Mamoru Munakata

Routine extended graft replacement for an acute type a aortic dissection and the patency of the residual false channel

BACKGROUND Recent surgical progress has had an impact on the mortality of acute type A aortic dissection. Routine aortic arch replacement, irrespective of the location of the intimal tears, may improve not only the outcome of the residual dissection but the operative mortality, because complete resection of intimal tears, including those invisible through the aortotomy in the ascending aorta is achieved. METHODS During the past 7 years, total aortic arch replacement was performed in 50 consecutive patients with acute type A aortic dissection. Cerebral protection was achieved by deep hypothermia associated with pharmacologic cerebroplegia. Computed tomography and aortic angiography were performed to examine 48 patients for the possible presence of residual false channels before discharge. RESULTS The duration of circulatory arrest ranged from 30 to 84 minutes. The hospital mortality was 10%, and a cerebral complication was observed in 1 patient. No evidence of a persisting false channel was detected in 27 patients (54%) who were totally thrombosed. During the follow-up period (range: 2 months to 7 years), 2 patients died of hepatoma or pneumonia, respectively, and 2 patients underwent reoperation for recurrence of a dissection at the sinus of Valsalva. The Kaplan-Meier method estimated a 7-year survival of 82%, and a 7-year freedom from reoperation of 93%. CONCLUSIONS These results suggest that our aggressive use of routine aortic arch grafting can be accomplished with an acceptable risk and that our strategy not only improved the late results but the mortality associated with repairs for acute type A aortic dissection.

Risks and benefits of bilateral internal thoracic artery grafting in diabetic patients.

BACKGROUND There is a tendency to avoid the bilateral internal thoracic artery (ITA) grafting in diabetics. However, we no longer consider diabetes a reason for excluding the bilateral use of ITAs. We compare the early and long-term results in diabetic cases treated by coronary artery bypass grafting (CABG) using unilateral and bilateral ITA grafts. METHODS A total of 303 consecutive diabetic cases of CABG using ITA grafts between April 1991 and January 2003 were reviewed. Of these, 149 (49%) were being treated with insulin. The cases were divided into two groups: 179 cases in which bilateral ITA grafts had been used and 124 in which a unilateral ITA graft had been used. RESULTS The mortality for the bilateral ITA group and unilateral ITA group were 1.7% and 1.6%, respectively. The fact that patients were receiving insulin had no effect on the mortality of CABG. A review of morbidity revealed that no differences were found between the two groups. The survival curves, cardiac-death-free curves, and cardiac-event-free curves showed that there was no difference between the use of one or two ITA grafts in diabetics, while bilateral use of ITA grafts was significantly better than unilateral use in a comparable group of nondiabetics operated during the same time period. CONCLUSIONS There was no significant difference in operative mortality related to single or double ITA grafting in diabetics. There was also no difference between the use of one or two ITA grafts in diabetics in regard to long-term follow-up.

Post-ischemic PKC inhibition impairs myocardial calcium handling and increases contractile protein calcium sensitivity

OBJECTIVE Protein kinase C (PKC) activation impairs contractility in the normal heart but is protective during myocardial ischemia. We hypothesized that PKC remains activated post-ischemia and modulates myocardial excitation-contraction coupling during early reperfusion. METHODS Langendorff-perfused rabbit hearts where subjected to 25 min unmodified ischemia and 30 min reperfusion. Total PKC activity was measured, and the intracellular translocation pattern of PKC-alpha, -delta, -epsilon, and -eta assessed by immunohistochemistry and fractionated Western immunoblotting. The PKC-inhibitors chelerythrine and GF109203X were added during reperfusion and also given to non-ischemic hearts. Measurements included left ventricular function, intracellular calcium handling measured by Rhod-2 spectrofluorometry, myofibrillar calcium responsiveness in beating and tetanized hearts, and metabolic parameters. RESULTS Total PKC activity was increased at end-ischemia and remained elevated after 30 min of reperfusion. The translocation pattern indicated PKC-epsilon as the main active isoform during reperfusion. Post-ischemic PKC inhibition affected mainly diastolic relaxation, with lesser effect on contractility. Both PKC inhibitors increased the Ca(2+) responsiveness of the myofilaments as indicated by a leftward shift of the calcium-to-force relationship and increased maximum calcium activated tetanic pressure. Diastolic Ca(2+) removal was delayed and the post-ischemic [Ca(2+)](i) overload further exacerbated. Depressed systolic function was associated with a lower amplitude of [Ca(2+)](i) transients. CONCLUSION PKC is activated during ischemia and remains activated during early reperfusion. Inhibition of PKC activity post-ischemia impairs functional recovery, delays diastolic [Ca(2+)](i) removal, and increases Ca(2+) sensitivity of the contractile apparatus, resulting in impaired diastolic relaxation. Thus, post-ischemic PKC activity may serve to restore post-ischemic Ca(2+) homeostasis and attenuate contractile protein calcium sensitivity during the period of post-ischemic [Ca(2+)](i) overload.

Protective effects of protein kinase C during myocardial ischemia require activation of phosphatidyl-inositol specific phospholipase C

BACKGROUND Protein kinase C (PKC) activation during myocardial ischemia is thought to be cardioprotective. However, the mechanism of ischemia-induced PKC activation remains unclear. We hypothesized that ischemic PKC activation occurs through activation of phosphatidyl-inositol specific phospholipase C (PI-PLC) and protects the heart from ischemic injury. METHODS Isolated rabbit hearts were subjected to 20 minutes of normothermic ischemia and reperfusion. The PI-PLC inhibitor U73122 (0.5 micromol/L), its inactive analogue U73343 (0.5 micromol/L), or the PKC inhibitor chelerythrine (2 micromol/L) were given just before ischemia. Another group received U73122 plus the direct PKC activator phorbol 12-myristate-13-acetate (PMA, 10 pmol/L). Measurements included contractile function, intracellular calcium, PI-PLC activity, and translocation of PKC isoforms. RESULTS PI-PLC activity increased during myocardial ischemia and was inhibited by U73122. PI-PLC inhibition prevented the ischemic translocation of PKC-alpha, PKC-epsilon, and PKC-eta, and impaired cardiac recovery and cytosolic calcium regulation without significant changes in energy metabolism. PMA restored both contractile function and PKC translocation pattern in U73122-treated hearts. Direct PKC inhibition with chelerythrine mimicked the effects of U73122. CONCLUSIONS PI-PLC mediates PKC translocation during myocardial ischemia. Inhibition of PI-PLC or PKC activation, or both, during ischemia significantly impairs postischemic myocardial recovery.

Stent graft treatment for abdominal pseudoaneurysm near the celiac artery

pledget-supported suture. We did not use this method because of suspected infection and the severely damaged PA wall. The histologic findings also support our decision. However, the PA wall was extensively abnormal, and the suture line was disrupted. Resuturing incorporating the pulmonary valve annulus caused mild residual stenosis that could not be tolerated in the presence of severe right ventricular dysfunction. Pulmonary root replacement can be a method of choice in such patients. Therefore, we believe that a pulmonary allograft should also be made available whenever possible and should be implanted during the initial operation, if necessary. The last problem was the timing of the operation. Emergency intervention was required in most reported patients with aortopulmonary fistulae and in this patient also, although the history of the present illness was rather long, and his general condition was fair

Nafamostat mesilate modulates the release of platelet-activating factor during left ventricular assistance with hemofiltration in canine heart failure.

OBJECTIVE The enhanced generation of various chemical mediators is regarded as one of the mechanisms by which severe heart failure progresses to multiple organ failure. Platelet-activating factor is a phospholipid mediator which plays an important role in inflammatory reactions and circulatory shock. We studied the changes in platelet-activating factor levels in a canine heart failure model treated with a left ventricular assist device and hemofiltration, and assessed the effect of a protease inhibitor, nafamostat mesilate. METHODS Twenty dogs underwent multiple coronary ligations, and at 2 hours after the ligations they were maintained on left ventricular assist device support with continuous hemofiltration. The animals were divided into two groups: a nafamostat group (n = 10) that received nafamostat mesilate (2 mg/kg/hr), and a control group (n = 10) that received vehicle only. RESULTS The blood platelet-activating factor level, before coronary ligations, in the control and nafamostat groups was 2.3 +/- 0.4 and 2.0 +/- 0.7 ng/ml, respectively, and the coronary ligations had little effect on the platelet-activating factor. However, after the initiation of left ventricular assist device, the platelet-activating factor in the control group (5.6 +/- 2.2) was significantly higher (p < 0.05) than that in the nafamostat group (1.1 +/- 0.3). Nafamostat administration was also effective in controlling the increase in the blood lactate level. Hemofiltration did not change the platelet-activating factor. CONCLUSIONS We concluded that platelet-activating factor may play a critical role in the development of severe heart failure with left ventricular assistance, and nafamostat administration is likely to be beneficial in such a critical condition by suppressing the platelet-activating factor level.

Thrombosis of biatrial appendages due to heparin-induced thrombocytopenia.

An 81-year-old woman underwent off-pump multivessel coronary artery bypass. Paroxysmal atrial fibrillation occurred on postoperative day (POD) 1, and we started continuous administration of heparin (10,000Uday ). Her platelet count fell rapidly from 184,000/mL to 38,000/mL by POD 6. Simultaneously, fibrin/fibrinogen degradation products and D-dimer were elevated to 325.7 mg mL 1 and >40 mg mL , Asian Cardiovascular & Thoracic Annals 21(2) 245–246 The Author(s) 2012 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0218492312450700 aan.sagepub.com

Aortic valve perforation due to latent infective endocarditis

A 64-year-old man underwent aortic valve replacement for aortic regurgitation. The aortic valve was perforated in the noncoronary cusp. Pathological findings showed that the perforation probably occurred due to infective endocarditis. However, the patient had no obvious inflammatory signs preoperatively, to suggest latent infective endocarditis.

Mycotic Inferior Mesenteric Aneurysm Penetrating to Duodenum: Observation of the Formative Course

症例は64歳, 女性. 腰痛, 発熱で発症し, 腹部CT上, 腎動脈下大動脈および下腸間膜動脈起始部の周囲 の低吸収域と, 肝門部の肝膿瘍を認めた. 入院当初より感染性動脈瘤を疑っていたが, 確診は得られず, 抗 生剤の投与を開始した. 炎症所見の消退と解熱がみられたが, 第12病 日に吐血 し, ショック状態となった. 緊急CTを 施行 したところ, 腹部大動脈周囲低吸収域は拡大 し, 下腸間膜動脈根部に最大径16mmの 拡 張 ・瘤化が認められた. 感染性動脈瘤切迫破裂の診断のもと, 緊急手術を施行 した. 腹部大動脈周囲には壊 死組織 と血塊からなる6cmの 腫瘤を認め, 腫瘤は十二指腸水平脚に接 していた. 大動脈内腔には潰瘍形成 を認め, 十二指腸へ穿通 していた. 腹部大動脈を腎動脈下大動脈と大動脈末端で縫合閉鎖し, 左腋窩-大腿 動脈バイパスをおいた. 開放 した腹部大動脈と十二指腸の間には大網を充填 した. 大動脈周囲壊死組織の培 養検査では, Klebsiella pneumoniae が検出され, 抗生剤の投与を継続 した. 術後経過は良好で, 術後46 日目に退院した. 感染性動脈瘤の十二指腸穿通例は死亡率も高 く予後不良であり, 早期診断, 治療開始が最 も肝要と考えられる. 感染初期から感染性動脈瘤形成および十二指腸穿通までの経時的経過を観察 し, 緊急 手術により救命しえたので報告する. 日心外会誌33巻4号=287-290(2004)