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

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

To evaluate the hypotensive effect of dilevalol which has a nonselective blocking action on beta receptors with selective beta2 agonist actcvity, We performed a prospective clinical study for 8 weeks in 31 patients with essential hypertension(mean age : 52+/-9, mean sitting blood pressure : 158/101mmHg) without concomitant heart failure, coronary heart disease, conduction disturbance or renal impairment. The daily dose of dilevalol was 200-400mg. The results were as follows ; 1) After 8 weeks of treatment with dilevalol, average sitting systolic and diastolic blood pressures reduced to 138+/-8mmHg(13%), 84+/-5mmHg(17%) respectively(p<0.01, 0.01). 2) After 8 weeks of treatment with dilevalol, 28(90%) out of the 31 hypertensives showed good hypotensive effect ie, : sitting diastolic blood pressure decreased to below 90mmHg. 3) Pulse rate decreased slightly from pretreatment average of 75+/-8 beats per minute to 70+/-6 beat per minute at the end of 6 weeks of treatment but went back to pretreatment value lastly. 4) Average body weight, serum levels of total cholesterol, HDL cholesterol, triglyceride, AST, ALT, BUN, creatinine, sodium and potassium were not significantly changed from the pretreatment values. 5) A few side effects in order of frequency were epigastralgia, fatigue, cold extremities and dizziness. These results suggest that dilevalil may be used as an effective first line monotherapeutic antihypertensive agent in mild to moderate hypertensives without significant limitations.
Blood Pressure ; Body Weight ; Cholesterol ; Cholesterol, HDL ; Coronary Disease ; Creatinine ; Dizziness ; Extremities ; Fatigue ; Heart Failure ; Heart Rate ; Humans ; Hypertension* ; Labetalol* ; Potassium ; Prospective Studies ; Sodium ; Triglycerides

Coronary spasm may be induced by a variety of physiologic and pharmacologic stimuli but specific receptor blockade has not been consistently shown to prevent the attacks. Most patients with variant angina respond well to treatment with calcium antagonists and nitrates. A small proportion of patients are refractory to this therapy. We report a case of the patient with a 9-year-history of variant angina who has been refractory to high doses of calcium antagonists and nitrates. The repeated addition of clonidine was consistently effective in abolishing both symptoms and objective evidence of myocardial ischemia in this particular patient.
Calcium ; Clonidine* ; Humans ; Myocardial Ischemia ; Nitrates ; Spasm

BACKGROUND AND PURPOSE: Valproic acid (2-propylpentanoic acid) which enhances GABA synthesis and blocks it's degradation has been useful treatment of migraine and may activate GABA receptors to modulate trigeminal nociceptive neurons innervating the meninges. But the mechanism and action of sodium valproate in headache is not clear. To investigate the mechanism of valproic acid action in headache model, we compared the change of dural plasma protein extravasation in both substance-P neurogenic inflammation rats with valproic acid pretreatment and without valproic acid pretreatment. METHOD: Sprague-Dawely rats were pretreated with valproate 30 minutes prior to substance-P administration in order to test the effects of sodium valproate on dural plasma protein extravasation by detecting the amount of extravasated Evans blue in the dura matter. To examine the abilities of either bicuculine (GABAA antagonist) and phaclofen (GABAB antagonist) to reverse the effect of valproate, they were administered 5 min before valproate administration. After then we also test the effect of muscimol (GABAA agonist) and bicuculine (GABAA antagonist) in substance-P induced neurogenic inflammation rats. RESULTS: Intraperitoneal injection of sodium valproate and muscimol reduced dural plasma protein extravasation after intravenous substance-P administration. The GABAA antagonist bicuculine completely reversed the effect of valproate and muscimol on plasma extravasation following substance-P administration, whereas the GABAB receptor antagonist, phaclofen, did not. CONCLUSION: We concluded that the attenuation of dural plasma protein extravasation by valproate and muscimol is mediated by via GABAA receptors within the meninges. Agonists and modulators at the GABAA receptor may become useful for the development of selective therapeutic agents for migraine headache.
Animals ; Evans Blue ; gamma-Aminobutyric Acid ; Headache* ; Injections, Intraperitoneal ; Meninges ; Migraine Disorders ; Muscimol ; Neurogenic Inflammation ; Nociceptors ; Plasma ; Rats* ; Receptors, GABA ; Sodium* ; Valproic Acid*

To analyze the effects of the characteristics of the systolic anterior motion(SAM) of the mitral valve on the left ventricular outflow pressure gradient and to determine the relation between the anatomical characteristics of the left ventricle and the left ventricular outflow pressure gradient, mitral valve and left ventricular M mode echocardiogram and continuous wave Doppler echocardiogram of the left ventricular outflow tract were recorded in 7 patients with hypertrophic obstructive cardiomyopathy(HOCM), aged 19 to 66 years(mean 37 years). Mitral-septal distance at the closest apposition(S-SAM;1.1+/-2mm), duration of mitral-septal apposition(89+/-20 msec), time interval from the peak of the R-wave to initial apposition of the mitral valve against the interventricular septum(R-SAM interval ; 222+/-32 msec) and left ventricular posterior wall thickness(LVPWT; 1.1+/-0.5mm) were observed on mitral valve and left ventricular M-mode echocardiograms and peak flow velocity in the left ventricular outflow(V-LVOT; 3.5+/-1.5 m/sec) was measured from the Doppler echocardiograms of the left ventricular outflow tract. V-LVOT was correlated significantly with degree of mitral-septal apposition(r=-0.70, p<0.05), duration of mitral-septal apposition(r=0.74, P<0.05), R-SAM interval(r=-0.80, p<0.05) and LVPWT(r=0.78, p<0.05). These results suggest that the closer apposition of mitral valve against interventricular septum, the more prolonged mitral-septal apposition, the earlier onset of SAM of the mitral valve and the thicker the left ventricular posterior wall, the more increase the LV outflow pressure gradient in HOCM.
Cardiomyopathy, Hypertrophic* ; Heart Ventricles ; Humans ; Mitral Valve*

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

BACKGROUND: The diastolic transmitral flow velocity pattern has been commonly used to assess left ventricular(LV) diastolic function. The effects of multiple factors(such as, LV preload, afterload and heart rate, etc.) make difficulties in accurate interpretation. METHODS: In order to investigate the diastolic transmitral filling patterns according to the changes of the proload or heart rate, we studied 27 normal subjects with pulsed Doppler echocardiography after the administration of nitroglycerin(0.6mg/tab.) sublingually or atropine(0.5mg/amp.) intravenously. RESULTS: 1) After nitroglycerin administration, the folowings were obtained. ; The systolic blood pressure and LV diastolic filling time(DFT) decreased by 10.1% and 15.3%, respectively(p<0.001), compared with baseline data. The ratio of peak early to late diastolic transmitral flow velocities (E/A) and time-velocity integrals(TVIE/TVIA) decreased by 10.3% and 14.8%, respectively(p<0.01). The early diastolic filling time(Time E) was unchanged. Therefore, we suggest that time E is helpful, compared with the increments of the preload or the diastolic dysfunction. 2) After atropin administration, the heart rate, peak late diastolic transmitral flow velocity(PA) and percent atrial contribution(%AC) significantly increased by 43.6%, 25.1% and 41.4%, respectively(p<0.001). The E/A, TVIE/TVIA and DFT significantly decreased by 42.9%, 38.9% and 43.0%, respectively(p<0.001) compared to the data before drug administration. 3) The heart rate correlated negatively to the E/A, TVIE/TVIA and DFT. It was correlated positively to %AC(r=+0.63; p<0.001). The normalized E/A ratio by DFT(E/A/DFT) didn't correlate. Therefore, E/A/DFT is helpful on the exclusion of the influences of heart rate by the administration of the atropine. CONCLUSION: The decrement of preload or the increment of heart rate changes the diastolic transmitral flow velocity patterns. Therefore, when the diastolic function is assessed by interpretation of the Doppler transmitral flow velocity pattern with pulsed Doppler echocardiogram, the potential influences of preload and heart rate must be taken into account.
Atropine* ; Blood Pressure ; Echocardiography ; Echocardiography, Doppler* ; Echocardiography, Doppler, Pulsed ; Heart Rate ; Humans* ; Nitroglycerin* ; Time

Torsade de pointes (TdP) is a form of polymorphic ventricular tachycardia that is associated with prolongation of the QT interval. Although it occurs in many clinical settings, torsade de pointes is most commonly caused by drugs. The second generation antihistamines, including terfenadine and astemizole, have little sedation or other adverse effects on the CNS. They have been used widely to treat various allergic diseases, but it has been reported that overdoses or combinations with antifungal agents or macrolide antibiotics may lead to TdP. We report a case of TdP that occured during com-bination therapy of terfenadine and ketoconazole.
Anti-Bacterial Agents ; Antifungal Agents ; Astemizole ; Histamine H1 Antagonists, Non-Sedating ; Ketoconazole* ; Tachycardia, Ventricular ; Terfenadine* ; Torsades de Pointes*

No abstract available.
Coronary Artery Bypass* ; Coronary Vessels* ; Echocardiography*