WPW syndrome: the 'Rosetta stone' of rhythmology. The history of the Rosetta stone.

Prior to the 'discovery' of the Wolff-Parkinson-White syndrome, interpreting the respective phenomena was akin to reading hieroglyphic characters; thus a clear pathophysiological understanding and practical clinical diagnosis were impossible. The epochal work by Wolff, Parkinson, and White, which resulted in the electrophysiologically correct interpretation of circus movements as the cause of tachycardic rhythm disorders, can therefore indeed be compared to the deciphering of hieroglyphic writing by Champollion in 1822 with the aid of the Rosetta stone. After intensive archaeological and graphological examinations by the Society of Antiquaries, the Rosetta stone finally made its way to the British Museum, where it can still be viewed and admired today.

Recovery from ultra-high dose organophosphate poisoning after "in-the-field" antidote treatment: potential lessons for civil defense.

Organophosphate poisoning is associated with a high mortality rate due to respiratory failure, dysrhythmias, and multi-organ failure. We report two cases of survival after "in-the field" antidote treatment of very severe organophosphate poisonings. Two patients orally ingested large amounts of the organophosphorous agent oxydemeton-methyl in suicide attempts, resulting in the hypercholinergic syndrome in both. Resuscitation included early administration of antidote by emergency medical personnel as well as high-dose atropine. Plasma levels of pseudo cholinesterase were initially very low in both patients. Long-term mechanical ventilation was necessary, and both patients developed aspiration pneumonia. At discharge, no major neurological deficits were present. Prompt antidote treatment and aggressive supportive emergency and intensive care unit therapy contribute to improved survival after acute organophosphate poisoning. We believe that in cases of mass poisonings--for example, terrorist activity--therapy must be available on the scene as soon as possible. This also may require decentralized antidote storage.

Patients with atrial fibrillation and dense spontaneous echo contrast at high risk a prospective and serial follow-up over 12 months with transesophageal echocardiography and cerebral magnetic resonance imaging.

OBJECTIVES: We sought to assess the prognosis of patients with atrial fibrillation (AF) and dense spontaneous echo contrast (SEC) and to determine the incidence of cerebral embolism under continued oral anticoagulation. BACKGROUND: Patients with AF and dense SEC have an increased risk of cerebral embolism. However, there is little knowledge about the long-term fate and the rate of clinical silent cerebral embolism under continued oral anticoagulation. METHODS: Between 1998 and 2001, all consecutive patients with AF and dense SEC were included in the study. We performed serial and prospective transesophageal echocardiography, cranial magnetic resonance imaging, and clinical examinations during a period of 12 months. RESULTS: A total of 128 patients with dense SEC and AF were included. The control group consisted of 143 patients with faint SEC and AF. During the follow-up period, three patients (2%) had cerebral embolism with neurologic deficits. A total of eight patients (6%) died due to embolic events, and 19 (15%) patients had silent embolism, as documented on cerebral magnetic resonance imaging. Patients with an event had significantly lower left atrial appendage peak emptying velocities and more commonly had a history of previous thromboembolism and denser SEC, as compared with patients without an event. CONCLUSIONS: Patients with AF and dense SEC have a high likelihood of cerebral embolism (22%) and/or death, despite oral anticoagulation. Low peak emptying velocities of the left atrial appendage and dense SEC are independent predictors of an event.

Persistence of iatrogenic atrial septal defect after pulmonary vein isolation--an underestimated risk?

BACKGROUND: According to present knowledge, pulmonary vein isolation (PVI) bears a low interventional risk and has a high feasibility. For completion of PVI, left atrial access is achieved via single or double transseptal puncture. We sought to determine the incidence and echocardiographic characteristics of persistent iatrogenic atrial septal defect (iASD) after PVI. Further objectives were to define clinical and periprocedural risk factors for the development of iASD. METHODS: Every patient admitted for PVI at our hospital was screened for eligibility for study participation. Exclusion criteria were inability for undergoing transesophageal echocardiography, preexisting atrial septal defect, open-heart surgery or another transseptal procedure during the follow-up period. Transesophageal echocardiography was performed before PVI and after 9 months. Interatrial shunt was characterized by echocardiographic parameters; right-to-left-shunting (RLS) was quantified by contrast echocardiography. RESULTS: Forty-two patients were included, 27 patients underwent PVI with single transseptal puncture and additional advancement of a second electrophysiologic catheter (group A) 15 patients underwent PVI with double transseptal puncture (group B). In 8 patients of group A, iASD persisted after the follow-up period, including 6 patients with distinct RLS. We saw no iASD in group B (P = .011, CI -0.79 to -0.11). Preprocedural pulmonary artery pressure was significantly higher in patients with iASD and accompanying RLS, compared with patients with iASD and no evidence of RLS (23.75 +/- 0.50 vs 17.59 +/- 5.82, P = .048, CI 0.048-12.27). CONCLUSION: This is the first study that demonstrates a high incidence of long-term persistent iatrogenic atrial septal defect with RLS after PVI. All interatrial shunts occurred after single transseptal puncture with passage of 2 electrophysiologic catheters into the left atrium. Increased preprocedural pulmonary artery pressure seems to promote the occurrence of RLS across iASD.

Identification of "substrate fibrillators" and "trigger fibrillators" by pacemaker diagnostics.

BACKGROUND: The population of patients likely to respond to selected pacing algorithms for maintenance of sinus rhythm is unknown. OBJECTIVES: The purpose of this study was to identify patients with specific onset patterns of paroxysmal atrial fibrillation (AF). METHODS: Dual-chamber pacemakers with advanced diagnostic functions were implanted in 112 patients with conventional indications for antibradycardia pacing and a history of paroxysmal AF. Pacemaker diagnostic data were analyzed after 97.5 +/- 40.9 days. According to the frequency of premature atrial contractions (PACs) during the 5 minutes before AF onset, patients were assigned to one of three groups: group A (high PAC activity), group B (moderate PAC activity), or group C (low PAC activity). RESULTS: AF burden was lower in group A (4.6% +/- 2.4%) than group B (15.8% +/- 3.0%, P = .003) and group C (15.5% +/- 3.1%, P = .003). Fewer AF episodes occurred in group A (2.1 +/- 1.3 per day) than group B (3.8 +/- 1.2 per day, P = .006). Mean AF episode duration was shorter in group A (11.4 +/- 10.2 hours) than group C (41.4 +/- 27.5 hours, P = .03). CONCLUSION: The coincidence of low PAC activity before AF onset, high AF burden, and extended arrhythmia episode duration appears to be the consequence of a high atrial substrate factor. In these "substrate fibrillators," the efficacy of pacing algorithms for maintenance of sinus rhythm may be limited. In contrast, "trigger fibrillators" exhibiting low AF burden despite high PAC incidence may represent the target population for specific PAC-suppressing pacing algorithms.

Creatine phosphokinase elevation in obstructive sleep apnea syndrome: an unknown association?

STUDY OBJECTIVES: To evaluate the impact of obstructive sleep apnea syndrome (OSAS) on serum creatine phosphokinase (CK) levels. DESIGN: Single-center prospective cross-sectional study. SETTING: Academic sleep disorder center. PATIENTS: Two hundred one consecutive patients (mean [+/- SD] age, 54.9 +/- 11.0 years; 155 men and 46 women; mean body mass index, 31.3 +/- 6.9 kg/m(2)) with suspected sleep-disordered breathing. MEASUREMENTS AND RESULTS: OSAS was confirmed in182 patients (apnea-hypopnea index [AHI], > 5 events per hour) and was ruled out in 19 patients (control subjects) by standard polysomnography. Sixty-six OSAS patients and 1 control patient showed an unexplained CK elevation. The mean baseline CK level was significantly higher in patients with severe OSAS (AHI, > 30 event per hour; n = 89) compared to those with mild-to-moderate OSAS (AHI, 5 to 30 events per hour; n = 93) and control subjects (191.4 +/- 12.9 vs 134.3 +/- 7.5 vs 107.1 +/- 7.9 U/L, respectively; p < 0.01). Receiver operating curve analysis identified an optimal cutoff value of > 148 U/L (r = 0.660) for CK, which yielded a positive predictive value of 99%, a sensitivity of 43%, and a specificity of 95% for the diagnosis of OSAS. The mean nocturnal oxyhemoglobin saturation was the main predictor of CK level (r = 0.47; p < 0.001). Continuous positive airway pressure (CPAP) treatment resulted in a significant decline of CK levels both in patients with mild-to-moderate OSAS (n = 38; 129.7 +/- 13.4 vs 96.7 +/- 7.6 U/L, respectively; p < 0.001) and in patients with severe OSAS (n = 39; 187.7 +/- 18.9 vs 132.2 +/- 12.9 U/L, respectively; p < 0.001). CONCLUSIONS: One third of our study population showed a mild-to-moderate elevation in CK level, which was highly predictive of OSAS. The application of CPAP therapy in OSAS patients resulted in a significant decrease in CK level. We speculate that OSAS may account for a substantial number of cases of unexplained CK elevation (ie, hyperCKemia). Further studies should address the prevalence of OSAS in patients with mild-to-moderate hyperCKemia.

Diagnosis of ischaemic heart disease by myocardial contrast echocardiography during supine bicycle stress.

INTRODUCTION: Myocardial contrast echocardiography (MCE) is a new imaging modality for diagnosing ischaemic heart disease (IHD). AIM: The aim of this study was to assess 1) the feasibility of MCE during supine bicycle stress and 2) the value of this method in the diagnosis of IHD. METHODS: Supine bicycle stress was performed in 44 consecutive patients (pts) referred for coronary angiography with an intermediate pre-test probability of IHD. MCE was carried out at peak stress and during recovery (once the heart rate returned to the pre-exercise value). During MCE an ultrasound contrast agent (Sonovue) was administered intravenously in a continuous mode using an infusion pump (BR-INF 100, Bracco Research). The acquired images were qualitatively assessed for perfusion and wall motion abnormalities. The 18-segment division of the left ventricle was used in the analysis. Coronary angiography was performed in all pts within 15 days of the exercise test. A quantitative analysis of coronary artery stenoses was carried out using the CAAS system. RESULTS: MCE could not be performed in 2 pts due to technical difficulties. Coronary angiography revealed significant coronary artery stenosis in 25 pts. The sensitivity and specificity of MCE in the diagnosis of IHD were 92.0% and 82.4%, respectively. The positive and negative predictive values were found to be 88.5% and 87.5%, respectively, while the agreement between coronary angiography and MCE was 88.1% (kappa=0.75). CONCLUSIONS: MCE during supine bicycle stress and continuous intravenous administration of an ultrasound contrast agent is a feasible technique and allows accurate diagnosis of IHD in pts in whom the pre-test probability of the disease is intermediate.

[Atrial fibrillation: current therapeutic options]. / Vorhofflimmern: therapeutische Möglichkeiten.

The treatment of atrial fibrillation still remains challenging in everyday practice. Even after the introduction of catheter ablation, the decision making about the type of therapy became more complex. The recently published guidelines of the American Heart Association, the American College of Cardiology, and the European Society of Cardiology clearly show therapeutic approaches for different types of atrial fibrillation. The fear of thromboembolism still forces the physician to restore sinus rhythms and perform a perfect anticoagulation. Based on large studies, we are able to decide for each patient individually whether oral anticoagulation or acetylsalicylic acid/clopidogrel are required. Future studies in a large cohort of patients are still necessary to clarify the value of interventional therapy in conjunction with antiarrhythmic drug therapy. These will provide patients with a safe therapy and high quality of life despite presenting paroxysmal or persistent atrial fibrillation.

Caspase-3 and tissue factor expression in lipid-rich plaque macrophages: evidence for apoptosis as link between inflammation and atherothrombosis.

BACKGROUND: Macrophages associated with arterial wall lipid deposition contribute to inflammatory processes. Tissue factor (TF) has been implicated in the thrombogenicity of atherosclerotic plaques. Intimal cells undergoing apoptosis have been postulated as a source for TF. However, there is only limited knowledge of cell type, plaque component, and conditions associated with TF expression and apoptosis. We examined the hypothesis that macrophages exposed to conditions of lipid-rich plaque undergo apoptosis and express TF. METHODS AND RESULTS: In human carotid (n=15) and coronary (n=6) atherosclerotic plaques, TF and caspase-3 mRNA and protein expression (evaluated by in situ hybridization and immunohistochemistry) were increased significantly in lipid-rich compared with fibrous plaque components (P<0.01) and correlated with high macrophage content (P<0.05). Double-labeling studies demonstrated colocalization of TF and active caspase-3. In hyperlipidemic mice, expression of TF and active caspase-3 was observed simultaneously and colocalized in neointimal macrophages after arterial injury. In neointima of normolipidemic animals, TF and active caspase-3 were absent after arterial injury. In monocytes cultured in the presence of oxidized LDL, strong induction and colocalization of TF and active caspase-3 were found compared with baseline (P<0.05). Both antigens were significantly decreased after cotreatment with a caspase inhibitor (P<0.05) and were absent in untreated control cells. CONCLUSIONS: The expression of TF as the primary cell-associated activator of the coagulation pathway proves to be closely related to macrophages undergoing apoptosis in conditions of lipid-rich plaque, pointing to a key role of lipid content and inflammatory cell viability in determining plaque thrombogenicity.

Radiation exposure during catheter ablation of atrial fibrillation.

BACKGROUND: The purpose of this study was to determine the radiation exposure during catheter ablation of atrial fibrillation (AF) using the pulmonary vein (PV) approach. METHODS AND RESULTS: The study included 15 patients with AF and 5 patients each with atrial flutter and atrioventricular nodal reentrant tachycardia (AVNRT) who underwent fluoroscopically guided procedures on a biplane x-ray system operated at a low-frame pulsed fluoroscopy (7.5 frames per second). Radiation exposure was measured directly with 50 to 60 thermoluminescent dosimeters (TLDs). Peak skin doses (PSDs), effective radiation doses, and risk of fatal malignancies were all computed. Mean fluoroscopy durations for AF procedures were 67.8+/-21 minutes in the right anterior oblique (RAO) and 61.9+/-16.6 minutes in the left anterior oblique (LAO) projection, significantly different from that required for atrial flutter and AVNRT. The mean PSDs measured with the TLDs were 1.0+/-0.5 Gy in the RAO and 1.5+/-0.4 Gy in the LAO projection. The lifetime risk of excess fatal malignancies normalized to 60 minutes of fluoroscopy was 0.07% for women and 0.1% for men. CONCLUSIONS: The relatively small amounts of the patient's radiation exposure in this study, despite the prolonged fluoroscopy durations, can be attributed to the use of very-low-frame pulsed fluoroscopy, the avoidance of magnification, and optimal adjustments of the fluoroscopy exposure rates. The resulting lifetime risk of fatal malignancy is within the range previously reported for standard supraventricular arrhythmias.

Dendritic cells in neointima formation after rat carotid balloon injury: coordinated expression withanti-apoptotic Bcl-2 and HSP47 in arterial repair.

OBJECTIVES: We sought to evaluate: 1) the contribution of dendritic cells (DCs); and 2) the impact of B-cell lymphoma 2 protein (Bcl-2), a central anti-apoptotic protooncogene, and of heat shock protein 47 (HSP47), indicating subsequent collagen deposition, in neointima formation after angioplasty. BACKGROUND: The origin of neointimal cells and the factors that promote their accumulation are still unclear. Previous studies reported intimal presence of DCs and suggested cells of primarily extravascular origin to contribute to arterial repair. METHODS: Sprague-Dawley rats underwent carotid balloon angioplasty. At different times after angioplasty, tissue sections were analyzed by immunohistochemistry using OX-62 and S100 as DC markers and antibodies against Bcl-2 and HSP47, supplemented by electron microscopic analysis of cell type and apoptosis. RESULTS: Four days after injury, DCs adhered along the internal elastic lamina and demonstrated intense Bcl-2 and HSP47 expression, consistent with low apoptosis. With ongoing neointima enlargement, luminal DCs remained prevalent and were colocalized with Bcl-2 and HSP47, while signaling decreased to basal regions. Media showed no DCs and only low Bcl-2 and HSP47 immunoreactivity. Adventitia transiently revealed a structural separation between day 4 and 7. Whereas the inner layer demonstrated sparse cellularity, apoptosis and no DC, Bcl-2, and HSP47 labeling, the outer layer was characterized by high myofibroblast density with strong Bcl-2 and HSP47 expression but absence of DCs. CONCLUSIONS: We identify DCs as novel components in early neointima formation, promoted by coordinated anti-apoptotic Bcl-2 and HSP47 expression. Despite intense adventitial remodeling, there is no evidence of adventitial cell transmigration.

Post mortem analysis of a left atrial appendage occlusion device (PLAATO) in a patient with permanent atrial fibrillation.

Thromboemoblism is the most feared complication of atrial fibrillation. Percutaneous left atrial appendage occlusion is a new interventional procedure for reducing thromboembolic risk in patients with atrial fibrillation. The paper reports of a post mortem analysis of the device demonstrating that one year after implantation the atrial surface of the device is completely covered by neo-endothelium and the device occludes the appendage completely.

[A case of arteria cerebri aneurysm, sepsis, and miliary lung infiltrates in a 32-year-old woman]. / Arteria-cerebri-Aneurysma, Sepsis und miliare Lungenrundherde bei einer 32-jährigen Patientin.

BACKGROUND: Miliary tuberculosis is a rare manifestation of tuberculosis with a high mortality rate. Diagnosis may easily be missed when severe neurologic symptoms are the first clinical manifestation. A typical case of miliary tuberculosis is reported, with special regard to the problems of diagnostic work-up. The need for an early empirical therapy for suspected military tuberculosis is emphasized in particular. CASE REPORT: A 32-year-old Moroccan woman was admitted to the hospital with aphasia and a hemiparesis due to an intracerebral hemorrhage caused by a ruptured septic A. cerebri media aneurysm. Despite intensive work-up no septic focus could be found. Chest radiograph and computerized tomography (CT) showed miliary consolidations in the lungs. Skin testing (Tuberkulin Behring GT5) and smears for acid-fast bacilli and polymerase chain reaction (PCR) for tuberculosis of bronchoalveolar lavage (BAL) were negative. A four-drug antituberculous regimen (rifampicin [RMP], isoniazid [INH], pyrazinamide [PZA], ethambutol [EMB]) was initiated, and resulted in normalization of temperature, blood pressure, and C-reactive protein. Subsequently, cultures of BAL yielded Mycobacterium tuberculosis. The patient was discharged, a two-drug regimen was conducted (RMP, INH) after 2 months. Follow-up of the patient showed a significant improvement of the miliary lung consolidations after 5 months in CT of the lung. Only minor neurologic symptoms persisted after cessation of the therapy. CONCLUSION: In developed countries, miliary tuberculosis is a very rare cause of septic infiltrative lung disease. However, due to the nonspecific nature of the presentation and despite improved diagnostic techniques, a high clinical suspicion is essential for successful treatment.

[Long-term outcome of intrapleural fibrinolytic therapy via small-bore catheter drainage in the management of complicated parapneumonic effusion and empyema-a case series]. / Langzeitergebnisse der intrapleuralen Fibrinolytikatherapie komplizierter parapneumonischer Pleuraergüsse und Empyeme über kleinlumige Katheter.

BACKGROUND AND PURPOSE: Complicated parapneumonic effusions (PPE) and pleural empyemas (PE) are associated with increased morbidity and mortality. Intrapleural fibrinolytic therapy (IFT) has been established, besides video-assisted thoracoscopy (VATS), in the management of PPE and PE. Combination of IFT and small-bore catheter drainage has previously not been investigated. PATIENTS AND METHODS: 15 patients consecutively referred for PPE and PE were managed with simultaneous IFT via small-bore catheter drainage (9, 12, 14 F). In addition to evaluation of primary outcome, lung function testing and radiologic studies were obtained after 3 months to predict potential pulmonary restrictive impairment and residual pleural thickening. RESULTS: Primary outcome of all 15 patients was positive. Only one patient showed a significant residual pleural thickening. None of the patients showed a restrictive lung function pattern. CONCLUSION: Proven applicability of IFT via small-bore catheter drainage seems to be effective in the face of long-term outcome. Further prospective and multicentric studies should be initiated to investigate the practicability of IFT via small-bore catheter drainage.

Presence of bone-marrow- and neural-crest-derived cells in intimal hyperplasia at the time of clinical in-stent restenosis.

OBJECTIVE: Intralesional data of coronary target lesions following stent implantation are infrequent. In addition, there is ongoing controversy on the origin of neointimal cells. In this respect, several lines of evidence revealed bone-marrow-derived endothelial progenitor and dendritic cells (DCs) as well as neural-crest-derived cells (NCCs) to contribute to atherosclerosis. Therefore, the objective of the present study was to assess cellularity, cell type and origin of neointimal cells in in-stent restenosis (ISR). METHODS: Atherectomy specimens from 17 patients with coronary in-stent restenosis (n=10; time post-stenting 5+/-3 months) and with peripheral in-stent restenosis (n=7; 7+/-3 months) versus those from 10 patients with primary lesions were immunohistochemically examined for the presence of the determinants CD34, AC133, S100, glial fibrillary acidic protein (GFAP), neuron-specific enolase (NSE), nerve growth factor receptor (NGFR) and alpha-smooth muscle actin followed by computer-assisted morphometry. RESULTS: In-stent restenosis probes consistently demonstrated homogeneous hypercellularity (942+/-318 cells/mm(2)) compared to de novo lesions (347+/-120 cells/mm(2), P<0.001). alpha-smooth muscle actin positive cells occupied 67% of intimal cells in in-stent restenosis. As a key finding, expression of endothelial progenitor cells (CD34: 7.1+/-2.5% positive/total cells vs. 0.6+/-0.7%, P<0.001; AC133: 7.0+/-3.4% vs. 1.0+/-0.7%, P<0.001), dendritic cells (S100: 9.8+/-5.6% vs. 1.4+/-1.1%, P<0.001) and neural-crest-derived cells (GFAP: 7.9+/-2.4% vs. 3.1+/-1.0%; NSE: 4.4+/-2.6% vs. 1.3+/-1.6%; NGFR: 4.2+/-2.5% vs. 1.1+/-0.7%; each P<0.001) was significantly increased in in-stent restenosis compared to primary lesions. CONCLUSIONS: Bone-marrow- and neural-crest-derived cells, the most dendritic cells, are consistently present in in-stent restenosis, whereas alpha-smooth muscle actin positive cells constitute the largest intimal cell pool. Our data suggest the recruitment of primarily extravascular cells within neointima formation in human in-stent restenosis.

Antiplatelet effects of angiotensin-converting enzyme inhibitors compared with aspirin and clopidogrel: a pilot study with whole-blood aggregometry.

BACKGROUND: Although specific antiplatelet drugs are well-established and effective in atherosclerosis prevention, recent clinical trials have also shown that use of angiotensin-converting enzyme (ACE) inhibitors results in a decrease in cardiovascular events. Therefore, in this study, we sought to assess the coagulative activity of patients with cardiovascular disease grouped for treatment with either ACE inhibitors, aspirin, clopidogrel/aspirin, or none of these medications. METHODS: Blood samples from 303 patients with cardiovascular disease were analyzed with whole-blood aggregometry. Platelet aggregation was determined by the increase in impedance across paired electrodes in response to the aggregatory agents adenosine diphosphate (ADP) or collagen. RESULTS: As the central finding, platelet aggregation was attenuated by ACE inhibitors and by aspirin or clopidogrel/aspirin, which was indicated by a lower impedance increase compared with no medication. With ACE inhibition, platelet aggregation decreased by 33% (P =.042) after ADP induction. No significant antithrombotic effect was seen with aspirin alone (17%, P = 1.0), whereas a decrease in ADP-induced platelet aggregation was extensive with clopidogrel/aspirin (85%, P =.001). After collagen induction, platelet aggregation was reduced by 16% (P =.028) in the presence of ACE inhibitor therapy, whereas inhibition with aspirin and clopidogrel/aspirin was 23% (P =.004) and 35% (P =.026), respectively, compared with participants who were not treated. CONCLUSIONS: These ex vivo data on whole-blood aggregometry provide direct evidence that ACE inhibitors decrease platelet aggregation, whereas aspirin and clopidogrel are confirmed as established antithrombotics. Pleiotropic effects of ACE inhibition on platelet function may contribute to the clinical benefit observed with this drug class on major cardiovascular end points.

A prospective and randomized comparison of the safety and effects of therapeutic levels of enoxaparin versus unfractionated heparin in chronically anticoagulated patients undergoing elective cardiac catheterization.

Consecutive patients with atrial fibrillation and/or prosthetic heart valves, receiving chronic anticoagulation with phenprocoumon and scheduled to undergo cardiac catheterization, were randomized to subcutaneous enoxaparin twice daily (n = 32) or intravenous UFH (n = 36). Cardiac catheterization was performed at an international normalized ratio <1.5. Activated partial thromboplastin times and levels of anti-Factor Xa activity were measured daily. The time until effective anticoagulation (primary endpoint) was significantly shorter for enoxaparin than for UFH (1.1 +/- 0.4 days versus 3.7 +/- 2.5 days, p<0.0001). The percentage of days of effective anticoagulation was significantly higher in the enoxaparin group than in the UFH group (93.3 +/- 9.5% versus 53.7 +/- 26.6%, p <0.0001). In conclusion, enoxaparin achieves therapeutic levels of anticoagulation more rapidly and consistently than UFH in chronically anticoagulated patients with prosthetic heart valves and/or atrial fibrillation undergoing cardiac catheterization.

Fate of left atrial thrombi in patients with atrial fibrillation determined by transesophageal echocardiography and cerebral magnetic resonance imaging.

Patients with atrial fibrillation (AF) and atrial thrombi have an increased risk for cerebral embolism. However, there is little knowledge about the long-term fate of atrial thrombi and the incidence of cerebral embolism in patients receiving continued oral anticoagulation. Forty-three consecutive patients with AF and atrial thrombi were enrolled in the study. Serial and prospective transesophageal echocardiographic studies, cranial magnetic resonance imaging (MRI), and clinical examinations were performed during a period of 12 months. Oral anticoagulation was continued or initiated in all patients. An international normalized ratio of 2.0 to 3.0 was regarded as effective. During follow-up, 56% of the thrombi disappeared (7 [16%] at 1 month, 18 [42%] at 3 months, 21 [49%] at 6 months, and 24 [56%] at 12 months). Patients with the disappearance of thrombi had significantly smaller thrombi compared with patients with persistent thrombi (1.5 +/- 0.8 cm in length and 0.8 +/- 0.5 cm in width vs 1.9 +/- 0.6 cm in length and 1.3 +/- 0.4 cm in width, p = 0.04), reduced echogenicity of thrombi (46% vs 89%, p <0.01), and smaller left atrial (LA) volume (83 +/- 27 vs 116 +/- 55 cm(3)). Seven patients (16%) had embolic lesions during follow-up MRI. Six of these patients (86%) had clinically apparent embolisms, and 1 died from stroke. The only independent predictors of cerebral embolism were an elevated peak emptying velocity of the LA appendage (p <0.01) and previous thromboembolic events (p = 0.02). Patients with AF and atrial thrombi have a large likelihood of cerebral embolism (16%) and/or death despite oral anticoagulation therapy. Thrombus size may predict thrombus resolution under continued anticoagulation.

D-Ribose improves diastolic function and quality of life in congestive heart failure patients: a prospective feasibility study.

Patients with chronic coronary heart disease often suffer from congestive heart failure (CHF) despite multiple drug therapies. D-Ribose has been shown in animal models to improve cardiac energy metabolism and function following ischaemia. This was a prospective, double blind, randomized, crossover design study, to assess the effect of oral D-ribose supplementation on cardiac hemodynamics and quality of life in 15 patients with chronic coronary artery disease and CHF. The study consisted of two treatment periods of 3 weeks, during which either oral D-ribose or placebo was administered followed by a 1-week wash out period, and then administration of the other supplement. Assessment of myocardial functional parameters by echocardiography, quality of life using the SF-36 questionnaire and functional capacity using cycle ergometer testing was performed. The administration of D-ribose resulted in an enhancement of atrial contribution to left ventricular filling (40+/-11 vs. 45+/-9%, P=0.02), a smaller left atrial dimension (54+/-20 vs. 47+/-18 ml, P=0.02) and a shortened E wave deceleration (235+/-64 vs. 196+/-42, P=0.002) by echocardiography. Further, D-ribose also demonstrated a significant improvement of the patient's quality of life (417+/-118 vs. 467+/-128, P< or =0.01). In comparison, placebo did not result in any significant echocardiographic changes or in quality of life. This feasibility study in patients with coronary artery disease in CHF revealed the beneficial effects of D-ribose by improving diastolic functional parameters and enhancing quality of life.