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Resume Introduction Les liens entre cœur et thyroide sont etroits et les complications cardiaques de la maladie de Basedow sont essentiellement representees par des troubles du rythme supra-ventriculaires ou une insuffisance cardiaque a debit cardiaque augmente, sans veritable atteinte myocardique. Observation Un homme de 40 ans ayant une maladie de Basedow resistante au traitement conventionnel etait hospitalise pour douleur thoracique aigue avec elevation des biomarqueurs cardiaques, le bilan initial excluant une cause coronaire. Le diagnostic de myocardite aigue etait confirme par IRM cardiaque, sans element pour une cause infectieuse. L’hypothese d’une myocardite aigue auto-immune au cours d’une maladie de Basedow active etait retenue. Conclusion La myocardite aigue est une complication exceptionnelle de la maladie de Basedow, dont le mecanisme auto-immun est le plus probable. Ses consequences rythmiques ou hemodynamiques sont parfois fulminantes, justifiant de realiser un bilan cardiologique minimal avant l’introduction d’un traitement beta bloquant.

Interactions between heart and thyroid are strong. Main cardiac complications of Graves' disease are supra-ventricular tachycardia or high output cardiac failure, without real myocardial involvement.A 40-year-old man with history of refractory Graves' disease was hospitalized for an acute chest pain with elevated cardiac biomarkers and normal coronarography. Acute myocarditis was confirmed by cardiac MRI. We found no evidence for an infectious etiology. We retained the hypothesis of acute autoimmune myocarditis in the context of active Graves' disease.Acute myocarditis is an exceptional complication of Graves' disease, with most likely an autoimmune mechanism. Possible occurrence of fulminant rhythmic or hemodynamic complications justify minimal cardiological check-up before introducing beta blockers.

Background: In normal subjects, systolic longitudinal regional velocity profiles (SVP) (measured both based on pulsed or tissue Doppler) have a non-uniform pattern. SVP from the right ventricle (RV), the septal (Sep) and the inferior wall are similar in shape and tend to be monophasic. Their shape differs markedly from the lateral wall (LW), the posterior wall and the anterior wall, which are biphasic. We studied the hypothesis that the double-peaked SVP in the left ventricular free walls are caused by interventricular interaction. This might have additional implication in understanding the measurements of the timing of SVP maxima in pathology as, for example, used to determine intraventricular dyssynchrony in heart failure. Methods: 38 healthy individuals underwent a standard echo examination and a tissue Doppler study. SVP from the RV, Sep and LW basal segments were acquired in an apical four-chamber view. The amplitude and timing of the peak velocities were measured. If a double peak was present, the amplitude and timing of the dip was calculated. Results: RV and Sep had a single systolic velocity peak, while the LW had two peaks with a clear dip between both peaks. The first peak in the LW was the earliest event in the cycle (119 (19) ms) followed by the peak Sep (123 (20) ms; p = 0.34). Peak RV velocity occurred at the same time as the dip in the LW (200 (30) vs 203 (30) ms, respectively; p = 0.53). Conclusion: Our study suggests that the biphasic SVP in the free walls is probably caused by interventricular interaction. Therefore the timing of maxima on SVP should be used with great caution when looking for intraventricular dyssynchrony as the peaks are influenced by RV function.

A 72-year-old female renal transplant recipient was admitted with asthenia and low-grade fever. Two months earlier, she developed nodular pulmonary infiltrates (Figure 1), and microbiological examination of bronchoalveolar lavage fluid established the diagnosis of pulmonary nocardiosis. She had been taking ciprofloxacin and minocycline since that time. Physical examination was unremarkable, and the ECG revealed normal sinus rhythm with atrial bigeminy and no conduction abnormalities (Figure 2). Because of persistent fever, cerebral and thoracoabdominal computed tomography scans were performed and revealed multiple cystic lesions in the brain and mediastinum. Subcutaneous nodular lesions were also seen in the thoracoabdominal wall. Needle aspiration of one of the latter revealed gram-positive bacilli and grew Nocardia farcinica. Figure 1. Chest radiograph performed 2 months before admission, when pulmonary nocardiosis was diagnosed ( A ), showing right superior lobe nodular infiltrate (white arrows), which regressed on the chest radiograph performed on admission ( B ). The cardiothoracic index (black arrows) is increased because of …

Heart failure (HF) is a growing clinical condition resulting from a variety of primary or systemic disorders that impair the ability of the heart to meet systemic demands. Coronary artery disease(CAD), hypertension, and dilated cardiomyopathy (DCM) represent the most common aetiologies in the Western world, with a genetic background found in up to 30% of DCM. Although HF is largely a clinical diagnosis, imaging has become an essential part of patients’ work-up complementing more invasive testing (e.g. coronary angiography, endomyocardial biopsy) and genetic testing. It is key to characterize myocardial and valvular structure and function; identify an underlying treatable substrate; risk-stratify patients; and guide decision-making for medical, surgical, or device therapies such as internal cardioverter-defibrillators (ICD) and cardiac resynchronization therapy (CRT). In addition, it provides measurements for assessing the effect of treatment, including percutaneous or surgical procedures. As the prognosis of HF remains poor, particular emphasis has been placed on detection of early disease in patients at risk and in those with asymptomatic evidence of left ventricular damage as well as screening of relatives. Although echocardiography remains the first imaging step, cardiac magnetic resonance imaging (CMR) is now widely available and appears as an ideal complementary technique with the potential to address in a single 45–60 min scan an exhaustive evaluation of three-dimensional cardiac anatomy, function, tissue characterization, coronary and microvascular perfusion, valve disease, and coronary angiography. The diagnostic and prognostic strengths of CMR as an integral part of the clinical workup of a HF patient are reviewed in a stepwise approach.

Background and objectives Early changes in left atrial function in hypertension are difficult to assess quantitatively. Measuring atrial reversal flow into the pulmonary veins and regional left atrial deformation parameters assessed by Tissue Doppler-derived strain/rate (S/SR) imaging could provide quantitative assessment of left atrial deformation. We aimed to quantify changes in left atrial volume and deformation and pulmonary flow reversal (PV REVERS ) in hypertension to detect subclinical left atrial dysfunction. Design, setting and patients In 74 hypertensive and 34 age-matched normotensive patients (mean age 49 ± 1.4 vs. 44.2 ± 2.1 years) echo studies were performed, including measurements of LAV during reservoir, conduit and pump phases and standard indices reflecting left ventricular filling. S/SR was measured in the lateral left atrial wall. Total deformation (S TOTAL ) and the contribution to early (S E - index ) and late (S A - index ) filling were calculated. Results Hypertensive patients had significantly impaired diastolic function and increased left atrial volume during all phases. Only LAV CONDUIT significantly correlated with both ventricular hypertrophy and parameters of diastolic function. Velocity time integral of PV REVERS correlated with blood pressure and LAV CONDUIT · In hypertensive patients S TOTAL was significantly higher (54.9 ± 2.6 vs. 45.5 ± 2.7%, P

AIMS: Myocardium contracts in the beginning of ejection causing outflow acceleration, resulting in asymmetric outflow velocity profiles peaking around one-third of ejection and declining when force development declines. This article aimed to demonstrate that decreased contractility in coronary artery disease (CAD) changes outflow timing and profile symmetry. ----- METHODS AND RESULTS: Seventy-nine patients undergoing routine full dose dobutamine stress-echo (DSE) were divided into two groups based on resting wall motion and DSE response: DSE negative (DSE(neg)) (35 of 79 patients) and positive (DSE(pos)) (44 of 79 patients) which were compared with 32 healthy volunteers. Aortic CW-Doppler traces at rest were analysed semi-automatically; time-to-peak (T(mod)), ejection-time (ET(mod)), rise-time (t(rise)), and fall-time (t(fall)) were quantified. Asymmetry (asymm) was calculated as the normalized difference of left and right half of the spectrum. Normal curves were triangular, early-peaking, whereas patients showed more rounded shapes and later peaks. T(rise) was longest in DSE(pos). T(fall) was shortest in DSE(pos), followed by controls and DSE(neg). Asymm was lowest in DSE(pos), followed by controls and DSE(neg). Abnormally symmetric profiles (asymm

International audience; AIM: To date, most published echocardiographic methods have assessed left ventricular (LV) dyssynchrony (DYS) alone as a predictor for response to cardiac resynchronization therapy (CRT). We hypothesized that the response is instead dictated by multiple correctable factors. METHODS AND RESULTS: A total of 161 patients (66 +/- 10 years, EF 24 +/- 6%, QRS > 120 ms) were investigated pre- and post-CRT (median of 6 months). Reduction in NYHA Class >/=1 or LV reverse remodelling (end-systolic volume reduction >/= 10%) defined response. Four different pathological mechanisms were identified. Group1: LVDYS characterized by a pre-ejection septal flash (SF) (87 patients, 54%). Elimination of SF (77 of 87 patients) resulted in reverse remodelling in 100%. Group 2: short-AV delay (21 patients, 13%) resolution (19 of 21 patients) resulted in reverse remodelling in 16 of 19. Group 3: long-AV delay (16 patients, 10%) resolution (14 of 16 patients) resulted in NYHA Class reduction >/=1 in 11 with reverse remodelling in five patients. Group 4: exaggerated LV-RV interaction (15 patients, 9%) reduced post-CRT. All responded clinically with fall in pulmonary artery pressure (P = 0.003) but did not volume respond. Group 5: patients with none of the above correctable mechanisms (22 patients, 14%). None responded to CRT. CONCLUSION: CRT response is dictated by correction of multiple independent mechanisms of which LVDYS is only one. Long-axis DYS measurements alone failed to detect 40% of responders.

Cardiac resynchronisation therapy (CRT) is a recognised treatment for symptomatic left ventricular (LV) failure associated with a broad QRS.It has been suggested that >15% myocardial scarring predicted failure to respond to CRT. To determine if the scar burden is a major determinant in response to CRT, we prospectively studied 50 pts (66± 1 years, ischaemic aetiology 57%) undergoing CRT for standard indications at baseline (NYHA: 3±0.4, EF: 23±0.8%, QRS: 150±7 ms, BNP: 495±461 pmol/l) and 6 months post-CRT. Clinical response was defined by a reduction in NYHA class >1 and in BNP level >30%. Reverse LV remodelling was defined as a reduction in end-systolic volume ≥10%. All patients had an echocardiographic examination, including an assessment of dyssynchrony. Additionally, a Cardiac Magnetic Resonance (CMR) study, with delayed enhancement, was performed in patients without contraindications. Of the 30 patients that had CMR, 23 pts (77%) responded clinically to CRT (reduction in NYHA: 1.6±0.6, reduction in BNP: 34±0.4%) and 19/30 (63%) additionally displayed reverse LV remodelling. Among the clinical responders 8 pts (35% of responders) were found to have extensive full thickness myocardial scarring on CMR (in 7 ±1 segments), predominantly in the anteroseptum and apex (86%). Three of these patients also showed significant echocardiographic reverse remodelling. The mechanism of response to CRT in these patients with extensive infarction was more frequently interventricular resynchronisation (43%) or atrio-ventricular resynchronisation (43%) rather than intra-ventricular resynchronisation (14%).The previously suggested 12 segment dyssynchrony index (DI) would have identified none of these responders with extensive myocardial infarction. The DI identified only 7/23 responders (30%). Conclusion : Even patients with extensive myocardial scar are potential responders to CRT and should not be excluded if they fulfil the standard AHA/ESC criteria for biventricular pacing. Intraventricular resynchronisation is not the only mechanism by which patients respond to CRT and measures of intraventricular dyssynchrony alone are inadequate for identifying potential response

Detecting changes in the contractility of the heart muscle, especially in the presence of coronary artery disease, is an important medical task. From isolated myocytes, it was suggested that chronic ischemia decreases but prolongs contraction. Additionally, severe aortic stenosis shows higher but often prolonged outflow velocities. From this, we hypothesize that there is a correlation between the morphology of the aortic outflow velocity profile and myocardial function. To test this hypothesis, we (semi-) automatically analyzed continuous wave Doppler aortic outflow traces from 112 individuals. The traces were segmented and a set of morphology features were extracted. Areas under ROC curve were used as a measure of quality of each feature for detecting changes in cardiac function related to coronary artery disease. Signal analysis has shown that the probabilistic distributions of the various features are different for normal individuals and patients with ongoing disease. This result shows that aortic outflow profiles provide information on cardiac function and that the presented signal analysis and feature extraction method might be used to provide additional diagnostic information in the clinical management of coronary artery disease.

A 79-year-old woman was admitted for progressive asthenia and weight loss over a 3-month period. Her past medical history was remarkable for episodes of recurrent chest pain with unobstructed coronaries and a gastric ulcer with oesophagitis leading to upper gastrointestinal bleeding 5 years earlier. Physical examination and standard …