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Biomedical subjects

F J van Capelle

Publications and source records attributed to F J van Capelle.

At least 37 records · Page 2Linked to original sources
PubMed1990

Determinants of prognosis in symptomatic ventricular tachycardia or ventricular fibrillation late after myocardial infarction. The Dutch Ventricular Tachycardia Study Group of the Interuniversity Cardiology Institute of The Netherlands.

In a multicenter study, 390 patients with sustained symptomatic ventricular tachycardia or ventricular fibrillation late after acute myocardial infarction were prospectively followed up to assess determinants of mortality and recurrence of arrhythmic events. Patients were given standard antiarrhythmic treatment, which consisted primarily of drug therapy. During a mean follow-up period of 1.9 years, 133 patients (34%) died; arrhythmic events and heart failure were the most common cause of death (41 patients [11%] died suddenly, 31 [8%] died because of recurrent ventricular tachycardia or ventricular fibrillation and 23 [6%] died of heart failure). One hundred ninety-two patients (49%) had at least one recurrent arrhythmic event; 85% of first recurrent arrhythmic events were nonfatal. Multivariate analysis of data from patients who developed the arrhythmia less than 6 weeks after infarction identified five variables as independent determinants of total mortality: 1) age greater than 70 years (risk ratio 4.5); 2) Killip class III or IV in the subacute phase of infarction (risk ratio 3.5); 3) cardiac arrest during the index arrhythmia (risk ratio 1.7); 4) anterior infarction (risk ratio 2.2); and 5) multiple previous infarctions (risk ratio 1.6). Multivariate analysis of data from patients developing the arrhythmia greater than 6 weeks after infarction identified four variables as independently predictive of total mortality: 1) Q wave infarction (risk ratio 2.1); 2) cardiac arrest during the index arrhythmia (risk ratio 1.7); 3) Killip class III or IV in the subacute phase of infarction (risk ratio 1.7); and 4) multiple previous infarctions (risk ratio 1.4). The results of the two multivariate analyses were used in a model for prediction of mortality at 1 year. The average predicted mortality rate varied considerably according to the model: for 243 patients (62%) with the lowest risk, it was 13%, corresponding to an observed mortality rate of 12%; for 92 patients (24%) with intermediate risk, it was 27%, corresponding to an observed rate of 28%; for 55 patients (14%) with the highest risk, it was 64%, corresponding to an observed rate of 54%. This study shows that patients with symptomatic ventricular tachycardia or ventricular fibrillation late after myocardial infarction who are given standard antiarrhythmic treatment have a high mortality rate. The predictive model presented identifies patients at low, intermediate and high risk of death and can be of help in designing the appropriate diagnostic and therapeutic strategy for the individual patient.

Aged↗
PubMed1990

Ventricular tachycardia in the infarcted, Langendorff-perfused human heart: role of the arrangement of surviving cardiac fibers.

Electrophysiologic and histologic studies were performed on Langendorff-perfused human hearts from patients who underwent heart transplantation because of extensive infarction. In nine hearts, 15 sustained ventricular tachycardias could be induced by programmed stimulation. In all hearts, mapping of epicardial and endocardial electrical activity during tachycardia was carried out. Histologic examination of the infarcted area between the site of latest activation of one cycle and the site of earliest activation of the next cycle revealed zones of viable myocardial tissue. In two hearts in which the time gap between latest and earliest activation was small, surviving myocardial tissue constituted a continuous tract that traversed the infarct. In three other hearts in which the time gap was large, surviving tissue consisted of parallel bundles that coursed separately over a few hundred micrometers, then merged into a single bundle and finally branched again. The direction of the fibers within the bundles was perpendicular to the direction of the activation front in that area. A similar type of inhomogeneous anisotrophy and activation delay was found in an infarcted papillary muscle removed from one of the explanted hearts and studied in a tissue bath during basic stimulation. Histologic examination of this preparation revealed that the delay was caused by a zigzag route of activation over branching and merging bundles of surviving myocytes separated by connective tissue.

Cardiac Pacing, Artificial↗
PubMed1988

Reentry as a cause of ventricular tachycardia in patients with chronic ischemic heart disease: electrophysiologic and anatomic correlation.

In this report we describe electrophysiologic and histologic findings in hearts and endocardially resected preparations from patients with sustained ventricular tachycardias in the chronic phase of myocardial infarction. We recorded simultaneously from 64 endocardial sites during tachycardia in 72 patients that were operated on for medically intractable ventricular tachycardias. Two other patients underwent heart transplantation, and mapping was performed on the explanted isolated heart connected to a Langendorff perfusion set-up. During operation 139 tachycardias with different morphologies could be induced. Although the majority of evidence supports the concept of a reentrant mechanism for these tachycardias, we found that 105 tachycardias appeared to arise at a focal area of less than 1.4 cm2. In only three cases macroreentry around the infarction scar could be detected. Of 21 tachycardias in which the "origin" appeared to be focal, earliest subendocardial activation was preceded by discrete electrograms of low amplitude (presystolic activity). In three tachycardias presystolic activity was detected at several sites, permitting reconstruction of its route. Histology of the endocardial resected preparation in one of these cases revealed separate zones of viable myocardial fibers in areas in which presystolic activity was recorded. These zones were located intramurally and subendocardially, supporting the concept that reentry occurred via isolated bundles of surviving myocytes at the border of the infarct and the larger subendocardial muscle mass. Conduction velocity through the isolated tracts was on the order of 25 cm/sec. Similar reentrant pathways were found in the two isolated hearts. Extracellular and intracellular recordings were made from 20 endocardial preparations that were excised from areas in which tachycardia originated. Preparations were superfused in a tissue bath. These experiments showed that action potentials were usually close to normal, but occasionally action potentials with reduced amplitude and slow upstrokes were found. In addition, there were cells that exhibited both fast and slow upstrokes, depending on the direction of the wavefront. Histology of seven resected preparations and the isolated hearts showed subendocardially as well as intramurally located zones of viable myocardium. Fractionation of extracellular electrograms and slow conduction were found in areas where surviving muscle fibers and strands of fibrous tissue were interwoven, and in zones where muscle fibers were oriented in parallel but isolated by strands of connective tissue.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1986

Propagation through electrically coupled cells. How a small SA node drives a large atrium.

Each normal cardiac cycle is started by an action potential that is initiated in the sino-atrial (SA) node by automaticity of the SA nodal cells. This action potential then propagates from the SA node into the surrounding atrial cells. We have done numerical simulations of electrically coupled cells to understand how a small SA node can be spontaneously active and yet be sufficiently electrically coupled to the surrounding quiescent atrial cells to initiate an action potential in the atrial cells. Our results with a simple model of two coupled cells and a more complex model of a two-dimensional sheet of cells suggest that some degree of electrical uncoupling of the cells within the SA node may be an essential design feature of the normal SA-atrial system.

Action Potentials↗
PubMed1983

Risk of operative mortality in surgery for coronary heart disease (a multiple regression analysis of perioperative hemodynamic and electrocardiographic data).

Using multiple regression analysis, we examined perioperative hemodynamic and electrocardiographic variables as predictors of operative mortality in surgery for coronary heart disease. Data were first analyzed as univariates and, if significantly related to mortality, they were subjected to stepwise logistic multivariate regression analysis. The preoperative predictor variables were: heart rate, ventricular arrhythmia and ST-T shift. The intraoperative predictor variables were: ventricular arrhythmia and ST-T shifts; and the postoperative predictor variables were: left ventricular stroke work index, blood pressure, mixed venous oxygen content and intrapulmonary shunt. When only electrocardiographic data were analyzed, the preoperative variables were: ventricular arrhythmia, ST-T shift and anterior wall infarction. The intraoperative variables were: ventricular arrhythmia and ST-T shift. The postoperative electrocardiogram did not give additional information. The common denominator of the relevant hemodynamic and electrocardiographic variables appears to be an accumulation of pre- and perioperative myocardial damage, which leads to operative mortality.

Cardiac Surgical Procedures↗
PubMed1983

Infarct size estimation from serial CK MB determinations: peak activity and predictability.

In 198 patients with acute myocardial infarction serial measurements of plasma creatine kinase isoenzyme MB (CK MB) were performed at four hour intervals. In every patient, maximal CK MB activity (peak activity) was compared with calculated total release per litre plasma. In 28 patients (group 1) sufficient plasma samples were available for calculation of the apparent first order inactivation constant kd. Mean apparent kd in group 1 patients was 0 . 085 +/- 0 . 018 h-1 (mean +/- SD). Total release in group 1 was calculated with individual apparent kd values (Q) and with the mean kd value (Q*). In the remaining 170 patients (group 2), Q* only was calculated. A linear relation between peak activity P and total release (both Q and Q*) was found, extending over the whole range of CK MB peak activities that are routinely observed (4-216 U/l). It was immaterial whether a one or a two compartment model was used: both yielded a close linear relation. Though the mean ratio between Q* and peak activity depends on the value of kd chosen for calculation of total release (the ratio increasing with increasing kd), linearity between peak activity and Q* was found for any value of kd up to 0 . 4 h-1. In group 1, shapes of calculated CK MB release curves Q*(t), expressed relative to maximal release Q(40), were sufficiently similar so as to be superimposable; the section of the release curves extending from 12 hours before until two hours after peak time could be tentatively described by a linear time course with a slope of 4 . 2 +/- 0 . 5% per hour (mean +/- SD). We conclude that peak activity of CK MB is a reliable estimate of cumulative CK MB release and may be clinically more practicable than calculation of Q(40). Both the similarity and the large apparently linear section of the calculated enzyme release curves possibly permit early prediction of Q(40), with acceptable precision.

Creatine Kinase↗
PubMed1982

Effect of sodium nitroprusside on mortality in acute myocardial infarction.

We gave sodium nitroprusside by intravenous infusion to 163 randomly selected patients during the first 24 hours after hospitalization for typical acute myocardial infarction, and we studied its effects on mortality at one week, on the incidence of cardiogenic shock, on clinical signs of left ventricular failure, and on peak levels of creatine kinase isoenzyme MB. A control group of 165 patients received standard medical treatment and infusion of 5 per cent glucose. The end point of the study was a significant reduction in mortality in the nitroprusside group; this was reached when five deaths had occurred in this group, as compared with 18 among the controls (P less than 0.05). The incidence of cardiogenic shock, clinical signs of left-heart failure, and mean peak levels of creatine kinase isoenzyme MB were all reduced (P less than 0.05). The results indicate that infusion of nitroprusside in the early phase of acute infarction limits complications, possibly by reducing infarct size. The drug was particularly effective in anterior-wall infarction.

Aged↗
PubMed1982

Electrotonic interactions across an inexcitable region as a cause of ectopic activity in acute regional myocardial ischemia. A study in intact porcine and canine hearts and computer models.

We recorded 60 DC simultaneous electrograms from isolated porcine and canine hearts in the first minutes after coronary occlusion. Ventricular premature beats (VPB) originated from the normal side of the ischemic border, which was frequently separated from the central ischemic area showing delayed activity by a small zone of inexcitable tissue. We attempted in a computer model to generate VPB's at one side of an area showing conduction block. In computer simulations,,, the presence of elements capable of automatic activity greatly facilitated the induction of VPB's. By coupling automatic elements to nonautomatic elements, overt pacemaking activity could be suppressed. Subthreshold depolarizations transmitted through a zone of conduction block could, when properly timed, trigger the latent automatic elements into overt automatic activity, resulting in single or repetitive VPB's. The ventricular premature beats in the intact hearts with acute regional ischemia may be caused by "triggered automaticity" in which the trigger is provided by the "injury current" flowing from ischemic cells showing delayed repolarization via a segment of inexcitable ischemic cells in the border zone to normally perfused cells with suppressed automaticity.

Animals↗
PubMed1981

Treatment of acute myocardial infarction with sodium nitroprusside during 24 hours, followed by isosorbide dinitrate.

In a controlled randomized study of 328 consecutive patients admitted within 24 hours after the onset of acute myocardial infarction, 163 patients received a sodium nitroprusside infusion during 24 hours, followed by six times a day 5 mg isosorbide dinitrate for seven days and 165 patients received a glucose 5% infusion. Excluded from the study were patients with either pulmonary edema and/or cardiogenic shock, two or more previous myocardial infarctions or a systolic blood pressure of less than 95 mmHg just before entering the study. Sodium nitroprusside was titrated in such a way that systolic blood pressure was kept between 95 and 105 mmHg. Standard medical treatment for both groups was the same. CK-MB was sampled every four hours until peak value was reached. Endpoint of the study was a significant reduction in mortality within a week after starting treatment.

Clinical Trials as Topic↗
PubMed1980

Computer simulation of arrhythmias in a network of coupled excitable elements.

Arrhythmias were simulated in sheets or cables, consisting of coupled excitable elements, which were characterized by a simple regenerative mechanism. The geometry of the network, the amount of coupling among individual elements, and the properties of the elements relating to excitability, automaticity, and duration of the refractory period could be adjusted arbitrarily in an interactive computer program. When a critical amount of coupling was present between automatic and non-automatic cells, sustained repetitive activity could be initiated and stopped by stimulation of the elements. Using this mechanism, it also was possible to evoke reciprocal activity in a one-dimensional cable. In uniform sheets of coupled elements, circus movement of the activation front could be evoked. The presence of an obstacle or dispersion of the refractory periods of the elements was not a prerequisite for the initiation of circus movements. The vortex of circus movements in the homogeneous sheets consisted of elements which were inactivated by depolarizing currents from the circulating wavefront. In sheets of sufficient size, multiple vortices could be present.

Action Potentials↗
PubMed1976

A combined electrophysiological and anatomical study of the human fetal heart.

Five human fetal hearts of gestational ages ranging from 12 to 16 weeks were studied with both electrophysiological and anatomical techniques. The electrophysiological behavior of these hearts was comparable with results obtained with other animal species and adult human hearts. This indicates that the fetal heart is functionally mature from an early stage of development; however the tissues are not fully differentiated from an anatomical standpoint. Results of mapping experiments indicated that atrial activation occurred through broad wave fronts, and no electrophysiological evidence was found to support the concept of "specialized internodal conduction." In two hearts, the node and bundle were found to be anatomical contiguity with ventricular myocardium throughout their length, but the conducting tissues were already functionally insulated from the ventricles. The results have significance with regard to concepts of the "sudden death in infancy syndrome" and ventricular pre-excitation.

Action Potentials↗
PubMed1976

Cycle-length-dependent properties of AV nodal activation in rabbit hearts.

Cycle-length-dependent changes in AV nodal cell activation were studied in isolated preparations from rabbit hearts. Transmembrane action potentials were recorded from the node while it was propagating impulses initiated in the atrium with an accelerating train of stimuli. This train consisting of five successive stimuli separated by progressively shorter intervals was uniformly repeated at every 10th basic beat, each time reproducing a sequence of five different increasing AV nodal delays. The AN and NH cells were found to contribute only slightly to the cycle-length-dependent AV nodal delay which developed mainly in the small N zone, located centrally in the AV node. With the increasing delay, the action potentials from this N zone typically dissociated into two components synchronous with late AN and early NH activity, respectively. The amplitude of the first component decreased, wheareas that of the second increased progressively in N cells activated progressively later. No cells were activated at an intermediate time between the two components. This dissociation was not accompanied by changes in the activation pattern of the AV node. The different nodal cells classified according to their response to the accelerating train delineated functional zones corresponding to different anatomic structures. The possible mechanisms which would explain the cycle-length-dependent AV nodal delay are discussed.

Action Potentials↗