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Objective: The Edwards Duromedics valve (Baxter Healthcare Corp., Edwards Division, Santa Ana, Calif.) was designed with a self-irrigating hinge mechanism to reduce thromboembolic complications. After good initial clinical results, distribution was suspended in 1988 after reports of valve fracture after 20,000 valves had been implanted. The manufacturer conducted extensive studies to improve the Edwards Duromedics and reintroduced a modified version, which is available as Edwards Tekna. The purpose of the study was the evaluation of long-term results of the original Edwards Duromedics that might be important for the current version, the Edwards Tekna valve. Methods: A prospective clinical 10-year follow-up was performed of 508 patients who underwent valve replacement with the Edwards Duromedics valve in the aortic ( n = 268), mitral ( n = 183), and aortic and mitral ( n = 56) position. Results: The perioperative mortality rate was 6.9%; follow-up was 98% complete, comprising 3648 patient-years for a mean follow-up of 86 months (range: 33 to 144 months). The actuarial freedom from complications at the 10-year follow-up and the incidence rate (percent per patient-year) were as follows: late mortality rate, 69.2% ± 2.4% (3.5% per patient-year); thromboembolism, 90.7% ± 1.6% (0.96% per patient-year); anticoagulation-related hemorrhage, 87.7% ± 1.7% (1.34% per patient-year); prosthetic valve endocarditis, 96.7% ± 0.09% (0.38% per patient-year); valve-related mortality rate, 89.3% ± 1.6% (1.21% per patient-year); valve failure, 86.2% ± 1.85% (1.54% per patient-year); and valve-related morbidity and mortality rate, 71.1% ± 2.3% (3.2% per patient-year). Three leaflet escapes were observed (one lethal, two successful reoperations; 99.1% ± 0.05% freedom, 0.08% per patient-year). All patients functionally improved (86% in New York Heart Association classes I and II), and incidence of anemia was insignificant. Conclusions: These results confirm that the Edwards Duromedics valve shows excellent performance concerning thromboembolism, hemolysis, and functional improvement and will serve as a reference for the last version, the Edwards Tekna valve, where comparable long-term data are currently not available. (J Thorac Cardiovasc Surg 1998;115:1121-9)

Following the implantation of biodegradable vascular grafts, macrophages and fibroblasts are the major two cell types recruited to the host-biomaterial interface. In-vitro biocompatibility assessment usually involves one cell type, predominantly macrophages. In this study, macrophage and fibroblast mono- and co-cultures, in paracrine and juxtacrine settings, were used to evaluate a new biodegradable thermoplastic polyurethane (TPU) vascular graft. Expanded-polytetrafluoroethylene (ePTFE) grafts served as controls. Pro/anti-inflammatory gene expression of macrophages and cytokines was assessed in vitro and compared to those of an in vivo rat model. Host cell infiltration and the type of proliferated cells was further studied in vivo. TPU grafts revealed superior support in cell attachment, infiltration and proliferation compared with ePTFE grafts. Expression of pro-inflammatory TNF-α/IL-1α cytokines was significantly higher in ePTFE, whereas the level of IL-10 was higher in TPU. Initial high expression of pro-inflammatory CCR7 macrophages was noted in TPU, however there was a clear transition from CCR7 to anti-inflammatory CD163 expression in vitro and in vivo only in TPU, confirming superior cell-biomaterial response. The co-culture models, especially the paracrine model, revealed higher fidelity to the immunomodulatory/biocompatibility behavior of degradable TPU grafts in vivo. This study established an exciting approach developing a co-culture model as a tool for biocompatibility evaluation of degradable biomaterials. Electronic supplementary material The online version of this article (doi:10.1007/s10439-016-1601-y) contains supplementary material, which is available to authorized users.

A randomized study was performed on 70 patients undergoing elective coronary bypass surgery to examine whether the combined, perioperative, 24-hour infusion of the calcium-channel blocker nifedipine (10 micrograms/kg/h) and the beta 1-blocker metoprolol (12 micrograms/kg/h) reduces the incidence of perioperative myocardial ischemia and arrhythmias (group NM, n = 34). The control group received nifedipine only (n = 36). Repeated assessment of serum enzyme levels (CK, CK-MB) and 12-lead ECG, together with 3-channel Holter monitoring over 48 h were used to define perioperative myocardial ischemia (transient ischemic event, myocardial infarction) and supraventricular and ventricular arrhythmias. The two groups did not significantly differ with respect to preoperative anamnestic and surgical data. No perioperative myocardial infarction was detected in either group. However, a significantly lower incidence of transient ischemic events was observed in the NM group as compared to the nifedipine group (3% versus 11%; p < 0.05). In addition, there was a tendency towards lower CK-MB levels and peak-values of CK- and CK-MB in the NM group. With regard to perioperative dysrhythmias, there was a significantly lower incidence of sinus tachycardia (9%) and atrial flutter/fibrillation (6%) in the NM group as compared to the nifedipine group (33 and 27%, p < 0.05). In addition, postoperative heart rate was lower in the NM group starting from the 6th hour after opening of the aortic cross-clamp. In conclusion, the combined perioperative infusion of nifedipine and metoprolol is superior in preventing perioperative myocardial ischemia and decreasing the incidence of supraventricular arrhythmias as compared to a single-drug regimen with nifedipine.

In the present study the effect of oxygenated Bretschneider cardioplegia on high-energy phosphates [adenosine triphosphate (ATP), adenosine diphosphate (ADP) and creatine phosphate (CP)] and hemodynamics was evaluated in the isolated working rabbit heart. Hearts were obtained from 37 adult white Elco rabbits (3,100 +/- 110 g). After a 20-min working period 14 hearts were arrested with Bretschneider cardioplegia (8 degrees C) oxygenated with 98% oxygen (O2) and 2% carbon dioxide in comparison to 14 hearts receiving Bretschneider solution saturated with 98% nitrogen (N2) and 2% carbon dioxide as a control group for either 60 or 90 min (O(2)60, O(2)90, N(2)60, N(2)90 groups, n = 7). Seven hearts were used to determine preischemic baseline values of ATP, ADP and CP, 2 were excluded. The results showed a significantly poorer preservation of high-energy phosphates in hearts receiving oxygenated Bretschneider cardioplegia as compared to hearts receiving nitrogenated cardioplegia (p0.05). Postischemic recovery of hemodynamics did not demonstrate any statistically significant differences between the groups. However, the intragroup analysis showed a tendency towards weaker hemodynamic recovery in hearts treated with oxygenated cardioplegia. in contrast to the beneficial effect of oxygenated St. Thomas solution. In conclusion our findings suggest that oxygenated Bretschneider cardioplegia leads to significantly poorer preservation of high-energy phosphates and depressed hemodynamic recovery.

7 healthy pigs, anesthetized with ketamine/azaperon/thiopentone and ventilated with O2/N2O by volume control, underwent anterior resection of the descending colon by laparoscopic view. During operation of pneumoperitoneum by inflating CO2 to an abdominal pressure of 14 mm Hg was installed. Immediately (+2 min) after the onset of insufflation, both systemic and pulmonary arterial pressure increased. However, pulmonary artery pressure started to decrease after 10 min, whereas systemic arterial pressure remained elevated until the end of the experimental protocol. Left ventricular (LV) pressure and LV dp/dt increased in parallel with the systemic arterial pressure. Peak inspiratory pressure and central venous pressure increased in parallel with the abdominal pressure. Blood gas analysis of arterial and pulmonary blood demonstrated increased pCO2 associated with mild acidosis. Arterial pO2 did not change significantly indicating that the decreased pulmonary distensibility did not endanger the oxygenation. Pulmonary pO2 and pulmonary O2 saturation increased early (+10 min) after start of insufflation and were stable during the 2 h of observation indicating either increased cardiac output or decreased O2 extraction. We conclude that the sharp initial rise of both arterial pressures could be the effect of a mechanical action, whereas sustained hemodynamic alterations would involve complex regulatory mechanisms like an increase of sympathetic activity, baroreceptor control, or a response to acidosis. The acute and, in the systemic circulation, stable increase of ventricular afterload should be considered in patients with underlying cardiac diseases such as ischemic heart disease or valvular dysfunction or in patients taking drugs which interfere with normal compensatory processes.

Although the anatomy, histology and pathology of human coronary arteries have been studied extensively, little is known about the functional relationship between vessel radius and wall thickness. It is the purpose of this study to present detailed measurements and to describe this relationship covering the range from the feeding coronary artery to the arterioles. Human hearts of 10 adults less than 36 ± 3 years old were investigated immediately postmortem. Ten cubic tissue blocks, measuring about 10 mm in length on each side, were dissected from the left ventricular wall. After fixation by immersion, 15-µm sections were prepared and outer and inner perimeters of 52 arterial segments were digitalized. Vessel radius and wall thickness were calculated and plotted to show their relationship over the whole range of vessel calibers. Outer vessel radii ranged from 100 to 3,000 µm and wall thickness from 80 to 800 µm. Plotting the outer vessel radius against the wall thickness, the data points were found to cluster around a straight line. A significant correlation between the two parameters was found (R2 = 0.79). This mathematical correlation and the good agreement of the presented results with data from other species indicate a common physiologic concept.

In a randomized prospective experimental study on 48 adult white Elco rabbits biochemical and rhythmic changes after bolus administration of the phosphodiesterase inhibitor piroximone were investigated using a working heart model. The treatment group (n = 21) intravenously received 1 mg/kg of piroximone 15 min before thoracotomy. Twenty-three untreated hearts served as the control group. From 6 hearts of each group myocardial biopsies were taken before ischemia, 4 (2/2) hearts were excluded. Hemodynamic results of a previous study with an identical protocol were reanalyzed; a biochemical analysis of myocardial high-energy phosphates was investigated after 60 min of global ischemia and at the end of the experiments after 45 min of reperfusion. Already prior to ischemia, in the treatment group depletion of high-energy phosphates was detected. After 60 min of ischemia during early reperfusion in the treatment group ATP and creatine phosphate depletion became even more evident and increased until the end of the experiments. The incidence of reperfusion-induced arrhythmias was significantly lower in the treatment group. Consequently these results and the hemodynamic results of prior studies indicate a possible positive effect of piroximone during the early reperfusion period by optimizing hemodynamics and arrhythmias.