Biomedical subjects

J M Fauvel

Publications and source records attributed to J M Fauvel.

At least 37 records · Page 2Linked to original sources

PubMed2000

[Utilization of heart rate at the ventilatory threshold for the prescription of intensity of exercise training in cardiac failure].

Physical exercise is a treatment for cardiac failure but a large range of intensities of exercise is proposed. The aims of this study were to determine the range of intensities of effort used and to individualize the intensities used. Thirty patients with stable cardiac failure (NYHA Classes II-III, age: 53 +/- 2.1 years, ejection fraction: 31 +/- 1.4%) underwent a cardiorespiratory exercise stress test before and after individualized training at the ventilatory threshold. However, before and after the training period, standard methods of calculation of the intensities at the ventilatory threshold showed individual differences greater than +/- 2 standard deviations, indicating different metabolic stimulations. After the individualized training programme, peak oxygen consumption on exercise (1679 +/- 100 vs 1487 +/- 89 ml.min-1, p = 0.0001) and at ventilatory threshold increased (1365 +/- 85 vs 1133 +/- 65 ml.min-1, p = 0.0001), the ventilatory threshold/peak exercise ratio increased (81.2 +/- 1.3 vs 76.7 +/- 1.4%, p = 0.0008), and there was a decrease in heart and ventilatory rates at submaximal metabolic levels (p = 0.0001). The authors conclude that protocols using intensity of effort at the ventilatory threshold give similar results with respect to improvement of aerobic capacity as other methods of indirect calculation, based on maximal heart rate of oxygen consumption. The value of this particular method lies in the adequation between aerobic capacity of the patient and the intensity of training. The results obtained attain the physiopathological aims of rehabilitation.

Calibration↗

PubMed1999

[Hyperinsulinism, heart rate variability and circadian variation of arterial pressure in obese hypertensive patients].

AIMS: During insulin resistance, sympathetic nerve activity is increased. However insulin resistance is a common feature of obesity and essential hypertension, it is unclear if chronic hyperinsulinemia per se contributes to sympathetic overactivation. The purpose of our study was to explore++ the relationships between chronic hyperinsulinemia and heart rate variability (HRV), a non-intensive tool to assess autonomic function, in obese and hypertensive subjects. METHODS: 24 hours Holter ECG for HRV time and frequency domain analysis was performed in 77 patients, mean age 53 +/- 10 years, 52 men and 25 women, free of diabetes, without beta-blockers, divided in four groups according to three parameters, body mass index (BMI > 27 kg/m2 in man and > 25 kg/m2 in woman defined obesity), arterial pressure and insulinemia (fasting insulinemia > 25 mUI/L defined hyperinsulinemia): 27 patients obese, hypertensive, with hyperinsulinemia; 28 patients obese, hypertensive, without hyperinsulinemia; 12 patients non obese, hypertensive, without hyperinsulinemia; 10 patients obese, normotensive, without hyperinsulinemia. RESULTS: In comparison with the three other groups, patients with hyperinsulinemia showed a significant decrease (p < 0.05) of SDNN and the power of total spectrum (0.01-1 Hz) band, which are indexes of global HRV, and a significant decrease (p < 0.005) of SD and the normalized power of the low frequency (0.04-0.15 Hz) band, both indexes reflecting sympathetic modulation of HRV. In contrast, no significant difference was observed between the four groups for indexes of HRV reflecting parasympathetic tone. These relations were independent of mean RR. Fasting insulinemia was significantly (p < 0.0001) related with HRV in time domain (SDNN; r = -0.43; SD: r = -0.49) and spectral domain (total spectrum: r = -0.49; low frequency: r = -0.52). CONCLUSION: Chronic hyperinsulinemia appears to be an important determinant of HRV, particularly for the indexes reflecting sympathetic influence, independent of obesity and hypertension.

Adult↗

PubMed1999

[Evaluation of arrhythmic risk in coronary insufficiency].

Half of all deaths occurring in patients with heart failure are sudden deaths probably related to a malignant ventricular arrhythmia. The pathophysiological mechanisms of these arrhythmias are unclear, but left ventricular function, hypokalaemia accentuated by diuretics and treatments altering inotropism play a definite role. Because of the diversity of aetiologies generating heart failure, the multiplicity of fatal arrhythmias and the multifactorial origin of these arrhythmias, there is no formal marker for the risk of sudden death in patients with heart failure, at the present time. In addition to the NYHA classification and detection of episodes of syncope, assessment of these patients must be as complete as possible, at least including repeated evaluation of the ejection fraction, Holter ECG monitoring and detection of delayed ventricular potentials.

Arrhythmias, Cardiac↗

PubMed1998

QT interval dispersion as a predictor of arrhythmic events in congestive heart failure. Importance of aetiology.

AIMS: Identification of patients with congestive heart failure at risk of sudden death remains problematic and few data are available on the prognostic implications of QT dispersion. We sought to assess the predictive value of QT dispersion for arrhythmic events in heart failure secondary to dilated cardiomyopathy or ischaemic heart disease. METHODS AND RESULTS: Twelve-lead ECGs calculated for QT dispersion, 24 h Holter ECGs and signal-averaged ECGs were prospectively recorded in 205 heart failure patients in sinus rhythm. The 86 patients with ischaemic heart disease and the 119 with dilated cardiomyopathy were not significantly different as regards NYHA grades (51 vs 49% in grades III-i.v.), cardiothoracic ratio (57 +/- 7 vs 57 +/- 6%) and ejection fraction (28 +/- 8 vs 29 +/- 9%). The mean QT dispersion (66 +/- 29 vs 65 +/- 27 ms), the frequency of non-sustained ventricular tachycardia (37 vs 38%) and ventricular late potentials (41 vs 40%) were not significantly different in patients with ischaemic or dilated cardiomyopathy. QT dispersion was significantly related to other arrhythmogenic markers. During follow-up (24 +/- 16 months), 66 patients died, 22 of them died suddenly and seven presented a spontaneous sustained ventricular tachycardia. In patients with dilated cardiomyopathy, in multivariate analysis, only a QT dispersion > 80 ms was an independent predictor of sudden death (RR: 4.9, 95% CI 1.4-16.8, P < 0.02) and arrhythmic events (RR: 4.5, 95% CI 1.5-13.5, P < 0.01). In patients with ischaemic heart disease, no studied parameter was found significantly related to sudden death or arrhythmic events. CONCLUSIONS: In congestive heart failure, abnormal QT dispersion can identify patients with dilated cardiomyopathy who are at high risk of arrhythmic events.

Adult↗

PubMed1998

Nasal nitric oxide concentration is decreased in heart failure patients receiving nitrates.

Nitric oxide (NO) is a free radical gas and a short-lived messenger which has many paracrine functions. Direct assessment of NO production is very difficult in vivo. However, the paranasal cavities generate a high amount of NO which diffuses in the nasal cavity where it can be easily measured. Several studies have suggested alterations of the NO production in heart failure. Thus, we assessed nasal NO concentration in normal subjects and in heart failure patients. The nasal NO concentration averaged 227 +/- 10 ppb in the control group (n = 20), and 210 +/- 10, 198 +/- 20 and 159 +/- 54 ppb in New York Heart Association (NYHA) class II (n = 30), III (n = 28) and IV (n = 7) patients, respectively (mean +/- standard error [SE], not significant using analysis of variance [ANOVA]). Nasal NO level was not influenced by age, sex or etiology of the heart failure or by treatment with frusemide, angiotensin-converting enzyme inhibitor or digoxin. However, treatment with NO-releasing drugs (nitrates or molsidomine) significantly decreased the nasal NO level in heart failure patients. A two-way ANOVA revealed that treatment with a NO-releasing drug influenced nasal NO concentration (P = 0.0005), whereas NYHA class did not (P = 0.23), with a trend towards an interaction between the two parameters (P = 0.09): the inhibitory effect of NO-releasing drug on nasal NO concentration was more pronounced in severe heart failure. In an additional group of 12 patients (NYHA class II or III), the nasal NO concentration was 174 +/- 19 ppb during NO-releasing drug treatment and increased to 231 +/- 27 ppb 3 days after withdrawal of the nitrates (P = 0.0007 using paired t-test). Conversely, the nasal NO concentration in another group of seven patients (NYHA class II or III) was 219 +/- 32 ppb without nitrate treatment and decreased to 188 +/- 28 ppb 7 days after nitrate addition (P = 0.02 using paired t-test). In contrast, the nasal NO concentration in another group of ten ischemic patients without heart failure was 203 +/- 25 ppb without nitrate treatment and was similar (207 +/- 28 ppb) 7 days after nitrate addition (not significant using paired t-test). In conclusion, nasal NO production is normal in heart failure, except in patients receiving NO-releasing drugs. Nasal NO concentration could be useful for investigating the mechanism(s) by which exogenous NO donors decrease endogenous NO production.

Adult↗

PubMed1998

[Functional decoupling of left ventricular beta-adrenoceptor in a canine model of obesity-hypertension].

OBJECTIVE: To assess cardiac beta-adrenoceptors (beta-AR) in an obesity-hypertension model. METHODS: Six male beagle dogs (aged 35 +/- 5 months) receiving during 30 weeks a high-fat diet with 60% uncooked beef fat were compared to 6 normal beagle dogs. With right auricular and left ventricular samples we analysed cardiac beta-AR density through binding study using [125I]-cyanopindolol. beta 1 and beta 2 densities were obtained by competition with CGP 20712A. Affinity state of beta-AR was assessed by competition with isoproterenol. Noradrenaline plasma level was assayed by HPLC. Left ventricular mass (LV mass) was measured by echocardiography. Results are expressed as mean +/- SE. All comparisons were performed using a variance analysis (*: p < 0.05). RESULTS: Systolic blood pressure was significantly higher in obesses (245 +/- 8 vs 197 +/- 10 mmHg in controls). Diastolic blood pressure did not differed between both groups (93 +/- 3 vs 84 +/- 3 mmHg in controls). Noradrenaline plasma levels were similar in both groups (276 +/- 30 vs 235 +/- 50 pg/mL in controls). Obesses were characterized by higher LV mass (80 +/- 24 vs 67 +/- 15 g in controls*). Right auricular and left ventricular beta-AR densities were not different in obesses (57 +/- 6 and 67 +/- 4 fmoles/mg protein) and in controls (68 +/- 7 and 63 +/- 9 fmoles/mg protein). The beta 1-AR proportion was the same in obesses and controls in right auricule (63 +/- 4 vs 64 +/- 3% in controls) and left ventricule (59 +/- 3 vs 60 +/- 4% in controls). The proportion of beta-AR receptors in a high affinity state was similar in right auricular samples (69 +/- 4 vs 67 +/- 3%) in controls) but was significantly different in left ventricule (28 +/- 6 vs 74 +/- 6%) in controls). CONCLUSION: Left ventricular beta-adrenoceptors came under a specific desensibilisation independent of plasma noradrenaline levels. This functional decoupling of beta-adrenoceptors may account for the progressive systolic dysfunction of hypertensive cardiomyopathy.

Animals↗

PubMed1998

[Sudden death and chronic cardiac insufficiency].

Sudden death accounts for about 35% of the mortality of cardiac failure and its incidence does not decrease with the use of angiotensin converting enzyme inhibitors. Non-sustained ventricular tachycardia on Holter monitoring, late ventricular potentials and tachycardia induced by programmed ventricular stimulation have no formal predictive value of sudden death, underlining the varied character of the mechanisms underlying sudden death during cardiac failure. Sustained ventricular tachycardia degenerating to ventricular fibrillation is only one of the rhythmic factors implicated together with inaugural ventricular fibrillation, bradyarrhythmias and electromechanical dissociation. The underlying cardiac disease plays a role in the initiation of the fatal arrhythmia. In coronary artery disease, recurrent acute ischaemia is the principal trigger factor in patients who often have triple vessel disease. This explains the fact that classic markers of arrhythmia in the post-infarction period, which are only the reflection of the arrhythmogenic substrate of ventricular tachycardia, usually due to reentry around the fibrous scar of the infarct, are not valid in patients with progressive ischaemic cardiomyopathy. The most effective antiarrhythmic treatment in this type of patient is the prevention of ischaemia, when possible. In primary dilated cardiomyopathy, the mechanism underlying sudden death could be different at each stage. In NYHA Stages I and II, ventricular tachyarrhythmias could play a major part in unexpected sudden death in patients whose stable haemodynamic status suggested a more prolonged survival. The value of an implantable defibrillator would seem to be proved in this group of patients, at least in secondary prevention. In Stages III and IV, ventricular arrhythmias only indicate the degree of ventricular dysfunction and sudden death may follow bradyarrhythmias and electromechanical dissociation due to the precarious haemodynamic status.

Cardiac Output, Low↗

PubMed1997

Prognostic value of arrhythmogenic markers in systemic hypertension.

OBJECTIVE: To evaluate the prognostic value of arrhythmogenic markers in hypertensive patients. DESIGN: Two hundred and fourteen hypertensive patients without symptomatic coronary disease, systolic dysfunction, electrolyte disturbances or anti-arrhythmic therapy were included. Recordings were made of 12-lead standard ECGs with calculations of QT interval dispersion, 24 h Holter ECGs (204 patients), echocardiography (187 patients) and signal-averaged ECGs (125 patients). RESULTS BASELINE DATA: echocardiographic left ventricular hypertrophy was found in 63 patients (33.7%), non-sustained ventricular tachycardia (Lown class IV b) in 33 patients (16.2%), ventricular late potentials in 27 patients (21.6%). Mortality: after a mean follow-up of 42.4 +/- 26.8 months, global mortality was 11.2% (24 patients), cardiac mortality 7.9% (17 patients), sudden death 4.2% (nine patients). Univariate analysis: predictors of global, cardiac and sudden death were age > or = 65 years, ECG strain pattern, Lown class IV b and QT interval dispersion > 80 ms (P < or = 0.01). Left ventricular mass index was closely related to cardiac mortality (P = 0.002). Multivariate analysis: only Lown class IV b was an independent predictor of global (RR 2.6, 95% CI 1.2-6.0) and cardiac mortality (RR 3.5, 95% CI 1.2-9.7). CONCLUSION: In hypertensive patients, non-sustained ventricular tachycardia has a prognostic value.

Aged↗

PubMed1997

Prognostic value of ventricular arrhythmias in systemic hypertension.

OBJECTIVE: Hypertensive left ventricular hypertrophy is associated with an increased risk of arrhythmias and mortality. However, no clinical study has demonstrated a significant relationship between ventricular arrhythmias and mortality in systemic hypertension. DESIGN AND METHODS: To evaluate the prognostic value of arrhythmogenic markers, we included, prospectively, 214 hypertensive patients aged (mean+/-SD) 59.1+/-12.8 years, without symptomatic coronary disease, myocardial infarction, systolic dysfunction or electrolyte disturbances. At inclusion, a 12-lead electrocardiogram (ECG) with QT dispersion calculation, a 24 h Holter ECG (204 patients) with Lown classification of ventricular arrhythmias, echocardiography (reliable in 187 patients) and a signal-averaged ECG (125 patients) with ventricular late potentials were recorded. RESULTS: At baseline, echocardiographic left ventricular hypertrophy was found in 63 patients (33.7%). Non-sustained ventricular tachycardia (Lown class IVb) was recorded in 33 patients (16.2%) and late potentials in 27 patients (21.6%). After a mean follow-up of 42.4+/-26.8 months, all-cause mortality was 11.2% (24 patients); 17 patients died of cardiac causes (7.9%); of these, nine (4.2%) died suddenly. In univariate analysis, age, Lown class IVb and a QT dispersion > 80 ms were significantly related to global, cardiac and sudden death (P < 0.01). The left ventricular mass index was related to cardiac mortality (P= 0.002). In multivariate analysis, only Lown class IVb was an independent predictor of global and cardiac mortality, increasing the risk of global death 2.6-fold (95% confidence interval 1.2-6.0) and cardiac death 3.5-fold (95% confidence interval 1.2-9.7). CONCLUSION: In hypertensive patients the presence of non-sustained ventricular tachycardia has prognostic value.

Echocardiography↗

PubMed1997

[Prognostic value of ventricular arrhythmia in hypertensive patients].

OBJECTIVE: Hypertensive left ventricular hypertrophy (LVH) is associated with increased risk of arrhythmias and mortality. However, no clinical study demonstrated a significant relation between ventricular arrhythmias and mortality in systemic hypertension. DESIGN AND METHODS: To evaluate the prognostic value of arrhythmogenic markers in systemic hypertension, we included between 1987 and 1993. 214 hypertensive patients, 59.1 +/- 12.8 years old, without symptomatic coronary disease, myocardial infarction, systolic dysfunction, electrolyte disturbances or antiarrhythmic therapy. At inclusion, an ECG, a 24 h Holter ECG (204 patients) with Lown classification of ventricular arrhythmias, an echocardiography (reliable in 187 patients) with left ventricular mass index and ejection fraction calculation, a SAECG (125 patients, enrolled after 1988) with ventricular late potentials (LP) were recorded. QT interval dispersion (QTd) was calculated on 12 leads standard ECG and LVH was appreciated. RESULTS: At baseline echocardiographic LVH was recorded in 63 patients (33.7%) with normal ejection fraction (75 +/- 7.4%). Non-sustained ventricular tachycardia (Lown IVb) was found in 33 pts (16.2%) and LP in 27 patients (21.6%). After a mean follow up of 42.4 +/- 26.8 months, all-cause mortality was 11.2% (24 patients); 17 patients died of cardiac causes (7.9%); of these 9 patients (4.2%) died suddenly. In univariate analysis, age, strain pattern of LVH, advanced Lown classes and abnormal QT dispersion (> 80 ms) were significantly related to global, cardiac and sudden death (p < or = 0.01). Left ventricular mass index was closely related to cardiac mortality (p = 0.002). LP failed to predict mortality. In multivariate analysis, only Lown class IVb was an independent predictor of global and cardiac mortality, increasing the risk of global death 2.6 fold [1.2-6.0] (CI 95%) and the risk of cardiac death 3.5 fold [1.2-9.7] (CI 95%). CONCLUSIONS: In hypertensive patients the presence of non-sustained ventricular tachycardia on 24 h Holter has a prognostic value.

Aged↗

PubMed1996

Prognostic value of late potentials in patients with congestive heart failure.

To investigate whether detection of ventricular late potentials could provide prognostic information in patients with congestive heart failure with or without bundle branch block, we prospectively obtained a signal-averaged ECG from 151 patients with congestive heart failure, using specific criteria in 57 patients with bundle branch block. Late potentials were detected in 49 patients (32.5%); their incidence was not significantly different in patients without (31%; 29 patients) or with bundle branch block (35%; 20 patients). Late potentials were present in 25 of 73 patients (34%) with idiopathic dilated cardiomyopathy, in 20 of 57 patients (35%) with ischaemic cardiomyopathy and in four of 21 patients (19%) with hypertensive heart disease (ns). Age, NYHA class, ejection fraction and use of amiodarone were not statistically different among patients with or without late potentials. In contrast, patients with late potentials had more past episodes of sustained ventricular tachycardia (8.2%; four patients) than those without late potentials (1.9%; two patients). Twenty four hour ambulatory ECGs were obtained in 135 patients (89%). Non-sustained ventricular tachycardia was not correlated with the presence of late potentials found in 45 of 88 patients (51%) without late potentials and in 29 of 47 patients (62%) with late potentials (ns). The mean follow-up was 27 +/- 12 months; 51 patients died, 31 from progressive congestive heart failure and 13 suddenly; seven prospectively had sustained ventricular tachycardia. The total mortality rate, the cardiac mortality rate and sudden death risk were not significantly related to the presence of late potentials; their incidence were respectively 35% (36 patients), 32% (33 patients) and 10% (10 patients) in patients without late potentials and 31% (15 patients), 23% (11 patients) and 6% (three patients) in those without late potentials. The incidence of sustained ventricular tachycardia during follow-up was 2% (two patients) in patients without late potentials and 10% (five patients) in those with late potentials. The incidence of sustained ventricular tachycardia experienced by the patients before the study or seen during follow-up was significantly increased in the presence of late potentials: 18% (nine patients) vs 2% (two patients) in the absence of late potentials (P < 0.001). Removal from the study of data from patients with bundle branch block, patients with severe congestive heart failure (NYHA 3 or 4) or patients taking amiodarone did not alter these results. Thus, signal-averaged ECG results only improved risk stratification for sustained ventricular tachycardia in patients with congestive heart failure and failed to identify patients at high risk for sudden death.

Action Potentials↗

PubMed1996

[Correlation between QT interval dispersion and ventricular arrhythmia in hypertension].

OBJECTIVE: To evaluate the correlation between QT interval dispersion (QTd) and ventricular arrhythmias in hypertensive patients (pts) with or without left ventricular hypertrophy (LVH). A secondary aim was to investigate correlations of QTd with other markers of arrythmogenic propensity: ventricular late potentials (LP) and heart rate variability (HRV). METHODS: We retrospectively measured the QTd on the 12 standard surface ECG leads in 230 hypertensive pts (94F, 136M; 59.6 +/- 12.7 years old). A 24 hours ECG Holter recording was performed in 218 pts and ventricular arrhythmias were appreciated using the Lown classification. Left ventricular mass was determined by echocardiography (LVM-Devereux formula) and left ventricular mass index (LVMI) were determined in 202 subjects. LP (122 pts) and HRV (55 pts) were investigated. RESULTS: The QTd varied between 20 and 160 msec (57.8 +/- 32.7 msec). The distribution of pts classified using Lown criteria was: 29 pts (13.3%) class O; 106 pts (48.6%) class I; 8 pts (3.6%) class II; 13 pts (6%) class III; 29 pts (13.3%) class IVa; 33 pts (15.1%) class IVb; 116 pts (69.5%) had LVH determined by echocardiography. The QTd was strongly correlated with the Lown classes (p < 0.0001). The QTd was significantly broader in Lown classes III, IVa and IVb compared to classes O, I and II cumulated (p < 0.002); there was no difference concerning QTd between Lown classes III, IVa and IVb. The QTd was also correlated with the absolute number of premature ventricular depolarizations/24 hours (p = 0.02; r = 0.16). The 75 pts with an increased LVMI had significantly elevated QTd compared to pts without it (p < 0.0001). Qtd was correlated with LVMI (r = 0.37; p < 0.0001). There was no correlation between QTd and the existence of LP (which were correlated with the Lown classes; p < 0.03) and HRV parameters. CONCLUSION: Elevated QT interval dispersion is associated with more severe ventricular arrhythmias in hypertensive subjects with LVH. The mechanism of an increased inhomogeneity of repolarisation is probably related to the anatomic modifications induced by LVH. No significant correlation between QTd, LP and HRV was observed.

Aged↗

PubMed1996

[Transesophageal cardiac echography and paracardiac tumor masses. Apropos of a case].

Computed tomography is currently the reference examination in the investigation of mediastinal tumours. We report a case of pericardial tumour revealed by transoesophageal echocardiography. This investigation immediately defined the limits of this mass and its relations with cardiac cavities and large vessels and suggested the main features of its tissue structure. However, the aetiological diagnosis is still based on CT-guided needle biopsy or investigation by mediastinoscopy or thoracotomy. Our case consisted of a non-Hodgkin lymphoma. Transoesophageal echocardiography is a non-irradiating technique, which can be performed at the patient's bed and which allows a precise assessment of the pericardial regions, especially the right pericardial regions.

Adult↗

PubMed1995

[Myocardial infarction in non-menopausal women. Coronary lesions and prognosis].

Between 1977 and 1990, 64 premenopausal women, under 50 years of age (42 +/- 5.6 years), were admitted for typical acute myocardial infarction with pathological Q waves. Twenty one patients had attempted myocardial revascularisation either by intravenous thrombolysis or primary angioplasty (n = 3). All patients underwent coronary angiography with selective left ventriculography during their hospital admission. This group of 64 women was characterised by the association of coronary risk factors (2.8 per patient): smoking (89%), hyperlipidaemia (67%), diabetes (45%) and oral contraception (35%). Coronary angiography showed single vessel occlusion in 86% of patients receiving oral contraception, multiple vessel disease in 36.5% and single or double vessel disease in 31.7% of the other patients. There were 3 deaths during the hospital period (4.6%), 12 cases of left ventricular failure, 2 ventricular aneurysms, 2 operated ischaemic mitral regurgitations and 9 recurrences of pain treated by angioplasty. During follow-up (36.5 +/- 4 months), 22 patients were readmitted to hospital and there were 3 further deaths, 12 cases of persistent cardiac failure, 10 cases of latent ventricular dysfunction and 9 ischaemic reoccurrences treated by angioplasty or surgery. The results in this group of patients suffering from myocardial infarction at an unusually early age for women showed that although the mortality was similar to that observed in men of the same age (9%) there was a very high morbidity and a high risk of cardiac failure. The prognosis of myocardial infarction in women, though better than 10 years ago, should improve with immediate revascularisation, the correction of cardiovascular risk factors and the rapid application of all techniques of modern cardiology.

Adult↗

PubMed1995

[Absence of the effect of nitric oxide on pulmonary and systemic hypertension induced by sino-aortic denervation].

Inhaled nitric oxide, a selective pulmonary vasodilator, reverses hypoxic pulmonary vasoconstriction and is an effective treatment in some cases of human pulmonary hypertension. Localization of nitric oxide synthase had indicated a neural role for nitric oxide. Thus, we studied the interactions between inhaled nitric oxide and systemic and pulmonary vascular reactivity in acute neurogenic hypertension. In 6 male beagle dogs (mean weight: 15 +/- 1 kg), anesthetized by chloralose (8 cg/kg) and in spontaneous ventilation, the hemodynamic effects on systemic and pulmonary circulation of inhaled nitric oxide (12 ppm) were studied before and after acute sino-aortic denervation. The hemodynamic effects of intravenous propranolol (300 micrograms/kg) were studied after denervation. Mean arterial pressure (MAP), pulmonary capillary pressure (PCP), mean arterial pulmonary pressure (MAPP), cardiac input (CI) and oxygen venous saturation (SvO2) were measured. [table: see text] Sino-aortic denervation causes an acute and transitory pulmonary hypertension due to a double mechanism: a post-capillary hypertension (increase PCP) secondary to an increase left ventricular post-charge by systemic hypertension and a precapillary hypertension. In fact, vascular pulmonary resistances increase from 1.8 +/- 0.1 to 3.4 +/- 0.8 uW after denervation (p < 0.05). Change in pulmonary vascular reactivity induced by catecholamines is probably involved. Propranolol but not inhaled nitric oxide reverse pulmonary hypertension due to sino-aortic denervation.

Administration, Inhalation↗

PubMed1992

[Hypertensive cardiopathy and ventricular late potentials].

Ventricular arrhythmias occur with increased frequency in hypertensive patients with left ventricular hypertrophy (LVH). The aim of this work is to study the incidence of ventricular late potentials (LP) and their relation to ventricular arrhythmias in 148 hypertensive patients, 87 men and 55 women, without evidence of a coronaropathy. For each patient we carried out a signal-averaged electrocardiography, an echocardiogram to determine the LV mass index (LVMI) and the LV end-diastolic dimension (EDD), and 24 hours Holter monitoring to record ventricular arrhythmias filed according to Lown's classification. LP were considered present if the root-mean-square voltage during the last 40 ms of the QRS was: < 20 uV in absence of bundle branch block, or < or = 17 uV in presence of bundle branch block. [table: see text] The frequency of LP appears exceptional in hypertensive patients without LVH (5%) and remains uncommon in patients with concentric LVH (13%). The incidence of LP is only frequent at the end stage of hypertensive cardiopathy with eccentric LVH (48%). The severity of ventricular arrhythmias is only correlated to the presence of LP in patients with concentric LVH (p < 0.02).

Action Potentials↗

PubMed1992

[Ambulatory blood pressure monitoring and left ventricular hypertrophy: correlations and trial of predictive value].

The purpose of the study is to make a selection of patients with left ventricular hypertrophy from Ambulatory Blood Pressure Monitoring (ABPM) values. We studied 39 patients, 23 men and 16 women, without treatment. These patients had systolic pressure > 140 mmHg and/or diastolic pressure > 90. With ABPM we measured mean systolic (MS) and diastolic (MD) pressure during the day (D) and the night (N), the percentages of systolic values (%S) > 160 mmHg and of diastolic values (%D) > 95 mmHg. With echocardiography we measured left ventricular mass index (LVMI: Devereux) and with pulsed Doppler peak of early (E) and late (A) ventricular filling and the ration A/E. We found the same amount of correlations between ABPM and echocardiographic parameters as other authors. [table: see text] The study of LVMI found a difference between groups when MD were > 140/90 (*) and A was significantly greater in patients with MSD > 140 (*). LVMI was greater in patients with MDD > 80 (*) and A was greater in patients with MSN > 120 (*). Predictive value of MSD > 140: 53% specificity: 79%. Predictive value of MSN > 120: 80% specificity: 45.8%. We concluded that the correlations between ABPM and echocardiographic disturbances are not very strong, but significant. If the predictive value of MSF is low, his specificity is rather high and conversely MSN has a good predictive value for selection of hypertrophic patients.

Adult↗

PubMed1991

[Idiopathic chylopericardium. Apropos of a new case. Review of the literature].

The authors report a new case of primary chylopericardium in an asymptomatic 26 year old male. In view of the negativity of the complementary etiological investigations a surgical subxiphoid window was performed and this confirmed the diagnosis. After failure of isolated evacuatory drainage, the patient was cured by pericardectomy. The anatomo-clinical, biochemical and diagnostic features of this condition are described based on a review of the other cases of primary chylopericardium reported in the literature. Surgical pericardectomy seems to be the only effective long term treatment.

Adult↗