Yukio Okazaki

Platelets are deposited early post-operatively on the leaflet of a mechanical heart valve in sheep without post-operative anticoagulants or antiplatelet agents: A scanning electron microscopic observation of the pyrolytic carbon surface in a mechanical heart valve

Pyrolytic carbon has been used for mechanical heart valves as a thromboresistant, wear resistant, and fatigue resistant material. Thrombosis and thromboembolism, however, remain major mechanical heart valve associated complications and may frequently occur during the early post-operative period. In depth morphologic studies on blood-pyrolytic carbon surface interactions are limited. The purpose of this study was to evaluate the blood compatibility of the pyrolytic carbon surface of St. Jude Medical mechanical heart valves that were implanted in the mitral position of sheep without the administration of post-operative anticoagulants or antiplatelet agents for 2, 4, and 6 weeks. Almost the entire leaflet and orifice ring surfaces were observed by scanning electron microscopy. Although the surfaces appeared clean macroscopically, when observed by electron microscopy, the surface were mottled, mainly by solitary platelets and aggregations. There were only a few leukocytes or red blood cells observed. No fibrin clots were observed on the leaflets. The density of platelet deposition was higher in the vicinity of the pivots and near the edges of the leaflets. The sizes of the platelet aggregations decreased with longer duration. The outer surfaces of the pivot guards were covered by various amounts of deposition composed of platelet aggregations and thrombi. Thus, the administration of antiplatelet agents is recommended during the early post-operative period after mechanical heart valve implantation.

Heat from an implanted power source is mainly dissipated by blood perfusion.

Heat dissipation and its effects on tissue and blood interfaces are common problems associated with the development and increased use of artificial hearts, because all of the implantable actuators for artificial hearts generate waste heat due to inefficiencies of energy conversion. To determine the mechanisms of heat dissipation from artificial hearts, heated disks producing constant heat fluxes of 0.08 watts/cm2 were implanted adjacent to the left lung and the latissimus dorsi muscle in calves for 2 weeks, 4 weeks, and 7 weeks. At the end of each experiment, a series of acute studies was performed in which blood perfusion to the heated tissue was decreased or stopped to observe the contribution of blood perfusion to heat dissipation. The cooling effect of ventilation was also examined to determine its relative contribution to heat dissipation in lung tissue by decreasing the minute ventilation volume. The importance of blood perfusion for heat dissipation was demonstrated by the temperature rise after cessation of blood perfusion to the heated tissue. The contribution of ventilation to heat dissipation in the heated lung tissue was minimal. Contribution of total blood perfusion to heat dissipation was increased with time in the muscle tissue, which has relatively low resting blood perfusion, but not in the lung tissue, which has relatively high blood perfusion. In the heated muscle tissue, the in vivo adaptive response to chronic heat was functionally shown by the increased perfusion. In conclusion, blood perfusion was the main mechanism of heat dissipation from tissues that were adjacent to an implanted power source. ASAIO Journal 1997; 43:M585-M588.

Anatomic fitting studies of a total artificial heart in heart transplant recipients. Critical dimensions and prediction of fit.

Anatomic fitting studies of the Cleveland Clinic-Nimbus total artificial heart were performed in 33 patients undergoing heart transplantation. The pump fit in the pericardial space in 20 men (80%) and 4 women (50%). There was no significant difference between the Fit and Non-Fit groups in external chest dimensions. Among 42 intrathoracic dimensions, the distance from the center of the mitral valve to the diaphragm (Fit: 5.6 +/- 2.2 cm, Non-Fit: 3.6 +/- 0.4 cm, p < 0.00001) and the distance from the caudal end of the pulmonary valve to the diaphragm (Fit: 9.4 +/- 1.6 cm, Non-Fit: 6.3 +/- 0.8 cm, p < 0.0001) were the most critical. To predict anatomic fit, an index (A x B x C) was obtained from chest X-ray measurements (A, the craniocaudal distance from the dorsal region of the 8th left rib to the left diaphragm; B, the maximum left chest width; and C, the maximum anteroposterior sternum-vertebrae dimension). The pump fit in 88.5% of the patients with an index above 1200 cm3, whereas it fit in only 14.3% of the patients with an index below 1200 cm3 (p < 0.001). This index was an easily obtainable, good predictor of anatomic fit.

Heat Dissipation from Artificial Hearts: Characterizing Tissue Responses and Defining Safe Levels

Mechanical artificial hearts generate heat, imposing unprecedented biomedical problems. Experiments were conducted in calves to study the effects of chronic heating and the mechanisms of the adaptation response, and to determine the safe levels for device-tissue interfacial temperatures. Electric heat sources which dissipated three different levels of constant heat flux (0.04, 0.06, or 0.08 W/cm2) were implanted adjacent to lung and muscle for up to seven weeks. The tissue temperatures were continuously monitored at the heater surface and 1, 3, and 7 mm from the surface. Correlating the local tissue temperatures with histologic features, the safe upper limit was identified to be 43°C, or 4°C above the body temperature. There were significant differences in tissue temperatures between the lung and muscle at all distances and with all three fluxes (P = 0.0001), reflecting a higher blood perfusion in the lung tissue. With the highest heat flux of 0.08 W/cm2, and the resultant initial surface temperature of 42.8°C ± 0.9°C, the lung showed no sign of tissue damage or necrosis, while the muscle, with a surface temperature of 45.3°C ± 2.2°C, was necrotic to a distance of 18.1mm and 3.0mm from the surface at 2 and 4 weeks, respectively. By the seventh week this muscle necrosis was totally replaced by fibrosis. Gradual decreases in the surface temperatures with the two higher heat fluxes and enhanced angiogenesis have suggested that the tissues adapt to chronic heating by increased perfusion. The expression of heat shock proteins by the tissue repair cells in the tissue capsule also suggests that cellular adaptation to heating is occurring.

Systemic hypertension as a risk factor for complications with an aortic mechanical valve.

We sought to determine the effect of preoperative systemic hypertension on prosthesis related complications or postoperative aortic dissection after valve replacement in patients with aortic regurgitation. The patients were divided into two groups according to the presence or absence of systemic hypertension: Group I, with hypertension (n = 35), and Group II, without hypertension (n = 37). The survival rate and event free rate were examined for 72 patients who were alive 30 days after valve replacement with a St. Jude Medical valve for aortic regurgitation. The cumulative 10 year survival rate of Group I (65% +/- 12%) was lower than that of Group II (79% +/- 15%). The 10 year event free rate of all prosthesis related complications was 62% +/- 13% in Group I, and 96% +/- 3% in Group II (p < 0.05). The 10 year event free rate for ascending aortic dissection was 73% +/- 12% in Group I and 100% in Group II (p < 0.05). The linearized event rate of all prosthesis related complication was 3.8% per patient-year in Group I and 0.5% per patient-year in Group II. In conclusion, systemic hypertension was a risk factor for prosthesis related complications and for complicated aortic lesions after aortic valve replacement. Careful postoperative management for hypertension is necessary in patients with systemic hypertension after aortic valve replacement. Tissue valves may be recommended in patients with aortic valve disease and severe hypertension.

Surgical Treatment for a Trauma-Caused Cardiac Rupture

鈍的外傷による心破裂の救命率は低い.救命率の向上のためには診断,治療方針を明確にする必要がある.われわれは鈍的外傷による心破裂例8例を経験した.来院時,全例経胸壁心エコーにより心嚢液貯留を認め,心タンポナーデの状態であった.受傷から来院までの平均時間は186±185分,来院から手術室搬入までの平均時間は82±49分.術前に心嚢ドレナージを行ったのは2例,経皮的心肺補助装置を使用したのは2例であった.破裂部位は,右房3例,右房-下大静脈1例,右室2例,左房1例,左室1例であった.4例に体外循環を用い損傷部位を修復した.8例中6例を救命することができた(救命率75%).診断において経胸壁心エコーが簡便かつ有効であった.多発外傷例が多いが,心タンポナーデによるショック状態を呈している場合,早急に手術室へ搬送すべきである.手術までの循環維持が重要であり,心嚢ドレナージ,PCPSが有効である.