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An 82-year-old woman was admitted to the hospital due to repeated episodes of syncope with incontinence. Electrocardiography showed torsades de pointes, complete atrioventricular (AV) block, T-wave inversions and a prolonged QTc interval. Urgent coronary angiography showed no significant coronary stenosis and left ventriculography demonstrated typical abnormal wall motion of takotusbo cardiomyopathy. Electrophysiology study suggested that the damaged structure might be the bundle of His. After temporary transvenous pacing and administration of intravenous lidocaine, no recurrence of torsade de pointes was found. Symptoms of worsening heart failure were not found. Although abnormal left ventricular wall motion improved, a complete AV block remained and the patient needed pacemaker implantation on Day 18 after admission. This case demonstrated that complete AV block associated with takotsubo cardiomyopathy may persist after improvement of left ventricular wall motion, and implantation of a pacemaker may be needed.

Background: There has not been a comparison of the electrocardiographic (ECG) finding of ST-segment elevation in the precordial leads in patients with takotsubo cardiomyopathy (TC) and those with anterior acute myocardial infarction (AMI), with regard to the location of the culprit lesion., Methods and Results: The present study evaluated 18 patients with TC, and 85 with anterior AMI who were divided into 3 groups: group A had the culprit lesion proximal to both the first septal branch (S1) and the first diagonal branch (D1), group B had the culprit lesion proximal to either S1 or D1, and group C had the culprit lesion distal to both S1 and D1. In patients with TC, reciprocal ST-segment depression in the inferior leads was observed less frequently than in patients in groups A (p<0.0001) and B (p=0.0002), and abnormal Q waves and ST-segment elevation in the inferior leads were observed more frequently than in group A (p=0.0007, p=0.0057, respectively). The ECG findings in TC did not differ from those in group C., Conclusion: Electrocardiographic findings may differentiate TC from AMI with a proximal lesion of left anterior descending coronary artery, but not those with distal lesions.

Although gallium-67-citrate (67Ga) scanning and single-photon emission computed tomography (SPECT) are useful in the assessment of disease activity in cardiac sarcoidosis, a patient with cardiac sarcoidosis in whom SPECT imaging with 67Ga failed to predict the deterioration in the clinical course is presented. A 53-year-old woman diagnosed with cardiac sarcidosis had 67Ga scanning and 67Ga SPECT, both of which showed abnormal high uptake. After treatment with corticosteroid, there was an apparent improvement in the 67Ga SPECT findings, and the dose of the corticosteroid was reduced. Subsequently, the disease activity of the cardiac sarcoidosis was thought to be well controlled, because abnormal uptake was not found on repeat 67Ga SPECT. However, 4 years after initial diagnosis, thinning at the basal ventricular septal wall and complete atrioventricular block were noted. Despite repeating the evaluation with 67Ga SPECT and additional fluorine-18-fluorodeoxyglucose positron emission tomography (18FDG PET) after discovering this progression, neither of these examinations showed any abnormality. Unfortunately, in this patient, the disease activity of cardiac sarcoidosis was underestimated by the diagnostic imaging modalities.

Hemolytic anemia following mitral valve repair and annular ring placement is uncommon compared with mitral valve replacement. A 60-year-old man, who had undergone mitral valve repair with a Duran ring, developed hemolytic anemia and needed a blood transfusion. Transesophageal echocardiography revealed a paravalvular mitral regurgitation jet colliding with the Duran ring. Most cases of severe hemolysis after mitral valve repair have undergone reoperation, but in the present case study, the hemolysis after mitral valve repair reduced without the need for reoperation, although the paravalvular mitral regurgitation jet continued to collide with the Duran ring.

A 49-year-old female presented with a 1-month history of cough and low-grade fever. Echocardiography showed a large mass in the right ventricle and percutaneous right ventricular endomyocardial biopsy provided the histologic diagnosis. Despite radiotherapy and chemotherapy, the patient died. At autopsy, the metastatic deposit in the heart was larger than the primary cervical carcinoma.

A 56-year-old Japanese woman with an acute inferior myocardial infarction was admitted to hospital. Emergency coronary angiography revealed an anomalous origin of the right coronary artery from the left sinus of Valsalva, but there was no stenosis or thrombus in either the right or left coronary artery. Coronary spasm was provoked at the site of the proximal portion of the anomalous coronary artery, which was located between the aorta and pulmonary trunk. This was thought to be the cause of the myocardial infarction.

Anomalous origin of the coronary artery can lead to angina pectoris, acute myocardial infarction or even sudden death in the absence of atherosclerosis. However, in Japan, this anomaly is usually treated medically rather than surgically. To clarify the clinical features of anomalous origin of the coronary artery in Japanese and the prognosis of such patients who are treated medically, we reviewed 56 patients with anomalous origin of the coronary arteries. The mean age of these patients was 55.9 +/- 11.5 years. Anomalous origin of the right coronary artery from the left sinus of Valsalva was seen most frequently (78.6%). In contrast, we found no cases of anomalous origin of the left coronary artery from the right sinus of Valsalva traversing between the aorta and the pulmonary trunk. A history of syncope (14.3%) and aorta regurgitation (21.4%) was frequent and serious complications during exercise stress testing occurred in 5 patients. These patients were treated medically, such as by limiting exercise or by the oral administration of medicine. During the follow up period (mean 5.6 +/- 4.2 years), death directly related to anomalous origin of the coronary artery was not found despite the lack of surgical treatment. Our results suggest that the prognosis of these middle-aged-to-elderly patients without atherosclerosis is relatively good, despite the lack of surgical treatment.

A 50-year-old woman was transported to a hospital complaining of marked general malaise and epigastralgia with diarrhea and vomiting. Her electrocardiogram showed sinus arrest with a duration of nearly 8 sec. Atrial pacing with an external pacemaker improved her symptoms promptly. Following transfer to our hospital 3 days later, bradyarrhythmia was not detected despite the removal of the external pacemaker. Transient atrial fibrillation was found in our hospital, and she was diagnosed as hyperthyroidism based on findings of finger tremor, exophthalmos, diffuse goiter and an abnormally high level of thyroid hormone. On cardiac catheterization, left ventriculography showed anterior wall hypokinesis and mild mitral regurgitation. Coronary arteriography showed the absence of organic stenosis. Right ventricular endomyocardial biopsy showed myocardial hypertrophy and partial disarray, but no findings of myocarditis. Electrophysiological study showed the normal upper range of AH-time (120 msec) and HV-time (50 msec), and prolongation of corrected sinus recovery time (CSRT, 955 msec). After a euthyroid state was successively induced for about 10 days by methylmercaptoimidazole therapy, AH-time, HV-time and CSRT were shortened to 85, 35 and 290 msec respectively. Her complaints and sick sinus syndrome disappeared after the treatment of hyperthyroidism without a pacemaker.

A 60-year-old woman on chronic dialysis consulted our department for closer examination of transient atrial fibrillation and a mitral regurgitant murmur. Echocardiography revealed a left atrial abnormal dense echogenic spherical mass, the diameter of which was 2 cm. She died of cerebral bleeding 3 months later. At autopsy, the submitral mass-like structure consisted of light-gray pasty material, which was liquefaction necrosis of a mitral annular calcification. These findings were different from those of the so-called mitral annular calcification found in the elderly or in chronic renal failure patients. The existence of such calcification must be kept in mind and not be mistaken for cardiac tumor.

Ultrastructural localization and intensity of ATPase activity were studied in myocardial cells from biopsies with reference to fine-structural alterations and cardiac functions in patients with various heart diseases. ATPase activity was found to be intense in the sarcoplasmic reticulum (SR), the matrices of the mitochondria (Mt), on the myofilaments (Mf) and along the gap-junctions of intercalated discs in the control myocardial cells. ATPase activity was more intense in cardiac myocytes from well-functioning or ultrastructurally well preserved hearts. In failing and degenerating hearts, ATPase activity was decreased. ATPase activity was more intense in clinically-improving than in clinically-worsening patients. However, the localized pattern of ATPase activity was similar in each heart disease. These results suggest that cytochemical observation of ATPase activity can reflect not only fine structural changes in cardiac myocytes, but also the metabolic state in the diseased heart, and is valuable therefore from the standpoint of clinical medicine.

A case of cardiac sarcoma was reported. The tumor, which arose from the posterior wall of the left atrium, was demonstrated by echocardiography, contrast-enhanced computed tomography and direct observation during surgery. The tumor was successfully excised under emergency operation and was diagnosed as malignant fibrous histiocytoma after histologic examination. The patient had been free of symptoms for several months, but died of rapidly progressive congestive heart failure 6 months after surgery.

In the present study, we demonstrated that hypertensive left ventricular hypertrophy can be divided angiographically into symmetrical (SH) and asymmetrical septal hypertrophy (ASH) groups. In the SH group, the dynamics of the septal wall and the free wall were almost the same as those of the control group. On the other hand, the ASH group rather resembled the HCM group in the thickness and dynamics of the septal wall and the free wall as well as in the septal configuration. The most characteristic difference of the ASH and HCM groups from the SH group was in the significantly greater thickness of the septal wall at end diastole. However, in view of the developmental mechanism of hypertensive heart, it is interesting to note that the more the septal-free wall ratio increases, the more the thickness of the septal wall increases in the SH group.