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Biomedical subjects

K I Lie

Publications and source records attributed to K I Lie.

At least 145 records · Page 8Linked to original sources
PubMed1995

Exploratory study of the effects of single doses of isomazole on hemodynamics and heart rate variability parameters in chronic heart failure.

Ventricular arrhythmias and disturbed autonomic control, as reflected by abnormal heart rate variability (HRV), are related to hemodynamic impairment in chronic heart failure (CHF). We investigated the effects of orally (p.o.) administered isomazole, a new phosphodiesterase (PDE) inhibitor with calcium-sensitizing properties, on hemodynamics, ventricular arrhythmias, and HRV and examined a possible interaction between these parameters. Hemodynamic measurements and ambulatory ECG monitoring were performed in 12 patients with stable CHF class III-IV after single doses of isomazole 5-30 mg. Pulmonary wedge pressure decreased after 5, 10, 20, and 30 mg, but cardiac output, (CO) increased only after the higher doses [20 mg, + 20% (p = 0.031)] of isomazole. HR did not change. Mean arterial and pulmonary artery pressure, (MAP, PAP) decreased significantly in the 10- and 20-mg groups [10 mg, -6% (p = 0.035) and -14% (p < 0.001) respectively; 20 mg, -13% (p = 0.047) and -31% (p = 0.006), respectively]. Isomazole did not exert a significant effect on ventricular arrhythmias in the subsequent 24 h after acute dosing. Analysis of HRV showed that rMSSD and pNN50 (parameters of vagal tone) tended to increase after isomazole administration. Normalized high-frequency power during the day increased from 17.4 to 22.3 nu (p < 0.05), whereas low frequency tended to decrease from 52.7 to 48.2 nu (p = 0.06). Acute isomazole administration improves hemodynamics but has no effect on ventricular arrhythmias. The HRV variability data suggest development of an increase in vagal control of HR, parallel to the acute hemodynamic improvement after isomazole. Withdrawal of vagal control of HR in CHF may be a reversible process.

Administration, Oral↗
PubMed1995

Effects of spirapril and captopril on regional blood flow in chronic congestive heart failure: a comparison between a short- and a long-acting angiotensin-converting enzyme inhibitor.

Spirapril is a new angiotensin-converting enzyme (ACE) inhibitor with a long duration of action. To determine whether duration of inhibition of serum ACE activity may affect regional blood flow (RBF), we compared spirapril with captopril, an ACE inhibitor with a short duration of action. Both the short- and long-term effects were studied in patients with mild to moderate congestive heart failure (CHF). Calf, renal, and hepatic BF measurements were performed in the morning before intake of the study medication; 24 h after the previous dose of spirapril (n = 9 patients) and 12 h after the previous dose of captopril (n = 9 patients). Serum ACE activity after 1, 6, and 12 weeks was significantly reduced in patients receiving spirapril, but not in those receiving captopril. The decrease in mean arterial pressure (MAP) was more pronounced in the spirapril group. Calf BF showed a slight but not significant increase in both spirapril- and captopril-treated patients. Effective renal BF increased significantly only in patients treated with spirapril. Although filtration fraction (FF) tended to decrease in the spirapril group, the decrease was significant only in the captopril group. No changes were observed in hepatic BF. Cerebral BF (CBF) measurements were performed after intake of the first dose of study medication and after 12 weeks, immediately after drug intake. Significant reduction in MAP in the two treatment groups both after the first dose and after 12 weeks did not affect CBF. Despite a significantly prolonged decrease in MAP and serum ACE activity in spirapril-treated patients, no marked differences in RBF were noted between the two ACE inhibitors.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Renal and systemic hemodynamic effects of ibopamine in patients with mild to moderate congestive heart failure.

To study the hemodynamic and renal effects of the orally (p. o.) active dopamine (DA) agonist ibopamine, we examined 10 patients with mild to moderate congestive heart failure (CHF), who were stable while treated with digoxin and diuretics. All patients were in New York Heart Association (NYHA) functional class II-III; their mean age was 63 years (range 51-79 years), and mean left ventricular ejection fraction (LVEF) was 28% (range 18-36%). The protocol consisted of a control study-day with measurements of renal characteristics including glomerular filtration rate (GFR), effective renal plasma flow (ERPF), and filtration fraction (FF). One week later, systemic and renal hemodynamics were measured simultaneously before and after patients received one 100-mg tablet of ibopamine. Ibopamine caused a slight but significant increase in both ERPF (from 288 +/- 32 ml/min/1.73 m2 at baseline to 316 +/- 32 ml/min/1.73 m2 after ibopamine) and GFR (from 77 +/- 8 to 85 +/- 8 ml/min/1.73 m2; both p < 0.05); FF was not affected (mean value 0.26 +/- 0.02). Sodium excretion was not influenced by ibopamine, but diuresis increased significantly. Cardiac output (CO) increased significantly (from 4.0 +/- 0.4 L/min at baseline to a maximum of 5.0 L/min after ibopamine, p < 0.05), mainly due to decreased systemic vascular resistance (SVR). Heart rate (HR) and blood pressure (BP) were unchanged throughout the studies. The percentage of contribution of CO to renal blood flow (RBF) was not significantly affected by ibopamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

Comparative effects of diltiazem and lisinopril on left ventricular structure and filling in mild-to-moderate hypertension.

The comparative effects on echocardiographically determined left ventricular (LV) mass and pulsed Doppler derived indexes of LV diastolic filling were studied in previously untreated hypertensive patients after 6 months of treatment with diltiazem 300 mg once daily (o.d.) (n = 16), and lisinopril 20 mg o.d. (n = 20). LV mass index decreased in the lisinopril group (from 98 to 96 g/m2; mean difference after 6 months of treatment with diltiazem-lisinopril was 13.7 g/m2 [95% confidence interval (CI) 0.8 to 26.6, p < 0.05]. In both groups diastolic filling parameters improved, but there was no statistically significant difference between the groups. Both treatment regimens showed a similar decrease in office and maximal exercise systolic blood pressure (SPB). Ambulatory daytime BP was lower after lisinopril treatment (from 147/96 to 126/83 mm Hg) than after diltiazem treatment (from 142/93 to 135/87 mm Hg); mean difference between diltiazem and lisinopril after 6 months of treatment was 9.7 (95% CI 3.4 to 16.0, p < 0.05)/9.4 (95% CI 2.5 to 16.3, p < 0.05) mm Hg. Nighttime BP decreased from 129/81 to 113/70 mm Hg in the lisinopril group, but not in the diltiazem group (from 125/79 to 122/77 mm Hg); mean difference between diltiazem and lisinopril after 6 months of treatment was 4.4 (95% CI - 0.2 to 8.9)/6.6 (95% CI 1.1 to 12.0) mm Hg. Changes in diastolic filling parameters were significantly correlated with changes in LV mass index in the lisinopril group, suggesting that the improvements in diastolic filling in the diltazem group may be partly due to an effect on factors other than LV mass.

Adult↗
PubMed1995

Increased dispersion of refractoriness in the absence of QT prolongation in patients with mitral valve prolapse and ventricular arrhythmias.

BACKGROUND: The mechanism responsible for the reported high incidence of ventricular arrhythmias in mitral valve prolapse is not clear. Electrocardiographic studies show an increased occurrence of repolarisation abnormalities on the 12 lead surface electrocardiogram, indicating regional differences in ventricular recovery. The purpose of this study was to investigate whether dispersion of refractoriness was an arrhythmogenic mechanism. METHODS: QT dispersion was measured in 32 patients with echocardiographically documented mitral valve prolapse and ventricular arrhythmias on 24 hour Holter recordings. QT dispersion was defined as the difference between the maximum and minimum average QT interval in any of the 12 leads of the surface electrocardiogram. QT dispersion corrected for heart rate was calculated by Bazett's formula. The results were compared with the data from 32 matched controls without a history of cardiac disease. Patients taking drugs that influence the QT interval and patients with a QRS duration > 120 ms were excluded. RESULTS: QT dispersion was greater in patients with mitral valve prolapse than in matched controls (60 (20) v 39 (11 ms) respectively, P < or = 0.001) as was corrected QT (64 (20 ms) v 43 (12 ms) respectively, P < or = 0.001). There was no significant difference in minimum or maximum QT intervals between the two groups. CONCLUSIONS: QT dispersion on the 12 lead surface electrocardiogram was greater in patients with mitral valve prolapse with ventricular arrhythmias than in normal controls, but the maximum QT interval was not increased. The results accord with the hypothesis that regional shortening and lengthening of repolarisation times in patients with mitral valve prolapse may account for the increased dispersion of refractoriness.

Arrhythmias, Cardiac↗
PubMed1995

Differential autonomic mechanisms underlying early morning and daytime transient myocardial ischaemia in patients with stable coronary artery disease.

OBJECTIVES: To see whether autonomic regulatory mechanisms play a part in transient myocardial ischaemia in patients treated with beta blockers. DESIGN: Prospective study. SETTING: Outpatients' clinic. PATIENTS: 51 consecutive patients with angiographically documented coronary artery disease, stable angina, and transient myocardial ischaemia despite beta blockade. INTERVENTIONS: 24 hour ambulatory electrocardiographic monitoring for analysis of variability in ST depression and heart rate. MAIN OUTCOME MEASURES: Numbers of episodes of ischaemia, with an ST depression of > or = 0.1 mV 80 ms after the J point that lasted > or = 60 s at an interval of > or = 60 s from a previous ischaemic episode. Heart rate at onset of ischaemia. Normalised spectral analysis of heart rate variability; ratio of low to high frequency power to assess the sympathovagal balance. RESULTS: Despite treatment, 258 episodes of transient ischaemia were recorded. At heart rates at onset of ischaemia of < 70 beats per minute a high ratio of low to high frequency power accompanied the ischaemic events and was paralleled by a remarkably reduced high frequency power. The high ratio--that is, enhanced sympathetic tone during ischaemia--was mainly found in the early morning. By contrast, ischaemic episodes with heart rates at onset of > or = 70 beats per minute were not associated with significant changes in the parameters of autonomic function. CONCLUSIONS: During beta blockade the residual transient ischaemia is associated with decreased variability in heart rate. In particular, in ischaemic episodes with a low heart rate at onset the neural regulation of the heart plays a part. Apparently, variability in heart rate is not sufficiently modified by beta blockers to prevent all ischaemia. The ischaemia related change in the autonomic nervous system during the early morning is in agreement with previous studies, showing increased cardiovascular risk at this time of the day.

Adrenergic beta-Antagonists↗
PubMed1995

Effect of exercise on cycle length in atrial flutter.

OBJECTIVE: To examine the effect of exercise on cycle length in atrial flutter. PATIENTS: 15 patients with chronic atrial flutter. Seven patients were taking digoxin and six verapamil; two were not taking medication. METHODS: All patients underwent bicycle ergometry. Flutter cycle length was measured at rest and at peak exercise. RESULTS: Mean flutter cycle length increased from 245 ms to 256 ms (P = 0.002). Six patients developed 1:1 atrioventricular conduction. Significant increases in flutter cycle length were observed irrespective of development of 1:1 atrioventricular conduction and use of digoxin and verapamil. CONCLUSION: Exercise prolongs flutter cycle length. This effect would promote development of 1:1 atrioventricular conduction during exercise, causing inordinately high ventricular rates.

Adult↗
PubMed1995

Favourable outcome in idiopathic ventricular fibrillation with treatment aimed at prevention of high sympathetic tone and suppression of inducible arrhythmias.

OBJECTIVE: In the absence of an obvious cause for cardiac arrest, patients with idiopathic ventricular fibrillation are difficult to manage. A subset of patients has inducible arrhythmias. In others sympathetic excitation plays a role in the onset of the cardiac arrest. This study evaluates a prospective stepped care approach in the management of idiopathic ventricular fibrillation, with therapy first directed at induced arrhythmias and secondly at adrenergic trigger events. SETTING: University Hospital. PATIENTS: 10 consecutive patients successfully resuscitated from idiopathic ventricular fibrillation. INTERVENTIONS: Programmed electrical stimulation to determine inducibility, followed by serial drug treatment. Assessment of pre-arrest physical activity and mental stress status by interview, followed by beta blockade. Cardioverter-defibrillator implantation in non-inducible patients not showing significant arrest related sympathetic excitation. MAIN OUTCOME MEASURE: Recurrent cardiac arrest or ventricular tachycardia. RESULTS: Five patients were managed with serial drug treatment and four with beta blockade. In one patient a defibrillator was implanted. During a median follow up of 2.8 years (range 6 to 112 months) no patient died or experienced defibrillator shocks. One patient had a recurrence of a well tolerated ventricular tachycardia on disopyramide. CONCLUSIONS: Idiopathic ventricular fibrillation may be related to enhanced sympathetic activation. Prognosis may be favourable irrespective of the method of treatment. Whether the present approach enhances prognosis of idiopathic ventricular fibrillation remains to be determined. However, it may help to avoid potentially hazardous antiarrhythmic drugs or obviate the need for implantation of cardioverter-defibrillators.

Adult↗
PubMed1995

Oral ibopamine substitution in patients with intravenous dopamine dependence.

In a prospective open study we evaluated whether intravenous dopamine infusions can be safely switched to enterally administered ibopamine in dopamine-dependent patients. Six patients defined as being clinically stable, normovolaemic, but dopamine dependent, i.e. with repeated inability to stop intravenous dopamine, were included. Ibopamine was administered via a nasogastric or nasoduodenal tube. During the initial 48-hour period of ibopamine administration the dopamine infusion was gradually decreased and then discontinued. Arterial blood pressure was continuously recorded via a 20-gauge cannula in the radial artery. Urine output was measured each hour. In all 6 patients it was possible to decrease and then discontinue the dopamine infusion whilst maintaining haemodynamic stability and an appropriate diuresis. It was then possible to discharge the patients from the intensive care unit. Normovolaemic, clinically stable but dopamine-dependent patients may be weaned off intravenous dopamine by substitution of enterally administered ibopamine, allowing discharge from the intensive care unit.

Administration, Oral↗
PubMed1995

Thrombolytic therapy of right heart emboli-in-transit.

Currently, no consensus exists for the appropriate treatment of echocardiographically diagnosed mobile right heart masses giving rise to a high suspicion of migrant thromboembolism in patients with pulmonary embolism. This may lead to unnecessary delay in the implementation of the most appropriate treatment for these patients. Several earlier studies have supported the beneficial role of thrombolytic therapy. We report on an additional two patients with mobile right heart thromboemboli, refractory to systemic anticoagulation, who recovered quickly after initiation of thrombolytic therapy.

Aged↗
PubMed1995

Does the potential for development of streptokinase antibodies change the risk-benefit ratio in older patients?

In patients with acute myocardial infarction (MI), quick initiation of thrombolytic therapy is the best strategy for improvement of survival and reduction of morbidity. Streptokinase, a purified product of haemolytic streptococci, is the most commonly administered agent. The compound anistreplase (a complex of streptokinase to plasminogen), is available but currently not often used. The non-antigenic competitor for these two compounds for the indication of MI is alteplase (recombinant tissue plasminogen activator, rt-PA). Due to former use of streptokinase or its derivative anistreplase, patients may develop specific antibodies to the foreign protein, whereas cross-reacting antibodies may be due to streptococcal infections. These antibodies may neutralise streptokinase or its derivative in case of (re)administration and may mediate adverse events, sometimes serious. Since advanced age by itself is certainly not a contraindication to thrombolytic therapy, and because reinfarction occurs frequently, the benefit-risk ratio of re-exposure to streptokinase or its derivative is decreased in the elderly who present with reinfarction. In the framework of tailored thrombolytic therapy, alteplase or urokinase appear to be the drugs of choice in these patients.

Aged↗
PubMed1995

Relation between myocardial beta-adrenoceptor density and hemodynamic and neurohumoral changes in a rat model of chronic myocardial infarction: effects of ibopamine and captopril.

OBJECTIVES: The purpose of this study was to investigate the changes in beta-adrenoceptor density (Bmax) and distribution in a model of chronic myocardial infarction in rats, and to relate possible changes to hemodynamic and neurohumoral abnormalities. In addition, we examined the effects of 8 weeks treatment with ibopamine and captopril. METHODS: There were 3 experiments: (1) Bmax and plasma catecholamines were examined (n = 46), (2) Bmax was compared in infarcted and non-infarcted tissue (n = 13), and (3) contractile function was evaluated by isolated heart perfusion (n = 40). Of rats in Expts. (1) and (3), 50% had myocardial infarction induced by coronary ligation and 50% were controls. Each group was divided between ibopamine, ibopamine and captopril, or standard (no drug) treatment. RESULTS: Bmax was not decreased in rats with myocardial infarction (10.8 +/- 0.8 fmol/mg protein), compared to normal rats (11.4 +/- 0.6 fmol/mg protein), and the ratio beta 1/beta 2 was also unaffected. In infarcted tissue, Bmax was significantly (P = 0.03) lower than in non-infarcted tissue. Baseline left ventricular pressure, systolic and diastolic dP/dT were all impaired (P < 0.001), and plasma norepinephrine levels were elevated in rats with myocardial infarction (16.03 +/- 230 vs. 1287 +/- 83 pg/ml; P < 0.05), compared to normals. Both ibopamine alone and in combination with captopril reduced the elevated plasma norepinephrine levels in infarcted rats (P < 0.001), but only the combination of the 2 drugs significantly increased Bmax in infarcted rats (14.7 +/- 0.8 fmol/mg protein; P = 0.03 vs. untreated myocardial infarction), while ibopamine alone had no significant effect (13.1 +/- 1.1 fmol/mg protein; p = ns). Also, active drug treatment had no significant effect on the hemodynamic changes. CONCLUSIONS: In this coronary artery ligation model of myocardial infarction in rats, no beta-adrenoceptor down-regulation is observed, despite marked abnormalities in baseline left ventricular function and plasma norepinephrine levels. The combination of ibopamine and captopril significantly increases Bmax in infarcted rats, which is accompanied by a reduction in plasma norepinephrine levels, but not by an improvement in hemodynamic parameters.

Adrenergic beta-Agonists↗
PubMed1995

Posterolateral defect of the normal human heart investigated with nitrogen-13-ammonia and dynamic PET.

UNLABELLED: The posterolateral defect is a common artifact seen when static 13N-ammonia imaging with PET is used to assess myocardial perfusion. The aim of this study was to compare dynamic and static. 13N-ammonia PET and to obtain more insight into the cause of the posterolateral defect. METHODS: Dynamic 13N-ammonia PET was performed in 19 healthy nonsmoking volunteers at rest. Perfusion was assessed in the early phase of the study using a curve fit method over the first 90 sec. Nitrogen-13 accumulation (static PET) was assessed 4 to 8 min after injection. Each study was normalized to a mean of 100. The average distribution of normalized perfusion and activity was calculated in 24 segments. Heterogeneity of both activity and perfusion distribution were assessed and the activity distribution was compared with perfusion distribution. RESULTS: Perfusion distribution was homogeneous, with the exception of the inferior and apical regions. Activity distribution was inhomogeneous, with a lower activity in the posterolateral and apical regions. In the whole left ventricle, significant differences in distribution were found between static and dynamic imaging. CONCLUSION: Perfusion distribution was significantly different on dynamic images compared to static images. The posterolateral defect was not found on dynamic images. The posterolateral defect and other inhomogeneities in activity distribution are caused by tracer-dependent features, probably a redistribution of metabolites of 13N-ammonia.

Adult↗
PubMed1995

Quantitative myocardial mapping of perfusion and metabolism using parametric polar map displays in cardiac PET.

UNLABELLED: Most efficacy studies of cardiac PET in demonstrating myocardial ischemia and viability have been performed using one or more transversal static images of the heart. In contrast, in this paper we describe a method of functional imaging of the complete left ventricular myocardium for perfusion with nitrogen-13-ammonia, both at rest and during a dipyridamol stress test, and of glucose metabolism with 18F-fluorodeoxyglucose (18FDG). METHODS: This was performed by using the data of each of 48 radial segments of 10 short-axis images as tissue data and LV cavity data of three basal planes as blood pool data. The study describes the results of 19 normal volunteers and 36 patients with coronary artery disease. From the data of the normal volunteers a 95% normal confidence interval was calculated for each imaging modality. These intervals were then used to describe the patient data as normal, ischemic or infarcted. RESULTS: The results of analysis of the parametric images was compared with the results of static analysis of the same patient data and found to be less dependant on the detection threshold used. CONCLUSION: The described method enables the routine application of functional PET imaging of the total myocardium by the semi-automatic construction of parametric flow and metabolism polar maps. It thus provides an increased performance in the diagnosis, quantification and localization of myocardial ischemia and viability over conventional PET imaging.

Adult↗
PubMed1994

Comparison between felodipine and isosorbide mononitrate as adjunct to beta blockade in patients > 65 years of age with angina pectoris.

Coronary artery disease is an increasingly common medical problem in the elderly, and relatively few studies investigating drug therapy focus on this population. To assess the efficacy and safety of the calcium channel blocker, felodipine, and isosorbide mononitrate (ISMN), as adjunct to optimal beta-blocker therapy in elderly patients, a placebo-controlled, double-blind study was conducted in 46 patients, aged between 65 and 80 years, with documented stress-induced angina pectoris and myocardial ischemia. With use of a latin-square design, with 3 periods of 4 weeks each, exercise testing was performed after each period. Felodipine, 5 mg once daily, significantly improved both time to ischemic threshold and pain threshold (p = 0.02 and p = 0.003, respectively, vs placebo), and tended to increase total exercise time (p = 0.06 vs placebo). In contrast, ISMN, 20 mg twice daily, did not significantly affect these parameters. Comparison of the 2 active treatment arms showed that, overall, felodipine was more effective than ISMN, with a statistically significant difference for time to ischemic threshold (p = 0.02). With regard to safety, felodipine was also better tolerated than ISMN, which led to more patients discontinuing study medication with ISMN (p < 0.05 between ISMN and felodipine). It is concluded that in elderly patients who are treated with optimal beta blockade, felodipine, but not ISMN, leads to an additional significant reduction in ischemic parameters during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗