Hideaki Uchino

Spontaneous splenic rupture after mitral valve replacement for infective endocarditis

We report a successful treatment of massive bleeding due to spontaneous splenic rupture after mitral valve replacement. A 61-year-old man was admitted to our hospital for intermittent high fever. An echocardiogram demonstrated a large vegetation on the posterior cusp of the mitral valve and mitral regurgitation of moderate degree. Staphylococcus epidermidis was cultured from his arterial blood. He underwent a mitral valve replacement after 3 weeks of antimicrobiological therapy with penicillin G crystalline and minocycline hydrochloeide. The patient fell into hemorrhagic shock on postoperative day 11 after complaining dull pain on his left upper abdomen for 3 days. A computed tomography demonstrated a splenic rupture and massive hematoma in the retroperitoneum. A splenic arterial embolization was done before splenectomy. The blood and clot of 2800 g were sucked from peritoneal and retroperitoneal cavities. There were no mycotic aneurysms nor abscess but the torn capsule on the swelled and partially necrotic spleen. The patient discharged uneventfully on postoperative day 43. Infective endocarditis frequently causes splenic infarction but rarely splenic rupture. Anticoagulation therapy after mitral valve replacement might have emphasized the bleeding in the patient.

In vitro evaluation of phosphate, bicarbonate, and hepes buffered storage solutions on hypothermic injury to immature myocytes

SummaryIn this study we evaluated cardiac myocyte viability and function under hypothermic conditions using three types of buffer solutions: phosphate buffer solution (PBS), Krebs-Henseleit bicarbonate buffer solution (KHB), and Hepes buffered minimum salt solution (MSS). As a control, normal saline solution (NSS) was used. Cardiac myocytes were isolated from neonatal rat ventricles. Myocytes (12.5 × 105 myocytes/culture flask) were then incubated at 4°C for 6, 12, 18, and 24 hours in various buffer solutions. After each incubation time, CPK and LDH were measured. The myocytes were then incubated for an additional 24 hours at 37°C to evaluate the recovery of the myocyte beating rate. Group MSS had a significantly better beating rate recovery than group NSS (control) after 18 hours (MSS, 32.7%, NSS, 0.0% of control; i.e., beating rate prior to hypothermic incubation). In contrast, group KHB showed a significantly lower recovery ratio than group NSS at 12 hours (41.0%, 78.8%, respectively), and the lowest recovery was observed in group PBS beginning at 6 hours of hypothermic incubation (27.6%). Group MSS significantly suppressed the release of CPK and LDH compared to group NSS at 24 hours (MSS, 246.7 and 440.2 mIU/flask; NSS, 369.7 and 821.3 mIU/flask, respectively). In contrast, groups PBS and KHB showed significantly increased CPK and LDH levels compared to group NSS after 12 hours (PBS, 388.6 and 721.4 mIU/flask; KHB, 340.5 and 540.5 mIU/flask; NSS, 91.5 and 222.7 mIU/flask, respectively). In conclusion, Hepes buffer has cytoprotective characteristics that may be suitable for long-term hypothermic preservation of immature myocardium compared to phosphate or bicarbonate buffer.

Prevention of postischemic reperfusion injury: The improvement of myocardial tissue blood flow after ischemia by terminal Nicorandil-Mg cardioplegia

We evaluated the preventive effect of postischemic reperfusion injury by Nicorandil-Mg cardioplegia given just prior to reperfusion as “terminal cardioplegia.” Twenty seven dogs were placed on cardiopulmonary bypass and the aorta was cross-clamped for 90 min under hypothermic (17–19°C) cardioplegic arrest. The canine hearts were divided into three groups: in group A (n=10) the hearts were reperfused without any treatment; in group B (n=9) the hearts received coronary perfusion with Nicorandil-Mg solution (Nic, 8 mg/l; Mg, 20 mEq/l; glucose, 50 g/l) for 2 min just prior to reperfusion; and in group C (n=8) the hearts received coronary perfusion with Nicorandil-Mg free solution (glucose, 50g/l). During and after ischemia, the myocardial tissue PCO2 (t-PCO2) was continuously monitored by an ion-sensitive field effective transistor (ISFET) sensor. In addition, the myocardial tissue blood flow (TBF), oxygen consumption, and lactate flux were then calculated at 5, 10, 20, and 40 min of reperfusion. In the initial reperfusion period, Group B showed an improved TBF compared to group A and C (at 5 min, group B was 42.7±11.9; group A was 29.4±11.2, P<0.025; and group C was 33.9±9.2% of the preischemic control level, P<0.05). T-PCO2 in group B was significantly decreased at 5 min of reperfusion (group B, 127.5±22.5 → 42.5±9.7; group A, 117.5±23.0 → 85.2±17.4, P<0.001; group C, 122.3 mmHg → 68.2±18.7 mmHg, P<0.01), and group B had a better metabolic recovery. These results suggest that terminal Nicorandil-Mg cardioplegia might reduce the rate of postischemic reperfusion injury.

In vitro evaluation of diltiazem on hypothermic injury to immature myocytes

SummaryThe purpose of the present study was to evaluate the functional and biochemical effects of diltiazem (DTZ) on cardiac myocytes incubated under hypothermic conditions. Cardiac myocytes were isolated from neonatal rat ventricles and cultured for 4 days with MCDB 107 medium. Then, myocytes (12.5×105 myocytes/flask) were incubated at 4°C for 24 hours in media with or without DTZ at concentrations of 0 M (group C), 10−7 M (Group D1), 10−6 M (group D2), 10−5 M (group D3), or 10−4 M (group D4). After 24 hours at 4°C, CPK and LDH were measured. The myocytes were then cultured for 24 hours at 37°C to evaluate the recovery of the myocyte beating rate. In group C (n=7), the recovery ratio of the myocyte beating rate was 29.9% of control (beating rate prior to hypothermic incubation). Groups D1 and D2 (n=7 each) had approximately the same recovery ratios as group C (24.0% and 24.7%, respectively); however, groups D3 and D4 (n=7 each) showed no beating rate recovery. Release of CPK and LDH in group C was 112.3 mIU/flask and 457.4 mIU/flask, respectively. Groups D1 and D2 showed no significant differences in both enzymes compared to group C. However, the levels of CPK were significantly higher in group D4 (203.3, p<0.05), and LDH levels were significantly higher in groups D3 and D4 (669.3, p<0.05; 883.4, p<0.02). In conclusion, DTZ showed no protective effects on hypothermic injury to immature cardiac myocytes; moreover, it accelerated cellular injury at the concentrations of 10−5 and 10−4 M both functionally and biochemically. Therefore, diltiazem may not be suitable for cardiac preservation during the neonatal period.

Quadricuspid aortic valve illustrated by 64-slice multidetector computed tomography: Surgical treatment of a rare cause of severe aortic regurgitation

The quadricuspid aortic valve (QAV) is a rare congenital malformation that usually presents with aortic regurgitation (AR). The first case was reported in 1862. Most cases were diagnosed at the time of surgery or postmortem examination. With advances in imaging techniques, more cases have been diagnosed before surgery. We describe a 59-year-old man whose QAV had not been noted until the current admission. Transthoracic echocardiography revealed dilation of the left ventricle, severe AR, and suspected QAV. The QAV was confirmed by transesophageal echocardiography and 64-slice multidetector computed tomography. This case was a QAV with three equal cusps and one smaller cusp (type B in Hurwitz and Roberts classification). Because the cardiac catheterization and aortography showed severe AR and a QAV, the patient underwent elective surgery. The surgery consisted of replacing the QAV by a mechanical prosthesis. There were no post-operative complications. The patient revealed no symptoms in the post-operative 7 months.

Possible Deleterious Effects of Glucose on Immature Myocytes Under Hypothermic Conditions

The purpose of the present study was to evaluate the functional and biochemical effects of glucose-based solutions in combination with potassium or insulin (or both) on immature myocytes under hypothermic conditions. Myocytes were isolated from neonatal rat ventricles and cultured for 4 days with MCDB 107 (University of Colorado solution). Initially, myocytes (12.5 x 10(5) myocytes/flask) were incubated at 4 degrees C for 6 hours in 5% glucose solution containing various potassium concentrations ranging from 0 to 80 mEq/L to evaluate the protective effects. Next, myocytes were incubated at 4 degrees C for 3, 6, 12, 18, and 24 hours in three types of solutions: normal saline solution (control), glucose-potassium solution, and glucose-insulin-potassium solution (glucose: 50 g/L; NaHCO3, 20 mEq; potassium, 20 mEq; insulin, 20 IU/L). After each incubation, creatine kinase and lactate dehydrogenase levels were measured in the incubation solutions. The myocytes then were cultured for an additional 24 hours at 37 degrees C to evaluate the recovery of myocyte beating rate. The 20-mEq potassium treatment showed significantly better beating rate recovery and lower enzymal release than the glucose-only control. The saline solution showed the best protection of all three solutions, both functionally and biochemically, by 12 hours. The greatest damage was observed with glucose-potassium solution, beginning at 3 hours of hypothermic incubation. Although potassium and insulin have additional protective effects on hypothermic preservation, the high concentration of glucose has noxious characteristics for immature myocytes that may not be suitable for cardiac preservation in the neonatal period.