ABSTRACT
BACKGROUND: This study was designed to evaluate the safety and the efficacy of fosinopril(Monopril(R)) in the treatment of mild to moderate essential hypertension. METHOD: Fosinopril(10mg) once a day was administrated as a starting dose in 20 patients with essential hypertension in the morning and a one step upward titration was performed(fosinopril 20mg once a day, after 4 weeks treatment). RESULT: After 2 weeks treatment with dose of 10mg, the systolic blood pressure(SBP) was decreased(183.8+/-28.5 vs, 161.5+/-25.9mmHg, p<0.05) and the diastolic blood pressure(DBP) was also decreased significantly(108.3+/-9.3 vs, 96.6+/-10.3mmHg, p<0.05). The effect of fosinopril were maintained. The SBP an DBP were decreased in 14 out of 20 patients till 8 weeks. There was no significant change in heart rate before and after fosinopril treatment(74.3+/-10 vs, 76.4+/-7.9beats/min). Fosinopril had no significant effects on laboratory findings such as serum creatinin, BUN, AST/ALT, WBC, Platelet and lipid profiles. Mild dry coughing was noticed only in 5 patients and it did not disturb continuing medication. CONCLUSION: Fosinopril is an effective antihypertensive agent, as monotherapy once a day in patients with mild to moderate hypertension.
Subject(s)
Humans , Blood Platelets , Cough , Fosinopril , Heart Rate , HypertensionABSTRACT
BACKGROUND: In previous study, hypertensive patients with left ventricular diastolic dysfunction showed delayed relaxation time intervals and increased relaxation nonuniformity of regional wall motion. In this point of view, the effects of amlodipine on the regional wall motion and mitral flow patterns were evaluated. METHODS: Before and 32weeks after the antihypertensive medication of amlodipine, M-mode & Doppler echocardiogram were performed in 14 patients with moderate hypertension. We measured A2 to the peak thinning rate point of left ventricular(LV)posterior wall [A2-(-)dpw/dt] and the peak lengthening rate point of mitral annulus [A2-dL/dt] on M-mode echocardiogram and we defined nonuniformity as the time interval, (-)dpw/dt-dL/dt. RESULTS: 1) Mitral flow velocity E/A ratio was increased (0.95+/-0.4 vs 1.42+/-0.6, p<0.05) after amlodipine medication. 2) Heart rate and LV posterior wall thickness was decreased (79+/-9.3 vs 72+/-10.8 beats/min, 10.7+/-1.5 vs 9.4+/-2.0mm, p<0.05 respectively). 3) Long axis relaxation was improved (A2-dL/dt ; 165+/-44 vs 140+/-23msec, p<0.05) and nonuniformity index was decreased ((-)dpw/dt-dL/dt ; 63+/-49 vs 41+/-30msec p=0.07). CONCLUSION: Amlodipine improved E/A ratio of mitral flow (E/A ratio) in hypertensive patients with diastolic dysfunction, which could be attributed to the decreased heart rate, the decrease in wall thickness and the improvement in relaxation movement of LV long axis.
Subject(s)
Humans , Amlodipine , Axis, Cervical Vertebra , Heart Rate , Hypertension , RelaxationABSTRACT
BACKGROUND: Viral myocarditis is considered as a cause of dilated cardiomyopathy. At present, two pathogenic mechanisms may be involved in the pathogenesis of viral myocarditis and subsequent cardiomyopathy. First, the virus infection of myocyte may directly lead to either cell death or persistent metabolic dysfunction. Second, virus-induced immune or autoimmune mechanism may play a role. METHODS: To test the therapeutic efficacy of immunosuppression with cyclophophamide(CYP) on coxsackievirus B3(CB3) myocarditis, 10-14 week-old Balb/c mice were inoculated with 4000 plaque-forming units of CB3. In experiment 1, CYP (100mg/kg/day subcutaneous injection, s.c) was administrated daily on days 1-7(group 2, n=16). In experiment 2, CYP 30mg/kg/day s.c(group 3, n=32) or CYP 100mg/kg/day s.c(group 4, n=32) were administrated on days 8-14. The animals of infected controls(group 1, n=26) and group 2, 3, 4 were dissected at days 4, 7, 15, 22 and spleen, heart, thymus and body weights were measured. RESULTS: In experiment 1. survival rate in group 2 on day 7, 15 were low compared with group 1(85%, 0% vs 100%, p<0.05). and myocardial virus titers in group 2 on day 4 was 50 times, and on day 7, 1000 times higher compared with group 1, Histologically, on day 7, focal cellular infiltrations were prominent findings in group 1, but diffuse myocardial necrosis without cellular infiltration were observed in group 2. In experiment 2, survival rate, cardiac histopathology myocardial virus titer and serum neutralizing antibody titers did not differ among groups 1, 3 and 4. In experiment 1 and 2, the spleen-to-body-weight and thymus-to-body-weight ratios were significantly lower in CYP treated groups than those in controls and marked cellular depletions in spleens and thymus were observed in CYP treated groups. CONCLUSIONS: As the results of above, it can be concluded that the immunosuppression during viremic phase of murine viral myocarditis aggravated the myocardial necrosis, and during aviremic phase, the administration of CYP didnot affect the process of viral myocarditis. Thus, direct viral mechanisms in the production of cardiomyocyte injury in CB3-infected mice appear to bo more important than cell mediated immune mechanism. To understand relevant pathogenic mechanisms of clinical myocarditis and dilated cardiomyopathy resulting from viral infection, the experimental study expanding into nonmurine animals and into various models using other infectious agents may be required.
Subject(s)
Animals , Mice , Antibodies, Neutralizing , Body Weight , Cardiomyopathies , Cardiomyopathy, Dilated , Cell Death , Cyclophosphamide , Heart , Immunosuppression Therapy , Injections, Subcutaneous , Muscle Cells , Myocarditis , Myocytes, Cardiac , Necrosis , Spleen , Survival Rate , Thymus Gland , Viral LoadABSTRACT
BACKGROUND: To evaluate the safety and the efficacy of amlodipine, a dihydropyridine calcium antagonist, monotherapy in the treatment of moderate essential hypertension. METHOD: Amlodipine 5mg once a day was administered as a starting dose in 30 patients with essential hypertension in the morning and a one step upward titration was performed (amlodipine 10 mg once a day) was done at the end of 4weeks treatment. Final evaluation was done at 12weeks with laboratory test and echocardiogram. RESULT: Within 4weeks treatment with dose of 5mg amlodipine once a day, the systolic blood pressure (SBP) was decreased(184.5+/-23.3/150.5+/-16.0mmHg,p<0.000), and the diastolic blood pressure(DBP) was also decreased significantly (109.9+/-04.6/92.3+/-11.5mmHg, P<0.001). After 12 weeks of treatment with a mean dosage of 6.6mg once a day, SBP and DBP was maintained comparing with basal level (147.0+/-15.8/88.1+/-0.9mmHg, respectively). The efficacy of amlodipine treatment was noted an excellent in 16 patients(53.3%), good in 4 patient(13.3%), fair in 4 patients(13.3%), and failed in 2 patients(6.7%). There was no significant change in heart rate before and after amlodipine treatment. (80.0+/-2.3/80.9+/-10.4 beats/minute n.s). Amlodipine had not significant effects on laboratory findings such as serum creatinine, BUN, ALT/AST, hemoglobin, leukocyte count,platelet and lipid profiles. There was facial flushing 2 patients, but no need to discontinue administration of amlodipine and all patients completed for 12weeks therapy. CONCLUSION: It is concluded that amlodipine is an effective antihypertensive agent, as monotherapy once a day in patients with moderate essential hypertension.