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Coronary effects of Ca 2+ -channel blockers mibefradil and amlodipine were compared in conscious dogs. Ten dogs were instrumented for measurement of aortic and left ventricular pressures, circumflex coronary blood flow velocity (CBFv), and coronary diameter (CD). A permanent catheter was implanted in the circumflex coronary artery. At doses having no systemic effects (7.5-150 μg/kg), mibefradil and amlodipine increased CBFv and CD dose dependently. At the same dose, mibefradil increased less CBFv than amlodipine. However, for a similar increase in CBFv induced by amlodipine, mibefradil increased CD more. BAY K8644, an L-type Ca 2+ -channel agonist, prevented the CBFv and CD responses to amlodipine, but minimally affected the coronary responses to mibefradil. Intracoronary isoproterenol (6 ng/kg) increased LV dP/dt max, CBFv, and CD. Amlodipine markedly altered these responses, while mibefradil did not affect LV inotropic response and slightly altered CBFv response to isoproterenol. Thus, in conscious dogs, both mibefradil and amlodipine exert coronary vasodilation, with different patterns on coronary conductance and resistance vessels and during β-adrenergic stimulation. These differences could be related to their actions on different Ca 2+ channels.

Background: An 80-mg dose once or twice daily is the dose of valsartan frequently administered for treatment of hypertension. The target dose selected for the Val-HeFT trial in patients with chronic heart failure is 160 mg twice daily. The level and time course of angiotensin II type 1 (AT 1 )-receptor blockade achieved by 160 mg valsartan have not been reported. Methods and Results: Seven normotensive healthy subjects were assigned in random order to receive a single dose of placebo, 80 mg valsartan, and 160 mg valsartan at 7- to 10-day intervals. AT 1 -receptor blockade level (%) was determined by the pressure response to administration of exogenous angiotensin II. The pressure response to angiotensin II was measured at baseline and 2, 6, 12, and 24 hours after oral administration of placebo, 80 mg valsartan, and 160 mg valsartan. Eighty and 160 mg valsartan resulted in a significant and similar level of AT 1 -receptor blockade at 2 and 6 hours compared with placebo. The 160-mg dose resulted in a significantly greater level of AT 1 -receptor blockade than 80 mg at 12 and 24 hours. Conclusions: During the first 6 hours after oral administration of 80 and 160 mg valsartan the level of AT 1 -receptor blockade is similar. However, only 160 mg valsartan provides sustained AT 1 -receptor blockade over 24 hours.

OBJECTIVES We sought to determine whether the benefit of training for vasodilation in the skeletal muscle vasculature of patients with chronic heart failure (CHF) is likely to be caused at the molecular level primarily by increased nitric oxide (NO) production or decreased inactivation of NO. BACKGROUND Physical training reverses endothelium dysfunction in patients with CHF, mediated by increased NO bioactivity. Some animal studies support a mechanism whereby training results in increased vascular NO levels by sustained transcriptional activation of the endothelial NO synthase (eNOS) gene, presumably due to shear stress. The mechanism has not been addressed in patients with CHF. METHODS The steady state transcript levels for eNOS and two other shear stress regulated genes (angiotensin-converting enzyme [ACE] and prostacyclin synthase [PGI2S]) were measured in samples of skeletal muscle from patients with CHF before and after 12 weeks of training. Transcript levels were measured in the same samples for two genes encoding antioxidant enzymes, copper zinc superoxide dismutase (Cu/Zn SOD) and glutathione peroxidase (GSH-Px). Untrained patients served as controls. RESULTS As expected, training significantly enhanced peak oxygen uptake in the patients with CHF. Training did not increase steady-state transcript levels for eNOS, ACE or PGI2S. In striking contrast, training increased the expression of the antioxidative enzyme genes by approximately 100%. CONCLUSIONS Our results do not support a model of benefit from training by increased eNOS expression. However, the data are entirely consistent with the alternative hypothesis, that reduced oxidative stress may account for the increase in vascular NO-mediated vasodilation. Insight into the mechanism may be relevant when considering therapies for exercise-intolerant patients with CHF.

Losartan, an angiotensin II type 1 receptor (AT1) antagonist, was developed as a more specific alternative to angiotensin-converting enzyme (ACE) inhibitors. At a daily dose of 50 mg, losartan is currently evaluated in large outcome trials involving patients with hypertension and postmyocardial infarction. The current study evaluated the level and duration of blockade of a pressor response to angiotensin II by 50 and 150 mg of losartan, compared with 32 mg of candesartan. Eight normotensive volunteers were randomly assigned to a single dose of losartan 50 or 150 mg, candesartan 32 mg, or placebo. Subjects were re-randomized after a 2-week washout period to complete all four study arms. Radial artery systolic pressure response to exogenous angiotensin II was measured at 2, 6, 12, and 24 h after administration of drug. Losartan 50 mg reduced the pressure response to exogenous angiotensin II significantly only at 6 h. In contrast, candesartan and losartan 150 mg produced a greater reduction in the pressure response to angiotensin II throughout the 24-h period. This suppression was not paralleled by a reduction in resting systemic arterial pressure. Higher doses than 50 mg of losartan might be evaluated to elicit optimal clinical effects.

Multiple cardiac papillary fibroelastomas (PFEs) are thought to account for less than 10% of patients with PFE. We aimed at evaluating the frequency and location of multiple PFEs and the reliability of transthoracic (TTE) and transoesophageal (TEE) echocardiography in diagnosing multiple PFEs. Twenty-six consecutive patients (52±14 years, 65% males) with pathologically confirmed PFE had 21 PFEs diagnosed by TTE, 33 by TEE, and 62 at surgery. Eight patients (31%) had multiple PFEs found either by TEE or at surgery. Aortic valve was involved in 75% of patients with multiple PFEs and left ventricle in 38% of patients. The sensitivity of TTE in diagnosing any PFEs was 51.3% and 76.9% for TEE. Our study emphasizes the high frequency of multiple PFEs, the need of TEE for all presumed PFE and the need for careful assessment of left-sided endocardial surfaces, especially of the aortic valve, during PFE excision.

Native double-orifice mitral valve is an exceedingly rare valvular abnormality. A 77-year-old patient was referred for a severe mitral regurgitation, and a double-orifice mitral valve with a central fibrous bridge was unexpectedly found. A flail anterior leaflet with 2 ruptured chordae was observed on the anterolateral mitral valve orifice, the leaflets on the posterior valve orifice were normally thin. Mitral valve repair was successfully performed with replacement of the 2 torn chordae by two 4/0 expanded polytetrafluoroethylene neochordae. We accordingly suggest that current mitral valve repair techniques remained a valuable option, even on central bridge double-orifice mitral valve regurgitation.

MOTS CLES Cardiomyopathie hypertrophique ; Echo-doppler A 38-year-old man was admitted to the cardiology emergency department for palpitations. He had been diagnosed 3 years earlier with hypertrophic cardiomyopathy and was receiving chronic treatment with beta-blockers and low-dose aspirin. Physical examination was unremarkable. Electrocardiogram showed right bundle branch block associated with diffuse abnormal ST-segment changes (Fig. 1). Troponin I was increased slightly, at 0.11 ng/mL (normal < 0.05). Transthoracic echocardiographic examination revealed concentric left ventricular hypertrophy with maximal midventricular thickening without significant left ventricular obstruction and a large apical aneurysm (Video 1). Coronary angiography was normal. The left ventricular cine-angiogram showed midcavitary obliteration at end-systole and a large aneurysm (Video 2). Late gadolinium enhancement cardiac magnetic resonance imaging found transmural fibrosis of the apex and confirmed maximal left ventricular wall thickening at the midventricular level (Video 3, Fig. 2). Exercise testing did not produce arrhythmias. Treatment with a vitamin K antagonist was

Background —Vascular remodeling occurs in the skeletal muscle of patients with severe congestive heart failure (CHF); this remodeling is mediated in part by increased activity of the renin-angiotensin system. Animal models suggest that in the vasculature, angiotensin II receptor type 2 (AT2-R) expression may be upregulated in pathological states associated with vascular remodeling. The therapeutic effects of an AT1-R antagonist may, therefore, be in part due to increased plasma angiotensin II levels, which stimulate AT2-R. However, whether AT2-R is expressed in the skeletal muscle vasculature of patients with severe CHF is unknown. Methods and Results —The steady-state transcript levels of the AT1-R and AT2-R genes were analyzed by reverse transcription–polymerase chain reaction in RNA samples prepared from the skeletal muscle of 12 patients with severe CHF (V̇O 2 −1 · min −1 ) and 5 age-matched healthy subjects who underwent vastus lateralis biopsies. Human fetal skeletal muscle RNA served as a positive control for the expression of AT1-R and AT2-R gene transcripts. Transcripts from the AT1-R gene were detected readily in all samples. In contrast, transcripts from the AT2-R gene were only detected in fetal skeletal muscle samples and could not be detected in the skeletal muscle vasculature of healthy subjects or that of CHF patients, who were treated with either angiotensin-converting enzyme inhibitors or AT1-R antagonists. Conclusions —The AT2-R gene is not expressed in the skeletal muscle of patients with CHF. In the absence of detectable AT2-R gene transcripts, the AT2-R pathway is unlikely to contribute to the effects of AT1-R antagonists on the skeletal muscle vasculature in patients with severe CHF.

Abstract —We quantified the repolarization time (so-called QT interval) in a rat, an animal species that does not show a well-characterized T wave on surface ECG. We used spontaneously hypertensive rats (SHR) and converting enzyme inhibition to demonstrate a reversible increase in QT interval in pressure-overloaded hearts in the absence of ischemia. An implanted telemetry system recording ECG data in freely moving rats was used to automatically calculate the RR interval. The QT duration was manually determined by use of a calibrated gauge, and a time-frequency domain analysis was used to evaluate heart rate variability. Left ventricular mass was sequentially assessed by echocardiography. Before treatment, 12-month-old SHR had higher left ventricular mass, QT and RR intervals, and unchanged heart rate variability compared with age-matched Wistar rats. A 2-month converting enzyme inhibition treatment with trandolapril reduces systolic blood pressure, left ventricular mass, and QT interval. The RR interval and heart rate variability remains unchanged. There is a positive correlation between the QT interval and left ventricular mass. The SHR is suitable for longitudinal studies on the QT interval. Thus, the detection of the QT interval reflects the phenotypic changes that occur during mechanical overload and, on the basis of these criteria, allows an in vivo determination of the adaptational process.

The level of inhibition of the angiotensin-converting enzyme (ACE) provided by standard doses of ACE inhibitors may only be partial during long-term treatment in patients with severe chronic heart failure (CHF). Partial ACE inhibition with time is often referred to as escape from ACE inhibition and labeled ACE escape. Several lines of evidence suggest that ACE escape occurs in patients with severe CHF. Plasma levels of angiotensin II rise above initial values during long-term ACE inhibition, and the effects of ACE inhibitors on cardiac remodeling and lowering of sympathetic nervous system activity attenuate after 1 year of treatment. Moreover, angiotensin II type I receptor blockade (ARB) produces clinical and hemodynamic benefits in patients with CHF who are already receiving ACE inhibitors. The therapeutic implications of ACE escape include evaluation of higher- than-standard doses of ACE inhibitors and routine addition of ARB to ACE inhibition in patients with severe CHF. Data are reviewed to demonstrate that ACE escape reflects inadequate ACE dosage rather than a decrease in ACE inhibition occurring with time.

Myocardial infarction occurring with angiographically normal coronary arteries is rare and often described in young people. This report describes a case of myocardial infarction with normal coronary arteries in a young female patient related to coronary thrombosis complicated by left ventricular apical thrombus in the setting of an unknown and subclinical Graves disease. A 23-year-old overweight female patient without history of alcohol, tobacco, recreational drug abuse or inherited cardiovascular risk factors presented with chest pain. On presentation, heart rate was 78 beats per minute and blood pressure 130/65 mm Hg. Diffuse ST segment elevation was found on electrocardiogram (Fig. A). Echocardiography showed apical akinesia filled with thrombus despite normal ejection fraction (video 1). Coronary angiography revealed a distal left anterior descending artery thrombosis with no sign of coronary dissection or atherosclerosis (Fig. B, videos 2, 3). Thromboaspiration was not the chosen option with a TIMI III flow artery and a distal thrombosis. Medical treatment was then decided. Troponin I levels rose to 16.35 ng/mL (normal b0.05 ng/mL) and C-reactive protein to 7 mg/L. Lipid profile was normal. Cardiac magnetic resonance imaging (MRI) showed transmural apical late enhancement related to myocardial infarction (Fig. C) and apical thrombus. There were no clinical or biological signs suggestive of myocarditis, Behcet's disease, lupus erythematosus, antiphospholipid syndrome, Takayasu disease, nor Kawasaki disease. Graves disease was diagnosed on laboratory findings without any clinical sign of hyperthyroidism (thyroid stimulating hormone b0.005 μUI/mL, presence of specific auto-antibodies: anti-thyroid peroxidase, anti-thyroglobulin and anti-thyrotropin binding-inhibitory immunoglobulin). Followup was uneventful while the patient received antiplatelet, warfarin, angiotensin-converting enzyme inhibition and beta blockade therapy in addition to carbimazole. Thrombus disappearance was confirmed on 3-month cardiac MRI (Fig. D). The patient is doing well at 3-year follow-up. Myocardial infarction occurring with angiographically normal coronary arteries is rare and often described in young people [1]. Smoking, cocaine and alcohol abuse have been shown to trigger coronary vasospasm in normal coronary arteries [2]. Prolonged coronary vasospasm itself may in turn induce endothelial damage and platelet aggregation resulting in local thrombosis [3]. Oral contraceptives and inherited thrombophilia are also factors that may promote coronary thrombosis [4]. Hyperthyroidism results in a physiologic state that resembles activation of the sympathetic nervous system. Rare observations have reported an association between hyperthyroidism and myocardial infarction with normal coronary arteries [5]. The complex pathogenesis of coronary thrombosis in patients with hyperthyroidism associates coronary vasospam and hypercoagulable state [6]. Hyperthyroidism was found to be associated with increased plasma factor X activity, increase in plasma concentrations factor VIII, von Willebrand antigen and activity, and decreased tissue plasminogen activator inhibitor-1 activity [7]. Abnormal endothelial NO release and exaggerated vasoconstrictive response have also been demonstrated in the setting of hyperthyroidism [7]. Return to a euthyroid state may result in complete resolution of vascular abnormalities [7]. Lastly, local stasis due to a dysfunctional infarcted myocardium along with endocardial inflammation favors local thrombosis in our patient. In conclusion subclinical hyperthyroidism may be an under recognized etiology of acute myocardial infarction with normal coronary arteries. Supplementary data to this article can be found online at http://dx.

Background and aim: Recent evidence suggests that overweight is not associated with increased risk of premature death in the general population. We assessed 5-year mortality in AMI hospital survivors according to body mass index (BMI) category and waist circumference (WC). Methods: FAST-MI is a French nationwide registry of STEMI and NSTEMI patients included at the end of 2005 in 223 institutions (60% of all institutions taking care of AMI patients). Of 3,670 patients enrolled, 3,463 were discharged alive, of whom 3102 had BMI and 1647 WC recorded. BMI was categorized into 5 groups (

A 46-year-old man who was diagnosed with familial hypertrophic cardiomyopathy (HCM) related to a heterozygote MYBPC3 (cardiac myosin-binding protein-C) gene mutation at the age of 18 was admitted with cardiogenic shock. A progressive decline in functional capacity started 2 years earlier while successive cardiac magnetic resonance (CMR) imaging performed in 2006, 2010, and 2012 showed focal and progressive myocardial fibrosis ( Panel 1 A ). At admission, bedside echocardiography showed severe HCM and biventricular dysfunction. Femoro-femoral extracorporeal life support …

Purpose In the prospective KaRen registry of heart failure with preserved ejection fraction (HFPEF), changes in clinical and biological parameters and medications were assessed between acute presentation and out-patient follow-up in stable state. Methods The KaRen study included patients presenting with acute heart failure (HF) according to inclusion criteria: Framingham criteria for HF, left ventricular ejection fraction > or=45% and brain natriuretic peptide (BNP)>100 pg/mL or NT-proBNP>300 pg/mL. Once stabilized, 4-8 weeks after the index presentation, patients returned as out-patients for repeat assessment. Changes in clinical and biological parameters and medications between inclusion and follow-up were assessed with Students t-test and Chi-square tests Results 577 patients were recruited and 458 returned for the 4-8 weeks visit. 56% were women. The median [25-75pctl] age was 79 [72-84] years. Medical history included 78% hypertension, 58% atrial arrhythmia, 26% type II diabetes and 27% serum creatinin >100 micromol/l. The table provides inclusion and follow-up data Conclusions Patients presenting with HFPEF are elderly and a majority are women, with a high rate of hypertension and atrial arrhythmias. Blood pressure is incompletely controlled. At follow-up, blood pressure and NT-proBNP were reduced, but patients remain symptomatic. Still, efforts are needed to improve symptoms in HFPEF. Table (abstract 85) – Inclusion and follow-up data. Variable Mean (IQR) NYHA I / II / III / IV SBP Creatinine NT-proBNP ACEI /ARB B-blocker ANTICOAG Inclusion 0.8 / 9.4 / 40 / 49.8% 148 [130-170] 93 [74-128] 2433 [1272-4790] 60% 65% 41% Follow-up 13 / 62.5 / 22.2 / 2.3 140 [120-150] 95 [75-129] 1409 [514-2641] 68% 67.5% 51.3% p 0.003

A 54-year-old obese woman with a history of hypertension dialed ambulance service for headache and vomiting. EKG found diffuse ST segment elevation (figure 1A). Prehospital management consisted of intravenous aspirin, oral antiplatelet therapy (prasugrel) and subcutaneous low-molecular-weight heparin. She was transferred in our intensive care unit. Echocardiography showed impaired left ventricular ejection fraction (30%) with apical dysfunction but preserved basal function (figure 1B–D). Coronary angiography showed normal epicardial coronary arteries (figure 1E,F …

We report here two cases of patients admitted in our institution for heart failure. The first had been previously diagnosed with severe aortic valve stenosis and was referred for aortic valve replacement. The myocardial and valvular anatomy combined with the Doppler profiles allowed, however, to suggest the diagnosis of a discrete subaortic membrane that was confirmed by surgical findings. In the second case, the use of real-time three-dimensional transoesophageal echocardiography (3D TEE) provided superb 3D visualization quality of the subaortic membrane and allowed assessing the stenosis area using the multiplanar review mode. Hence, the use of live real-time 3D TEE is likely to be key in the spatial assessment of this complex lesion.

Purpose There is a paucity of data regarding consequences of mitral stenosis (MS) on respiratory function and exercise capacity. In view of frequent discrepancies between symptoms and anatomy in MS, identification of determinants of aerobic capacity could be useful in the clinical-decision making process. Our objective was to evaluate the role of cardiac and pulmonary alterations on aerobic capacity in MS. Methods Twenty-eight patients (53±7 y) with history of MS were prospectively included. A comprehensive echocardiography was performed at rest and during exercise. Right ventricular (RV) systolic function was assessed with tricuspid lateral annulus S wave velocity (STric). Respiratory function was assessed at rest with measure of transfer of carbon monoxide (DLCO). We analyzed the two components of DLCO: membrane diffusion (DM) and capillary volume (VCAP). Maximal oxygen uptake (VO2max) was determined during cardio-pulmonary exercise test. Results Ten patients were examined before (native MS group) and 18 after corrective treatment (treated MS group). The mitral valve functional area (MVA) was 1.3±0.3 cm2 in native MS group and 1.6±0.1 cm2 in treated MS group. Overall, NYHA class was 1.8±0.3, VO2max 18±3 ml/kg/min, maximal workload 85±13 Watts. There were no differences between groups in NYHA class, maximal workload, VO2max, trans-mitral and trans-tricuspid gradients and DLCO. DM and VCAP were impaired in patients with a history of MS. In univariate analysis determinants of VO2max were gender (r=0.6, p=0.001), DM (r=0.65, p=0.04), VCAP (r=0.69, p=0.001), exercise cardiac output (r=0.55, p=0.003), and exercise STric (r=0.56, p=0.008). In multivariate analysis, independent determinants of VO2max were exercice STric (r=0.55, p=0.005) and VCAP (r=0.46, p=0.01). Conclusion DM and VCAP are impaired in MS. RV contractile reserve and VCAP are the main determinants of aerobic capacity in MS. Theses parameters could be used in the clinical-decision making process in MS.

We report here the worsening of functional mitral regurgitation (MR) during dynamic exercise Doppler echocardiography in four female patients with heart failure and preserved ejection fraction. MR worsened concomitantly to an increase in systolic mitral tenting area and in E / E a ratio, whereas local left ventricular (LV) remodelling was not substantially aggravated by exercise. We accordingly suggest that exercise-induced increase in LV filling or left atrial pressure that in turn leads to increase in mitral tenting area worsens functional MR during exercise.

Bioprosthetic valve thrombosis is considered extremely unlikely, thus usually allowing patients to avoid long-term anticoagulation. The authors report the case of a patient with late bioprosthetic mitral valve thrombosis associated with a history of postoperative heparin-induced thrombocytopenia. The patient successfully underwent mitral valve replacement.

Type A acute aortic dissection (AAD) requires prompt diagnosis to initiate life-saving treatment. However, the diagnosis of AAD is clinically challenging in the emergency room or prehospital setting. Pulse oximetry using a finger probe is routinely used to assess …

Contexte Le systeme renine-angiotensine-aldosterone constitue une cible therapeutique majeure dans le traitement de la maladie coronarienne. Des travaux recents suggerent l’interet pronostique de l’aldosterone dans les syndromes coronariens aigus (SCA). Nous avons etudie la valeur pronostique potentielle de l’aldosterone dans une population de coronariens plus large : ceux beneficiant d’une angioplastie coronaire programmee. Methodes De juin 2000 a Septembre 2001, nous avons inclus les patients hospitalises au CHRU de Lille beneficiant d’une angioplastie coronaire non urgente. Des prelevements sanguins etaient realises durant la coronarographie pour dosage de l’aldosterone plasmatique et le suivi etait d’au moins 12 mois, le critere de jugement etant la mortalite cardiovasculaire. Resultats 807 patients ont ete inclus, âges en moyenne de 61 ans, essentiellement des hommes (78 %) fumeurs (71 %) hypertendus (53 %). 32 % etaient diabetiques, la FEVG moyenne etait de 58 ± 15 % et 93 % des patients ont recu une endoprothese. 50 % des patients etaient des coronariens stables. Le taux moyen d’aldosterone etait de 25 (13-5) pg/mL. Les facteurs associes a une augmentation de l’aldosterone etaient l’IMC (p = 0.003), une classe NYHA > 1 (p = 0.0001) et une elevation de la troponine (p = 0.01). Inversement un âge eleve (p = 0.0001), une fonction renale normale (p = 0.01) et la prise de betabloquants (p = 0.01) etaient associes a une diminution de l’aldosterone. Le suivi moyen etait de 14.9 mois et il y a eu 40 deces d’origine cardiovasculaire. Les facteurs predictifs independants de mortalite cardiovasculaire en analyse multivariee etaient un âge eleve (RR = 1.42, p = 0.04), la presence d’un diabete (RR = 2.20, p = 0.04), une fraction d’ejection alteree (RR = 1.58, p = 0.001), la survenue recente d’un SCA (RR = 3.23, p = 0.02), une CRP elevee (RR = 2.59, p = 0.004) et un taux d’aldosterone eleve (RR = 3.48, p = 0.004). Conclusion L’aldosterone plasmatique semble etre un facteur pronostique independant chez les patients beneficiant d’une angioplastie coronaire non urgente et son utilisation permettrait d’ameliorer la stratification du risque cardiovasculaire. Cela pourrait n’etre que le reflet de l’activation generale du systeme neurohormonal mais l’aldosterone induit divers effets extrarenaux (developpement d’une dysfonction endotheliale, d’une fibrose vasculaire et myocardique, effets pro-thrombotiques et proinflammatoires) qui en font un marqueur de risque cardiovasculaire tres seduisant. Download : Download full-size image

Cardiac arrest remains a challenging diagnostic issue when not triggered by a myocardial ischaemia due to coronary artery disease. We report a 41-year-old woman who was admitted to the intensive care …

A 65 year old man was admitted to our hospital for recurrent syncope. Two years before presentation, he had placement of a Le Veen shunt for an intractable ascite complicating liver cirrhosis. On physical examination he appeared well. His blood pressure was 130/80 …

SummaryLeft ejection fraction (LVEF) – resulting from the difference between end-diastolic volume (EDV) and end-systolic volume (ESV), divided by EDV – is a poor index of left ventricular (LV) systolic performance due to its dependency on load conditions, inotropic state and LV remodelling. The characteristic impedance of the ascending aorta (Zc) integrates factors opposing LV ejection during the early ejection period when arterial wave reflection can be neglected. Zc is related to the pressure wave velocity (C) and the cross-sectional area of the aorta. The aim is to demonstrate that LV performance and geometry are closely related to the physical properties of the arterial system. LV pressure-volume loops were obtained from simultaneous measurements of LV (or aortic) pressure and LV volume. The slope Ees (also called LV end-systolic elastance) of the ESP-ESV relationship was assessed. Aortic diameters, pressure and flow measurements were synchronized to evaluate C, aortic forward and backward pressure waves, the elasticity of the aorta (Ep) and thereby Zc. In contrast to LVEF, LV end-systolic elastance (Ees), which reflects the stiffness of the chamber at maximal myofilament activation, is relatively insensitive to load conditions and may be considered as an index of ventricular chamber contractility. For a given Ees value, the end-systolic pressure (ESP) determines the LV end-systolic volume. Ees is determined by cardiac myocytes contractility and density, and thereby concentric remodelling. A tight correlation between Zc and the degree of LV concentric remodelling was found in hypertensive and in normal subjects. Zc was found to increase throughout the full lifespan and also with hypertension. Both Zc and wave reflections determine aortic input impedance estimated from the aortic pressure-flow relationship. Increased arterial stiffness resulted in increasing C and overlap of forward and backward waves and thereby in greater pulse pressure and ESP and a greater difference between ESP and diastolic pressure. Ees is an accurate index of LV systolic performance. Besides the inotropic state of myofibers, Ees depends on the concentric remodelling and thereby on the characteristic impedance of the aorta.

To the Editor: Patients with chronic heart failure (CHF) due to left ventricular (LV) systolic dysfunction develop skeletal muscle alterations that contribute to lower peak aerobic capacity ([1][1]). Patients with type 2 diabetes develop skeletal muscle alterations similar to those of patients with

Background Benfluorex was withdrawn from European markets in June 2010 following reports of an association with heart valve lesions. The link between benfluorex and valve regurgitations was based on small observational studies and retrospective estimations. We therefore designed an echocardiography-based multicenter study to compare the frequency of left heart valve regurgitations in diabetic patients exposed to benfluorex for at least three months and in diabetic controls never exposed to the drug. Methods This reader-blinded controlled study conducted in ten centres in France included prospectively between November 2009 and September 2011 393 consecutive diabetic subjects previously exposed to benfluorex referred by primary care physicians for echocardiography screening and 393 diabetic controls. Using propensity scores, 303 patients and 303 controls were matched for age, gender, body mass index, smoking, dyslipidemia, hypertension, coronary artery disease, and previous use of other drugs associated with valve lesions. The main outcome measure was the frequency of mild or greater left heart valve regurgitations. Findings In the matched sample, the frequency and relative risk (OR) of mild or greater left heart valve regurgitations were significantly increased in benfluorex patients compared to controls: 30·0% vs. 13·5% (OR 2.96[1·94-4·53]) for aortic and/or mitral regurgitation; 21·1% vs. 5·0% (OR 5·63[3·08-10·3]) for aortic regurgitation, and 17·2% vs. 10·2% (OR 1·99[1·22-3·25]) for mitral regurgitation. The frequency of moderate left heart valve regurgitations was also increased among benfluorex patients vs. controls (7·3% vs. 0·7%; OR 13·9[3·21-60·7]. Interpretation Our results indicate that use of benfluorex is associated with significant increase in the frequency of left heart valve regurgitations. The natural history of benfluorex-induced valve abnormalities needs further research. Download : Download full-size image Figure . Left heart regurgitations in patients vs. controls

J Thorac Cardiovasc Surg Pierre-Vladimir Ennezat, Christophe Decoene and Henri Warembourg Georges Fayad, Thomas Modine, Thierry Le Tourneau, Sharif Al-Ruzzeh, ischemic mitral regurgitation Chordal cutting technique through aortotomy: A new approach to treat chronic http://jtcs.ctsnetjournals.org/cgi/content/full/129/5/1173 located on the World Wide Web at: The online version of this article, along with updated information and services, is

The renin-angiotensin-aldosterone system is a major therapeutic target in coronary artery disease (CAD). Recent data suggest that plasma aldosterone has a high prognostic value in acute coronary syndrome (ACS). We tested whether plasma aldosterone could predict clinical outcome in patients undergoing scheduled percutaneous coronary revascularization (PCR). Methods From June 2001 to September 2002, we included all consecutive patients referred to Lille's University Hospital for scheduled PCR. Blood samples were taken during the PCR. The primary endpoint was cardiac death throughout at least 12 months of follow-up. Results 807 patients were included, with a mean age of 61 years. Most were men (78%), smokers (71%). 32% were diabetics, mean LVEF was 58±15% and 93% received stents. 50% had stable angina. The mean plasma aldosterone level was 25(13-45)pg/mL. BMI (p=0.003), NYHA class>1 (p=0.0001) and elevated baseline troponine (p=0.01) were associated with increased aldosterone level. Old age (p=0.0001), normal GFR (p=0.01) and betablockers (p=0.01) were associated with decreased aldosterone level. The mean follow-up was 14.9 months and there were 40 cardiac deaths during this period. In multivariate analysis, old age (HR=1.42, p=0.04), low LVEF (HR=1.58, p=0.001), diabetes mellitus (HR=2.2, p=0.04), a recent history of ACS (HR=3.23, p=0.02), high usCRP (HR=2.59, p=0.004) and high plasma aldosterone (HR=3.48, p=0.004) were independent predictors of cardiac mortality. Conclusion Plasma aldosterone level seems to have an independent prognostic value in patients referred for PCR and could be useful in determining the individual cardiovascular risk. Whether this is the result of direct deleterious effects (promotion of endothelial dysfunction, pro-fibrotic, pro-inflammatory and pro-thrombotic effects) or the marker of a global activation of the neuroendocrine system remains to be determined. However plasma aldosterone appears to be an attractive risk marker in CAD. Download : Download full-size image

La dyspnée inexpliquée est le premier symptôme faisant suspecter une insuffisance cardiaque à fraction d’éjection préservée. L’évaluation des pressions de remplissage du ventricule gauche en échocardiographie reste approximative. Le cathétérisme cardiaque droit est incontournable dans la prise en charge diagnostique et peut être sensibilisé par un test de remplissage afin d’évaluer la réponse du ventricule gauche à la surcharge volumétrique. L’objectif principal de ce travail est d’évaluer si un seuil de pression capillaire pulmonaire moyenne (PCPM) post remplissage supérieure à 20mmHg permettent de prédire la survenue d’évènements cliniques. Il s’agit d’une étude monocentrique rétrospective. Nous avons inclus les patients ayant bénéficié d’un cathétérisme droit avec test de remplissage au CHUG, entre le 1er janvier 2011 et le 30 septembre 2014. Les patients ont été répartis en 2 groupes en fonction de leur PCPM post remplissage. Un suivi téléphonique a été réalisé entre mars et juillet 2015. Le critère principal d’évaluation comprenait la survenue de décès, l’aggravation de la dyspnée et les hospitalisations pour décompensation cardiaque. 57 patients ont été inclus. 17 patients ont présenté un événement. Le nombre d’évènements n’étaient pas significativement supérieur dans le groupe PCPM post-remplissage >20mmHg. En régression linéaire, il n’y avait pas de relation entre une PCPM>20mmHg après remplissage et la survenue d’événements. Le test de remplissage a permis de démasquer une dysfonction diastolique chez 12 patients. Notre étude n’a pas mis en évidence de relation entre une élévation excessive de la PCPM après remplissage et la survenue d’événements.