During the period of two years from 2001 to 2003, we treated nine cases of takotsubo-type myocardiopathy. In this paper, the clinical characteristics and patients' conditions are described, and the mechanisms leading to dyskinesia of the muscular walls of the heart are discussed. All the cases were female. The mean age was 73 years. Physiological as well as psychological stress was implicated as a major cause of the disease, with onset occurring when some members of their family were suddenly taken ill or when they started quarreling with others. Echocardiograms revealed sigmoid septa in almost half of the nine patients. The prognosis was good. Only one patient had cardiac insufficiency as a sequela, but her condition improved. No one died.Eight patients got over dyskinesia of the left ventricular walls in two weeks. From our experience and studies of literature, we ruled out the possibility of the involvement of circulatory disorder and myocarditis in the onset of the disease. Women of advanced age are apt to have sigmoid septa and left ventricular walls thinning. When the old patient in this condition suffer psychosomatic stress, catecholamines will be released, causing the hypercontraction of the left ventricle, the pressure difference in the chamber, and the collapse of the apical of the heart. We concluded that these physiopathological states may be responsible for the abnormal movements of the muscular walls of the heart peculiar to the disease taken up in this study.
Heart ; Patients ; Dyskinetic syndrome ; Age, NOS ; Heart insufficiency

  During the period of two years from 2001 to 2003, we treated nine cases of takotsubo-type myocardiopathy. In this paper, the clinical characteristics and patients' conditions are described, and the mechanisms leading to dyskinesia of the muscular walls of the heart are discussed. All the cases were female. The mean age was 73 years. Physiological as well as psychological stress was implicated as a major cause of the disease, with onset occurring when some members of their family were suddenly taken ill or when they started quarreling with others. Echocardiograms revealed sigmoid septa in almost half of the nine patients. The prognosis was good. Only one patient had cardiac insufficiency as a sequela, but her condition improved. No one died.Eight patients got over dyskinesia of the left ventricular walls in two weeks. From our experience and studies of literature, we ruled out the possibility of the involvement of circulatory disorder and myocarditis in the onset of the disease. Women of advanced age are apt to have sigmoid septa and left ventricular walls thinning. When the old patient in this condition suffer psychosomatic stress, catecholamines will be released, causing the hypercontraction of the left ventricle, the pressure difference in the chamber, and the collapse of the apical of the heart. We concluded that these physiopathological states may be responsible for the abnormal movements of the muscular walls of the heart peculiar to the disease taken up in this study.

A 48-year-old man was readmitted to the hospital because of severe intraventricular conduction defects (QRS duration was 0.30 sec). The patient had been given pilsicainide hydrochloride (150 mg/day) prior to the hospitalization. The blood tests revealed that the concentration of pilsicainide was 3.30 μg/ml, which was several times higher than the average value in patients given in a dosage of 150 mg per day. Five months before the second admission, impaired left ventricular (LV) myocardial function and paroxymal atrial fibrillation were observed in the patient. His illness was diagnosed as myotonic dystrophy as the patient presented with skeletal muscle atrophy, premature frontal baldness, hatchet face, cataract, and testicular atrophy. The trial of remedication with pilsicainide in the same dosage for seven days did not produce the toxic effects as seen previously. Both load-dependent LV dysfunction in myotonic muscular dystrophy and moderately impaired renal function in the patient probably underlay the state of intoxication.

We examined the clinical features, 12-leads ECG, Holter ECG, monitor ECG, and electrophysiologic study (EPS) in nine consecutive paroxysmal atrioventricular block (PAVB) patients treated in our hospital between 1995 and 2000. In some of them, parasympathetic nerve stimulating maneuvers, drug administration and head-up tilt test (HUT) were performed as provocative tests. EPS documented that the sites of AV block were within the His-Purkinje system (H-PSB) in five patients, proximal to the His bundle potential (AHB) in three patients. In the remaining one patient, the His bundle potential was not recorded. The main features of the patients with H-PSB were as follows: 1) often wide QRS complex with or without axis deviation; 2) variable degrees of AV conduction disturbance in a short period; 3) sinus tachycardia, and normal length and constant PQ intervals in a daytime being apt to precede PAVB; 4) rather long ventricular asystoles leading to abrupt syncope; 5) easy induction of the block by intravenousadministration of atropine. In the other hand, the features of the patients with AHB included: 1) narrow QRS; 2) progressively increasing or decreasing in PQ intervals preceding PAVB; 3) ventricular asystole lasting about 3 to 10 seconds; 4) the failure to induce PAVB by any probale provocative tests.
Although we treated all the patients with permanent pacemakers, there might have been other management method for AHB patients who had about 3-second ventricular asystole.

Four patients with fulminant myocarditis (two males and two females, age 21-67 years old) were examined during 1995-2001. Fulminant myocarditis was diagnosed based on clinical features, abnormal electrocardiographic and echocardiographic findings, and increased serum enzyme levels. In three of four cases, the diagnoses were confirmed histologically in autopsy. All four patients had flu-like symptoms and fever at the start. One patient died suddenly next day. Other three patients went into cardiogenic shock five and seven days after the onset of symptoms and hospitalized, and treated with temporary pacing, steroid pulse therapy, catecholamine (in all three patients) and percutaneous cardiopulmonary support : PCPS (in one patient), but they died within ten days. Electrocardigrams showed ventricular escape rhythm, ST elevation associated with Q wave, and low voltage of the QRS complex. Markedly increased serum enzyme levels, severe metabolic acidosis and disseminated intravascular coagulation were thought to be indicative of poor prognosis. Early recognition of cardiac involvement and using of PCPS without hesitation in an acute phase could improve the outcome of fulminant myocarditis.
Myocarditis ; Clinical ; Therapeutic brand of coal tar ; symptoms <1> ; Serum

A 73-year-old man was admitted to the hospital on March 31, 2000 because of nonsustained ventricular tachycardia (VT). In 1983, he was diagnosed as having apical hypertrophic cardiomyopathy (APH). Electrocardiograms showed high amplitude of R waves and giant negative T waves (GNT), and left ventriculography (LVG) revealed spade like configuration. He stopped medication without leave six months after the diagnosis. The latest ECG showed a decrease in amplitude of R waves, no signs of GNT, ST elevation in precordial leads, and an increase in QRS duration. LVG demonstrated midventricular obstruction, apical aneurysm, and the intraventricular pressure gradient in systolic phase was 56 mm Hg. No stenotic lesion was observed in coronary arteriography. Early diastolic paradoxic flow from the apical chamber toward the outflow of the left ventricle was detected by pulsed Doppler echocardiography. VT was successfully treated with beta-blocker and amiodarone, but he needed hospital treatment again one month later because of congestive heart failure. During the follow-up of APH, the decrease in amplitude of R waves and disappeasance of GNT, ST elevation, and the increase in QRS duration in electrocardiograms, and the detection of early diastolic paradoxic flow by echocardiography could be the predictors of developing apical aneurysm and/or left ventricular dysfunction.

A19-year-old man was admitted to the hospital because of severe congestive heart failure on 7 April 2000. In the previous year his case had been diagnosed as Churg-Strauss syndrome (allergic granulomatous angiitis, AGA) with bronchial asthma and mononeuritis multiplex. Echocardiography revealed the dilatation of the left ventricle (LVDd 74 mm) and impaired left ventricular systolic function (LVEF 20%). On the 21st hospital day, the irregularity of peripheral branches of left and right coronary arteries was detected by coronary arteriography. Right ventricular endomyocardial biopsy yielded little fibrosis and no infiltration of eosinophil. Although all the laboratory tests showed lower activity of AGA, steroid pulse therapy was tried and the use of steroids was tapered at intervals of two weeks. Left ventricular function was slowly improved (LVDd 60 mm, LVEF 36%). He was discharged on foot on the 71st hospital day.