[Chlamydia infection: An uncommon cause of sexually transmitted myopericarditis]. / Infection à Chlamydia: une cause rare de myopéricardite sexuellement transmissible.

INTRODUCTION: The vast majority of myopericarditis are thought to be caused by viral infection. CASE REPORT: We here report a 46-year-old woman who was admitted twice for clinical presentations compatible with acute coronary syndromes despite normal coronary arteries at angiography. Diagnosis of myopericarditis caused by Chlamydia trachomatis was based on cardiac magnetic resonance and laboratory findings. Treatment with levofloxacin allowed for a full recovery. CONCLUSION: Chlamydia trachomatis infections affect young, sexually active individuals and are responsible for a large proportion of salpingitis, ectopic pregnancy or infertility. Myopericarditis in the setting of chlamydial infection has been seldom reported. Its identification is needed allowing for a specific treatment.

[Heart failure with preserved ejection fraction: a systemic disorder?]. / L'insuffisance cardiaque à fraction d'éjection préservée : une maladie de système ?

When the syndrome of heart failure (HF) is due to left ventricular (LV) systolic dysfunction the clinical manifestations and natural history of the syndrome depend primarily on the severity of LV systolic dysfunction. In contrast, when the syndrome is attributed to LV diastolic dysfunction multiple comorbidities are responsible for the clinical manifestations and the natural history of the syndrome. The present review underscores the multifactorial pathogenesis of the syndrome of HF associated with LV diastolic dysfunction that nowadays is more properly referred to as HF with preserved LV ejection fraction (HFpEF) than to diastolic HF. The prognosis is similarly poor whether HF is due to systolic dysfunction or associated with diastolic dysfunction. The cause of death that is commonly non-cardiovascular in HFpEF supports the pathogenic importance of comorbidities in this condition. Hypertension, chronic kidney disease (CKD), diabetes, obesity and sleep disorder breathing are among the most frequent comorbidities in HFpEF. These comorbidities account for the multiple clinical presentations of the syndrome of HFpEF. Limited functional capacity is in HFpEF largely related to the downward spiral between CKD mediated fluid accumulation and LV stiffness as well as altered ventricular-vascular coupling. The diagnosis of HFpEF currently relies on 2D-Doppler echocardiography findings of impaired LV relaxation and increased LV stiffness and to a lesser extent on biomarkers. Owing to both lack of stringent inclusion and exclusion enrollment criteria and mistaken therapeutic target, placebo-controlled randomized therapeutic trials have been so far negative in HFpEF.

Elevated left atrial pressure estimated by Doppler echocardiography is a key determinant of mitral valve tenting in functional mitral regurgitation.

BACKGROUND: Functional mitral regurgitation (FMR) may occur in patients with reduced or preserved left ventricular ejection fraction (LVEF) and has been associated with excess valvular tenting only in patients with reduced LVEF. This study aimed at identifying the predictors of FMR and to determine whether or not they are different in patients with reduced versus preserved LVEF. METHODS: 190 consecutive patients free of congenital or primary valvular disease had a comprehensive echocardiographic assessment of LV remodelling and function, diastolic function and FMR severity. RESULTS: 112 patients had depressed LVEF (<50%) and 78 had preserved LVEF. FMR was present in 30 patients with preserved LVEF and in 65 with reduced LVEF. Higher E/Ea, E/A and larger mitral tenting were independent predictors of FMR regardless of LVEF. The mitral tenting area was an independent predictor of FMR severity in patients with reduced or preserved LVEF (p = 0.04 and p = 0.0045) in addition to E/A (p = 0.0007), E/Ea (p = 0.004) in patients with reduced and preserved LVEF, respectively. Higher E/Ea was independently associated with larger mitral tenting in patients with reduced and preserved LVEF. Mitral tenting area was linearly related to E/Ea (r = 0.30, p<0.0001) and E/A (r = 0.43, p<0.0001) and LA enlargement (r = 0.54, p<0.0001) after having paired 96 patients with and without FMR on indices of LV remodelling. CONCLUSIONS: In both patients with preserved and reduced LVEF, mitral tenting that leads to FMR is mainly determined by both mitral tethering forces-that is, displacement of papillary muscles and by pushing forces-that is, increased left atrial pressure. This study underscores that LV preload is a key determinant of FMR.

Exercise testing and exercise stress echocardiography in asymptomatic aortic valve stenosis.

Management of asymptomatic patients with severe aortic valve stenosis (AVS) remains a source of debate. Exercise testing is no longer contraindicated and needs now to be considered when evaluating asymptomatic patients with AVS. Several studies have clearly demonstrated that exercise-elicited symptoms during conventional upright exercise portends clinical events. Semi-supine exercise with continuous Doppler echocardiography monitoring elicits cardiovascular abnormalities that are not detected at rest. Abnormal left ventricular response to exercise and/or major increase in mean transvalvular gradient add to the prognostic value of elicited symptoms in asymptomatic patients with severe AVS. However, preliminary experience needs to be confirmed to warrant routine use of exercise Doppler echocardiography in the evaluation of patients with asymptomatic AVS.

[Pulmonary embolism and right diaphragmatic paralysis: "one train can hide another"]. / Embolie pulmonaire et paralysie diaphragmatique droite "un train peut en cacher un autre".

The authors report the case of an 84 year old woman admitted for a mild pulmonary embolism associated with severe hypoxaemia. The association of a right diaphragmatic paralysis with renewed patency of a foramenovale and creation of a right-to-left shunt is probably an underestimated cause of refractory hypoxaemia.

[Myocardial infarction with normal coronary arteries: role of transesophageal echocardiography]. / Infarctus du myocarde à artères coronaires saines: place de l'échographie cardiaque transcesophagienne.

We report the case of 74 years-old female patient hospitalized for a ST+ acute coronary syndrome with normal coronary angiography. The association of a patent foramen ovale, a deep venous thrombosis and a pulmonary embolism led us to conclude the diagnosis of paradoxical coronary embolism. This case allows us to remind different etiologies to be considered in case of myocardial infarction with normal coronary arteries, and the interest of transesophageal echocardiography for the diagnosis of its etiology.

[Heparin-induced thrombocytopenia: a case of persistent thrombocytopenia]. / Thrombopénie induite à l'héparine: à propos d'une thtombopénine persistante.

Heparin-induced thrombocytopenia is rare. It should be considered if there is a reduction of at least 40% in the number of platelets and/or a level<100,000/mm3 in any patients who have received heparin in the previous 100 days. On stopping heparin, the rise in platelets is classically rapid, and normal levels are usually obtained in under 7 days. We report a case of heparin-induced thrombocytopenia, which was marked by a severe thrombocytopenia that only returned to normal 19 days after stopping heparin, in a patient treated initially with non-fractionated heparin for a pulmonary embolism secondary to an extensive deep venous thrombosis of the right lower limb.

Functional mitral regurgitation and chronic heart failure.

Functional mitral regurgitation (MR) frequently develops during the progression of chronic heart failure and predicts poor outcome. Impaired left ventricular (LV) function, LV remodeling associated with papillary muscle apical displacement and annular enlargement result in decreased mitral closing forces and tenting of the mitral valve at closure. Reduced closing forces and tenting both promote MR. Active myocardial ischemia, myocardial asynchronism and excessive loading conditions worsen MR at rest and during exercise. The therapeutic target in functional MR is the left ventricle and not the valve.

[Tako-tsubo syndrome and left ventricular obstruction: report of one case]. / Syndrome de tako-tsubo et obstruction intraventriculaire gauche: mécanisme de pérennisation? A propos d'un cas.

We report here the case of an 80 year old female suffering from Tako-tsubo syndrome diagnosed following type B aortic dissection, treated surgically with an aortic endoprosthesis. The recovery was marked by the secondary development of left intraventricular obstruction. Regression of the electrical and ultrasound anomalies was slow, taking 4 months of treatment with a beta-blocker. The intraventricular obstruction seemed to occupy a central role in this case, and we discuss the significance of this mechanical phenomenon in the pathophysiology of this syndrome.

Cardiac resynchronisation therapy reduces functional mitral regurgitation during dynamic exercise in patients with chronic heart failure: an acute echocardiographic study.

OBJECTIVES: To assess non-invasively the acute effects of cardiac resynchronisation therapy (CRT) on functional mitral regurgitation (MR) at rest and during dynamic exercise. METHODS: 21 patients with left ventricular (LV) systolic dysfunction and functional MR at rest, treated with CRT, were studied. Each patient performed a symptom-limited maximal exercise with continuous two dimensional Doppler echocardiography twice. The first exercise was performed with CRT; the second exercise was performed without CRT. Mitral regurgitant flow volume (RV), effective regurgitant orifice area (ERO) and LV dP/dt were measured at rest and at peak exercise. RESULTS: CRT mildly reduced resting mitral ERO (mean 8 (SEM 2) v 11 (2) mm(2) without CRT, p = 0.02) and RV (13 (3) v 18 (3) ml without CRT, p = 0.03). CRT attenuated the spontaneous increase in mitral ERO and RV during exercise (1 (1) v 9 (2) mm(2), p = 0.004 and 1 (1) v 8 (2) ml, p = 0.004, respectively). CRT also significantly increased exercise-induced changes in LV dP/dt (140 (46) v 479 (112) mm Hg/s, p < 0.001). CONCLUSION: Attenuation of functional MR, induced by an increase in LV contractility during dynamic exercise, may contribute to the beneficial clinical outcome of CRT in patients with chronic heart failure and LV asynchrony.

Tissue Doppler echocardiography in patients with long QT syndrome.

BACKGROUND: Congenital long QT syndrome (LQTS) is a well-defined clinical entity associated with a high mortality among untreated patients. Tissue Doppler (TD) echocardiography that has been recently introduced, facilitates wall motion analysis. Therefore, to further characterize myocardial velocity abnormalities associated with LQTS, using TD and conventional echocardiography, we compared control subjects and LQTS patients. METHODS AND RESULTS: Ten patients with mild LQTS and 14 control subjects were examined with standard and TD echocardiography. We studied myocardial velocities in basal and mid-segments of the septal, lateral, inferior and anterior walls. Peak velocity and time intervals were measured in each segment. We confirmed previously described M-mode abnormalities, demonstrated by an increase of the wall thickening time index. TD analysis demonstrated increased systolic and diastolic peak velocities for all segments in LQTS patients. Regional isovolumic relaxation time and systolic velocity half time (VHT) were significantly longer in LQTS group associated with a prolonged late systolic phase, resulting in a plateau morphology. CONCLUSION: We demonstrated that TD allows the characterization of myocardial velocity abnormalities in LQTS patients. TD measurements could become part of the routine clinical evaluation for patients potentially affected by the LQTS as a new phenotypic marker.

Angiotensin II type 1 receptor blockade with 80 and 160 mg valsartan in healthy, normotensive subjects.

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.

Physical training in patients with chronic heart failure enhances the expression of genes encoding antioxidative enzymes.

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.

Dose-dependent blockade of the angiotensin II type 1 receptor with losartan in normal volunteers.

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.