To analyse the rate of changes of left atrial demension in ventricular diastole in hypertensive heart disease, the velocities of early diastolic(OR) slope and presystolic(AV) slope of the motions of the posterior aortic wall were measured using M-mode echocardiogram. 18 normal subjects(Group I), 17 hypertensive patients without left ventricular thickening(Group II), 16 hypertensive patients with thickening of either interventricular septum or left ventricular posterior wall(Group III), 15 hypertensive patients with both interventricular septum and left ventricular posterior wall without dilation of left ventricle(Group IV) and 5 hypertensive patients with thickening and dilation of left ventricle(Group V) were compared. Whereas %fractional shortening and AV slope decreased in only Group V, there was a progressive increase in left atrial dimension and a progressive decrease in the OR slope and patients without left atrial dilation in Group I also decrease in OR slope. The velocity of OR slope was correlated strongly with the thickness of left ventricular posterior wall(r=-0.62, p<0.001), and weakly with left atrial dimension(r=0.379, p<0.01) but not with heart rate and %fractional shortening and the velocity of AV slope with %fractional shortening(r=0.433, p<0.001). These data suggest that the velocity of OR slope appears to be an early indicator of abnormalities of left ventricular diastolic compliance and the velocity of AV slope and indicator of systolic abnormality and rapid filling of the left ventricle is reduced early in hypertension, even before left atrial dilation or left ventricular thickening are detectable.
Compliance ; Diastole ; Heart Diseases* ; Heart Rate ; Heart Ventricles ; Heart* ; Humans ; Hypertension

The effect of left ventricular hypertrophy resulting from essential hypertension upon left ventricular performance was studied in 30 normotensive normal control subjects and 34 hypertensive patients; 14 hypertensive patients without left ventricular hypertrophy, 8 hypertensive heart disease patients with compensation and 12 hypertensive heart disease patients with decompensation. In hypertensive heart disease patients with decompensation, ejection fraction and mean rate of circumferential shortening was reduced(0.45+/-0.12, 0.67+/-0.20 circ/sec respectively) compaired with normal control(0.70+/-0.05, 1.16+/-0.15 circ/sec respectively), hypertensive patients without left ventricular hypertrophy(0.67+/-0.05, 1.16+/-0.15 circ/sec respectively) and hypertensive heart disease patients with compensation(0.67+/-0.07, 1.09+/-0.14 circ/sec respectively). In contrast, ejection fraction and mean rate of circumferential shortening were not significantly different among the last three groups. These results indicate that left ventricular performance measured by ejection fraction and mean rate of circumferential shortening is well preserved in hypertensive patients without left ventricular hypertrophy and hypertensive heart disease patients with compensation.
Compensation and Redress ; Heart Diseases ; Humans ; Hypertension* ; Hypertrophy, Left Ventricular*

The systolic time intervals, hemodynamics, and indices of myocardial contractility were measured in 158 normal Koreans with average age of 34(14~69) years by non-invasive technique, i.e. simultaneous recording of ECG, PCG, and carotid and femoral pulse tracing with paper speed 100mm/sec. by cardiograph. 1. Normal values of systolic time intervals were as follows(M+/-SD): QS1was 61.5+/-10.8, ICT 41.9+/-12.0, PEP 10.+/-14, LVET 281+/-24, and QS2 385+/-26 msec. 2. Regression equations of systolic time intervals to pulse rate were as follows: QS1; 0.04 x PR + 60.0 (r=+0.038, p>0.05), ICT; -0.2 x PR + 59.6 (r=-0.234, p<0.01), PEP; -0.2 x PR + 117 (r=-0.162, pp<0.05), LVET; -1.5 x PR + 389 (r=-0.725, pp<0.001), QS2; -1.7 x PR + 507 (r=-0.745, pp<0.001). 3. Each phase of systolic time intervals was affected by various factors: ICT and PEP by pulse rate, diastolic pressure and stroke volume, LVET by pulse rate and stroke volume, QS1by diastolic pressure, and QS2by pulse rate. Multiple linear regression analysis results in the following formulas for prediction of the systolic time intervals from the pulse rate, diastolic pressure and stroke volume: ICT; -0.299PR+0.230Pd-0.139Vs+28.1(r=0.38), PEP; -0.272PR+0.356Pd-0119Vs+104.8 (r=0.39), LVET; -1.475PR+0.167Vs+376.6 (r=0.74). 4. Systolic time intervals were not influenced by height, weight or body surface, but LVET and QS2were prolonged significantly in female group. 5. Normal values of hemodynamics calculated by Wezler's formula were as follows: stroke volume was 68.1+/-21.7ml, stroke index 50.2+/-14.9ml/m2, cardiac output 4.9+/-1.71/min., cardiac index 3.6+/-1.3 1min/m2, peripheral resistance 1696+/-507 dyne sec. cm(-5), and volume elasticity coefficient 1916+/-422 dyne cm(-5). 6. Normal values of non-invasive indices of myocardial contractility were as follows: ICT was 42+/-21 msec. PEP 10.+/-14 msec., 1/PEP2 9.87x10-5+/-2.79x10-5msec., 1/ICT28.56x10-3+/-1.65+/-10-3msec-2., Pd/ICT 1.96+/-0.92 mmHg/msec., Pd/PEP 0.723+/-0.125 mmHg/msec., PEP/LVEE 0.37+/-0.06, LVET/PEP 2.77+/-0.47, and LVET/ICT 7.45+/-3.19. 7. Each index of myocardial contractility was affected by various factors: ICT, PEP, 1/PEP2, PEP/LVET, LVET/PEP and LVET/ICT by pulse rate, diastolic pressure and stroke volume, 1/ICT2by pulse rate, and Pd/ICT and PD/PEP by pulse rate and diastolic pressure. 8. Correlation coefficients between PEP/LVET and other indices were relatively high in PEP, 1/PEP2and LVET/PEP, and relatively low in ICT, 1/ICT2Pd/ICT, Pd/PEP and LVET/ICT.
Blood Pressure ; Cardiac Output ; Elasticity ; Electrocardiography ; Female ; Heart Rate ; Hemodynamics* ; Humans ; Linear Models ; Reference Values ; Stroke ; Stroke Volume ; Systole* ; Vascular Resistance

Parameters of the left ventricular performance were evaluated by echocardiographic examination in 66 normal subjects. Effects of pulse rate, systemic arterial pressure, peripheral resistance and left ventricular end-diastolic dimension on the parameters were also observed. Normal value(mean+/-SD) of fractional shortening was 34.0+/-5.2%, ejection fraction 0.71+/-0.07, mean rate of circumferential fiber shortening 1.15+/-0.19 circ/sec, mean posterior wall velocity 4.05+/-0.70cm/sec, maximal posterior wall velocity 6.31+/-1.26cm/sec, mean normalized posterior wall velocity 0.82+/-0.14/sec, and maximal normalized posterior wall velocity 1.28+/-0.24/sec. There were negative correlations of peripheral resistance to fractional shortening, ejection fraction and mean rate of circumferential fiber shortening. Pulse rate and left ventricular end-diastolic dimension did not have significant effects on these parameters. Mean and maximal posterior wall velocity had negative correlations to peripheral resistance and positive correlations to left ventricular end-diastolic dimension. But mean and maximal normalized posterior wall velocity had no correlations to any of them.
Arterial Pressure ; Echocardiography* ; Heart Rate ; Vascular Resistance

To evaluate the changes of Doppler echocardiographic parameters of left ventricular(LV) filling in hypertensive subjects, 34 patients(M : F=17 : 17) with and without LV hypertrophy and 19 healthy, age-matched control subjects(M : F=10 : 9) were examined by M-mode, 2 dimensional and Doppler echocardiography. From the Doppler recording, A2 D(time from second heart sound to the onset of early diastolic mitral flow), peak velocity at early diastole(E) and late diastole(A), ratio of E to A velocity, diastolic filling times, early diastolic deceleration rate(EDDR) and flow velocity integral(FVI) were measured. In the patients without LV hypertrophy, A2 D only was significantly prolonged(127+/-21 vs 83+/-24 msec P<0.01) as compared with the normal subjects, but the patients with LV hypertrophy had more prolonged A2 D(149+/-31 vs 83+/-24 msec P<0.01), higher late diastolic peak velocity(A : 0.58+/-0.17 vs 0.47+/-0.09m/sec, P<0.01) and lower E/A velocity ratio(0.95+/-0.19 vs 1.24+/-0.29, P<0.01) than the normal subjects. There was a significant correlation between A2 D and LV muscle mass index in entire patients with hypertension(r=0.42P<0.01). These data suggest that A2D is the earliest parameter indicating abnormality of LV diastolic function and E/A ratio is not likely to be a definite index of LV diastolic dysfunction but rather be a reliable index of LV hypertrophy in hypertensive patients with preserved LV systolic funtion.
Deceleration ; Echocardiography* ; Echocardiography, Doppler ; Heart Sounds ; Humans ; Hypertrophy

To determine the level of exercise for dynamic exercise echocardiography and to evaluate the changes of cardiac work loads in normal subjects, the authors performed M-mode echocardiography at rest and during 20degrees supine bicycle exercise in 10 normal subjects with good image of left ventricle. A special, self-made 20degrees supine exercise table was used on which the subject's chest could be immobilized to record echocardiograms during exercise. The recordings were always performed just below the tip of the anterior mitral leaflet. Interpretable left ventricular M-mode echocardiograms were obtained at a submaximal exercise level with mean heart rate of 132+/-21 beat/min. Left ventricular end-diastolic dimension, an index of preload, showed no significant change during exersise. But left ventricular end-systolic dimension decreased significantly(p<0.01) and % fractional shortening increased significantly(p<0.01). Peak-systolic left ventricular wall stress increased signficantly(p<0.01) during exercise but end-systolic wall stress did not. Both end-systolic wall stress/end systolic dimension ratio and systolic blood pressure/end-systolic dimension ratio increased during exercise(p<0.01). The results suggest that dynamic exercise echocardiography is a suitable method measuring various parameters of cardiac mechanics during submaximal exercise, whereas it's not available during maximal exercise.
Echocardiography* ; Heart Rate ; Heart Ventricles ; Mechanics ; Thorax ; Ventricular Function, Left*

BACKGROUND AND OBJECTIVES: The relationship of cold pressor, hyperventilation and exercise test responses to circadian patterns and types of angina in vasospastic angina have still not been known. The aim of this study was to identify subgoups of patients who have similar clinical features and provocation test response. MATERIALS AND METHODS: Twenty-one consecutive patients with pure vasospastic angina were studied. Six exercise tests were performed in the early morning, late morning, and late afternoon in consecutive days, and 2 hyperventilation tests and 2 cold pressor tests in the early morning. Circadian distribution and types of angina(at rest, on physical activity or both) were evaluated by clinical history, clinical records and ambulatory ECG recordings during admission and follow-up periods(mean 19+/-9 months). RESULTS: Three patterns of circadian distribution of anginal attacks were identified during all observation periods together(morning and night: MN n=, morning and afternoon or evening: M+/E n=, morning, night and afternoon and/or evening: MN+/E n=1). Exercise test was positive in 36%(40/111) without circadian variation, hyperventilation test in 66%(23/35) and cold pressor test in 6%(2/33). Neither hyperventilation test nor cold pressor test was related to circadian patterns, types or activity of angina, or numbers of spastic artery. But positive exercise test increased significantly in patients with angina on physical activity(43% vs 21%, p<0.05), high activity(57% vs 18%, p<0.01), multivessel spasm(50% vs 27%, p<0.05 ) and circadian patterns of M+/E and MN+/E(29%, 55% vs 4%, p<0.05, p<0.01). All patients with MN had rest angina and single vessel spasm. All 6 patients with M+/E had angina both at rest and on physical activity and 5 single vessel spasm. Eight of 11 patients with MN+/E had angina both at rest and on physical activity and 8 multivessel spasm. CONCLUSION: These findings suggest that hyperventilation test is highly sensitive in vasospastic angina without any relationship to clinical features, but exercise test response is related well to circadian patterns of angina attacks which are associated with characteristic clinical features.
Arteries ; Electrocardiography ; Exercise Test ; Follow-Up Studies ; Humans ; Hyperventilation ; Motor Activity ; Muscle Spasticity ; Spasm

BACKGROUND: The heart rate adjusted ST segment criteria(Delta ST/HR index and rate-recovery loop or R-R loop) compared to standard ST segment criteria may improve the ability of the exercise electrocardiogram for the prediction of severe coronary artery disease and future cardiac events in patients with chronic angina pectoris, but the predictive value of these criteria for predicting these issues has not been studied in patients with acute myocardial infarction. METHODS: 64 patients with first uncomplicated myocardial infarction were studied. All patients performed predischarge(mean 8+/-4 days) symptom-limited exercise test and coronary angiography(mean 11+/-15 days). During the follow-up period(mean 449+/-273 days), the occurrence of the major cardiac events(death, reinfarction, coronary artery bypass surgery) and minor cardiac event(angina, heart failure) were recorded, and then univariate and multivariate analysis of several clinical and exercise variables known to be as prognostic markers were performed. RESULTS: The results are as follows : 1) The sensitivities of Delta ST/HR index and R-R loop(92%, 83% respectively) for predicting multivessel disease showed no significant difference compared to that of standard ST segment criteria(83%). 2) Major cardiac events occurred in 12(20%) of 64 patients and only single independent predictive factor for its prediction was multivessel coronary artery disease(p=0.0001), whereas total cardiac event occurred in 32(50%), multivessel disease(p=0.003), and maximal workload <5mets(p=0.038). 3) For the prediction of total cardiac event, DeltaST/HR index and R-R loop(all 97%) were significantly more sensitive(p<0.05) than standard ST segment criteria(78%), and there was a tendency to increase in specificity in R-R loop(84%) compared to DeltaST/HR index(59%) or standard ST segment criteria(66%). 4) The negative predictive value of all negative test of three ST segment criteria for predicting total cardiac event was 100%. CONCLUSION: Although the heart rate-adjusted ST segment criteria have no advantage over standand ST segment criteria for the prediction of severe coronary artery disease, they can be more useful prognostic markers by enhancing the accuracy of the predischarge exercise electrocardiogram for the prediction of subsequent cardiac events after a first acute myocardial infarction.
Angina Pectoris ; Coronary Artery Bypass ; Coronary Artery Disease ; Coronary Vessels ; Electrocardiography ; Exercise Test* ; Follow-Up Studies ; Heart ; Heart Rate ; Humans ; Multivariate Analysis ; Myocardial Infarction* ; Prognosis ; Sensitivity and Specificity

To investigate relationship between alpha1-acrenoceptors and nicardipine, an 1,4-dihydropyridine calcium antagonist, effects of nicardipine, on phenylephrinne(PE)-induced vasoconstriction in isolated arterial rings and pressor response of rabbits were observed. In normal physiological salt solution(NPSS), 35mM KCI produced persistent contractions of thoracic aorta and carotid artery and the contractions were dose-dependently inhoboted by cumulative admini-stration of nicardipine in the range of doses from 10(-10)M to 10(-4)M, IC50s of nicardipine in the thoracic aorta and carotid artery were 3.3x10(-7)M and 4.6x10(-7)M, respectively and there was no difference between both values. Constant contractions induced by 10(-5)M PE in both rings were inhibited by the same doses of nicardipine in a dose-dependent fashion. The IC50s were 2.8x10(-4)M in thoracic aorta and 2.9x10(-5)M in carotid artery respectively, and the former was about 10 times greater than the latter. In Ca2+ free PSS, KCI did not produce any contractionn. Though constant and reproducible in NPSS, PE-induced contraction was transient and not reproducible in Ca2+ free PSS. The contraction in both rings were weakened to about 70% of those in NPSS. Pretreatment with nicardipine in the range of doses from 10-8M to 10-5M hardly affected the PE-induced contraction and the largest dose 10(-4)M slightly inhibited the contraction. Intravenous injection of nicardipine 10 to 1000microg/kg decreased blood pressure and heart rate of rabbits in a dose-dependent manner. The % decrease of heart rate was much smaller in comparison with the %decrease of blood presseure. Pressor effect of 30microg/kg PE was dose-dependently inhibited after treatment with nicardipine 10 to 1000microg/kg and ID50 was 314microg/kg(6.1x10(-7)mole/kg). Above results suggest that nicardipine blocks extracellulr Ca2+ influx by membrane depolarization and in a part by alpha1-adrenceptors, then relaxes arterial smooth muscles in rabbits.
Aorta, Thoracic ; Blood Pressure ; Calcium ; Carotid Arteries ; Heart Rate ; Inhibitory Concentration 50 ; Injections, Intravenous ; Membranes ; Muscle, Smooth ; Nicardipine* ; Rabbits ; Vasoconstriction

To evaluate the antihypertensive effect, side effects and metabolic changes of arotinolol, a combined alpha and beta blocker, 10-15mg of arotinolol twice a day was administered for 8 weeks in 27 hypertensives (168+/-16/106+/-10mmHg) without heart failure, bradycardia, conduction disturbance, coronary heart disease or renal impairment. Blood pressure decreased to 137+/-10/90+/-6mmHg and average reduction of systolic BP and diastolic BP were 31 mmHg(18%) and 16mmHg(15%) respectively. Pulse rate reduced significantly(p<0.01) after 2weeks' treatment of arotinolol and average reduction of pulse rate was 10 beats/min after 8weeks treatment. There were no significant changes of serum ALP, AST and ALT, BUN, and serum creatinine, Na+, K+, total cholesterol, HDL cholesterol and triglyceride. But in 8 patients(30%), insomina, sleepness, cold extrimities or numbness on extremities developed or aggravated. These results suggest that arotinolol be an useful antihypertensive agent in hypertensives without heart failure, bradyarrhythmais or peripheral vascular disease.
Blood Pressure ; Bradycardia ; Cholesterol ; Cholesterol, HDL ; Coronary Disease ; Creatinine ; Extremities ; Heart Failure ; Heart Rate ; Hypertension* ; Hypesthesia ; Peripheral Vascular Diseases ; Triglycerides