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SummaryA 62-year-old man presented to hospital with chest oppression. Coronary angiography revealed total occlusion of the right coronary artery and inferior myocardial infarction was diagnosed. He was treated by percutaneous coronary intervention with stenting for myocardial infarction. After four months, echocardiography revealed a huge aneurysm protruding below the inferior surface of the left ventricle. It was considered to be a pseudoaneurysm from the echocardiographic findings. The patient had no symptoms and he refused surgery, so progression of the aneurysm was monitored carefully. At seven months after revascularization, the aneurysm showed a marked increase in size, with a maximal diameter of 48mm and orifice diameter of 22mm. Accordingly, the patient agreed to undergo surgical excision. The aneurysm was resected and the defect was closed with a pericardial patch. Pathological examination revealed all of the myocardial elements in the aneurysm wall and thrombus in its lumen. In conclusion, this was a rare case of venricular subepicardial aneurysm.

症例は73歳，男性．突然の前胸部痛を主訴に当院に救急搬送となり，同日の緊急カテーテル検査で左主幹部病変を伴う3枝冠動脈病変を認める急性心筋梗塞と診断され，責任病変と考えられた右冠動脈のインターベンション後，残存病変に対する冠動脈バイパス手術目的に当科紹介となった．術前精査で左鎖骨下動脈閉塞による盗血現象 （subclavian steal phenomenon)，および両側外腸骨動脈に閉塞病変を認める閉塞性動脈硬化症 （ASO） を合併し，左主幹部分岐部の冠動脈瘤を疑う左主幹部狭窄病変を伴う重症3枝病変の虚血性心疾患 （IHD） と診断した．治療戦略として， LAD および LCX 領域の冠動脈血行再建と同時に，冠動脈瘤切除を予定した．術後心機能低下時の補助循環に備え，上行大動脈-右大腿動脈人工血管バイパス術を併施し，患者への手術侵襲を軽減するために左上肢および左下肢への血行再建は後日に施行する2期的手術を選択した．術中所見で冠動脈瘤は認めず，瘤切除は施行しなかったが，予定どおりの手術を施行し，術後補助循環を使用することなく，術後24日目に2期目の手術を施行し，術後経過良好で2期目術後20日目に退院された．本症例のように複雑な IHD と ASO の合併した症例は手術侵襲と術後補助循環挿入ルートを十分に考慮した治療戦略をたてる必要があると考えられた．

This report describes the successful treatment of a case of cardiac adenocarcinoma with the clinical presentation as Budd-Chiari syndrome. Complete surgical excision of the atriocaval mass was successfully achieved under deep hypothermic circulatory arrest. Histopathological diagnosis of this tumor was tubular adenocarcinoma with positive immunostaining by carcinoembrionic antigen. Subsequent systemic search could not detect any evidence of extra-cardiac primary site and distant metastatic lesion. A 2-year follow-up without any adjuvant therapy revealed no sign of recurrence.

完全左脚ブロックを伴う重症虚血性心筋症に対して,冠動脈バイパス術に自己骨髄単核球細胞移植術(BMCI)による血管新生療法と両心室ペーシング(BVP)を用いた心臓再同期治療を同時施行し,良好な結果を得たので報告する.症例は67歳,男性.心不全増悪による呼吸困難を主訴とし,左冠動脈の広範囲びまん性閉塞病変に起因する虚血性心筋症に対する外科的治療目的で当科紹介となった.心臓超音波検査ではLVDd 71mmと左室腔の拡大を認め,心電図検査はQRS幅180msの完全左脚ブロックを呈していた.冠動脈造影検査で#5:50%,#6,7,8:90%(ステント内多発病変),#12:100%(枯れ枝状末梢性びまん性閉塞),#14:75%の有意狭窄病変を認めた.当大学倫理委員会の承認を得て,冠動脈バイパス術(1枝:#14)と同時に,末梢性びまん性閉塞病変を有する左室高側壁領域へのBMCIとBVPを施行した.術後15ヵ月が経過,自覚症状および心機能の著明な改善を認めた.

The role of protein kinase C (PKC) isoforms in myogenic tone of the ferret coronary microcirculation was investigated by measuring fura 2 Ca2+signals, PKC immunoblots, contractile responses, and confocal microscopy of PKC translocation. Phorbol ester-evoked contractions were completely abolished in the absence of extracellular Ca2+but involved a Ca2+sensitization relative to KCl contractions. Immunoblotting using isoform-specific antibodies showed the presence of PKC-α and -ι and traces of PKC-ɛ and -μ in the ferret coronary microcirculation. PKC-β was not detectable. When intraluminal pressure (40 to 60 and 80 mmHg) was increased, ferret coronary arterioles showed a transient increase in fura 2 Ca2+signals, whereas the myogenic tone remained sustained. The increase in Ca2+and tone was sustained at 100 mmHg. Isolated ferret coronary arterioles were fixed and immunostained for PKC-α at 40 and 100 mmHg intraluminal pressure. PKC translocation was determined by confocal microscopy. Increased PKC translocation was observed when vessels were exposed to 100 mmHg relative to that at resting pressure (40 mmHg). These results suggest a link between the Ca2+sensitization that occurs during the myogenic contraction and activation of the α-isoform of PKC.

Background: The purpose of this study was to determine the influence of oxygenation of a hyperkalemic cardioplegic solution (K-CP) on endothelial modulation of vasomotor tone and to correlate these changes with the intracellular calcium concentration ([Ca++]i) in microvascular smooth muscle. Methods: Rat coronary arterioles were studied in a pressurized, no-flow normothermic state. Simultaneous monitoring of luminal diameter and [Ca++]i (fura-2) was performed with use of microscopic image analysis. Vessels were subjected to 60 minutes of oxygenated or hypoxic K-CP (K+ = 25.0 mmol/L) and were then reperfused with oxygenated Krebs–physiologic saline solution for 60 minutes. Results: In oxygenated K-CP, the K-CP–induced contraction and [Ca++]i accumulation were significantly increased in endothelium-denuded (ED) vessels compared with endothelium-intact vessels. The effect of ED in oxygenated K-CP was mimicked by administration of the nitric oxide synthase inhibitor NG-monomethyl-L -arginine. Conversely, in hypoxic K-CP the contraction was significantly attenuated in ED vessels compared with endothelium-intact vessels, although there was no significant difference in [Ca++]i. Indomethacin did not affect the endothelium-dependent contraction during hypoxic K-CP. Conclusions: Endothelium-derived nitric oxide modulates the vascular tone during K-CP by regulating the vascular smooth muscle [Ca++]i, whereas endothelium-derived contracting factor(s), which is not predominantly a product of cyclo-oxygenase, may play a prominent role under hypoxic K-CP by increasing vascular smooth muscle Ca++ sensitivity. (Surgery 1999;126:264-71.)

The effects of calcium and magnesium ions in cardioplegic solutions on cardioprotection and intracellular calcium ion handling during ischemia and reoxygenation were investigated in cultured neonatal rat myocardial cells. Myocytes were subjected to simulated ischemia for 60 min at 37 degrees C in hyperkalemic cardioplegic solutions containing various concentrations of calcium and magnesium ions, followed by 30 min of reoxygenation. For each Ca2+ concentration (0.1, 0.6, 1.2, or 2.4 mM), the Mg2+ concentration was either 0, 1.2, 8, or 16 mM. The increase in intracellular Ca2+ concentration during ischemia and reoxygenation was suppressed by the addition of magnesium ion, independent of cardioplegic Ca2+ concentration. The recovery of spontaneous contraction rate and enzyme leakage (creatine phosphokinase and lactate dehydrogenase) during both ischemia and reoxygenation correlated with the degree of inhibition of intracellular Ca2+ accumulation. However, in the 0.1 mM Ca2+ groups in which the Mg2+ concentration was greater than 8 mM, the intracellular Ca2+ concentration increased during reoxygenation in a dose-dependent fashion of Mg2+, and was associated with increased enzyme leakage. The findings suggest that in immature cardiac myocytes, the concentrations of Ca2+ and Mg2+ present in cardioplegic solutions control the intracellular Ca2+ concentration during ischemia and reoxygenation, which, in turn, influences the cardioprotective effect of the cardioplegic solution.

Coronary artery bypass grafting (CABG) in patients with severely diseased ascending aorta has been associated with high risk for cerebral vascular accidents due to atheromatous embolism. In this situation, aortic no-touch techniques are widely employed as most important surgical strategy to prevent these complications. A case of 75-year-old man with effort angina associated with porcelain ascending aorta was reported here. He successfully underwent off-pump axillo-coronary bypass grafting with saphenous vein graft and has remained uneventful during his follow-up period. The off-pump axillo-coronary artery bypass grafting seemed to be an appropriate procedure for coronary revascularization with severely diseased ascending aorta.

症例は77歳,男性である.腹部大動脈瘤術後9年目に中枢側吻合部瘤のため入院した.吻合部瘤は腎動脈より3cm末梢側に存在し,最大径55mmであった.再手術症例で脳梗塞の既往があり,また解剖学的にも適応があったためステントグラフト内挿術を施行した.術後endoleakやmigrationは認めず,現在外来通院中である.ステントグラフト内挿術は腹部大動脈瘤の再手術症例に対し有効な手段であり,解剖学的に可能であれば積極的に試みるべき治療手技であると考えられた.

We characterized the interaction of 2,5-di(tert-butyl)-1,4-benzohydroquinone (tBuBHQ) with the sarcoplasmic reticulum (SR) Ca(2+)-ATPase from rabbit fast-twitch skeletal and canine cardiac muscles by examining the effect of this agent on the ATPase reaction. tBuBHQ at less than 10 microM inhibited ATP hydrolysis by both isoforms of Ca(2+)-ATPase by up to 80 and 90%, respectively. The half maximal inhibition of these enzymes was observed at about 1.5 microM tBuBHQ. Thus, this agent potently inhibits the fast-twitch skeletal and slow-twitch skeletal/cardiac isoforms of SR Ca(2+)-ATPase. tBuBHQ at 5-10 microM inhibited the rate of decomposition of the phosphoenzyme intermediate (EP), measured as a ratio between ATPase activity and the EP level in the steady state, by 35-40%. It also inhibited formation of EP by decreasing the rate of Ca2+ binding to the Ca(2+)-deficient, nonphosphorylated enzyme to about 1/8 of the control value. These results indicate that tBuBHQ has at least two sites of action in the reaction sequence for the SR Ca(2+)-ATPase.

Calcium overload during reperfusion after prolonged ischemia has been associated with the Na + Ca 2+ exchange system. It has been proposed that the promotion of Na + Ca 2+ exchange at reperfusion may be mediated by Na + H + exchange. To evaluate whether this hypothesis is applicable for stunned myocardium, we examined the influence of temporary suppression of Na + H + and/or Na + Ca 2+ exchange during early reperfusion in isolated rat hearts. Myocardial stunning was produced by global ischemia for 15 min at 37°C. The initial reperfusate was given during the subsequent 10 min after ischemia, and followed by reperfusion with normal Krebs—Henseleit buffer solution for 40 min. Hemodynamic indices, creatine kinase in coronary effluent, and myocardial water content were measured during reperfusion. The functional recovery of stunned myocardium was improved with higher extracellular Na + concentration and/or lower Ca 2+ concentration of the initial reperfusate. Aortic flow recovery of group II (135 m M Na + -0.5 m M Ca 2+ ) was 77.0 ± 3.4%, which was substantially greater ( P M Na + -1.5 m M Ca 2+ ), 68.2 ± 2.4%; group III (25 m M Na + -0.5 m M Ca 2+ ), 48.7 ± 2.9%; group IV (25 m M Na + -1.5 m M Ca 2+ ), 21.6 ± 1.5%. Administration of amiloride, an inhibitor of Na + H + exchange, in the initial reperfusate ameliorates cardiac damage and improved aortic flow recovery in a dose-dependent manner (10 −6 , M , 70.1 ± 3.7%; 10 −5 M, 77.3 ± 1.7%; 10 −4 , M , 82.0 ± 2.1% vs control 68.2 ± 2.4%). These data are consistent with the hypothesis that Na + H + and/or Na + Ca 2+ exchange may be involved in the mechanism for myocardial stunning.

虚血心再灌流障害の発生機序を明らかにすることを目的に, 細胞膜Na+-Ca2+交換機構の観点から実験的検討を行った. ラット摘出心を用いた isolated working heart model を使用した. 37℃-15分間の global ischemia の後, 再灌流の初期10分間の冠灌流液中Na+濃度, Ca2+濃度を段階的に変化せしめ, 再灌流後の心機能, 心筋代謝に及ぼす影響を検討した. その結果, 再灌流障害はNa+濃度25～135mMにおいて濃度依存性に軽減され, Ca2+濃度0.5～1.5mMにおいて濃度依存性に増悪した. また, 細胞膜Na+-Ca2+交換阻害物質として amiloride を再灌流の初期に投与した結果, 心筋障害は有意に抑制された. 以上の結果より, 再灌流障害発生機序の原因として細胞膜Na+-Ca2+交換機構の役割は重要であり, 交換阻害物質を投与し, Ca2+の細胞内流入を抑制することは, 再灌流障害の発生予防に有効な手段になりうると考えられた.

The effects of metabolic acidosis and alkalosis in the initial reperfusate on post-ischemic stunned myocardium were investigated in isolated rat hearts. Metabolic acidosis and alkalosis were produced by altering the doses of artificial buffer (Tris) in place of sodium bicarbonate. All hearts were subjected to global ischemia for 15 min at 37 degrees C. The initial reperfusate under study was given during the subsequent 10 min of reperfusion, just prior to release of the aortic clamp. After that, reperfusion using normal Krebs-Henseleit buffer solution was carried out for 40 min. The acidotic initial reperfusate (pH 6.8) resulted in better protection than the alkalotic initial reperfusate (pH 7.8), as demonstrated by 1) a higher recovery of aortic flow (80.6% +/- 3.8% vs 32.7% +/- 4.8%, p less than 0.01), 2) a smaller leakage of creatine kinase during the initial reperfusion phase (6.0 +/- 0.7 vs 14.6 +/- 2.1 IU/10 min/g dry weight, p less than 0.05) and during the post-ischemic Langendorff perfusion phase (8.8 +/- 1.7 vs 37.3 +/- 5.2 IU/10 min/g dry weight, p less than 0.05), and 3) a lower myocardial water content at the end of reperfusion (84.8% +/- 0.2% vs 85.7% +/- 0.3%, p less than 0.05). Not only Tris buffer system, but also HEPES buffer system indicated that acidotic initial reperfusate was effective to protect against myocardial injury. These results suggest that 1) the extracellular pH during initial reperfusion profoundly influences the reversible myocardial dysfunction (stunned myocardium), and 2) the acidotic initial reperfusate improves post-ischemic myocardial performance.

A case of bilateral persistence of the sciatic artery in association with a DeBakey type III dissecting aortic aneurysm is presented. Arteriography demon strated a patent persistent left sciatic artery with an aneurysm, and this artery connected to the popliteal artery. The sciatic artery was also present on the right side but had been occluded in the pelvis, so the hypoplastic superficial femoral artery provided the main route to the popliteal artery. Aneurysm or occlusion of a sciatic artery is common. However, the combination of a dissecting aortic aneurysm and a persistent sciatic artery has never been reported previously. When a persistent sciatic artery provides the main blood supply to the lower limb, anticoagulant therapy is recommended to prevent its occlusion.

The effects of the potassium (K+) channel opener pinacidil (Pin) on the coronary smooth muscle Ca2+-myosin light chain (MLC) phosphorylation pathway under hypothermic K+cardioplegia were determined by use of an in vitro microvessel model. Rat coronary arterioles (100–260 μm in diameter) were subjected to 60 min of simulated hypothermic (20°C) K+cardioplegic solutions (K+= 25 mM). We first characterized the time course of changes in intracellular Ca2+concentration, MLC phosphorylation, and diameter and observed that the K+cardioplegia-related vasoconstriction was associated with an activation of the Ca2+-MLC phosphorylation pathway. Supplementation with Pin effectively suppressed the Ca2+accumulation and MLC phosphorylation in a dose-dependent manner and subsequently maintained a small decrease in vasomotor tone. The ATP-sensitive K+(KATP)-channel blocker glibenclamide, but not the nitric oxide (NO) synthase inhibitor Nω-nitro-l-arginine methyl ester, significantly inhibited the effect of Pin. K+cardioplegia augments the coronary Ca2+-MLC pathway and results in vasoconstriction. Pin effectively prevents the activation of this pathway and maintains adequate vasorelaxation during K+cardioplegia through a KATP-channel mechanism not coupled with the endothelium-derived NO signaling cascade.

This study was designed to compare the effects of hyperpolarizing versus depolarizing cardioplegic solutions on the coronary vasomotor regulation, specifically focusing on coronary myoplasmic Ca2+-myosin light chain (MLC) phosphorylation pathway and beta-adrenergic signal transduction.With the use of an in vitro cardioplegic model, rat coronary microvessels loaded with fura-2 were subjected to simulated cold (20 degrees C) cardioplegia and reperfused with Krebs solution for 60 minutes at 37 degrees C. Cardioplegia consisted of either (1) Krebs solution alone (control), (2) Krebs plus adenosine triphosphate-sensitive potassium channel opener (100 micromol/L pinacidil [PCO-CP]), (3) hyperkalemic cardioplegia (K(+) = 25 mmol/L [K-CP]), or (4) K-CP plus magnesium (Mg(2+) = 25 mmol/L; [K/Mg-CP]).At the endpoint of the cardioplegic period, K-CP resulted in a significant increase both in [Ca(2+)](i) and in MLC phosphorylation compared with control (both P.05). In contrast, PCO-CP did not make any significant difference in these indices compared with control. After reperfusion, the relaxation responses to isoproterenol and forskolin after K-CP were significantly reduced (both P.05 vs control) but were preserved after PCO-CP. K/Mg-CP provided comparable effects to PCO-CP.These results suggest that neither an activation of the coronary myoplasmic Ca(2+)-MLC phosphorylation pathway nor beta-adrenergic desensitization seen after exposure to depolarizing cardioplegia occurs with exposure to hyperpolarizing cardioplegia and magnesium-supplemented depolarizing hyperkalemic cardioplegia.

The use of Mg2+-supplemented hyperkalemic cardioplegia preserves microvascular function. However, the mechanism of this beneficial action remains to be elucidated. We investigated the effects of Mg2+supplementation on the regulation of intracellular calcium concentration ([Ca2+]i) and vascular function using an in vitro microvascular model. Ferret coronary arterioles (80–150 μm in diameter) were studied in a pressurized (40 mmHg) no-flow, normothermic (37°C) state. Simultaneous monitoring of internal luminal diameter and [Ca2+]iusing fura 2 were made with microscopic image analysis. The microvessels ( n = 6 each group) were divided into four groups according to the content of MgCl2(nominally 0, 1.2, 5.0, and 25.0 mM) in a hyperkalemic cardioplegic solution ([K+] 25.0 mM). After baseline measurements, vessels were subjected to 60 min of hypoxia with hyperkalemic cardioplegia (equilibrated with 95% N2-5% CO2) containing each concentration of Mg2+([Mg2+]) and were then reoxygenated. During hyperkalemic cardioplegia, [Ca2+]iincreased in a time-dependent manner in all groups. In the lower [Mg2+] cardioplegia groups, [Ca2+]iwas significantly increased at the end of the 60-min cardioplegic period (247 ± 44 nM and 236 ± 49 nM in [Mg2+] 0 and 1.2 mM groups, respectively; both P < 0.05 vs. baseline) with 19.6–17.2% vascular contraction. Conversely, there was no significant [Ca2+]iincrease in the higher [Mg2+] cardioplegia groups and less vascular contraction (5.4–4.1%, both P < 0.05 vs. [Mg2+] 1.2 mM group). After reperfusion, agonist (U-46619, thromboxane A2analog)-induced vascular contraction was significantly enhanced in the lower [Mg2+] cardioplegia groups (both P < 0.05 vs. control) but was normalized in the higher [Mg2+] cardioplegia groups. Intrinsic myogenic contraction was significantly decreased in the lower [Mg2+] cardioplegia groups (both P < 0.05 vs. control) but was preserved in the higher [Mg2+] cardioplegia groups. These results suggest that supplementation of the solution with >5.0 mM [Mg2+] may prevent hyperkalemic cardioplegia-related intracellular Ca2+overloading and preserve vascular contractile function in coronary microvessels.

The plasma concentrations of brain natriuretic peptide (BNP), a cardiac hormone, were measured in 30 consecutive adult patients undergoing cardiac surgery with cardiopulmonary bypass (CPB) during the perioperative period. BNP concentrations remained unchanged until 6 h after the cessation of bypass, and were elevated 12, 24, and 48 h post-bypass (P < 0.0001 versus baseline). They had returned to the baseline values when measured 3 weeks postoperatively. The preoperative plasma BNP concentration correlated significantly with the left ventricular ejection fraction (r = -0.895). The peak plasma BNP concentration 24 h after bypass correlated with the cardiac index (r = -0.64), stroke volume index (r = -0.62), injection rate of dopamine hydrochloride (r = 0.65), and aortic crossclamp time (r = 0.57). There was also a significant correlation between the preoperative BNP concentration and the plasma BNP concentration 24 h post-CPB. These findings led us to conclude that the plasma concentrations of BNP become markedly and acutely elevated after cardiac surgery with CPB, and reflect the state of left ventricular function. Moreover, the severity of acute heart failure after cardiac surgery can be predicted by the preoperative plasma BNP concentration.

The effects of calcium (Ca) on a hyperkalemic cardioplegic solution for continuous cardioplegia were examined in an isolated perfused working rat heart model. The coronary arteries were perfused with a modified Krebs-Henseleit bicarbonate buffer (K-H) solution, containing various concentrations of Ca (0.1, 0.6, 1.2, and 2.5 mmol/l) and a high concentration of potassium (20 mmol/l), for 180 min, after which cardiac arrest was induced at 37 degrees C for 180 min. Cardiac function and creatine kinase (CK) were measured. In the control group, K-H solution was infused in place of the cardioplegic solution, and cardiac arrest was not induced. No significant differences were observed between the groups infused with the K-H solution containing Ca concentrations of 0.6, 1.2, and 2.5 mmol/l in the percent recovery of aortic flow (82.1 +/- 2.9%, 80.6 +/- 2.0%, and 71.5 +/- 3.7% (mean +/- SEM) respectively) or in the recovery of other indices of cardiac function, or in CK leakage. There were also no significant differences in the recovery of cardiac function and CK leakage between these groups and the control group. In the Ca 0.1 mmol/l group, however, the characteristic Ca paradox was observed. These findings suggest that if the Ca concentration in a cardioplegic solution is higher than 0.6 mmol/l during continuous cardioplegia, excellent cardioprotective effects will be achieved.

Congenital pericardial defect is a rare and little-known anomaly. Here we describe the unique clinical presentation of a 64-year-old man with partial defect of the left pericardium associated with ruptured acute type A aortic dissection manifesting massive left hemothorax. In this patient, the pericardial defect played the role of a pericardial draining window, which incidentally prevented the heart from cardiac tamponade. Emergent surgery was successfully performed with a prosthetic graft replacement.