The aortic arch has 3D distortions in the transverse arch in the axial view, and we previously reported that this distortion is a risk factor in the pathogenesis of arch aneurysms. In this study, we evaluated blood flow and movement of the aortic arch. In 10 healthy young volunteers, ECG-gated cine magnetic resonance imaging was carried out in the axial plane of the transverse arch, the coronal plane of the ascending arch, and the long axial plane along the entire arch. 1. Left anterolateral movements around the midpoint of the transverse arch in the systolic phase were observed in all of the men (6.3±1.59 mm) and women (4.8±0.73 mm). 2. A jet flow was detected in the systolic phase along the right side of the aortic wall. At the top of the plane, this jet flow turned to the left in a clockwise rotation in the anterior view. 3. In the long axial plane, a turbulent flow in the systolic phase was observed distal to the left subclavian arterial orifice in 6 of the 7 cases. In conclusion, this turbulent flow and left anterolateral wall motion of the transverse arch are due to anatomical three-dimensional distortion of the transverse arch. We propose that these phenomena may be important risk factors in the pathogenesis of arch aneurysms. (Jpn Circ J 1996; 60: 553 - 559)

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To determine whether myocardial changes in patients with supraventricular tachycardia (SVT) are primary or secondary to persistent tachycardia, 11 patients with SVT were studied. These patients were divided into 2 groups with respect to the type of SVT. Group I consisted of 5 patients with incessant SVT and one with multifocal atrial tachycardia, while group II consisted of 4 patients with paroxysmal supraventricular tachycardia and one with short-run supraventricular premature contraction. All of the patients underwent electrbphysiological study and endomyocardial biopsy from the right ventricle following routine cardiac catheterization. In group II, there were no significant abnormalities in the clinical and hemodynamic parameters. In group I, 3 patients had clinical features of dilated cardiomyopathy including abnormal ECG, chest X-ray and hypokinesis on left ventriculography. Induction and termination of SVT were possible in 2 patients in group I and in 4 of the 5 patients in group II. The only significant histologic difference between group I and group II was fibrosis. A high incidence of histopathological abnormalities, such as hypertrophy, degeneration, interstitial fibrosis and disarray was observed in both groups. The incidence of significant pathology was higher in group I than in group II. Almost all of the patients were given antiarrhythmic drugs. One patient underwent a successful surgical procedure and normal cardiac function returned after resection of the foci of the right atrium. Our present results suggest that patients with SVT who have incessant or recurrent SVT should undergo not only intracardiac electrophysiologic study but also endomyocardial biopsy for the evaluation of myocardial damage, since SVT might be the initial sign of cardiomyopathy. (Jpn Circ J 1996; 60: 560 - 566)

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To identify a subset of patients with a high probability of extensive calcification for further intravascular ultrasound (IVUS) examination, the frequency and extent of target lesion calcification as assessed by IVUS and its correlations with age, gender and risk factors as well as the value of angiography in identifying ultrasound calcification were analyzed in 88 patients undergoing balloon angioplasty for significant coronary atherosclerotic stenosis. The extent of calcification was semi-quantitatively graded as 0: no calcification; +: calcification arc <90°; ++: calcification arc from 90° to 180°; +++: calcification arc >180°. The distribution pattern of calcification was classified as superficial, deep or mixed. The results indicate: (1) the frequency of target lesion calcification was 38.6%, of which 52.9% showed a superficial pattern and 56.0% had a calcification arc <90°; and (2) only age was significantly associated with target lesion calcification in all of the patients. The frequency of calcification was remarkably higher in patients ≥ 60 years old than in patients ≤ 60 years old (61.9% vs 17.4%, p<0.001); (3) among patients less than 60 years old, those with calcification had a higher average number of risk factors than those without; and (4) the total sensitivity of angiography in identifying ultrasound calcification was 43.6%, with a significantly higher sensitivity for calcification arc >180° and mixed pattern. In conclusion, pre-intervention IVUS may be necessary in patients ≥60 years old and in those <60 years old with more than two risk factors in selecting devices to optimize interventional strategies. (Jpn Circ J 1996; 60: 567 - 574)

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To evaluate the accuracy of intravascular ultrasound (IVUS) for the measurement of coronary luminal area, we compared IVUS with quantitative coronary angiography (QCA). We studied 46 segments in 21 patients who underwent coronary intervention. In each lesion, coronary luminal areas were evaluated by both IVUS and QCA. To quantitate the differences between the two modalities , we calculated a difference index (intraluminal area by IVUS - intraluminal area by QCA|/intraluminal area by IVUS). We also calculated an eccentricity index (the thinnest thickness of plaque divided by the width of the opposite plaque) using IVUS. All samples were classified into 2 groups according to the lumen diameter by QCA. In Group I (lumen diameter≥3.0 mm), we found a close correlation between the intraluminal areas obtained by the two modalities (r=0.95, p<0.001). In Group II (lumen diameter<3.0 mm), we found a lower correlation between the intraluminal areas obtained by the two techniques (r=0.61, p<0.005), and the intraluminal area by IVUS was significantly larger than that from QCA (p<0.001). Furthermore, there was an inverse correlation between the eccentricity index and the difference index in Group II (r=0.83, p<0.001). These findings indicate that the differences between ultrasonic and angiographic measurements the coronary luminal area were greater in coronary arteries with a narrow lumen due to plaque eccentricity. (Jpn Circ J 1996; 60: 575 - 584)

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This study investigated vasoreactivity modulated by endothelium in pulmonary arteries from isolated monocrotaline (MCT)-induced pulmonary hypertensive rats. The responses to KC1, 5-hydroxytryptamine (5-HT), acetylcholine (ACh), and nitroglycerin (NTG) were studied in the pulmonary artery with and without endothelium for 3 weeks following MCT-treatment. The sensitivity of the con-tractile response to KCI markedly increased in the arteries with endothelium at 2 and 3 weeks after treatment, but only slightly in the arteries without endothe-lium. In addition, the sensitivity of the contractile response to 5-HT peaked 2 weeks after treatment in the arteries with endothelium, but at I week in those without endothelium. Although the removal of endothelium shifted the concentration-response curve for KCI and 5-HT to the left both in the control state and at I week, it did not shift the curves at 2 or 3 weeks. The relaxation responses to ACh and NTG, indicative of endothelium-dependent and -independent relaxation, respectively, as well as the content of tissue CGMP were reduced 2 weeks after treatment. These results suggest that the impair-ment of both the endothelium-dependent and -independent relaxation re-sponses contributes to hyperreactivity of the pulmonary artery, and may in part contribute to the development of MCT-induced pulmonary hypertension. (Jpn Circ J 1996; 60: 585 - 592)

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We studied the subcellular mechanisms of the negative force-frequency relation-ship in rat myocardium by measuring 1) intracellular Ca²⁺ transients by indo-1 fluorometry and 2) intracellular pH (pHi) and phosphate compounds with ³¹P-nuclear magnetic resonance (NMR). The data were compared with those from guinea pig hearts, which show a positive force-frequency relationship. By increasing the pacing rate from 3 Hz to 5 Hz, the peak positive first derivative of left ventricular pressure (LVdP/dt) in rat heart decreased by 10±1% (n=6). In contrast to this negative inotropic response, simultaneously measured peak Ca²⁺ transients increased by 6±1%. Guinea pig heart (n=6) showed an increase in peak positive LVdP/dt (331%) which was associated with an increase in peak Ca²⁺ transients (8±1%). Under equivalent experimental conditions in an NMR spectrometer, this increase in the pacing rate did not affect intracellular levels of phosphate compounds in either rat (n=6) or guinea pig heart (n=6). In contrast, pH_i showed a decrease of 0.031±0.006 pH units in rat heart, while no changes were observed in guinea pig heart. These results suggest that in physiological rat myocardium, pH_i is susceptible to changes in the stimulus frequency and may affect the Ca²⁺ -responsiveness of contractile proteins, which results in the negative force-frequency relationship. (Jpn Circ J 1996; 60: 593 - 603)

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The purpose of this study was to develop an experimental model of neonatal right ventricular hypertrophy which was similar to human congenital heart disease associated with pulmonary hypertension. Monocrotaline (200 mg/kg), a pyrrolizidine alkaloid, was injected into neonatal Hartley guinea pigs on the day of delivery. The occurrence of pulmonary hypertension and right ventricular hypertrophy was confirmed by pressure studies and a determination of the right ventricular wet weight and myocyte diameter on the seventh day after delivery. Right ventricular systolic pressure was significantly increased at 7 days after monocrotaline treatment compared with the untreated control group. The ratio of right ventricular systolic pressure to left ventricular systolic pressure, an indicator of pulmonary hypertension, was significantly elevated from 0.32±0.02 in the controls to 0.59±0.03 in the monocrotaline group. Right ventricular wet weight was also significantly increased, indicating right ventricular hypertrophy. The diameter of cardiac myocytes was significantly increased in the right ventricle, and was decreased in the left ventricle and interventricular septum in the monocrotaline group. Neonatal guinea pigs developed pulmonary hypertension and marked right ventricular hypertrophy within 1 week after treatment with monocrotaline. This simple experimental model may have features similar to those of human congenital heart disease associated with pulmonary hypertension. (Jpn Circ J 1996; 60: 604 - 608)

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To clarify the pathogenetic mechanism of chronic ongoing myocarditis, we produced Coxsackievirus B3-induced myocarditis in A/J mice and immunopathologically examined the microcirculation in the chronic phase of myocarditis. Forty-two 3-week-old A/J mice were inoculated intraperitoneally with Coxsackievirus B3 (Nancy strain) 2×10⁴ PFU (plaque-forming units) and sacrificed 7, 14, 21, 50, 90, or 120 days later. To evaluate myocardial microcirculation, 18 of the hearts were perfused from the thoracic aorta with warm 2% gelatin/carbon solution. The remaining hearts were quickly frozen for immunologic analysis with an enzyme immunostaining assay using monoclonal antibodies against CD4, CD8, macrophages, intercellular adhesion molecule-1 (ICAM-1) and major histocompatibility complex class I or II. The presence of viral RNA genome in the myocardium at 40, 50, or 60 days after inoculation was evaluated using the polymerase chain reaction. The lesions in chronic ongoing myocarditis consisted of myocardial damage, myocardial calcification, interstitial fibrosis, and infiltration of mononuclear cells. These infiltrated lymphocytes were predominantly CD4+ T cells. Furthermore, microvascular abnormalities, including dilatation, tortuosity, constriction, and abrupt termination, were observed around the lesions. There was marked infiltration by mononuclear cells around the microvessels. ICAM-1 was strongly expressed in the endothelial cells of the vessels. Coxsackie B3 viral genome was not detected in the myocardium of mice with chronic ongoing myocarditis in each stage examined. These results suggest that an autoimmune mechanism is involved in the persistent inflammation seen in chronic ongoing myocarditis. (Jpn Circ J 1996; 60: 609 - 617)

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An 87-year-old woman was admitted to our hospital on an emergency basis with atypical chest pain and dyspnea. She had a continuous precordial murmur. Electrocardiogram showed no evidence of myocardial ischemia, but chest X-ray showed marked enlargement of the cardiac silhouette and an abnormal calcified vascular structure. Computed tomography of the chest revealed large abnormal masses next to the heart. Two-dimensional echocardiography showed enlargement of the main trunk of the left coronary artery and 2 giant saccular aneurysms. Abnormal diastolic inflow to the main pulmonary trunk was also observed by color flow imaging. These findings were supported by data obtained using magnetic resonance imaging and transesophageal echocardiography. Based on the above findings, we diagnosed this case as a coronary artery fistula originating from the proximal left anterior descending artery associated with 2 giant saccular aneurysms draining into the pulmonary artery. To our knowledge, this is the oldest patient ever reported with such an anomaly. This case emphasizes that a good prognosis is possible even with a very pronounced visible structural abnormality. (Jpn Circ J 1996; 60: 618 - 623)

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A 42-year-old Japanese man was diagnosed as tetralogy of Fallot (TOF). Coronary arteriography demonstrated coronary artery-ventricular fistulas (left coronary artery to left ventricle, right coronary artery to right ventricle). A radical operation for TOF was performed, including a patch closure of the ventricular septal defect, right ventricular muscle resection and a patch enlargement of the right ventricular outflow tract. After the operation, coronary arteriography showed a marked decrease in the shunt flow through the coronary artery-ventricular fistulas. Six months later, the patient was diagnosed as postoperative constrictive pericarditis, while the fistulas had almost completely disappeared. After pericardiectomy, when all hemodynamic variables were normal, the fistulas did not reappear. This is the first repor of TOF complicated with multiple coronary artery-ventricular fistulas which completely disappeared after a radical operation. It is conceivable that in our case coronary artery-ventricular fistulas partially compensated for reduced arterial O₂ Saturation and disappeared after surgical correction with an improvement in hemodynamic variables. (Jpn Circ J 1996; 60: 624 - 627)

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