Objective Percutaneous treatment of coronary chronic total occlusions (CTO) remains one of the major challenges in interventional cardiology. The strategies of recanalisation in CTO have changed drastically due the development of new techniques such as the retrograde approach via collaterals. In this single-centre experience we sought to analyse the success rates with the use of different CTO techniques, the complication rates, and we evaluated predictors of failed CTO recanalisation attempts.Methods and Results In this single-centre observational study we analysed the prospectively entered data of 331 consecutive patients, undergoing percutaneous coronary intervention (PCI) for CTO in 338 lesions at the Heart Center Wuppertal between June 2007 and July 2010. Nineteen lesions were attempted twice and one lesion three times (=358 procedures). The lesion-related success rates were 81.1%. Single-wire usage was the predominant strategy used in 198 antegrade cases (65.6%) followed by parallel wire technique and see-saw technique in 94 cases (31.1%). In the retrograde procedures, the reverse CART technique was predominantly used (35.7%), followed by retrograde wire passage (17.9%), marker wire (17.9%) and CART (14.3%). The in-hospital complications were low and comparable with conventional PCI data. The presence of blunt stump, severe calcification, severe tortuosity and occlusion length > 30 mm were independent predictors of procedural failure.Conclusions A high degree of success with low in-hospital complications comparable with conventional PCI data can be expected in the hands of experienced CTO operators. A second try with a retrograde approach after antegrade failure should be considered.

Background Recent genome-wide association studies have identified several genetic loci linked to coronary artery disease (CAD) and myocardial infarction (MI). The 9p21.3 locus was verified by numerous replication studies to be the first common locus for CAD and MI. In the present study, we investigated whether six single nucleotide polymorphisms (SNP) rs1333049, rs1333040, rs10757274, rs2383206, rs10757278, and rs2383207 representing the 9p21.3 locus were associated with the incidence of an acute MI in patients with the main focus on the familial aggregation of the disease. Methods The overall cohort consisted of 976 unrelated male patients presenting with an acute coronary syndrome (ACS) with ST-elevated (STEMI) as well as non-ST-elevated myocardial infarction (NSTEMI). Genotyping data of the investigated SNPs were generated and statistically analyzed in comparison to previously published findings of matchable control cohorts. Results Statistical evaluation confirmed a highly significant association of all analyzed SNP's with the occurrence of MI (p < 0.0001; OR: 1.621-2.039). When only MI patients with a positive family disposition were comprised in the analysis a much stronger association of the accordant risk alleles with incident disease was found with odds ratios up to 2.769. Conclusions The findings in the present study confirmed a strong association of the 9p21.3 locus with MI particularly in patients with a positive family history thereby, emphasizing the pathogenic relevance of this locus as a common genetic cardiovascular risk factor.

BACKGROUND:In the era of fibrinolysis, women suffered from higher early and late mortality rates than men after acute ST-elevation myocardial infarction (STEMI). Primary percutaneous coronary intervention (PCI) has been determined to be the most effective therapy strategy in STEMI. It is not clear if female gender is an independent predictor of a worse long-term prognosis among patients who were systematically treated with PCI. We, therefore, examined the effect of PCI on long-term outcome between women and men.METHODS:Between 1999 and 2001, 500 consecutive patients at the Wuppertal Heart Centre were treated with PCI after acute STEMI. A long-term follow-up (up to 7 years) was achieved in 97% of the patients.RESULTS:In comparison to men, women were 7 years older (65 +/- 12 vs. 58 +/- 11) and had significantly more diabetes mellitus. The time between onset of symptoms and intervention tended to be longer in women than men. There was no difference in 30-day mortality (8.9% vs. 6.6%), cardiac late mortality (3.6% vs. 3.2%), and long-term cardiac overall mortality up to 7 years (12.1% vs. 9.6%). Stepwise regression analysis did not identify female gender as an independent predictor of late mortality. The quality of life was comparable.CONCLUSIONS:There was no gender-related difference in the long-term outcome if patients were sytematically treated with PCI in STEMI. PCI in STEMI has a long-lasting positive effect in women and should, therefore, be considered the treatment of choice for women with acute myocardial infarction.

Purpose: Coronary metal stents generally hamper lumenvisibility in coronary MR angiography (cMRA); yet, there is considerable scientific interest, clinical need and economic implication in early detection of in-stent stenosis. Therefore we sought to develop a systematic and standardized approach to evaluate which factors need to be optimized for quantification of in-stent stenosis by analysis of lumenvisibility in a static MRI in-vitro model of coronary in-stent stenosis.Materials and methods: Six different types of stents (all with a diameter of 3.5 mm) were mechanically fixed parallel to the static magnetic field B-0 of the MRI within a static phantom. A artificial material, corresponding to smooth muscle cells and neointima, was used to simulate an artificial stenosis 50% and 75% in diameter. The MRI protocol was carried out by usage of different sequences in a 1.5 Tesla system. The prepared stents were filled with NaCl solution. Signal intensities inside and outside the stents were measured.Results: Quantification of in-stent stenosis using MRI was limited in stainless steel stents and cobalt-chromium stents by artifacts. Tantalum stent showed a lower rate of artifacts and measuring the degree of stenosis was possible.Discussion: Whereas MRI is not clinically used for coronary imaging, our specific ex-vivo test procedure indicated a feasibility to quantify the degree of in-stent stenosis. Image quality was strongly depended from stent material and stent design. Therefore further research on coronary stents is needed to optimize the MRI protocol and to test the accuracy in a clinical setting.

Restenosis represents the major limiting factor for the long-term efficacy of percutaneous coronary intervention (PCI). Several genetic factors involved in the regulation of the vascular system have been described to play a role in the pathogenesis of restenosis. We investigated whether the EPHX2 K55R polymorphism, previously linked to significantly higher risk for coronary heart disease (CHD), was associated with the occurrence of restenosis after PCI. The association with incident CHD should have been confirmed and a potential correlation of the EPHX2 K55R variant to an increased risk of hypertension was analysed.

We aimed to assess the additive diagnostic value of measuring the serum levels of soluble human heart-type fatty acid binding protein (H-FABP) in the early diagnosis of acute myocardial infarction (AMI) in unselected patients with chest pain. A total of 97 consecutive patients with acute ischemic-type chest pain were prospectively enrolled and classified according to the American Heart Association/American College of Cardiology guidelines. The test characteristics of H-FABP and cardiac troponin T serum levels at admission revealed a greater sensitivity of H-FABP in the first 4 hours of symptoms (86% vs 42%, p <0.05). Combining H-FABP and cardiac troponin T also improved the sensitivity in the detection of AMI (97% vs 71%, p <0.05) but demonstrated a greater misclassification rate (25% vs 9%, p <0.05). The specificity of H-FABP was poor (65%, 95% confidence interval 58% to 71%). Receiver operating characteristics revealed a poor performance of H-FABP in patients with non-ST-elevation myocardial infarction. Classification tree analysis demonstrated that an H-FABP-related improvement in the early definite rule-out of AMI (reduction of false-negative rate from 11% to 3%) was at the expense of an increase in the false-positive rate to 5%. In conclusion, measurement of H-FABP, in addition to cardiac troponin T, serum levels within the first 4 hours of symptoms improves the sensitivity and negative predictive value for the detection of AMI at the cost of test accuracy and precision, especially in patients with non-ST-elevation myocardial infarction.

Inflammation contributes to the development of atherosclerosis and cardiovascular events. Counteracting pro- and anti-inflammatory responses of serum cytokines have been reported, but the relevance of TNF-alpha, TGF-beta and IL-6 gene expression in peripheral blood leukocytes and their contribution to systemic inflammation in atherosclerosis, especially after acute myocardial infarction (AMI), has not been investigated yet. Using quantitative RT-PCR, we determined temporal cytokine mRNA expression alterations in blood cells from patients with AMI (n = 51). Serum cytokine concentrations were analyzed in parallel using the ELISA technique. TNF-alpha mRNA expression rates and serum concentrations were significantly elevated in AMI patients compared to controls (n = 77), while mRNA expression and serum content of TGF-beta were decreased. Interestingly, we found no statistically significant correlation between transcript and protein levels, indicating that gene expression in leukocytes may be an independent sign for systemic inflammation. While IL-6 was significantly increased in serum from AMI patients with positive correlation to left ventricular dysfunction and negative correlation to ejection fraction, IL-6 mRNA levels did not differ between patients and controls. Gene expression alterations indicate a sophisticated regulation of counteracting TNF-alpha and TGF-beta cytokine expression in peripheral blood leukocytes after AMI with bias towards a pro-inflammatory situation.

BACKGROUNDThe combined use of anticoagulants, antiplatelet agents, and invasive coronary procedures reduces ischemic coronary events but also increases bleeding in patients with acute coronary syndromes. We therefore assessed whether fondaparinux would preserve the anti-ischemic benefits of enoxaparin while reducing bleeding.METHODSWe randomly assigned 20,078 patients with acute coronary syndromes to receive either fondaparinux (2.5 mg daily) or enoxaparin (1 mg per kilogram of body weight twice daily) for a mean of six days and evaluated death, myocardial infarction, or refractory ischemia at nine days (the primary outcome); major bleeding; and their combination. Patients were followed for up to six months.RESULTSThe number of patients with primary-outcome events was similar in the two groups (579 with fondaparinux [5.8 percent] vs. 573 with enoxaparin [5.7 percent]; hazard ratio in the fondaparinux group, 1.01; 95 percent confidence interval, 0.90 to 1.13), satisfying the noninferiority criteria. The number of events meeting this combined outcome showed a nonsignificant trend toward a lower value in the fondaparinux group at 30 days (805 vs. 864, P=0.13) and at the end of the study (1222 vs. 1308, P=0.06). The rate of major bleeding at nine days was markedly lower with fondaparinux than with enoxaparin (217 events [2.2 percent] vs. 412 events [4.1 percent]; hazard ratio, 0.52; P<0.001). The composite of the primary outcome and major bleeding at nine days favored fondaparinux (737 events [7.3 percent] vs. 905 events [9.0 percent]; hazard ratio, 0.81; P<0.001). Fondaparinux was associated with a significantly reduced number of deaths at 30 days (295 vs. 352, P=0.02) and at 180 days (574 vs. 638, P=0.05).CONCLUSIONSFondaparinux is similar to enoxaparin in reducing the risk of ischemic events at nine days, but it substantially reduces major bleeding and improves long term mortality and morbidity. (ClinicalTrials.gov number, NCT00139815.).

Here we report a parallel cytokine analysis on transcription and translation level. We could show a bias towards Th1 cytokine expression in peripheral blood leukocytes from acute myocardial infarction (AMI) patients indicating a systemic activation of the immune system.

Hypertrophic cardiomyopathy (HCM) is a dominantly inherited disease defined by unexplained myocardial hypertrophy. The prevalence is about 0.2% in the general population. The condition is characterised by a heterogeneous disease expression, and common symptoms include angina, dyspnoea, palpitations, syncope, and exercise limitation. Hypertrophic cardiomyopathy is a frequent cause of sudden cardiac death in young people.1 More than 200 mutations associated with the disease have been identified in sarcomeric contractile protein genes: TNNT2 (troponin T), MYL3 (essential myosin light chain), MYBPC3 (myosin binding protein C), MYL2 (regulatory myosin light chain), MYH7 (β myosin heavy chain), TPM1 (α tropomyosin), ACTC (α cardiac actin), and TNNI3 (troponin I).2–4 In addition, mutations recently have been reported in two non-sarcomeric genes.5–7 Mutations in ACTC have also been reported to cause the inherited form of idiopathic dilated cardiomyopathy (DCM). It has been suggested previously that ACTC mutations that affect sarcomere contraction lead to HCM, whereas ACTC mutations that affect force transmission from the sarcomere to the surrounding syncytium lead to DCM.3,8 We report the clinical and genetic characteristics of ACTC mutations in 206 consecutive patients with HCM. Informed consent was obtained from each participant in accordance with local institutional review committee guidelines. We investigated 206 consecutive Caucasian probands with HCM from Germany (n = 146) or Denmark (n = 60) by mutation analysis of ACTC . We physically and genetically investigated relatives of probands who carried ACTC mutations. The diagnosis of HCM was based on the presence of unexplained myocardial hypertrophy.3,9,10 In brief, a person was defined as having HCM if the maximal left ventricular wall thickness by echocardiography or cardiac magnetic resonance scan was ⩾13 mm or the electrocardiogram (ECG) showed major Q wave abnormalities, left ventricular hypertrophy, or marked repolarisation alterations. One patient (pedigree B, participant I-1) was …

Wir berichten über Verlauf und mögliche Therapieoptionen bei einem 46-jährigen Patienten mit Zustand nach überlebtem plötzlichen Herztod auf dem Boden rezidivierender ventrikulärer Tachyarrhythmien bei Prinzmetal-Angina. Nach Diagnosestellung erhielt der Patient einen Implantierbaren Cardioverter-Defibrillator, der im Verlauf trotz additiver medikamentöser Therapien weiterhin gehäuft Episoden detektierte und diese jeweils mittels Schockabgaben terminierte. Auch eine perkutane transluminale Koronarangioplastie mit Stentimplantation im vasospastischen Bereich der rechten Koronararterie blieb ohne anhaltenden Effekt. Schließlich wurde der Patient einer operativen Myokardrevaskularisation in Kombination mit einer Sympathektomie zugeführt. In einem Nachbeobachtungszeitraum von 6 Monaten war der Patient komplett beschwerdefrei, ventrikuläre Tachyarrhythmien wurden nicht mehr dokumentiert.

Increasing use of bilateral internal mammary arteries for coronary surgery will increase the number of interventions in these grafts. Such interventions may be technically challenging because of often tortuous and angulated vessels. We describe a technique to intubate an acutely angulated right internal mammary artery that was inaccessible with conventional catheters.

Echocardiographic assessment of regional systolic left ventricular function is usually performed qualitatively and depends on investigator experience. In this study, we investigated a new method for quantifying regional systolic wall motion based on color kinesis. In this study, regional systolic wall motion velocity (Vsys) was determined by dividing end-systolic color width by systolic time. High regional wall motion velocity (Vhigh) was determined by dividing the width of the widest color by its duration of 40 ms. First, in vitro measurements with an acrylic glass model were obtained; these demonstrated a high correlation between echocardiographically determined and real "wall motion velocities" (R = 0.99, p<0.001, R2 = 0.99). Then, 17 healthy, young persons were examined, and normal values for each left ventricular wall segment (16-segment model) were determined. The mean Vsys and Vhigh of all 272 wall segments were 2.3+/-0.6 and 7.4+/-1.8 cm/s, respectively. Finally, in 12 patients with coronary artery disease and prior myocardial infarction, Vsys and Vhigh of each left ventricular wall segment were determined and compared with conventional echocardiographic wall motion analysis using the usual 4-grade score system. Analysis of data showed that quantitative color kinesis measurements demonstrated significantly lower velocity values in pathologic than in normal wall segments (Mann-Whitney U test, p<0.05). Measurements discriminated between pathologic and normal wall motion, with an accuracy of 89% for Vsys and 83% for Vhigh (chi-square test, p<0.05). To summarize, in this first study, measurements of regional wall motion velocities with color kinesis demonstrated reliable results for the quantification of regional left ventricular systolic function.

Crit Care 1999, 3 3 ( (s su up pp pl l 1 1) ):P1 I In nt tr ro od du uc ct ti io on n: : Critically ill patients requiring intensive care are at risk of iatrogenic ocular damage.Studies have reported an incidence of eye problems of up to 40% in critically ill ventilated patients.We conducted this study to assess the incidence of ocular complications in our intensive care unit where all patients are cared for according to an eye care standard.M Me et th ho od ds s: : All ventilated patients over a 2 month period were included.Ophthalmic assessment was performed on admission and repeated every other day during the period of ventilation.At each assessment the average Ramsey sedation score over the previous 24 h, the presence of tracheal secretions and the presence of ventilation associated pneumonia was noted.Eye care performed was recorded.R Re es su ul lt ts s: : Sixty patients were included.One patient developed corneal exposure keratopathy.No patient developed conjunctivitis or corneal ulceration.Further advice on appropriate measures of eye care was given in five cases (8%).Nine patients (15%) had large amounts of respiratory secretions with positive microbiological results.C Co on nc cl lu us si io on n: : This study confirms that the use of an eye care standard is associated with a low incidence of ocular surface complications.The incidence of ocular complications in this group of patients is far lower than previously described.

Overestimation of flow velocity through leaks in mechanical prosthese and other small orifices

The purpose of this study was to determine the influence of polarity reversal on DFT in patients undergoing implantation of nonthoracotomy defibrillators with biphasic shocks. Previous studies have shown higher defibrillation efficacy with using the distal electrode as anode implantation of nonthoracotomy defibrillators and monophasic shocks. However, it is as yet unclear whether biphasic shock defibrillation will also be influenced by polarity reversal. Using a transvenous lead system with a proximal electrode in the superior caval vein and a distal electrode in the RV apex, 27 patients undergoing defibrillator implantation were randomized to DFT testing "initial" (distal electrode = cathode) or "reversed" polarity (distal electrode = anode). Defibrillation energy was reduced stepwise until defibrillation failure occurred. At this point, polarity was switched and testing continued until the lowest energy requirement was determined for both polarities. With reversed polarity, DFT was 11.1 +/- 5.7 J versus 13.3 +/- 5.8 J with polarity (P = 0.033). This means a 17% reduction of the DFT. In 10 patients, the threshold was lower with reversed, whereas in 3 patients it was lower with initial polarity. In conclusion, changing electrode polarity in transvenous implantable defibrillators with biphasic shocks may significantly influence defibrillation energy requirements. Therefore, polarity reversal should always be attempted before considering patch implantation.

The Mahaim syndrome is a rare variant of accessory pathways. Typically, a normal surface ECG and paroxysmal tachycardias with left bundle branch block morphology are found. The anatomic correlate is an atrioventricular or atriofascicular fiber with decremental conduction properties. Criteria for intracardiac mapping of the atrial insertion of such a fiber include: 1) maximal preexcitation and a short stimulus-QRS interval with differential pacing from the atrial aspect of the tricuspid annulus, and 2) recording of an accessory pathway potential ("M" potential). We report a case of a patient that underwent successful radiofrequency ablation of a Mahaim fiber at the tricuspid annulus.

The Mahaim syndrome is a rare variant of accessory pathways. Typically, a normal surface ECG and paroxysmal tachycardias with left bundle branch block morphology are found. The anatomic correlate is an atrioventricular or atriofascicular fiber with decremental conduction properties. Criteria for intracardiac mapping of the atrial insertion of such a fiber include: 1) maximal preexcitation and a short stimulus-QRS interval with differential pacing from the atrial aspect of the tricuspid annulus, and 2) recording of an accessory pathway potential (''M'' potential). We report a case of a patient that underwent successful radiofrequency ablation of a Mahaim fiber at the tricuspid annulus.