Isolated coronary artery aneurysms (CA) are defined as non-obstructive lesions with luminal dilation ≥2-fold of normal coronary diameters.

BACKGROUND:N-terminal pro-brain natriuretic peptide (NT-ProBNP) has emerged as an important marker of cardiac stress and may reflect the severity of underlying cardiac dysfunction, which is thought to be associated with obstructive sleep apnoea syndrome (OSAS).METHODS:This study evaluated the plasma concentration of NT-ProBNP in 60 consecutive patients (median age 55.7 years, median body mass index (BMI) 31.8) who were referred to a sleep laboratory with a suspicion of OSAS. Each subject underwent measurement of morning NT-ProBNP plasma levels, polysomnography and echocardiography. Patients were treated with nasal continuous or bilevel positive airway pressure ventilation (nCPAP/BIPAP) or without mechanical respiratory support, depending on clinical symptoms and results of polysomnography. Three months after treatment of OSAS 28 of the patients were reassessed for re-evaluation of NT-ProBNP and polysomnography.RESULTS:Low or high levels of NT-proBNP were not associated with AHI and other sleep related indices (p>0.3). There was no correlation between NT-proBNP and AHI or other sleep related indices. In multiple regression analysis, NT-proBNP was significantly correlated with left ventricular ejection fraction, creatinine clearance and the presence of systemic arterial hypertension but not with AHI.CONCLUSIONS:Our results show by a robust multiple regression analysis, that NT-pro BNP is not associated with OSAS and NT-pro BNP cannot be used as a sensitive marker for underlying cardiovascular abnormalities in patients with OSAS.

BACKGROUND:Bacterial DNA has been repeatedly detected in atheromatous lesions of coronary heart disease (CHD) patients. Phylogenetic signatures in the atheroma lesions that are similar to those of bacterial biofilms on human barrier organs, including the respiratory or gastrointestinal tract, raise the question of a defective barrier function in CHD. NOD2 plays a major role in defense against bacterial invasion. Genetic variation in the CARD15 gene, which encodes NOD2, was previously shown to result in a barrier defect that causes chronic inflammatory disorders (e.g. Crohn disease). In the present study, we investigated the possible involvement of NOD2/CARD15 in the pathology of CHD by i) analyzing the local expression of NOD2 in atherectomy versus healthy tissue (n = 5 each) using histochemical immunofluorescence and ii) by testing the three major functional CARD15 variants (R702W, G908R and 1007fs) for association with early-onset CHD in 900 German patients and 632 healthy controls.RESULTS:In atherectomy tissue of CHD patients, NOD2 was detected in inflammatory cells at the luminal sides of the lesions. However, the allele and genotype frequencies of the three major CARD15 polymorphisms did not differ between CHD patients and controls.CONCLUSION:The NOD2 up-regulation in atheroma lesions indicates an involvement of this protein in the pathology of CHD. Although NOD2 could be important in local immune response mechanisms, none of the analyzed CARD15 variants seem to play a significant role in the etiology of CHD.

BACKGROUND:The concept of initiating fibrinolytic therapy in patients who cannot undergo immediate percutaneous coronary intervention (PCI) in the setting of acute ST-segment-elevation myocardial infarction (STEMI) has been proposed as a strategy to improve outcomes. However, evidence supporting the use of this strategy is not conclusive, and the results of recent randomized controlled trials are apparently contradictory. Probably, the time points of administration of the adjunctive thrombolytics and antiplatelet agents and the time loss until coronary intervention have a major influence on the discrepancy of outcomes in different trials. Therefore, the relationship between therapeutic time intervals and outcome in patients treated with facilitated PCI has been analyzed. METHODS:In this single center retrospective study, 131 patients with STEMI were treated with a combined pharmaco-mechanical reperfusion strategy using half-dose r-tPA combined with a glycoprotein (GP) IIb/IIIa antagonist prior to PCI. Specific time points were recorded for each patient, including the time of symptom onset, the time of first medical contact, the start of intravenous thrombolysis, the time of administration of the GP IIb/IIIa antagonist and the start of coronary intervention. We then examined the relationship between the time delay from symptom onset to the initiation of various steps of treatment and the residual myocardial damage as expressed by the severity of both global and regional myocardial dysfunction calculated from a left ventriculography study performed 3 months later. RESULTS:The median time from symptom onset to the first medical contact, with 25th and 75th percentiles in parentheses, was 1.25 h (0.75, 3), from symptom onset to initiation of thrombolytic therapy 2.25 h (1.25, 3), to initiation of GP IIb/ IIIa inhibitor therapy 3.5 h (2, 5.69), and to the start of coronary intervention 4.81 h (2.85, 7.91). The time between symptom onset and initiation of both thrombolytic therapy and coronary intervention was significantly related to the global ejection fraction and to the extent of regional hypokinesia at the 3-month follow-up (p<0.05). The time to the initiation of GP IIb/IIIa inhibitors was only significantly related to the global ejection fraction (p<0.05), while the time to the first medical contact did not show a similar relationship (p>0.05). Furthermore, we observed a significant relationship between the infarct-related artery (IRA) patency at the initial angiogram and the residual regional myocardial damage at follow-up; normokinesia at follow-up was found in 61.3% of patients with an initially patent IRA and in 41.2% of patients with an initially occluded IRA, whereas severe hypokinesia was found in 13.8% and 37.3%, respectively (p<0.05). CONCLUSION:In patients with STEMI treated with a facilitated PCI strategy using half dose r-tPA in combination with a glycoprotein IIb/IIIa receptor blocker, the 3-month global and regional residual myocardial dysfunction is significantly related to the time elapsed between the onset of symptoms and the start of both fibrinolytic therapy and coronary intervention.

Liberation of plaque debris during PCI in native coronary arteries is supposed to be a possible mechanism of the no-reflow phenomenon, which can cause impairment of the distal and microvascular circulations.Therefore, ten consecutive patients undergoing PCI for complex lesions in their native right coronary arteries were enrolled in a pilot trial, using the triActiv system (Kensey Nash Company) for distal protection.For all patients, device success (device was successfully delivered to the target location, device operated as intended and was successfully retrieved) could be documented. For the primary (MACE rate at 30 days) and secondary endpoints no events were reported, neither in hospital nor during the follow-up period of 30 days.Debris was found in all patients in whom the extracted fluid could be investigated (7/10), the average particle size being 28 x 68 mu m. This observation suggests that embolization can occur during PCI of native coronary vessels and may be more often present than so far expected. Larger studies, however, are needed to confirm the relevance of this finding.

Bacterial DNA has been found in coronary plaques and it has therefore been concluded that bacteria may play a role as trigger factors in the chronic inflammatory process underlying coronary atherosclerosis. However, the microbial spectrum is complex and it is not known whether microorganisms other than bacteria are involved in coronary disease. Fungal 18S rDNA signatures were systematically investigated in atherosclerotic tissue obtained through catheter-based atherectomy of 38 patients and controls (unaffected coronary arteries) using clone libraries, denaturating gradient gel analysis (DGGE), in situ hybridization and fluorescence in situ hybridization (FISH). Fungal DNA was found in 35 of 38 (92.11%) coronary heart disease patients by either polymerase chain reaction (PCR) with universal primers or in situ hybridization analysis (n = 5), but not in any control sample. In a clone library with more than 350 sequenced clones from pooled patient DNA, an overall richness of 19 different fungal phylotypes could be observed. Fungal profiles of coronary heart disease patients obtained by DGGE analysis showed a median richness of fungal species of 5 (range from 2 to 9) with a high interindividual variability (mean similarity 18.83%). For the first time, the presence of fungal components in atherosclerotic plaques has been demonstrated. Coronary atheromatous plaques harbour diverse and variable fungal communities suggesting a polymicrobial contribution to the chronic inflammatory aetiology.

OBJECTIVE:Interventions in aorto-coronary venous bypass grafts (CABG) can cause acute procedural complications due to distal embolization of debris. In the FIRST (First European Investigation Regarding the Systematic use of the TriActiv device) multicenter trial the distal endovascular protection system TriActiv (Kensey Nash) was evaluated during intervention of CABG.METHODS:195 patients in 17 centers in Germany with significant disease of a vein graft were enrolled. Inclusion and exclusion criteria were comparable to the SAFER trial.RESULTS:Acute procedural success was achieved in 98% of cases. Aspirated debris was found in 96.5% of patients. Primary endpoints (MACE at 30 days) occurred in 8.7% of all pts. (ITT). No patient died and 7.2% of patients suffered from MI. The rate of early revascularization was 1.5%. Secondary endpoints (MACCE at 30 days) were found in 9.2% and at hospital discharge in 8.7% of patients.CONCLUSIONS:The TriActiv system is safe and effective. Normal post procedural flow can be preserved and the MACE rate is with 8.7% considerably low. The FIRST trial supports the growing belief that PCI of CABG should be performed with protection systems.

Infection and innate immunity have been suggested as playing an important role in the pathogenesis of atherosclerosis. The recently discovered pattern-recognition receptor (PRR) proteins initiate signalling after host-pathogen interactions and several PRRs, especially the Toll-like receptor 4 (TLR4), have been shown to be involved in the development and progression of atherosclerosis. A new addition to the PRRs is CARD4, a gene that encodes the protein nucleotide-binding oligomerization domain 1 (NOD1) and that seems to be associated with barrier function in chronic inflammatory disorders. Recently, a functional variant in the CARD4 gene, the insertion-deletion polymorphism ND1+32656, has been associated with inflammatory barrier diseases (inflammatory bowel diseases and asthma). We analysed the frequencies of this known functional mutation in the CARD4 gene and of the two adjacent variants, rs2075822 and rs2907748, in a German sample of 1440 unrelated early onset coronary heart disease (CHD) patients and healthy controls. Genotype and haplotype data showed no evidence for a significant association of these CARD4 variants with CHD. Our results suggest that the analysed CARD4 mutations do not play a major role in the aetiology of CHD.

Recently, we generated cells with multipotent properties from blood monocytes that in vitro differentiate into various somatic cell types. This experimental study investigated whether these programmable cells of monocytic origin (PCMO) succeed to restore left ventricular function after myocardial infarction (MI). PCMO were generated from monocytes by exposition to RPMI medium containing M-CSF and IL-3 for 6 days. MI was induced in female Lewis rats ligating the left coronary artery. PCMO of male Lewis donors were injected either intramyocardially (i.my.) or intravenously (i.v.) 24 h or 6 days post-infarction. Hemodynamic assessment after 60 days demonstrated significant improvement of left ventricular function following i.my. transplantation of PCMO as well as early (24 h post-infarction) i.v. application while nonmodulated monocytes failed to restore heart function. The Y-chromosome-specific SRY gene of male donor PCMO was detected exclusively in infarcted hearts of animals, which demonstrated improved cardiac function. Subdivision of infarcted hearts by microdissection localized the SRY gene-containing department to the left ventricle adjacent to the infarcted area whereas the right ventricle remained negative. Successful generation of PCMO in access numbers allows their autologous use as a new additive treatment for early restoration of cardiac function after MI.

Background— Bacterial infection has been discussed as a potential etiologic factor in the pathophysiology of coronary heart disease (CHD). This study analyzes molecular phylogenies to systematically explore the presence, frequency, and diversity of bacteria in atherosclerotic lesions in patients with CHD. Methods and Results— We investigated 16S rDNA signatures in atherosclerotic tissue obtained through catheter-based atherectomy of 38 patients with CHD, control material from postmortem patients (n=15), and heart-beating organ donors (n=11) using clone libraries, denaturating gradient gel analysis, and fluorescence in situ hybridization. Bacterial DNA was found in all CHD patients by conserved PCR but not in control material or in any of the normal/unaffected coronary arteries. Presence of bacteria in atherosclerotic lesions was confirmed by fluorescence in situ hybridization. A high overall bacterial diversity of >50 different species, among them Staphylococcus species, Proteus vulgaris , Klebsiella pneumoniae , and Streptococcus species, was demonstrated in >1500 clones from a combined library and confirmed by denaturating gradient gel analysis. Mean bacterial diversity in atheromas was high, with a score of 12.33±3.81 (range, 5 to 22). A specific PCR detected Chlamydia species in 51.5% of CHD patients. Conclusions— Detection of a broad variety of molecular signatures in all CHD specimens suggests that diverse bacterial colonization may be more important than a single pathogen. Our observation does not allow us to conclude that bacteria are the causative agent in the etiopathogenesis of CHD. However, bacterial agents could have secondarily colonized atheromatous lesions and could act as an additional factor accelerating disease progression.

Wir berichten über einen 67-jährigen Patienten, der mit dem Bild eines akuten Vorderwandmyokardinfarktes im Rahmen eines akuten Koronarsyndroms in die Klinik eingeliefert wurde. Die sofort durchgeführte Herzkatheteruntersuchung zeigte einen frischen Thrombus im proximalen Ramus interventrikularis anterior (RIVA) bei sonst unauffälligen Koronararterien. Nach PTCA mit Stent-Implantation in den proximalen RIVA war der Patient vollkommen beschwerdefrei. Die CK, CKMB sowie das Troponin T blieben im Normbereich. Im Verlauf entwickelte der Patient eine Podagra des rechten Großzehengrundgelenkes, welches mit Colchicin, Diclofenac und lokaler Kühlung behandelt wurde. Fünf Stunden nach Gabe von Colchicin sowie Diclofenac klagte der Patient über heftige Angina pectoris-Symptomatik mit elektrokardiographischen Zeichen eines akuten Hinterwand- und Vorderwandmyokardinfarktes. Eine erneute durchgeführte Herzkatheteruntersuchung zeigte ausgeprägte Vasospasmen der rechten Koronararterie. Nach intrakoronarer Verapamil- und Nitroglycerin-Gabe waren die Koronarspasmen deutlich rückläufig und der Patient war beschwerdefrei. Anamnestisch berichtete der Patient, dass er am Abend ca. 6 h vor dem akuten Koronarsyndrom ebenfalls Diclofenac eingenommen hätte. Bei zweimaliger in unmittelbarem Zusammenhang mit der Diclofenac-Einnahme stehenden akuten Koronarsymptomatik ist von einem Diclofenac induziertem Vasospasmus auszugehen.

Problemstellung: Die Gefäßwandverletzung ist nach der Virchow-Trias ein wichtiger Auslöser für eine Thrombose. Bei jeder Katheterintervention über die Leiste besteht ein erhöhtes Risiko eine lokale Thrombose auszubilden. Es ist anzunehmen, dass das Thromboserisiko vor allem bei aufwendigeren Katheteruntersuchungen wie der elektrophysiologischen Untersuchung (EPU) aufgrund des Durchmessers, der Anzahl und der langen Liegezeit von Kathetern und Zugangsschleusen erhöht ist.

Coronary collateral connections occur frequently in the presence of occlusive coronary artery disease. If functionally sufficient, these collaterals are able to reduce or prevent myocardial ischemia in case of proximal vessel occlusion. Developement of collateral connections will be triggered of multiple ischemic episodes that stimulate the growth of new vessels. However, none of these mechanisms are found in patients with non-stenosed coronary arteries. Therefore, we report on a 74-yr old man who was admitted to the hospital due to atypical chest pain. No history of a cardiac event was reported by the patient. An echocardiogram showed normal left ventricular function with signs of wall thickening. Cardiac enzymes were normal. During coronary angiography (BP 140/62, mean

The first interoperability demonstration of the Cardiology profiles of the "Integrating the Healthcare Enterprise" (IHE) initiative was held in conjunction with the annual scientific sessions of the American College of Cardiology (ACC) in March, 2005.The IHE Cardiology Planning Committee identified clinical problems to be addressed: the ability to view an ECG from anywhere in the enterprise, and the effective integration of patient, order and procedure information for echocardiography and for cardiac catheterization. The IHE Cardiology Technical Committee developed a set of Integration Profiles to address the retrieval and display of ECG's as well as scheduled and unscheduled echo and cath for registered and unregistered patients. The demonstration used clinical scenarios to demonstrate the integration of the participating systems: (1) Emergent Angioplasty (2) Change of Procedure Room; (3) Add-on Mobile Echo Procedure; and (4) Stress Echo Images.