were recruited at eight German centres and randomized to PTCA or CABG. From 337 patients undergoing the planned procedure, 324 patients could be followed-up (96%). Baseline parameters were identical in both groups, 2.2+/-0.6 vessels were treated in CABG patients, whereas 1.9+/-0.5 vessels were treated in PTCA patients. Thirty-seven per cent of surgical patients received internal mammary artery grafts, while no stents were used in patients undergoing PTCA. At the end of the 13-year follow-up period, the degree of angina, the degree of dyspnea, and the utilization of nitrates were comparable in both groups. With a total number of 76 deaths, Kaplan-Meier analysis revealed a comparable distribution in both groups. Although time to first re-intervention was significantly shorter in the PTCA group, P<0.001, frequencies of re-intervention (CABG, n=94; PTCA, n=136) and crossover rates (CABG to PTCA, n=49; PTCA to CABG, n=51) were comparable in both groups. CONCLUSION: The results of our 13-year follow-up suggest that in patients with symptomatic multi-vessel disease, both PTCA and CABG are associated with a comparable long-term survival and symptomatic efficacy. How far these results may be altered by developments such as drug-eluting stents or off-pump surgery remains to be determined.

Adult↗

PubMed2005

Effect of syncope-related traumatic injuries on the diagnostic evaluation and syncope recurrence of patients with syncope and apparently normal hearts.

The aims of this study were to assess the frequency of traumatic injuries in patients with syncope and apparently normal hearts and their influence on the diagnostic evaluation and recurrence of syncope. Patients presenting with syncope before head-up tilt testing frequently had a history of syncope-related injuries. Syncope-related injuries seemed to be random: they was not related to patients' histories, including the number of previous syncopal attacks, and they had no predictive value for the outcome of head-up tilt testing or for the recurrence of syncope during 1-year follow-up.

Female↗

PubMed2005

Elevation of asymmetric dimethylarginine in patients with unstable angina and recurrent cardiovascular events.

AIMS: We investigated the role of asymmetric dimethylarginine (ADMA) for clinical outcome of patients with unstable angina. METHODS AND RESULTS: Forty-five patients with stable angina, 36 patients with unstable angina, and 40 healthy controls were included in this study. Coronary artery disease (CAD) patients were prospectively followed for 1 year. ADMA levels were measured at baseline and after 6 weeks using a validated ELISA. Baseline ADMA concentration in controls was significantly lower than in patients with CAD (0.59+/-0.23 vs. 0.76+/-0.17 micromol/L; P<0.001). Patients with unstable angina had significantly higher baseline ADMA levels than patients with stable angina (0.82+/-0.18 vs. 0.73+/-0.15 micromol/L; P=0.01). There was a significant reduction of ADMA levels at 6 weeks after percutaneous coronary intervention (PCI) in patients with unstable angina who experienced no recurrent cardiovascular event (from 0.81+/-0.14 to 0.73+/-0.19 micromol/L; P<0.05). In contrast, patients with unstable angina who had an event showed no significant decrease in ADMA at 6 weeks. Actuarial survival analysis showed a significantly higher event rate in patients with persistently elevated ADMA plasma concentrations. CONCLUSION: ADMA is significantly elevated in patients with unstable angina. A reduced ADMA level at 6 weeks after PCI may indicate a decreased risk of recurrent cardiovascular events.

Adult↗

PubMed2005

Systemic endothelial dysfunction as an early predictor of adverse outcome in heart failure.

OBJECTIVE: Endothelial dysfunction is an early event in the natural progression of heart failure. Increased oxidative stress has been linked to impaired endothelial function and both may play a prognostic role. METHODS AND RESULTS: Endothelium-dependent and endothelium-independent vasodilatation were determined in 289 patients with mild left ventricular dysfunction by measuring forearm blood flow responses to acetylcholine and sodium nitroprusside using venous occlusion plethysmography. Vascular effects of the coadministration of the antioxidant vitamin C at pharmacological doses (24 mg/min) were assessed. Occurrence of death, heart transplantation, and readmission with worsening heart failure were recorded as clinical outcome parameters during a follow-up period of 4.8 years. Patients experiencing adverse events (n=79) had lower vasodilator responses to acetylcholine (P<0.001) and to sodium nitroprusside (P=0.03) compared with patients without events. However, beneficial effects of vitamin C did not differ between both groups. Cox proportional hazards model demonstrated that age (P=0.001), renal function (P=0.001), and blunted acetylcholine-induced vasodilatation (P=0.007) remained independent predictors of adverse outcome. CONCLUSIONS: Impaired peripheral endothelial function independently predicts long-term adverse outcome in patients with early-stage heart failure. The findings suggest that assessment of peripheral endothelial function may represent an additional mean for risk stratification and therapy management in these patients.

Acetylcholine↗

PubMed2005

A randomized trial in patients undergoing percutaneous coronary angioplasty: roxithromycin does not reduce clinical restenosis but angioplasty increases antibody concentrations against Chlamydia pneumoniae.

BACKGROUND: Elevated antibodies against Chlamydia pneumoniae have been associated with coronary artery disease. In patients undergoing percutaneous coronary angioplasty, we therefore investigated the effect of roxithromycin on symptomatic restenosis and determined antichlamydial antibodies as well as inflammatory and immunological parameters. METHODS: A total of 327 patients undergoing coronary angioplasty were randomized to roxithromycin or placebo and followed-up for 1 year. Antibodies were determined by microimmunofluorescence and enzyme-linked immunosorbent assay; C-reactive protein, interleukin-10, tumor necrosis factor-alpha (TNF-alpha), and eotaxin were determined by enzyme-linked immunosorbent assay. RESULTS: Although the frequency of restenosis was not affected by roxithromycin (25 restenoses vs 32 in the control group), antichlamydial antibodies increased during follow-up (anti-CP IgG +12 +/- 2%, P < .001). Concentrations of TNF-alpha and eotaxin increased as well (TNF-alpha +9 +/- 1% and eotaxin +10 +/- 2%) and correlated with antichlamydial antibody concentrations (TNF-alpha, r = 0.23, P = .02; eotaxin, r = 0.32, P = .002). CONCLUSIONS: Treatment with roxithromycin was not associated with a reduction of symptomatic restenoses. During follow-up, a marked increase in antichlamydial antibodies, TNF-alpha, and eotaxin was observed, suggesting that angioplasty-induced plaque rupture induces a specific immunological response without activation of inflammatory mechanisms as represented by C-reactive protein. Whether this mechanism occurs in all plaque ruptures remains to be determined.

Angioplasty, Balloon, Coronary↗

PubMed2005

Targeted pharmacological reversal of electrical remodeling after cardioversion--rationale and design of the Flecainide Short-Long (Flec-SL) trial.

Persistent atrial fibrillation (AF) causes relevant mortality and cardiovascular and noncardiovascular morbidity. Therefore, maintenance of sinus rhythm is an important clinical goal, especially when the patient is symptomatic, despite the fact that current treatment strategies are not sufficient to completely prevent recurrent AF. In addition to underlying atrial disease that predisposes to AF, AF in itself induces structural and electrical adaptations ("electrical remodeling" and "structural remodeling"). Underlying disease processes and parts of structural remodeling are not always reversible. Electrical remodeling, in contrast, is reversed by a few weeks of maintenance of sinus rhythm under experimental conditions. This corresponds to the period when most of the recurrent episodes of AF occur after cardioversion. Antiarrhythmic drugs that prolong the atrial action potential can assist in the prevention of recurrent AF by promoting the reversal of electrical remodeling. Such drugs, which are currently used over long periods after cardioversion, may only be needed until the physiological action potential duration is restored, for example, during the first few weeks after cardioversion of persistent AF. This treatment concept that we call "targeted pharmacological reversal of electrical remodeling" would limit both cost and drug-induced side effects of antiarrhythmic drug therapy after cardioversion. The Flec-SL trial, ISECTN62728743, therefore tests the main hypothesis that targeted pharmacological reversal of electrical remodeling by short-term antiarrhythmic drug therapy for 4 weeks after cardioversion is not inferior to standard long-term antiarrhythmic drug therapy for the prevention of recurrent AF after cardioversion in a parallel group, randomized, multicenter, open, blinded end point analysis design. Based on its effectiveness and pharmacokinetic profile, flecainide is used to test the study hypothesis. The trial uses daily transtelephonic electrocardiographic monitoring for all patients and will be conducted within the German Atrial Fibrillation Competence NETwork (AFNET) to facilitate inclusion of patients from electrophysiologically oriented cardiology centers, ordinary hospitals, and office-based physicians.

Anti-Arrhythmia Agents↗

PubMed2005

Impact of amiodarone on electrophysiologic properties of pulmonary veins in patients with paroxysmal atrial fibrillation.

INTRODUCTION: Pulmonary veins (PVs) are the predominant location of triggers for atrial fibrillation (AF), but little is known about the electrophysiologic properties of PVs. In addition, the influence of amiodarone on the electrophysiologic properties of PVs has not been elucidated. METHODS AND RESULTS: Fifty-five patients with symptomatic and drug-resistant AF were divided into two groups: group 1 patients (n=29) without antiarrhythmic drug therapy at the time of electrophysiologic study (EPS), and group 2 patients (n=26) undergoing continuous long-term treatment with amiodarone. EPS including programmed stimulation of both atria and within the PVs was performed in both groups. In group 1, the effective refractory period (ERP) of all PVs (174 +/- 62 msec) was significantly shorter than the ERP of the left atrium ([LA] 254 +/- 30 msec, P=0.0001) and right atrium ([RA] 221 +/- 29 msec, P=0.0001). The same pattern was observed in group 2 (PV: 210 +/- 58 msec; LA: 259 +/- 35 msec, P=0.0001; RA: 246 +/- 37 msec, P=0.0255). The ERP of all stimulated PVs was significantly lower in group 1 (174 +/- 62 msec) than in group 2 (210 +/- 58 msec; P=0.0001). The ERP of the left superior and right superior PVs and RA but not the left inferior PV and LA were significantly increased in patients treated with amiodarone. Decremental conduction properties were observed in all stimulated PVs, and there were no significantly differences between the maximal decrement of both groups. CONCLUSION: The distinctive electrophysiologic properties of PVs are emphasized by amiodarone therapy. Long-term amiodarone treatment is responsible for heterogeneous alteration of the PV electrophysiology, which may account for the individual antiarrhythmic responses in a subset of patients with paroxysmal AF.

Amiodarone↗

PubMed2005

Moderate exercise induces different autonomic modulations of sinus and AV node.

BACKGROUND: The routine determination of heart rate variability (HRV) from surface ECGs is based on RR intervals because of the difficulty to precisely locate the P-wave fiducial point on surface ECG recordings. The aim of the study was to assess the changes of RR, PP, and PR intervals at rest and during moderate exercise. The time intervals were determined from atrial and ventricular pacemaker-mediated intracardiac electrograms. METHODS: Ten patients in sinus rhythm with intrinsic AV node conduction who had received the dual-chamber pacemaker Logos (Biotronik) were included. High-resolution atrial and ventricular intracardiac electrograms were transmitted at rest in supine position and during walking to a portable external recorder. Recording sequences of 150 successive heart cycles were used for HRV analyses after computer-assisted triggering of P and R events. The HRV-index SDNN and power spectral densities for the low (LF; 0.04-0.15 Hz) as well as high (HF; 0.15-0.40 Hz) frequency bands were determined. RESULTS: SDNN decreased from 26.0 +/- 8.1 ms at rest to 18.3 +/- 4.2 ms during exercise for the PP intervals (P < 0.05) and from 26.8 +/- 8.1 to 18.4 +/- 4.1 ms for the RR intervals (P < 0.05). The LF/HF ratio increased from 2.02 +/- 1.3 to 4.5 +/- 1.5 in the atrium (P < 0.05) and from 2.0 +/- 1.2 to 5.2 +/- 1.9 in the ventricle P < 0.05). Comparing atrial and ventricular HRV at both activity levels, no significant differences were observed for the power of LF and HF spectral components. Regarding the PR intervals SDNN, the total power and the LF/HF ratio did not significantly change during exercise. CONCLUSIONS: The described technique enabled to record intracardiac electrograms not only at rest, but also during moderate exercise and to use them for HRV evaluation. The changes of PP and RR, but not of the PR intervals, during exercise indicate that autonomic inputs to the sinus node and AV node are independent from each other. The ventricular HRV seems to derive mainly from variations of the sinus node pulse formation.

Aged↗

PubMed2005

Efficacy and safety of radiofrequency catheter ablation of atrioventricular nodal reentrant tachycardia in the elderly.

INTRODUCTION: Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common regular supraventricular tachycardia in the general population as well as in elderly patients. The purpose of the study was to investigate the success and complication rate particularly regarding the induction of an atrioventricular (AV) block by radiofrequency (RF) ablation in elderly patients with and without a preexisting AV block. METHODS AND RESULTS: Between February 1998 and July 2004, all patients with symptomatic AVNRT referred for slow-pathway ablation in our institution were included and divided into two groups: group 1 patients younger than 75 years (n = 508) and group 2 patients > or =75 years (n = 70). A preexisting prolonged PR interval was present in 17 (3.3%) patients of group 1 and in 26 (37%, P < 0.0001) patients of group 2. Following successful slow-pathway ablation (follow-up time group 1: 37 +/- 22, group 2: 37 +/- 24 months) no induction of an AV block was observed in group 2 but in four patients of group 1 (0.79%) a complete heart block was induced requiring a pacemaker implantation. In group 1, 15 (2.95%) patients with a recurrence of AVNRT were readmitted for a repeat ablation procedure. No recurrences occurred in group 2. CONCLUSION: Despite a higher incidence of preexisting prolonged PR intervals slow-pathway ablation in elderly patients is both effective and safe and should be considered as the first line therapy also in this patient population.

Age Factors↗

PubMed2004

Myeloperoxidase mediates neutrophil activation by association with CD11b/CD18 integrins.

Recruitment and activation of polymorphonuclear neutrophils (PMNs) reflects a primary immunological response to invading pathogens and has also emerged as a hallmark of vascular inflammation. One of the principal enzymes released upon PMN activation is myeloperoxidase (MPO), a heme protein that not only generates cytotoxic oxidants but also impacts deleteriously on nitric oxide-dependent signaling cascades within the vasculature. Because MPO also associates with the membrane of PMN, we evaluated whether MPO could also function as an autocrine modulator of PMN activation. The extent of PMN membrane-associated MPO was elevated in patients with acute inflammatory vascular disease compared with healthy individuals. Isolated PMNs bound free MPO by a CD11b/CD18 integrin-dependent mechanism. PMNs exposed to MPO were characterized by increased tyrosine phosphorylation and p38 mitogen-activated protein kinase activation. Also, nuclear translocation of NFkappaBin PMN was enhanced after incubation with MPO, as was surface expression of CD11b. Binding of PMN to MPO-coated fibronectin surfaces amplified PMN degranulation, as evidenced by increased release of MPO and elastase. MPO also augmented PMN-dependent superoxide (O(2)(*-)) production, which was prevented by anti-CD11b antibodies, but not MPO inhibitors. Collectively, these results reveal that binding of MPO to CD11b/CD18 integrins stimulates PMN signaling pathways to induce PMN activation in a mechanism independent of MPO catalytic activity. These cytokine-like properties of MPO thus represent an additional dimension of the proinflammatory actions of MPO in vascular disease.

CD11b Antigen↗

PubMed2004

Sulfatides activate platelets through P-selectin and enhance platelet and platelet-leukocyte aggregation.

OBJECTIVE: Sulfatides are sulfated glycosphingolipids present on the surface of a variety of cells; however, their exact physiological function is not known. Recently, we have shown that the inhibition of sulfatide-P-selectin interactions leads to disaggregation of platelet aggregates. METHODS AND RESULTS: In this study, we show that sulfatides activated platelets as they increased activation of GPIIb/IIIa (PAC-1 epitope) and expression of P-selectin on the platelet surface. Furthermore, sulfatides aggregated washed platelets in a dose-dependent manner and enhanced platelet aggregation in platelet-rich plasma. Previous activation of platelets was necessary for this effect. Monoclonal anti-P-selectin antibodies inhibited not only sulfatide-induced PAC-1 binding to platelets but also sulfatide-induced platelet aggregation, suggesting that sulfatides activate platelet GPIIb/IIIa via signaling through P-selectin. The proaggegatory effect of sulfatides was also observed in an ex vivo thrombosis model using whole blood and pulsatile flow at 37 degrees C. In this model, sulfatides significantly enhanced platelet aggregation and the formation of platelet-leukocyte aggregates. CONCLUSIONS: We show that sulfatide-P-selectin interactions lead to subsequent platelet activation and P-selectin expression, forming a positive feedback loop that can potentiate formation of stable platelet aggregates. In addition, sulfatides enhance the aggregation of platelet-leukocyte aggregates. These mechanisms may play a significant role in hemostasis and thrombosis.

Adenosine Diphosphate↗

PubMed2004

Myeloperoxidase enhances nitric oxide catabolism during myocardial ischemia and reperfusion.

Impaired microvascular function during myocardial ischemia and reperfusion is associated with recruitment of polymorphonuclear neutrophils (PMN) and has been attributed to decreased bioavailability of nitric oxide (NO). Whereas myeloperoxidase (MPO), a highly abundant, PMN-derived heme protein facilitates oxidative NO consumption and impairs vascular function in animal models of acute inflammation, its capacity to function in this regard during human myocardial ischemia and reperfusion remains unknown. Plasma samples from 30 consecutive patients (61 +/- 14 years, 80% male) presenting with acute myocardial infarction were collected 9 +/- 4 h after vessel recanalization and compared to plasma from healthy control subjects (n = 12). Plasma levels of MPO were higher in patients than in control subjects (1.4 +/- 0.9 vs 0.3 +/- 0.2 ng/mg protein, respectively, p < 0.0001). The addition of hydrogen peroxide to patient plasma resulted in accelerated rates of NO consumption compared to control subjects (0.53 +/- 0.25 vs 0.068 +/- 0.039 nM/s/mg protein, respectively, p < 0.0001). Myocardial tissue from patients with the same pathology revealed intense recruitment of MPO-positive PMN localized along infarct-related vessels as well as diffuse endothelial distribution of non-PMN-associated MPO immunoreactivity. Endothelium-dependent microvascular function, as assessed by an acetylcholine-dependent increase in forearm blood flow in 75 patients with symptomatic coronary artery disease, inversely correlated with MPO plasma levels (r = -0.75, p < 0.005). Plasma from patients undergoing myocardial reperfusion contained increased levels of MPO, which catalytically consumed NO in the presence of H(2)O(2). Given the correlation between intravascular MPO levels and forearm vasomotor function in patients with coronary artery disease, MPO appears to be an important modulator of vasomotor function in inflammatory vascular disease and a potential therapeutic target for treatment.

Aged↗

PubMed2004

Tissue resident cells play a dominant role in arteriogenesis and concomitant macrophage accumulation.

Collateral growth is characterized by macrophage accumulation, suggesting an important role of circulating cells. To study origin and function of macrophages during arteriogenesis, we related the extent of macrophage accumulation to vascular proliferation and investigated the fate of fluorescently (CMFDA) labeled blood cells that were injected at the time of femoral artery occlusion. The effect of bone marrow depletion via cyclophosphamide before femoral artery occlusion on collateral proliferation and macrophage accumulation was studied, and we looked for the presence of bone marrow-derived stem cells in the vicinity of growing collateral vessels. Finally, we investigated the arteriogenic effect of macrophage activation via MCP-1 in bone marrow-depleted animals. Maximal macrophage accumulation occurred during the first 3 days after femoral artery occlusion and paralleled the extent of vascular proliferation. Fluorescently labeled leukocytes homed to spleen and wound but they were absent in proliferating collateral arteries during maximal macrophage accumulation. Depletion of circulating cells did neither affect macrophage accumulation nor collateral growth. Staining of monocyte-depleted animals for BrdUrd and ED2, alphaSMA, or VE-Cadherin demonstrated local proliferation of macrophages and vascular cells, whereas C-Kit, SSEA1, or Thy1-positive bone marrow-derived stem cells were not detectable. Enhancement of macrophage accumulation via MCP-1 was independent of circulating monocytes and promoted arteriogenesis in the absence of direct effects on vascular cells. We propose that the initial phase of vascular growth is characterized by local proliferation of tissue resident precursors rather than by migration of blood born cells. The full text of this article is available online at http://circres.ahajournals.org.

Actins↗

PubMed2004

Acute myocardial infarction: evaluation with first-pass enhancement and delayed enhancement MR imaging compared with 201Tl SPECT imaging.

PURPOSE: To evaluate acute myocardial infarction by using first-pass enhancement (FPE) and delayed enhancement (DE) magnetic resonance (MR) imaging compared with thallium 201 ((201)Tl) single photon emission computed tomography (SPECT). MATERIALS AND METHODS: Contrast material-enhanced FPE MR, inversion-recovery DE MR, and rest-redistribution (201)Tl SPECT images were obtained in 60 consecutive patients (53 men, seven women; mean age [+/- SD], 56 years +/- 13; range, 30-78 years) at 6 days +/- 3 after reperfused first myocardial infarction. Presence of microvascular obstruction was determined on FPE MR images. Infarct size was defined on DE MR images as percentage of left ventricular (LV) area and compared with uptake defect on redistribution (201)Tl SPECT images. Differences in continuous data were analyzed with Student t test. Linear regression and Bland-Altman analysis were used to compare measurements of infarct size. RESULTS: Mean infarct size was not significantly different between DE MR imaging (20.7% +/- 11.5% of LV area) and (201)Tl SPECT (19.4% +/- 14.3% of LV area; P =.26); good correlation (r = 0.73; P <.001) and agreement were found, with a mean difference of +1.3% +/- 9.8% of LV area. (201)Tl SPECT failed to depict infarct in six (20%) of 30 patients with inferior myocardial infarction (mean size, 6.4% +/- 5.7% of LV area on DE MR images), whereas DE MR images showed the infarct in all patients (P <.01). FPE MR images depicted microvascular obstruction in 23 (38%) of 60 patients; these patients had larger infarctions at DE MR imaging than did patients without microvascular obstruction (30.4% +/- 9.0% vs 15.1% +/- 8.4% of LV area, P <.001). (201)Tl SPECT showed larger infarcts in patients with microvascular obstruction (26.7% +/- 16.2% vs 15.0% +/- 11.2% of LV area, P <.01). CONCLUSION: Good correlation and agreement with (201)Tl SPECT indicate DE MR imaging may be used to estimate infarct size 6 days after reperfused acute myocardial infarction. DE MR imaging is more sensitive for detection of inferior infarction than is (201)Tl SPECT. Patients with microvascular obstruction on FPE MR images have larger infarcts.

Adult↗

PubMed2004

Chest radiography for the diagnosis of acute aortic syndrome.

PURPOSE: We sought to assess the diagnostic accuracy of routine chest radiography for the acute aortic syndrome (dissection, intramural hematoma, penetrating ulcer, or nondissecting aneurysm). METHODS: During a 6-year period, 216 patients (143 men, 73 women; mean [+/- SD] age, 58 +/- 17 years) underwent chest radiography for suspected acute aortic syndrome. Chest films were re-evaluated blindly for aortic disease, based on an overall impression using standard criteria such as widening of the aortic contour and mediastinal shadow. Findings were matched to tomographic images, anatomical inspection, or both, as the criterion standard; aortic disease was confirmed in 109 (50%) of the patients. RESULTS: Chest radiography had a sensitivity of 64% (70/109) and a specificity of 86% (92/107) for aortic disease. Sensitivity was 67% (38/57) for overt aortic dissection, 61% (22/36) for nondissecting aneurysm, and 63% (10/16) for intramural hemorrhage or penetrating ulcer. However, sensitivity was lower for pathology confined to the proximal aorta (47% [21/45]) than for disease involving distal aortic segments (77% [49/64]). A receiver operating characteristic curve analysis of aortic diameters failed to identify a threshold for the diagnosis of aortic disease. CONCLUSION: Chest radiography is of limited value for diagnosing the acute aortic syndrome, particularly for conditions confined to the ascending aorta. Since a definitive diagnosis is required in any patient with clinically suspected acute aortic syndrome, routine chest radiography should be replaced by tomographic aortic imaging.

Acute Disease↗

PubMed2004

Surgical revision of an uncommonly dislocated self-expanding Amplatzer septal occluder device.

Open heart surgery is the standard procedure for closure of ostium secundum atrial septal defects. Recently, percutaneous transcatheter procedures emerged as therapeutic alternatives for closure of both atrial septal defects and patent foramen ovale. Unfortunately, however, such percutaneous procedures may require surgical intervention for early or late complications. We report a case with emergent surgery for dislocation of the Amplatzer septal occluder into the aortic arch diagnosed 30 days after percutaneous closure of an atrial septal defect.

Aorta, Thoracic↗

PubMed2004

Three-dimensional color Doppler echocardiography for assessing shunt volume in atrial septal defects.

Background Three-dimensional color Doppler echocardiography has been used to assess cardiac blood flow in experimental settings. We tested whether this technique can be applied to assess transatrial shunt flow in patients with atrial septal defect in a clinical setting. Methods In 46 consecutive patients with atrial septal defects, shunt flow was assessed during cardiac catheterization using the Fick method and by conventional 2-D quantitative transesophageal Doppler echocardiography. The averaged values for shunt flow obtained by both methods were used as a reference. Transesophageal 3-D color Doppler echocardiography was performed for analysis of the 3-D flow velocity field of transatrial shunt flow. Shunt volume was calculated by application of the Gauss theorem. Results We found a close correlation between shunt volume (L/min) obtained by either 3-D color Doppler echocardiography or the reference methods ( r = 0.981, P < .001). Using 3-D color Doppler data to predict the reference values, 95% confidence limits were -11.5 to +11.6%. Conclusions Shunt flow in patients with atrial septal defects can be assessed in a clinical setting by transesophageal 3-D color Doppler echocardiography.

Adolescent↗

PubMed2004

Prevention of atrial fibrillation after cardioversion: results of the PAFAC trial.

AIMS: In patients with persistent atrial fibrillation (AF), the efficacy and safety of two anti-arrhythmic drugs in preventing the recurrence of AF after successful direct current (DC) cardioversion was prospectively assessed in a multi-centre double-blind, placebo-controlled, randomised trial using daily trans-telephonic monitoring. METHODS AND RESULTS: 1182 patients with persistent AF were prospectively enrolled, 848 patients were successfully cardioverted and then randomised to either sotalol (383 patients), quinidine plus verapamil (377 patients) or placebo (88 patients). The primary outcome parameter was AF recurrence or death. All patients received an event recorder (Tele-ECG) and had to record and transmit via telephone at least one ECG per day during follow-up. The mean follow-up period was 266 days. A total of 191,103 Tele-ECGs were recorded and transmitted. The primary outcome parameter (AF recurrence of any kind or death) was observed in 572 patients (67%) in whom at least one episode of AF recurrence was documented during follow-up, in 348 patients (41%) AF recurrence was persistent. The recurrence rates after one year for any AF were 83% for placebo, 67% for sotalol and 65% for quinidine plus verapamil, the latter being statistically superior to placebo but not different from sotalol. The recurrence rates for the secondary outcome parameter persistent AF were 77%, 49% and 38%, respectively. Quinidine plus verapamil was significantly superior to placebo and to sotalol. About 95% of all AF recurrences were initially detected in the daily Tele-ECG, about 70% of all AF recurrences occurred completely asymptomatic. Adverse events on sotalol and quinidine plus verapamil were comparable with the exception that all torsade de pointes tachycardias occurred on sotalol. CONCLUSION: Anti-arrhythmic treatment after DC cardioversion of persistent AF significantly decreases the recurrence rates of persistent AF compared to placebo with superiority of quinidine plus verapamil compared to sotalol. Symptoms were not reliable as clinical surrogates to detect episodes of AF.

Adolescent↗