Journal of Anesthesia

A coronary artery aneurysm (CAA) is defined as dilatation of a coronary artery to a diameter >1.5 times that of the adjoining normal coronary artery. Giant CAAs with a diameter ≥50 mm are quite rare. Coronary artery fistulas are also uncommon, and affected patients require prompt diagnosis and treatment. Coronary angiography is the most common method of diagnosing coronary artery fistulas; however, transesophageal echocardiography (TEE) can also be a key intraoperative tool. In the present report, we describe the case of an 83-year-old man urgently admitted to our hospital with pericardial tamponade. Enhanced computed tomography and coronary angiography revealed a bulging left main and circumflex artery that was connected to a 50-mm diameter CAA. Emergency intraoperative TEE clearly showed a CAA with a surrounding hematoma, bulging circumflex artery, and a fistulous connection to the coronary sinus; the fistulous vessel contained a thrombus. Surgical repair was successful. This case demonstrates that CAA can rupture because of spontaneous closure of a thrombus-containing fistula and that intraoperative TEE could help to clearly identify the location of the CAA and fistulous connection.

We have developed a new detection method of blood remifentanil concentration using a gas chromatography-mass spectrometry(GC–MS) with fentanyl as the internal standard(IS). The detection was performed at m/z 168 and 245 for remifentanil and fentanyl, respectively. In addition, the retention times of remifentanil and fentanyl were 5 min 45 s and 6 min 51 s, respectively. The standard curve of relationship between remifentanil concentration and the ratio of the peak area of remifentanil to fentanyl was satisfactorily fitted as linear regression (R 2 = 0.998, p < 0.01). Intra- and inter-assay CV was 10.5 and 11.5 %, respectively. In the clinical setting, 21 adult patients undergoing elective surgery under propofol–remifentanil TIVA were enrolled. To determine blood remifentanil concentrations, arterial blood was obtained at 0–30 min after cessation of remifentanil infusion at 0.2 μg/kg/min. Blood samples were given into sample tubes(chilled on ice) containing citric acid 50 % 60 μl which inactivates all esterase, and then stored at −20 °C until assay. Measured blood remifentanil concentration was 3.59 ± 0.74 ng/ml at the end of remifentanil infusion, and the ime for a decrease in blood remifentanil concentration by half was ~2 min. Remifentanil concentration was below the detection limit 30 min after the cessation. Thus, we have confirmed that this new method is clinically applicable.

This study was conducted to elucidate the effects of KB-R9032, a newly developed Na+-H+ exchange inhibitor, on reperfusion-induced ventricular arrhythmia in the isolated perfused rat heart. Male Wistar rat hearts (n = 48; 12 for each group) were perfused with modified Krebs-Ringer’s solution equilibrated with 5% carbon dioxide in oxygen by means of the Langendorff technique. An occluder was placed around the left anterior descending coronary artery (LAD). Heart rate, coronary flow, and ECG were monitored. Drug-free perfusate was used for 10 min before switching to a perfusate containing various concentrations of KB-R9032. The added concentrations of KB-R9032 varied in the range of 0 (control) to 1 × 10−5 mol·l−1. Each heart was subjected to regional ischemia (occlusion of LAD for 11 min) and to 3 min of reperfusion (release of the ligation). In the control group, reperfusion-induced ventricular fibrillation (VF) occurred in 91.7%, and the duration was 158.2 ± 14.4 s (mean ± SEM); however, 1 × 10−7, 1 × 10−6, and 1 × 10−5 mol·l−1 KB-R9032 reduced the incidence of VF to 75.0%, 42.9%, and 6.7%, respectively (P < 0.05 at 1 × 10−5 mol·l−1 of KB-R9032) and reduced the duration of VF to 64.8 ± 22.1, 16.8 ± 10.1, and 1.2 ± 1.2 s, respectively (P < 0.05 at 1 × 10−6 and 1 × 10−5 mol·l−1 of KB-R9032). It was shown in this study that the Na+/H+ exchange inhibitor KB-R9032 suppresses reperfusion arrhythmias in the ischemia-reperfusion model of isolated rat heart.

New-onset atrial fibrillation (NOAF) is the most common perioperative complication of heart surgery, typically occurring in the perioperative period. NOAF commonly occurs in patients who are elderly, or have left atrial enlargement, or left ventricular hypertrophy. Various factors have been identified as being involved in the development of NOAF, and numerous approaches have been proposed for its prevention and treatment. Risk factors include diabetes, obesity, and metabolic syndrome. For prevention of NOAF, β-blockers and amiodarone are particularly effective and are recommended by guidelines. NOAF can be treated by rhythm/rate control, and antithrombotic therapy. Treatment is required in patients with decreased cardiac function, a heart rate exceeding 130 beats/min, or persistent NOAF lasting for ≥ 48 h. It is anticipated that anticoagulant therapies, as well as hemodynamic management, will also play a major role in the management of NOAF. When using warfarin as an anticoagulant, its dose should be adjusted based on PT-INR. PT-INR should be controlled between 2.0 and 3.0 in patients aged < 70 years and between 1.6 and 2.6 in those aged ≥ 70 years. Rate control combined with antithrombotic therapies for NOAF is expected to contribute to further advances in treatment and improvement of survival.

Using an implanted Doppler crystal, we evaluated emodynamic changes induced by subconvulsive doses of bupivacaine and lidocaine in awake and pentobarbitalanesthetized rats. Low doses of lidocaine (2.0 mg·kg−1) and bupivacaine (0.5 mg·kg−1) changed hemodynamics minimally. However, a high dose of lidocaine (8.0 mg·kg−1) reduced heart rate, cardiac output, and regional myocardial wall thickening for a short period with or without anesthesia. In contrast, a high dose of bupivacaine (2.0 mg·kg−1) increased mean arterial pressure and did not change heart rate or regional myocardial wall thickening in the awake state. Under pentobarbital anesthesia, a high dose of lidocaine reduced mean arterial pressure significantly shortly after the injection, but bupivacaine did not. Thus, it is unlikely that bupivacaine has more potent cardiotoxicity than lidocaine in subconvulsive doses.

Prostaglandin E1-induced hypotension (25% reduction from the preadministration level in mean arterial pressure) was applied to thirteen patients. Eight patients among them were operated in the supine position (group I) and other five in the prone position (group II). The maintenance dose of PGE1 was considerably lower in group II than in group I (0.067 μg·kg−1·min−1 vs. 0.119 μg·kg−1·min−1). In group I, there was a significant increase in CI, with a significant decrease in SVRI and PVRI during PGEI-induced hypotension. Such a high dose of PGE1 (0.119 μg·kg−1·min−1) was considered to have a direct dilating action on the systemic resistance bed as well as on the pulmonary vasculature. It was considered that the suppression of hypoxic pulmonary vasoconstriction could be a mechanism to increase venous admixture during PGE1-induced hypotension. In group II, there was no significant increase in CI, and no significant decrease in SVRI and PVRI. PGE1-induced hypotension can be safely applied to the anesthetized patients, but we should be careful to apply it to the patients in the prone position, because lower dose of PGE1 can induce severe hypotension, which is not accompanied by the increase in CI as occures in the patients in the supine position.