Biomedical subjects

C A Morillo

Publications and source records attributed to C A Morillo.

27 records · Page 2Linked to original sources

PubMed1994

Time and frequency domain analyses of heart rate variability during orthostatic stress in patients with neurally mediated syncope.

The role of autonomic balance during upright tilt in patients with neurally mediated syncope is unclear. To assess the characteristics of autonomic tone during orthostatic stress, 15 patients (mean age 32 years) with recurrent episodes of syncope (> or = 2) and a positive response to a 30-minute 60 degrees upright tilt were compared with the following control groups: (1) 15 patients (mean age 33.5 years) with > or = 2 episodes of recurrent syncope and a negative tilt response, and (2) 15 age- and sex-matched healthy volunteers (mean age 34 years) with no previous history of presyncope or syncope. Time domain measurements assessed were mean RR interval, standard deviation of normal RR intervals, and percentage of normal consecutive RR intervals differing by > 50 ms. Frequency domain measurements of the low-frequency (LF) and high-frequency (HF) bands were obtained, and the LF/HF ratio was also calculated. All variables were calculated in the supine position and during the first 5 minutes of upright tilt. No significant difference was observed in the time and frequency domain variables in the supine position between control groups with a negative head-up tilt response and the group with a positive response. The percentage of normal consecutive RR intervals differing by > 50 ms during the first 5 minutes of head-up tilt was significantly higher in the group with positive tilt tests than in the controls (25 +/- 12% vs 7 +/- 4%, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Effect of shock timing on efficacy and safety of internal cardioversion for ventricular tachycardia.

OBJECTIVES: We examined the effect of shock timing within the QRS complex on cardioversion efficacy in a randomized crossover test of shocks delivered at two timing intervals relative to QRS onset. BACKGROUND: The local ventricular electrogram is used in implantable cardioverter-defibrillators to synchronize cardioversion shocks to terminate ventricular tachycardia. However, the timing of the local electrogram relative to global ventricular depolarization is variable, depending on the site of ventricular tachycardia origin. METHODS: Transvenous defibrillation leads were positioned in the right ventricular apex (cathode), coronary sinus and superior vena cava (anodes) of patients with sustained monomorphic ventricular tachycardia. After repeat ventricular tachycardia induction, sequential shocks with energy settings of 0.5 to 22 J were delivered simultaneously with QRS onset (QRS + 0 shock) or 100 ms after QRS onset (QRS + 100 shock). QRS onset was determined from the surface electrocardiogram. Cardioversion threshold, defined as the lowest shock energy for successful ventricular tachycardia termination, was measured for these two timings. RESULTS: Fifteen patients (13 men, 2 women; mean [+/- SD] age 60.5 +/- 7.7 years) completed testing. Cardioversion threshold was significantly lower with QRS + 100 shocks than QRS + 0 shocks (3.1 +/- 3.5 vs. 10.5 +/- 7.4 J, p < 0.01). Thirteen patients (87%) experienced ventricular tachycardia acceleration with QRS + 0 shocks, but only three patients (20%) had ventricular tachycardia acceleration using QRS + 100 shocks (p < 0.01). Of the 32 failed QRS + 0 shocks, 25 (78%) caused ventricular tachycardia acceleration, whereas only 5 (36%) of the 14 failed QRS + 100 shocks caused ventricular tachycardia acceleration (p < 0.05). Cardioversion threshold was not correlated with ventricular tachycardia cycle length, QRS duration, left ventricular ejection fraction or left ventricular diastolic volume (p = NS). CONCLUSIONS: Internal cardioversion shocks delivered late in the QRS complex during ventricular tachycardia are more effective and have a lower risk of ventricular tachycardia acceleration than those delivered near QRS onset.

Aged↗

PubMed1994

Effect of adenosine or adenosine triphosphate on antidromic tachycardia.

OBJECTIVES: This study was designed to determine the effect of adenosine or adenosine triphosphate (ATP) on antidromic tachycardia. BACKGROUND: Adenosine and adenosine triphosphate are useful for differential diagnosis of wide QRS tachycardia. It has been believed that tachycardia termination caused by these agents is due to the preferential depressive effect on the atrioventricular (AV) node, whereas their effect on accessory pathways is minimal. METHODS: We studied the effect of adenosine or ATP on the termination pattern of antidromic tachycardia in 17 patients (10 men, 7 women; mean age [+/- SD] 32 +/- 11 years) with one or more accessory pathways. Adenosine (6 to 12 mg [n = 10]) or ATP (8 to 20 mg [n = 7]) was injected rapidly through a central venous line and followed by 10 ml of saline flush after induction of sustained antidromic tachycardia. RESULTS: Tachycardia was terminated in < 2 min in 14 patients (82%) after the injection and remained unchanged in 3 (18%). Tachycardia termination was due to conduction block in the accessory pathway (anterograde limb) in seven patients (50%) and in the AV node (retrograde limb) in another seven. Adenosine or ATP caused accessory pathway block in seven (88%) of the eight patients lacking retrograde accessory pathway conduction and in none of the nine patients having retrograde accessory pathway conduction (p < 0.01). All five patients with an atriofascicular accessory pathway and unidirectional anterograde conduction had tachycardia termination due to anterograde accessory pathway block after injection of adenosine or ATP. CONCLUSIONS: 1) Adenosine or ATP effectively terminates antidromic tachycardia; 2) the termination is related to block in either the accessory pathway or the AV node; 3) accessory pathway block occurs in patients with a unidirectional, anterogradely conducting accessory pathway, especially an atriofascicular accessory pathway.

Adenosine↗

PubMed1994

Radiofrequency catheter ablation of accessory pathways during entrainment of AV reentrant tachycardia.

Radiofrequency ablation of accessory pathways must sometimes be done during orthodromic atrioventricular reentrant tachycardia when manifest anterograde accessory pathway conduction is absent or retrograde fusion obscures accessory pathway location during ventricular pacing. Unfortunately, abrupt heart rate slowing upon radiofrequency induced termination of atrioventricular reentrant tachycardia often causes catheter dislodgment. We report our experience in circumventing this problem during radiofrequency ablation by using entrainment of atrioventricular reentrant tachycardia. The latter maintains retrograde activation pattern over the accessory pathway while preventing abrupt ventricular rate change. Eight patients (4 men and 4 women, mean age 37.3 +/- 17.9) with eleven left-sided accessory pathways were included. Ablation during entrainment was used as the first approach in three patients with concealed accessory pathways and one patient with a bidirectional accessory pathway. In another four patients, ablation during entrainment was used after technical difficulties in ablating during tachycardia. Only 1-3 radiofrequency applications were required to eliminate the accessory pathway using the entrainment technique. The catheter remained stable when accessory pathway conduction was interrupted by radiofrequency current. In conclusion, entrainment of atrioventricular reentrant tachycardia during radiofrequency application is useful for maintaining catheter position for accessory pathway ablation during atrioventricular reentrant tachycardia.

Adolescent↗

PubMed1994

Mechanism of 'inappropriate' sinus tachycardia. Role of sympathovagal balance.

BACKGROUND: "Inappropriate" sinus tachycardia (IST) is an uncommon and poorly defined atrial tachycardia characterized by inappropriate tachycardia and exaggerated acceleration of heart rate with "normal" P wave. The mechanism of this tachycardia is unknown. The purpose of the present study was to determine the role of autonomic balance in the genesis of IST. METHODS AND RESULTS: Six female patients aged 23 to 38 years with IST and 10 age- and sex-matched control subjects were assessed with the following autonomic function tests: (1) sympathovagal balance to the sinus node assessed by calculating the LF/HF (low frequency/high frequency) ratio using power spectral analysis both in the supine position and after 10 minutes of head-up tilt to 60 degrees, (2) cardiovagal reflex assessed by cold face test (CFT), (3) beta-adrenergic sensitivity as determined by calculating isoproterenol dose-response curves and isoproterenol chronotropic dose 25 (CD25), and (4) intrinsic heart rate (IHR) assessed after autonomic blockade with atropine 0.04 mg/kg and propranolol 0.2 mg/kg administered as an intravenous bolus. No significant differences in the LF/HF ratio both in the supine position (2.8 +/- 0.3 versus 2.6 +/- 0.4) and during upright tilt (8.7 +/- 1.3 versus 8.5 +/- 0.5) were observed between control subjects and IST patients. Cardiovagal response to CFT was markedly depressed in all patients (6.3% IST patients versus 24.2% control subjects, P < .001). beta-Adrenergic hypersensitivity to isoproterenol was noted in all patients (mean CD25, 0.29 +/- 0.10 microgram IST patients versus 1.27 +/- 0.4 microgram control subjects; P < .001), and high IHR was noted in all cases. The patients were treated with high doses of beta-blockers with adequate short-term control. Radiofrequency catheter ablation of the sinus node area was performed in one drug-refractory patient. CONCLUSIONS: These findings suggest that the mechanism leading to IST is related to a primary sinus node abnormality characterized by a high IHR, depressed efferent cardiovagal reflex, and beta-adrenergic hypersensitivity.

Adrenergic beta-Antagonists↗

PubMed1993

A prospective randomized comparison of autodecremental pacing to burst pacing in device therapy for chronic ventricular tachycardia secondary to coronary artery disease.

A number of modes of antitachycardia pacing therapies are available in the newer generations of implantable cardioverter/defibrillators. The efficacy of synchronized burst overdrive pacing for the termination of induced and spontaneous monomorphic ventricular tachycardia (VT) was compared with synchronized autodecremental (ramp) pacing in 21 patients who received an implantable antitachycardia pacemaker/cardioverter/defibrillator for treatment of recurrent sustained monomorphic VT. Patients undergoing serial noninvasive VT induction studies after device implantation were prospectively randomized to receive trials of burst or ramp pacing therapies in a crossover study design. Antitachycardia pacing therapies were equally efficacious in treating induced VT (68% for ramp, 76% for burst pacing trials). The efficacy of ramp (93%) and burst (96%) pacing therapies was significantly higher in terminating spontaneously occurring episodes of VT than in terminating induced episodes (p = 0.001). The incidence of tachycardia acceleration was similar for both modes of pacing. The incidence of VT acceleration was lower for spontaneously occurring episodes of VT (0.01%) than for induced episodes of VT (6%, p < 0.01). Thus, antitachycardia pacing is an effective therapy for episodes of monomorphic VT, and the risk of accelerating VT to a hemodynamically unstable form is low. Antitachycardia pacing therapies are more effective against spontaneously occurring episodes than induced episodes of VT. Differences in tachycardia cycle length and duration may contribute to these effects.

Adult↗

PubMed1993

A placebo-controlled trial of intravenous and oral disopyramide for prevention of neurally mediated syncope induced by head-up tilt.

OBJECTIVES: A double-blind randomized trial was designed to determine the efficacy of intravenous and oral disopyramide phosphate in preventing neurally mediated syncope induced by a head-up tilt test. BACKGROUND: Neurally mediated syncope is a frequent cause of syncope and may be induced by head-up tilt testing. Recent uncontrolled trials have suggested that disopyramide may be an effective therapy in patients with neurally mediated syncope. METHODS: Twenty-two consecutive patients with recurrent neurally mediated syncope and two or more successive positive head-up tilt test responses were randomly allocated to receive either intravenous disopyramide or placebo. Head-up tilt testing at 60 degrees was performed for 15 min. If presyncope or syncope was not provoked, isoproterenol infusion was started at a rate of 1 microgram/min and the rate gradually increased until a 25% increase in heart rate was achieved. Eleven patients were subsequently randomized in crossover fashion to receive oral disopyramide (800 mg/day) or placebo during 1 week. The primary end point was prevention of syncope or presyncope provoked by head-up tilt testing. RESULTS: Head-up tilt test results were positive for syncope in 12 (75%) of 16 patients receiving intravenous placebo and in 12 (60%) of 20 patients receiving disopyramide (p = 0.55 Fisher exact test, 95% confidence interval [CI] -14% to 40%). In the intravenous phase, complete crossover was achieved in 15 patients. Head-up tilt test results during this phase were positive in 13 patients (87%) receiving placebo and in 12 patients (80%) receiving disopyramide (p = 0.50 Fisher exact test, 95% CI -19% to 32%) and were positive in all patients receiving their initially randomized drug or placebo. In the oral phase, head-up tilt results were positive in only two patients (18%) assigned to placebo and in three patients (27%) receiving disopyramide (p = 0.54 Fisher exact test, 95% CI -42% to 24%). A mean follow-up time of 29 +/- 8 months was obtained in 21 of the 22 patients. Syncope recurred in 3 (27%) of the 11 patients receiving disopyramide and 3 (30%) of the 10 patients not treated pharmacologically (p > 0.05). CONCLUSIONS: Intravenous disopyramide was ineffective for the prevention of neurally mediated syncope provoked by head-up tilt testing. No significant effect was observed after oral therapy with disopyramide. There was a striking decrease in the incidence of positive tilt test results over time regardless of intervention, thus discouraging the use of head-up tilt as the single method of assessing therapeutic efficacy. Recurrence of syncope after the investigative protocol was infrequent over long-term follow-up regardless of treatment group.

Administration, Oral↗

PubMed1993

Elimination of slow pathway conduction: an accurate indicator of clinical success after radiofrequency atrioventricular node modification.

OBJECTIVES: The purpose of this study was to determine the optimal end point of radiofrequency atrioventricular (AV) node modification using anatomically guided slow pathway approaches in patients with AV node reentrant tachycardia. BACKGROUND: The optimal end point for AV node modification using radiofrequency energy is uncertain, although elimination of inducible AV node reentrant tachycardia has been used. METHODS: We followed up 51 consecutive patients (40 women, 11 men, mean age +/- SD 41 +/- 16 years) with symptomatic AV node reentrant tachycardia for 12 +/- 6 months (range 4 to 24) after radiofrequency AV node modification using an anatomically guided slow pathway approach. Inducible AV node reentrant tachycardia was eliminated in all patients, whereas residual slow pathway conduction persisted in 12 patients (24%) after ablation. One study was complicated by complete AV block and two patients were lost to follow-up (one with and one without residual slow pathway conduction). RESULTS: Clinical recurrence of AV node reentrant tachycardia was documented in seven patients (14%) 3 days to 3 months (median 1 month) after ablation. The recurrence rate was significantly higher in patients with than in those without residual slow pathway conduction (6 [55%] of 11 vs. 1 [3%] of 37, p < 0.01). The recurrence rate was not different between patients with only residual slow pathway conduction and those with residual slow pathway conduction and inducible single echo cycles (three [60%] of five in both groups, p = NS). The number of radiofrequency energy applications was not significantly different between those without and those with recurrence (20 +/- 17 vs. 16 +/- 9, p = NS). Junctional tachycardia during application of radiofrequency energy tended to be more frequently observed in those with a successful outcome (77% vs. 57%, p > 0.05). Of the 22 patients who underwent modification before 1992, residual slow pathway conduction was present in 9 (41%) of 22 patients. Atrioventricular node reentrant tachycardia recurred in five (56%) of these nine patients. A greater effort made in 1992 to eliminate slow pathway conduction in 29 patients resulted in residual slow pathway conduction in only 3 (11%) with recurrence in 2 (4%). CONCLUSIONS: Complete elimination of slow pathway conduction is feasible in the majority of patients. Elimination of slow pathway conduction is highly predictive of long-term success after AV node modification using an anatomically guided approach.

Adult↗

PubMed1993

Malposition of transvenous pacing lead in the left ventricle.

Malposition of pacemaker leads has been described in several locations but rarely in the left ventricle. The incidence and clinical course of this pacemaker complication are unknown. We describe clinical, electrocardiographic, chest X ray, and echocardiographic findings in four patients in whom the transvenous pacing lead was inadvertently placed through the interatrial septum and mitral valve into the left ventricle. In these patients, lead misplacement was not recognized at the time of implantation and lead malposition was diagnosed a mean of 2 years later. All four patients had right bundle branch block configuration paced complexes. In retrospect, chest X rays suggested atypical lead position in all, but the initial posterior-anterior and lateral chest X rays were misinterpreted and contributed to the delay in diagnosis. When lead misplacement in the left ventricle was considered it was confirmed by two-dimensional echocardiography. One patient subsequently presented with a stroke and the remainder were diagnosed when they presented with other unrelated problems. Pacing thresholds were normal at the time of implantation and behaved normally during follow-up. The patient presenting with stroke was anticoagulated and the other three have been managed expectantly without anticoagulation. Diagnosis of left ventricular lead malposition is not difficult but requires a high index of suspicion. A 12-lead ECG and posterior-anterior and lateral chest X rays after implantation can be diagnostic. Patients with pacing lead in the left ventricle may remain asymptomatic with normal lead function during long-term follow-up. Anticoagulation should be considered when this problem comes to attention for the first time during follow-up.

Aged↗