Successful interhospital transfer for extracorporeal cardiopulmonary resuscitation of a patient who had a cardiac arrest after cesarean section.

BACKGROUND: Studies describing the effectiveness of extracorporeal cardiopulmonary resuscitation (ECPR) for peripartum cardiopulmonary arrest are lacking. CASE PRESENTATION: A 39-year-old woman underwent elective cesarean section. Right after surgery, she fell into a cardiac arrest and was promptly transferred to our institute by ambulance. On arrival, we immediately initiated ECPR, within 63 min of the cardiac arrest. Return of spontaneous circulation was achieved 80 min after induction of extracorporeal membrane oxygenation. As the hemodynamics of the patient stabilized, extracorporeal membrane oxygenation was discontinued on day 3 of hospitalization. The patient's cerebral performance category score was 3 at discharge, which improved to 2 after 3 months. CONCLUSION: This case suggests that prompt interhospital transfer and ECPR might be effective for peripartum cardiac arrest due to nonhemorrhagic events.

Sudden Cardiac Arrest in a Patient With Sarcoidosis and Familial Hypercholesterolemia.

A 32-year-old Japanese man experienced out-of-hospital cardiac arrest. On arrival, computed tomography (CT) showed ground-glass opacity in the right lung. Emergency coronary angiography revealed triple vessel disease, then he underwent percutaneous coronary intervention. We also diagnosed him with heterozygous familial hypercholesterolemia and administered rosuvastatin and evolocumab. His clinical course was uncomplicated, and he was discharged on the 21st day of admission. Follow-up CT performed two years later revealed multiple areas of consolidation with sarcoid galaxy sign and mediastinal lymphadenopathy. We diagnosed him with pulmonary sarcoidosis by histopathological evaluation of the biopsied specimen via endobronchial ultrasound-guided transbronchial fine-needle aspiration of enlarged subcarinal lymph nodes. After we administered oral prednisolone with a gradual taper, his CT findings improved.

Transcatheter Atrial Septal Defect Closure in a 'Nonagenarian' with Intractable Heart Failure.

A 92-year-old man was referred to our hospital with decompensated heart failure. He was treated with diuretics and inotropic agents, but the clinical response was unsatisfactory. Echocardiography incidentally revealed an atrial septal defect (ASD) with a significant left-to-right shunt and pulmonary-to-systemic-blood-flow ratio of 2.36. Because the ASD was considered to be the primary cause of his treatment-resistant heart failure, the patient underwent transcatheter ASD closure. Shortly after shunt closure, his hemodynamics significantly improved, and he was discharged nine days later. This is an extremely rare case of a nonagenarian who showed an excellent clinical course after transcatheter ASD closure.

[Investigation of Computed Tomography Exposure Dose for Whole-body 18F-FDG PET/CT Examination in Chugoku-Shikoku Regions].

PURPOSE: We investigated the way of thinking about the CT dose setting, the exposure dose (CTDIvol, DLP) and the image quality (standard deviation of liver: SDliver) of whole-body PET/CT examinations in the Chugoku and Shikoku regions for the optimized CT dose setting. METHOD: It was researched in the target 29 facilities which is equipped with 18F-FDG, PET/CT scanner in that regions. We examined how to determine the dose of complete physical PET/CT setting, the CT radiation dose (CTDIvol and DLP) and the image quality of CT fusion image that is the standard deviation of liver CT value in each facility. RESULT: The optimized CT dose was lower than the diagnostic CT in many facilities. The 75th percentile CTDIvol was 6.01 mGy. The 75th percentile DLP was 560.9 mGy ×cm. The SDliver was 14.6±5.3 HU. CONCLUSION: The CT condition was low setting in comparison with diagnostic CT in many facilities. The exposure dose was lower than the diagnostic CT dose. The image quality of the normal region of liver was very close to the diagnostic CT. Even though it was low dose, images were less noise components.

The lesion characteristics assessed by LGE-MRI after the cryoballoon ablation and conventional radiofrequency ablation.

Background: Rhythm outcomes after the pulmonary vein isolation (PVI) using the cryoballoon (CB) are reported to be excellent. However, the lesions after CB ablation have not been well discussed. We sought to characterize and compare the lesion formation after CB ablation with that after radiofrequency (RF) ablation. Methods: A total of 42 consecutive patients who underwent PVI were enrolled (29 in the CB group and 13 in the RF group). The PVI lesions were assessed by late gadolinium enhancement magnetic resonance imaging 1-3 months after the PVI. The region around the PVs was divided into eight segments: roof, anterior-superior, anterior-carina, anterior-inferior, bottom, posterior-inferior, posterior-carina, and posterior-superior segment. The lesion width and lesion gap in each segment were compared between the two groups. Lesion gaps were defined as no-enhancement sites of >4 mm. Results: As compared to the RF group, the overall lesion width was significantly wider and lesion gaps significantly fewer at the anterior-superior segment of the left PV (LAS) and anterior-inferior segment of the right PV (RAI) in the CB group (lesion width: 8.2 ± 2.2 mm vs 5.6 ± 2.0 mm, P = .001; lesion gap at LAS: 7% vs 38%, P = .02; lesion gap at RAI: 7% vs 46%, P = .006). Conclusions: The PVI lesions after CB ablation were characterized by extremely wider and more continuous lesions than those after RF ablation.

A Case with Recurrent Free-Floating Ball Thrombi in Left Atrium.

BACKGROUND A free-floating ball thrombus in the left atrium is a rare clinical condition. However, the diagnosis of this condition has been facilitated by the advent and development of echocardiography and multi-detector row computed tomography (MDCT) and several cases have been reported. CASE REPORT We report a case of a 75-year-old woman who had recurrent giant spherical thrombi in the left atrium. She was diagnosed with chronic atrial fibrillation at 52 years of age. A pacemaker implantation was performed at 54 years of age because of a complete atrioventricular block; and mitral valve replacement was performed for severe mitral regurgitation at 62 years of age. She had a history of cerebral infarction and she was under treatment for chronic heart failure. Despite intensive anticoagulant therapy, she developed ball thrombi in the left atrium three times in six months. During hospitalization for acute myocardial infarction treated with percutaneous catheter intervention, transthoracic echocardiography and computed tomography (CT) revealed a free-floating giant spherical thrombus in the left atrium. She was treated with intensive anticoagulation therapy and the left atrial ball thrombus disappeared; however, two ball thrombi in the left atrium and left atrial appendage recurred after three months. Surgical removal of the thrombi and closure of the left atrial appendage were performed. Unfortunately, a ball thrombus in the left atrium recurred again after a further three months. CONCLUSIONS The present case highlights the difficulty of treating refractory thrombi in the left atrium.

Candesartan restored cardiac Hsp72 expression and tolerance against reperfusion injury in hereditary insulin-resistant rats.

AIMS: We tested the hypothesis that candesartan, an angiotensin II (AII) type 1 receptor antagonist, would restore the depressed phosphatidylinositol 3 (PI3) kinase-dependent Akt phosphorylation, an essential signal to induce heat-shock protein 72 (Hsp72) in response to hyperthermia, in Otsuka Long-Evans Tokushima fatty (OLETF) rats. METHODS AND RESULTS: At 14 weeks of age, male OLETF rats and Long-Evans Tokushima Otsuka (LETO) rats were treated with candesartan (0.25 mg/kg/day) for 2 weeks. Thereafter, hyperthermia (43°C for 20 min) was applied. We observed the following: (i) Candesartan did not improve insulin sensitivity in OLETF rats. (ii) Candesartan restored depressed PI3 kinase-dependent Akt phosphorylation and Hsp72 expression in OLETF rat hearts. (iii) Cardiac ventricular tissue contents of AII were greater in OLETF rats, which were suppressed by candesartan. (iv) Cardiac levels of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) phosphorylation were greater in OLETF rats, which were suppressed by candesartan. In cultured cardiomyocytes, application of AII induced PTEN phosphorylation, which was suppressed by candesartan. (v) In high-fat diet insulin-resistant rats, similar results were observed with respect to Hsp72 expression, Akt phosphorylation and PTEN phosphorylation. (vi) In isolated, perfused heart experiments, reperfusion-induced cardiac functional recovery was suppressed in OLETF rat hearts, which was improved by candesartan. CONCLUSION: Our results suggest that the depression of PI3 kinase-dependent Akt activation in response to hyperthermia in OLETF rats can be restored by candesartan. Substantial activation of the renin-angiotensin system, represented by increased myocardial AII content and subsequent PTEN phosphorylation, may underlie the pathogenesis which is ameliorated by candesartan.

Gender differences in the ST segment: effect of androgen-deprivation therapy and possible role of testosterone.

BACKGROUND: ST-segment elevation in a structurally normal heart is observed in Brugada- and early repolarization syndrome. The incidence of both syndromes is much higher in males than females. Clinical and basic studies suggest that testosterone plays an important role in ventricular repolarization. METHODS AND RESULTS: Standard surface 12-lead electrocardiograms recorded in 640 healthy subjects were studied (310 males, 330 females ranging in age from 5 to 89 years) (Study 1). The 3 ST levels (ST-J, -M, and -E) were measured in leads V(2) and V(5), which are representative of the right and left ventricles, respectively. The effect of androgen-deprivation therapy on the ST segment was also evaluated in 21 prostate cancer patients (Study 2). In both leads, the 3 ST levels were significantly higher in adult males than females (P<0.0001) due to a marked increase after puberty in males. As their age increased, males manifested a gradual reduction in the ST level in both leads; in females, there was a reduction in lead V(5) only. In both sexes, all 3 ST levels were significantly higher in lead V(2) than V(5) (P<0.0001). Androgen-deprivation therapy significantly decreased all 3 ST segments in both leads. CONCLUSIONS: Significant age- and gender differences in the ST segment in healthy adults were found, suggesting that testosterone modulates the early phase of ventricular repolarization.

Gender differences in the effect of auditory stimuli on ventricular repolarization in healthy subjects.

INTRODUCTION: Gender differences in the incidence of ventricular arrhythmias have been reported and torsade de pointes associated with long-QT syndrome (LQTS) is more common in women than men. Although auditory stimulation has been recognized as an important trigger of torsade de pointes in LQT2 patients, the normal response and gender differences in ventricular repolarization induced by auditory stimuli remained to be evaluated systematically. METHODS: Holter ECGs were recorded in 30 healthy volunteers (14 men aged 25 +/- 4 years and 16 women aged 23 +/- 2 years). They were awakened by an alarm clock at 5:00 am. The RR and QT (QTc) intervals and the T-wave amplitude were measured before and after alarm ringing. RESULTS: The morphology of the T-wave changed dynamically and transiently during awakening. The RR interval significantly decreased just after sounding of the alarm in both sexes (P < 0.0001). The QT interval changed little after the alarm ringing and was significantly longer in women than men (P < 0.0001). The QTc intervals were significantly prolonged just after alarm ringing in both sexes (P < 0.0001); QTc prolongation was significantly longer and more sustained in women than men (P < 0.0001). The T-wave amplitude decreased after the alarm and was significantly lower in women than men (P = 0.0001). CONCLUSION: Auditory stimulation abruptly and abnormally modulated the dynamics of ventricular repolarization in healthy subjects; the effect was more pronounced in women than men. This gender difference may partially account for the increased susceptibility of women with electrically unstable hearts to arrhythmogenesis.

Mitochondria are targets for geranylgeranylacetone-induced cardioprotection against ischemia-reperfusion in the rat heart.

It has been shown that orally administered geranylgeranylacetone (GGA), an anti-ulcer drug, induces expression of heat shock protein 72 (HSP72) and provides protection against ischemia-reperfusion in rat hearts. The underlying protective mechanisms, however, remain unknown. Mitochondria have been shown to be a selective target for heat stress-induced cardioprotection. Therefore, we hypothesized that preservation of mitochondrial function, owing to an opening of a putative channel in the inner mitochondrial membrane, the mitochondrial ATP-sensitive potassium (mitoK(ATP)) channel, could be involved in GGA- or heat stress-induced cardioprotection against ischemia-reperfusion. Rats were treated with oral GGA or vehicle. Twenty-four hours later, each heart was isolated and perfused with a Langendorff apparatus. GGA-treated hearts showed better functional recovery, and less creatine kinase was released during a 30-min reperfusion period, after 20 min of no-flow ischemia. Concomitant perfusion with 5-hydroxydecanoate (5-HD, 100 microM) or glibenclamide (10 microM) abolished the GGA-induced cardioprotective effect. GGA also showed preserved mitochondrial respiratory function, isolated at the end of the reperfusion period, which was abolished with 5-HD treatment. GGA prevented destruction of the mitochondrial structure by ischemia-reperfusion, as shown by electron microscopy. In cultured cardiomyocytes, GGA induced HSP72 expression and resulted in less damage to cells, including less apoptosis in response to hypoxia-reoxygenation. Treatment with 5-HD abolished the GGA-induced cardioprotective effects but did not affect HSP72 expression. Our results indicate that preserved mitochondrial respiratory function, owing to GGA-induced HSP72 expression, may, at least in part, have a role in cardioprotection against ischemia-reperfusion. These processes may involve opening of the mitoK(ATP) channel.

[Evaluation of autonomic function using posture change].

There are several examinations to evaluate cardiac autonomic function. Autonomic neuropathy is a common complication of diabetes mellitus and is associated with increased mortality. Baroreflex sensitivity (BRS) is a marker for the ability to augment vagal activity. Several studies have shown that BRS is impaired in diabetes with autonomic neuropathy. The head-up tilt test is the most useful tool to diagnose the neurally mediated syncope. We have developed a new non-invasive method to evaluate the baroreflex using downward tilting (DT-BRS). In our previous study conducted in healthy volunteers and diabetic patients, we demonstrated a strong correlation between systolic blood pressure increase and corresponding RR interval lengthening during downward tilting, which yielded DT-BRS values that correlated well with the BRS value obtained by the phenylephrine method (Phe-BRS). Heart rate responses observed after both squatting and standing (squatting test) are assumed to be a simple and useful tool to assess autonomic activity. We reported that indices of the squatting test showed a significant correlation with BRS assessed by Phe-BRS in diabetes. DT-BRS and the squatting test may provide promising information for the assessment of reflex vagal activity in diabetes.

Pioglitazone but not glibenclamide improves cardiac expression of heat shock protein 72 and tolerance against ischemia/reperfusion injury in the heredity insulin-resistant rat.

We tested the hypothesis that pioglitazone could restore expression of heat shock protein (HSP)72 in insulin-resistant rat heart. At 12 weeks of age, male Otsuka Long-Evans Tokushima Fatty (OLETF) rats and control (LETO) rats were treated with pioglitazone (10 mg x kg(-1) x day(-1)) or glibenclamide (5 mg x kg(-1) x day(-1)) for 4 weeks. Thereafter, hyperthermia (43 degrees C for 20 min) was applied. In response to hyperthermia, the activation of serine/threonine kinase Akt depending on phosphatidylinositol 3 (PI3) kinase was necessary for cardiac expression of HSP72. Hyperthermia-induced activation of Akt and HSP72 expression were depressed in OLETF rat hearts. Pioglitazone but not glibenclamide improved insulin sensitivity in OLETF rats, which was associated with the restoration of Akt activation and HSP72 expression. In experiments with isolated perfused heart, reperfusion-induced cardiac functional recovery was suppressed in OLETF rat hearts, which was improved by pioglitazone but not glibenclamide. Our results suggest that PI3 kinase-dependent Akt activation, an essential signal for HSP72 expression, is depressed in the heart in insulin-resistant OLETF rats, and the results suggest also that the restoration of HSP72 expression and tolerance against ischemia/reperfusion injury by treatment with pioglitazone might be due to an improvement of insulin resistance, leading to restoration of impaired PI3 kinase-dependent Akt activation in response to hyperthermia.

Influence of menstrual cycle on QT interval dynamics.

OBJECTIVES: The aim of this study was to investigate the effects of the menstrual cycle on QT interval dynamics and the autonomic tone in healthy women. METHODS: Holter ECGs were recorded in 11 healthy women aged 18-32 years during the follicular and luteal phases of their regular menstrual cycle. The interval from QRS onset to the apex (QaT) and to the end of the T-wave (QeT), the interval between the apex and the end of the T-wave (Ta-e), and RR intervals were measured automatically in the course of 24 hours by Holter ECGs. The QeT/RR, QaT/RR, and Ta-e/RR relationships were evaluated in each subject. The autonomic tone was assessed by the serum catecholamine level at rest and heart rate variability was measured by Holter ECGs. RESULTS: (1) The follicular and luteal phases did not differ significantly with respect to the slopes of the QeT/RR, QaT/RR, and Ta-e/RR relationships. However, QeT and QaT intervals were significantly shorter for all RR intervals in the luteal than in the follicular phase (P < 0.0001). (2) The serum progesterone concentration was significantly higher in the luteal than in the follicular phase (P < 0.001). (3) Noradrenaline was significantly higher in the luteal than in the follicular phase (P < 0.05). There was no significant difference in the follicular and luteal phases with respect to heart rate variability measurements. CONCLUSIONS: Our results suggest that the menstrual cycle affects the QT intervals. The observed shorter QT interval during the luteal than the follicular phase may be attributable to the increase in serum progesterone and sympathetic tone.

Effects of insulin resistance on geranylgeranylacetone-induced expression of heat shock protein 72 and cardioprotection in high-fat diet rats.

We investigated the effects of insulin resistance on the expression of heat-shock proteins (HSPs) and myocardial protection against ischemia/reperfusion injury. Male Sprague-Dawley rats received normal chow (CNT) or high-fat (HiF) diet. HiF diet for 6 weeks resulted in the development of insulin resistance, which was evaluated by oral glucose test and insulin tolerance test. Twenty-four hour after oral administration of geranylgeranylacetone (GGA) (200 mg/kg), the heart was isolated and perfused retrogradely with two different doses of insulin (0.1 or 1 mU/ml). Myocardial expression of HSP72 was examined using Western blot analysis. In the HiF group, the expression of HSP72 in response to GGA was decreased. The recovery of left ventricular developed pressure (LVDP) 30 min after reperfusion was tended to be lower in HiF group than in CNT group. Although GGA improved the recovery of LVDP in both CNT and HiF rats, LVDP during reperfusion period was significantly lower in HiF group than in CNT group. High-dose insulin perfusion caused deterioration of post-ischemic functional recovery and LVDP was not different between the two groups, but GGA-induced cardioprotection was preserved irrespective of the dose of insulin both in the CNT and HiF rats. This is the first demonstration that expression of HSP72 was depressed in the heart and that reduced HSP72 was related with less cardioprotection against ischemic insult in high-fat diet-induced insulin resistance rats.