The endomyocardial biopsy (EMB) method was first developed by Japan's Dr. Souji Konno in 1962. Since then, this technique has been used worldwide in clinical cardiology for the recognition and diagnosis of cardiomyopathies, arrhythmias, and other heart conditions. Many studies relating to the EMB have been published at the global level, including a large review by Cooper, et al.,¹⁾ wherein a limited selection of Japanese papers were cited despite considerable pioneering work on the EMB having been done in Japan. Following this, the Cardiac Biopsy Conference (CABIC) organization, which was founded in Japan in 1979, conducted a nationwide survey of the English language literature on the EMB. Among the collection of 500 studies compiled, approximately 40 abstracts have been selected by the co-editors in CABIC for further discussion. This report aims to supplement Cooper's work and bring to light other prominent contributions of Japanese researchers on the EMB.

Hypertrophic cardiomyopathy patients rarely have left ventricular apical aneurysms without coronary artery disease and the pathophysiological processes responsible for apical wall thinning and aneurysm formation are not known exactly today. Here we present a rare nonobstructive hypertrophic cardiomyopathy case with an apical thrombotic aneurysm.

A 60-year-old Japanese man with obstructive hypertrophic cardiomyopathy was found to have a mutation in the cardiac myosin binding protein C gene: a single base deletion of a thymidine residue at nucleotide 11645 (codon 593) in exon 18. He was diagnosed at the age of 43 and has been followed for 17 years. During this follow-up period, echocardiograms and mechanocardiograms revealed progressive hypertrophy until the age of 54, then gradual dilation of the left ventricle associated with a decrease in the obstruction. Paroxysmal atrial fibrillation occurred at the age of 52 and progressed to chronic atrial fibrillation at the age of 53. He had congestive heart failure at the age of 58.

A 71-year-old woman had hypertrophic cardiomyopathy associated with midventricular obstruction and an apical aneurysm in the left ventricle. She had had abnormal electrocardiograms for more than 30 years and for the past year had been suffering from occasional attacks of dizziness and low systemic blood pressure. Holter 24-h electrocardiographic monitoring revealed ventricular paroxysmal contractions (676/day) with nonsustained ventricular tachycardia. Doppler echocardiography revealed paradoxical jet flow from the apical aneurysm to the left ventricular outflow during early diastole. Magnetic resonance imaging depicted midventricular hypertrophy and a dyskinetic thin apical wall, which were confirmed by angiography. Coronary angiograms showed no narrowing of the major extramural coronary arteries, but there was compression of aberrant coronary arteries apparently feeding the hypertrophic portion of the left ventricular wall. Stress thallium-201 myocardial imaging showed a persistent severe defect in the left ventricular apex. A hemodynamic study revealed low cardiac output and an intraventricular pressure gradient (approximately 90 mmHg) between the left ventricular apical high-pressure chamber and the subaortic low-pressure chamber. The present case represents a rare combination of hypertrophic cardiomyopathy, midventricular obstruction, and an apical aneurysm in an elderly woman. Myocardial ischemia may have played an important role in the genesis of the apical aneurysm.