Pathogen burden in degenerative aortic valves is associated with inflammatory and immune reactions.

BACKGROUND AND AIM OF THE STUDY: The presence of five pathogens was assessed, together with a possible correlation of the total pathogen burden on inflammation and (auto)immunity in aortic stenosis (AS) and degenerative aortic valve bioprosthesis (BP). METHODS: Diseased valve specimens from a total of 68 patients (52 with AS, 16 with BP) were studied. The presence and localization was assessed of Chlamydia pneumoniae (cHSP60), Helicobacter pylori (HP), cytomegalovirus (CMV), Epstein-Barr virus (EBV) and herpes simplex virus (HSV), as well as of macrophages (CD68), C-reactive protein (CRP) and human heat shock protein 60 (hHSP60), by using immunohistochemical and morphometric analyses. RESULTS: In the majority of degenerative aortic valves, specific pathogens, inflammation and immunity were localized predominantly in the fibrosa of AS patients, and in superficial regions of the BP. The categorization of valves as having four or more pathogens (n = 37) or fewer pathogens (n = 31) demonstrated an increased signaling of CD68 (p = 0.03) and CRP (p = 0.02). Specifically, cHSP60, HP and hHSP60 levels were increased in valves where one or two bacteria were identified (n = 59) compared to those without bacterial presence (n = 9) (p = 0.04). CONCLUSION: The pathogen burden may contribute to valvular degeneration by promoting further deleterious inflammatory and (auto)immune processes at the level of the valvular fibrosa.

Evaluation of fractal-coated temporary pacing leads in the early postoperative course.

BACKGROUND: The performance of temporary pacing wires is still limited by capture and sensing problems. Fractal coating can enhance electrical properties and reliability. We therefore investigated fractal-laminated wires in comparison with conventional wires. METHODS: In 21 patients two unipolar, fractal-coated pacing wires (fe) and one conventional bipolar electrode (se) were implanted in ventricular position. Afterward pacing threshold (V), R-wave sensing (mV), lead impedance (ohm), and slew-rate (mV/s) were measured. Loss of capture or sensing and dislocation was documented. fe wires were examined with energy dispersive x-ray diffraction (EDX)-analysis and scanning electrode microscopy (SEM). RESULTS: Failure in pacing was less frequent in fe wires. Also fe leads had lower pacing thresholds at implantation (0.76 +/- 0.15 V vs 1.51 +/- 0.95 V, P< 0.0001) and afterward. Furthermore fe wires showed lower increase of pacing threshold/time (0.25 V/day vs 0.42 V/day). R-wave sensing and slew-rate values in the fe group on day of operation (5.81 +/- 4.80 mV; 0.63 +/- 0.71 V/s) were lower than in the se group (10.37 +/- 6.89 mV; 1.85 +/- 1.71 V/s P< 0.0001) and afterward. Nevertheless, decrease of amplitude/time was lower in fe wires (0.17mV/day vs 0.46 mV/day). fe wires always had lower impedance values. CONCLUSIONS: Lower pacing threshold and increase of threshold/time in fe wires indicate more reliable function. Initial lower sensitivity values are still not understandable and must be investigated. However, fe wires, constancy of sensing and impedance values was more stable, so fe epicardial wires can be recommended for safe and feasible use.

A rare case of skin cancer above a subcutaneously implanted pacemaker: implications for future implants.

BACKGROUND: The occurrence of a skin neoplasm close to the position of an implanted pacemaker or cardioverter-defibrillator device is not very common. CASE REPORT: We report on an 82-year-old patient who developed a basal cell carcinoma in the skin directly above a subcutaneously implanted pacemaker generator. The patient presented with a history of recurrent basalioma at various locations. The pacemaker (Kappa KDR 731; Medtronic) was implanted 17 months before and represented a series that was recalled because of problems occurring after submuscular implantation. CONCLUSION: Primary submuscular implantation of pacemaker devices should be carefully considered in elderly patients with a history of previous skin tumors.

Persistence of Chlamydia pneumoniae in degenerative aortic valve stenosis indicated by heat shock protein 60 homologues.

BACKGROUND AND AIMS OF THE STUDY: Based on the concept of chronic persistent infections with Chlamydia pneumoniae among variable stressors for aortic valve degeneration, the study aim was to assess the presence of chlamydial heat shock protein (cHSP) 60 and its human homologue (hHSP60) in diseased valvular tissue. METHODS: Surgical specimens of high-grade stenosed, native (n = 33) and bioprosthetic (n = 10) aortic valves were examined immunohistochemically for the localization of cHSP60, hHSP60 and macrophages (CD68), supplemented by polymerase chain reaction (PCR) and electron microscopy to prove microbial presence. RESULTS: Degenerated valves showed specific immunostaining of cHSP60 in 27 cases (65%), of hHSP60 in 26 (63%), and of CD68 in 36 (84%). Both HSP60 homologues were predominantly detected in valvular fibrosa, consistently co-localized with macrophages and, quantitatively, showed a strong correlation (r = 0.81, p < 0.001). Presence of C. pneumoniae was demonstrated by PCR in a subset of 11 of 18 valves (61%). Microbial persistence was confirmed by ultrastructural analysis. Degenerated prosthetic valves revealed markedly higher macrophage infiltration and cHSP60 signaling compared with degenerated native valves (each p < 0.05). CONCLUSION: Beyond detection of C. pneumoniae, the present data on co-localization and valvular predilection sites (fibrosa) of both HSP60 homologues indicate the presence of chronic persistent C. pneumoniae infection as well as regional stressor effects, and suggest their involvement in native and prosthetic valve degeneration.

Detection of (reversible) myocardial ischemic injury by means of electrical bioimpedance.

The scope of this paper was to determine whether ischemic and reperfusion damage in cardiac surgery can be detected by measurement of electrical bioimpedance (EBI). Conventional pacing wires were replaced by pacing wires with sputtered iridium coating in order to reduce polarization associated with two-electrode impedance measurements. A custom-built bioimpedance analyzer (Osypka Medical GmbH, Berlin, Germany) measured the real part of impedance Re(Z) and the phase (ϕ) at three frequencies (1, 10, and 1000 kHz) and determined an extracellular space index (EZRI) as the quotient of Re(Z) at 1000 kHz and Re(Z) at 1 kHz. Our study included six patients (conventional coronary artery bypass graft, age 68.1 ± 8.3 years) subject to routine cardioplegic ischemia and reperfusion. Preischemic bioimpedance measurements were not impaired by interference of the beating heart. Intraischemically, bioimpedance at 1 kHz and phase at 10 kHz increased until opening of a bypass graft, which is probably induced by closure of gap junctions and cell swelling processes. After cross clamping, EZRI slowly decreased as an effect of mild cell swelling. After ischemia, values returned almost to baseline measurements, indicating sufficient reperfusion processes. Measurement of EBI correlates with myocardial ischemic injury and is applicable in a two-electrode setup providing low-polarization pacing wires.

Perioperative monitoring of primary and secondary hemostasis in coronary artery bypass grafting.

On-pump cardiac surgery is accompanied by complex alterations of hemostasis. The excessive postoperative bleeding has been attributed to acquired platelet dysfunction, impaired plasmatic coagulation, and increased fibrinolysis. The characterization of the hemostatic defects responsible for bleeding is crucial for specific treatment and optimal clinical management of the patient. For rapid determination of platelet-dependent primary hemostatic capacity (PHC), the Platelet Function Analyzer PFA-100 system is available. To evaluate the PFA performance in perioperative monitoring, a study was performed in 49 patients selected for low bleeding risk undergoing selective primary coronary artery bypass grafting (CABG). We compared PHC with Simplate bleeding time (BT) and platelet aggregometry. Furthermore, we analyzed global hemostasis by thromboelastography (TEG) and plasmatic coagulation by standard clotting tests prothrombin time (PT, Quick), activated partial thromboplastin time (aPTT), thrombin time (TT) and clotting factors and fibrinolysis by batroxobin (reptilase) time (RT). In all patients BT was postoperatively increased by 1.5- to 2-fold irrespective of perioperative complications and decreased to mildly prolonged values on the first postoperative day (1st day). In patients without complications, PHC in both collagen-adenosine diphosphate closure time (CADP-CT: 83 seconds preop, 78 seconds postop, and 74 seconds 1st day) and collagen-epinephrine closure time (CEPI-CT: 98 seconds preop, 95 seconds postop, 85 seconds 1st day) remained nearly stable. Apart from a patient with postoperative moderate thrombocytopenia, in bleeding patients no other significant defect of postoperative platelet hemostatic capacity was observed. However, on 1st day, the PHC of those patients was significantly reduced compared with non-bleeding patients. In patients with postoperative myocardial ischemia, increased PHC was identified by significantly shorter postoperative CADP-CT (66 seconds vs. 83 seconds) than in uncomplicated patients. By aggregometry, partial platelet dysfunction was observed in some patients without correlation to bleeding complications. In seven of 9 patients the postoperative bleeding complication was attributed to prolonged heparin anticoagulation and/or mildly enhanced fibrinogenolysis/fibrinolysis by TEG and standard plasmatic coagulation tests (TEG: k time 18 minutes vs. 8 minutes; aPTT: 47 seconds vs. 32 seconds; TT: 18.0 seconds vs. 12.3 seconds) and (RT: 19.5 seconds vs. 17.7 seconds). The impairment of PHC, platelet aggregation, and clotting factors observed on the 1st day in bleeding and in intra-aortic balloon pump (IABP) patients are most likely secondary effects, for example, loss of active platelets and clotting factors, to the primary postoperative bleeding or implantation of the IABP. In conclusion, our data indicate that in standard CABG procedures highly variable alterations of the hemostatic system occur after cardiopulmonary bypass (CPB) even in patients with assumed low operative risks. For identification of post-CPB bleeding complications, thromboelastography, aPTT, and TT and heparin and batroxobin (reptilase) time as fibrinolysis-sensitive assays are useful. Platelet function appears to be rapidly restored in uncomplicated CABG. PHC determination by PFA-100 demonstrates a high specificity for adequate platelet function and, therefore, could be beneficial in improved transfusion of platelet concentrates. PHC testing by PFA-100 may help identify postoperative platelet hyper-reactivity associated with myocardial lesion.

Cells of primarily extra-valvular origin in degenerative aortic valves and bioprostheses.

AIMS: We assessed aortic valves from patients with non-rheumatic aortic valve stenosis (AS) and with degenerative aortic valve bioprostheses (BP) for the presence of progenitor cell and leukocyte subtype-specific markers. METHODS AND RESULTS: Diseased valve probes from a total of 87 patients (60 AS and 27 BP) were studied. We assessed presence and localization of endothelial progenitor cells (EPCs: CD34, CD133), dendritic cells (DCs: S100), T-lymphocytes (CD3), and macrophages (CD68) by immunohistochemical and morphometric analyses. In the majority of valves, we detected cell-bound signals of CD34 (48% of AS, 74% of BP, respectively), CD133 (58%/81%), S100 (58%/93%), CD3 (62%/81%), and CD68 (78%/93%). Labelled cells were predominantly localized within the valvular fibrosa. As key results, frequency of EPCs, DCs, macrophages, and lymphocytes was found significantly higher in BP when compared with AS (CD34: 19.2+/-23.2 vs. 5.7+/-13.0%; CD133: 13.7+/-12.4 vs. 5.5+/-8.3%; S100: 15.2+/-12.2 vs. 5.7+/-8.9%; CD3: 3.3+/-2.7 vs. 1.1+/-1.4%; CD68: 35.3+/-26.6 vs. 3.4+/-4.1%; each P

Radiofrequency catheter ablation of an incessant ventricular tachycardia following valve surgery.

Sustained monomorphic ventricular tachycardia (VT) after valve surgery represents a clinical entity with different tachycardia mechanisms. This case report describes an incessant VT after tricuspid and aortic valve replacement that did not respond to antiarrhythmic drug treatment. The tachycardia exhibited VA block and a right bundle branch block pattern with left-axis deviation, suggesting ventricular excitation via the left posterior fascicle. The electrophysiological study was limited by the prosthetic tricuspid and aortic valve replacement, therefore a transseptal approach was necessary to obtain access to the ventricular myocardium. Radiofrequency catheter ablation was performed in the proximal left bundle or distal His region with termination of the incessant VT followed by complete AV block. After pacemaker implantation using a transvenous right atrial and an epicardial ventricular lead, no VT reoccurrence could be documented.

An unusual case of pacemaker failure: complete disconnection of connector block and battery of a subpectorally implanted dual chamber pacemaker.

Local trauma to patients with implanted pacemaker devices may result in lead fracture or breakage of the lead socket with leakage of fluid into the connector system. This report describes an unusual case of complete entrance and exit block in a subpectorally implanted dual chamber pacemaker due to total disconnection and dislodgement of header block and battery part. Damage may be caused by an interaction of machine fatigue/manufacturing defective and fixation of the header with unusual movability of the battery, leading to breakage with intermittent malfunction and consecutive bradycardia and syncope.