[Two cases of primary artery dissection].

We experienced two cases of primary coronary artery dissection. (Case 1) 55-year-old man had frequent episodes of chest oppression at early morning and midnight. During chest oppression, electrocardiogram showed transient ST-segment elevation in leads II, III, and a VF. Then, he was diagnosed as having angina pectoris. This diagnosis was based on the fact that he presented coronary spastic syndrome. Right coronary angiogram demonstrated an intimal flap and false lumen at segment 3, and primary coronary dissection was confirmed. (Case 2) A 27-year-old woman complained of back pain while taking a bath. Electrocardiogram showed ST-segment elevation and abnormal Q in leads V2, V3 and V4. She was diagnosed as having acute anterior wall myocardial infarction. Presence of coronary artery dissection at segment 6 was identified by left coronary angiogram. Primary coronary artery dissection is clinically diagnosed by coronary angiogram very rarely. Only 27 such cases have been reported. It was speculated that, in case 1, vasospastic angina may be associated with primary coronary artery dissection. Case 2 had primary coronary artery dissection at segment 6 of the left anterior descending artery. Thus, her clinical picture was similar to those of previously reported cases.

[Significance of negative U-waves during anginal attacks: correlation with severity, location and prognosis of coronary stenosis].

Negative U-waves (NU) are not infrequently observed during anginal attacks. Correlations of prevalence of NU and coronary arteriographic findings were observed in 84 patients whose 12-lead electrocardiograms were obtained during anginal attacks. The left anterior descending coronary artery (LAD) was involved in 27 patients, the left circumflex artery (LCX) in 23 and the right coronary artery (RCA) in 34. NU were observed in 44 (52%) of 84 patients with angina; 17 (63%) with LAD, 13 (57%) with LCX, and 14 (41%) with RCA stenosis. The majority (91%) of patients with angina-induced NU had severe (greater than or equal to 90%) coronary stenosis. In the patient group with LAD stenosis, NU were most frequently observed in V4 (59%) greater than V5 (56%) greater than V6 (37%) greater than V3 (33%), while more frequent in V6 (52%) greater than V5 (48%) in the group with LCX stenosis, and in III (29%) greater than a VF (24%) greater than V6 (21%) in the group with RCA stenosis. Thus, the location of the stenosed vessel could be predicted electrocardiographically from the sites of the NU. Coronary revascularization was performed in 10 patients (59%) with LAD stenosis, in nine (69%) with LCX stenosis and in eight (57%) with RCA stenosis. Both anginal attacks and NU resolved after successful coronary revascularization. We concluded that NU proves a highly predictive parameter for detecting and locating significant coronary artery stenosis.

[The effect of bunazosin vs captopril on hemodynamic and neurohumoral parameters in patients with congestive heart failure].

The hemodynamic parameters (right atrial pressure, mean pulmonary artery pressure, pulmonary capillary wedge pressure, cardiac index, heart rate, blood pressure) and neurohumoral responses (alpha-ANP, plasma renin activity, aldosterone, angiotensin II) of Captopril, oral ACE inhibitor, and Bunazosin, oral alpha 1-blocker, were investigated in 28 patients with congestive heart failure at rest and after exercise. These data were analysed in both acute and chronic phases. 1) Acute effect. Captopril produced significant improvement of neurohumoral factors at rest and also after exercise. Bunazosin reduced alpha-ANP, but other neurohumoral factors did not change. Bunazosin produced significant hemodynamic improvement both at rest and after exercise. 2) Chronic effect. Captopril produced significant hemodynamic improvement both at rest and after exercise. Improvement of neurohumoral factors in acute phase was also preserved at chronic phase. On Bunazosin, improvement of hemodynamics at acute phase was also preserved at chronic phase without deterioration of neurohumoral factors.

[Severe hyponatremia associated with captopril therapy in dilated cardiomyopathy: a case report].

A 47-year-old man, with dilated cardiomyopathy developed severe hyponatremia and hypoosmolarity during captopril therapy. He also had an inappropriate elevation of antidiuretic hormone and urine osmolarity, but no evidence of dehydration, renal or suprarenal disturbances. The hyponatremia and hypoosmolarity improved after withdrawal of captopril alone, and recurred after readministration of captopril. We conclude that the hyponatremia may be caused by high secretion of prostagrandin and bradykinin associated with captopril therapy.

[Significance of decreased washout rate in hypertrophic cardiomyopathy by exercise Tl-201 myocardial scintigraphy].

UNLABELLED: A clinical significance of decreased washout rate (WR) in hypertrophic cardiomyopathy by exercise thallium-201 myocardial scintigraphy was evaluated. Thirty-six patients with hypertrophic cardiomyopathy and normal coronary angiogram were categorized into 3 groups according to initial distribution (ID) and WR: decreased ID group (17 patients, ID group), normal ID but decreased WR group (9 patients, WR group) and normal ID and normal WR group (10 patients, N group). RESULTS: (1) Cardio-thoracic-ratio and left ventricular end-diastolic pressure were higher in WR group than in other 2 groups. (2) Resting ejection fraction and left ventricular end-diastolic volume index did not differ in three groups. (3) Exercise ejection fraction was increased in N group, whereas it was not increased in ID or WR groups. It was increased in 47% of ID group, but were decreased or not changed in all patients of WR group. In conclusion, decreased WR in patients with hypertrophic cardiomyopathy may strongly suggest left ventricular myocardial damage.

[A marked Hegglin syndrome in pheochromocytoma].

A 46-year-old man was hospitalized with paroxysmal headache and chest discomfort. His blood pressure varied, occasionally being up to 300/160 mmHg. Cardiac examination revealed a decrescendo type of diastolic murmur (aortic regurgitation) and S4 gallop. Both blood and urine catecholamine levels were extremely high. Electrocardiogram and echocardiogram showed severe left ventricular hypertrophy pattern presenting hypertrophic cardiomyopathic changes. The phonocardiogram showed marked Hegglin syndrome (QT; 450 msec and QII; 310 msec). Right adrenal tumor, pheochromocytoma was found on the abdominal CT scanning and 131I-metaiodobenzylguanidine (MIBG). In the post-operative period, Hegglin syndrome was completely abolished (QT; 360 msec and QII; 345 msec,), and also electrocardiographic left ventricular hypertrophy pattern improved immediately after surgical removal of the pheochromocytoma.

[Clinical significance of electrocardiographic P-terminal force in V1 in patients with hypertrophic cardiomyopathy].

The clinical usefulness of P-terminal force in lead V1 (P-TF) was evaluated in 49 patients with hypertrophic cardiomyopathy. These 49 patients were categorized as 17 with an abnormal P-wave (P-TF greater than or equal to 3.0 msec.mV: group A) and 32 with a normal P-wave (P-TF less than 3.0 msec.mV: group B). Systolic blood pressure response (delta SBP) during the treadmill exercise test was significantly less in the group A than in the group B (delta SBP: 36 +/- 22 mmHg, 58 +/- 26 mmHg, respectively). Left atrial dimension measured from the M-mode echocardiogram was 37.8 +/- 5.0 mm in the group A and 31.0 +/- 5.2 mm in the group B. These differences were statistically significant (p less than 0.05). Left ventricular end-diastolic pressure averaged 19.5 +/- 7.9 mmHg in the group A and 13.5 +/- 4.0 mmHg in the group B (p less than 0.05). When comparing the group A and B, negative dp/dt / positive dp/dt of the group A was significantly less (0.69 +/- 0.14, 0.90 +/- 0.18, respectively) and the time constant T of the group A was significantly prolonged (86 +/- 30 msec, 56 +/- 10 msec, respectively). According to classifications of hypertrophic cardiomyopathy, all patients with the obstructive type had an abnormal P-wave. On the contrary, the majority of patients with apical hypertrophy had a normal P-wave.(ABSTRACT TRUNCATED AT 250 WORDS)

Right ventricular outflow obstruction secondary to post-infarction aneurysm: a possible new syndrome.

Two patients with extensive anterior myocardial infarction developed a hitherto unreported type of right ventricular outflow tract obstruction. A 71-year-old woman, who had had an acute infarction 10 years before, was admitted for sustained ventricular tachycardia. A loud ejection murmur was heard in the mid-precordium. The echocardiogram and left ventriculogram showed a septal aneurysm, with a systolic gradient of 21 mmHg between the right ventricular outflow tract and apex. The ejection murmur was detected in the outflow tract by intracardiac phonocardiography. The second patient was a 60-year-old man who had had an acute infarction at age 47. He was also referred because of ventricular tachycardia, and his clinical situation was almost the same as that of the first case. Our search of the literature failed to disclose any similar case with a loud ejection murmur confirmed by intracardiac phonocardiography to be due to an obstructive septal aneurysm.

[Mid-systolic ejection murmur with thrill caused by right ventricular outflow tract obstruction secondary to septal aneurysm following myocardial infarction: a case report].

A 71-year-old woman with a history of previous myocardial infarction was transferred to our hospital for evaluation of chest pain and ventricular tachycardia. On admission, a loud mid-systolic ejection murmur accompanied by a thrill was found at the left sternal border in the third intercostal space, and it was significantly accentuated in the post-extrasystolic beat. Abnormal Q waves and ST elevations were noted in leads I, aVL and V5,6 on electrocardiograms. Echocardiograms, confirmed a septal-to-apical aneurysm, and a thin interventricular septum (IVS) with paradoxical motion. Right ventricular (RV) catheterization showed a pressure gradient of 21 mmHg between the outflow tract (RVOT) and the apex, and a mid-systolic ejection murmur was recorded in the RVOT on an intracardiac phonocardiogram. Coronary arteriograms revealed total occlusion of the left anterior descending artery in its proximal portion, and a 90% stenosis of the circumflex artery. A left ventriculogram demonstrated a septal-to-apical aneurysm with a markedly reduced ejection fraction of 0.16. A right ventriculogram showed obstruction to RVOT caused by systolic ballooning of the IVS. In this patient, the mid-systolic ejection murmur was probably caused by the obstruction of the outflow tract secondary to septal aneurysm following old myocardial infarction.

[Reversed Hegglin syndrome in Takayasu arteritis].

To study the "reversed Hegglin syndrome" in Takayasu arteritis, 57 patients were selected, and divided into four groups; Group I: 12 with Takayasu arteritis with aortic regurgitation (AR), Group II: 27 with Takayasu arteritis without AR, Group III: six with annuloaortic ectasia and severe AR, and Group IV: 12 with severe AR of other miscellaneous etiologies. QII-QT intervals were compared among the four groups. The reversed Hegglin syndrome (QII-QT greater than or equal to 40 msec) was observed in 58 percent of Group I patients and 37 percent of Group II patients. This phenomenon was not seen in any patients in Group III or IV. Sixteen of the 17 patients who had the reversed Hegglin syndrome belonged to the thoracic aortic type or diffuse type of Takayasu arteritis. Most patients who did not have this syndrome either had a localized lesion or a prolonged QT interval. The reversed Hegglin syndrome, therefore, is related to widespread lesions involving the thoracic aorta due to Takayasu arteritis, and may be attributed to a delay in closure of the aortic second heart sound due to a decrease in aortic impedance of the diseased proximal aorta.