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Biomedical subjects

P Maisonblanche

Publications and source records attributed to P Maisonblanche.

17 recordsLinked to original sources
PubMed1996

Molecular basis of the regression of cardiac hypertrophy.

Cardiac failure is a disease which involves three different mechanisms: (1) the limits and imperfections of the general process of myocardial adaptation to mechanical stress, which includes various changes in genetic expression, including an increased collagen mass, but an unchanged collagen concentration; (2) the limits and imperfections of the adaptational process at the peripheral level which allows the entire organism to adapt to the low cardiac output; (3) fibrosis, an augmented collagen concentration, which is not a direct consequence of mechanical overload, but depends on aging, myocardial ischemia or hormonal changes. Middle-aged spontaneously hypertensive rats (SHRs) represent a good model of the common clinical situation. Three-month treatment with a CEI reduces, in parallel, arterial hypertension, left ventricular hypertrophy and ventricular fibrosis. Holter monitoring was also performed in these animals. Untreated SHRs when compared to age-matched Wistar rats have an increased number of ventricular premature beats which are suppressed by the treatment. In addition, heart rate variability has been quantified by using the pseudo Wigner-Villé transformation, a time and frequency domain method. The low frequency oscillations are hampered in SHRs. CEI normalizes this parameter.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Microgravity and orthostatic intolerance: carotid hemodynamics and peripheral responses.

A ground-based model [24 h of bed rest (BR) with head-down tilt (HDT)] was used to investigate the cardiovascular deconditioning responsible for orthostatic intolerance, frequently observed after weightlessness flights. This experimental deconditioning is shown to be distinguished by an increase of mean blood pressure (P < 0.05), with increased total peripheral resistances (TPRs). Systolic tangential tension of the carotid arterial wall, cardiac output and frequency (spectral analysis), and plasma norepinephrine and epinephrine were not significantly altered, while plasma dopamine was increased (P < 0.05). Cardiovascular homeostasis was challenged before and after 24 h of BR with HDT through -40 mmHg lower body negative pressure (LBNP). Systolic tangential tension of the carotid wall was decreased, with a decrease of systolic pressure and cardiac output; increased heart rate was likely due to an increase of sympathetic drive with a decrease of vagal braking. The overall picture was not changed after 24 h of BR with HDT, except for a lack of increase of TPRs: their increase (+13.7%, P < 0.05) before was no longer observed after (-2.6%) 24 h of BR with HDT. This apparent deficiency cannot be explained. However, a heterogeneity in the response of TPR should be considered because the magnitude of the increase of blood pressure to cold pressor test was the same after 24 h of BR with HDT as it was before.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Long-term follow-up after sustained monomorphic ventricular tachycardia: Causes, pump failure, and empiric antiarrhythmic therapy that modify survival.

We analyzed the actuarial cardiac mortality rate of 295 consecutive patients with sustained monomorphic ventricular tachycardia who were referred to us between 1978 and 1988. Patients were divided into four groups: group I of 156 patients with coronary disease, group II of 55 patients with nonischemic left ventricular disease, group III of 65 patients with right ventricular disease, and group IV of 19 patients without detectable heart disease. Patients were treated empirically according to a prospective schema: (1) class I antiarrhythmic drugs, (2) in case of recurrence of ventricular tachycardia: amiodarone or beta-blockers, (3) in case of recurrence of ventricular tachycardia: drug combinations or surgery. The mean follow-up duration was 61 +/- 40 months after the first occurrence of ventricular tachycardia, and the clinical outcome was known in 67.5% of patients at 5 years. The actuarial mortality rates were considerably higher in groups I and II compared with those in groups III and IV (p less than 0.01). The mortality rate was slightly higher in group I than in group II (p less than 0.05). In groups I and II, actuarial mortality rate were much higher when left ventricular ejection fraction was less than 0.30 (p less than 0.01). Comparisons between treatments showed no difference in actuarial mortality rates in patients with ventricular tachycardia and left ventricular ejection fraction greater than 0.30.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1989

[Sinus rhythm and standard deviation in cardiac cycles. Influence of myocardial status and beta-blocker treatment].

The efficacy of beta-blockers in preventing sudden death after myocardial infarction would seem to be greater in patients with cardiac failure and proportional to the reduction in heart rate induced by these drugs. In addition, a reduction in heart rate variability measured by the standard deviation from the average cardiac cycle over 24 hours has been reported to be an independent bad prognostic factor after myocardial infarction. This study compares the heart rates and the standard deviations from the mean cardiac cycle over 24 hours in 41 patients divided into 3 groups of comparable age (group I: normal subjects, n = 15; group II: hypertrophic cardiomyopathy without cardiac failure, n = 13; group III: cardiac failure, n = 13) before and after administration of acebutolol (10 mg/kg). The average 24 hour heart rates, the maximum 8-hour diurnal and minimum average 4-hour nocturnal heart rates, day-night ratio and standard deviations from the average 24 hour heart rate and at the hours of maximum and minimum average heart rates were measured by Holter monitoring with an ATREC II system. The 24 hour heart rates were slower in groups II (-18.1 p. 100) and III (-19.1 p. 100) than in group I (-9.5 p. 100), p less than 0.01, the basal heart rates being comparable and the heart rates after acebutolol being significantly lower in groups II and III. The degree of change was comparable during the diurnal and nocturnal periods.(ABSTRACT TRUNCATED AT 250 WORDS)

Acebutolol↗
PubMed1988

Respective role of sympathetic tone and of cardiac pauses in the genesis of 62 cases of ventricular fibrillation recorded during Holter monitoring.

Sixty-two Holter recordings of sudden death due to ventricular fibrillation (VF) were analysed by full disclosure and computerized processing. Thirteen sudden deaths were due to torsades de pointes in noncoronary subjects (11/13), related to quinidine-like drugs and/or hypokalaemia: they were always initiated by a long RR cycle due to a post-extrasystolic pause, and announced by a progressive decrease of mean heart rate (from 77.5 +/- 2.5 to 60.6 +/- 2.7 beats min-1, P less than 0.001), in the three preceding hours. The other cases occurred in coronary patients (45/49), with acceleration of ventricular tachycardia (VT), monomorphic in 24 cases, polymorphic in 13, the ventricular rate increasing from 220.6 +/- 55 to 241.5 +/- 69 beats min-1, rather than with primary VF (12 cases). A cardiac pause (RR cycle exceeding 125% of the mean five preceding cycles) was present in 22/49 cases immediately before the onset of VT/VF. The coupling interval of the extrasystole initiating VT/VF was shorter than the shortest value encountered before: 377.6 +/- 94.5 ms vs 421.4 +/- 92.3. The prematurity index (coupling interval/preceding RR cycle ratio) was lower in primary VF than in VT leading to VF. In the last hour preceding VF, ST changes were unusual (five cases), whereas heart rate increased from 82.8 +/- 20 to 92.0 +/- 26.7 beats min-1, (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

[Characteristics and prognosis of ventricular arrhythmia in arrhythmogenic right ventricular dysplasia].

The authors report their findings in 47 cases of ventricular arrhythmias due to arrhythmogenic dysplasia. The 47 patients were selected on the presence of ventricular tachycardia or fibrillation associated with dysplasia affecting selectively (44/47) or predominantly (3/47) the right ventricle at angiography. In this series males were predominant (38/47, 81 p. 100), familial incidence was high (13/47, 28 p. 100) and ECG abnormalities were constant. Most of the dysrhythmias (40/47) consisted of sustained ventricular tachycardia (VT) with left bundle branch block pattern (96 p. 100), occurring at the rate of 1.6 per patient on average and seldom with extreme axial deviation, as seen in post-infarction VT or VT associated with cardiomyopathy. The QRS complex was slightly prolonged (151 +/- 28 ms) and of high amplitude (2.5 +/- 1 mV on a VR, a VL and a VF leads), these values being intermediate between those of mild VT bursts and those of post-infarction or cardiomyopathy-related VT. The tachycardia was easily tippered by EP study, Intercritical Holter recordings showed frequent ventricular extrasystoles in the vast majority of cases; these were usually polymorphous and grouped into short bursts in one-half of the patients. On an 8.3 +/- 7 years' follow-up starting with the first attack of VT, it was found that only during the initial phase the spontaneous onset of VT was mediated by the adrenergic system (triggered by sports). Only 3 patients died during the follow-up period: one of ventricular fibrillation, 2 of right heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Decreased incidence of supraventricular arrhythmias achieved by selective atrial cooling during aortic valve replacement.

Inadequate atrial hypothermia and subsequent ischemic injury have been recognized as the major causes of supraventricular arrhythmias (SVAs) and conduction defects following cold chemical cardioplegia. This study was designed to assess the effects of right atrial cooling (15 degrees-20 degrees C) during cardioplegic arrest upon the incidence of postoperative SVAs and conduction defects in 40 consecutive patients undergoing isolated aortic valve replacement. Atrial preservation was ensured by combining systemic (24 degrees C) and topical hypothermia with snared double caval cannulation during arrest. Myocardial temperatures in the right atrial septum and anterior wall of the right ventricle were recorded before and after each cardioplegic infusion and upon release of caval tapes. Postoperatively, the incidence of SVAs and conduction defects was assessed by continuous rhythm monitoring, bipolar atrial electrograms and, in ten patients, 24-h Holter recordings during the first postoperative day. With the venae cavae snared, temperatures in the right atrial septum were not significantly different from those measured simultaneously in the right ventricle. Release of caval tapes resulted in right atrial temperatures increasing to systemic temperature (from 17.1 +/- 2.9 degrees C to 25.9 +/- 5.6 degrees C [m +/- SD]; P less than 0.01). Atrial rewarming between cardioplegic infusions did not exceed 2.9 degrees +/- 3.2 degrees C. Postoperatively, four patients (10%) developed sustained atrial fibrillation. One additional patient had a single episode of paroxysmal atrial fibrillation and two patients experienced asymptomatic episodes of junctional rhythm.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Determinants of the spontaneous ectopic activity in repetitive monomorphic idiopathic ventricular tachycardia.

Twenty-four hour ambulatory electrocardiographic tape recordings of 30 patients (16 men and 14 women, mean age 42 +/- 17 years) with repetitive monomorphic idiopathic ventricular tachycardia were analyzed using a new computerized system designed to study 15 RR cycles and mean heart rate of the 3 minutes preceding any defined event. The mean (+/- SD) number of events analyzed per patient in 24 hours was 610 +/- 483 for single premature ventricular complexes, 622 +/- 490 for couplets, 260 +/- 411 for runs of 3 complexes, 186 +/- 476 for runs of 4, 108 +/- 173 for runs of 5, 82 +/- 129 for runs of 6 to 10 and 83 +/- 116 for runs of more than 10 complexes. The heart rate was faster before runs of ventricular tachycardia than before isolated extrasystoles (p less than 0.01) and a positive linear correlation was observed between the mean preceding heart rate and the type of extrasystolic activity, the length of the runs increasing with increasing preceding heart rate (r = 0.98, p less than 0.001). A long RR interval just before the occurrence of runs was present in 77% of the cases (23 of 30) with or without an oscillatory pattern of RR intervals due to bigeminy or trigeminy, and the length of the runs correlated positively with the duration of this long preceding diastole (r = 0.90, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

The QRS morphology in post-myocardial infarction ventricular tachycardia. A study of 100 tracings compared with 70 cases of idiopathic ventricular tachycardia.

A hundred tracings of ventricular tachycardia (VT) belonging to 85 patients with myocardial infarction (MI) were compared with 70 cases of incessant, benign, idiopathic VT. The two groups of tracings differed in terms of QRS axis, most often normal in idiopathic VT (75%) and outside normality in MIVT (74%). The sum of QRS amplitude in unipolar limb leads was greater in idiopathic VT (4.3 +/- 1.3 mv, mean +/- S.D.) than in MIVT (2.6 +/- 0.8 mv, P less than 0.001). The QRS width was also different: 135 +/- 11 ms in idiopathic VT vs. 171 +/- 32 ms in MIVT (P less than 0.001). The QRS morphology in MIVT was characterized by the presence of a QR pattern in leads other than VR, or a QS pattern in V5-V6. These two aspects were constantly absent in idiopathic VT, and they were present in 89% of MIVT. In only 38 MIVT tracings were the ECG signs of MI observed in the same leads during sinus rhythm and during VT. In 51 MIVT tracings the location of the MI indicated by the VT tracing differed from that displayed in sinus rhythm. Rather than indicating an extension of the infarcted area not apparent in the tracings in sinus rhythm, such a discrepancy suggests that the QRS pattern during VT strongly depends on the point of origin of the VT. Conversely, this explains why the morphology of the QRS is an unreliable means for localizing the VT origin if the location of the MI is not taken into account. We conclude that both factors should be taken into consideration, and this might theoretically permit a better though complex approach to the VT origin in coronary heart disease using surface tracings.

Adult↗
PubMed1984

[Ventricular rhythm disorders in congestive myocardiopathy].

The authors studied 32 patients with ventricular arrhythmias--ventricular tachycardia (VT) or frequent ventricular extrasystoles (VES) and/or runs of extrasystole and cardiomyopathy with dilatation. This diagnosis was retained on the following criteria: absence of angina or electrical changes in infarction, normal coronary angiography in patients over the age of 50, diffuse abnormalities of ventricular contraction on 2D echocardiography or angiography, and on the absence of organic valvular heart disease. Thirteen patients had sustained paroxysmal VT, 18 patients had runs of VT and only 8 patients had isolated VES without repetition. The arrhythmia was polymorphic in 25 patients. All possible combinations of morphology of right of left sided delay with variable axes were observed. There were 25 right sided delays and 18 left sided delays; the association of left sided delay and vertical axis was only present in 5 occasions. Twelve patients underwent electrophysiological investigations for sustained VT but the arrhythmia could only be induced by ventricular extrastimulation in 4 cases. Eight patients were investigated during VT; the arrhythmia could only be terminated easily in 2 cases. Three of these 12 patients had biventricular tachycardia. Of the 11 patients with chronic alcoholism, only 2 had sustained VT, 8 had polymorphic VES and 1 monomorphic VES. Conversely, of the 21 patients without alcoholism, 11 had sustained VT, 6 had polymorphic VES, and 4 had monomorphic VES. There was a correlation between the polymorphism of the arrhythmia and the degree of ventricular dysfunction: of the 16 patients in overt cardiac failure (EF less than 30%), only 1 had monomorphic VT; the 15 others all had polymorphic arrhythmias. Only 2 had sustained VT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

[Value of long-term electrocardiography in patients with cerebral ischemic accidents].

Continuous 24 hour electrocardiography (Holter monitoring) was performed in 226 patients aged 20 to 85 years (mean 61 years) presenting with focal signs of a cerebrovascular accident (CVA). The technique was the same in all patients; the study was limited to paroxysmal atrial arrhythmias. Eighty four of the 226 patients examined had atrial arrhythmias which were already known in 39 patients before Holter monitoring. In the other 187 cases, the following results were obtained: 1) 9 patients (4,8%) had paroxysmal atrial fibrillation (AF), 2) 6 patients (3,2%) had paroxysmal atrial tachycardia (PAT), 3) 11 patients (5,9%) had runs of atrial extrasystoles, 4) 19 patients (10%) had isolated atrial extrasystoles (IAE). When patients with underlying cardiac disease constituting a diagnostic indicator for arrhythmia were excluded, the following incidences were obtained: AF = 3,7%, PAT = 2,7% and runs of atrial extrasystoles = 4,3%. The majority of these arrhythmias occurred in elderly patients in whom atrial arrhythmias are known to occur and may be asymptomatic. There were practical consequences of these results, i.e. antiarrhythmic and anticoagulant therapy in 12 patients (6,4%) alone. As Holter monitoring is also associated with a number of false negative results with respect to paroxysmal atrial tachycardia, we do not believe that this investigation should be offered routinely to patients with CVA in the absence of other clinical or electrocardiographic indications.

Adult↗
PubMed1984

[Polymorphic familial incessant ventricular rhythm disorders with ventricular repolarization abnormalities: borderline form of the congenital long QT syndrome?].

Two cases of polymorphic ventricular tachycardia (VT) are reported in siblings: the elder sister (18 years) was admitted to hospital because of syncope and ECG showed incessant attacks of VT. There was no obvious cardiac disease on echocardiography or cardiac catheterisation. A second syncopal attack occurred during Holter monitoring: this showed prolonged torsades de pointe which terminated spontaneously after a few minutes. Both syncopal attacks occurred at moments of intense emotional stress. Concomitantly, the duration of ventricular repolarisation was also observed to be increased. The attacks of polymorphic VT disappeared when the atrial rhythm accelerated, for example during exercise of isoprenaline infusion. It was not possible to induce VT by ventricular extrastimulation. The arrhythmia was controlled by nadolol and propafenone or flecainide. A familial investigation revealed that a younger brother had attacks of incessant VT with a long QT interval. The mother had frequent polymorphic ventricular extrasystoles and abnormal ST-T wave changes. The association of familial ventricular arrhythmias and long QT interval is suggestive of the Romano-Ward syndrome, but in this condition the intercritical ECG is normal except for the long QT. Conversely, in benign VT, the arrhythmia disappears during atrial pacing and exercise but there have been a few reports of sudden death. Our two cases could represent an intermediary form between these two pathological entities.

Adolescent↗
PubMed1984

[Anti-arrhythmic effect of oral propafenone. Apropos of 70 cases].

During a 3 year period, seventy patients aged 53 +/- 16 years with a total of 73 arrhythmias were treated over a mean period of 6.8 months (maximum 27 months) with oral propafenone, the usual dose being 900 mg/day. The study covered the whole spectrum of cardiac arrhythmias (32 supraventricular, 41 ventricular), and their relation to the autonomic nervous system. The efficacy was scored from 1 (no effect) to 5 (complete control) as judged by the clinical response, the results of Holter monitoring (175 control and 133 test recordings on therapy), and a comparison was made between the effects of propafenone and other antiarrhythmics: quinidine-like drugs, beta-blockers and amiodarone. With respect to supraventricular arrhythmias: 9 cases of vagally-induced atrial flutter and fibrillation were unaffected by propafenone (mean score = 1.1). On the other hand, the drug was very effective (mean score = 4.1) in 8 cases of adrenergic atrial arrhythmias. In 12 arrhythmias with more varied mechanisms (extrasystoles, tachysystole, paroxysmal atrial fibrillation) an intermediate score was obtained (2.8). Three cases of resistant junctional tachycardia due to reentry were improved. At ventricular level, 5 cases of extrasystole sensitive to quinidine were also improved by propafenone (4.6); the difference was more clearcut in 8 cases of benign idiopathic tachycardia (propafenone: 4.1, and quinidine: 2.4). This was more marked in 13 cases of more severe arrhythmia in diseased hearts in which the effect of propafenone (4.1) was superior even to that of amiodarone. However, propafenone was less effective (3.3) than amiodarone in 4 cases of severe polymorphic idiopathic ventricular tachycardia closely related to the autonomic nervous system. The antiarrhythmic effect of propafenone was appreciable in 10 cases of resistant post-infarction ventricular tachycardia, eventually in association with amiodarone. Slowing of the sinus rhythm (-11.6%) with no change in the day/night ratio was due to beta-inhibition. However, in toxic doses this may progress to sinoatrial block (9 cases). A lengthening of the PR interval and duration of QRS was common, but this was not complicated by torsade de pointes, one case of which was successfully treated by propafenone. Secondary gastro-intestinal effects and vertigo were rarely severe enough to warrant stopping therapy. In conclusion, these results show that the introduction of propafenone is a valuable therapeutic advance in the treatment of arrhythmias, especially in those with a favoring adrenergic mechanism.

Administration, Oral↗