Biomedical subjects
Publications and source records attributed to F Paganelli.
An interelectrode fracture was diagnosed 7 years after the implantation of an Accufix lead. The lead body separated from the tip with the helix screwed into the atrial wall. The retention wire was intact and may have contributed to the lead rupture.
Resistance to vitamin K antagonists is a rare phenomenon. In general, it is the result of poor patient compliance, malabsorption, a diet rich in vitamin K, or the use of enzyme inducers. Occasionally, the diagnosis of resistance is made when plasma levels are high. The authors report a case of hereditary resistance to vitamin K antagonists in a 43 year old man admitted for atrial fibrillation. The precise prevalence of this anomaly is unknown. However, the existence should be known to clinicians who often use this important family of drugs.
BACKGROUND: Type 1 plasminogen activator inhibitor (PAI-1) is considered to be risk factor for acute myocardial infarction (AMI). A rebound of circulating PAI-1 has been reported after rt-PA administration. We investigated the relationships between PAI-1 levels before and after thrombolytic therapy with streptokinase (SK) as compared to rt-PA and the patency of infarct-related arteries. METHODS AND RESULTS: Fifty five consecutive patients with acute MI were randomized to streptokinase or rt-PA. The plasma PAI-1 levels were studied before and serially within 24 h after thrombolytic administration. Vessel patency was assessed by an angiogram at 5+/-1days. The PAI-1 levels increased significantly with both rt-PA and SK as shown by the levels obtained from a control group of 10 patients treated with coronary angioplasty alone. However, the area under the PAI-1 curve was significantly higher with SK than with rt-PA (p<0.01) and the plasma PAI-1 levels peaked later with SK than with rt-PA (18 h versus 3 h respectively). Conversely to PAI-1 levels on admission, the PAI-1 levels after thrombolysis were related to vessel patency. Plasma PAI-1 levels 6 and 18 h after SK therapy and the area under the PAI-1 curve were significantly higher in patients with occluded arteries (p<0.002, p<0.04 and p<0.05 respectively). The same tendency was observed in the t-PA group without reaching significance. CONCLUSIONS: This study showed that the PAI-1 level increase is more pronounced after SK treatment than after t-PA treatment. There is a relationship between increased PAI-1 levels after thrombolytic therapy and poor patency. Therapeutic approaches aimed at quenching PAI-1 activity after thrombolysis might be of interest to improve the efficacy of thrombolytic therapy for acute myocardial infarction.
OBJECTIVES: Assess the efficacy of an anesthetic cream for cardiac catheterization. PATIENTS AND METHODS: Percutaneous anesthesia was studied in a series of 100 consecutive patients undergoing cardiac catheterization. The anesthesia was composed with an eutetic mixture of local anesthetics and applied precisely over the puncture area in a randomized controlled study. After admission, patients were randomized into two groups: 50 patients received lidocaine infiltration and 50 patients received associated cream and infiltration. Percutaneous anesthesia was to be applied 2 hours before entering the operating room. RESULTS: No complication developed with this cream combined with lidocaine infiltration. Serum concentration indicated very low levels which were very well tolerated. Patient comfort improved with the anesthetic cream-lidocaine infiltration association. CONCLUSION: The use of an anesthetic cream is safe and effective, especially combined with lidocaine infiltration during cardiac catheterization. Cost is high and the association might be reserved for special indications (obesity, children).
Cicletanine, a furopyridine-derivative drug, was shown to enhance the production of endogenous prostacyclin. The potent vasodilating properties of prostacyclin are used to treat severe primary pulmonary hypertension. Prostacyclin has a short half-life and can be administered only as an i.v. infusion. The aim of this study was to evaluate the effects of cicletanine on pulmonary artery hypertension (PAH) resulting from chronic obstructive lung disease (COLD). In a double-blind controlled study, we evaluated the effects of short- and long-term administration of cicletanine (50 mg daily, orally) on hemodynamics and blood gases of patients with PAH resulting from COLD. The initial dose of 50 mg of cicletanine had no effect. A significant decrease in the mean pulmonary artery pressure (15%) and in total pulmonary resistance (20%) was observed after 3 or 12 months of treatment in the cicletanine group (11 patients), when compared with placebo (12 patients). PaO2 decreased slightly in the cicletanine group, but the difference from the control group was not significant. These results suggest that long-term treatment with cicletanine can induce effective pulmonary vasodilation in patients with PAH caused by COLD and that this is probably responsible for a small venous admixture.
INTRODUCTION: Circulating autoantibodies against myosin heavy chain have been detected in patients with ventricular myocarditis and in patients with dilated cardiomyopathy. This study investigated the presence of antibodies against myosin in sera of healthy control persons as compared with patients with idiopathic paroxysmal atrial fibrillation refractory to antiarrhythmic therapy. METHODS AND RESULTS: An SDS-PAGE (sodium dodecylsulfate polyacrylamide gel electrophoresis) procedure, followed by Western blotting with homogenates and membrane fractions of human left ventricular and atrial specimen as antigens, was used to analyze sera of 10 patients with idiopathic paroxysmal atrial fibrillation and 10 age-matched healthy control subjects. Circulating immunoglobulin G reactivity against cardiac myosin heavy chain was detected in 6 patients (60%) as compared with 1 control subject (10%). This difference was statistically significant (P < 0.05). All patients with idiopathic paroxysmal atrial fibrillation who showed reactivity against myosin heavy chain also had specific reactivity in their sera that exhibited reactivities to both ventricular and atrial cardiac myosin heavy chain isoforms. CONCLUSION: This study demonstrates the presence of circulating autoantibodies against myosin heavy chain in a significant percentage of patients with idiopathic paroxysmal atrial fibrillation and raises the possibility of an autoimmune process in some patients with paroxysmal atrial fibrillation.
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BACKGROUND: Recent studies have suggested that induced atrial fibrillation (AF) could be successfully terminated by using a two-catheter electrode system and low energy (< 400 V). This study evaluated the efficacy and safety of low-energy cardioversion in spontaneous chronic and paroxysmal AF. METHODS AND RESULTS: Forty-two consecutive patients with spontaneous AF underwent low-energy electrical cardioversion. AF was chronic (> or = 1 month) with a mean duration of 9 +/- 19 months in 28 patients (group I) or paroxysmal with a history of recurrent attacks and a mean duration of the present episode of 7 +/- 16 days in 14 patients (group II). An underlying heart disease was present in 28 patients. A 3/3-ms biphasic shock was delivered between catheters positioned in the right atrium and the coronary sinus in 32 patients. In 10 patients, the left pulmonary artery branch was used. The catheters were connected to a custom external defibrillator. The shocks were synchronized to the R wave. Following a test shock of 60 V, the energy was increased in 40-V steps until a maximum of 400 V or restoration of sinus rhythm. Sinus rhythm was restored in 22 of the 28 patients (78%) of group I by using a mean leading-edge voltage of 297 +/- 57 V (mean energy 3.3 +/- 1.3 J) and in 11 of 14 patients (78%) of group II by using a mean leading-edge voltage of 223 +/- 41 V (mean energy, 1.8 +/- 0.7 J). The energy required for terminating chronic AF was significantly (P < .001) higher than that required for terminating paroxysmal AF. Among the other variables studied, the duration of AF significantly affected the successful voltage. Ventricular proarrhythmia occurred in 1 patient with atrial flutter due to an unsynchronized shock. Of the 22 patients of group I in whom sinus rhythm was restored, 14 (63%) remained in sinus rhythm with a mean follow-up of 9 +/- 3 months. Pain level showed a good correlation with increasing voltage. However, a marked inter-individual variation was noted. CONCLUSIONS: Atrial defibrillation using low energy between two intracardiac catheters with an electrical field between the right and left atria and the protocol used is feasible in patients with persistent spontaneous AF. The technique is safe provided synchronization to the R wave is achieved. A low recurrence rate of AF was seen in patients in whom sinus rhythm was restored.
This study demonstrates that shocks <200 J often are effective for transthoracic cardioversion of atrial fibrillation (AF). Lower energy shocks are more likely to be effective when the AF is <24 hours in duration or in patients with idiopathic AF.
This report describes the case of a patient in whom, after an unsuccessful attempt through the subclavian vein, a permanent pacing lead was inserted through the femoral vein and a left inferior vena cava with azygos continuation. The procedure was followed 4 months later by a pulmonary embolism complicating a right femoroiliac thrombosis. The patient was successfully treated by a percutaneous lead extraction procedure combined with an inferior vena caval surgical interruption.
Several reports have suggested that radiofrequency ablation could prevent atrial flutter resistant to antiarrhythmic therapy. The usual recommendation is to apply the radiofrequency current in a zone situated between the tricuspid valve and orifice of inferior vena cava. The aim of this study was to assess the efficacy of another site of ablation of flutter extending from the tricuspid valve to the orifice of the coronary sinus, either alone or associated with a site between the coronary sinus and the lateral wall of the right atrium. Twenty patients aged 42 to 78 years (mean : 6 +/- 11 years) were included. Atrial flutter was paroxysmal in 15 patients and chronic in 5 patients. Each patients had documented failure of 1 to 5 antiarrhythmic agents (average 3.1 +/- 1.6). The site of ablation was localised by anatomical criteria alone. During follow-up of 7 +/- 5 months (range 1 to 18 months), 13 patients had no recurrence of atrial flutter after ablation, 5 patients had recurrence and 2 patients had paroxysmal atrial fibrillation alone: the success rate was 15/20 (75%). This study suggests that the zone between the tricuspid valve and coronary sinus may be a site for radiofrequency ablation of atrial flutter. It is valuable alternative to the usually recommended technique.
The intraoperative and early postoperative mechanical complications of a procedure combining an atrial screw-in lead and a ventricular screw-in lead insertion were prospectively evaluated. The procedure was performed in 119 consecutive patients (mean age 69 +/- 8 years), at first implant in 100 patients and at reoperation in 19. Nine patients had previously undergone cardiac surgery and three underwent transvenous ventricular defibrillator implantation. The double sets of leads were introduced through 2 separate veins in 5 cases, through a single venous route in 114 cases, using a percutaneous approach in 75 cases and a venous cutdown in 49, and a guidewire procedure following the venotomy in 19. The screw was mannitol coated in 102 cases, exposed in 111, and extendable/retractable in 25. The fixation of the ventricular lead was performed at the apex in 108 cases, at the outflow tract in 11, and was followed by the fixation of the atrial lead at the appendage in 112 cases and at the lateral wall in 7 cases. The lead positioning and fixation were successful at first attempt in 103 cases and after repeated lead manipulation in 19 cases. The rotational torque could be transferred to the helix in all cases except in one patient who required a second vein puncture. Unintentional fixation in the ventricular chamber with subsequent failure to remove the lead occurred in one patient. Reoperation for lead dislodgment was required in two patients. In one patient, symptomatic pericarditis with pericardial effusion was observed 1 day after the procedure and resolved spontaneously. Dual active fixation is feasible with a low incidence of mechanical complications.
Aborted sudden death as the presenting manifestation of hypertrophic cardiomyopathy in a 14-year-old child is reported. Documented ventricular fibrillation was the cause of cardiac arrest. No ventricular arrhythmia was induced during programmed electrical stimulation. An implantable cardioverter-defibrillator was indicated. As the patient had a family history of myocardial disease, he had undergone a cardiovascular evaluation 4 years before the major event, and was found normal. It is suggested that normal physical examination, ECG, echocardiogram should not rule out the diagnosis of hypertrophic cardiomyopathy when a family history is present. Left ventricular hypertrophy may develop during childhood in patients with hypertrophic cardiomyopathy.
OBJECTIVES: There is no consensus on heart explorations required before infra-renal reconstruction surgery of the aorta. We proposed a selective approach in 81 consecutive patients undergoing elective surgery. METHODS: Four clinical criteria were recorded: age over 70 years, diabetes mellitus and a clinical history of coronary artery disease or heart failure. RESULTS: For 23 patients (group 1), none of the criteria were positive. Surgery was performed in all without prior exploration. There was one death (4.8%) and one post-operative cardiac event (4.8%) in this group. The 58 other patients (group 2) had at least one of the criteria and had complementary heart explorations before surgery. There were 2 deaths (3.4%) and 5 cases of cardiac morbidity (8.6%) in this group. CONCLUSION: The lack of any statistical difference between the two groups with and without risk criteria has led us to propose selective indications for preoperative explorations based on specific clinical criteria.
Intravenous cibenzoline was evaluated in 37 patients with acute supraventricular tachyarrhythmias and a ventricular rate > 120 beats/min. The presenting arrhythmia was atrial fibrillation in 15 patients, atrial flutter in 5, ectopic atrial tachycardia in 11, and paroxysmal atrioventricular (AV) junctional reentrant tachycardia in 6 patients. Intravenous cibenzoline was administered as a bolus given over 2 minutes, at a dose of 1 mg/kg in the first 26 patients and 1.2 mg/kg in the subsequent 11 patients, 15 minutes following failure of placebo (isotonic glucose). The results were evaluated 15 minutes after the intravenous injection. Restoration of sinus rhythm was obtained in 3 out of 6 patients with paroxysmal AV junctional tachycardia (50%) and in 7 out of 31 patients (23%) with atrial tachyarrhythmias (5 out of 15 patients with atrial fibrillation and 2 out of 16 patients with ectopic atrial tachycardia or atrial flutter). Five additional patients with atrial tachyarrhythmias had slowing of ventricular rate below 100 beats/min. Therefore, a satisfactory result, that is, restoration of sinus rhythm or slowing of ventricular rate, occurred in 15 patients (40.5%). Side effects were transient, including visual disturbance (one patient), asymptomatic widening of QRS complex (three patients), incessant reciprocating tachycardia (one patient), and acceleration of ventricular rate (eight patients), resulting in 1:1 flutter, with poor tolerance in two patients.(ABSTRACT TRUNCATED AT 250 WORDS)
In addition to pain and stress, endogenous opiates and in particular beta-endorphin could be involved in the modulation of cardiovascular parameters. Several studies have thus shown increases in plasma beta-endorphin levels in the course of septic or hypovolemic shock. Our study involving 44 multiple trauma patients indicates that even in the absence of any hemodynamic disorders, there is a correlation between systolic blood pressure and plasma beta-endorphins. These results argue in favor of the existence of feedback between systolic blood pressure and plasma beta-endorphins.
UNLABELLED: Classification of Atrial Fibrillation. INTRODUCTION: Clinical aspects of paroxysmal atrial fibrillation are heterogeneous. The attacks of atrial fibrillation may differ in their duration frequency and presence and severity of symptoms. Therefore, a proposal for a clinical classification of paroxysmal atrial fibrillation may be helpful. We tested a new classification system in a cohort of 51 consecutive hospitalized patients with paroxysmal atrial fibrillation. METHODS AND RESULTS: Paroxysmal atrial fibrillation was subdivided into three classes. Class I included a first attack of symptomatic atrial fibrillation either with spontaneous termination (IA) or requiring cardioversion because of poor tolerance (IB). Class II included recurrent attacks in untreated patients within three subgroups: IIA with no symptoms, IIB with < 1 symptomatic attack per 3-month period, and IIC > with 1 symptomatic attack per 3-month period. Class III included recurrent atrial fibrillation unresponsive to one or more antiarrhythmic agents for prevention of recurrences. Class III also consisted of three subgroups: IIIA with no or mild symptoms, IIIB with < 1 symptomatic attack per 3-month period, and IIIC with > 1 symptomatic attack per 3-month period. The criteria for paroxysmal atrial fibrillation (episode > 2 minutes and < 7 days in duration) were fulfilled by 51 patients (29 men, 22 women; mean age 61 +/- 14 years). Structural heart disease was present in 31 patients; the atrial fibrillation was idiopathic in 18 (35%). All 51 patients could be classified within the three classes and their subgroups: 14 patients (27%) in Class I, 13 (25%) in Class II, and 24 (47%) in Class III. The incidences of idiopathic atrial fibrillation were 21%, 30%, and 45% of the patients in Classes I, II, and III, respectively. CONCLUSIONS: Based on this new classification system, all hospitalized patients with paroxysmal atrial fibrillation could be classified. This classification may be useful to delineate better the clinical subgroups of patients with paroxysmal atrial fibrillation, to characterize better the patient population in future studies, and to improve treatment strategies.