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

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 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

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

Hypertensive left ventricular hypertrophy(LVH) was considered to be a physiologic adaptation to the increased afterload of left ventricle, but recent studies revealed that LVH was one of the most important target organ damage in essential hypertensive patients & cardiovascular morbidity was increased in patients with hypertensive LVH. Hypertensive LVH could be classified into three types : concentric LVH, disproportionate septal thickening(DST), and left ventricular dilatation. Relatively high incidence of DST in hypertension has bee reported after clinical introduction of echocardiogram. But, the mechanisms for the development of DST and its clinical significance have not been elucidated exactly. In order to assess left ventricular diastolic function in hypertensives with DST, the authors performed phonocardiogram, M-mode, and pulsed Doppler echocardiogram in 15 normotensive control(group A : 5 male, 10 female, 44.4+/-7.7 years), 15 hypertensives without LVH(group B : 5 male, 10 female, 45.5+/-8.6 years), 85 hypertensives with DST(group C : 9 male, 16 female, 47.5+/-8.6 years) and 15 hypertensives with concentric LVH(group D : 8 male, 7 female, 47.7+/-6.1 years). The obtained results were as follows : 1) Left ventricular ejection fraction was 71.6+/-6.3% in group A, 71.9+/-7.5% in group B, 731+/-7.0% in group C, and 70.3+/-10.3% in group D. Ejection fraction was not significantly different in each other group. 2) Left ventricular mass index(LVMI) by echocardiogram was 87.8+/-20.6g/m
Adaptation, Physiological ; Bees ; Deceleration ; Dilatation ; Female ; Heart Ventricles ; Humans ; Hypertension ; Hypertrophy ; Incidence ; Male ; Relaxation ; Stroke Volume

Two factors of the ventricular function, systolic contractile and diastolic relaxing functions, cooporate in pumping the adequate blood volumes to suffice bodily demands. In some hypertensive patients with marked left ventricular hypertrophy, the intact systolic function of the ventricle associated with clinical symptom of congestive heart failure(CHF), which is considered to be a consequence of diastolic dysfunction. In this study 10 hypertensive patients(group A) complaining of exertional dyspnea or chest pain with increased left ventricular mass index and normal systolic function and 6 normotensive controls(group B) were examined by cardiac catheterization and echocardiography to assess the left ventricular systolic and diastolic function and ventricular responses to constant infusion of nitroprusside. Various systolic and diastolic function indices were measured by cardiac catheterization and echocardiography. 1) The ejection fraction(EF), fractional fiber shortening, mean velocity of circumferential fiber shortening, left ventricular(LV) peak+dp/dt, change of slope of LV peak systolic pressure-volume and pressure-dimension relations in group A were not different from those of group B in the resting states. 2) Diastolic dysfunction was evidenced by prolonged A2D time, decreased OR slope, decreased peak negative dp/dt and increased diastolic time constant 'T' in group A. 3) Cardiac index by thermodilution method was negatively related to left ventricular mass index(LVMI) measured by echocardiography, whereas time constant T was positively related to LVMI. 4) With constant infusion of nitroprusside, LV systolic pressure, LV end-diastolic pressure and pulmonary arterial pressure were decreased, and left ventricular end-systolic stress and stroke work index(SWI) derived from left ventricular pressure-volume loop area were decreased, EF was increased, but time constant T was prolonged and cardiac output(CO) by thermodilution method was decreased in group A. 5) In group B, with constant infusion of nitroprusside, EF, SWI and CO were pratically unaffected and time constant T was not prolonged significantly. These reults suggest that patients with hypertensive hypertrophic left ventricle is associated with diastolic dysfunction, which could further be exacerbated by a vasodilator such as nitroprusside.
Arterial Pressure ; Blood Pressure ; Blood Volume ; Cardiac Catheterization ; Cardiac Catheters ; Chest Pain ; Dyspnea ; Echocardiography ; Estrogens, Conjugated (USP) ; Heart Diseases* ; Heart Ventricles* ; Heart* ; Humans ; Hypertension ; Hypertrophy, Left Ventricular ; Nitroprusside* ; Stroke ; Theophylline ; Thermodilution ; Ventricular Function

Cardiac output depends on the ability of systolic ejection and diastolic filling of the heart. M-mode echocardiography can provide accurate clinical assessment of left ventricular systolic and diastolic functions. To see whether there are changes of the left ventricular function in asymptomatic hypertensives and if any kind of dysfunction and whether any relationship between the pattern of the ventricular hypertrophy and type of ventricular dysfunction exists, the authors examined the systolic and diastolic function indices of the left ventricle in 50 normotensives and 88 hypertensives composed of 18 patients without left ventricular hypertrophy(group 1), 40 patients with disproportionate septal thickening (group 2) and 30 patients with concentric left ventricular hypertrophy(group 3). Obtained results were as follows : 1) Blood pressure & left ventricular mass index were increased significantly in each hypertensive group compared to normal control. 2) Ejection fraction & fractional shortening in the hypertensive groups were not different from the normotensive control group. 3) Left ventricular isovolumic relaxation time(A2D time) was prolonged in each hypertensive group, especially in group 3. 4) Left atrial emptying index (AEI) was decreased in each hypertensive group. 5) Left ventricular percent ventricular A wave (% VAW) was increased in all hypertensive groups. Above study suggested that the left ventricular diastolic function could be impaired in the hypertensives without associated systolic dysfunction, and the degree of the diastolic dysfunction was not much affected by the type of left ventricular hypertrophy, but the more prolonged A2D time in the concentric hypertrophy group.
Blood Pressure ; Cardiac Output ; Echocardiography ; Heart ; Heart Ventricles ; Humans ; Hypertrophy ; Hypertrophy, Left Ventricular ; Relaxation ; Ventricular Dysfunction ; Ventricular Function, Left

The hypotensive effect of tripamide(Normonal(R)) were evaluated in 31 cases of essential hypertension. Fifteen to thirty mg of tripamide per day were administered continuously for 8 weeks. The results were as follows; 1) The systolic blood pressure was significantly lowered from 175+/-15 mmHg(Mean+/-SD) before treatment to 144+/-17 mmHg after treatment(p<0.01), and the diastolic blood pressure was significantly lowered from 106+/-11 mmHg before treatment to 90+/-12 mmHg after treatment(p<0.01). 2) The systolic blood pressure was lowered 20 mmHg or more in 25 out of 31 cases(80.7%), and the diastolic blood pressure was decreased 10 mmHg or more in 25 out of 31 cases(80.7%) at the end of 8 weeks treatement. 3) There was no significantl differences in the level of SGOT, serum cholesterol, serum electrolytes(Na+, K+, Cl-), BUN, creatinine and urinc acid before and after treatment with tripamide. 4) In most cases the subjective symptoms disappeared or became easier after tripamide treatment. 5) Profound weakness was developed in 2 cases during tripamide administration.
Aspartate Aminotransferases ; Blood Pressure ; Cholesterol ; Creatinine ; Hypertension*

No abstract available.

No abstract available.
Tomography, Emission-Computed, Single-Photon*