Effectiveness of Saireito, a Traditional Japanese Kampo Herbal Medication, on Pacemaker-Related Pleural Effusion: A Case Report.

BACKGROUND Post-cardiac injury syndrome, including pleural effusion as a delayed complication of permanent pacemaker implantation, has rarely been reported. To resolve pleural effusion, prolonged chest tube placement is often required. Anti-inflammatory agents combined with diuretics are also often prescribed. Saireito, a Japanese herbal medication, which is a combination of Goreisan and Shousaikoto, has both anti-inflammatory and water-modulation properties and has been used for edema (lymph edema, cerebral edema) and inflammation (chronic nephritis). CASE REPORT We describe a 71-year-old woman with a history of syncope and bradycardia who underwent dual permanent pacemaker implantation (placed in the right chest because of a persistent left superior vena cava) without complications. Two months later, she came to the hospital as an outpatient with a dry cough, and was diagnosed with right-sided pleural effusion. A pleural fluid analysis revealed exudative effusion, according to Light's criteria. The fluid was negative for infectious etiology. Chest X-ray, computed tomography, and echocardiography revealed no signs of pericardial effusion or perforation of the pacemaker lead to outside the heart. The pleural effusion persisted despite use of anti-inflammatory medication for several weeks and diuretics for a short period. Saireito was administered with good response; the pleural effusion resolved completely and there was no deterioration of renal function. CONCLUSIONS The present case highlights the clinical significance of Saireito as an effective therapeutic agent for late-onset pacemaker-related pleural effusion, without adverse effects such as renal dysfunction.

A Case of Takotsubo Cardiomyopathy with a Rare Transition Pattern of Left Ventricular Wall Motion Abnormality.

BACKGROUND Takotsubo cardiomyopathy is characterized by apical ballooning and excessive constriction of the base of heart. However, reverse takotsubo cardiomyopathy, wherein ballooning from the mid-ventricle to the base of the heart occurs with excessive constriction of the apex, has also been reported. We report a case of a transition from atypical wall motion abnormality to a typical takotsubo cardiomyopathy pattern. CASE REPORT A 54-year-old woman was following excessive sugar and dietary restrictions because of concerns regarding her blood sugar levels while receiving treatment for diabetes at another hospital. She presented at our hospital with general malaise and chest discomfort after several days of significantly increased workload. On admission, blood tests showed elevated cardiac enzymes. Electrocardiogram showed ST elevation of V2-V3 and poor R-wave enhancement of the anterior precordial lead. Coronary angiography showed no significant stenosis; however, left ventricular (LV) angiography showed a decrease in mid-ventricular wall motion. On the basis of these findings, she was diagnosed with a reverse takotsubo cardiomyopathy. We initiated conservative treatment for her condition. During her treatment, the LV wall motion showed a typical pattern of the apical ballooning that is characteristic of takotsubo cardiomyopathy. This LV wall motion was normalized on day 22 of the onset. CONCLUSIONS We observed a rare case of takotsubo cardiomyopathy where the pattern of LV wall motion abnormality changed over time. This case suggests that it is necessary to follow up LV abnormality over time rather than rely on single-point observations in cases with takotsubo cardiomyopathy.

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.

Transplantation of cardiotrophin-1-expressing myoblasts to the left ventricular wall alleviates the transition from compensatory hypertrophy to congestive heart failure in Dahl salt-sensitive hypertensive rats.

OBJECTIVES: We investigated whether autologous transplantation of skeletal myoblasts (MB) transferred with cardiotrophin-1 (CT-1) gene could retard the transition to heart failure (HF) in Dahl salt-sensitive (DS) hypertensive rats. BACKGROUND: Although MB is a therapeutic candidate for chronic HF, little is known about the efficiency of this strategy when applied in nonischemic HF. Cardiotrophin-1 has potent hypertrophic and survival effects on cardiac myocytes. We hypothesized that transplantation of CT-1-expressing myoblasts could provide cardioprotective effects against ventricular remodeling in DS hypertensive rats. METHODS: The DS rats were fed a high salt diet for 6 weeks and developed left ventricular (LV) hypertrophy at 11 weeks. At this stage, animals underwent MB to the myocardium with skeletal myoblasts transferred with CT-1 gene using retrovirus (transplantation of CT-1-expressing myoblasts [MB + CT], n = 31) or myoblasts alone (MB, n = 31). The sham group rats were injected with phosphate-buffered saline (n = 24). RESULTS: At 17 weeks, MB and MB + CT groups showed a significant alleviation of LV dilation and contractile dysfunction compared with the sham group. The degree of alleviation was significantly greater in the MB + CT group than the MB group (LV end-diastolic dimension: sham 7.06 +/- 0.14 mm, MB 6.51 +/- 0.16 mm, MB + CT 6.24 +/- 0.07 mm; fractional shortening: sham 32.1 +/- 1.4%, MB 38.5 +/- 1.5%, MB + CT 43.2 +/- 0.8%). Histological examination revealed that the myocyte size was 20% larger in the MB + CT group at 17 weeks than in the age-matched sham group. Upregulation of renin-angiotensin and endothelin systems during the transition to HF was attenuated by myoblast transplantation, and this effect was enhanced in the MB + CT group. CONCLUSIONS: Transplantation of skeletal myoblasts combined with CT-1-gene transfer could be a useful therapeutic strategy for HF.

Zinc finger protein Prz1 regulates Ca2+ but not Cl- homeostasis in fission yeast. Identification of distinct branches of calcineurin signaling pathway in fission yeast.

Calcineurin is an important mediator that connects the Ca(2+)-dependent signaling to various cellular responses in a wide variety of cell types and organisms. In budding yeast, activated calcineurin exerts its function mainly by regulating the Crz1p/Tcn1 transcription factor. Here, we cloned the fission yeast prz1(+) gene, which encodes a zinc finger transcription factor highly homologous to Crz1/Tcn1. Similar to the results in budding yeast, calcineurin dephosphorylated Prz1 and resulted in the trans-location of Prz1 from the cytoplasm to the nucleus. Prz1 expression was stimulated by high extracellular Ca(2+) in a calcineurin-dependent fashion. However, unlike in budding yeast, the prz1-null cells did not show any phenotype similar to those previously reported in calcineurin deletion such as aberrant cell morphology, mating defect, or hypersensitivity to Cl(-). Instead, the prz1-null cells showed hypersensitivity to Ca(2+), consistent with a dramatic decrease in transcription of Pmc1 Ca(2+) pump. Interestingly, overexpression of Prz1 did not suppress the Cl(-) hypersensitivity of calcineurin deletion, and overexpression of Pmp1 MAPK phosphatase suppressed the Cl(-) hypersensitivity of calcineurin deletion but not the Ca(2+) hypersensitivity of prz1 deletion. In addition, mutations in the its2(+)/cps1(+), its8(+), and its10(+)/cdc7(+) genes that showed synthetic lethal genetic interaction with calcineurin deletion did not exhibit synthetic lethality with the prz1 deletion. Our results suggest that calcineurin activates at least two distinct signaling branches, i.e. the Prz1-dependent transcriptional regulation and an unknown mechanism, which functions antagonistically with the Pmk1 MAPK pathway.