Multivessel disease and decreased left ventricular ejection fraction(LVEF) are believed to be significant predictors of the outcome in patients with acute inferior myocardial infarction(AIMI). We attempted to determine new electro-cardiographic(ECG) markers for detecting concomitant left anterior descending(LAD) disease and/or decreased left ventricular function in patients with AIMI. Eighty patients with AIMI were evaluated within 6 h of the onset of symptoms and grouped according to the presence (Group 1) or absence (Group 2) of concomitant LAD disease. All of the patients underwent coronary angiography and left ventriculography 4-6 weeks from the onset of their infarction. We studied the validity of two new ECG markers : S-T depression deeper in lead V5 than in V4 (S-T↓V5>V4) and negative U waves (NUs)>0.5mm (50 pμV) in leads V4-6. The sensitivity and specificity of S-T↓V5>V4, NUs in V4-6, or both, in detecting concomitant LAD disease were 56% and 83%, 59% and 87%, and 35% and 98%, respectively. LAD lesions in patients who showed either of these new markers (74% of those with S-T↓V5>V4 and 80% of those with NUs in V4-6) were mostly in the proximal segments (AHA segments #6 or #7). Patients with either S-T↓V5>V4 or NUs in V4-6 tended to have asynergy in the anterolateral segment, while there was a strong correlation between the asynergy of the anterolateral and septal segments in patients who showed both ECG markers. On the other hand, there were no significant differences in LVEF between patients with or without LAD disease on angiography. In addition, there was also no difference in LVEF between patients with or without S-T↓V5>V4, and between patients with or without NUs in V4-6. However, the mean LVEF of patients with both of these new markers (47.4±16.4%) was significantly less than that in those without (56.4±11.5%) (p=0.0365). These findings demonstrate that S-T↓V5>V4 and/or NUs in V4-6 may be useful new markers for detecting concomitant LAD disease in patients with AIMI. In addition, the absence of both markers was highly specific for the absence of LAD disease and appears to indicate a relatively preserved LVEF.

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Endocardial catheter ablation has been recently been proposed for the treatment of arrhythmias originating in the right atrium. In this study, we used this technique in 5 patients with paroxysmal common atrial flutter and 3 patients with paroxysmal uncommon atrial flutter. Various antiarrhythmic agents had failed to prevent the recurrence of these episodes. In each procedure, we used a large-tip 7 F quadripolar catheter electrode that was introduced via the femoral vein into the lower part of the right atrium. The two distal electrodes were used to record double-spike potentials or fragmented electrograms. A unipolar electrogram recording from a distal electrode of the same catheter was also used to identify local activation. The targets for ablation were sites which showed double-spike potential and fragmented electrogram 40-60 msec earlier than the onset of the F wave. Application of radiofrequency(RF) energy (25-40 watts) (3-17 applications) terminated atrial flutter and prevented reinduction of atrial flutter in the 5 patients with common atrial flutter. However, atrial flutter could not be terminated with the application of RF energy in the 3 patients with uncommon atrial flutter. The sites at which ablation was successful were located inferior or posterior to the coronary sinus ostium between the inferior vena cava and the tricuspid valve annulus, and were characterized by double-spike potentials and fragmented electrograms with activation times ≥40 msec before the onset of the F wave. This area may represent the exit site from the area of slow conduction, since pacing from this site showed concealed entrainment of the F wave, and a local electrogram to the onset of the F wave coincided with the pacing spike to the onset of the F wave. Follow-up of these 5 patients (19.4±10.4 weeks) revealed recurrence of the original atrial flutter in 1 patient and a new type of atrial flutter in 1 patient. The other 3 patients have been episode-free, although an antiarrythmic agent was given for the treatment of paroxysmal atrial fibrillation in 2 patients. We conclude that the application of RF energy to the presumed critical area in the atrial flutter reentrant circuit seems to be effective in terminating and preventing common atrial flutter. Long-term follow-up is required for the recurrence of atrial flutter.

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The relation between isolated negative U waves and the severity of induced coronary artery spasm was investigated in 24 patients with variant angina to determine the grade of myocardial ischemia during the appearance of isolated negative U waves. Coronary artery spasm was induced by injections of either incremental doses of acetylcholine or ergonovine into the left coronary artery. Coronary spasm was quantified into 4 grades : Grade 0=complete perfusion, Grade 1=partia1 perfusion, Grade 2=penetration without perfusion, and Grade 3=no perfusion. Induction with acetylcholine was discontinued when a coronary spasm of Grade ≥2 was induced. Electrocardiogram in leads V1 to V6 and systemic blood pressure were recorded continuously. Provocations of coronary spasm with at least 2 doses'of acetylcholine could be performed in 15 patients. All acetylcholine-induced coronary spasms of Grade ≤1 disappeared spontaneously within 3 min. Negative U waves developed in 19 (79%) patients, in whom 37 trials with acetylcholine or ergonovine injection were performed. Isolated negative U waves were detected in 10 trials, negative U waves and ST depression in 8 trials, and negative U waves and ST elevation in 14 trials. The induced coronary spasms associated with isolated negative U waves were of Grade 1 in 9 of the 10 trials. In contrast, all of the coronary spasms associated with negative U waves and ST elevation had a Grade of ≥2. In conclusion, the coronary angiographic finding associated with isolated negative U waves is coronary spasm with delayed filling of the distal coronary artery, with opacification of the entire coronary bed.

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We investigated the nature of the contraction produced by 5-hydroxytryptamine(5-HT) in the rat pulmonary artery, and compared it with that produced in the rat aorta. Both ketanserin and ritanserin inhibited 5-HT-induced contraction in the pulmonary artery non-competitively. In contrast, ketanserin competitively antagonized the contraction in the aorta. Bunazosin, a selective α₁-blocker, partially inhibited 5-HT-induced contraction in the pulmonary artery, but not in the aorta. In both the pulmonary artery and aorta, 8-OH-DPAT, a 5-HT_1A selective agonist, produced a concentration-dependent contraction. In the pulmonary artery, 5-HT and 8-OH-DPAT produced contractions with similar potencies. In contrast, 8-OH-DPAT was less potent than 5-HT in the aorta. Bunazosin inhibited 8-OH-DPAT-induced contraction in both vessels. However, pindolol, a 5-HT_1A antagonist, did not inhibit 8-OH-DPAT-induced contraction in the pulmonary artery. These results suggest that 5-HT produces contraction via not only 5-HT₂ receptor, but also non-5-HT₂ receptor (probably α₁-adrenoceptor) in the rat pulmonary artery. Furthermore, 8-OH-DPAT does not activate the 5-HT_1A receptor to produce a contraction, but does activate other receptors which interact with α₁-adrenoceptor.

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The NZW×BXSB F1 male mice that a model for systemic lupus erythematosus(SLE) develop myocardial infarction. To determine whether the gene(s) linked to the major histocompatibility complex(MHC) of NZW mice are involved in myocardial infarction, we developed an H-2-congenic NZW. H-2^d strain and compared the incidence of myocardial infarction in NZW×BXSB F1 (H-2^z/b) male mice to that in NZW. H-2^d×BXSB F1 male mice (H-2^d/b). H-2^z/b heterozygous F1 male mice showed a higher incidence of myocardial infarction than H-2^d/b F1 male mice. This observation suggests that the myocardial infarction seen in SLE may be related to MHC.

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Phorbol ester, which activates protein kinase C(PKC), modulates vasoconstrictor-induced tension in vascular smooth muscle. Recently, Staphylococcal aureus α-toxin, which produces too small pores in the plasma membrane to allow passage of proteins, such as PKC, is used to investigate the signal transduction system in vascular smooth muscle cells. In order to elucidate the role of PKC on vascular smooth muscle contraction, we examined whether PKC activation influences the relationship between intracellular Ca²⁺ ([Ca²⁺]_i) and tension in Wistar rat superior mesenteric artery(SMA) using vascular smooth muscle permeabilized with Staphylococcal α-toxin. [Ca²⁺]_i was clamped at specified values (10^-8.5-10^-4mol/L) using EGTA-Ca²⁺ buffer. In α-toxin non-treated rings of SMA, isometric tension was evoked by 10 mmol/L caffeine and 10-30 mmol/L external potassium (high K⁺) in the absence or presence of phorbol 12, 13-dibutyrate (PDBu), a PKC activator, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), and staurosporine (PKC inhibitors). PDBu significantly augmented caffeine- and high K⁺-evoked contractions. H-7 and staurosporine significantly attenuated caffeine- and high K⁺-evoked contractions augmented by PDBu. Moreover, H-7 significantly suppressed high K⁺-induced contraction in the absence of PDBu. In α-toxin permeabilized artery, PDBu shifted the [Ca²⁺]_i-force relationship curve to the left. These results suggest that PKC activates vascular smooth muscle contraction by increasing the sensitivity of the contractile apparatus to Ca²⁺ .

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In this study, the middle cerebral artery(MCA) of adult male Sprague-Dawley rats was occluded by the modified Koizumi method to determine the temporal thresholds of reperfusion for the treatment of cerebral embolism. Regional cerebral blood flow(rCBF) and pathological findings were measured at I and 2 h of ischemia and after 24 h and 7 days of reperfusion following 1 or 2 h of ischemia. rCBF was decreased the most (less than 10% of control CBF) in the parietal cortex (Pcor) and the lateral caudoputamen(Lcp) at both 1 and 2 h of ischemia. There was no significant difference in rCBF in these areas between the 2 ischemic groups. The 2 h ischemia group clearly showed infarction in the area perfused by the middle cerebral artery (including the Pcor and Lcp) after 24 h and 7 days of reperfusion, while the 1 h ischemia group showed only slight infarction. These findings suggest that temporal thresholds of reperfusion in this model exist between 1 and 2 h (of ischemia, and that rCBF levels during ischemia and the duration of ischemia are the most important factors in producing brain infarction.

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