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Biomedical subjects

I C van Gelder

Publications and source records attributed to I C van Gelder.

17 recordsLinked to original sources
PubMed2001

Quality of life in patients with paroxysmal atrial fibrillation and its predictors: importance of the autonomic nervous system.

AIMS: To determine the impact of paroxysmal atrial fibrillation on quality of life and to determine the predictors of quality of life, particularly the role of symptomatology and autonomic function. METHODS AND RESULTS: The study group comprised 73 patients with paroxysmal atrial fibrillation (mean age 54.1 years, 51 males). On average, patients had a 3-year history of one paroxysm per week lasting 2 h. Quality of life was assessed using the SF-36 (Medical Outcomes Study Short-Form Health Survey) and compared with age-matched controls. Autonomic function was assessed using Holter monitoring with analysis of heart rate variability and autonomic function tests. Symptoms during paroxysms of atrial fibrillation were also scored. Multivariate analysis was performed to identify independent predictors of quality of life. Quality of life scores were markedly lower in patients than in controls in four of the eight subscales (P<0.001): physical role function, emotional role function, vitality and general health. Structural heart disease did not predict quality of life, whereas frequency of paroxysms was predictive only of physical role function. In contrast, autonomic variables (baroreflex-sensitivity, total power (heart rate variability), response to deep breathing, 30-15 ratio (standing up)) were predictive in all four respective subscales (P<0.05), depressed vagal function being predictive of low scores. Symptoms, particularly severe perspiration, were also predictive of low scores (P<0.05). CONCLUSIONS: This study shows that paroxysmal atrial fibrillation causes significant impairment of quality of life. Further, symptomatology and autonomic function are important predictors of quality of life in this patient group.

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PubMed2000

Electrophysiological changes of angiotensin-converting enzyme inhibition after myocardial infarction.

To investigate whether prevention of remodeling would translate into a more stable electrophysiological profile, the investigators randomized 56 patients to treatment with angiotensin-converting enzyme (ACE) inhibition or placebo for 3 months after myocardial infarction. Programmed electrical stimulation revealed no significant differences in inducibility of monomorphic sustained ventricular tachycardia (VT), whereas ventricular fibrillation (VF) tended to be lower in the ACE-inhibitor group. Effective refractory periods were consistently longer, and dispersion of refractoriness was significantly shorter in the ACE-inhibitor group. The investigators conclude that in this small patient group ACE inhibition may mildly add to a more stable electrophysiological profile.

Action Potentials↗
PubMed2000

Prognostic value of the presence and development of atrial fibrillation in patients with advanced chronic heart failure.

AIMS: To examine whether the presence, or development, of atrial fibrillation in patients with advanced chronic heart failure, is associated with a poorer prognosis, compared to patients with sinus rhythm and chronic heart failure. METHODS AND RESULTS: We examined 409 patients with moderate to severe chronic heart failure, and compared patients with sinus rhythm (n=325) to those with atrial fibrillation (n=84). At baseline, the two groups were similar regarding most indices of severity of chronic heart failure, such as left ventricular ejection fraction (0.23) and New York Heart Association (NYHA) functional class, while they were different for age (70 years for atrial fibrillation vs 67 years for sinus rhythm patients), aetiology of chronic heart failure, blood pressure, concomitant treatment, and plasma neurohormones (all P<0.05). During a mean follow-up of 3.4 years (range 2.0-5.4), 203 patients (50%) died. The majority of deaths was due to progressive chronic heart failure (55%) or was sudden (28%), but there was no difference in mode of death between sinus rhythm and atrial fibrillation patients. Overall mortality was higher in atrial fibrillation patients (60%), than in those with sinus rhythm (47%; risk ratio 1.40, 95% CI 1.01-1.92, P=0. 04). After adjusting for important prognostic variables, such as age, left ventricular ejection fraction, NYHA class, renal function, and blood pressure, the presence of atrial fibrillation was no longer related to increased mortality (risk ratio 0.86, range 0.59-1.24, P=ns). Of the 325 patients who had sinus rhythm at baseline, 30 (9%) developed atrial fibrillation during the study. These patients were older (70 vs 66 years, P<0.007), and had slightly lower blood pressure and plasma norepinephrine concentrations (P<0.05), but were otherwise similar. During follow-up, mortality was similar in these two groups (47% in those with new onset atrial fibrillation, vs 47% in those who had sinus rhythm throughout the study). CONCLUSIONS: The present data do not support the concept that the presence, or the development of atrial fibrillation in patients with advanced chronic heart failure is independently related to an adverse outcome during long-term follow-up. The generally observed higher mortality in patients with atrial fibrillation thus seems to be related to other factors, associated with atrial fibrillation.

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PubMed1999

Gene expression of proteins influencing the calcium homeostasis in patients with persistent and paroxysmal atrial fibrillation.

OBJECTIVE: Persistent atrial fibrillation (AF) results in an impairment of atrial function. In order to elucidate the mechanism behind this phenomenon, we investigated the gene expression of proteins influencing calcium handling. METHODS: Right atrial appendages were obtained from eight patients with paroxysmal AF, ten with persistent AF (> 8 months) and 18 matched controls in sinus rhythm. All controls underwent coronary artery bypass grafting, whereas most AF patients underwent Cox's MAZE surgery (n = 12). All patients had a normal left ventricular function. Total RNA was isolated and reversely transcribed into cDNA. In a semi-quantitative polymerase chain reaction the cDNA of interest and of glyceraldehyde-3-phosphate dehydrogenase were coamplified and separated by ethidium bromide-stained gel electrophoresis. Slot blot analysis was performed to study protein expression. RESULTS: L-type calcium channel alpha 1 and sarcoplasmic reticulum Ca(2+)-ATPase mRNA (-57%, p = 0.01 and -28%, p = 0.04, respectively) and protein contents (-43%, p = 0.02 and -28%, p = 0.04, respectively) were reduced in patients with persistent AF compared to the controls. mRNA contents of phospholamban, ryanodine receptor type 2 and sodium/calcium exchanger were comparable. No changes were observed in patients with paroxysmal AF. CONCLUSIONS: Alterations in gene expression of proteins involved in the calcium homeostasis occur only in patients with long-term persistent AF. In the absence of underlying heart disease, the changes are rather secondary than primary to AF.

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PubMed1999

Human SCN5A gene mutations alter cardiac sodium channel kinetics and are associated with the Brugada syndrome.

BACKGROUND: Primary dysrhythmias other than those associated with the long QT syndrome, are increasingly recognized. One of these are represented by patients with a history of resuscitation from cardiac arrest but without any structural heart disease. These patients exhibit a distinct electrocardiographic (ECG) pattern consisting of a persistent ST-segment elevation in the right precordial leads often but not always accompanied by a right bundle branch block (Brugada syndrome). This syndrome is associated with a high mortality rate and has been shown to display familial occurrence. METHODS AND RESULTS: Pharmacological sodium channel blockade elicits or worsens the electrocardiographic features associated with this syndrome. Hence, a candidate gene approach directed towards SCN5A, the gene encoding the alpha-subunit of the cardiac sodium channel, was followed in six affected individuals. In two patients missense mutations were identified in the coding region of the gene: R1512W in the DIII-DIV cytoplasmic linker and A1924T in the C-terminal cytoplasmic domain. In two other patients mutations were detected near intron/exon junctions. To assess the functional consequences of the R1512W and A1924T mutations, wild-type and mutant sodium channel proteins were expressed in Xenopus oocytes. Both missense mutations affected channel function, most notably a 4-5 mV negative voltage shift of the steady-state activation and inactivation curves in R1512W and a 9 mV negative voltage shift of the steady-state activation curve in A1924T, measured at 22 degrees C. Recovery from inactivation was slightly prolonged for R1512W channels. The time dependent kinetics of activation and inactivation at -20 mV were not significantly affected by either mutation. CONCLUSIONS: Two SCN5A mutations associated with the Brugada syndrome, significantly affect cardiac sodium channel characteristics. The alterations seem to be associated with an increase in inward sodium current during the action potential upstroke.

Action Potentials↗
PubMed1997

Efficacy, safety, and determinants of conversion of atrial fibrillation and flutter with oral amiodarone.

Amiodarone is effective for long-term maintenance of sinus rhythm after electrical cardioversion of refractory atrial fibrillation or flutter. To examine its efficacy and safety for pharmacologic conversion of these arrhythmias, we studied 129 patients with refractory atrial fibrillation or flutter who had failed previous intensive conventional antiarrhythmic treatment. In anticipation of electrical cardioversion, patients were loaded with amiodarone, 600 mg/day during a 4-week period. The main outcome measure was pharmacologic conversion during this period. During the loading period, 23 patients (18%) converted to sinus rhythm. When analyzed in a multivariate model, conversion was related to desethylamiodarone plasma level (p = 0.0006), arrhythmia duration (p = 0.04), left atrial area (p = 0.02), and concomitant treatment with verapamil (p = 0.01). During ongoing atrial fibrillation after loading, the ventricular rate decreased from 100 +/- 25 to 87 +/- 27 beats/ min (p <0.001). Amiodarone appeared to be safe and did not have to be discontinued because of intolerable side effects. Thus, amiodarone loading is safe and is still able to convert refractory atrial fibrillation or flutter. Conversion is related to increased desethylamiodarone plasma levels and concomitant treatment with verapamil. Because prolonged loading may increase desethylamiodarone plasma concentrations, this may enhance efficacy and obviate the need for electrical cardioversion.

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PubMed1994

Benefits and risks of antiarrhythmic drug therapy after DC electrical cardioversion of atrial fibrillation or flutter.

Electrical cardioversion is the method of choice to restore sinus rhythm in patients with chronic atrial fibrillation. After cardioversion, long-term maintenance of sinus rhythm is troublesome since many patients relapse. In addition, haemodynamic complications associated with recurrence and hazards of prophylactic antiarrhythmic drug therapy are among the problems threatening these patients. Several new antiarrhythmics have become available but their safety remains to be established. Advantages of prophylactic antiarrhythmic treatment must be carefully weighed against the hazards. As a consequence, non-pharmacological modalities like serial electrical cardioversions (no drugs) and His bundle ablation may become important treatment modalities. The present report summarizes current antiarrhythmic strategies, focusing primarily on feasibility of prophylactic treatment and on early and late proarrhythmia.

Anti-Arrhythmia Agents↗
PubMed1990

Patency of arm vein grafts used in aorto-coronary bypass surgery.

Arm veins have been used in myocardial revascularisation procedures as a last resort bypass conduit because of their associated low patency. Nevertheless, leg veins and mammary arteries, which are the most commonly used, are sometimes not sufficient, leaving little choice as to the bypass conduit. To assess the properties of arm veins in bypass surgery, we compared a group of 28 patients that underwent an arm vein graft coronary bypass procedure with a matched group of patients in which leg veins were used. In 28 patients, 40 arm vein grafts with 77 distal anastomoses were used (mean 1.9 +/- 0.9; range 1-5). A cerebrovascular accident was the cause of the sole death (2%) during the study period. The mean follow-up was 4.6 years (Standard deviation, SD: 1.5 years). More antianginal medication was used in the arm vein group (P = 0.017). Additionally, the percentage of the expected maximal frequency during exercise testing was lower in the arm vein group as compared to the leg vein group. Digital subtraction angiography showed that the patency of the arm vein bypass grafts was 47% (70% confidence limits, CL: 32%-62%) while the patency of the leg vein grafts was 77% (CL: 64%-87%), which was statistically significant (P = 0.051). Comparison of these figures with the few published reports on arm veins used as coronary bypass grafts reveals similar results. We conclude that the arm vein as a coronary bypass graft is only to be used when mammary arteries and leg veins are not available.

Arm↗
PubMed1990

Flecainide: long-term effects in patients with sustained ventricular tachycardia or ventricular fibrillation.

Efficacy of flecainide was investigated in 50 patients with sustained ventricular tachycardia (n = 38) or ventricular fibrillation (n = 12) during a 4-week in-hospital and 1-year follow-up period. Furthermore, the predictive value of programmed electrical stimulation, Holter monitoring, and exercise testing on outcome of long-term treatment was studied. Etiology of the tachyarrhythmia was coronary artery disease in 37 patients and other etiologies in 13 patients. The success rate of flecainide after 1 year, based on intention to treat, was 54%. The success rate during the in-hospital phase was 84% (in six patients flecainide was discontinued because of tachyarrhythmia and in two because of side effects). Calculated after 4 weeks hospitalization, the success rate was 78% for patients with tachyarrhythmias based on coronary artery disease and 55% for patients with tachyarrhythmias based on other etiologies (11 patients showed recurrences and two patients severe side effects). Patients with tachyarrhythmias based on coronary artery disease showed a lower ejection fraction and earlier recurrence than patients with arrhythmias based on other etiologies. Proarrhythmic effects developed in six patients (12%). Electrophysiological evaluation was performed in 28 patients at baseline and after intravenous flecainide. Negative predictive value of the electrophysiological evaluation after intravenous flecainide for patients with inducible tachyarrhythmias at baseline (n = 21) was 40%. For Holter monitoring (n = 24) this value was 86%. Non-ischemia-related induction of tachycardia by exercise was present in two of 30 patients on flecainide; both patients showed recurrence of the tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1988

Abnormal pharmacokinetics of flecainide in a "nonresponder".

Flecainide is well absorbed after oral administration. Following rapid infusion of flecainide, there is a short distribution phase. Plasma levels of flecainide are proportional to dose. Both QRS durations and flutter wave intervals are lengthened after flecainide administration. We report an abnormal pharmacokinetic response to oral as well as intravenous flecainide in a patient who was treated with flecainide for several episodes of atrial flutter. In contrast to the usual pattern, this patient did not show a significant increase in QRS duration, flutter wave interval, or plasma concentration. We could not explain this abnormal pharmacokinetic response, but excluded a rapid and complete renal clearance, an excessively high rate of metabolization, and an abnormal binding mechanism as possible mechanisms. We concluded that flecainide may produce abnormal pharmacokinetic mechanisms, preventing appearance of unbound substance in plasma, thereby preventing occurrence of electrophysiological effects.

Administration, Oral↗
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↗