Biomedical subjects
Publications and source records attributed to E Andries.
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BACKGROUND: Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common form of regular narrow complex tachycardia. It is due to dual atrioventricular nodal conduction over two pathways with different electrophysiological properties. The first pathway ('fast' pathway) conducts faster but has longer refractory period than the second pathway ('slow' pathway). OBJECTIVES: To review AVNRT. Clinically, AVNRT patients usually have palpitations in their neck during attacks. On the surface electrocardiogram, the diagnosis is suggested by the absence of P waves during tachycardia or very discrete P waves immediately after the QRS or an rSr' pattern in lead VI. Electrophysiologically, it can be reproducibly initiated or terminated by cardiac pacing. The reentrant circuit is limited to the atrioventricular node and a small amount of perinodal atrial tissue. Acute termination of tachycardia can be achieved by vagal manoeuvres or drugs. Adenosine compounds are excellent drugs, as are calcium channel blockers, for acute termination of the arrhythmia. If chronic therapy is indicated, digitalis, calcium blockers and beta-blockers are effective and simple initial options. Catheter ablation, especially using radiofrequency energy, antitachycardia pacing and surgery are therapeutic alternatives for the resistant patient. CONCLUSION: Because of its high success rate and low incidence of complications, radiofrequency ablation is becoming the therapy of first choice for the treatment of AVNRT.
Radiofrequency catheter ablation was used to treat 179 patients aged 5 to 79 (37 +/- 17) years. Six patients had multiple accessory pathways. The total number of accessory pathways was 188, 47 conducting only retrogradely; among them, 8 had retrograde decremental properties. The location of the accessory pathways was: 81 at the left lateral position; 13 left posterior; 15 left posteroseptal; 24 posteroseptal; 16 midseptal; 16 right posteroseptal; 17 anteroseptal and 6 right lateral. All patients were symptomatic and six had congenital heart disease. Initial success was achieved in 159 patients (88.8%). Ten out the 20 patients in whom ablation failed underwent a second attempt and success was obtained in all but 3 patients. Final success was accomplished in 166 patients (92.7%). There were 14 recurrences (7.8%) all successfully ablated during a second procedure. The mean procedure duration time was 80 +/- 60 minutes, the mean radiation exposure time was 31 +/- 26 minutes and the mean number of radiofrequency applications was 9 +/- 10. Three patients developed complete atrioventricular block during the procedure requiring permanent pacing, one patient had a perforation of a previously unknown congenital aneurysm of the aorta solved by surgery and one patient had a transient amaurosis after the procedure attributed to microembolization. Radiofrequency ablation of accessory pathways is a safe and effective treatment.
Catheter ablation using radiofrequency energy became the non-pharmacological therapy of first choice for patients with supraventricular tachycardias. Modification of the atrioventricular nodal conduction using this source of energy can be performed to treat patients with atrioventricular nodal reentrant tachycardia. In this article the authors present an updated review of radiofrequency catheter ablation of atrioventricular nodal reentrant tachycardia and report their own experience in this field.
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The uncomfortable awareness of a beating heart--palpitations--is a common complaint that can occur under normal or abnormal circumstances. For example, normal palpitations occur with exercise, emotions, and stress, or after taking substances that increase adrenergic tone or diminish vagal activity (coffee, nicotine, and adrenergic or anticholinergic drugs). Normal palpitations are recognised as such because individuals who experience them realise or are told that something happened to accelerate the normal rhythm of the heart. However, some people find sinus tachycardia troublesome enough to seek medical attention. In other situations palpitations are clearly abnormal. The heart beat which is felt for no apparent reason, may be fast, or strong and slow, or feel like a missed or extra beat. Although these abnormal palpitations usually point to a cardiac arrhythmia, this is not always the case. Moreover, many patients with arrhythmias do not have palpitations but manifestations such as syncope, shock, and chest pain (sudden death is also possible). We will discuss the approach to the patient who seeks medical attention because of a history of palpitations, with special emphasis on the history, physical examination, and 12-lead electrocardiogram (ECG) because they are simple and inexpensive diagnostic tools that are available to most physicians.
The goal of this study was to test the hypothesis that class I drugs modify the electrophysiological substrate of atrial fibrillation. The effects of a single intravenous dose (1.4 +/- 0.3 mg.kg-1) of the new class I drug, cibenzoline, were studied in 20 patients with spontaneous (n = 11) or induced (n = 9) atrial fibrillation, during an electrophysiological study. In one additional patient with chronic atrial fibrillation, the effects of a single intravenous dose of 2 mg.kg-1 of cibenzoline were studied intra-operatively before undergoing a 'corridor' operation. High resolution epicardial mapping (248 channels) was used to reconstruct the atrial activation patterns before and after administration of the drug. In 18 out of 20 patients administration of cibenzoline resulted in conversion of atrial fibrillation into regular monomorphic atrial tachycardia. In these 18 patients, the mean atrial cycle length was prolonged from 147 +/- 34 ms during atrial fibrillation to 302 +/- 34 ms after cibenzoline (P < 0.001). In eight out of the 18 patients, spontaneous (n = 3) or pacing induced (n = 5) conversion into sinus rhythm was observed after administration of the drug. In the patient undergoing the 'corridor' operation, epicardial mapping of both atria showed that the multiple wavelets present during atrial fibrillation fused into a single broad wavefront circulating counterclockwise around the caval veins after cibenzoline. In conclusion, cibenzoline transforms random re-entry into ordered re-entry in the atria. This effect seems related to the depression of conduction produced by the drug.
The increasing technological developments have made it possible to have implantable defibrillators with a wide range of diagnostic and therapeutic capabilities, which can be implanted without the need for a thoracotomy. It is not surprising, therefore, that the indications for implantation of a defibrillator have rapidly evolved. Defining populations of patients in whom a true "prophylactic" implantation (before the first episode of ventricular tachycardia or ventricular fibrillation) may be justified is still difficult. However, the time has certainly come to provide a cardioverter defibrillator to all patients who have suffered from one episode of ventricular tachycardia or ventricular fibrillation and who are at real risk of sudden arrhythmic death. Identification of these patients is relatively easy. It can be done using simple variables from the clinical history. Results from an ongoing multicenter trial testing the hypothesis that clinical variables can indeed be used to stratify the risk of sudden death and to select candidates for a defibrillator have proven the validity of this approach. There is no medical justification to withhold implantation of a cardioverter defibrillator in the truly "high risk" patient. One has to realize, however, that the concept of "high risk" is relative, and that the indications for the implantable defibrillator will continue to broaden.
OBJECTIVES: The purpose of this study was to assess the value of the Belgium system to control the indications for the implantable defibrillator. METHODS: We reviewed the answers of our official organization (Riijksinstituut voor Ziekte en Invaliditeitsverzekering-RIZIV) to our requests of implantable defibrillators in 49 patients in 1990, 1991 and the first months of 1992. In 1988 and in agreement with the RIZIV, 15 implants per year were allowed, but this number had been extended to 100 in 1992. RESULTS: There was an increasing first refusal rate from 1990 (0%) to 1991 (25%) and 1992 (42%), which was caused by: a) Difficulties to deal with indications for unusual diseases, particularly young patients with cardiac arrest and a structural normal heart; b) Possible distrust by the RIZIV towards the physician when the number of requests increases over time. However, all patients for whom a defibrillator was requested ultimately had it implanted. CONCLUSIONS: In the most ideal type of cooperation between official organisms and implanting physicians, such as the Belgian system, the official organization has to realize that uncommon patients with disputable indications exist. To avoid refusal of reimbursement in these cases, the decision taken by the treating physician can be accepted only on condition that the mutual relationship between both parties is based on open communication, mutual respect, and trust. The Belgian system provides care to all patients requiring a defibrillator with costs to society which are very acceptable. The Belgian system may be an excellent model for countries without clear regulations for reimbursement of implantable defibrillators.
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The treatment of ventricular arrhythmias remains a major challenge in cardiology. Several very helpful pieces of information can be obtained from the clinical history. The left ventricular function and the hemodynamic effects of a ventricular tachycardia are the two main factors affecting survival. Therefore, if a patient with sustained ventricular tachycardia presents with syncope or cardiac arrest, or if his functional class for dyspnea is III-IV (NYHA classification), he is a candidate for an implantable defibrillator while otherwise medical therapy is advised.
UNLABELLED: Radiofrequency (RF) ablation of the His bundle was attempted in 30 consecutive patients with atrial flutter or fibrillation. A 7 French quadripolar catheter with a 4-mm distal electrode was advanced from the right femoral vein (21 patients), or subclavian vein (two patients) and positioned across the tricuspid valve. Adequate His-bundle potentials were obtained in all patients. However, in six patients atrioventricular (AV) block could not be obtained after multiple (mean = 8) applications of RF energy from the conventional right-sided approach. In these patients the same catheter was advanced to record a His potential through a retrograde arterial approach. AV block was created in all patients with one to three applications of RF energy. The duration of the procedure was 22 to 90 minutes for the right-sided approach and 5 to 10 for the left-sided approach (P < 0.005). Subsequently, in seven patients a left-sided approach was used first. One to six applications of RF energy were required to create AV block. The radiation exposure time was 3 to 20 minutes. No complications occurred. CONCLUSIONS: RF ablation of the His bundle seems easier using a left-sided than a right-sided approach, reduces procedure and radiation time, and avoids recovery of conduction. These data suggest that a left-sided approach, in spite of requiring arterial catheterization, may be preferable to a right-sided approach.
Two cases are presented where ablation of severely symptomatic ventricular arrhythmias not responding to medical therapy was accomplished with radiofrequency current application. After a routine programmed stimulation protocol, a quadripolar ablation catheter with a 4-mm tip was advanced percutaneously into the left ventricle in one case and into the right ventricle in the second case; and after precise pace mapping, the arrhythmogenic focus was successfully ablated using radiofrequency current. The postablation ambulatory recording revealed virtual eradication of ventricular ectopy in both cases. In conclusion, in severely symptomatic cases of "benign" ventricular arrhythmias, radiofrequency ablation offers an effective therapeutic alternative.
BACKGROUND: Chemical or electrical ablation of an arrhythmogenic ventricular area and the atrioventricular (AV) node is still an experimental technique. After we introduced alcohol ablation in the clinical situation we conducted this study to develop the catheter technique for delivering alcohol in patients with incessant ventricular tachycardia after myocardial infarction and patients with atrial fibrillation and flutter with uncontrollable ventricular rates. METHODS: In patients with incessant ventricular tachycardia, the coronary artery supplying blood to the site of origin of the tachycardia could be identified by the combined information from coronary and left ventricular angiography and from programmed electrical stimulation, including endocardial mapping and pace mapping. In the 12 patients with incessant ventricular tachycardia we selected, the coronary artery supplying blood to the site of origin of the tachycardia could be identified and catheterized in ten patients. Ethanol ablation was successful in all of them. With a follow-up from 2 to 44 months, seven of the ten treated patients are still alive and six remain free of tachycardia. In patients with atrial fibrillation or flutter and uncontrollable ventricular rates, the AV artery could be catheterized and ethanol injected in 13 of the 19 patients. Complete block was produced in ten patients and AV conduction was sufficiently modified to control symptoms in three patients. Long-term results with ethanol ablation have remained excellent in this setting. CONCLUSION: Chemical ablation is a technique that may be of enormous value and even lifesaving for patients with an incessant form of tachycardia not responding to any form of medical therapy. Transcoronary ablation of AV conduction should be considered in patients with a right dominant coronary circulation in whom radiofrequency ablation has failed.
The effects of balloon aortic valvuloplasty on orifice variability of the stenotic sclerocalcific aortic valve were evaluated by hemodynamic measurements of aortic valve function in 14 patients before balloon aortic valvuloplasty, during nitroprusside infusion before valvuloplasty, 48 h after valvuloplasty and during nitroprusside infusion 48 h after valvuloplasty. Aortic valve function was assessed by aortic valve area calculations with use of the Gorlin and Cannon formulas. Nitroprusside infusion before balloon aortic valvuloplasty caused no change in mean aortic valve gradient but a significant increase in mean aortic transvalvular flow from 186 +/- 46 to 202 +/- 61 ml/s (p less than 0.05), in Gorlin aortic valve area from 0.49 +/- 0.17 to 0.53 +/- 0.21 cm2 (p less than 0.05) and in Cannon aortic valve area from 0.45 +/- 0.18 to 0.49 +/- 0.22 cm2 (p less than 0.05). Nitroprusside infusion 48 h after valvuloplasty induced no change in mean aortic valve gradient but a significant increase in mean aortic transvalvular flow from 214 +/- 61 to 254 +/- 78 ml/s (p less than 0.005), in Gorlin aortic valve area from 0.71 +/- 0.25 to 0.83 +/- 0.32 cm2 (p less than 0.01) and in Cannon aortic valve area from 0.78 +/- 0.33 to 0.88 +/- 0.40 cm2 (p less than 0.05). Forty-eight hours after valvuloplasty, nitroprusside infusion induced a larger increase (40 +/- 40 ml/s) in mean transvalvular flow than before valvuloplasty (16 +/- 27 ml/s; p less than 0.05) and a larger increase (0.12 +/- 0.14 cm2) in Gorlin aortic valve area than before valvuloplasty (0.05 +/- 0.07 cm2; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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To assess the effects of left ventricular (LV) load on isovolumic relaxation rate of the hypertrophied LV, wide range LV load shifts were imposed by the sequential use of balloon aortic valvuloplasty (BAV) and arterial vasodilation in 14 patients with severe sclerocalcific aortic stenosis (aortic valve area, 0.45 +/- 0.16 cm2). Micromanometer tip-catheter LV pressure recordings (n = 14) and simultaneous LV angiograms (n = 9) were obtained before BAV, during nitroprusside infusion (NIT) before BAV, 48 hours after BAV, and 48 hours after BAV during NIT. LV peak systolic pressure (LVPSP) decreased from 237 +/- 33 mm Hg before BAV to 200 +/- 33 mm Hg (p less than 0.01) during NIT before BAV, to 201 +/- 27 mm Hg (p less than 0.01) after BAV and to 165 +/- 26 mm Hg (p less than 0.01) during NIT after BAV.LV end-systolic volume (LVESV) decreased from 55 +/- 34 ml before BAV to 25 +/- 23 ml (p less than 0.01) during NIT before BAV, to 30 +/- 32 ml (p less than 0.025) after BAV and to 15 +/- 12 ml (p less than 0.025) during NIT after BAV. LV end-systolic wall stress (LVESs) decreased from 90 +/- 30.10(3) dyne/cm2 before BAV to 41 +/- 13.10(3) dyne/cm2 (p less than 0.01) during NIT before BAV, to 55 +/- 16.10(3) dyne/cm2 (p less than 0.025) after BAV and to 26 +/- 6.10(3) dyne/cm2 (p less than 0.01) during NIT after BAV. Only after sequential BAV-NIT was the time of LV electromechanical systole (LVEST), which marked the onset of the LV isovolumic relaxation period, significantly reduced (from 419 +/- 26 msec before BAV to 363 +/- 28 msec after BAV-NIT [p less than 0.01]). The time constants of LV pressure decay with zero or nonzero asymptote pressure (TO and TPB) remained unchanged after BAV and during NIT before BAV. At the lowest LVPSP, LVESV, and LVESs after sequential BAV-NIT, both TO and TPB significantly prolonged from 35.7 +/- 6.3 to 46.7 +/- 12.6 msec (p less than 0.025) and from 46.6 +/- 12.5 to 73.2 +/- 23.3 msec (p less than 0.01). Phase-plane plots (LV dP/dt vs. LVP) of the LV pressure (P) signal during isovolumic relaxation were constructed for the four different loading states by matching corresponding LVP and LV dP/dt points. For a given LVP value, the corresponding LV dP/dt values on the phase plane plots were comparable before BAV, during NIT before BAV, and after BAV. The corresponding LV dP/dt value was higher during NIT after BAV, impling a slower relaxation rate at the same LVP after sequential BAV-NIT. A shift in the control of isovolumic LV relaxation kinetics from myofilamentary detachment to myoplasmic calcium removal, which proceeds slower in hypertrophied myocardium, could explain the observed slowing of LV isovolumic relaxation after drastic LV unloading of sequential BAV-NIT.