Rapid pacing from the high right atrium was performed in 7 patients with atrial flutter in whom potentials with multicomponent high-frequency deflections were recorded at the high right atrium to examine the origin of these potentials during transient entrainment in atrial flutter. In all of the patients with relatively slow rapid pacing, the potentials were captured orthodromically through the atrial flutter reentry circuit with a long conduction time. With more rapid pacing, the potentials were split into 2 associated components: P1 and P2. P1 was captured antidromically with a short conduction time whereas P2 was captured persistently in an orthodromic direction through the reentry circuit with a progressively long conduction time. In 3 of the 7 patients, atrial flutter was converted into another atrial flutter by rapid pacing. During this other atrial flutter, the potentials at the high right atrium were split from the beginning to form double potentials: D1 and D2. During rapid pacing, D1 and D2 were fused, and D1 was captured antidromically whereas D2 was captured orthodromically through the reentry circuit. In sinus rhythm, the potentials at the high right atrium formed fractionated potentials. These findings suggest that 1) fractionated potentials may represent 2 atrial regions with different conductivity properties, 2) fractionated potentials may be able to change into double potentials, and 3) double potentials may be attributable to their conductivity properties rather than refractoriness.

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Four pediatric cases of congenital coronary artery fistula were surgically treated and followed for 8 years. In the 3 cases of right coronary artery to right ventricle fistula, regression of coronary artery dilatation was observed postoperatively. In the 1 case of circumflex artery to right atrium fistula, aneurysmal dilatation of the abnormal vessel persisted for 8 years. A reduction in vessel size is expected if the fistula-related coronary artery has a normal course and normal branchings. When the aneurysmal vessel takes an abnormal course without branches, it should be removed surgically along with fistula closure.

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We investigated the vasodilative effects of various doses of intracoronary diltiazem on coronary resistance vessels. Nine patients with normal angiograms were studied. A coronary Doppler guide wire was inserted into the left anterior descending coronary artery. Diltiazem, in doses of 0.1 mg, 0.5 mg, 1.0 mg, 2.0 mg and 4.0 mg, was injected into the left coronary artery at 10 min intervals and coronary blood flow velocity was measured. The coronary artery was pretreated with intracoronary nitroglycerin to avoid changes in the cross-sectional area. As a measure of the change in coronary vascular resistance, a coronary vascular resistance index (CVRI) was calculated as mean aortic pressure/coronary blood flow velocity. An injection of diltiazem into the left coronary artery caused a significant dose-dependent decrease in CVRI. A dose of 2.0 mg was the lowest dose on the plateau of the dose-response curve. In conclusion, the injection of diltiazem into the left coronary artery causes a dose-dependent dilatation of coronary resistance vessels, and the maximal effect can be produced with a dose of 2.0 mg.

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In 9 patients with the common type of atrial flutter (AF), a zone of slow conduction was observed proximal to the coronary sinus orifice. Class IA antiarrhythmic drugs were administrated intravenously in all 9 patients. AF was converted to sinus rhythm in only 1 patient. In the remaining 8 patients, although IA drugs suppressed conduction velocity, this effect was not preferential with regard to the zone of slow conduction. Conversion of AF to sinus rhythm by rapid pacing was achieved in these 8 patients. At a critical pacing cycle length, AF was interrupted just after conduction block developed in the zone of slow conduction. A progressive decrease in conduction velocity was observed in the zone of slow conduction for several beats just before the onset of conduction block. In conclusion, class IA drugs facilitate the interruption of AF by rapid atrial pacing by inducing conduction block in the zone of slow conduction.

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To clarify the relationship between the dilatation of angiographically non-steno-tic coronary artery segments in response to isosorbide dinitrate (ISDN), and serum lipids, 5 coronary segments in 7 patients with familial hypercholesterolemia (FH) and 43 patients with non-familial hypercholesterolemia (non-FH), who had either 1-or 2-vessel coronary heart disease, were investigated. The serum total cholesterol level was significantly greater in FH than in non-FH. Before and after the direct intracoronary injection of ISDN, coronary diameter was measured by a computer-assisted coronary angiography analysis system. The order of the dilative responses in coronary segments in non-FH patients (segments: #5> #11> #6> #13> #7) was exactly the same as the order of their original diameters, while the ratio of the increase in diameter (after/before ISDN injection) did not differ among any of the segments (mean: 1.08-fold increase). In the non-FH group, no correlation was found between the serum total cholesterol, triglyceride, low-density lipoprotein-cholesterol, or high-densi-ty lipoprotein-cholesterol, and the ratio of the coronary diameter after and before injection of ISDN. Moreover, hypercholesterolemia in non-FH did not affect the coronary dilative response to ISDN injection. In the FH group, although the original diameter of each segment did not differ from that in the non-FH group, the ratio of the diameter after and before injection of ISDN was significantly smaller in FH than in non-FH (p<0.01). These results suggest that a non-stenotic coronary artery in FH has a lower capacity for vasodilation in response to ISDN. Although hypercholesterolemia was excluded as a factor which may suppress the capacity for coronary dilation in non-FH, spontaneous hypercholesterolemia in FH may affect medial smooth muscle functions of the coronary artery.

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Myocardial injury after heart storage has been known to contribute to an increase in myocardial calcium content or oxygen free radical production. The present experiment was designed to determine the inhibitory effect of steroid in the preservation solution on myocardial injury during simple immersion of isolated rat hearts. The experimental group was divided into 5 sub-groups according to the concentration of steroid added to the solution. Group I was stored in preservation solution containing no steroid. Groups II to V were stored in preservation solutions containing methylprednisolone in concentrations of 50 mg/L, 100 mg/L, 150 mg/L, and 200 mg/L, respectively. After the rat hearts were isolated, crystalloid cardioplegic solution at 4 °C was used for cardiac arrest, and the hearts were immersed in 4°C Euro-Collins solution for 8 h. Hearts were then maintained under ischemic conditions at 25°C for 15 min. After 60 min of reperfusion at 37°C, cardiac function was measured and biochemical analyses of coronary effluent and myocardium were performed. The cardiac outputs in groups IV and V were significantly higher than those in groups I and 11 (p< 0.01). Creatine kinase-MB in coronary effluent in groups IV and V were significantly lower than those in groups I and II at 15, 30 and 60 min after reperfusion (p<0.05). The level of arachidonic acid at 1 and 5 min, and the level of malon-dialdehyde at 5 min, after reperfusion in groups III, IV and V were significantly lower than those in groups I and II. Myocardial adenosine triphosphate was most preserved in group IV, and myocardial arachidonic acid, malondialdehyde, and calcium levels and water content in groups IV and V were lower than those in groups I and II. Ultrastructural observations also showed that myofilaments and mitochondria were well preserved in groups III, IV and V at 15 min after reperfusion compared with those in groups I and II. These results indicate that the addition of steroid to preservation solution might be effective in preventing myocardial injury during preservation of rat hearts, and the optimal concentration appears to range from 150 mg/L to 200 mg/L.

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A 50-year-old woman was transported to a hospital complaining of marked general malaise and epigastralgia with diarrhea and vomiting. Her electrocar-diogram showed sinus arrest with a duration of nearly 8 sec. Atrial pacing with an external pacemaker improved her symptoms promptly. Following transfer to our hospital 3 days later, bradyarrhythmia was not detected despite the removal of the external pacemaker. Transient atrial fibrillation was found in our hospital, and she was diagnosed as hyperthyroidism based on findings of finger tremor, exophthalmos, diffuse goiter and an abnormally high level of thyroid hormone. On cardiac catheterization, left ventriculography showed anterior wall hypokinesis and mild mitral regurgitation. Coronary arteriography showed the absence of organic stenosis. Right ventricular endomyocardial biopsy showed myocardial hypertrophy and partial disarray, but no findings of myocarditis. Electrophysiological study showed the normal upper range of AH-time (120 msec) and HV-time (50 msec), and prolongation of corrected sinus recovery time (CSRT, 955 msec). After a euthyroid state was successively induced for about 10 days by methylmercaptoimidazole therapy, AH-time, HV-time and CSRT were shortened to 85, 35 and 290 msec respectively. Her complaints and sick sinus syndrome disappeared after the treatment of hyperthyroidism without a pacemaker.

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Ventricular tachycardia (VT) with right bundle branch block QRS morphology and left axis deviation originating in the inferolateral apical segment of the left ventricle was found in a 24-year-old man without overt structural heart disease. Intracardiac recordings during VT showed atrioventricular dissociation with the earliest activation at an apical inferolateral site in the left ventricle, where Purkinje fiber potentials were recorded fusing in the ventricular electrogram. Ventricular pacing was performed at this site, and yielded a QRS morphology identical to the VT. Radiofrequency current was applied and resulted in the complete elimination of VT.

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A 55-year-old man had been previously admitted at the age of 44 because of chest pain on effort. He was diagnosed as hypertrophic obstructive cardiomyopathy with a left ventrlcular outflow pressure gradient of 65 mmHg. We analyzed the cardiac β-myosin heavy chain gene in this patient using polymerase chain reaction-single strand conformation polymorphism analysis (PCR-SSCP analysis). PCR-SSCP analysis revealed a sequence variation within exon 16. A G-to-A transversion with replacement of Val by Met at codon 606 was confirmed by sequencing analysis. Previously, a ⁶⁰⁶Val&roarr;Met mutation has been reported to give a benign prognosis because of the neutral charge substitution. However, there have been some premature deaths in this patient's kindred. Thus, despite the absence of a change in charge, this mutation may be malignant in some kindreds.

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