Search PubMed⌕ Search

Biomedical subjects

K I Lie

Publications and source records attributed to K I Lie.

At least 289 records · Page 16Linked to original sources
PubMed1988

Diltiazem in comparison with metoprolol in stable angina pectoris.

The efficacy of diltiazem in comparison with metoprolol in chronic stable angina was assessed in 33 male patients during a 15-week blind cross-over study. After an initial two-week run-in period, baseline measurements were made. Subsequently, the patients entered a blind cross-over study consisting of two six-week treatment periods with diltiazem 240 mg (60 mg q.i.d.) or metoprolol 200 mg (100 mg b.i.d.). Dose adjustment to either 360 mg diltiazem (120 t.i.d.) or 400 mg metoprolol (200 b.i.d.) was allowed two weeks after the start of treatment. There was a one-week washout period between the two treatment periods. Compared to baseline values both drugs reduced the number of anginal attacks (diltiazem - 55%, P = 0.02; metoprolol - 73%, P = 0.01) and showed improvement of the measured exercise variables (exercise duration: diltiazem + 16%, P less than 0.001; metoprolol + 4%, P = NS; time to angina: diltiazem + 21%, P = 0.02, metoprolol + 14%, P = NS; maximal ST-depression: diltiazem + 13%, P = NS, metoprolol + 33%, P = 0.002). No significant change in LVEF was noticed. Both drugs reduced the mean heart rate on Holter tape (diltiazem - 11%, P = 0.006; metoprolol - 14%, P = 0.004). No effects on conduction were noticed. Although at the borderline of significance, diltiazem increased the total exercise duration as compared to metoprolol (16 vs. 4%, P = 0.05). It is concluded that diltiazem improves exercise tolerance in patients with stable angina pectoris and appears to be a safe and effective alternative to the beta-blocking agent metoprolol.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Acute conversion of atrial fibrillation to sinus rhythm: clinical efficacy of flecainide acetate. Comparison of two regimens.

The efficacy and safety of oral (up to 400 mg in 3 h) and intravenous regimens (up to 150 mg in 10 min) of flecainide acetate were compared in the acute conversion of atrial fibrillation to sinus rhythm. Acute conversion was defined as conversion occurring within 5 h (oral) or within 30 min (intravenous regimen). Following classification in recent onset (duration less than 24 h) atrial fibrillation (n = 27) and chronic (greater than 24 h) atrial fibrillation (n = 13), patients were randomly assigned to one of the two regimens. In the group of patients with recent onset atrial fibrillation, 10 out of 14 (oral treatment) and 10 out of 13 (intravenous treatment) responded acutely. Approximately half of responding patients converted after the first oral dose or within the infusion time. In contrast, no patient with chronic atrial fibrillation showed conversion on flecainide. No serious adverse effects were encountered with the regimens used, not even in patients concomitantly using digitalis or verapamil. Thus, patients with recent onset atrial fibrillation can safely be converted to sinus rhythm using oral or intravenous regimens of flecainide.

Administration, Oral↗
PubMed1987

Acute hemodynamic and hormonal effects of ramipril in chronic congestive heart failure and comparison with captopril.

Acute hemodynamic and hormonal responses to ramipril in comparison with captopril were studied in 10 patients with moderate to severe congestive heart failure in an open, randomized study. Both drugs were given to 5 patients each in 2 increasing doses on 2 successive days. After 5 mg of ramipril angiotensin converting enzyme (ACE) activity was significantly decreased during 24 hours with a maximum decrease 4 hours after administration. Mean arterial blood pressure decreased from 84 +/- 5 to 62 +/- 5 mm Hg at 4 hours and 71 +/- 4 mm Hg at 12 hours, respectively, after this dose. Capillary wedge pressure decreased from 19 +/- 1 mm Hg to 13 +/- 1 mm Hg at 4 hours with a maximum increase in cardiac output from 3.8 +/- 0.3 liters/min to 4.4 +/- 0.3 liters/min at 2 hours. No significant cardiac effects were present 8 hours after administration. After 10 mg of ramipril, cardiac and hormonal effects showed a quicker onset of action and longer duration compared with the 5 mg dose. Mean arterial pressure decreased to 61 +/- 6 mm Hg. Similar effects were seen after captopril, but with a significantly shorter duration. Mean arterial pressure decreased from 82 +/- 4 mm Hg to 64 +/- 5 mm Hg after 12.5 mg and to 58 +/- 6 mm Hg after 25 mg of captopril. In patients with congestive heart failure ramipril has the hemodynamic profile of a long-acting and potent ACE inhibitor. Significant cardiac effects are present during 4 to 8 hours and ACE activity is still significantly inhibited 24 hours after a single dose of ramipril.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Prevalence of antibody to Chlamydia trachomatis in spontaneous abortion and infertility.

A higher prevalence of Chlamydia trachomatis antibody occurred in 57.6% of women with recurrent abortion, but not in their male partners, compared to 33.7% of normal pregnant women (p less than 0.01) and 44.2% of infertile women (NS). The mean titer for the recurrent abortion group was not significantly elevated, compared to controls. Women with blocked fallopian tubes had the highest prevalence of elevated titers (p less than 0.01) and the highest mean titer (p less than 0.001). Despite multiple testing, no women or men were chlamydia culture-positive. The lack of isolation among patients with antibody could be due to cryptic infection at a site not amenable to culture or to inhibition by secretory IgA. There could also be nonspecific stimulation of chlamydial antibody caused by other infections such as mycoplasma. The presence, though at a low level, of antibody in culture-negative patients suggests chlamydia may not be directly associated with recurrent abortion but reflect previous exposure to chlamydia or an altered immune system.

Abortion, Habitual↗
PubMed1987

Comparison of the effects of two doses of bisoprolol on exercise tolerance in exercise-induced stable angina pectoris.

Recently, bisoprolol has been investigated regarding its effects on exercise tolerance and the duration of action in patients with coronary heart disease (CHD) following single oral administration. It appears, however, that the extent of effects of 5 mg bisoprolol is not fully established yet. Therefore, the effects of 5 and 10 mg bisoprolol and the duration of action were assessed in 12 patients (10 male, 2 female; mean age 60.2 years) with stable angina pectoris due to CHD after repeated administration. Patients were given 5 or 10 mg bisoprolol once daily for 2 weeks according to a double-blind, randomized cross-over design. At entry one exercise tolerance test (ETT) served as baseline measurement and following each treatment period ETTs were performed before (24-hour value) and 3 hours after tablet intake. Exercise capacity (in W X min) was calculated until the onset of angina, 0.1 mV ST-segment depression and at peak exercise. Compared to baseline all workload values during active therapy were significantly improved (P less than or equal to 0.05) except for the workload till onset of angina with bisoprolol 5 mg at 24 hours. The effects at 3 hours were significantly stronger than those after 24 hours for both dosages. Significantly stronger effects were observed 3 hours as well as 24 hours after intake during treatment with 10 mg compared to 5 mg: at peak exercise on heart rate (P less than or equal to 0.05) and exercise capacity (P less than or equal to 0.01), at identical workload on heart rate (P less than or equal to 0.01) and rate-pressure product (P less than or equal to 0.01). It was found that bisoprolol 5 mg once daily leads to therapeutic effects with a clearly maintained duration of action over 24 hours, but further increase of peak exercise capacity may be achieved with 10 mg.

Administration, Oral↗
PubMed1987

Orthodromic pacemaker circus movement tachycardia.

We report on the case of a 33-year-old woman with sick sinus syndrome who had an orthodromic pacemaker circus movement tachycardia (PCMT), with antegrade atrioventricular (AV) conduction and a retrograde pathway by means of a DDD (AV universal) pacemaker. This PCMT was provoked and sustained by premature ventricular contraction-synchronous atrial stimulation (PVC-SAS), which is a new feature for the prevention of antidromic PCMTs. The conditions for occurrence of this tachycardia were: PVC-SAS; atrial undersensing; first degree AV block. Recommendations for prevention of this pacemaker-mediated tachycardia are given.

Adult↗
PubMed1986

Effects of nifedipine on left ventricular performance in unstable angina pectoris during a follow-up of 48 hours.

In 1981, a large, double-blind, randomized, multicenter trial was started in The Netherlands to evaluate the therapeutic effects of nifedipine or metoprolol in patients with unstable angina. This study, called the Holland Interuniversity Nifedipine Trial (HINT), included several hundred patients to establish potential therapeutic effects. From December 1982 until January 1984 the effects of nifedipine on left ventricular (LV) performance in a subgroup of 37 HINT patients were studied using radionuclide techniques. All patients (18 treated with nifedipine, 19 with placebo) underwent radionuclide angiography and 33 underwent thallium-201 scintigraphy just before and 48 hours after the start of treatment with the experimental medication. Radionuclide angiographic studies were also performed 1 hour (29 patients) and 4 hours (31 patients) after the start of treatment. The thallium-201 images showed defects in 24 (73%) of the baseline images and in 21 (64%) of the 48-hour images. No significant differences were seen between patients receiving nifedipine or placebo in the incidence of new defects or in the disappearance of defects at 48 hours. Changes in thallium-201 images were not related to recurrence of myocardial ischemia or the development of acute myocardial infarction. Nineteen of the 37 patients (51%) with baseline blood pool images had a reduced LV ejection fraction (EF) (38 +/- 10%) and 18 patients (49%) had a normal LVEF of 56 +/- 5%. LVEF improved after 48 hours in 8 patients receiving nifedipine and in only 1 patient receiving placebo (p less than 0.02). This effect was not present at 1 and 4 hours after treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1986

Influence of nifedipine on left ventricular perfusion and function in patients with unstable angina: evaluation with radionuclide techniques.

In 1981, a large, double-blind, randomized trial was started in The Netherlands to evaluate the therapeutic effects of nifedipine and/or metoprolol in patients with unstable angina. This study has been called the Holland Interuniversity Nifedipine/metoprolol Trial (HINT) and required several hundred patients to establish potential therapeutic effects. From December 1982 to January 1984 the effects of nifedipine on left ventricular (LV) performance in a subgroup of 52 HINT patients were studied using radionuclide techniques. All patients (23 on nifedipine, 29 controls) underwent thallium-201 scintigraphy or radionuclide angiography just before and 48 h after the start of experimental medication. The radionuclide angiographic studies were also performed at 1 and 4 h after treatment. Nifedipine did not influence the incidence or disappearance of perfusion defects on the 48-h thallium images. No significant differences in overall LV ejection fraction (EF) were seen at any time between nifedipine-treated patients and controls. However, paired observations in 37 patients showed improvement of LVEF after 48 h in 8 patients on nifedipine and in only 1 control patient. Scintigraphic measurements on admission were not related to clinical outcome after 48 h. Concomitant administration of metoprolol did not influence LVEF in either group. It is concluded that nifedipine improves LVEF after 48 h in a subset of patients with unstable angina without affecting myocardial perfusion. This finding indicates that nifedipine has a predominant effect on afterload reduction in patients with unstable angina. However, early scintigraphic measurements had no significant predictive value for subsequent cardiac events.

Angina Pectoris↗
PubMed1986

Intractable ventricular tachycardia in a patient with giant cell myocarditis, thymoma and myasthenia gravis.

A 48-year-old man presented with a malignant thymoma in combination with myositis, myasthenia gravis, a giant cell myocarditis and recurrent intractable ventricular tachycardias. Despite various therapies (chemical, electrical and surgical), arrhythmias supervened in the presence of a normal coronary arteriogram. Active myocarditis was believed to be the mechanism of the ventricular tachycardias.

Granuloma, Giant Cell↗
PubMed1986

Intrinsic sympathomimetic activity (ISA) of pindolol in patients with sinus node dysfunction.

The effects of pindolol treatment on mean heart rate (MHR) and the number of paced heart beats were investigated in a group of 12 patients, with frequency programmable pacemakers implanted to control symptomatic bradyarrhythmias resulting from sinus node dysfunction. In a randomized double blind cross over experiment the patients were treated with pindolol (5 mg t.i.d.) or with placebo. Before the study the pacemaker was programmed to its lowest frequency in the demand mode. In the pretreatment period and after 2 weeks treatment with either pindolol or placebo a 24-hour ambulatory ECG was recorded. MHR during the night (24.00-8.00) was slightly but significantly increased by pindolol treatment by 6.0% when compared to placebo (P less than 0.05). There was no difference in the daytime MHR during either treatment period. During pindolol treatment the number of paced beats was reduced in 8/12 patients and in 4 of these the reduction exceeded 98%. In 2 patients the number of paced beats increased. The results indicate that in some patients with sinus node dysfunction pindolol can effectively reduce the number of paced beats thereby preserving the atrial contribution to pump function.

Adult↗
PubMed1985

Combination of metoprolol with molsidomine in the treatment of angina pectoris.

In a randomized controlled trial 31 patients, who were unsuccessfully being treated with metoprolol for severe angina pectoris, were also given molsidomine or placebo. During an exercise test, there was no difference between the groups in heart rate or blood pressure. There was a tendency towards a mild, significant improvement in exercise performance in the molsidomine-treated group, in whom both workload and exercise duration increased after two weeks of treatment. In the placebo-treated group, these parameters decreased.

Aged↗
PubMed1985

Lidocaine and prevention of ventricular fibrillation complicating acute myocardial infarction.

Prehospital prevention of primary ventricular fibrillation using 400 mg lidocaine i.m. may be effective in subjects aged under 70, but routine administration is not yet recommended since mortality was unaffected. Although in-hospital prevention of ventricular fibrillation can be achieved by routine i.v. administration of lidocaine in rather high dosages, this regimen is still controversial in well-equipped CCUs in view of conflicting results on mortality.

Aged↗
PubMed1985

Left ventricular performance in unstable angina: assessment with radionuclide techniques.

In a clinical trial we studied left ventricular performance at rest in 50 patients with unstable angina by radionuclide techniques. Thallium-201 scintigraphy was performed on admission in 38 patients and repeated after 48 hr in 32 patients. Also dynamic blood pool scintigraphy was performed in 37 patients on admission and in 45 patients after 48 hr. Of the 50 patients, 27 (54%) had no recurrent episodes of myocardial ischemia, but 23 (46%) patients showed recurrent ischemic episodes of whom 11 (22%) patients developed a myocardial infarction. The thallium-201 images showed perfusion defects in 27 (71%) of the 38 patients studied on admission and in 20 (63%) of the 32 patients studied at 48 hr. No relation between clinical outcome and presence or absence of defects was observed. Left ventricular ejection fraction was abnormal (less than 50%) in 19 (51%) of the 37 patients on admission and in 29 (64%) of the 45 patients studied at 48 hr. As with thallium-201, no relation could be established between clinical outcome and left ventricular ejection fraction. It is concluded that radionuclide techniques are useful to provide insight into the pathophysiological mechanism of unstable angina, but they are not helpful for the short-time assessment of clinical outcome.

Angina Pectoris↗
PubMed1985

Quantification of myocardium at risk in unstable angina: comparison of patients with and without previous infarction.

We studied two subgroups of patients with unstable angina pectoris: 35 without (Group A) and 73 with (Group B) previous myocardial infarction. The severity of coronary artery disease was assessed by means of a previously described scoring system. This scoring system was used to calculate the proportion of left ventricular myocardium fed by significantly (greater than 75% luminal area reduction) stenosed coronary arteries (called percent myocardium threatened). To estimate the amount of myocardium lost by previous infarction we used a four-point wall motion score for each of seven left ventricular wall segments: a value of 2 was given to normokinetic segments, 1 for hypokinetic segments, 0 for akinetic and -1 for dyskinetic segments. The deficit in wall motion score was used to estimate the amount of myocardium infarcted. This was then subtracted from the proportion of myocardium threatened to yield the proportion of myocardium still in jeopardy. We found a different extent and severity of coronary artery disease between the two subgroups. In the group without previous infarction, the numbers of patients with one-, two- and three-vessel disease were 15, 9, and 11, respectively (or 43, 26, and 31%). In those with a previous infarction, the respective numbers were 11, 23, and 39 (or 15, 31.5, and 53.5%). This difference is statistically significant (P less than 0.01). The mean number of stenotic arteries was 1.9 +/- 0.9 in the patients without previous infarction and 2.4 +/- 0.7 in those with an infarction (P less than 0.05). Using the above-mentioned scoring system the score was 3.2 +/- 1.4 in patients without previous infarction and 4.0 +/- 1.6 in those with previous infarction (P less than 0.05). The percent myocardium threatened was 53.6 +/- 24.1 vs. 68.7 +/- 24.7 (P less than 0.01). Wall motion score was 13.8 +/- 0.6 in Group A and 10.6 +/- 3.1 in Group B (P less than 0.01), which gives values for the proportion of myocardium infarcted of 1.6 +/- 4.2 and 24.2 +/- 22.0%, respectively. The percentage still in jeopardy (after subtracting that infarcted from that threatened) was 51.8 +/- 22.7 in those without and 44.2 +/- 31.1 in those with a previous infarction: this difference is not statistically significant. We conclude that patients with unstable angina pectoris who have sustained a previous myocardial infarction have more severe coronary artery disease than similar patients without previous infarction. The amount of left ventricular myocardium still in jeopardy of becoming infarcted is, however, the same.

Aged↗