A linear lesion created at the right atrial isthmus by radiofrequency current application can successfully eliminate common atrial flutter (AF). The mechanism of unsuccessful cases has not yet been well delineated. This study sought to investigate the cause of unsuccessful cases of radiofrequency catheter ablation of AF. Sixty-six patients with refractory common AF were referred for radiofrequency catheter ablation. Radiofrequency current was applied to the right atrial isthmus between the inferior vena cava and tricuspid annulus or between the coronary sinus orifice and tricuspid annulus. In 5 (8%) of the 66 patients, a morphological change of the flutter wave was observed in the 12-lead ECG concomitant with the change of the atrial excitation sequence during the delivery of radiofrequency energy without the termination of atrial flutter. In 8 (12%) patients, the morphology of the new AF wave, which was provoked electrically after the termination of the original AF, was different, and the average flutter cycle length also differed in 3 cases (2%). The results of radiofrequency application could be misinterpreted as unsuccessful when the occurrence of another, different type of AF has been overlooked following the elimination of the original AF during the radiofrequency catheter ablation procedure. It is possible that the flutter circuit can take an alternative pathway despite the complete conduction block at the right atrial isthmus. (Jpn Circ J 1998; 62: 795 - 800)

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The fibrinolytic capacity of patients with acute myocardial infarction (AMI) is known to be impaired. The primary regulatory element of the fibrinolytic system is plasminogen activator inhibitor (PAI). It has been previously observed that there are 2 peaks in the plasma PAI level of AMI patients at 4 h and 16 h after thrombolytic therapy with recombinant tissue plasminogen activator (rtPA). Lanoteplase/SUN9216 is a mutant tPA with a biological half-life longer than that of rtPA. Thrombolytic therapy with mutant tPA or rtPA was carried out consecutively in 21 patients with AMI (8 patients as the mutant tPA group, and 13 patients as the rtPA group). The recanalization time of the mutant tPA group was significantly faster than that of the rtPA group (16.1±3.9 min vs 39.6 ±4.8 min, p<0.01). The PAI activity at 4 h after the initiation of thrombolysis was significantly lower in the mutant tPA group than in the rtPA group (8.74±5.46 IU/L vs 26.74±3.35 IU/L, p<0.01). There was a one mild peak in serial plasma PAI activity levels 24 h after the initiation of thrombolysis. The results suggest that thrombolytic therapy with mutant tPA reduced the impairment of fibrinolytic capacity. The mutant tPA gives faster recanalization and lower PAI activity after successful thrombolysis, compared with rtPA. (Jpn Circ J 1998; 62: 801 - 806)

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Under continuous ECG and oxygen saturation (SpO ₂) monitoring, the following measurements were taken by Doppler echocardiography in 6 consecutive patients with tetralogy of Fallot (TF) before and after intravenous administration of disopyramide (2 mg/kg): left ventricular shortening fraction (LVSF); peak velocities in the right ventricular outflow tract (RVOT); diastolic and systolic internal diameters of the right ventricular outflow tract (dRVOT, sRVOT); and systolic blood pressure. SpO₂ increased (p<0.01) from 78 to 98 (89±7, mean ± standard deviation)% to 86-99 (94±5)%. LVSF decreased (p<0.05) from 0.34-0.56 (0.42±0.08) to 0.22-0.54 (0.33±0.13). The systolic blood pressure fell slightly (p<0.05) from 68-92 (79±8) to 64-92 (71±11) mmHg. The sRVOT increased (p<0.05) from 2.1-4.8 (2.7±1.5) mm to 3.0-8.1 (4.9±2.4) mm, while RVOT peak velocity decreased (p<0.05) from 2.20-4.88 (3.70±0.97) m/sec to 2.05-4.07 (2.92±0.72) m/sec. Disopyramide alleviates hypoxia in patients of TF through its negative inotropic action on right ventricular outflow obstruction. (Jpn Circ J 1998; 62: 807 - 810)

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Patients can present with hypertrophied papillary muscles in the left ventricle, even without hypertrophy in other segments, and they have electrocardiographic (ECG) abnormalities suggestive of hypertrophic cardiomyopathy (HCM). This study was performed to evaluate whether the solitary papillary muscle hypertrophy was related to HCM. By analyzing 6731 echocardiographic studies between 1990 and 1994, the incidence of patients with papillary muscle hypertrophy was retrospectively examined, as well as the ECG features and family history related to HCM in these patients. After the normal size of the anterolateral and posteromedial papillary muscles was obtained from echocardiographic studies in 40 healthy subjects (0.7±0.2 cm for each of the vertical and horizontal axis), papillary muscle hypertrophy was defined as follows: either the vertical or horizontal diameter of at least one of the 2 papillary muscles was more than 1.1 cm (mean + 2SD in the normal subjects). Using this definition, 29 patients with papillary muscle hypertrophy were identified, of whom 14 (48%) showed high voltage QRS complexes, 10 (34%) showed T wave inversion, and 6 (21%) showed abnormal Q waves. Ten patients (34%) had a family history of HCM. In 2 patients that were followed for 18 and 11 years, respectively, the voltages of the QRS complexes and inverted T waves progressed with the hypertrophy of the papillary muscle. These findings suggest that solitary papillary muscle hypertrophy is related to HCM and that papillary muscle hypertrophy is a newly identified subtype of or an early form of HCM. (Jpn Circ J 1998; 62: 811 - 816)

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The issue of valve prosthesis-patient mismatch in small annular patients is still controversial. The hemodynamic function of bileaflet mechanical valves in the aortic position was examined using dobutamine-stress echocardiography. Forty-four patients were enrolled in the study and divided into 5 groups, according to prosthesis size, from 21 mm to 29 mm. The aortic peak pressure gradient (APG) increased significantly in all groups with dobutamine-stress and exceeded 50 mmHg in 83% of the 21-mm group, in 64% of the 23-mm group, and in 33% of the 25-mm group. The APG even exceeded 80 mmHg in 22% and 18% of the 21-mm and 23-mm groups, respectively. In these cases, the potential of `valve prosthesis-patient mismatch' was considered. From the relationship between the APG and the prosthesis valve area index (VAI), `critical VAIs' were found where patients were likely to enter the `mismatch' status; that is, 1.22 and 1.77 cm<sup>2</sup>/m<sup>2</sup>, respectively, for the 5 and 10μg/kg per min stages of dobutamine stress. This critical VAI range is useful in predicting the `mismatch' patients preoperatively. Alternative procedures or prostheses should then be selected for them. (Jpn Circ J 1998; 62: 817 -823)

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Orthostatic hypotension can be caused by an inadequate vasoconstrictor response. The effects of amezinium on vasoconstrictor response to sympathetic stimulation and to exogenous noradrenaline were investigated and compared with those of midodrine. In 8 healthy men, the following experiments were performed after a single oral dose of 10 mg of amezinium, 2 mg of midodrine or a placebo. First, finger-tip blood flow (FTBF) was recorded using a laser Doppler flowmeter before and during the contralateral hand cooling and a reduction ratio of FTBF was calculated as an index of the vasoconstrictor response. Second, dose-response curves to increasing doses (1-512 ng/min) of noradrenaline infused locally to the dorsal hand vein were determined using a linear variable differential transformer. The reduction ratio of FTBF was significantly increased (p<0.05) by amezimium [placebo, 75.9±9.8(mean ± SD)%; amezinium, 85.1±7.9%; midodrine, 78.1±9.3%]. The infusion rate of noradrenaline producing a half-maximum venoconstriction was significantly decreased (p<0.05) by amezinium (placebo, 40.6±33.9 ng/min; amezinium, 21.0±21.3 ng/min; midodrine, 33.2±31.5 ng/min). These findings indicate that amezinium increases the vasoconstrictor response to sympathetic stimulation and to noradrenaline in normal subjects, and this mechanism might contribute to the improvement by amezinium of the symptoms of orthostatic hypotension. (Jpn Circ J 1998; 62: 824 - 828)

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The effects of verapamil administration or vagal stimulation on the mechanical restitution curve (MRC) were studied in order to better understand the modulation of left ventricular (LV) function by interventions that lower the ventricular rate of atrial fibrillation. The MRC and the postextrasystolic MRC were obtained in 11 dogs using peak single beat elastance (Emax). The MRC was fitted by a monoexponential curve. Vagal stimulation or verapamil administration decreased the peak of the MRC and right-shifted the MRC. The postextrasystolic MRC was located upward compared with the control MRC, and was shifted downward by vagal stimulation or verapamil administration. If interventions having a negative inotropic effect effectively slow a rapid heart rate, the net effect of the ventricular contractile state may not always be negative. It was concluded that the MRC is useful in understanding LV contractility during irregular rhythm, especially when assessing the net effect of the negative dromotropic and inotropic action of antiarrhythmic drugs. (Jpn Circ J 1998; 62: 829 - 836)

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To assess the expression of cell adhesion molecules and the appearance of leukocytes adhering to the left atrial endothelium with atrial fibrillation (AF), 10 Japanese white rabbits were anesthetized and 3 pacing leads were placed in the right atrium. For the AF model, the right atrium was stimulated by electrical pacing (the stimulation frequency of each lead being adjusted to different intervals) for 8 h while the control model was subjected to a sham operation without atrial stimulation. The left atrial appendage was excised from the heart and examined immunohistochemically. P-selectin staining of the endothelium in both models was linear and regional, and intracellular adhesion molecule-1 (ICAM-1) in the AF model was confined to leukocytes and endothelial cells with adherent leukocytes. The expression of P-selectin (p<0.05) and the appearance of positively ICAM-1 stained adherent leukocytes (p<0.05) were significantly greater in the AF model than in the control model. In conclusion, AF could regulate the expression of at least 2 critical adhesion molecules, P-selectin and ICAM-1, and the appearance of adherent leukocytes; suggesting that these molecules may play an important role in left atrial thrombus formation with AF. Although anticoagulant therapy has generally been carried out with warfarin in AF patients, neutralizing antibodies to cell adhesion molecules should be tried to prevent thromboembolic complications. (Jpn Circ J 1998; 62: 837 - 843)

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The high frequency components contained in the QRS complex (HF-QRS) are a powerful indicator for the risk of sudden cardiac death. However, it is controversial whether conduction delay increases or decreases the HF-QRS. In 21 anesthetized, open-chest dogs, the right atrium was constantly paced. A cannula was inserted into the left anterior descending artery and flecainide, lidocaine or disopyramide was infused to slow the local conduction. Sixty unipolar electrograms were recorded from the entire ventricular surface and were signal-averaged. Data were filtered (30-250 Hz) by using fast-Fourier transform. The HF-QRS was calculated by integrating the filtered QRS signal. Activation time (AT; dV/dt minimum) was delayed and the HF-QRS was reduced in the area perfused by flecainide, lidocaine or disopyramide. The percent increase in AT closely correlated the percentage decrease in the HF-QRS; the correlation coefficients were 0.75, 0.83 and 0.76 for flecainide, lidocaine and disopyramide infusion, respectively, (p<0.001). Decrease in the HF-QRS linearly correlated with the local conduction delay. This study proved that conduction delay decreases the HF-QRS, and that the HF-QRS is a potent indicator of disturbed local conduction. (Jpn Circ J 1998; 62: 844 - 848)

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A premenopausal female patient presented with acute myocardial infarction of 3 different coronary vessels at different times within 1 year. These events were caused not by restenotic lesions after balloon angioplasty but by new lesions, which were successfully treated by primary angioplasty. Although she had a history of hypertension, type IIB hyperlipidemia, and diabetes, they had been well-controlled on medication. An elevated serum lipoprotein(a) level may have played a role in this rapid angiographic progression. (Jpn Circ J 1998; 62: 849 - 853)

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Chest pain in patients with hypertrophic cardiomyopathy seems to be caused by relative myocardial ischemia due to the left ventricular outflow pressure gradient and myocardial hypertrophy. However, in 2 cases of hypertrophic cardiomyopathy chest pain was associated with coronary vasospasm. Thus, chest pain in these cases was decreased not by a beta-blocker but by isosorbide dinitrate and a calcium antagonist. Because beta-blockers are commonly used for hypertrophic obstructive cardiomyopathy and chest pain may be aggravated by beta-blockers in patients with coronary vasospasm, a combination of beta-blocker, isosorbide dinitrate and calcium antagonist was necessary for this hypertrophic cardiomyopathy with variant angina. (Jpn Circ J 1998; 62: 854 - 857)

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Should antihypertensive therapy be based on home blood-pressure monitoring in hypertensive patients with marked white-coat phenomenon? A 53-year-old hypertensive woman with marked white-coat phenomenon had been treated on the basis of blood pressure at home without measurements of clinic blood pressure for 5 years. The target of her treatment was changed to clinic blood pressure because of marked electrocardiographic abnormalities, which were subsequently normalized by the treatment given for the office hypertension. Thus, the experience of this case suggests that treatment of cases of hypertension with white-coat phenomenon should not be based only on home recordings. (Jpn Circ J 1998; 62: 858 - 859)

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A 67-year-old man was admitted to hospital for the treatment of exertional dyspnea. He suffered from congestive heart failure due to an old inferior myocardial infarction with type B Wolff-Parkinson-White syndrome. Asynchronous wall motion caused by pre-excitation through a right-side bypass tract caused his cardiac function to deteriorate. Catheter ablation of the bypass tract increased the ejection fraction, and improved his symptoms, prior to surgical revascularization. (Jpn Circ J 1998; 62: 860 - 862)

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In patients with malignant lymphoma, the first signs and symptoms are frequently noncardiac and clinical manifestations of cardiac involvement are often nonspecific. This case report presents a patient with malignant lymphoma whose first manifestation was characteristic of heart failure, mainly due to diastolic dysfunction, and whose postmortem examination revealed massive myocardial invasion. (Jpn Circ J 1998; 62: 863 - 867)

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Pacemaker oversensing with inappropriate inhibition is commonly caused by sensing of either T-waves or polarization potentials, which are difficult to distinguish from one another. Decisive evidence, obtained from telemetered electrograms and subthreshold pacing, is presented to support sensing of the polarization potential alone and the exclusion of the T-wave as the cause of oversensing in a patient. (Jpn Circ J 1998; 62: 868 - 870)

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The cardiac function of an adult patient with fulminant myocarditis requiring a mechanical circulatory support was improved, along with the suppressed release of inflammatory mediators, after intravenous infusion with high-dose immunoglobulin. This therapy may have immunomodulatory effects and serve as a potential adjunctive therapy for patients with fulminant myocarditis. (Jpn Circ J 1998; 62: 871 - 872)

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