No abstract available.
Korea* ; Myocardial Infarction*

No abstract available.
Diagnosis* ; Estrogens, Conjugated (USP)* ; Heart Failure*

No abstract available.
Estrogens, Conjugated (USP)* ; Heart Failure*

No abstract available.
Renal Artery Obstruction* ; Renal Artery* ; Stents*

Serial meanurements of the pacing threshold have been considered as essential for follow-up of the patients in whom the pacemaker had been implanted because pacing threshold is directly related to the success of long-term pacemaker therapy and reflects the alterations in electrobiologic factors influencing it. The development of the noninvasive technique of measuring pacing threshold such as Vario system made the noninvasive follow-up of it feasible and therefore has contributed to understanding of long-term threshold behavior. This study was performed to get the knowledge of acute and chronic pacing threshold behavior by measuring it serially in 46 patients after pacemaker implantation using a non invasive technique of Vario system. Patients subjected to the present study were 46(18 males, 28 females) comprising 21 sick sinus syndromes, 24 A-V blocks, and 1 combined disorder. All were received a multiprogrammable pacemaker of VVI mode (OPTIMA-MP, Telectronics). Pacing threshold was increased significantly from initial threshold(0.65+/-0.22) 2 days after implantation and reached to peak(1.65+/-0.75 volts) in the fourth week, thereafter it was maintained around twice the initial value. In the 30 patients followed more than 3 months, the maximum increase and difference in pacing thresholds were 0.86+/-0.62 volts and 0.93+/-0.56 volts respectively and the ratios of peak threshold and threshold at the end of follow-up to initial threshold were 2.56+/-1.23 and 2.30+/-1.30 respectively. Pacing threshold exceeded 2.0 volts in 7 patients(15.2%), but transiently in 3 of 5 patients in whom it happened within 6 weeks after implantation. Safety margins of long-term thresholds were acceptable(more than 3) in all patients at 5.0 volts and 19(63.3%) at 2.5 volts of programmed output.
Follow-Up Studies ; Humans ; Male

BACKGROUND: The electrophysiological effects of purinergic receptor agonists, adenosine triphosphate(ATP) and adenosine were examined using conventional microelectrode technique in rat atrial muscle fibers under superfused with a normal or a simulated ischemic(hypoxic, hyperkalemic and acidotic) physiologic salt solution(PSS) in vitro. METHODS: Action potential parameters, such as maximal diastolic potential(MDP), action potential amplitude(APA), rate of phase 0 depolarization(dv/dtmax) and action potential duration(APD90) were measured in electrically paced, physiologic salt solution(Tyrode's) superfused left rat atrium. In the experiment of ischemic simulation in vitro, normal physiologic salt solutions(NPSS0 were modified(MPSS) and superfused in substitute for normal Tyrode's solution. To investigate the effects of purinergic receptor agonists, ATP or adenosine was added to the superfused tyrode's solutions(NPSS or MPSS) in molar concentration. RESULTS: Under superfused with normal PSS, ATP(10(-3), 10(-4)M) elicited slight hyperpolarization in MDP, and both ATP(10(-6)-10(-3)M) and adenosine(10(-6)-10(-3)M) shortened the duration of normal action potential in a dose-dependent manner. The other paramaters were not affected by the drugs. Superfusion with ischemic PSS caused reductions in MDP as well as APA, dv/dtmax and, especially, APD90. The effects produced by the initial 10 minutes of superfusion with ischemic PSS almost completely disappeared during a subsequent period of continued superfusion with normal PSS, but, those by the initial 20 min lasted in some degree. Both ATP(10(-4)M) and adenosine(10(-4)M) attenuated the reduction in the rate of phase 0 depolarization and the amplitude of the action potential amplitude produced by the ischemic PSS. CONCLUSION: Purinergic receptor agonists, ATP and adensoine, caused a concentration-dependent shortening of the action potential duration in rat atrial muscle fibers and they attenuated the reductions in the rate of phase 0 depolarization and action potential amplitude in fibers superfused with ischemic PSS.
Action Potentials ; Adenosine ; Adenosine Triphosphate ; Animals ; Ischemia ; Microelectrodes ; Molar ; Purinergic Agonists* ; Rats ; Receptors, Purinergic

To evaluate the lipid-lowering effect of lovastatin(Mevacor(R)), lovastatin was administered to 38 patients with non-familial hypertcholesterolemia(>220mg/dl). The analysis of the effect was made with 25 patients(58.2+/-7.5 years ; 13 male, 12 female)who had received lovastatin more than 12 weeks. The drug was administered as a single dose with evening meal 20mg at the begining and adding another 20mg if the total cholesterol level was persistently higher than 200mg/dl at the end of each 4 week-period. 1) Total cholesterol level was decreased from 256.6+/-36.9mg/dl to 20932+/-50.1mg/dl at the end of the 4th week, 201.9+/-44.2mg/dl the 8th week and 203.6+/-39.6mg/dl the 12th week (p<0.001), respectively). 2) Triglyceride level was decreased from 196.4+/-104.1mg/dl to 163.4+/-74.4mg/dl at the end of the 4th week(p<0.05) but no significant change at the end of the 8th week showing 169.8+/-73.2mg/dl and 162.7+/-54.8mg/dl the 12th week(p<0.05). 3) High density lipoprotein cholesterol(HDL-C) level was not significantly changed with the drug during the 12 week treatment period. 4) Low density lipoprotein cholesterol(LDL-C) level was decreased remarkably similar to that of total cholesterol. 5) Total cholesterol/HDL-C ratio was decreased from 5.05+/-0.92 to 4.06+/-1.40 at the end of the 4th week(p<0.05), 3.89+/-0.99 the 8th week(p<0.001). 4.20+/-1.10 the 12th week(p<0.01). 6) LDL-C/HDL-C ratio was decreased from 3.24+/-0.94 to 2.43+/-1.21 at the end of the 4th week(p<0.05), 2.23+/-0.86 the 8th week(p<0.001) and 2.54+/-0.98 the 12th week(p<0.05). 7) There was no significant side effect on lovastatin therapy of 12 weeks duration. 8) The laboratory findings including liver function test, uric acid, creatinine, creatine phosphokinase and blood glucose were not changed significantly. From above results we concluded that lovastatin is safe and effective hypocholesterolemic agent in its clinical use.
Blood Glucose ; Cholesterol ; Creatine Kinase ; Creatinine ; Humans ; Hypercholesterolemia* ; Lipoproteins ; Liver Function Tests ; Lovastatin ; Male ; Meals ; Triglycerides ; Uric Acid

The systolic time intervals and hemodynamics were measured in 10 cases of acute anemia and 28 cases of chronic anemia. The measurment was done by non invasive technique, i.e., simultaneous recording of ECG, PCG and carotid and femoral pulse tracing with paper speed 100mm/sec. Compared with healthy persons chronic anemia showed significant reduction of the systolic time intervals except QS1, but the systolic time intervals were unaltered when they were corrected by pulse rate, diastolic pressure and stroke volume. Acute anemia showed decreased of the systolic time intervals except QS1 also the decrease of isovolumic contraction time(ICT) and QS2 when corrected as above. The preejection period(PEP)/left ventricular ejection time(LVET) ratio were not altered. ICT, PEP and PEP/LVET ratio decreased in proportion to the levels of hemoglobin. The heart rate, stroke volume and cardiac output showed significant increase in chronic anemia but mild incease in acute one. The decrease of diastolic pressures and peripheral resistances were more pronounced in chronic anemia than in acute one.
Anemia* ; Blood Pressure ; Cardiac Output ; Electrocardiography ; Heart Rate ; Hemodynamics* ; Humans ; Stroke Volume ; Systole*

The development of aorticpulmonary bodies was studied by electron microscope in human fatuses ranging from 40mm to 260mm crowm-rump length. The aorticpulmonary bodies were observed in the wall of the aorta, and of the pulmonart trunk and arteries. At 40mm fetus, the aorticopulmonary bodies were composed of clusters of primitive glomus cells, primative supporting cells, unmyelinated nerve fibers, and capillaries. The primitive glomus cells possessed large nuclei, dense-cored vesicles, many Golgi complexes, rough endoplasmic reticulum, and, multivesicular bodies, the primitive supporting cells were agranular with attenuated cytoplasmic processed which partially ensheathed the primitive glomus cells. Synaptic contacts between the axon terminals and the aoma of primitive glomus cells were first observed. The primitive glomus cells increased somewhat in size and number by 90mm fetus, but retained essentially the same characteristics as at the earlier stage. Desmosome-like contacts between glomus cells and adjacent cells were commonly seen. At 160mm fetus, the glomus cells had increased accumulations of all organells and numerous dense cored vesicles. The supporting cells completely invested the glomus cells. Two types of nerve terminals were observed. One type contained small agranular vesicles which was identified as cholinergic axon terminal. The other contained a majority of small granular vesicles which was classfied as adrenergic axon terminal. Synaptic contacts between the cholinergic axon terminals and the soma of the glomus cell were observed. During next prenatal stage up to 260mm fetus the glomus cells and the supporting cells resembling those in adult were present. It is concluded that the ultrastructural features of these aorticopulmonary bodies are similar to those of the carotid body. It is therefore suggested that the aorticopulmonary bodies of the human fetures have a chemorecepter function similar to that of the carotid body.
Adult ; Aorta ; Arteries ; Capillaries ; Carisoprodol ; Carotid Body ; Cytoplasm ; Endoplasmic Reticulum, Rough ; Fetus* ; Golgi Apparatus ; Humans* ; Multivesicular Bodies ; Nerve Fibers, Unmyelinated ; Presynaptic Terminals

The pulmonary arterial pressure(PAP) was reported to be higher in essential hypertensives than in normotensives, but the underlying mechanisms for the higher PAP were not known exactly. In order to observe the changes of pulmonary hemodynamics and to get an insight into the mechanism of the pulmonary hypertension, if any, in essential hypertensive patients, the autors performed the cardiac catheterization in 13 normal controls(group A), 14 coronary patients with normal systolic left ventricular function and systemic blood pressure(group B), and 15 essential hypertensives with normal coronary artery and systolic left ventricular function(group C). 1)Pulmonary arterial pressure(PAP) was 19.2+/-3.2/8.1+/-1.9/12.0+/-1.9(s/d/m)mmHg in group A, 25.0+/-6.2/12.8+/-4.0/16.3+/-4.5mmHg in group B, 29.3+/-6.1/12.8+/-4.0/18.2+/-3.6mmHg in group C. The PAP was higher in group B and C than that of group A(p<0.005). 2) Pulmonary vascular resistance(PVR) was 88.2+/-34.9 dyne.sec.cm(-5) in group A. 137.8+/-74.5 dyne.sec.cm(-5) in group B and 173.9+/-77.5 dyne.sec.cm(-5) in group C. In group B and C, PVR was increased compared to that of group A(p<0.05, p<0.005, respectively). 3) Pulmonary capillary wedge pressure(PCWP) was 6.6+/-2.8 mmHg in groupa A. 9.9+/-2.9mmHg, and 9.6+/-3.6 mmHg in group C. PCWP in group B and C were higher than that of group A(p<0.005). 4) Systemic vascular resistance(SVR) was 1298+/-340 dyne.sec.cm(-5) in group A, 1466+/-362 dyne .sec.cm(-5) i group B and 2255+/-439 dyne.sec.cm(-5) in group C. In group C, SVR was increased compared to that of group A and B(p<0.002). 5) Significant correlation was demonstrated between PVR and PCWP in group A(r=-0.74, p<0.05). 6) In group B, significant correlations were shown between PAP and PCWp(r=0.55, p<0.05), between PAP and PVR(r=0.69, p<0.05). 7) In group C, significant correlations were demonstrated between PAP and PCWP(r=0.55, p<0.05), between PVR and SVR(r=<0.51, p<0.01). Above results revealed that PAP and PVR were increased in essential hypertensives without left ventricular failure and this elevated PAPseemed to be affected in part by increased PCWP, and increased PVR in accordance with increased SVR.
Capillaries ; Cardiac Catheterization ; Cardiac Catheters ; Coronary Vessels ; Hemodynamics* ; Humans ; Hypertension* ; Hypertension, Pulmonary ; Ventricular Function, Left