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Biomedical subjects

N M van Hemel

Publications and source records attributed to N M van Hemel.

At least 19 recordsLinked to original sources
PubMed1992

Surgical therapy of paroxysmal atrial fibrillation with the "corridor" operation.

Patients with paroxysmal atrial fibrillation may be extremely disabled despite medical therapy. Based on recent concepts of atrial fibrillation, a surgical open heart procedure was designed to isolate a "corridor" from the right and the left atrium. The corridor consists of the sinus node area, the atrioventricular nodal junction, and the connecting right atrial mass, small enough to prevent atrial fibrillation. Between 1987 and 1990, 20 patients with severely disabling symptoms due to frequent paroxysmal atrial fibrillation underwent the corridor operation, with permanent success in 16 patients. In 8 patients, left atrium to corridor conduction reappeared shortly after the procedure. Reoperation was performed in these patients without extracorporeal circulation. The site of persistent conduction between the left atrium and the corridor could consistently be localized adjacent to the coronary sinus. Nevertheless, reoperation failed to isolate permanently the corridor in 4 patients. During a mean follow-up of 20 months, atrial fibrillation dominating the ventricles was never observed nor inducible in the corridor in the 16 patients with a successful operation. In all cured patients, sinus node function remained undisturbed. Paroxysmal atrial flutter inside the corridor arose in 1 patient and a paroxysmal focal tachycardia in another. All 16 cured patients experienced a clear improvement in quality of life. Refinement of the surgical technique to obtain persistent isolation between the left atrium and the corridor is needed. These results demonstrate that the concept of the corridor operation is sound and justify its use in the treatment of drug-refractory paroxysmal atrial fibrillation.

Adult↗
PubMed1992

Increased dispersion of "refractoriness" in patients with idiopathic paroxysmal atrial fibrillation.

The average interval between local depolarizations during atrial fibrillation, the so-called atrial fibrillation interval, was used as an index for local "refractoriness." This was based on the assumption that during fibrillation, cells are reexcited as soon as their refractory period ends. A very good correlation was found between refractory periods determined with the extrastimulus technique at a basic cycle length of 400 ms and atrial fibrillation intervals measured at the same epicardial sites of the right atrium. This new technique was used to assess dispersion in atrial fibrillation intervals in 10 patients with idiopathic paroxysmal atrial fibrillation and in a control group of 6 patients who were undergoing cardiac surgery. After a routine median sternotomy a multiterminal grid with up to 40 electrodes was placed over the right atrium, and atrial fibrillation was induced by premature stimulation. The average fibrillation interval in the test group, recorded at 247 sites, was 152 +/- 3 ms and that in the control group, recorded at 118 sites, was 176 +/- 8.1 ms (p less than 0.05). Dispersion in atrial fibrillation intervals, defined as the variance of the fibrillation intervals at all the recording sites, was three times larger in the group with paroxysmal atrial fibrillation than in the control group. This study suggests that both a shorter refractory period and a larger dispersion in refractoriness are responsible for the recurrence of atrial fibrillation.

Atrial Fibrillation↗
PubMed1992

Body surface mapping of ectopic left ventricular activation. QRS spectrum in patients with prior myocardial infarction.

To improve electrocardiographic localization of the site of origin of ectopic left ventricular (LV) impulse formation in the heart with prior myocardial infarction, 62-lead body surface QRS integral maps were studied during LV pacing at a total of 221 endocardial sites in 14 patients with previous anterior (AMI), inferior (IMI), lateral (LMI), or anterior and inferior (AMI/IMI) myocardial infarction. The anatomic location of each pacing site was computed using digitized biplane fluoroscopic images and plotted on standardized LV endocardial polar projections. A data base of characteristic AMI and IMI mean QRS integral maps was developed after visually selecting subgroups with nearly identical QRS integral morphology from the ectopic activation sequences produced at 110 sites in eight patients with AMI and at 66 sites in four patients with IMI. Intrasubgroup pattern uniformity and intersubgroup pattern variability were statistically verified. The endocardial pacing site locations belonging to each AMI and IMI subgroup were depicted as segments on the respective LV polar projections. In patients with AMI, a total of 18 typical mean QRS integral patterns were obtained, whereas 22 different mean total QRS integral patterns showing more substantial intersubgroup variation were acquired in patients with IMI. Posterolateral regions exhibited a relatively low electrocardiographic sensitivity (six AMI and five IMI patterns) as compared with anteroseptal regions (12 AMI and 17 IMI patterns). Total QRS integral patterns obtained at 24 sites in one patient with LMI were largely compatible with the IMI mean total QRS integral patterns, whereas the majority of total QRS integral patterns acquired at 21 sites in one patient with AMI/IMI corresponded with the AMI mean total QRS integral patterns. The results show that total body surface QRS integral maps generated during LV pacing in patients with prior myocardial infarction cluster by pattern and that each QRS integral pattern is related to a circumscribed endocardial segment of ectopic impulse formation. The relation between a given QRS integral pattern and the position and size of the corresponding paced segment is dependent on infarct location. The present infarct-specific data base of characteristic total body surface QRS integral patterns provides a clinical tool to obtain detailed electrocardiographic localization of ventricular arrhythmias in patients with previous myocardial infarction.

Adult↗
PubMed1991

Effectiveness of sotalol in preventing supraventricular tachyarrhythmias shortly after coronary artery bypass grafting.

To investigate the effectiveness and safety of low-dose sotalol (a class III antiarrhythmic beta-blocking agent) in the prevention of supraventricular tachyarrhythmias (SVTs) and to identify predictors for the occurrence of these arrhythmias shortly after coronary artery bypass grafting, 300 consecutive patients were randomized in a double-blind, placebo-controlled fashion. Patients with severely depressed left ventricular function or other contraindications for beta blockers were excluded. Beginning at 4 hours and up to the sixth day after surgery, 150 patients received 40 mg of sotalol every 6 hours. SVT was observed in 24 (16%) of 150 low-dose sotalol-and in 49 (33%) of 150 placebo-treated patients [p less than 0.005]. In patients receiving sotalol, atrial fibrillation was the only noted tachyarrhythmia, whereas in the placebo group, 42 (28%) patients had atrial fibrillation, 3 (2%) atrial flutter, 1 (0.7%) atrial tachycardia and 3 (2%) sinus tachycardia. Drug-related adverse effects necessitating discontinuation of the drug were noted in only 2 (1%) sotalol-treated patients and 4 (3%) placebo-treated patients (p = not significant). For both groups, univariate analysis indicated that older age, 1- or 2-vessel coronary artery disease, long bypass (greater than or equal to 150 minutes) and aorta cross-clamp time (greater than or equal to 120 minutes) were predictive variables for the occurrence of SVTs. Multivariate analysis showed that male sex (odds ratio 2.3), 1- or 2-vessel coronary artery disease (odds ratio 2.0) and older age (odds ratio 1.1) were independent risk factors for increased occurrence of postoperative SVT.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Artery Bypass↗
PubMed1991

Is surgery for ventricular tachycardia too risky?

There is strong evidence that recurrent symptomatic ventricular tachycardia (VT) after acute myocardial infarction is associated with a poor prognosis (1-year mortality varying from 12% to 54%). When successive drug trials fail to suppress VT, cardiac surgery is considered but its therapeutical value appears disputable. Recent studies show inhospital mortality after surgery varying from 5% to 23%, and the 5-year actuarial survival ranging from 33% to 71%. However, using the quality of the residual left ventricular function as criterion for operability, our recent inhospital mortality diminished to 1.3%, while the 4-year actuarial survival was 85%. Arrhythmia freedom without drugs after 4 years after surgery is nowadays about 75%. These findings show that cardiac surgery might be a very acceptable alternative therapy in surgical candidates, in particular when one or more risk factors become apparent after acute myocardial infarction. This article describes the current position of arrhythmia surgery in relation to drug therapy and the implantable automatic defibrillator.

Anti-Arrhythmia Agents↗
PubMed1991

Macroreentry in the infarcted human heart: the mechanism of ventricular tachycardias with a "focal" activation pattern.

Endocardial mapping of electrical activity was carried out in 150 patients to guide antiarrhythmic surgery for drug-resistant ventricular tachycardia in the chronic phase of myocardial infarction. In 20 of these patients, the activation pattern of 27 distinct tachycardias was focal and diastolic potentials were recorded at three or more sites. In 26 tachycardias, the sequence of diastolic potentials progressed from the area of latest activation of one cycle toward the "origin" of the next cycle. In two patients, the heart was stimulated during tachycardia, resulting in entrainment of the tachycardia in both. Late potentials were recorded during entrainment at sites where diastolic potentials occurred during tachycardia. In 11 of the 20 patients, endocardial mapping was performed during sinus rhythm. In four of these, late potentials were observed during sinus rhythm at sites where diastolic potentials were recorded during tachycardia. In two patients without late potentials during sinus rhythm, late potentials were observed during stimulation and induced ectopic beats. The results support the concept that the mechanism of several of these tachycardias is based on reentry in a macrocircuit comprising a tract of surviving tissue traversing the infarct and the remaining healthy tissue. They also indicate that the absence of late potentials during sinus rhythm does not guarantee the absence of arrhythmogenic pathways.

Cardiac Catheterization↗
PubMed1991

Predictive value of ventricular arrhythmias for patency of the infarct-related coronary artery after thrombolytic therapy.

In animal studies reperfusion of coronary arteries is commonly accompanied by ventricular arrhythmias. It is not certain, however, whether ventricular arrhythmias can be used as a reliable non-invasive marker of reperfusion in humans. Two-channel Holter recordings were obtained from the start of an intravenous infusion of streptokinase until coronary angiography (2.8 (2.7) hours (mean SD)) afterwards) in 57 patients with acute myocardial infarction of less than four hours who were generally not treated with antiarrhythmic drugs. Ventricular arrhythmias occurred in 21 (37%) of the 57 patients: accelerated idioventricular rhythm in 13 patients and non-sustained ventricular tachycardia in 15 patients. Seven patients had both accelerated idioventricular rhythm and non-sustained ventricular tachycardia. Coronary angiography showed a patent infarct-related vessel in 12 (92%) of the 13 patients with accelerated idioventricular rhythm (95% confidence interval 66 to 99%), in 22 (50%) of the 44 patients without accelerated idioventricular rhythm (95% CI 34 to 66%), in 11 (73%) of the 15 patients with non-sustained ventricular tachycardia (95% CI 45 to 92%), and in 23 (55%) (95% CI 39 to 71%) of the 42 patients who did not have non-sustained ventricular tachycardia. Seventeen (81%) of the 21 patients with accelerated idioventricular rhythm, or non-sustained ventricular tachycardia, or both, had a patent infarct-related vessel (95% CI 58 to 94%) as did 17 (47%) of the 36 patients with no ventricular arrhythmia (95% CI 29 to 65%). In patients with accelerated idioventricular rhythm after thrombolysis the infarct-related vessel is almost certain to be patent; but the infarct-related coronary artery can still be patent when no arrhythmia is seen.

Acute Disease↗
PubMed1990

[10-year experience with the surgical treatment of ventricular tachycardia following acute myocardial infarction].

From 1980 to 1988 direct arrhythmia surgery was performed in 121 patients suffering from postinfarction drug-refractory ventricular tachycardia (VT). By 1986 the initially high in-hospital mortality of 26% (18 of 69 patients) had decreased to 1.9% (1 of 52 patients). The 3-year actuarial survival of patients operated since 1986 is 90%. From 1985 the results of surgical therapy of VT have improved: 86% of the patients remained arrhythmia-free without drugs; none died suddenly. Residual left ventricular function was related to the prognosis, but the interval between the last myocardial infarction and time of surgery or the surgical technique were not. These results demonstrate that direct surgery has become a valuable method in the treatment of postinfarction VT, at least in patients with sufficient residual left ventricular function.

Adult↗
PubMed1990

A double-blind randomized multicenter dose-ranging trial of intravenous streptokinase in acute myocardial infarction.

Intravenous streptokinase administration is now a widely applied therapy for patients in the early hours of acute myocardial infarction (AMI). The dosages used do not appear to be based on comparative clinical investigations. Therefore a double-blind randomized trial was carried out to establish the optimal dose of streptokinase. A total of 189 patients who had symptoms of AMI for less than 4 hours were treated with 200,000, 750,000, 1,500,000 or 3,000,000 IU streptokinase intravenously. At coronary angiography 2.8 +/- 2.7 hours (mean +/- standard deviation) after the start of streptokinase infusion, patency of the infarct-related coronary artery was observed in 38, 75, 60 and 82% of the patients, respectively, in the 4 groups. The result of the dosage of 200,000 IU was significantly poorer than that of the other dosages (p less than 0.01). The result of a dosage of 3,000,000 IU was significantly better than that of 1,500,000 IU (p less than 0.05), but the differences with 750,000 IU were not significant. Blood transfusion was required in 4 patients (2%), distributed over the 4 groups in 0, 2, 1 and 1 of the patients. One patient had major bleeding; this patient had been treated with 750,000 IU. The 3-month mortality-rate in the whole study population was 5%. Thus, of the 4 doses of streptokinase tested, 750,000 IU is the minimal therapeutic dosage, and the arguments for 1,500,000 IU as standard therapy for comparison with other fibrinolytic drugs are poor. The best results in this study were achieved with 3,000,000 IU, but further research will be needed to establish the efficacy and safety of this new regimen.

Aged↗
PubMed1990

The value of class IC antiarrhythmic drugs for acute conversion of paroxysmal atrial fibrillation or flutter to sinus rhythm.

In a single-blind randomized study, the efficacy and safety of intravenous propafenone (2 mg/kg body weight per 10 min) versus flecainide (2 mg/kg per 10 min) were assessed in 50 patients with atrial fibrillation or flutter. Treatment was considered successful if sinus rhythm occurred within 1 h. Conversion to sinus was achieved in 11 (55%) of 20 patients with atrial fibrillation treated with propafenone and in 18 (90%) of 20 with atrial fibrillation treated with flecainide (p less than 0.02). If atrial fibrillation was present less than or equal to 24 h, conversion to sinus rhythm was achieved in 8 (57%) of 14 patients in the propafenone group and 13 (93%) of 14 in the flecainide group (p less than 0.05). Atrial flutter was converted in two (40%) of five patients treated with propafenone and in one (20%) of five with flecainide (p = NS). Mean time to conversion was 16 +/- 10 min in the propafenone group versus 18 +/- 13 min in the flecainide group (p = NS). QRS lengthening (83 +/- 15 to 99 +/- 20 ms) was observed only in the patients treated with flecainide (p less than 0.001). Patients successfully treated with propafenone showed significantly higher plasma levels than those whose arrhythmia did not convert to sinus rhythm. Transient adverse effects were more frequent in the flecainide group (40%) than in the propafenone group (8%) (p less than 0.01). In conclusion, at a dose of 2 mg/kg in 10 min, flecainide is more effective than propafenone for conversion of paroxysmal atrial fibrillation to sinus rhythm. However, considering the propafenone plasma levels and very few adverse effects, the dose or infusion rate, or both, used in the propafenone group may not have been sufficient to achieve an optimal effect. Neither drug seems very effective in patients with atrial flutter.

Atrial Fibrillation↗
PubMed1990

Initial clinical experience with rate adaptive cardiac pacing using two sensors simultaneously.

UNLABELLED: In the rate adaptive pacemakers, all presently available sensors show one or more drawbacks. Combining two sensors in a single pacemaker, we tried to optimize its rate responsive characteristics. In this study, we present the rate adaptive behavior of a two sensor pacemaker system, using both QT interval and activity sensing. In addition, we compared the rate response with that of each sensor alone. Nine patients with an implanted QT interval sensing pacemaker, and an externally attached activity sensing pacemaker performed three exercise stress tests on treadmill. The QT interval, measured by the implanted pacemaker, and the activity level, were transmitted to an external computer. This computer contained the two sensor rate adaptive algorithm, and reprogrammed the implanted pacemaker on beat-to-beat basis. CONCLUSION: In the two sensor mode the rate increases immediately at the onset of exercise, caused by the prompt response of the activity sensor. Further rate increase is driven by the QT interval sensor and therefore proportional to the level of exercise. Furthermore, the rate decay during the recovery phase is more physiological.

Atrial Fibrillation↗
PubMed1990

Body surface mapping of ectopic left and right ventricular activation. QRS spectrum in patients without structural heart disease.

The value of simultaneous 62-lead electrocardiographic recordings in localizing the site of origin of ectopic ventricular activation in a structurally normal heart was assessed by examining body surface QRS integral maps in 12 patients during left and right ventricular (LV and RV) pacing at 182 distinct endocardial sites. A data base of 38 characteristic mean integral maps was composed after visually selecting subgroups with nearly identical total QRS integral morphology and numerically evaluating intrasubgroup pattern uniformity and intersubgroup pattern variability. Corresponding endocardial pacing site locations were computed by a biplane cineradiographic method and outlined as segments on a standardized LV and RV polar projection. LV pacing resulted in 25 markedly different mean total QRS integral patterns, showing higher electrocardiographic sensitivity for anteroseptal (18 patterns) compared with posterolateral regions (seven patterns). RV pacing demonstrated 13 mean total QRS integral patterns, exhibiting less intersubgroup variation and comparatively low electrocardiographic sensitivity for the basal anterior and outflow regions. Comparison of LV with RV pacing revealed that QRS configurations produced at LV apical and LV midseptal sites closely resembled QRS configurations generated at RV apical, RV septal, and RV anterior sites, respectively. Total QRS time integral amplitudes showed considerable intrasubgroup variation but permitted global differentiation of spatially similar QRS patterns obtained during pacing at LV and RV sites. This study demonstrates that the QRS pattern of the total body surface electrocardiogram allows discrimination among 38 different LV and RV segments of ectopic endocardial impulse formation in patients with normal cardiac anatomy.

Adult↗
PubMed1990

Efficacy and safety of low- and high-dose sotalol versus propranolol in the prevention of supraventricular tachyarrhythmias early after coronary artery bypass operations.

Supraventricular tachyarrhythmias are reported in up to 40% of patients early after coronary artery bypass graft operations. In a randomized study, we compared the efficacy and safety of the class III antiarrhythmic beta-blocking drug sotalol versus propranolol at low and high doses in the prevention of supraventricular tachyarrhythmias in 429 consecutive patients after coronary artery bypass graft operations. Patients with severely depressed left ventricular function and other contraindications for beta-blockers were excluded. From the fourth hour up to the sixth day after coronary artery bypass, 74 patients received low-dose sotalol (40 mg every 8 hours), 66 patients low-dose propranolol (10 mg every 6 hours), 133 patients high-dose sotalol (80 mg every 8 hours), and 156 patients high-dose propranolol (20 mg every 6 hours). Baseline characteristics were comparable in all groups. Supraventricular tachyarrhythmia was observed in 10 of 72 (13.9%) who received low-dose sotalol, 12 of 64 (18.8%) who received low-dose propranolol, 13 of 119 (10.9%) who received high-dose sotalol, and 19 of 139 (13.7%) who received high-dose propranolol (not significant). Drug-related adverse effects necessitating discontinuation of the drug occurred in four receiving low doses (2.9%) and in 31 receiving high doses (10.7%) (p less than 0.02). In conclusion, no medication was found to be superior, although supraventricular tachyarrhythmias tended to be less prevalent in patients treated with sotalol than in those treated with propranolol. Moreover, significantly fewer adverse effects were noted in both low-dose groups. Therefore, low-dose beta-blocking treatment, especially low-dose sotalol, seems preferable.

Administration, Oral↗
PubMed1989

Left ventricular segmental wall motion score as a criterion for selecting patients for direct surgery in the treatment of postinfarction ventricular tachycardia.

No indisputable criteria for selecting candidates for direct surgery in postinfarction ventricular tachycardia are yet available. We prospectively tested the result of surgery in patients showing normokinesia or slight hypokinesia in at least 3 of 9 segments of the left ventricle as determined on two oblique projections of the left ventricular angiogram. Sixty consecutive patients with recurrent symptomatic ventricular tachycardia were stratified on the basis of this criterion; 50 candidates were thus eligible for surgery. Direct surgery (endocardial resection and/or cryoablation) was performed in 23 patients (after a mean of 4.1 antiarrhythmic drug trials), while 27 patients were maintained on drug treatment (at discharge, a mean of 3.7 drug trials). Surgery was map-guided in 19 patients and non-map-guided in four emergency cases. No patients died in the immediate postoperative phase, but two (9%) died during follow-up. The actuarial survival at 12 months was 93%; the surgery-alone cure rate for ventricular tachycardia was 78%. Of the 27 non-operated surgical candidates, two died during in-hospital drug testing and five after discharge (total 26%). Actuarial survival at 12 months was 78% and did not differ significantly from that of the operated patients. After discharge, 80% of the non-operated surgical candidates still using the drug at discharge remained free of recurrence. In the 10 drug-treated non-surgical candidates (at discharge, a mean of 3.8 drug trials), survival and the number of arrhythmia-free patients were markedly lower than in surgical candidates. This study shows that the segmental wall motion score is of great clinical value and can be applied for stratification of patients with ventricular tachycardia after myocardial infarction for either surgery or medical therapy.

Aged↗
PubMed1988

Cryosurgery for ventricular bigeminy using a transaortic closed ventricular approach.

Disabling monomorphic ventricular bigeminy has not been described as an indication for surgery. Three young patients with this arrhythmia sometimes deteriorating into ventricular tachyarrhythmias and in whom drug therapy failed completely were accepted for surgical ablation of the arrhythmogenic area. The earliest endocardial site of origin was located preoperatively by catheter mapping of the spontaneously occurring ventricular bigeminy in the left and right ventricles. For maximum preservation of myocardial muscle and function, the preoperative mapping and surgical procedure were performed through the aortic root; mapping by transaortic multipolar balloon was done during normothermic coronary perfusion and cryocoagulation was done during cardioplegic arrest. Cryocoagulation of the endocardial site was performed using the transaortic approach and epicardial cryocoagulation at the opposite site was done afterwards. In the two patients in whom the preoperative mapping results were consistent with those of preoperative catheter mapping, the arrhythmia could be abolished, as documented during long-term follow-up. In the only patient in whom the mapping results were not in agreement, the ventricular arrhythmia reoccurred and was the cause of death at five months after surgery. Postoperative wall-motion studies performed in the two surviving patients showed limited scars in the area of cryocoagulation and minor damage to the coronary arteries in that area. The transaortic approach can be considered as a new and important surgical option for endocardial mapping and cryocoagulation which prevents the damaging effects of a left ventriculotomy.

Adolescent↗
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↗