It has not been determined if signal-averaged electrocardiograms (SAECGs) have a diurnal variation. We recorded 3-channel 24-hour ECGs in 30 healthy volunteers and calculated the following parameters for the first 500 sec of every hour over the 24-hour period: the mean heart rate, the filtered QRS duration (f-QRS), the root-mean-square voltage of the signals in the last 40 msec of the QRS (RMS40), and the duration of low-amplitude signals (< 40 microV) in the terminal portion of the QRS (LAS40). Heart rate and RMS40 increased in the daytime compared with the nighttime; f-QRS and LAS40 increased during the nighttime hours. The f-QRS and LAS40 were negatively correlated with heart rate in all and 22 (73%) of 30 subjects, respectively, and RMS40 was positively correlated with heart rate in 21 subjects (70%). In conclusion, SAECGs exhibit a clear diurnal variation in healthy subjects, which is closely related to changes in heart rate.
Although mitochondrial ATP-sensitive potassium (mitoK ATP ) channels have been reported to reduce the extent of apoptosis, the critical timing of mitoK ATP channel opening required to protect myocytes against apoptosis remains unclear. In the present study, we examined whether the mitoK ATP channel serves as a trigger of cardioprotection against apoptosis induced by oxidative stress. Apoptosis of cultured neonatal rat cardiomyocytes was determined by flow cytometry (light scatter and propidium iodide/annexin V-FITC fluorescence) and by nuclear staining with Hoechst 33342. Mitochondrial membrane potential (ΔΨ) was measured by flow cytometry of cells stained with rhodamine-123 (Rh-123). Exposure to H 2 O 2 (500 μM) induced apoptosis, and the percentage of apoptotic cells increased progressively and peaked at 2 h. This H 2 O 2 -induced apoptosis was associated with the loss of ΔΨ, and the time course of decrease in Rh-123 fluorescence paralleled that of apoptosis. Pretreatment of cardiomyocytes with diazoxide (100 μM), a putative mitoK ATP channel opener, for 30 min before exposure to H 2 O 2 elicited transient and mild depolarization of ΔΨ and consequently suppressed both apoptosis and ΔΨ loss after 2-h exposure to H 2 O 2 . These protective effects of diazoxide were abrogated by the mitoK ATP channel blocker 5-hydroxydecanoate (500 μM) but not by the sarcolemmal K ATP channel blocker HMR-1098 (30 μM). Our results suggest for the first time that diazoxide-induced opening of mitoK ATP channels triggers cardioprotection against apoptosis induced by oxidative stress in rat cardiomyocytes.
The purpose of this study was to elucidate the possible link between lipoprotein(a) (Lp(a)) and the occurrence of restenosis after initial elective percutaneous transluminal coronary angiopasty (PTCA). Serum lipids, including Lp(a), total cholesterol, triglyceride, HDL-cholesterol, LDL-cholesterol, apolipoprotein A-I (Apo A-I), and apolipoprotein B (Apo B), and the Apo B/Apo A-I ratio were examined in 63 consecutive patients (41 men and 22 women, average age 63±8 years) who underwent initial elective PTCA in our department. Forty two target lesions were in left anterior descending, 10 were in left circumflex and 11 were in right coronary branches. Restenosis was observed in 22 patients (35%) 6.4±2.6 months after PTCA. The serum Lp(a) level was significantly higher in the restenosis group than in the non-restenosis group (38.0 vs 19.9 mg/dl, p<0.05). A significant correlation was observed between serum Lp(a) levels and the degree of % restenosis after PTCA (r=0.557, p<0.001). However, other lipids showed no significant relationship to restenosis. In addition, the % stenosis before PTCA was found to be related to the occurrence of restenosis after successful PTCA. We conclude that the serum Lp(a) level has a close correlation with the degree of % restenosis after PTCA, and may be a useful index for predicting the possibility of restenosis after PTCA, especially in patients with an Lp(a) level above 30 mg/dl.
It is recognized that heart failure in patients with atherosclerotic lesion is the result of ischemia. However, there may also be cardiac cell dysfunction independent of ischemia, as factors advancing both of atherosclerosis and heart failure are discovered. The renin-angiotensin system is one of factor and angiotensin-converting enzyme inhibitor (ACEi) prevents progression of atherosclerotic lesion and heart failure. To elucidate the association of atherosclerosis and cardiac cell dysfunction, we investigated the effects of ACEi on cultured cardiac myocytes. Captopril increased beta-receptor density of myocytes and augmented the response to isoproterenol. CV-3480, a ACEi, also up-regulated beta-receptors but angiotensin I, angiotensin II and angiotensin type I receptor antagonist did not. Bradykinin B2 receptor blocker, HOE140, suppressed the effect of captopril on cultured cells. The results suggest that ACEi up-regulated beta-receptors and augmented the response to beta-receptor agonist through BK potentiation.
Postextrasystolic U wave augmentation is observed in patients with long QT syndrome and those with organic heart disease. This phenomenon is considered a marker of increased risk of arrhythmia. However, the characteristics of the U wave have not been evaluated in patients with idiopathic VT originating from the right ventricular outflow tract (RVOT-VT). The present study evaluated the dynamic change in the T-U wave in patients with RVOT-VT. Holter ECGs obtained from 14 patients with RVOT-VT and 11 healthy control subjects were analyzed. The amplitude of T and U waves (Tamp and Uamp) and preceding RR intervals were measured during stable sinus rhythm (rate dependent change) and in the postextrasystolic sinus complex (pause dependent change). Uamp correlated negatively and significantly with the preceding RR interval in 13 (93%) RVOT-VT patients but in only 2 (18%) control subjects. The average value of the slope of the Uamp/RR relationship was negative (-0.22 +/- 0.10 mV/s) in the RVOT-VT group, but was positive (0.04 +/- 0.07 mV/s, P < 0.001) in the control group. Pause dependent U wave augmentation was observed in 12 (86%) of 14 patients. Increased frequency of consecutive preceding premature ventricular contractions (PVCs) was associated with a larger postextrasystolic Uamp. PVC or the first ventricular beat of VT arose from near the peak of augmented U waves. The dynamic changes in the T-U wave were observed in patients with RVOT-VT. Further investigations are required to elucidate the precise role of the U wave in arrhythmogenesis in those patients.
