We studied 494 patients with lung cancer who had been treated in our hospital from January 1985 through December 1994. Of the total number of cases, 20.4% were stage I; 4.5%, stage II; 12.1%, stage IIIA; 23.8%, stage IIIB; and 34.3%, stage IV. The 5-year-survival rate of patients with non-small cell lung cancer (NSCLC) was 61.0% in stage I, 43.4% in stage II, 21.2% in stage IIIA, 0% in stage IIIB and 0.9% in stage IV. The 3-year-survival rate and median survival time (MST) of patients with small cell lung cancer was 10.3% and 13.7 months in limited disease, and 0% and 4.8 months in extensive disease.
By histologic type, the 5-year-survival rate of patients with NSCLC was 19.7% in squamous cell carcinoma, 19.5% in adenocarcinoma and 5.3% in large cell carcinoma. The 5-year-survival rate of patients who were discovered by health screening was 39.4%; by subjective symptoms, 9.8%; and during the observation of other diseases, 14.7%. The 5-year-survival rate and MST of the patients with NSCLC treated in the Department of Internal Medicine of our hospital (stage III or IV) from 1985 through 1989, and from 1990 through 1994, were 1.9% and 7.4 months in the former period, and 3.7% and 9.9 months in the latter. Approximately 75% of the cases of lung cancer treated in our hospital were stage III or IV disease, and prognosis was very poor. Therefore, prevention and detection in the early stage of lung cancer are important.

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.

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.

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

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.