[Acute myocardial infarction in women. Initial characteristics, management and early outcome. The FAST-MI registry]. / L'infarctus du myocarde chez la femme. Caractéristiques spécifiques, prise en charge et pronostic. Données de FAST-MI 2010.

AIM: To assess gender differences in characteristics, management, and hospital outcomes in patients participating in the French FAST-MI 2010 registry. POPULATION: Three thousand and seventy-nine patients hospitalised for ST-elevation (STEMI) or non-ST-elevation (NSTEMI) myocardial infarction in 213 French centres during a 1-month period at the end of 2010. RESULTS: Women account for 27% of the population and more frequently present with NSTEMI. They are 9 years older than men on average, although 25% of women with STEMI are less than 60 years of age. Management of STEMI is similar, after adjustment for baseline characteristics. However, fewer women are treated with primary percutaneous coronary angioplasty. In NSTEMI, although use of coronary angiography is similar, fewer women get treated with angioplasty. Most medications are used in a similar way in men and women, except thienopyridines, with fewer women receive prasugrel. After adjustment, in-hospital mortality is similar for men and women. CONCLUSION: Myocardial infarction is not specific to men: one out of four patients admitted for myocardial infarction is a woman. Initial management is rather similar for men and women, after taking into account differences in baseline characteristics. Percutaneous coronary angioplasty, however, remains less frequently used in women. In-hospital complications have become rarer and do not differ according to sex.

[Myonecrosis and inflammatory response following percutaneous coronary angioplasty. A protective role for betablockers?]. / Myonécrose et majoration de la réponse inflammatoire après angioplastie coronaire. Rôle protecteur des bêtabloquants?

INTRODUCTION: Percutaneous coronary intervention (PCI) is widely used actually for the treatment of coronary disease. Stent implantation in the vessel wall is associated with local healing processes and some myonecrosis. However, little is known about the relationships between systemic inflammatory response, myonecrosis and the patient's and procedural characteristics. OBJECTIVES: (i) To evaluate the level of C-Reactive Protein (hsCRP) and cardiac troponin I (cTnI) elevation after PCI; (ii) to determine the patient's and procedural factors associated with those elevations. METHOD: This is a prospective monocentric study carried out in patients hospitalised for elective PCI or for ACS without cTnI elevation. CRP and cTnI were assessed before, after and 24 hours after the procedure. RESULTS: Thirty-four patients (mean age 64+/-10.9 years; sex ratio 28 males/six females) were included. hsCRP increased in 26 patients (76.4%) and cTnI in 16 patients (47%) after PCI. cTnI elevation did not correlate with inflammatory response. Whereas none of the studied parameters were statistically linked with hsCRP increase, cTnI elevation was significantly associated with AHA-ACC B(2)/C type lesion, the number and the total length of stents implanted, the duration of procedure and treatment by betablockers. Multivariate analysis showed that the independent predictors of cTnI elevation were procedure duration (p=0.032 OR=14.2 CI 95% 7.69-100) and the absence of pretreatment with betablockers (p=0.036, OR=2,6 CI 95% 1.35-35). CONCLUSION: cTnI elevation following PCI is very frequent and related with the duration of the procedure. Our data suggest a protective role of betablockers in the occurrence of cTnI elevation after PCI. Confirmation of the protective role of betablockers in larger cohort is mandatory.

[Delays of treatment of acute myocardial infarction with ST elevation admitted to the CCU (coronary care unit) in Alsace]. / Délais de prise en charge de l'infarctus aigu du myocarde avec sus-décalage persistant du segment ST admis dans les USIC d'Alsace.

OBJECTIVE: to determine the time delay from symptom onset to diagnosis and treatment of patients with persistant ST segment elevation myocardial infarction (STEMI). DESIGN: prospective observational study. METHOD: patients with symptoms onset < 24 h admitted in all 10 cardiac intensive care units in one French administrative region (Alsace). Data were recorded by doctors on duty soon after hospital admission. Patients with STEMI during hospital stay or as a complication of cardiac interventional procedure were excluded. The Kruskal-Wallis test was used to assess statistical differences between the groups (p value < 0.05). RESULT: from April to October 2004, 326 patients were admitted for STEMI. Median time between the symptoms onset and the patient's call for medical help was 60 minutes. General practitioners were the first medical contact in 41%. The time from symptoms onset to first medical intervention and from first medical intervention to coronary care unit admission were markedly shorter in patients who had directly called the Emergency Medical Services (group 15-110 patients i.e. 33% of the study population): 44 min vs 75 min otherwise (p=0,003). Median transport time was 60 min. Sixty two percent of the pts were transported by the Emergency Medical Services. The median time from symptoms onset to initiation of reperfusion therapy was 240 min. It was significantly lower in group 15 (170 min vs 286 min - p < 0,001) and for thrombolytic therapy (190 min versus 245 min for primary angioplasty, p=0,007). When thrombolysis (THL) was used, 89% of the pts could be treated during 6 hours of symptoms onset and 44% in 3 hours. For angioplasty only 4% of the pts were treated in the first 90 minutes, 9% in the 2 hours and 30% in the 3 hours of symptoms onset. If the time delay is evaluated from the 1 st medical intervention, call to reperfusion intervention was significatly shorter for THL: 91 versus 157 min, p< 0,003. Angioplasty represented 75% of reperfusion strategy in our area and THL alone only 2,7% and combine therapy 5,4%. CONCLUSION: our study documents the beneficial effect of a direct call to Emergency Medical Services. Our results also underscore the need for an effort to reduce the time to offer the best appropriate reperfusion techniques in STEMI pts: speed up the admission in the cath-lab, think about pre-hospital thrombolysis followed by coronary angioplasty if necessary.

[Platelet responsiveness to clopidogrel in patients with coronary syndrome. Comparison of platelet aggregation induced by ADP and flow cytometric analysis of intraplatelet VASP phosphorylation]. / Evaluation de la réponse plaquettaire au clopidogrel au cours des syndromes coronariens. Comparaison de l'agrégométrie à l'ADP et de la méthode VASP.

UNLABELLED: Although antiplatelet therapy with ASA-clopidogrel reduces the risk of cardiovascular episodes after PCI, a substantial number of events occur during follow-up. Sustained platelet reactivity under dual antiplatelet therapy was recently associated with increased risk of recurrent atherothrombotic events after PCI. Whereas it appears significant to determine clopidogrel responsiveness, the accurate platelet function assay is still under investigation. OBJECTIVES: (i) to determine the proportion of "low-responders" or "resistants" patients during coronary syndrome (ii) to identify determinants of interindividual variability response to clopidogrel (iii) to compare aggregometry and VASP phosphorylation measured by flow cytometry. Patients were treated by clopidogrel (300 mg loading dose and 75 mg maintenance dose) and ASA (160 mg) (N=27). Additional treatment by GPIIbIIIa antagonists was given to high-risk patients (N=9). Platelet function was monitored by ADP aggregometry (5, 10, 20 microM) and VASP phosphorylation before any treatment by clopidogrel (d0) and at least five days after (d5). The platelet reactivity index (PRI), expressed as percentage, is the difference in VASP fluorescence intensity between resting (+ PGE1) and activated (ADP) platelets. At d5, low responsiveness to clopidogrel was defined by either (i) a PRI > 67.3% corresponding to the mean value -2SD measured in untreated patients (dO) (ii) or an absolute change (delta d0-d5) in aggregation (ADP 10 microM) < to 30%. RESULTS: PRI, platelet aggregometry to ADP was significantly reduced following clopidogrel treatment (P < 0.01). A wide inter-individual variability to clopidogrel was observed at d5 (PRI from 11 to 83%). Whatever the platelet function used, a large proportion of patients were detected as "low-responders" (37% by VASP, 44% by ADP aggregometry). Absolute change in ADP aggregation was correlated to the variation of PRI (R = 0.559; P = 0.02). Contrary to ADP aggregometry, PRI was not influenced by GPIIbIIIa antagonists or prior administration of ASA. However, the conformity of the two methods to evaluate clopidogrel responsiveness was only 66%. No differences in platelet aggregometry could be observed at d5 between "low" and "good-responders" defined by VASP analysis. At d5, a higher PRI value could be detected in male and patients with history of dyslipemia. CONCLUSION: During coronary syndrome, impaired platelet responsiveness to clopidogrel was observed in a large proportion of patients whatever the platelet function assay used. VASP analysis was found insensitive to GPIIbIIIa or aspirin administration. Possible mechanisms linking clopidogrel "resistance" measured by VASP assay and enhanced thrombogenicity remain to be characterized. Indeed, clopidogrel "resistance" defined by VASP analysis was not associated with higher platelet aggregation.

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.

[Value and limitations of coronary artery imaging with the MRI navigator technique. Comparison with coronary angiography results in 37 patients]. / Intérêt et limites actuelles de l'imagerie des artères coronaires avec la technique d'IRM du navigateur. Comparaison avec les données coronaro-angiographiques chez 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.

[Heart failure and vasopeptidase inhibitors]. / Insuffisance cardiaque et inhibiteurs des vasopeptidases.

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.

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.

[Cartography of absolute myocardial perfusion with magnetic resonance imaging. Methods and results]. / Cartographie de la perfusion myocardique absolue avec imagerie par résonance magnétique. Méthodes et résultats.

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.

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.

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.

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.

[MRI semeiology of segmental contraction abnormalities in arrhythmogenic dysplasia of the right ventricle]. / Séméiologie IRM des anomalies de la contraction segmentaire dans la dysplasie arythmogène du ventricule droit.

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.

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.

[Prognosis of diastolic cardiac insufficiency]. / Pronostic de l'insuffisance cardiaque diastolique.

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.

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.

[Terminal heart failure; therapeutic strategies. Drug therapy in cases of absence of possibility of heart transplantation: dobutamine therapy, aspects of compassion?]. / Insuffisance cardiaque terminale; stratégies thérapeutiques. Moyens médicaux en l'absence de possibilité de greffe cardiaque: cure de dobutamine, aspects compassionnels?

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.

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.