[Usefulness of diastolic deceleration time assessed by transthoracic Doppler measurement in the detection of sustained microvascular obstruction in STEMI patients treated by primary PTCA]. / Intérêt de la mesure du temps de décélération diastolique par Doppler transthoracique dans l'évaluation du phénomène de no-reflow au cours de l'infarctus du myocarde antérieur traité par angioplastie primaire.

AIMS: To assess the value of coronary flow measurement by transthoracic Doppler technique in the detection of "no-reflow" phenomenon. METHODS: Fourteen patients with first anterior wall infarction treated by successful (TIMI3) primary percutaneous angioplasty and left descending coronary artery stenting were investigated. Myocardial perfusion following PCI was assessed by (i) ST-segment resolution, (ii) MRI-detected microvascular obstruction (early hypoenhancement), (iii) coronary flow pattern measurement by transthoracic Doppler technique. RESULTS: Sustained impairment of myocardial perfusion following PCI was observed in a large proportion of the cohort (36% by MRI, 43% by ST regression analysis). Patients with a diastolic deceleration time inferior to 482 ms had higher troponin and CK peak value, higher wall motion index score, lower ST resolution and lower LVEF assessed by MRI. The concordance of the three methods was 80%. CONCLUSION: The measurement of diastolic deceleration time by transthoracic Doppler technique is a reliable technique to identify microvascular obstruction following PCI in acute anterior STEMI. A DDT inferior to 482 ms is associated with sustained "no-reflow" phenomenon.

[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.

[Value of left atrial dilation in the diagnosis of silent myocardial ischemia in diabetes mellitus patients]. / Facteurs prédictifs de l'existence d'une ischémie myocardique silencieuse chez le patient diabétique. Intérêt de l'évaluation de la surface de l'oreillette gauche.

BACKGROUND: Accelerated atherothrombosis is a common feature in diabetes mellitus patients (DM), which can be related to abnormalities in vascular cell apoptosis and activation leading to the release of procoagulant microparticles (MPs). In DM patients, we hypothesized that circulating levels of biomarkers involved in atherothrombosis processes as well as cardiac and carotid echocardiography variables could be useful in the detection of silent myocardial diagnosed by myocardial perfusion imaging. METHODS AND RESULTS: We investigated, in 55 patients with diabetes (mean age 62+/-10 years) and 15 nondiabetics (46+/-14 years) patients the prevalence of silent myocardial ischemia (SMI) detected by a treadmill exercise or dipyridamole (99m)Tc-sestamibi stress test. Echocardiographic and -carotid variables were obtained using standardized methods. Biomarkers assessing endothelial apoptosis or activation (CD31+-MPs, CD62+-MPs, VCAM-1), inflammatory status (CD11a +/- MPs, MCP-1, CRP), platelet activation (GPIb+/-MPs, CD40-L, P-selectin, GPV) ventricular stretch (BNP) were measured in the plasma. SMI was diagnosed in 23/55 (42%) diabetics patients and in 3/15 (20%) nondiabetics patients. Enhanced inflammatory status and leukocyte damage (CD11a+-MPs) were evidenced in diabetic patients. Within the diabetic population, biomarkers levels of atherothrombosis were not significantly associated to the detection of SMI. In multivariable analyses adjusted for LV hypertophy, left atrial surface (LA) remained independent predictor of silent myocardial ischemia (OR 4.14; IC [1.7-16.13]; P=0.039). CONCLUSIONS: In diabetes mellitus patients, LA surface independently predicted silent myocardial ischemia after adjustment for established echocardiographic, and inflammatory risk factors. This simple measure of LA dilation could be helpful in the identification of diabetes mellitus patients at heightened cardiovascular risk.

[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.

[Platelet response to aspirin and clopidogrel. Biochemical evaluation, clinical impact, and pharmacological modulation]. / Réponse plaquettaire à l'aspirine et au clopidogrel. Evaluation biologique, impact clinique, modulation pharmacologique.

In the vasculature, platelets contribute to thrombotic and inflammatory responses, key processes in atherothrombosis. During percutaneous coronary interventions, several studies have emphasized the deleterious impact of enhanced platelet aggregation on early clinical outcome. However, despite the significant interest of determining platelet responsiveness appears worth, the clinically accurate and practical platelet function assay is still not widespread available. Furthermore, standardized definitions of platelet "low-responders" are still lacking. Up to now, light transmission platelet aggregometry remains the "gold-standard". Platelets "points of care" assays might overcome the limitations of conventional optical platelet aggregation but need further validation in clinical settings. The most recent ACC/AHA guideline endorses a strategy of platelet monitoring in the highest risk patients (IIb C). In "low-responders" patients, clopidogrel dose escalation was demonstrated to improve platelet responsiveness. Others potential pharmacological solutions could include the switch for another thienopyridine. Indeed, prasugrel a P2Y12 receptor inhibitor was demonstrated to provide higher levels of inhibition of ADP-induced platelet aggregation.

[Variable extent of platelet responsiveness to clopidogrel inhibition: "clopidogrel resistance"?]. / Variabilité de la réponse plaquettaire au clopidogrel: "résistance" biologique?

During percutaneous coronary angioplasty, platelet inhibition by clopidogrel and aspirin has drastically decreased the risk of thrombotic occlusion of the stented vessels. However, despite the widespread use of these drugs, the incidence of acute or subacute stent thrombosis remains elevated, concerning 1 to 2% of the treated patients. Considerable differences in the responsiveness to clopidogrel could be observed, suggesting a possible underlying biological resistance. "Clopidogrel resistance" has recently been associated to an increased risk of thrombotic events following coronary angioplasty. Variations in enteric absorption, biotransformation in the liver by the CYP3A4, changes in the ADP receptor P2Y12, abnomalies of intraplatelet signal transduction, extent of platelet activation, class angina, diabetes mellitus may account for the considerable interindividual response variability widely reported. In this view, laboratory tests evaluating "clopidogrel resistance" might be useful tools for the identification and follow-up of patients at higher thrombotic risk. Indeed, in these patients, further platelet inhibition can be achieved by higher doses of clopidogrel.

[Microparticles and cardiovascular disease]. / Microparticules et pathologies cardiovasculaires.

Microparticles are membrane fragments liberated by activated or apoptopic cells. Thought for a long time to be cellular debris with no specific biologic function, in the vascular compartment they are a circulating reservoir of cellular effectors involved in thrombosis, inflammation, vascular remodelling and angiogenesis. High concentrations of circulating procoagulating microparticles found in many cardiovascular diseases indicate the importance of platelet, endothelial and monocytic activation and could contribute to the persistence of atherothrombotic disease. Pharmacological modulation of circulating microparticle concentrations could become a major therapeutic target in the future.

[Procoagulant membranous microparticles and atherothrombotic complications in diabetics]. / Microparticules membranaires procoagulantes et complications athérothrombotiques chez le patient diabétique.

Endothelial apoptosis and platelet activation play a key role in atherothrombotic event. These two mechanisms resulting membrane thickening leading to procoagulant microparticle (MP) liberation into the blood stream. In the vascular compartment, MP contribute to increased thrombin formation, to platelet activation, and prolong inflammation of the arterial wall by inducing the synthesis of cytokines and adhesion of glycoproteins by the endothelial cells. In diabetic patients, increased endothelial apoptosis associated with intense platelet and monocytic activation could contribute to accelerated atherothrombosis. Endothelial, platelet and monocytic derived MP, found in high concentrations in these patients, induce a prothrombotic, proadhesive and proinflammatory tendency in the vascular comportment which could directly impact on the vascular prognosis. In diabetes, increased platelet or monocytic MP is a marker for microvascular disease. Likewise, in acute coronary syndromes of diabetic patients, high concentrations of procoagulant MP could be associated with a poor cardiovascular prognosis. In these diabetic patients, many treatments (antioxidant, antiplatelet, lipid lowering, antihypertensive) significantly reduce the levels of MP and parameters associated with inflammation. MP are one of the key factors linking inflammation, oxidative stress, apoptosis and thrombosis in accelerated atherothrombotic disease of the diabetic. In future, the measurement of MP should help evaluate the efficacy of antioxidant and antiplatelet therapy, especially in diabetic patients.

[An unusual complication of coronarography: neuralgia of the internal saphenous]. / Une complication inhabituelle de la coronarographie: la névralgie du nerf saphène interne.

Many causes of saphenous nerve lesions at the knee or leg level have been reported. Proximal nerve lesions, especially after varicose vein stripping, are uncommon. We report a case of saphenous nerve lesion following catheterization of the femoral artery complicated with arterial spasm. The patient experienced pain for 10 years and only transdermal electroneural stimulation provided sedation. To our knowledge, this is the first published case of such an unusual complication after coronarography, despite the frequency of this procedure. We suggest nerve ischemia could explain the definitive neuralgia.

[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.

[Evaluation of a specific French scale of activity in chronic heart failure. A national multicenter study. Group for Cardiac Insufficiency and Cardiomyopathy of the French Society of Cardiology]. / Evaluation d'une échelle d'activité spécifique française de l'insuffisance cardiaque chronique. Etude multicentrique nationale. Groupe insuffisance cardiaque et cardiomyopathie de la Société française de cardiologie.

Many systems have been proposed to evaluate the functional incapacity caused by chronic cardiac failure. The classification of the New York Heart Association (NYHA) is the best known. It is subjective, poorly reproducible and has a poor predictive value on effort. The authors propose a Specific French Scale of Activity with the object of a more accurate functional evaluation of cardiac failure, easier to use by the doctor and more specific to French patients and their life styles. A French multicentre study was set up in hospital departments by the French Society of Cardiology working group on Cardiomyopathy and Cardiac Failure to assess this new classification with respect to the NYHA classification and peak VO2 (Weber's classification). Eight centres participated in the study. A total of 124 patients with chronic cardiac failure and a mean age of 61 years (102 men) were included. Cardiac failure was due to ischaemic heart disease in 72 cases, hypertension in 10 cases, dilated cardiomyopathy in 40 cases and aortic regurgitation in 2 cases. Eighty-two patients underwent a double evaluation using the French Scale: 40 patients by 2 physicians and 42 patients by a physician and a nurse. Good reproducibility was found between the assessment by the 2 physicians in 35 cases (87%) and between the physician and nurse in 30 cases (71%). When compared with peak VO2, the classification was concordant in 47% of cases using the NYHA and in 61% of cases using the French Scale, with variation of one class in 40% of cases with the NYHA and 35% of cases with the French Scale. These results show good reproducibility and correspondence of classification with the exercise test which was better using the French Scale than the NYHA classification.

Identification of a genetic risk factor for idiopathic dilated cardiomyopathy. Involvement of a polymorphism in the endothelin receptor type A gene. CARDIGENE group.

BACKGROUND: Idiopathic dilated cardiomyopathy is a frequent cause of heart failure, a major concern of public health. Although idiopathic dilated cardiomyopathy may be familial, most cases are sporadic and the disease is considered to be multifactorial, for which genetic factors may account for a significant part. METHODS AND RESULTS: We hypothesized that genetic abnormalities of the endothelin pathway may be involved in idiopathic dilated cardiomyopathy pathophysiology and therefore examined the possible association between idiopathic dilated cardiomyopathy and polymorphisms in genes encoding endothelin 1, endothelin type A and type B receptors, in a case-control study (433 patients and 400 age- and sex-matched control subjects). Analysis of the Exon 8 C/T polymorphism in the endothelin receptor type A gene indicated that individuals who are homozygote for the T allele were at significantly increased risk for the disease (odds ratio: 1.9; 95% confidence interval: 1.2 to 3. 01;P<0.006). Analysis of the other polymorphisms indicated that no significant difference was observed in genotype or allele frequencies between cases and controls. CONCLUSIONS: The variant in the Exon 8 of the endothelin receptor type A gene appears as a genetic risk factor for idiopathic forms of heart failure. These results provide a new approach to the pathophysiology of idiopathic dilated cardiomyopathy.

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.