A Novel Approach to Identifying How Equipment Disrupts the Airflow Patterns in the Operating Room.

A decrease in the infection rates in the operating room (OR) is attributable to advances in sterile technique; heating, ventilation, and air-conditioning (HVAC) filtration; and limiting the number of people entering and leaving the OR. However, some infection complications after open heart procedures have been linked to the discharge fans of surgical equipment, most notably from the LivaNova 3T. We believe that surgical infection within the OR may also be due to other devices with internal fans. The purpose of this study was to 1) identify surgical equipment with an internal fan and see how they affect the airflow in an OR, 2) use the equipment to positively affect airflow to possibly reduce the risk of surgical site infections, and 3) bring attention to the HVAC system ability to exchange air throughout the OR. By using a fog machine and multiple camera angles, we identified the devices that have an effect on the airflow. We saw that the direction of the intake vent of specific devices can change the direction of airflow and possibly help to remove air. Last, we showed how the current HVAC air exchange rate might not be enough to remove contaminated air within the OR. Understanding intake and discharge vents for all equipment is important because sterile contamination and wound infection may be minimized or mitigated completely by simply repositioning a few devices.

Association Between Time-in-Therapeutic Tacrolimus Range and Early Rejection After Heart Transplant.

BACKGROUND: Historically, there is perceived pressure to achieve therapeutic levels of tacrolimus quickly after heart transplant (HT). We evaluated the association between time within therapeutic tacrolimus range and time to therapeutic trough and rejection in the 30 days following HT. METHODS: This is a single-center retrospective cohort study of consecutive adult HT patients receiving immunosuppression. Goal trough tacrolimus levels were 10-15 ng/ml. Surveillance endomyocardial biopsies were performed weekly for 4 weeks. Outcomes included the effect of time to and time-in-therapeutic tacrolimus range (Rosendaal method) on 30-day clinical rejection, 1R/1B, and 2R or higher histologic occurrences. RESULTS: We reviewed 67 HT patients (median age 58.8 yrs). For clinical rejection versus no-rejection groups, the median (25th, 75th percentile) time to therapeutic tacrolimus levels was 9.5 (8, 12.3) days versus 9.0 (7, 13) days (p=0.623). The median time-in-therapeutic tacrolimus range was 34.1% (23.2, 42.2) versus 36.2% (19.9, 51.2), respectively (p=0.512). Similarly, we observed no significant differences in time to and time-in-therapeutic tacrolimus range in patients who developed grade 1R/1B (p=0.650 and p=0.725) or grade 2R or higher histology (p=0.632 and p=0.933). CONCLUSIONS: Our small single-center analysis suggests that neither time to nor time in therapeutic tacrolimus range predicted acute rejection within 30 days of HT.

Usefulness of Circulating Caspase-3 p17 and Caspase-1 p20 Peptides and Cardiac Troponin 1 During Cardioplegia to Gauge Myocardial Preservation.

Evidence is accumulating that cardiac apoptosis occurs and contributes to myocyte cell death during myocardial ischemia. Cardioplegia, defined as the temporary cessation of cardiac activity during cardiac surgery, is a clinically controlled condition with myocardial ischemia and reperfusion. Our goal was to determine whether the apoptotic biomarker caspase-3 p17 is elevated in the coronary sinus (CS) during cardioplegia and if any elevations were reflected in the peripheral venous (PV) blood. Levels of the necrotic biomarker cardiac troponin I (cTnI) and the inflammatory marker caspase-1 p20 were also quantified in CS and PV. Blood was drawn before and at the end of cardioplegia in PV and CS and levels of p20, p17, and cTnI were measured. cTnI, p20, and p17 PV levels were significantly elevated compared with the control population before and at the end of cardioplegia. PV levels of all 3 markers increased after cardioplegia. CS levels were higher than PV levels for all 3 markers at both time points. Our data are consistent with the occurrence of cardiac apoptosis and inflammation during cardioplegia, in addition to necrosis. The heart-derived markers contributed to the peripheral levels and suggest that measurement of PV biomarker concentrations can be used to gauge cardiac preservation.

TRPM7-mediated Ca2+ signals confer fibrogenesis in human atrial fibrillation.

RATIONALE: Cardiac fibrosis contributes to pathogenesis of atrial fibrillation (AF), which is the most commonly sustained arrhythmia and a major cause of morbidity and mortality. Although it has been suggested that Ca(2+) signals are involved in fibrosis promotion, the molecular basis of Ca(2+) signaling mechanisms and how Ca(2+) signals contribute to fibrogenesis remain unknown. OBJECTIVE: To determine the molecular mechanisms of Ca(2+)-permeable channel(s) in human atrial fibroblasts, and to investigate how Ca(2+) signals contribute to fibrogenesis in human AF. METHODS AND RESULTS: We demonstrate that the transient receptor potential (TRP) melastatin related 7 (TRPM7) is the molecular basis of the major Ca(2+)-permeable channel in human atrial fibroblasts. Endogenous TRPM7 currents in atrial fibroblasts resemble the biophysical and pharmacological properties of heterologous expressed TRPM7. Knocking down TRPM7 by small hairpin RNA largely eliminates TRPM7 current and Ca(2+) influx in atrial fibroblasts. More importantly, atrial fibroblasts from AF patients show a striking upregulation of both TRPM7 currents and Ca(2+) influx and are more prone to myofibroblast differentiation, presumably attributable to the enhanced expression of TRPM7. TRPM7 small hairpin RNA markedly reduced basal AF fibroblast differentiation. Transforming growth factor (TGF)-beta1, the major stimulator of atrial fibrosis, requires TRPM7-mediated Ca(2+) signal for its effect on fibroblast proliferation and differentiation. Furthermore, TGF-beta1-induced differentiation of cultured human atrial fibroblasts is well correlated with an increase of TRPM7 expression induced by TGF-beta1. CONCLUSIONS: Our results establish that TRPM7 is the major Ca(2+)-permeable channel in human atrial fibroblasts and likely plays an essential role in TGF-beta1-elicited fibrogenesis in human AF.

Ascending thoracic aneurysms are associated with decreased systemic atherosclerosis.

STUDY OBJECTIVES: We noted clinically that patients with aortic root aneurysms and dissections seemed to have little systemic atherosclerosis. It is our objective to determine whether there is a negative association between ascending thoracic aneurysms and systemic atherosclerosis. DESIGN: Atherosclerosis was quantified by evaluating non-contrast CT images of the chest and scoring the degree of calcifications as a marker for atherosclerosis in the coronary arteries and aorta. PATIENTS: The degree of calcification was compared in 64 patients with aortic root aneurysm (annuloaortic ectasia, 31 patients; type A dissection, 33 patients) vs 86 control subjects. Multivariable analysis was applied to test for an association between aortic root aneurysms and systemic calcification independent of risk factors for atherosclerosis. RESULTS: Multivariable analysis revealed that patients with ascending aortic aneurysms of the annuloaortic ectasia type and patients with type A dissections had significantly lower overall calcification scores in their arterial vessels compared to patients in the control group (p = 0.03 and p < 0.0001, respectively). These results were independent of all other risk factors for atherosclerosis. Smoking, dyslipidemia, diabetes, and age were all found to increase the degree of atherosclerosis (p < 0.01 to 0.05). CONCLUSIONS: Aortic root pathology (annuloaortic ectasia or type A dissection) is associated with decreased systemic atherosclerosis. It is possible that a mechanism exists whereby the same genetic mutations predisposing patients to ascending aortic aneurysms also exert a protective effect against systemic atherosclerosis.

Avoidable errors in cardiac surgery: anastomosis of the left internal mammary artery to a vein.

We report the case of a patient who had undergone a three-vessel coronary artery bypass graft surgery 6 years earlier, during which the left internal mammary artery was erroneously anastomosed to an epicardial vein instead of the intended target, an intramyocardial left anterior descending artery. Visually distinguishing artery from vein can be occasionally challenging and can lead to errors in distal anastomosis. This case report identifies two difficult problems in cardiac surgery and discusses the techniques to differentiate between arterial and venous targets.

A simpler solution to the old problem of frozen leads.

Pacemaker generator replacement is usually a straightforward and simple procedure. However, it is occasionally complicated by entrapment of the lead in the header. Solutions to this problem have been described previously. We describe a simpler and safer technique to solve this old problem.

Femoral cannulation is safe for type A dissection repair.

BACKGROUND: Recently, surgeons have embraced axillary artery cannulation for type A aortic dissection repair out of concern for malperfusion phenomena with traditional femoral artery cannulation. My colleagues and I sought to determine whether these concerns are justified. METHODS: Records of 86 consecutive patients (51 men and 35 women; age, 30 to 86 years; mean, 62 years) undergoing surgical repair for acute type A dissection were reviewed. Cannulation site, specific operative repair, and complications related to cannulation were noted. RESULTS: Seventy-nine cannulations were performed in the femoral artery (47 left, 23 right, and 9 unspecified), 3 in the axillary artery (1 left and 2 right), and 4 in the ascending aorta or arch. Deep hypothermic arrest was used in 64 operations. Seven involved re-sternotomy. Seventy patients had supracoronary grafts (2 with valve replacement and 10 with valve resuspension), and 16 underwent aortic root replacement. Fourteen patients were in shock from cardiac tamponade. Eighty patients survived the operation, and 71 were hospital survivors. Malperfusion on initiation of cardiopulmonary bypass was noted in 3 patients. In 1, the original cannulation site was the ascending aorta, and the cannula was moved to the femoral artery for correction. In 2, the original cannulation site was the femoral artery, and the cannula was moved to the ascending aorta. Malperfusion on clamping of the aorta or on resumption of aortic flow was noted in no patient. Postoperative ischemia of any vascular bed was noted locally only in 3 (cannulated) lower extremities. CONCLUSIONS: Straight femoral cannulation for all phases of type A dissection repair is appropriate and yields excellent clinical results. The anticipated malperfusion events are actually rare (2 of 79 with femoral artery cannulation, or 2.5%).