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Biomedical subjects

F Hagemeijer

Publications and source records attributed to F Hagemeijer.

At least 19 recordsLinked to original sources
PubMed1994

Hemodynamic performance during exercise in patients with severe chronic congestive heart failure before and after a single dose of pimobendan.

Duration of symptom-limited exercise on a bicycle ergometer (constant workload of 25 W) was determined in 12 patients with severe chronic congestive heart failure (CHF) due to dilated cardiomyopathy (CMP, 4 patients) or ischemic heart disease (IHD, 8 patients) undergoing hemodynamic monitoring. Mean exercise duration was 214 +/- 124 s and produced severe dyspnea lasting > 5 min in all patients. The next morning, each patient exercised again to the same level; pimobendan (10 mg orally) was then administered, and exercise to the same workload was repeated 4 and 10 h later. Mean +/- SD exercise-induced changes in heart rate (HR, min-1), pulmonary capillary wedge pressure (PCW, mm Hg), cardiac output (CO, L/min-1), and stroke volume index (SVI, ml.min-1) were as follows. At baseline, HR was 85 +/- 17-110 +/- 21 beats/min (p < 0.001), PCW 21 +/- 10-31 +/- 10 mm Hg (p < 0.05), CO 3.7 +/- 1.0-3.9 +/- 1.0 L.min-1 (NS), and SVI, 25 +/- 7-20 +/- 7 ml.m-2 (NS). Four hours after pimobendan administration, HR was 90 +/- 14-113 +/- 21 beats/min (p < 0.001), PCW 11 +/- 7-20 +/- 10 mm Hg (p < 0.05), CO 5.3 +/- 0.7-5.8 +/- 1.0 L.min-1 (NS), and SVI 33 +/- 3-29 +/- 7 ml.m-2 (NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1993

Calcium sensitization with pimobendan: pharmacology, haemodynamic improvement, and sudden death in patients with chronic congestive heart failure.

Calcium sensitization increases myocardial contractility by improving energy utilization of the myocardium, without an increase in intracellular concentrations of cyclic adenosine monophosphate. The calcium sensitizer most extensively studied up to now is pimobendan (UD-CG 115 BS). Vasodilatation results primarily from phosphodiesterase III inhibition. Orally administered pimobendan appears rapidly in plasma. A peak concentration is reached 1.5 h after drug intake; elimination from the plasma compartment has a half-life of 1.5 h. First-pass hepatic O-desmethylation of pimobendan produces the active metabolite UD-CG 212; plasma concentration curves of UD-CG 212 are similar to those of pimobendan, with a peak concentration 1-2 h later than the peak concentration of the parent compound. In patients with chronic congestive heart failure, pimobendan produces a dose-dependent and prolonged decrease in pulmonary capillary wedge pressure and an increase in cardiac output. Maintenance doses of pimobendan are well tolerated and may lead to lasting symptomatic improvement in patients with heart failure; open and blinded trials show that exercise tolerance increases. No attenuation of these effects is seen during long-term therapy with pimobendan. Patients in chronic congestive heart failure frequently die suddenly; many inotropic agents increase the incidence of sudden death in these patients. Although proarrhythmia has never been observed with pimobendan, arrhythmia suppression with amiodarone seems prudent in heart failure patients receiving maintenance doses of pimobendan.

Animals↗
PubMed1991

Intractable heart failure despite angiotensin-converting enzyme inhibitors, digoxin, and diuretics: long-term effectiveness of add-on therapy with pimobendan.

In 25 patients whose chronic congestive heart failure (CHF) had recently worsened to New York Heart Association class IV, pimobendan (5 to 20 mg/day) was added to maximum conventional therapy consisting of digoxin, diuretics, angiotensin-converting enzyme inhibitors, coumadin derivatives to prevent thromboembolic complications, and amiodarone to suppress serious ventricular rhythm disturbances. CHF was fatal in less than 1 month in five patients (two had shown some initial improvement). The other 20 had sustained improvement by at least one functional class, interrupted by episodes of CHF that usually responded to intravenous therapy. Median survival was 12 months (range 10 days to greater than 3 years); five patients died suddenly, 12 died of intractable CHF, and two died of other causes. Six patients were alive 3 years after the onset of treatment with pimobendan. Add-on therapy with pimobendan produced a sustained improvement in many patients with severe CHF that was no longer responding to a combination of digoxin, diuretics, and angiotensin-converting enzyme inhibitors.

Aged↗
PubMed1991

Lack of negative inotropic effects of the new calcium antagonist Ro 40-5967 in patients with stable angina pectoris.

We screened the antiischemic, hemodynamic, and inotropic effects of different dosages of the new calcium channel blocker Ro 40-5967 in 65 patients with stable effort-induced angina pectoris. In a double-blind way, patients were randomized to recieve a single oral dose of 50, 100, or 200 mg Ro 40-5967 or placebo, given as a drinking solution. Left ventricular ejection fraction (LVEF), blood pressure (BP), and heart rate (HR) were measured at rest and during a supine bicycle exercise test on day 0 (baseline) and 2 h after drug intake on day 1. Twenty-four hours later, the bicycle exercise test was repeated. Ro 40-5967 improved exercise duration and resting LVEF. After 200 mg, exercise time increased significantly from 8.4 +/- 0.8 min (mean +/- SEM) to 9.6 +/- 0.7 min (p = 0.018), and LVEF at rest increased from 54.5 +/- 2.2 to 58.1 +/- 2.6% (p = 0.045). Time to 0.1 mV ST-segment depression increased significantly from 4.3 +/- 0.8 to 5.5 +/- 0.9 min in the 100-mg group (p = 0.013) and from 4.3 +/- 1.3 to 5.4 +/- 1.5 min in the 200-mg group (p = 0.027). Maximum ST-segment depression decreased significantly at all dose levels (p = 0.01), with the maximum decrease noted in the 200-mg group (from 0.21 +/- 0.03 to 0.15 +/- 0.02 mV, p = 0.004). BP, HR, and rate-pressure product did not change significantly at rest or at maximum exercise. A single dose of Ro 40-5967 has antiischemic properties in patients with stable angina pectoris, with maximum effects obtained after 200 mg. No signs of negative inotropy were noted, and the drug was well tolerated.

Adult↗
PubMed1989

Hemodynamic effects of pimobendan given orally in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.

Pimobendan (UD-CG 115 BS) was administered orally to 23 patients with congestive heart failure (functional class IV) caused by coronary artery disease (11 patients) or idiopathic dilated cardiomyopathy (12). All patients received maintenance doses of digoxin, furosemide and warfarin. Baseline data, collected during 15 hours, stayed within a 10% range. A 10-mg oral dose of pimobendan increased the heart rate from 95 +/- 20 to 109 +/- 24 beats/min (p less than 0.003). The pulmonary artery wedge pressure decreased from 23.0 +/- 5.9 to 10.1 +/- 5.2 mm Hg (p less than 0.0001), the cardiac index increased from 1.9 +/- 0.4 to 3.3 +/- 0.7 liters/min/m2 (p less than 0.0001) and the left ventricular stroke work index increased from 2,005 +/- 927 to 3,065 +/- 1,161 ml/mm Hg/m2 (p less than 0.0001). Statistically significant improvements in hemodynamic variables were still present 10 hours after the administration of pimobendan. Most patients felt better and reported no angina or other side effect, the incidence of ventricular arrhythmias was unchanged and no electrocardiographic changes suggesting ischemia were observed. Patients with severe congestive heart failure experienced a prolonged improvement of their cardiovascular condition after a single dose of pimobendan.

Administration, Oral↗
PubMed1989

Cardiovascular effects and plasma level profile of pimobendan (UD-CG 115 BS) and its metabolite UD-CG 212 in patients with congestive heart failure after single and repeated oral dosing.

Pimobendan (10 mg on day 1, then 5 mg twice daily for 28 days) was administered orally to nine patients in class III-IV stable congestive heart failure. On day 1, pimobendan appeared in plasma within 30 min, its plasma concentration peaked at 39 +/- 23 ng/ml after 1.5 h, and then decreased with a half-life of 1.44 +/- 0.94 h. Concentrations of its major metabolite UD-CG 212 peaked 3 h after drug intake, at 24 +/- 7 ng/ml. The time course of plasma concentrations was similar on days 1, 2, and 28. Cardiac index increased from 2.2 +/- 0.5 to 2.8 +/- 0.4 L.min-1.m-2 (p = 0.0001) on day 1, from 2.8 +/- 0.5 to 3.4 +/- 0.4 L.min-1.m-2 (p = 0.0032) on day 2, and stayed at 2.7 +/- 0.6 and 2.7 +/- 0.9 L.min-1.m-2 (p = 0.7895) on day 28. On day 1, pulmonary capillary wedge pressure decreased from 16 +/- 7 to 6 +/- 5 mm Hg (p = 0.0001), from 10 +/- 7 to 7 +/- 8 mm Hg (p = 0.0001) on day 2, and from 9 +/- 7 to 5 +/- 3 mm Hg (p = 0.0275) on day 28. Cardiovascular effects of pimobendan were independent of plasma concentrations. All patients improved by at least one NYHA functional class; exercise tolerance increased. No side effect was observed, but two patients died suddenly: Arrhythmogenicity should be ruled out before pimobendan is recommended for treatment of heart failure.

Aged↗
PubMed1989

Correlations between the cardiovascular effects of pimobendan and plasma concentrations of the parent compound and of its major active metabolite, UD-CG 212 CL, in patients with congestive heart failure.

Pimobendan was administered orally (10 mg single dose on day 1, then 5 mg twice daily for 4 weeks) to nine patients with chronic heart failure undergoing hemodynamic monitoring. The time course of changes in plasma concentrations of pimobendan and of its major active metabolite. UD-CG 212 CL, was similar on days 1, 2, and 28. Pimobendan plasma levels peaked 1.5-2.0 h after drug intake: plasma concentrations of UD-CG 212 CL reached a maximum 1 h later; the terminal half-life of pimobendan in plasma varied between 1.44 +/- 0.94 h on day 1 and 1.19 +/- 0.36 h on day 2. Initially, cardiovascular variables changed with increasing plasma drug levels and reached a maximum 4 h after pimobendan intake; later, we found no correlation between plasma concentrations and hemodynamic effects. A steady state of hemodynamic improvement was achieved after 4 weeks of maintenance therapy with pimobendan. Baseline pulmonary capillary wedge pressure dropped from 16 +/- 7 mm Hg on day 1 to 5 +/- 3 mm Hg at noon on day 28 (-69%; p less than 0.001), and baseline cardiac index increased from 2.2 +/- 0.5 L/min/m2 on day 1 to 2.7 +/- 0.9 L/min/m2 on day 28 (+23%; p less than 0.01). Pimobendan is a long-acting drug that effectively improves cardiac performance in patients with chronic congestive heart failure.

Administration, Oral↗
PubMed1986

Prevalence of retrograde conduction in heart block after DDD pacemaker implantation.

Electrophysiologic studies were performed before DDD pacemaker implantation in 50 patients with symptomatic heart block. The patients were separated into 2 groups. Group I consisted of patients with intact retrograde conduction and group II consisted of patients with blocked retrograde conduction. After pacemaker implantation, postventricular atrial refractory periods in patients in group I were programmed at 50 to 100 ms, in excess of the retrograde conduction times measured during electrophysiologic studies. In group II patients, postventricular atrial refractory periods were routinely programmed at 300 ms. During follow-up, patients visited the outpatient clinic at 3-month intervals for noninvasive assessment of the prevalence of retrograde conduction, and to test the inducibility of pacemaker-mediated tachycardias. The mean follow-up of group I (15 patients) was 27 +/- 10 months, whereas the mean follow-up of group II (35 patients) was 19 +/- 9 months. The mean number of noninvasive tests performed during follow-up was 8 +/- 3 per patient for group I and 5 +/- 3 per patient for group II. In group I, retrograde conduction remained intact in 12 patients (p less than 0.01). In 29 of 31 patients in group II, retrograde conduction remained absent (p less than 0.01). In 4 patients in group II, chronic atrial fibrillation occurred during follow-up. Chronic atrial fibrillation did not occur in any patient in group I. During serial electrophysiologic testing, no pacemaker-mediated tachycardias could be induced in any patient in group I or II.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Pacemaker electrocardiography of rate smoothing during DDD pacing.

A rate smoothing option is available in a new bipolar AV universal (DDD) pacemaker. In three patients, two with intact retrograde conduction and one with retrograde block, rate smoothing values of 3% and 6% were programmed. Irregular pacemaker-mediated tachycardia occurred in one patient and AV synchrony was temporarily lost in the other two patients. In this report, we describe the pacemaker electrocardiography of rate smoothing during DDD pacing.

Aged↗
PubMed1984

Flecainide: one-year efficacy in patients with chronic ventricular arrhythmias.

During a one-week short-term in-hospital period, 60 patients with chronic ventricular arrhythmias were treated with 200 mg flecainide twice a day. Flecainide reduced premature ventricular complexes (PVCs) by more than 85% without causing important side-effects in 47 patients, who entered a one-year follow-up period and were followed with bimonthly 24-h ECGs. Median PVC-frequency remained reduced by more than 99% during the follow-up period. Repetitive ventricular beats and ventricular tachycardia were present in 83% and 42% of patients, respectively, before flecainide. During follow-up, these arrhythmias were seen in less than 32% and less than 10% of patients, respectively, at each 24-h ECG. Furthermore, the mean number of hours with repetitive ventricular beats and ventricular tachycardia remained reduced by more than 76% and more than 79%, respectively, throughout the follow-up period. Ventricular arrhythmias remained suppressed despite a gradual reduction in flecainide dosages (to a median of 300 mg day-1) and flecainide plasma levels. In nine out of 47 patients, an increase in ventricular arrhythmias above baseline values on one or more occasions was observed. During a flecainide withdrawal period, a 65-fold increase in median PVC-frequency was observed and ventricular tachycardia reappeared in 18 patients. Subjective side-effects were acceptable except for two patients. During the follow-up period, one patient developed reversible heart failure and sinus node dysfunction. During the total study period, four patients, with either severe coronary artery disease (2) or cardiomyopathy (2) developed lethal arrhythmias (3) or ischaemic events (1). We conclude that prolonged flecainide treatment is effective in a high proportion of patients with chronic ventricular arrhythmias. In some patients an arrhythmogenic effect may occur.

Adult↗
PubMed1984

Cardiovascular effects of sulmazol administered intravenously to patients with severe heart failure.

Ten patients with severe heart failure (NYHA class IV) received sulmazol intravenously under haemodynamic and electrocardiographic surveillance. All patients were on maintenance doses of digitalis and diuretics. At 30 min intervals we increased the infusion rate of sulmazol from 1 to 2, 4, 6, and 8 mg min-1, to a total of 630 mg of sulmazol administered over 150 min. Statistically significant changes (P less than 0.001) were found for heart rate (from 97 to 103 min-1); right atrial pressure (from 9.5 to 1.5 mmHg); pulmonary artery diastolic pressure (from 25.0 to 9.0 mmHg); pulmonary capillary wedge pressure (from 22.0 to 9.0 mmHg); aortic diastolic pressure (from 62.5 to 52.5 mmHg); pulmonary artery oxygen saturation (from 53.0 to 68.5%); cardiac output (from 2.83 to 4.38 l min-1), and for indices derived from these measurements. No correlation was found between the improvement in cardiac performance and sulmazol plasma concentrations. Haemodynamic improvement persisted for more than 7.5 h after cessation of sulmazol administration. Renal function was measured before and after sulmazol administration; creatinine clearance (from 47.5 to 52.0 ml min-1) and p-amino hippuric acid clearance (from 146 to 125 ml min-1) were unchanged. Side-effects included yellow-colored vision, ventricular extrasystoles, and possibly sulmazol-induced liver function disturbances. Even in severe heart failure sulmazol improved cardiac performance in patients who were treated with the maximum tolerated dose of digoxin.

Acute Disease↗
PubMed1984

Serial electrophysiologic studies after single chamber atrial pacemaker implantation in patients with symptomatic sinus node dysfunction.

After single chamber atrial pacemaker implantation, serial electrophysiologic studies were performed noninvasively at intervals of 3 months over a total period of 3 years in 24 patients with symptomatic sinus node dysfunction. All patients underwent invasive electrophysiologic studies before pacemaker implantation and demonstrated intact anterograde AV conduction. Patients were divided into 2 groups: group I did not require antiarrhythmic drugs during follow-up whereas group 2 received antiarrhythmic drugs. In group I (11 patients) the atrial paced heart rate producing AV Wenckebach phenomenon (AVWHR) remained stable during a mean follow-up of 22 +/- 10 months; with a variability not exceeding 10 beats min-1 with respect to the initial AVWHR obtained during preoperative electrophysiologic study. In group 2 (13 patients) with a mean follow-up of 15 +/- 8 months a mean decrease of AVWHR of 19.2 +/- 17.5 beats min-1 was present between AVWHR before and 3 months after initiation of oral antiarrhythmic drugs (P less than 0.01). During chronic (greater than 3 months) antiarrhythmic drug therapy the variability of the AVWHR never exceeded 10 beats min-1 with respect to the AVWHR obtained 3 months after the initiation of oral drug therapy. Deterioration of anterograde AV conduction during long-term follow-up of patients with symptomatic sinus node dysfunction and intact anterograde AV conduction at the time of pacemaker implantation is a consequence of orally taken antiarrhythmic drugs, rather than a consequence of degeneration of the AV conducting system.

Aged↗
PubMed1984

Responses of an AV universal (DDD) pulse generator (Cordis 233D) to programmed single ventricular extrastimuli.

To evaluate factors playing a role in initiation and perpetuation of pacemaker-mediated tachycardias (PMTs), 22 consecutive patients with symptomatic conduction disorders were studied after implantation of an AV universal (DDD) pulse generator (Cordis 233D). Patients were divided into two groups, depending upon the presence or absence of ventriculo-atrial (VA) conduction during electrophysiological study (EPS) performed before pacemaker implantation. PMTs could be initiated in six of eight patients of Group I and in none of 14 patients of Group II. Initiation and perpetuation of PMTs during DDD pacing were dependent upon the capacity of the patient to conduct ventricular premature beats (VPBs) and subsequent paced ventricular beats retrogradely to the atria, and upon three programmable parameters of the pulse generator (AV delay period, upper rate limit, tachycardia response). Programmed single ventricular extrastimulation demonstrated that: (1) merely the presence of VA conduction during EPS, although necessary, was not sufficient to induce PMTs after DDD pacemaker implantation; (2) VPBs introduced late rather than early in the cardiac cycle initiated PMTs in a different way; (3) the initiation of PMTs could be prevented during study by adjusting the programmable parameters (AV delay period, upper rate limit, tachycardia response); (4) one of the two available tachycardia responses of the pulse generator (gradual fall-back response) was able to terminate and initiate PMTs consistently. These observations helped in understanding the responses of the Cordis 233D pulse generator to ventricular premature beats. They indicate that additional refinement of the pulse generator is necessary to solve the problem of PMT.

Aged↗
PubMed1983

Right to left shunt, with severe hypoxemia, at the atrial level in a patient with hemodynamically important right ventricular infarction.

This report describes a patient with a massive right ventricular infarction, complicated by severe hypoxemia. Contrast echocardiography demonstrated a right to left shunt through a previously asymptomatic atrial septal defect. This phenomenon should be considered as a possible cause of hypoxemia in the presence of right ventricular infarction.

Echocardiography↗
PubMed1983

Atrioventricular and ventriculo-atrial conduction in patients with symptomatic sinus node dysfunction.

In 14 patients with symptomatic sinus node dysfunction--sinus bradycardia, sino-atrial exit block, or sinus arrest--electrophysiological studies were performed before implantation of a pacemaker. In 8 patients incremental high right atrial pacing showed AV-nodal Wenckebach at pacing rates equal to or above 130/min (group I); in 6 patients AV-nodal Wenckebach was reached at pacing rates less than 130/min (group II). During ventricular pacing at a rate 10-15% faster than the existing sinus rate, ventriculo-atrial (VA) conduction was present in all patients of group I, while VA conduction was present in only 2 patients of group II (p less than 0.05). Patients with symptomatic sinus node dysfunction but with intact AV conduction frequently show VA conduction during ventricular pacing and thus are particularly at risk for developing a pacemaker syndrome when a ventricular demand (VVI) pacemaker is implanted. This complication can be avoided by atrial demand (AAI) pacing or AV sequential (DVI) pacing. When adequate experience has been gathered with AV universal (DDD) pacemakers, the indications for selection of a pacemaker in patients with symptomatic sinus node dysfunction will probably change.

Adult↗