Biomedical subjects
Publications and source records attributed to C Suty-Selton.
We compared the prognostic significance of prior angina pectoris in 151 patients > or = 75 years of age admitted for acute myocardial infarction. There was a similar in-hospital course, but the long-term outcome was poorer in patients with prior angina.
OBJECTIVES: Analyze management of myocardial infarction in elderly subjects and assess long-term outcome. METHODS: We studied retrospectively a series of 151 consecutive cases of acute myocardial infarction in patients over 75 years of age and compared then with a group of young subjects under 65 years of age admitted for the same pathology during the same period (1989-1993). RESULTS: In the elderly population, female sex, past history of angina or infarction, atypical presentation and hemodynamic complications were more frequent in the elderly population (left ventricle failure 44 vs 13%, cardiogenic shock 17.2 vs 0.7% without any difference in localization. Mortality was higher in the elderly group (23.2 vs 2.6%) with 68.6% of the deaths due to primary cardiogenic shock. Beta-blockers were used less frequently in the elderly population (31.8 vs 83.0%) as was thrombolysis (26.5 vs 64.5%); coronography was performed less often (21.8 vs 92.7%) as was percutaneous revascularization (9.9 vs 36.4%) or surgery (1.3 vs 6.6%). Survival at 1, 2 and 5 years was 88, 76 and 57% in the elderly group (Kaplan-Meier plot). A past history of unstable angina and a critical episode of left ventricle failure were factors predicting overmortality. CONCLUSION: Acute myocardial infarction remains a severe condition in patients over 75 years of age with overmortality during hospitalization and poor long-term prognosis. Clinical signs of poor prognosis could help guide selection for more aggressive therapeutic management during the post-infarction period, notably in terms of coronary revascularization.
The purpose of the study was to report the prevalence of inducible supraventricular tachyarrhythmias (SVTA) in 827 consecutive patients aged 17 to 90 years who did not have spontaneous documented SVTA and who had unexplained presyncope and/or syncope. The electrophysiologic study (EPS) included programmed atrial and ventricular stimulation up to two extrastimuli at three cycle lengths, and the study of sino-atrial and AV conduction. The results were as follows. EPS was normal in 386 patients. Inducible junctional tachycardia or atrial flutter and fibrillation was the only finding in 187 patients (23%). In the remaining patients we found ventricular tachycardia in 103 (12%), heart block in 67 (8%), sick sinus syndrome in 56 (7%) and increased vagal tone in 28 (3%). The presence of an underlying heart disease (47%) and salvos of atrial premature beats on Holter monitoring (39%) were significantly correlated with the induction of SVTA. However, the comparison with similar groups without syncope indicates that only the induction of SVTA in patients with hypertrophic cardiomyopathy and mitral valve prolapse was significantly correlated with the history of syncope. In patients without heart disease or with prior myocardial infarction or decreased left ventricular function, the induction of SVTA, which is not associated with hypotension in the supine position, could require an induction after head-up tilting, because of the lack of specificity of programmed stimulation in these patients. Programmed atrial stimulation should be systematically performed in patients with unexplained syncope, in particular in those with hypertropic cardiomyopathy and mitral valve prolapse, who require a specific treatment, if a SVTA is induced. In other patients the results of programmed atrial stimulation should be interpreted cautiously.
Prolapsed mitral valve prolapse (PMV) is classically associated with disorders of ventricular excitability whose significance is unclear. However, syncope can suggest the possibility of a serious ventricular arrhythmia. The objective of this study was to try to identify the mechanisms of dizziness and syncope associated with PMV. We report the results of programmed atrial and ventricular stimulation performed under baseline conditions and after administration of Isuprel in 56 patients with PMV: 27 patients had a history of presyncope or syncope (group I), 14 had spontaneous atrial or supraventricular tachycardias without dizziness or syncope (group II) and 15 were asymptomatic and investigated for VEBs or conduction disorders (group III). The following results were obtained: In group I, 6 patients experienced sustained inducible ventricular tachycardia (VT); an atrial tachycardia (atrial tachycardia and/or atrial fibrillation) (AT) was also induced in 5 of them. In another 19 patients, a supraventricular tachycardia (SVT) and/or AT was induced. A total of 24 atrial or junctional tachycardias were triggered in this group. In group II, AT and/or SVT were reproduced in 13 out of 14 cases (93%). In group III, AT was triggered in 3 patients (20%). SVT were induced by Isuprel while AT were triggered prior to administration of Isuprel, under baseline conditions, and 3 of them were reproduced during vagal manoeuvres. A ventricular arrhythmogenic effect was observed in two cases in group II while taking class I antiarrhythmics. In conclusion, spontaneous AT and SVT of PMV are easily inducible with a sensitivity of 93%, but are difficult to induce in asymptomatic subjects. The high incidence of TA and SVT in the case of unexplained presyncope in subjects without documented tachycardia therefore appears to be suggestive of a relationship between these presyncopes and AT or SVT. However, the search for VT should take precedence. SVT appear to be catecholaminergic while AT tend to be vagal.
The prognostic significance of ventricular tachyarrhythmias induced by programmed ventricular stimulation was evaluated in 492 consecutive survivors of acute myocardial infarction (AMI). Holter monitoring, signal-averaged electrocardiogram (ECG) and measurement of left ventricular ejection fraction (EF) were also performed. The protocol used up to 3 extrastimuli. Sustained monomorphic ventricular tachycardia (VT) < 270 beats/min, > 270 beats/min (ventricular flutter) (VFI), and ventricular fibrillation (VF) were induced in 99, 66 and 52 patients, respectively. Long term follow-up (mean 3.7 +/- 2.2 years) showed that most episodes of VT occurred during the first months following AMI (n = 14), but some patients (n = 6) could develop VT as late as 4 years after AMI. Sudden death (SD) (n = 22) always occurred during the first year following AMI. Multivariate analysis demonstrated that EF < 30% and induction of a VT < 270 beats/min were the only predictors for total cardiac death (P < 0.001). EF < 30%, induction of a VT < 270 beats/min and also of VFI (P < 0.05) were predictors for VT and SD: the risk was 4% in patients without inducible VT, 12% in those with inducible VF1, and 21% in those with inducible VT < 270 beats/min. In conclusion, induction of a sustained monomorphic VT < 270 beats/min or > 270 beats/min is a predictor of arrhythmic events during the first year as well as 4 years after myocardial infarction. However the risk of arrhythmic sudden death decreases after the first year, while the risk of VT persists. Because of the low positive predictive value of programmed stimulation (respectively 21% and 12% for the induction of a sustained VT and VFI), we recommended the indication of programmed stimulation in only the patients with one abnormal non-invasive investigation.
Among 7467 consecutive coronary angiograms performed during an 8-year period, 61 patients had a myocardial bridge of the left anterior descending coronary artery. The overall prevalence of myocardial bridges was 0.82% (from 0.41% to 1.16% per year). Among these patients, 26 had coronary artery disease, 4 had valvular heart disease, and 3 had cardiomyopathy. We studied the long-term outcome (11 +/- 3 years) of the other 28 patients with isolated milking at baseline. Two groups were constituted according to the percentage of systolic reduction of the left anterior descending coronary artery lumen: group A, < 50% (15 patients) and group B, > or = 50% (13 patients). During follow-up, 1 group A patient (cancer) and 2 group B patients (1 cancer and 1 suicide) died. Moreover, 1 group B patient was lost to follow-up. None of the patients sustained a myocardial infarction during follow-up. In group A patients, 71% felt very well or well and 50% had clinical symptoms; 64% took antianginal medications. In group B patients, 50% felt well and 70% had clinical symptoms; 50% took antianginal drugs. The long-term prognosis of isolated myocardial bridges of the left anterior descending coronary artery is good and is independent of the severity of systolic narrowing of internal lumen diameter.
In order to determine whether signal-averaged electrocardiography was useful in the diagnosis of syncopal ventricular tachycardia, 244 subjects with malaise or unexplained syncope without documented ventricular tachycardia underwent endocavitary electrophysiological study and signal-averaged electrocardiography with a 25 Hz bandpass filter. Ninety-three patients had no apparent cardiac disease whereas 151 patients had cardiac problems. ventricular tachycardia was induced in 91 patients. Fifty-two of them (57%) had ventricular late potentials. Twenty-two patients without inducible ventricular tachycardia also had late potentials (14%). The diagnostic value of signal-averaged electrocardiography depended on the cardiac disease: in the absence of cardiac disease, its sensitivity was poor (31%) but the specificity was excellent (96%). In the presence of cardiac disease, the sensitivity improved (63%) but the specificity was not as good (67%). The lack of sensitivity in the group with cardiac disease generally concerned subjects with inducible rapid ventricular tachycardia. The authors conclude that signal-averaged electrocardiography should not be requested in the investigation of unexplained syncope in subjects without cardiac disease to demonstrate abnormal ventricular excitability which is very rate in these subjects. On the other hand it is more valuable in those with underlying cardiac disease although inducible rapid ventricular tachycardia may still escape detection.
The authors report a new method of studying the autonomic nervous system, especially vagal tone, during endocavitary electrophysiological studies. After termination of fixed ventricular pacing at incremental rates to 200/min, an initial acceleration of the heart rate is observed followed about 5 seconds later by a sudden slowing. This phenomenon was studied in 278 patients. Ninety seven patients had no cardiac disease: the variation in heart rate was 33 +/- 18%. In the 181 other patients with cardiac disease (ejection fraction 35 +/- 16%) the variation was only 21 +/- 16% (p < 0.01). When the ejection fraction was less than 30%, the variation was only 13 +/- 4%. When the heart rate variation was less than 10%, the prognosis was poor because, of the 48 patients with this sign, 13 died, whereas there were only 2 deaths in the 133 other patients with cardiac disease and preserved adaptation. In 14 patients without cardiac disease the injection of 2 mg of atropine suppressed all adaptation of the heart rate, whilst in 18 other patients, oral betablockers reduced the variation but it persisted to a significant degree. The authors conclude that the adaptation of the heart rate after rapid ventricular stimulation is probably a reflection of vagal tone and may be used to assess the prognosis of subjects undergoing electrophysiological investigations.
Rapid uniform ventricular tachycardia (VT) (> 270 beats/min) or ventricular flutter induced during electrophysiological studies is thought not to be clinically significant in patients without cardiac arrest or documented rapid VT. The purpose of the study was to follow up 73 patients with inducible ventricular flutter but without confirmed rapid spontaneous VT. A long follow up (mean 3.5 years) identified two groups of patients. The first group had an excellent outcome and was characterised by a normal 24 hour Holter monitoring. In the second group, however, the risk of cardiac mortality was high (35%) and spontaneous VT was < 270 beats/min (26%) and was characterised by couplets or salvos of extrasystoles on Holter monitoring. In this group the history of syncope and decreased left ejection fraction increased the risk of mortality and VT. The presence of late potentials increased the risk of spontaneous VT. Electrophysiologically guided antiarrhythmic therapy reduced the risk of VT. Ventricular flutter was a non-specific finding in patients with normal Holter monitoring. In contrast, in patients with salvos of extrasystoles, ventricular flutter was associated with a high risk of cardiac mortality and VT.
The authors report the prognostic value of ventricular arrhythmias induced by routine programmed ventricular stimulation after the acute phase of myocardial infarction. The protocol consisted of two extrastimuli in the first 185 patients and 3 extrastimuli in 308 patients. The use of 3 extrastimuli increased the incidence of inducible sustained monomorphic ventricular tachycardia (VT) < 270/mn, from 17 to 22% and, more importantly, that of ventricular fibrillation from 4 to 17%. Induction of ventricular flutter (monomorphic VT > 270/mn) was not increased. A long follow-up period (average 4 +/- 2 years) showed that the risk of VT was increased during the first months after infarction (n = 14), and that, 4 years later, other patients develop VT (n = 6). The risk of serious arrhythmias (VT and sudden death) was significantly higher in patients with inducible VT < 270/mn (20%) than in patients without inducible VT, but it was also higher in patients with inducible ventricular flutter (12.5%). The use of a third extrastimulus has a low positive predictive value for arrhythmic events (10%). This study confirms that the induction of sustained monomorphic VT after myocardial infarction is associated with an increased risk of arrhythmic events but the positive predictive value is relatively low (17%). In view of the risk of inducing non-specific ventricular fibrillation, the authors recommended using a stimulation protocol with only 2 ventricular extrastimuli.
In order to update our information about the incidence and demographic, microbiological and clinical characteristics of infective endocarditis (IE) in France, a 12 month long study was carried out in three regions: Ile de France, Rhône-Alpes and Lorraine. Four hundred and fifteen cases of IE were recensed: certain (32%), probable (53%) or possible (15%). The annual incidence was 24.3 per million. The average age was 56 +/- 19 years. There was no past history of cardiac disease in 34% of cases; 33% had native valvular heart disease and 22% had one or more valvular prostheses. The site of IE was mitral in 39%, aortic in 36%, tricuspid in 6% and other or multivalvular in 19% of cases. The causal microorganism was isolated in 92% of cases. It was a streptococcus in 58% of cases (S. viridans in 27%; group D streptococcus + enterococcus in 23%); a staphylococcus was isolated in 23% of cases (Staphylococcus Aureus in 18%) and another microorganism in 11% of cases. The presumed portal of entry was dental in 24%, gastro-intestinal in 13%, cutaneous in 6% and urinary in 4% of cases. Twenty patients were intravenous drug addicts. Forty-five patients had medical or surgical procedure. Twenty-four per cent of patients were operated during the first two months, 17% died during this period (15% of operated and 18% of non-operated patients). Despite the advances in antibiotic therapy and in cardiac surgical techniques, IE seems to be as common and as severe as ten years ago.(ABSTRACT TRUNCATED AT 250 WORDS)
Idiopathic dilated cardiomyopathy carries a high risk of sudden death. It is also associated with sustained ventricular tachycardia. A complex ventricular arrhythmia is recorded in 3/4 of cases on Holter monitoring which has a low specificity. The aim of the study was to determine whether signal-averaged electrocardiography could provide a better evaluation of the prognosis of this condition. The results of signal-averaged electrocardiography were compared with those of 24 hour Holter monitoring and of systematic programmed ventricular stimulation in 58 patients with idiopathic dilated cardiomyopathy. Late ventricular potentials were recorded in 13 of the 14 subjects with inducible and usually spontaneous sustained ventricular tachycardia. The sensitivity of the technique for evaluating the risk of sustained VT was therefore good (93%). Late potentials were also recorded in 9 patients with induced ventricular flutter or fibrillation, these patients being symptomatic (dizzy spells). Late potentials were also demonstrated in 14 of the 35 asymptomatic patients without inducible VT, indicating that this non-invasive investigation had a limited specificity (60%). In addition, during follow-up of the patients, the risk of sudden death was difficult to demonstrate. Late potentials were only found in subjects with inducible sustained VT but no in the other cases. In conclusion, signal-averaged electrocardiography seems to be valuable for evaluating the risk of sustained VT in subjects with idiopathic dilated cardiomyopathy and complex ventricular arrhythmias. The detection of the risk of sudden death is probably impossible by this technique.
The aim of this study was to report the probable mechanism of resuscitated cardiac arrest without acute myocardial infarction. Fifty-seven cases were recensed but the arrest was only documented in 44 subjects. Systematic non-invasive investigations and programmed stimulation showed that the diagnosis of cardiac arrest was probably false in 5 patients and, in the others, that a ventricular arrhythmia was probably the cause (63%). The occurrence of cardiac arrest under antiarrhythmic therapy may reveal an underlying abnormality requiring specific therapy (3/8). The absence of cardiac disease did not exclude the risk of VF (3 cases). When reproducible, ventricular arrhythmias were present during programmed stimulation, the prognosis was good if the arrhythmia could not be induced under antiarrhythmic therapy. It was easier to find an effective treatment for inducible ventricular fibrillation-flutter (13/17) than for inducible ventricular tachycardia (7/17). The prognosis was poor if the arrhythmia was unchanged during programmed stimulation under antiarrhythmic therapy and non-pharmacological treatment was required.
Arrhythmogenic right ventricular dysplasia (ARVD) is classically associated with ventricular tachycardia and the prevalence of supraventricular tachycardia in this condition is not well known. The aim of this study was to observe the response of 20 patients with ARVD to programmed atrial stimulation and compare it with 150 subjects without cardiac disease or spontaneous supraventricular tachycardia. The protocol used 2 atrial extra-stimuli delivered on 3 paced cycles. Programmed atrial stimulation with 1 extrastimulus was repeated after infusion of 20 to 30 micrograms of Isoproterenol. Sustained supraventricular tachycardia could be induced in 13 patients with ARVD (65%) and 17 control subjects (11%) (p < 0.001). It was not possible to distinguish patients with inducible supraventricular tachycardia from those without inducible arrhythmias by electrophysiologic parameters. Isoproterenol facilitated the induction of VT but not supraventricular tachycardia. Three patients with inducible supraventricular tachycardia developed spontaneous atrial fibrillation. In conclusion, there is a relatively high incidence of inducible supraventricular tachycardia in ARVD: Isoproterenol does not facilitate this tachycardia, contrary to ventricular tachycardia.
The authors report the case of a patient developing two successive left ventricular kinetic abnormalities secondary to acute or chronic ischemia, and reversible after transluminal coronary angioplasty. The concept of myocardial hibernation is suggested as a possible mechanism.
While attempting to recanalize a right coronary artery obstruction by using a low-speed rotating catheter (Rotacs), proximal rupture of the catheter body occurred with entrapment of the blunt tip in the obstruction. To retrieve the device, it was necessary to severe the guiding catheter and the flexible tube of the Rotacs. At low-speed rotation the flexible segment of the catheter was then pulled back.
The aim of this study was to identify the factors associated with the induction of ventricular tachycardia (TV) by programmed ventricular stimulation in patients with unexplained syncope. Sustained VT was induced in 71 out of 619 patients (11.5%) with syncope. A comparison of subjects with inducible VT and those without inducible VT showed underlying cardiac disease to be more common (89% versus 16%), more Holter abnormalities (Grade IVa ventricular extrasystoles) (60.5% versus 10%) in the first group but that signal-averaged ECG, recorded in 51 cases, was not sufficiently specific to differentiate the two groups (delayed potentials in 57% versus 43%). When syncope occurred in a subject without apparent cardiac disease with a normal Holter recording, inducible VT was rare (1%). On the other hand, when syncope was associated with cardiac disease and/or an abnormal Holter recording, VT could be induced in 45 to 64% of cases. In addition, as inducible VT was associated with severe infrahisian conduction defects in 3 cases, the following strategy is suggested in patients with unexplained syncope: programmed ventricular stimulation should be performed systematically during endocavitary electrophysiological investigation of AV conduction in patients with cardiac disease and if the non-invasive investigations, Holter monitoring or echocardiography, are abnormal.
Programmed ventricular stimulation risks inducing non-pathological ventricular fibrillo-flutter. The aim of this study was to determine if the induction of a non-sustained polymorphic ventricular tachycardia (over 5 intraventricular reentries) could prevent this incident. One hundred and thirty-three non-sustained polymorphic tachycardias were induced by 2 or 3 extrastimuli during 1450 programmed ventricular stimulation studies. Ventricular stimulation was continued and led to ventricular fibrillo-flutter in 46 cases (Group I); to induction of sustained ventricular tachycardia in 26 cases (Group II) or to no other arrhythmias excepting the non-sustained tachycardia in 61 cases (Group III). The duration of the salvo was similar in all 3 groups. The rate of the induced arrhythmia was significantly lower in Group II (234 vs 290/min). The essential difference between the three groups was the clinical context. Only patients in Group II had previously documented sustained ventricular tachycardia and only patients in Group III had no apparent underlying cardiac disease. These results suggest that the decision to stop programmed ventricular stimulation should be based on the clinical indications of the study. In patients with previously documented or probable sustained ventricular tachycardia, it would seem to be necessary to continue ventricular stimulation irrespective to the rate and duration of the induced non-sustained ventricular tachycardia.