Aortitis syndrome named in Japan is widely known as Takayasu's arteritis internationally. Based on the experiences accumulated since the report of eyeground changes by Takayasu, it has become clear that the clinical manifestations of the disease are quite variable, including pulseless disease, atypical coarctation of the aorta, renovascular hypertension, aneurysms, aortic regurgitation and coronary artery disease. Pulmonary artery involvement is not infrequently present. For an exact diagnosis, it must be kept in mind that two or more of these manifestations are combined in most of the patients. The data of several epidemiological studies are presented and some of the recent literature reviewed.

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It is not clear whether there is any relationship between cardiac output and myocardial blood flow in the infarcted heart. We measured regional myocardial blood flow (RMBF) quantitatively by positron emission tomography (PET) with ¹³N-ammonia at rest in 18 patients with prior myocardial infarction. RMBF was calculated using the radioactivity in myocardial tissue measured by PET and the radioactivity of arterial blood. Cardiac output was determined by the dilution method using ¹³NH3 as an indicator, and the relation between cardiac output and RMBF was evaluated at the same time during PET study. There was a good linear correlation between cardiac index (C.I) and mean RMBF in non-infarcted myocardium (r=0.45, p<0.05), and non-infarcted size (r=0.74, p<0.01). There was an even better linear correlation between C.I. and ∑RMBF (representing the product of mean RMBF and non-infarcted size) as follows: y=0.016x+1.94, r=0.76 (p<0.001). It was indicated that the value of C.I. may be related to RMBF of non-infarcted myocardium and its size

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Serum troponin T, a myocardial contractile protein, has been reported to be a sensitive marker for the diagnosis of acute myocardial infarction. However, there have been few reports on its ability to detect coronary reperfusion and to predict left ventricular function in the chronic stage.
Twenty two patients (20 males and 2 females, 61±10 y.o.) with acute myocardial infarction were enrolled in this study. They were divided into 2 groups, one with successful reperfusion (group A: n=13) and one without reperfusion (Group B: n=9) and the serial changes of their serum troponin T levels were evaluated. Serum myosin light chain was measured in another group of patients with acute myocardial infarction without history of old myocardial infarction (group C: n=8). The slope of the logarithm of serum troponin T on a time-value curve was calculated from the time of admission to the first peak within 24 hours of the onset of acute myocardial infarction. The correlation coefficient between the late peak of serum troponin T and the left ventricular ejection fraction in 11 patients with first Q wave acute myocardial infarction was compared with that between the serum myosin light chain peak and the left ventricular ejection fraction in group C.
1) The slope of the logarithm of serum troponin T on the time-value curve in group A was greater than that in group B (0.57±0.45 vs. 0.22±0.16) (p<0.05). 2) There was a good correlation between the late peak level of serum troponin T (78±10 hours after the onset) and the left ventricular ejection fraction in 11 patients with first Q wave acute myocardial infarction (r=-0.84, p<0.01), which was similar to that of the serum myosin light chain peak and the left ventricular ejection fraction (r=-0.72, p<0.05). On the other hand, there was no correlation between the peak level of serum creatine phosphokinase and the left ventricular ejection fraction (r=-0.55, NS). The serum troponin T levels 24, 36, 48 and 60 hours after the onset also correlated well with the left ventricular ejection fraction (r=-0.65, -0.7, -0.65 and -0.89, respectively). We conclude that the serial measurement of serum troponin T in patients with acute myocardial infarction is useful in the evaluation of left ventricular function in the chronic stage and that it is a potential non-invasive predictor of coronary reperfusion.

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Accessory pathway-mediated tachyarrhythmias and AV nodal reentrant tachycardia represent a large portion of supraventricular tachycardia in younger patients. Reports comparing electrophysiologic characteristics and results of radiofrequency ablation between teenagers and adults from the same electrophysiology laboratory are rare, and these deserve further study. This study included 49 teenage patients (mean age 17±3 years, range from 10 to 20) and 1008 adult patients (mean age 50±13 years, range from 21 to 92) referred for electrophysiologic study and radiofrequency ablation for treatment of accessory pathway-mediated and AV nodal reentrant tachycardia. The results showed that: (1) mean duration of tachyarrhythmia was shorter in teenagers, but incidences of syncope, cardioversion for hemodynamic compromise and associated cardiovascular diseases were similar in both groups; (2) teenagers had a higher incidence of right-sided free wall accessory pathways (34.1% vs 14.9%, p=0.048) and better conduction properties of accessory pathways and AV nodal pathways; (3) fast-slow and multiple forms of AV nodal reentrant tachycardia were significantly less frequent (p=0.026) in teenagers, whereas atrial fibrillation with ventricular preexcitation was common in adults; (4) success rate, incidence of recurrent tachycardia, total procedure time, radiation exposure time and number of radiofrequency pulses for successful ablation did not differ significantly between teenagers and adults. In conclusion: (1) different electrophysiologic characteristics were found between teenagers and adults; and (2) radiofrequency ablation was effective and safe in teenagers with paroxysmal supraventricular tachycardia.

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We designed this study to determine whether orally administered L- and DL-carnitine can improve exercise tolerance in a group of patients with exercise intolerance. Nineteen patients with cardiac disease were randomly divided into 2 groups, an L-carnitine treatment group (n=9) and a DL-carnitine treatment group (n=10). Eight additional age-matched patients served as an untreated control group. Subjects in both carnitine treatment groups under-went cardiopulmonary exercise testing on a cycle ergometer in order to deter-mine peak exercise time, peak oxygen uptake (VO₂), lactate threshold (LT) and ventilatory threshold (VT) before and after the oral administration of 900mg/day of L- or DL-carnitine for 2 weeks. Basal values of peak exercise time, peak VO₂, LT and VT did not differ significantly among the 3 groups. Peak exercise time and peak VO₂ tended to be increased in the L-carnitine treatment group, and tended to be decreased in the DL-carnitine treatment group. Both LT and VT (ml/kg/min) were significantly improved (LT: from 9.7±0.6 to 10.8±1.0, p<0.05; VT: from 9.8±0.8 to 11.8±1.9, p<0.02) by the administration of L-carnitine, while LT was significantly decreased (from 11.0±2.0 to 9.6±1.2, p<0.05) and VT tended to be decreased by the administration of DL-carnitine (from 11.6±2.0 to 10.8±2.4). In the untreated control group, no significant changes were observed in the values of exercise tolerance between the 2 series of exercise testings. In neither group did carnitine modify hemodynamic parameters at rest or during exercise.
In conclusion, this study demonstrated that L-carnitine increases and DL-carnitine decreases exercise tolerance in patients with impaired exercise tolerance.

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The electrocardiograms in 8 patients with Cushing's syndrome and 4 with Cushing's disease were studied. The patients were divided into group A with electrocardiographic abnormalities and group B without. The mean age was significantly higher in group B than in group A. However, blood pressure, mean heart rate and the plasma adrenocorticotropic hormone level showed no significant differences between the two groups. In group A, the plasma concentration of cortisol had a tendency to be higher than in group B (A vs. B: 281±100ng/m_l, 188±9ng/m_l, respectively). Echocardiography performed on three of four patients in group A revealed cardiac hypertrophy. While, in group B, echocardiography performed on two patients showed no hypertrophic findings. As a result, it seems that the electrocardiographic changes are correlated with the plasma level of cortisol via myocardial hypertrophy.

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The roles of protein kinase C and calcium in the T cells of patients suffering from Takayasu's arteritis (TA) in response to the mitogens phorbolmyristate acetate (PMA) and streptococcal antigens have been studied. In TA there was an increased basal activity of protein kinase C (1.074±0.223nmoles/mg protein/min) as compared with that of controls (0.570±12) (p<0.001). There was 75% translocation from the cytosol to membrane fraction in response to PMA. Intracellular calcium levels showed increased basal levels in TA (177.07±12.56nmoles) compared with the controls (112.83±10.6nmoles) (p<0.001) and there was a further rise on stimulation, indicating the T cells were in an activated state. There was a positive correlation between the calcium levels and the activity of protein kinase C (r<=0.71, p<0.05). Unlike the situation in patients with rheumatic fever, T cells in TA showed no stimulation in response to streptococcal antigens. The low level of cAMP (1.12±0.169pmoles/million cells) compared with that of controls (1.4±0.03) further supports the role of PKC-calcium in the T cell activation process. These findings suggest activation of the PKC-calcium pathway in TA.

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The objectives of this study were to examine the serial vectorcardiographic changes following acute myocardial infarct and to assess the relationship between QRS loop changes and infarct size. Fifty adult male Long-Evans rats of 250-350gm body weight were used to study experimental acute myocardial infarction induced by coronary artery ligation. Vectorcardiograms (VCG) of the Frank lead system were recorded before, and 1 day and 7 days after operation. Animals were sacrificed on the 7th day for histological quantitation of infarct area ratios. We found that (1) before operation, rats have ST elevation, probably due to early repolarization. (2) After coronary artery ligation, ECG showed characteristic dome-shaped ST elevation at 1hr after ligation which returned to normal during the first day. Abnormal Q waves appeared thereafter. (3) After ligation, maximum QRS vector, ST vector and maximum T vector were reduced in magnitude the first day and recovered by the 7th day. The vectors tended to shift their direction to the right and to the posterior. QRS-T angle, however, widened as time went on. About half of the rats revealed changes in the inscription direction of the QRS loop and abnormal QRS morphology also appeared in about half of the ligated rats. (4) Those in whom abnormal QRS loop morphology and/or biting appeared had signifi-cantly larger infarct area ratios (p<0.01). (5) Change in QRS loop inscription direction seemed not to be related to the infarct size. (6) In the LS plane, the difference in max QRS vector magnitude between the 1st and 7th days significantly correlated with the infarct area ratio (r=0.533, p<0.05). In the H plane, the change in the max QRS vector magnitude at the 7th day correlated with the infarct area ratio (r=-0.531, p<0.05). In the F plane, changes in the direction of the max QRS vector were significantly correlated to the infarct area ratio both on the first (r=0.431, p<0.05) and 7th days (r=0.531, p<0.05). It is concluded that the VCG, like the ECG, had evolutional changes in AMI and that the QRS loop seen on vectorcardiography has only a slight correlation with the histological myocardial infarct size.

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Left ventricular (LV) diastolic filling and left atrial (LA) contribution have been investigated in patients with heart disease. However, many of these studies were not conducted at a constant heart rate, and the effects of heart rate remain unclear. The purpose of this study was to clarify the effects of the heart rate on left atrial contractile performance and left ventricular filling during atrial systole. The changes in LA and LV dimensions and pulmonary venous (PV) flow were determined in 9 open-chest dogs by a sonomicrometer and an electromagnetic flowmeter. With a stepwise decrease in the pacing rate from 110 beats/minute to 70 beats/minute, the LA dimension just before atrial contraction increased from 21.4±0.6mm to 23.1±0.7mm (p<0.01), and the LA systolic shortening increased from 1.6±0.1mm to 2.1±0.1mm (p<0.01). However, the calculated LV filling volume during atrial systole decreased from 1.9±0.3ml to 1.4±0.2ml (p<0.01). The PV flow during atrial systole was directed toward the LA, and the LA influx volume from PV decreased from 0.6±0.1ml to 0.2±0.04ml (p<0.01).
With a decrease in the pacing rate, the LA Frank-Starling mechanism operated. However, LV filling during atrial systole decreased because of the decrease in PV flow to the LV via the LA. Thus, LA contractile performance cannot always be evaluated from LV filling.

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The uptake and release of Ca²⁺ were studied in EGTA-skinned aortic strips from spontaneously hypertensive rats (SHR strain: SAP=191±5mmHg, n=27) and normotensive control rats (WKY strain: SAP=131±2mmHg, n=25). 45Ca uptake was measured as a function of time (0.5 to 30min.), at pCa 6.6, in the presence of 10mM of K oxalate. Skinned aortic strips of SHRs accumulated more Ca²⁺ after 30min of uptake than those of WKY rats (0.66±0.05 vs 0.52±0.03nmole.mg^-1 wet tissue; p<0.05). A lower activity of the transport system in the hypertensive group was evidenced by the fraction of these maximal uptake values accumulated after 2 minutes of uptake, 56% compared with 98% in the normotensive group. ⁴⁵Ca release was assayed in skinned aortic strips preloaded for 30 minutes with ⁴⁵Ca in the absence of K oxalate and desaturated with washing solutions containing 3nM free Ca²⁺. 30mM of caffeine, 5μM of norepinephrine or 10μM of IP₃ resulted in greater increases in the rates of Ca²⁺ efflux in WKY than in SHR aortic strips. Net effluxes of Ca²⁺ upon stimulation with all these drugs were statistically significant only in the hypertensive group due to its slightly but consistently higher Ca²⁺ content. Changes in both rate of efflux and net efflux induced by 30mM of caffeine could be blocked by 0.6mM of ryanodine.
The sarcoplasmic reticulum is characterized in the genetically hypertensive rats by a low transport activity of its Ca²⁺-ATPase, a high Ca²⁺ content and a Ca²⁺ release mechanism with low responsiveness to stimulation by caffeine, norepinephrine and IP₃

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Immunohistochemical studies have shown expression of two different isoforms of NOS in the juxtaglomerular apparatus (JGA). Antibodies to a Ca⁺⁺-calmodulin dependent isoform purified from rat brain (B-NOS) label the macula densa cells whereas antibodies to an isoform purified from rat aortic smooth muscle cells in culture (VSM-NOS) induced with lipopolysaccharide and interferon γ label the afferent arteriole. Since dietary salt intake and angiotensin II (Ang II) are determinants of renal NO generation, we have tested the hypothesis that salt intake can regulate the immunohistochemical expression of these NOS isoforms through an effect of Ang II. In 4 of 5 paired studies, the immunostaining for both B-NOS and VSM-NOS was more intense in rats that had received a low salt (LS), compared to a high salt (HS), diet. Infusion of the Ang II type 1 (AT₁) receptor antagonist, losartan, enhanced the intensity of immunoreactive staining for both isoforms. In conclusion, the immunohisto-chemical expression of NOS isoforms in the JGA is increased by dietary salt restriction; this effect cannot be ascribed to Ang II acting on type 1 receptors.

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Left atrial thrombus, which is a frequent finding in patients with mitral valve disease, is generally attached to the atrial wall. Left atrial free-floating thrombus has rarely been reported. Since the risk of peripheral emboli is fairly high, patients with such a thrombus are candidates for emergency surgery. Our first case was a 45-year-old female with mitral stenosis and regurgitation. The typically appearing free floating thrombus with a diameter of 3.4cm was detected by two-dimensional and M-mode echocardiography, and an appropriate surgical procedure was performed. The surgical findings were consistent with the echocardiographic findings. Our second case was a 59-year-old female. A free floating thrombus with a diameter of 2cm was detected by echocardiography when this patient with mitral stenosis was hospitalized because of right hemiplegia and aphasia. The thrombus was extracted by an immediate surgical procedure.
Transthoracic echocardiographic (TTE) study was definitely specific in both cases; no other study was thus required.

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