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Thomas Meinertz

Publications and source records attributed to Thomas Meinertz.

At least 19 recordsLinked to original sources
PubMed2006

Event-recorder monitoring in the diagnosis of atrial fibrillation in symptomatic patients: subanalysis of the SOPAT trial.

In the SOPAT (suppression of paroxysmal atrial tachyarrhythmias) trial, a high number of asymptomatic atrial fibrillation (AF) episodes were registered in patients with symptomatic AF. This subanalysis was performed to answer three questions: (1) Does antiarrhythmic therapy influence the ratio of symptomatic to asymptomatic AF? (2) Are symptoms during AF dependent on the heart rate (HR)? (3) Do symptoms correlate with an episode of AF? Within 60 months 1,033 patients with symptomatic AF were randomized to either quinidine plus verapamil (Q+V) 480/240 mg/day, Q+V 320/160 mg/day, sotalol 320 mg/day, or placebo, and followed up by daily and symptom-triggered ECG event recording. Over 188,634 ECGs were analyzed (87% SR, 7% AF). Symptoms were reported in only 46% of AF-ECGs. Quinidine plus verapamil reduced the ratio of symptomatic to asymptomatic AF, whereas sotalol had no effect (median [%] (25/75% quartile): Q+V 480/240: 33 (0/79), Q+V 320/160: 45 (1/82), sotalol: 56 (7/93), placebo: 63 (8/92)). The HR during AF directly correlates with the occurrence of symptoms (P < 0.001) and was significantly lower during asymptomatic AF in all groups (mean +/- SD: sympt.: 113 +/- 27/minute, asympt.: 103 +/- 27/minute, P < 0.001). Both antiarrhythmics reduced the mean HR compared to placebo (P < 0.001). Analyzing all symptom-triggered ECGs, AF was diagnosed in only 37%, whereas the majority were SR. Taken together, in contrast to sotalol, Q+V reduces the ratio of symptomatic to asymptomatic AF compared with placebo, at least in part by decreasing the heart rate. Furthermore, patients' symptoms are not a reliable surrogate parameter for the prevalence of AF.

Anti-Arrhythmia Agents↗
PubMed2006

AT1-receptor blockade with irbesartan improves peripheral but not coronary endothelial dysfunction in patients with stable coronary artery disease.

Activation of the renin-angiotensin-aldosterone system plays an important role in the pathogenesis of endothelial dysfunction and atherosclerosis. Studies evaluating the effect of AT1-receptor blockers on endothelial dysfunction in patients with coronary artery disease (CAD) revealed mixed results. Studies addressing the effects of AT1-receptor blockers on the coronary and peripheral function in the same study population, are still lacking. We therefore aimed to test the effects of long-term therapy with the AT1-receptor blocker irbesartan (IRB) on both, the coronary and peripheral endothelial function in patients with CAD. Seventy-two patients with CAD were randomly assigned to double-blinded treatment for 6 months with IRB 300 mg per day or placebo, respectively. Coronary and peripheral endothelial function were measured by intracoronary infusion of acetylcholine (final intracoronary concentration 10(-7.3) to 10(-5.6)M) and by determining flow-dependent dilation (FMD) of the brachial artery, respectively. IRB significantly improved FMD, while no change of coronary endothelial function was observed. Interestingly, plasma levels of N(G),N(G)-dimethyl-arginine, and the isoprostane excretion rate were not modified. IRB treatment improves peripheral but not coronary endothelial dysfunction in patients with CAD. Since reduced FMD of the brachial artery has been shown to be associated with a high-cardiovascular event rate, improvement of FMD by IRB may lead to better prognosis of patients with CAD.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2006

[German Competence Network on Atrial Fibrillation (AFNET). A nationwide cooperation for better research and patient care].

The Atrial Fibrillation Competence Network is an interdisciplinary national research network funded by the Federal Ministry of Education and Research (BMBF). The aim of the network--founded in 2003--is to improve the treatment of atrial fibrillation, the most common clinically important arrhythmia of the heart. A decentralized patient registry has been established. This registry, which comprises the manifestation, diagnostics and therapy of atrial fibrillation in Germany, is being used as a data basis for epidemiologic clinical studies. Epidemiologic projects are being conducted to study, e.g., the prevalence of atrial fibrillation as well as the occurrence of complications. Four multicenter clinical trials have been started to optimize pharmacological treatments (ANTIPAF trial, Flec-SL trial), preventive pacing (BACE-PACE trial) and catheter-based ablation (GAP-AF trial). Other clinical projects are being conducted to study the risk of neurologic complications and to develop new diagnostic imaging techniques. Experimental basic research projects are focusing on different aspects of atrial remodeling in order to find out in which way the molecular mechanisms can be manipulated by new methods of treatment. First results are presented.

Atrial Fibrillation↗
PubMed2006

Inhibition of xanthine oxidase improves myocardial contractility in patients with ischemic cardiomyopathy.

Reactive oxygen species, in particular superoxide, have been closely linked to the underlying pathophysiology of ischemic cardiomyopathy: superoxide not only mediates mechanoenergetic uncoupling of the myocyte but also adversely impacts on myocardial perfusion by depleting endothelial-derived nitric oxide bioavailability. Xanthine oxidase generates superoxide upon oxidation of hypoxanthine and xanthine and has been detected in cardiac myocytes and coronary endothelial cells of patients with ischemic heart disease. Here we investigated the effects of oxypurinol, a xanthine oxidase inhibitor, on myocardial contractility in patients with ischemic cardiomyopathy. Twenty patients (19 males, 66+/-8 years) with stable coronary disease, severely suppressed systolic function (left ventricular ejection fraction 22+/-2%), and nonelevated uric acid plasma levels received a single intravenous dose of oxypurinol (400 mg). Cardiac MRI studies, performed before and 5.2+/-0.9 h after oxypurinol administration, revealed a reduction in end-systolic volumes (-9.7+/-4.2%; p=0.03) and an increase in left ventricular ejection fraction (+17.5+/-5.2%; p=0.003), whereas 6 patients (6 males, 63+/-3.8 years, ejection fraction 26+/-5%) who received vehicle only did not show significant changes in any of the parameters studied. Oxypurinol improves left ventricular function in patients with ischemic cardiomyopathy. These results underscore the significance of reactive oxygen species as important pathophysiological mediators in ischemic heart failure and point toward xanthine oxidase as an important source of reactive species that serve to modulate the myocardial redox state in this disease.

Aged↗
PubMed2006

Substrate modification combined with pulmonary vein isolation improves outcome of catheter ablation in patients with persistent atrial fibrillation: a prospective randomized comparison.

AIMS: To investigate the effectiveness of additional substrate modification (SM) by left atrial (LA) linear lesions as compared with pulmonary vein isolation (PVI) alone in patients with persistent atrial fibrillation (AF) in a prospective randomized study. Percutaneous PVI has evolved as an accepted treatment for paroxysmal AF but seemed to be less effective in patients with persistent AF. The benefit of PVI alone and additional linear lesions has not been validated in a randomized study so far. METHODS AND RESULTS: Sixty-two patients with persistent AF (median duration 7, range 1-18 months) were randomly assigned to either PVI alone (n = 30) or additional SM (n =32) consisting of a roof line connecting both left superior and right superior PV and LA isthmus ablation between left inferior PV and mitral annulus. Procedures including SM were performed using a three-dimensional mapping system (EnSite NavX, St Jude Medical, St Paul, MN, USA). Anti-arrhythmic drugs were discontinued within 8 weeks after ablation in both groups. Follow-up included daily trans-telephonic ECG transmitted irrespective of the patient's symptoms. PVI was successful in 98% of all targeted veins in both groups. Additional SM did not increase fluoroscopy time (72.1+/-18.7 vs. 72.9+/-17.3 min, P=0.92) because of the use of three-dimensional navigation in the PVI+SM group. AF recurrences within the first 4 weeks following ablation were more common after PVI alone (77%) than additional SM (44%, P=0.002). After a follow-up time of 487 (429-570) days, only 20% of patients undergoing stand alone PVI remained in sinus rhythm when compared with 69% following PVI combined with SM (P=0.0001). Two patients assigned to PVI+SM experienced procedure-related complications (cardiac tamponade and minor stroke) which resolved without sequelae. CONCLUSION: PVI alone is insufficient in the treatment of persistent AF. However, additional left linear lesions increase the success rate significantly. Early AF-relapses are associated with a negative outcome after PVI alone but not following additional SM.

Atrial Fibrillation↗
PubMed2006

NADPH oxidase accounts for enhanced superoxide production and impaired endothelium-dependent smooth muscle relaxation in BKbeta1-/- mice.

OBJECTIVE: Nitric oxide (NO)-induced vasorelaxation involves activation of large conductance Ca2+-activated K+ channels (BK). A regulatory BKbeta1 subunit confers Ca2+, voltage, and NO/cGMP sensitivity to the BK channel. We investigated whether endothelial function and NO/cGMP signaling is affected by a deletion of the beta1-subunit. METHODS AND RESULTS: Vascular superoxide in BKbeta1-/- was measured using the fluorescent dye hydroethidine and lucigenin-enhanced chemiluminescence. Vascular NO formation was analyzed using electron paramagnetic resonance (EPR), expression of NADPH oxidase subunits, the endothelial NO synthase (eNOS), the soluble guanylyl cyclase (sGC), as well as the activity and expression of the cyclic GMP-dependent kinase I (cGK-I) were assessed by Western blotting technique. eNOS, sGC, cGK-I expression and acetylcholine-induced NO production were unaltered in Bkbeta1-/- animals, whereas endothelial function was impaired and the activity of the cGK-I was reduced. Vascular O2- and expression of the NADPH oxidase subunits p67phox and Nox1 were increased. Endothelial dysfunction was normalized by the NADPH oxidase inhibitor apocynin. Potassium chloride- and iberiotoxin-induced depolarization mimicked the effect of BKbeta1-deletion by increasing vascular O2- in an NADPH-dependent fashion. CONCLUSIONS: The deletion of BKbeta1 causes endothelial dysfunction by increasing O2- formation via increasing activity and expression of the vascular NADPH oxidase.

Animals↗
PubMed2006

Clopidogrel improves systemic endothelial nitric oxide bioavailability in patients with coronary artery disease: evidence for antioxidant and antiinflammatory effects.

BACKGROUND: Platelet stimulation and activation are known not only as prerequisite of clot formation but are increasingly recognized as important contributors to inflammation and vascular injury. The present study in patients with symptomatic coronary disease investigated whether platelet adenosine diphosphate receptor blockade by clopidogrel exerts beneficial effects on endothelial nitric oxide bioavailability, oxidative stress, and/or inflammatory status. METHODS AND RESULTS: One hundred three consecutive patients with symptomatic coronary disease and long-term aspirin therapy were studied. Endothelium-dependent and -independent vasodilation was determined measuring forearm blood flow (FBF)-responses to acetylcholine with and without N(G)-monomethyl-L-arginin (L-NMMA) and sodium nitroprusside, by using venous occlusion plethysmography. Patients were randomized to receive additional treatment with clopidogrel or placebo. Vascular function tests were repeated after 5 weeks and showed significant improvement of acetylcholine-induced vasodilatation and L-NMMA responses in the clopidogrel-added group (max. FBF from 9.8+/-0.3 to 14.7+/-0.4; L-NMMA-response from 3.7+/-0.1 to 6.8+/-0.3 mL/100 mL/min). In contrast, no significant changes were observed in the placebo group. Sodium nitroprusside-induced vasodilation was not changed in either group. Urinary excretion of 8-iso-prostaglandin F2alpha and plasma levels of hsCRP, sCD40L, and RANTES were reduced in patients on additional treatment with clopidogrel, but not in patients on placebo. CONCLUSIONS: Clopidogrel improves endothelial nitric oxide bioavailability and diminishes biomarkers of oxidant stress and inflammation in patients with symptomatic coronary artery disease, suggesting that beyond inhibition of platelet aggregation, adenosine phosphate receptor blockade may also have promising vasoprotective effects.

Acetylcholine↗
PubMed2006

Carcinoembryonic antigen-related cell adhesion molecule 1 modulates vascular remodeling in vitro and in vivo.

Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1), a cellular adhesion molecule of the Ig superfamily, is associated with early stages of angiogenesis. In vitro, CEACAM1 regulates proliferation, migration, and differentiation of murine endothelial cells. To prove that CEACAM1 is functionally involved in the regulation of vascular remodeling in vivo, we analyzed 2 different genetic models: in Ceacam1-/- mice, the Ceacam1 gene was deleted systemically, and in CEACAM1(endo+) mice, CEACAM1 was overexpressed under the control of the endothelial cell-specific promoter of the Tie2 receptor tyrosine kinase. In Matrigel plug assays, Ceacam1-/- mice failed to establish new capillaries whereas in CEACAM1(endo+) mice the implants were vascularized extensively. After induction of hind limb ischemia by femoral artery ligation, Ceacam1-/- mice showed significantly reduced growth of arterioles and collateral blood flow compared with their WT littermates. In agreement with a causal role of CEACAM1 in vascular remodeling, CEACAM1(endo+) mice exhibited an increase in revascularization and collateral blood flow after arterial occlusion. Our findings indicate that CEACAM1 expression is important for the establishment of newly formed vessels in vivo. Hence CEACAM1 could be a future target for therapeutic manipulation of angiogenesis in disease.

Animals↗
PubMed2006

Heparins increase endothelial nitric oxide bioavailability by liberating vessel-immobilized myeloperoxidase.

BACKGROUND: Neutrophils and monocytes are centrally linked to vascular inflammatory disease, and leukocyte-derived myeloperoxidase (MPO) has emerged as an important mechanistic participant in impaired vasomotor function. MPO binds to and transcytoses endothelial cells in a glycosaminoglycan-dependent manner, and MPO binding to the vessel wall is a prerequisite for MPO-dependent oxidation of endothelium-derived nitric oxide (NO) and impairment of endothelial function in animal models. In the present study, we investigated whether heparin mobilizes MPO from vascular compartments in humans and defined whether this translates into increased vascular NO bioavailability and function. METHODS AND RESULTS: Plasma MPO levels before and after heparin administration were assessed by ELISA in 109 patients undergoing coronary angiography. Whereas baseline plasma MPO levels did not differ between patients with or without angiographically detectable coronary artery disease (CAD), the increase in MPO plasma content on bolus heparin administration was higher in patients with CAD (P=0.01). Heparin treatment also improved endothelial NO bioavailability, as evidenced by flow-mediated dilation (P<0.01) and by acetylcholine-induced changes in forearm blood flow (P<0.01). The extent of heparin-induced MPO release was correlated with improvement in endothelial function (r=0.69, P<0.01). Moreover, and consistent with this tenet, ex vivo heparin treatment of extracellular matrix proteins, cultured endothelial cells, and saphenous vein graft specimens from CAD patients decreased MPO burden. CONCLUSIONS: Mobilization of vessel-associated MPO may represent an important mechanism by which heparins exert antiinflammatory effects and increase vascular NO bioavailability. These data add to the growing body of evidence for a causal role of MPO in compromised vascular NO signaling in humans.

Aged↗
PubMed2006

Transient ST-segment-elevation during pulmonary vein ablation using circumferential coiled microelectrodes in a prospective multi-centre study.

AIMS: Paroxysmal atrial fibrillation (PAF) is predominantly triggered by focal ectopies located within the pulmonary veins (PV). The BITMAP Study (Breakthrough and Isolation Trial: Mapping and Ablation of Pulmonary Veins) investigated prospectively the safety and efficacy of a catheter design with circumferential mapping and ablation electrodes. We report the phenomenon of ST-segment-elevation during catheter placement in the left atrium (LA) and superior PVs in this multi-centre study. METHODS AND RESULTS: Forty-three patients (57+/-10 years) with PAF were included in this study. Radiofrequency catheter (RFC) ablation supported by the 4F REVELATION Helix microcatheter (Cardima Inc., Freemont, CA, USA) with eight distal-coiled microelectrodes for bipolar mapping and ablation. RFC was applied at the ostial region of PV (30 W, 45-50 degrees C) with a maximum of four RFC applications per electrode. In four of the 43 patients from three centres, we recorded the occurrence of ST-segment-elevation greater than 0.2 mV and accompanying left thoracic discomfort. The ECG changes and the symptoms started abruptly and lasted for 4.2+/-2.2 min. Pericardial effusion could instantaneously be excluded by echocardiography in all cases. Coronary angiograms were performed in three patients with the longest episodes; no thrombotic material or air emboli were present. The symptoms and the ECG changes resolved completely in all patients. CONCLUSION: The phenomenon of ST-segment-elevation during LA- and PV-mapping in patients with PAF may be a common occurrence. In this prospective multi-centre trial, we demonstrated the reversibility of this phenomenon; no cardiovascular or cerebral damage was reported during both the procedure and the follow-up. Although the mechanism is still unclear, vasospasm may contribute to this phenomenon because of autonomic dysregulation.

Adult↗
PubMed2006

[Syncope].

Syncope is a transient, self-limiting loss of consciousness usually leading to a fall. The onset of syncope is relatively rapid and the subsequent recovery is spontaneous, complete and usually prompt. As syncope is a symptom, the aim of the diagnostic work-up is to assess whether there is a syncope or another "nonsyncopal" condition, whether there are clinical features suggesting the diagnosis, whether the patient has an increased risk for mortality or recurrent episodes, and whether the patient must be admitted to hospital. The diagnostic work-up is given for two cases: a 68-year-old male with insulin-dependent diabetes experienced his first syncope after lunch. The clinical judgment suggested a neurocardiogenic syncope. The initial evaluation consisting of history, physical examination and twelve-lead ECG evidenced that the patient received several drugs for arterial hypertension so that an orthostatic hypotension had to be ruled out. The twelve-lead ECG showed a left bundle branch block suggesting an arrhythmic syncope and the need for additional diagnostics: an echocardiography mainly to assess the left ventricular function which was normal, and a 24-h long-term ECG to rule out arrhythmias which were not observed. The patient gets an explanation of his risk and the reassurance about his excellent prognosis and some preventive lifestyle modifications such as sufficient volume intake. The second case is a sick 58-year-old male with tracheal cough und aggravating breathing who had a syncope on his way to the toilette. The cause of the syncope was related to a bronchitis with high fever. The patient received a causative treatment and recovered completely.

Cardiology↗
PubMed2006

Intraoperative comparison of a subthreshold test pulse with the standard high-energy shock approach for the measurement of defibrillation lead impedance.

UNLABELLED: There are two methods to measure shocking lead impedance: delivery of high-energy shocks that require patient sedation, and the painless measurement of impedance from subthreshold test pulses. The aim of this study was to compare the two methods. METHODS: The study included 131 patients implanted with a standard DR (n = 71) or VR (n = 60) ICD connected to either single-coil (n = 39) or dual-coil (n = 92) defibrillation leads. The noninvasive high-energy impedance test was done using a 17 J shock after induction of ventricular tachyarrhythmias and compared to a 0.4 microJ test pulse used by the ICD for the subthreshold measurements. RESULTS: Defibrillation lead impedance measurements were not significantly different between patients with the same shocking vector configuration. In patients with a single-coil defibrillation lead the impedance was 62 +/- 9 Omega with the high-energy shock and 62 +/- 8 Omega with the subthreshold test pulses (P = 0.13). Patients with a dual-coil configuration recorded average impedances of 40 +/- 5 Omega from both tests (P = 0.44). While there was no difference in values recorded within each lead configuration, there was a significant difference in impedance between the single-coil and the dual-coil patient groups (P = 0.001). CONCLUSIONS: There was no significant difference between shocking lead impedances measured with the high-energy shock or the subthreshold test pulses. This offers the possibility of noninvasive, low-energy serial measurements of shocking lead impedance at follow-up visits and removing the need for sedation.

Defibrillators, Implantable↗
PubMed2006

Correlation of symptoms to ECG diagnosis following atrial fibrillation ablation.

INTRODUCTION: Currently, definition of success following atrial fibrillation (AF) ablation is commonly based on the lack of symptoms. The purpose of this study was to evaluate the correlation between symptoms and the underlying rhythm after AF ablation. METHODS AND RESULTS: Eighty consecutive patients (pts) were treated for paroxysmal episodes of AF by segmental ostial ablation of all pulmonary veins and right atrial isthmus ablation. For 6 months pts transmitted transtelephonic (T-) ECG recordings in combination with comments daily or in the event of symptoms. Eligible comments were classified as: (1) asymptomatic, (2) symptomatic. Analysis was performed at 1-month intervals, defining an acute (first month) and chronic period (second to sixth month) after ablation. Overall 6,835 T-ECGs were analyzed. Of these 5,437 (79.5%) showed sinus rhythm (SR) and 1,398 (20.5%) showed AF. Pts in SR reported symptoms for 593 (10.9%) episodes, whereas 4,844 (89.1%) episodes were asymptomatic. During AF, 646 (46.2%) episodes were associated with symptoms, and 752 (53.8%) episodes remained asymptomatic. Exclusively asymptomatic were 7 (8.8%) pts. In 30 (52.6%) of 57 pts with AF, arrhythmic events were confined to the acute phase. Of the remaining 27 pts 14 (52%) reported an improvement, 12 (44%) the same, and 1 (4%) worsened symptoms after 3 months. A significant change (P < 0.01) toward more asymptomatic episodes from the acute (43.5%) to the chronic (57.5 +/- 4.5%) period was evident. CONCLUSION: Assessment of success after AF ablation cannot be based on the absence of symptoms due to a high prevalence of asymptomatic episodes.

Atrial Fibrillation↗
PubMed2006

Association between eotaxin (CCL11), C-reactive protein, and antimicrobial antibodies in patients undergoing coronary angioplasty.

Eotaxin (CCL11) is a potent chemoattractant for eosinophils and lymphocytes. Apart from its functions in the eosinophilic system, eotaxin has been shown to be overexpressed in atherosclerosis. We therefore sought to determine whether chronic infection with Chlamydia pneumoniae or other infectious agents is correlated with concentrations of eotaxin or C-reactive protein since this mechanism could explain the finding that chronic infection stimulates smooth muscle cell migration and plaque development. Patients undergoing percutaneous coronary angioplasty (PCI) for acute coronary syndrome or stable angina were included in the study. Blood was drawn before PCI, at 6 weeks, and 6 and 12 months after coronary intervention. Eotaxin and C-reactive protein were determined by enzyme-linked immunosorbent assay (ELISA). Antibodies against Candida, C. pneumoniae, cytomegalovirus, Helicobacter pylori, and herpes simplex virus were measured by ELISA or immunofluorescence. Two hundred five consecutive patients undergoing PCI (stable angina, n = 136; acute coronary syndrome, n = 69) and 83 patients with normal coronary arteries were enrolled in the study. Eotaxin concentrations at inclusion were higher in patients with coronary artery disease than in control patients, p = .01, and comparable in patients with stable angina and those with acute coronary syndrome but did not correlate with C-reactive protein. Eotaxin concentrations at inclusion and during follow-up weakly correlated with concentrations of antibodies against C. pneumoniae, H. pylori, and herpes simplex virus but not with concentrations of antibodies against Candida or cytomegalovirus. Eotaxin concentrations and antibody titers against C. pneumoniae significantly increased following angioplasty and remained elevated thereafter. In conclusion, our data demonstrate that eotaxin concentrations are elevated independently from C-reactive protein in patients with coronary artery disease and correlate with antibodies against infectious agents known for chronic infection in humans.

Aged↗
PubMed2005

How to guide stent-graft implantation in type B aortic dissection? Comparison of angiography, transesophageal echocardiography, and intravascular ultrasound.

BACKGROUND: Despite growing interest in stent-graft implantation for type-B aortic dissection, there are no established recommendations to prepare and perform an implantation procedure. METHODS AND RESULTS: We directly compared angiography (ANGIO), transesophageal echocardiography (TEE), and intravascular ultrasound (IVUS) intraprocedually before and after placement of 48 stent grafts in 42 consecutive patients (12 women, 61+/-11 years of age) with acute and chronic type-B aortic dissection for both usefulness and capability to guide aortic stent-graft implantation. Both IVUS and TEE are superior to ANGIO to identify multiple entries (52 and 43 versus 34; P<0.005 each), to diagnose false-lumen slow flow after stent-graft implantation (32 and 31 versus 24; P<0.005 each) and to detect incomplete stent apposition (18 and 16 versus 8; P<0.005 each). In comparison with ANGIO, guide wire position over the entire length of the aorta was documented more frequently by TEE and IVUS (40 and 42 versus 25; P<0.001 each). In 4 patients with abdominal extension of the dissection, only IVUS was able to accurately identify the false lumen over the entire length of the diseased aorta. TEE was superior to IVUS and ANGIO in the detection of endoleaks (5 versus 0 and 1; P<0.05 each). Intraprocedural ANGIO, TEE, and IVUS had been performed without complications in all patients. CONCLUSIONS: TEE in conjunction with ANGIO appears to be advantageous and adds incremental information to safely guide stent-graft placement in type-B aortic dissection. Additional use of IVUS was found to be helpful in patients with complex anatomy and abdominal extension of the dissection.

Aged↗
PubMed2005

Oxypurinol improves coronary and peripheral endothelial function in patients with coronary artery disease.

Coronary endothelial dysfunction is a powerful prognostic marker in patients with coronary artery disease (CAD) that is centrally related to oxidative inhibition of nitric oxide (NO)-dependent vascular cell signaling. Xanthine oxidase (XO), which both binds to and is expressed by endothelial cells, generates superoxide and hydrogen peroxide upon oxidation of purines. Whether inhibition of xanthine oxidase activity results in improved coronary vasomotor function in patients with CAD, however, remains unknown. We assessed coronary and peripheral (brachial artery) endothelial function in 18 patients (pts; 65+/-8 years, 86% male) with angiographically documented CAD, preserved left ventricular function, and non-elevated uric acid levels (233+/-10 microM). Patients received incremental doses of intracoronary acetylcholine (ACh; 10(-7) to 10(-5) microM), and minimal lumen diameter (MLD) and coronary blood flow (CBF) were assessed before and after intravenous administration of oxypurinol (200 mg). Oxypurinol inhibited plasma XO activity 63% (0.051+/- 0.001 vs 0.019+/- 0.005 microU/mg protein; p<0.01). In pts who displayed endothelial dysfunction as evidenced by coronary vasoconstriction in response to ACh (n=13), oxypurinol markedly attenuated ACh-induced vasoconstriction (-23+/- 4 vs -15+/- 4% at ACh 10(-5) microM, p<0.05) and significantly increased CBF (16+/-17 vs 62+/-18% at ACh 10(-5) microM, p<0.05), whereas in patients with preserved coronary endothelial function, oxypurinol had no effect on ACh-dependent changes in MLD (+2.8+/- 4.2 vs 5.2+/- 0.7%, p>0.05) or CBF (135+/-75 vs 154+/-61%, p>0.05). Flow-mediated dilation of the brachial artery, assessed in eight consecutive patients, increased from 5.1+/-1.5 before to 7.6+/-1.5% after oxypurinol administration (p < 0.05). Oxypurinol inhibition of XO improves coronary vascular endothelial dysfunction, a hallmark of patients with CAD. These observations reveal that XO-derived reactive oxygen species significantly contribute to impaired coronary NO bioavailability in CAD and that XO inhibition represents an additional treatment concept for inflammatory vascular diseases that deserves further investigation.

Aged↗