Transient Regional Wall Motion Abnormality and Increased Wall Thickness of the Left Ventricle in Acute Myopericarditis Occurring in the Puerperium

An unusual sequence of echocardiographic abnormalities of a 25-year-old female with acute myopericarditis was described. She presented with shortness of breath and a high body temperature after the birth of her first child. Regional asynergy and increased thickness of the left ventricle were transiently observed by echocardiography. It is considered that these abnormalities resulted from inflammatory changes in heart muscle such as edema, which was ascribable to acute myopericarditis in the puerperium

非侵襲的新指標である E' max/V 100 を用いた高血圧性肥大心の左室機能評価 : 非肥心， ST-T 変化を伴わない肥大心および ST-T 変化を伴う肥大心における比較検討

In forty-one essential hypertensive (EHT) patients with and without left ventricular hypertrophy (LVH), the left ventricular (LV) contractile performance was determined noninvasively using echocardiography. Classification was made with respect to the LVH, as measured by the sum of end-diatolic posterior wall thickness and interventricular septal thickness, and the presence of ST-T changes on electrocardiogram. Patients who had neither LVH nor ST-T changes formed Hl-subgroup (H1; n=22), those who had LVH without ST-T changes served as HZ-subgroup (H2; n =8), and those with LVH accompanied by ST-T changes constituted HS-subgroup (H3; n = 11), Sixteen normal volunteers served as normal control (N). LV systolic phase indices such as ejection fraction (EF), mean velocity of circumferential fiber shortening (mVcf) and end-systolic wall stress (ESWS), and diastolic indices such as isovolumic relaxation time (IVRT) and PR-AC interval were compared among each subgroup and normal subjects. All systolic and diastolic indices showed a depressed LV function in H3. Of these variables, the only IVRT could separate H2 from H1, suggesting deteriorated diastolic function at an early stage of hypertrophy. By altering LV systolic loading, peak systolic pressure-end-systolic volume relation, E’ max, and E' max-volume intercept at 100 mmHg peak systolic pressure ratio, E' max/V 100, were designated and these indices were used for the expression of the myocardial contractile state. E' max and E’ max/V 100 were significantly lower in H2 and H3 than in the control group, indicating depressed myocardial contractility. The value of these variables in Hl did not differ from N, indicating a normal level of inotropic state. E’ max/V 100 in H3, 0.13±0.04 mmHg/ml2, was significantly less than in H2, 0.23±0.05 (p<0.01), and the value in H2 was significantly lower than that in H1, 0.36 ±0.07 (p< 0.01), indicating a validity of E' max/V 100 to differentiate each EHT subgroup. It is concluded that in patients with LVH induced by pressure overload the LV function is declined, furthermore, LV contractile performance is more impaired when LVH is accompanied by ST-T changes. E’ max/V 100 is highly sensitive in identifying the presence of LV contractile impairment and may be a useful approach to the quantitation of LV. performance

本態性高血圧症患者および正常血圧者の Nifedipine 1回経口投与に対する交感神経ならびに内分泌応答のレニン群間比較

Behaviors of sympathetic and renin-angiotensin-aldosterone systems to an acute sublingual administration of nifedipine (10 mg) were studied in essential hypertensive (EHT) and normotensive (NT) groups. Basal values of plasma norepinephrine (NE) and plasma renin activity (PRA) were not consistent with mean blood pressure (BP), indicating no important role of NE and PRA values for determining BP level. Nifedipine reduced BP, and increased NE and PRA in both groups. Simultaneously, nifedipine produced a significant decrease of plasma aldosterone concentration (PAC) and plasma cortisol. High-renin EHT subgroup showed greater responses of BP, NE and PRA than normal- or low-renin subgroup but not in NT group. In high-, normal- and low-renin subgroups of both groups, the correlations between mean BP and △mean BP (r= -0.85, p<0.001; r= -0.89, p<0.001 and r= -0.77, p<0.001, respectively), △mean BP and △NE (r= -0.76, p<0.01; r= -0.71, p<0.05 and r= -0.57, NS, respectively) and △mean BP and △PRA (r= -0.87, p<0.001; r=0.59, NS and r= -0.05, NS, respectively) were observed. A significant relationship between basal PRA and △PRA was demonstrated in EHT group (r=0.77, p<0.001) but not in NT group (r=0.37, NS). These data indicate the presence of high vascular tone in high-renin EHT subgroup which is probably produced by an increased vascular responsiveness to sympathetic and/or to angiotensin II or by some other factors. It is suspected that juxtaglomerular cell response to vasodilator may be altered in patients with low-renin essential hypertension. The present study also suggests that nifedipine blocked aldosterone and cortisol secretion through Ca++ influx inhibition into the adrenal cortex

カテコールアミン心筋症を合併した褐色細胞腫の1症例

A 40-year-old female with the left adrenal pheochoromocytoma showed ECG abnormalities and the clinical features similar to acute myocardial infarction. Enzymological studies and UCG findings in the acute phase revealed the same pattern as those in acute myocardial infarction. After finding the existence of the left adrenal pheochromocytoma, the differential diagnosis between myocardial infarction and catecholamine cardiomyopathy as the cause of ECG, UCG and enzymological changes was tried to make. However, the differential diagnosis was not established during the preoperative period. The continued ECG abnormilities until the surgical removal of the tumor disappeared one week after the operation. Norepinephrine infusion test performed one and two weeks and 21 months after the operation could evoke the T wave change which disappeared soonly after norepinephrine infusion was stopped. Coronary angiography and 201Tl myocardial scintigraphy revealed the normal findings. These findings suggested that catecholamines released from pheochromocytoma was the cause of the myocardial damages and ECG abnormalities. The patient with catecholamine cardiomyopathy due to the adrenal pheochromocytoma whose ECG abnormalities continued until surgical treatment was reported

Waardenburg Syndrome with Isolated Deficiency of Myenteric Ganglion Cells at the Sigmoid Colon and Rectum

Waardenburg syndrome (WS) has the characteristic clinical features caused by the embryologic abnormality of neural crest cells. WS patients sometimes suffer from functional intestinal obstruction. When it is Hirschsprung disease (HD), the WS is diagnosed as type 4 WS. We report a case of WS which did not have myenteric ganglion cells in the sigmoid colon and rectum. Whether to diagnosis this case as type 1 or 4 WS is controversial. Moreover, this is the third report which has peristalsis failure caused by abnormal myenteric plexus. In all three cases, the eosinophils had aggregated in the myenteric layer of the transition zone. During embryonic life, enteric ganglion cells migrate to the myenteric layer from the proximal to the distal side sequentially and, subsequently, to the submucosal layer through the circular muscle. Therefore, we hypothesize that myenteric ganglion cells that had already migrated were eliminated by an eosinophil-mediated mechanism in these three cases. We believe this report may be helpful to elucidate the pathogenesis of some types of HD

WPW Syndrome Complicated by Another Cardiac Disorder

During the past 28 months, 16 cases of WPW syndrome were operated on at Hiroshima University Hospital. Two cases were complicated by other cardiac disorders which accelerated tachycardia, making diagnosis difficult. One of these cases showed serious mitral regurgitation, due to infective endocarditis and the patient suffered cardiac failure accompanied by paroxysmal tachycardia not responsive to medical therapy or cardioversion. A complex rhythm with atrial fibrillation and antegrade conduction rhythm through the accessory pathway made diagnosis and therapy quite difficult. The condition of the other patient was associated with myocardial bridging which caused angina pectoris during paroxysmal tachycardia. Myocardial scintigraphy showed myocardial ischemia in the antero-lateral area of the left ventricle. In the former case, mitral valve replacement and interruption of the accessory pathway were undergone simultaneously. In the latter case, myotomy of the muscle on segment 7 was conducted, following interruption of the accessory pathway