Hirokazu Niitani

Clinical, electrophysiological, and histopathological observations in supraventricular tachycardia.

Fifty patients with supra ventricular tachycardia (SVT) underwent clinical electrophysiological studies (EPS), endomyocardial biopsies und cardiac catheterizations. EPS revealed AV nodal reentrant tachycardia (AVNRT) in seven patients, AV reentrant tachycardia utilizing concealed AV bypass tracts (AVR‐ CBT) in nine patients, AV reentrant tacycardia utilizing AV bypass tracts with ventricular preexcitation (manifest WPW) in 13 patients, sinus nodal or intra‐atrial reentrant tachycardia (SNRT or TART) in three patients, atrial flutter (AF) in nine patients, automatic atrial tachycardia (AAT) in jive patients, and multifocal atrial tachycardia (MAT) in four patients. According to the clinical observations, three patients with AVNRT (43%), six with AVH‐CBT (67%), six with manifest WPW (46%), two with SNRT or IART (67%), eight with AF (89%), two with AAT (40%), and two with MAT (50%) showed other accompanying clinical abnormalities. In all patients who were studied histologically, changes in the myocardium were seen; myocarditic changes, postmyocarditic changes and nonspecific abnormalities were present in six (12%). 15 (30%), and nine (18%) respectively. Myocardial changes were observed in four out of seven cases with AVNRT (57%), in six out of nine with AVR‐CBT (67%), in five out of 13 with manifest WPW (38%), in two out of three with SNRT or IART (67%), in six out of nine with AF (67%), in all five cases of AAT (100%), and in two out of four with MAT (50%). Nineteen out of 32 without clinical abnormalities except for arrhythmias (59%) had myocardial changes (six had myocarditic changes, ten had postmyocarditic changes, and three had nonspecific abnormalities). On the other hand, nine out of 21 with myocarditic or postmyocarditic changes were accompanied with various arrhythmias other than SVT (two had SSS, five had AV block or rBBB, and two had VT). Elevated LVEDP was present in 36% of the group with normal myocardium and in 53% of the group with myocardial changes. However, the low EF was shown in no patients with normal myocardium but in 21% of the group with myocardial changes. The low CI was also shown in only 9% of the group with normal myocardium but in 28% of the group with myocardial changes. These results suggest that patients with SVT may exhibit several histopathological changes in the myocardium, even in the absence of any clinical organic heart disease.

Acid Hydrolases in the Initiation of Ischemic Myocardial Necrosis

Alterations in myocardial acid hydrolases in acute ischemia were studied in relation to the evolution of cardiac cellular necrosis by the determination of cathepsin D, acid phosphatase (AcPase), and beta-glucuronidase activities of the myocardial fractions and by electron microscopic cytochemical studies on AcPase in the canine heart. In the normal myocardium, the same level of activity of acid hydrolases was found in sarcoplasmic reticulum (SR) as in the lysosome fraction. In electron microscopy, AcPase reaction products were observed markedly in SR and moderately in lysosomes, in residual bodies, and in Golgi apparatus. In the ischemic myocardium, at 20 to 30 min after coronary ligation, activation of these enzymes was observed in both SR and lysosomes, and at 60 to 90 min they were decreased in the particles and, in turn, increased in the cytoplasm accompanying the ischemic fine structural changes. At 2 to 3 hr those acid hydrolase activities in the cytosol were decreased, indicating the loss of enzymes from necrotic myocardial cells. Acid hydrolases are the most important factor for the evolution of ischemic myocardial necrosis by being activated not only in lysosomes but also in SR and by being released to the cytoplasm to disintegrate the cellular structures.

A case of ankylosing spondylitis complicated with mitral regurgitation

強直性脊椎炎に僧帽弁閉鎖不全症と多彩な不整脈を合併し,心筋生検で著明な心筋変性像を認めた1例を報告する.症例は58才,男性.リウマチ熱などの既往歴もない. 37才頃から腰痛出現し, 54才で強直性脊椎炎と診断. 5年前から労作時息切れと足背部の浮腫がみられ,今回心雑音と不整脈を指摘され入院.心尖部に全収縮期雑音,振戦と下腿浮腫を認め,腰背部痛と脊椎の運動制限がみられた.白血球数10400,血沈1時間値60mm, CRP 5 (+)であり,心電図上左室肥大像, I度房室ブロック,多彩な上室性および心室性の不整脈を認めた.心臓超音波検査で左室腔と左房の拡大を認めたが,弁尖の肥厚・変形等はなかつた.ヒス束心電図で房室結節の機能障害を認め,心臓カテーテル検査で肺動脈楔入圧16mmHg,左室拡張終期圧18mmHgと上昇していた.左室造影で僧帽弁逆流を認めたが,大動脈造影では異常を認めなつた.冠動脈造影では有意の狭窄性病変を認めず,心内膜心筋生検で著明な線維化と高度の心筋変性を認め,心筋炎後遺症が強く示唆された.強直性脊椎炎の心病変は大動脈弁閉鎖不全症や伝導障害が特異的であるとされている.僧帽弁閉鎖不全症のみの合併は極めてまれであり,本邦では最初の報告である.本例では左室の心筋炎が僧帽弁輪や刺激伝導系へ波及し,心病変を起こしたものと推察され,本疾患の心病変を考察する上に興味ある症例と思われた.