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Biomedical subjects

G Roul

Publications and source records attributed to G Roul.

At least 19 recordsLinked to original sources
PubMed2007

Role of pre-infarction angina and inflammatory status in the extent of microvascular obstruction detected by MRI in myocardial infarction patients treated by PCI.

BACKGROUND/OBJECTIVES: The extent of microvascular obstruction (MVO) during myocardial infarction referred to as the "no-reflow phenomenon", may determine myocardial damage. Our study aimed to investigate the incidence and the influencing factors of MVO in patients with ST-elevation myocardial infarction (STEMI) treated by primary percutaneous intervention (PCI). PATIENTS, METHODS: Using contrast-enhanced MRI, microvascular obstruction was defined as early hypoenhancement. Contrast defects were scored from 0 (no hypoenhancement) to 3 (strong hypoenhancement). 50 patients (56+/-11 years) with STEMI underwent PCI. Contrast-enhanced MRI (6+/-2 days after STEMI) and biochemical parameters were evaluated. RESULTS: Microvascular obstruction (score 1 to 3) was observed in 90% of the patients and major microvascular obstruction (score 2-3) in 54%. In univariate analysis, leukocytes and CRP levels were associated with MVO, whereas pre-infarction angina and prior medication by aspirin or calcium channel antagonist appeared protective. Microvascular obstruction intensity positively correlated with baseline inflammation status assessed by C-reactive protein and leukocytes (rho=0.43 and rho=0.44; p=0.003), the peak of CK (rho=0.56; p=0.01) or Troponin I (rho=0.59; p=0.01) and negatively correlated with LVEF (rho=-0.44; p=0.002). Multivariate analysis identified the absence of pre-infarction angina as the only independent predictor for microvascular obstruction (odds ratio, 8.35, 95% confidence interval 1.27-54.71; p=0.027). CONCLUSION: MRI-detected microvascular obstruction has a high incidence in patients with STEMI treated by primary PCI and determines post-MI LVEF even in patients with post PCI TIMI 3 flow score. Pre-infarction angina appears to be an independent determinant of the extent of MVO detected by MRI.

Adult↗
PubMed2002

[Heart failure and vasopeptidase inhibitors].

The morbidity and mortality of cardiac insufficiency remains such that it justifies the pursuit of finding new drugs and new sensitive techniques to slow or abolish its evolution. Bringing the vasopeptidases, such as omapatrilat, up to date results in a rational process aimed at simultaneously modulating certain interactive humoral systems. They represent drugs which simultaneously inhibit neutral endopeptidase and angiotensin converting enzyme with the effect of potentiating the natiuretic peptide system and bradykinin, and blocking the conversion of angiotensin I and angiotensin II. In the IMPRESS study, omapatrilat has been evaluated in patients with cardiac insufficiency versus lisinopril; there was no significant difference on the principal outcome measure which was exercise tolerance, however it was significantly more effective than lisinopril on the outcome measure combining death and hospital admission for deteriorating cardiac insufficiency. A wider study is underway, the OVERTURE study, which is evaluating omapatrilat versus enalapril on hospital admission and all-cause mortality. The Vanlev dossier has not yet been submitted to the regulatory authorities for obtaining its authorisation to be put on the market.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2002

[Value and limitations of coronary artery imaging with the MRI navigator technique. Comparison with coronary angiography results in 37 patients].

The introduction of a non-invasive method of imaging the coronary arteries would be a great advance in daily cardiological practice. The authors report their experience of imaging the coronary arteries with 1 Tesla MRI using the "navigator technique". Twenty-five sections 1.2 mm thick, focused on the proximal left coronary artery, were acquired with a 512 matrix, without injecting contrast during normal respiration with a tolerance on the portion of the right diaphragmatic cupola of 5 mm. Analysis of the coronary segments included in the field of view was performed on native sections after curve reconstruction and on targetedMIP series. A comparison of the results with respect to conventional coronary angiography showed a relatively limited visualisation of the proximal coronary segments because, in addition to the impossibility of carrying out the investigation in 24% of cases (faulty cardiac or respiratory synchronisation, poor signal/noise ratio), only 93% of the left main coronary and 75% of the proximal left anterior descending arteries could be visualised. In the analyzable segments, the diagnostic performances were modest with a global sensitivity of 60.8% and specificity of 91%. With the exception of the left main coronary artery, the sensitivities observed did not make MRI of the coronary arteries a rival to conventional coronary angiography. These limited performances may be explained by the lack of rapidity of the sequences of acquisition compared to the rapid motion of the structures under investigation whose dimensions are 5 to 10 times smaller than their amplitude of excursion. Technical developments are regularly accomplished in this domain, especially 3rd generation sequences in apnoea with injection of contrast media. At present, despite some results reported in the literature, angio-MRI of the coronary arteries cannot be used reliably to guide clinical decisions in coronary artery disease with the exception of some situations like congenital abnormalities of the coronary arteries, non-invasive follow-up of coronary aneurysms or analysis of the left main coronary artery.

Coronary Aneurysm↗
PubMed2001

Myocardial flow reserve parametric map, assessed by first-pass MRI compartmental analysis at the chronic stage of infarction.

Regional myocardial flow and flow reserve (MFR) were assessed by compartmental analysis of Gd-enhanced MRI first-pass data in 7 patients with atypical chest pain, and in 15 patients with previous transmural myocardial infarction. The FE product (Flow x Extraction coefficient), derived from the modified Kety equation, was measured in regions corresponding to the Tetrofosmine-SPECT fixed defect and in remote normal regions. The FE product at rest and hyperemic FE product were similar in healed revascularized tissues (70.5 +/- 15.6 and 112.5 +/- 19.5 ml/mn/100 g, respectively) and in normal myocardium (76.2 +/- 18.3 and 142.2 +/- 33.0, respectively). In contrast, the FE index (48.8 +/- 15.2 and 60.7 +/- 18.0, respectively, P < 0.01 versus the two previous groups) and the MFR (1.27 +/- 0.20 vs. 1.91 +/- 0.29 in normal regions) were reduced in healed fibrotic tissues when the infarct-related artery remained occluded. Myocardial flow reserve maps allowed correct identification of regions corresponding to an occluded infarct-related artery.

Aged↗
PubMed2000

[Cartography of absolute myocardial perfusion with magnetic resonance imaging. Methods and results].

Ultra-rapid dynamic MRI (one image per heart beat) can follow the progression of the intra-myocardial signal during the first passage of diffusable gadolinium chelates injected as a bolus through a peripheral vein. A quantitative evaluation of myocardial perfusion is possible using a compartmental model of analysis. Absolute myocardial flow can be measured at rest and during hyperaemia induced by dipyridamole. It is possible to associate functional mapping, corresponding to parametric images of the flow indices, to the global evaluation. The ratio between the values obtained during hyperaemia and under basal conditions correspond to the myocardial reserve. The principles, results and limitations of this method are discussed in the light of published results, underlining the advantages of absolute flow measurement and of the differences between the results of MRI and myocardial scintigraphy.

Coronary Circulation↗
PubMed1999

Neurohormonal profile before and after beta-blockade in patients with neurocardiogenic syncope.

Our objective was to evaluate the effects of beta-blockers on the neurohormonal profile, particularly vasopressin (VP) release, in vasovagal syncope and to gain further insight on the pathophysiology of this syndrome. Patients (< or =75 years) with no cardiovascular, neurological disorders, or contraindications to the use of isoproterenol or beta-blockers and being explored for unexplained syncope were included. An 80 degrees HUT was performed under identical conditions. After a 25-min period of passive tilt, isoproterenol was infused at a rate of 1-5 microg/mn if required. Two groups matched for age and sex were considered: a HUT-positive and a HUT-negative group. The HUT-positive group was then given beta-blockers, subsequently reassessed, and divided into two subgroups: alpha beta-blocker nonresponder group and a beta-blocker responder group. Blood samples for assays of norepinephrine (NE), epinephrine (E), and VP were taken at baseline and the end of the procedure. In all, 44 subjects entered the study, 22 in each group. The HUT-positive group exhibited an obvious lesser increase in plasma NE and a clear-cut rise in plasma E and VP compared to the HUT-negative group (P < 0.05). Even though no patient in the HUT-positive group reported recurrent symptoms under treatment, the second HUT could distinguish two subgroups: a beta-blocker nonresponder group (n = 12) whose HUT remained positive and a beta-blocker responder group (n = 10) whose HUT was normalized. The time course of plasma E and VP during the second HUT was similar to that for the HUT-positive and HUT-negative groups. In conclusion, the efficacy of beta-blockers is associated not only with a reduction of the sympathoadrenal stimulation seen in vasovagal syncope but also with a lower release of VP suggesting that low-pressure baroreceptors might be involved in VP release.

Adolescent↗
PubMed1999

Mechanism of Ca2+ release and entry during contraction elicited by norepinephrine in rat resistance arteries.

The intracellular Ca2+ stores and the mechanisms of Ca2+ entry produced by norepinephrine (NE) were investigated in small mesenteric resistance arteries of the rat. In Ca2+-free medium, NE (10 microM) elicited a transient increase in both intracellular free Ca2+ concentration ([Ca2+]i) and tension that were both drastically reduced by caffeine and only partially reduced by the two sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) blockers thapsigargin and cyclopiazonic acid, despite the presence of SERCA2a and SERCA2b isoforms in the medial smooth muscle layer of the artery. After depletion of intracellular Ca2+ stores with 10 microM NE, addition of exogenous CaCl2 (2.5 mM) produced large and sustained increases in both [Ca2+]i and contraction of the arteries provided that the agonist was continuously present. In these conditions, the responses to CaCl2 were inhibited by the voltage-dependent Ca2+ entry blocker nitrendipine (1 microM), the putative inhibitor of receptor-operated Ca2+ entry SKF-96365 (30 microM), and NiCl2 (1 mM). The inhibition produced by SKF-96365 and NiCl2 was greater than that of nitrendipine. Also, the responses to CaCl2 were greatly reduced or abolished in the presence of the Na+/Ca2+ exchanger inhibitors 1,3-dimethyl-2-thiourea, 3',4'-dichlorobenzamil, MgCl2, and amiloride or after omission of NaCl in the medium. Also, protein kinase C inhibitors, calphostin C and staurosporine, and tyrosine kinase inhibitors, genistein and tyrphostin 23, both reduced the responses to CaCl2. The inhibitory effect of protein kinase C inhibitor and tyrosine kinase were additive. These results suggest that NE releases Ca2+ from intracellular stores that are caffeine sensitive and partially sensitive to SERCA inhibitors. They indicate that in addition to Ca2+ influx via nitrendipine-sensitive and SKF-96365-sensitive channels, Na+/Ca2+ exchanger participates in the CaCl2-induced contraction produced in NE-exposed vessels. The pathway leading to Ca2+ entry probably involves tyrosine kinase and protein kinase C. All the above mechanisms require ongoing receptor stimulation.

Animals↗
PubMed1999

Myocardial bridging as a cause of acute transient left heart dysfunction.

The significance of myocardial bridging is still a matter of debate, and although several reports have underlined its pathologic potential, myocardial bridging is often considered to be a benign phenomenon. We present here the case of a 63-year-old woman with a history of acute left heart failure and ECG evidence of ischemia, and whose primary abnormality on extensive workup was myocardial bridging. This case further underlines that myocardial bridging can lead to significant cardiac events.

Acute Disease↗
PubMed1998

Does the 6-minute walk test predict the prognosis in patients with NYHA class II or III chronic heart failure?

BACKGROUND: We prospectively evaluated the potential of the 6-minute walk test compared with peak VO2 in predicting outcome of patients with New York Heart Association (NYHA) class II or III heart failure. METHODS AND RESULTS: Patients with a history of heart failure caused by systolic dysfunction were included. The combined final outcome (death or hospitalization for heart failure) was used as the judgment criterion. One hundred twenty-one patients (age 59+/-11 years; left ventricular ejection fraction 29.6%+/-13%) were included and followed for 1.53+/-0.98 years. Patients were separated into two groups according to outcome: group 1 (G1, 74 patients), without events, and group 2 (G2, 47 patients), who reached the combined end point. Peak VO2 was clearly different between G1 and G2 (18.5+/-4 vs. 13.9+/-4 ml/kg/min, p=0.0001) but not the distance walked (448+/-92 vs 410+/-126 m; p=0.084, not significant). Survival analysis showed that unlike peak VO2, the distance covered was barely distinguishable between the groups (p < 0.08). However, receiver operating characteristic curves revealed that the best performances for the 6-minute walk test were obtained for subjects walking < or =300 m. These patients had a worse prognosis than those walking farther (p=0.013). In this subset of patients, there was a significant correlation between distance covered and peak VO2 (r=0.65, p=0.011). Thus it appears that the more severely affected patients have a daily activity level relatively close to their maximal exercise capacity. Nevertheless, the 300 m threshold suggested by this study needs to be validated in an independent population. CONCLUSIONS: A distance walked in 6 minutes < or =300 m can predict outcome. Moreover, in these cases there is a significant correlation between the 6-minute walk test and peak VO2 demonstrating the potential of this simple procedure as a first-line screening test for this subset of patients.

Adolescent↗
PubMed1998

[MRI semeiology of segmental contraction abnormalities in arrhythmogenic dysplasia of the right ventricle].

The diagnosis of localized arrhythmogenic right ventricular dysplasia may be difficult to ascertain. Aside from electrophysiological arguments, visualization of an abnormal right ventricular contraction pattern is of crucial importance for diagnosis. Cine-MR is almost the only examination method which offers detailed informations on the right ventricular contraction pattern. Nine observations of segmental right ventricular contraction abnormalities assessed by cine-MR are described here: dyskinesia of the distal part of the anterior wall (2), of the inferior wall (2), of the right ventricular outflow tract (2); akinesia of the outflow tract (2) and of the inferior wall (1). Morphological abnormalities of the right ventricle are always associated with contraction abnormalities but seem to be less disease specific. Patients should be more readily referred for a cine-MR examination when the diagnosis of localized right ventricular dysplasia is suspected. Cine-MR sequences related to these observations may be reached via Internet at:http:@alsace.u-strasbg.fr/cardio/coeur.htm.

Adult↗
PubMed1998

[Prognosis of diastolic cardiac insufficiency].

The natural history and prognosis of diastolic cardiac failure are difficult to determine because of the large differences in the studies which have been performed in this field. The ten studies published to date concerning the prognosis have been performed on hospital populations and, consequently, only the most severe cases have been recruited. Moreover, the threshold values of indices of the ejection phase used to define systolic dysfunction vary from one study to another. A review of these papers provides a rather disconcerting appreciation of the annual mortality rate (from 1.3% to 17.5%). The differences in aetiology, age and threshold values of parameters of systolic function probably explain most of the variability observed. Taking unbiased studies alone in consideration, such as the Framingham study, the mean annual mortality of diastolic cardiac failure between 55 and 71 years, is 3 to 9%, much less than that observed with predominantly systolic dysfunction (15 to 20%). Other prospective studies, adjusting morbidity and mortality to age and other principal prognostic factors, are awaited.

Cardiac Output, Low↗
PubMed1997

Diltiazem slow-release and left-ventricular hypertrophy: a volumetric approach of left ventricular mass using magnetic resonance imaging.

AIMS: This study was designed to assess the changes in left ventricular mass (LVM) in hypertensive patients with left ventricular hypertrophy under drug therapy with once-daily slow-release diltiazem. Magnetic resonance imaging (MRI) was used for this purpose because of its higher reproducibility than M-mode or two-dimensional echocardiography. METHODS: Patients suffering from essential hypertension were included if their baseline LVM index (LVMI) was > or = 105 g/m2 in male or > or = 85 g/m2 in female patients, ie, equal or higher to the median values observed in hypertensive patients in our institution. MRI consisted in a true short-axis, electrocardiogram (ECG) gated spin-echo slice acquisition at baseline, after 3 and 6 months of therapy (M0, M3, and M6). Data were stored on magnetic tapes and read subsequently under blind conditions and the control of an external auditor. RESULTS: Thirty-five patients were included. Of these, 14 patients (40%) were not previously treated. Inter- and intra-observer variability for LVMI measurement were 5.6 +/- 4.3% and 2.1 +/- 3.0%, respectively. Mean baseline LVMI was 110 +/- 16 g/m2 in male and 96 +/- 16 g/m2 in female patients. It decreased by 3.6% at M3 (P = 0.05) and by 6.0% at M6 (P = 0.02). A trend towards a greater LVMI reduction was observed in previously untreated patients. CONCLUSION: This study confirms that MRI is a reproducible technique for the measurement of LVM. It demonstrates a significant reduction in LVMI as early as the 3rd month of therapy in hypertensive patients treated with once-daily sustained release (SR) diltiazem, although baseline LVMI in the majority of participating patients was only moderately increased.

Adult↗
PubMed1996

Comparison between abnormalities in segmental endocardial motion and abnormalities in segmental wall thickening after anterior myocardial infarction. A cine-magnetic resonance study.

In this study, two patterns of regional contract on of the left ventricle have been studied: endocardial motion and wall thickening, in order to check which of these was the most affected after myocardial infarction. The clinical relevance of this comparison was to assess which parameter of the regional contraction abnormality would best depict the severity of the infarction. Long axis cine-magnetic resonance slices were used to assess segmental systolic left ventricular endocardial motion and segmental systolic wall thickening in 39 normal subjects and in 30 patients at the chronic stage of an anterior myocardial infarction. In the group of normal subjects, endocardial motion and wall thickening showed significant regional heterogeneity. Overall endocardial motion was greater than overall wall thickening: 9.5 +/- 2.0 mm vs 7.1 +/- 1.8 mm. P = 4 x 10(-12) (3.1 +/- 1.2 mm vs 2.0 +/- 0.7 mm, P = 9 x 10(-5) after infarction). A significant linear correlation was found between these two parameters. In the infarction group, abnormality scores for endocardial motion and for wall thickening were calculated. These scores were defined as the average values exceeding the mean minus two standard deviations of the normal range for segments corresponding to the antero-septal-apical walls. The abnormality score for endocardial motion greater than the abnormality score for wall thickening: 0.31 +/- 0.12 vs 0.20 +/- 0.07, P = 9 x 10(-4). We conclude that, in clinical practice, endocardial motion is affected to a greater degree by myocardial infarction than is wall thickening and therefore constitutes a more discriminant index in the assessment of post-infarction patients.

Adult↗
PubMed1996

[Left ventricular diastolic dysfunction in cardiomyopathies].

Although physiologists have recognised for many years that cardiac performance is based on two functions, systolic and diastolic, it has only been in the last 15 years that clinicians have acknowledged the essentiel role of diastole in the physiopathology of cardiac disease. Many studies have shown that left ventricular diastolic dysfunction resulting from abnormal active relaxation or changes in passive visco-elastic properties of the myocardium modulating its rigidity were responsible for decreased distensibility of the ventricle and an increase in its filling pressures. Therefore, the symptoms of the majority of patients with cardiomyopathy are due, more or less, to diastolic dysfunction. This is particularly the case in hypertrophic cardiomyopathy, most case of which have diastolic dysfunction secondary to an often asymetric distribution of the hypertrophy, to the disorganisation of the myocardiofibres and to interstitial fibrosis. With respect to advanced forms of restrictive cardiomyopathy, as their clinical and haemodynamic characteristics resembling constrictive pericarditis show, they demonstrate caricatural diastolic dysfunction. Finally, although the main abnormality in dilated cardiomyopathies is poor contractility, a decrease in ventricular compliance is constantly observed.

Atrial Fibrillation↗
PubMed1996

[Terminal heart failure; therapeutic strategies. Drug therapy in cases of absence of possibility of heart transplantation: dobutamine therapy, aspects of compassion?].

Terminal cardiac failure, despite the gain obtained by angiotensin converting enzyme inhibitors, continues to carry a high annual mortality. Cardiac transplantation, with a 1 year survival of about 80% (a result which is sustained at 5 years), constitutes the treatment of choice for these patients. However, in view of the contraindications to transplantation and the cruel lack of donors organs, many cases of terminal cardiac failure are unable to benefit from transplantation. What are the pharmacological means available for these patients? This is a real therapeutic challenge. The essential objective in the management of these patients with a poor short-term prognosis is the reduction of mortality. However, this aim is not easily attained, at least in the short or medium-term in the present state of our knowledge. Other objectives can therefore by legitimately considered in the management of patients with cardiac failure in the terminal phase: the most important ones are to improve symptomatology and the quality of life. Terminal cardiac failure is a complex syndrome implicating a number of non-cardiac abnormalities. They may not only participate in the symptomatology and high mortality, but also make therapeutic management a delicate operation. Nevertheless, the abnormalities of cardiovascular function remain the cardinal problem. The treatment which we use aims to correct them. The authors propose a review of the possibilities available with reference to data in the medical literature.

Adrenergic beta-Agonists↗
PubMed1995

Prognostic factors of chronic heart failure in NYHA class II or III: value of invasive exercise haemodynamic data.

UNLABELLED: Various parameters have been found useful for establishing the prognosis of patients with chronic heart failure, in particular haemodynamic parameters measured at rest. However, few studies deal with the prognostic value of invasive exercise haemodynamic parameters in such patients. Our aim was to test the value of such parameters to assess the prognosis of patients with chronic heart failure in functional class II or III of the New York Heart Association. METHODS: Between December 1990 and June 1993, 50 patients fulfilled the criteria for inclusion in the study. The average age and ejection fraction of the population were 54 +/- 2 years and 20 +/- 0.5% respectively. All patients were examined clinically; their invasive haemodynamic parameters were measured at rest and during exercise, and their exercise peak VO2, validated by reaching the anaerobic threshold, was determined. They were followed up for 21.2 +/- 1.17 months (ranges 3-26 months). The assessment criteria employed were mortality and the occurrence of major events (heart failure, pulmonary oedema or severe ventricular arrhythmia). RESULTS: The population consisted of 32 men and 18 women. No gender-related differences were found. Two groups could be distinguished in terms of prognosis: G1: n = 31 living patients with no events, and G2: n = 19 deceased or with major events. G1 and G2 were comparable with regard to age, sex ratio and ejection fraction. Several of the 52 parameters tested were different in the two groups, in particular peak VO2, exercise duration, the workload developed during the cardiopulmonary test and all the invasive exercise haemodynamic parameters except heart rate (P < 0.0001). Haemodynamic parameters at rest had no prognostic value in this series. The ROC curves, the survival curves and the Cox analysis showed that exercise cardiac power output, exercise left ventricular work indices and exercise peak VO2 were the most useful factors for assessing the prognosis of patients with NYHA II or III chronic heart failure. An exercise cardiac power output < 2 watts accurately identified those patients with a short-term poor prognosis, and exercise peak VO2 was almost as accurate. To a lesser extent, the NYHA functional class was also an independent prognostic parameter during multivariate analysis. In conclusion, it appears that invasive haemodynamic parameters are best for determining the prognosis of patients with chronic heart failure. Peak VO2 can, however, be as useful. Moreover this is an easily obtainable non-invasive parameter, which makes it more useful in the evaluation and the follow up of such patients.

Adolescent↗