Cardiac dyspnea risk zones in the South of France identified by geo-pollution trends study.

The incidence of cardiac dyspnea (CD) and the distribution of pollution in the south of France suggests that environmental pollution may have a role in disease triggering. CD is a hallmark symptom of heart failure leading to reduced ability to function and engage in activities of daily living. To show the impact of short-term pollution exposure on the increment of CD emergency room visits, we collected pollutants and climate measurements on a daily basis and 43,400 events of CD in the Région Sud from 2013 to 2018. We used a distributed lag non-linear model (DLNM) to assess the association between air pollution and CD events. We divided the region in 357 zones to reconciliate environmental and emergency room visits data. We applied the DLNM on the entire region, on zones grouped by pollution trends and on singular zones. Each pollutant has a significant effect on triggering CD. Depending on the pollutant, we identified four shapes of exposure curves to describe the impact of pollution on CD events: early and late effect for NO2; U-shape and rainbow-shape (or inverted U) for O3; all the four shapes for PM10. In the biggest cities, O3 has the most significant association along with the PM10. In the west side, a delayed effect triggered by PM10 was found. Zones along the main highway are mostly affected by NO2 pollution with an increase of the association for a period up to 9 days after the pollution peak. Our results can be used by local authorities to set up specific prevention policies, public alerts that adapt to the different zones and support public health prediction-making. We developed a user-friendly web application called Health, Environment in PACA Region Tool (HEART) to collect our results. HEART will allow citizens, researchers and local authorities to monitor the impact of pollution trends on local public health.

Cardiac remodelling amongst adults with various aetiologies of pulmonary arterial hypertension including Eisenmenger syndrome-implications on survival and the role of right ventricular transverse strain.

AIMS: Survival in pulmonary arterial hypertension (PAH) and Eisenmenger syndrome (ES) relates to right ventricular (RV) function. Little is known about differences of ventricular function between ES patients and those suffering from other PAH aetiologies. In this study, we compared global ventricular function assessed by speckle-tracking in adult patients with ES, other PAH aetiologies, or healthy controls; and assessed the relationship between ventricular function and survival. METHODS AND RESULTS: We performed a prospective cohort study recruiting 83 adult PAH patients (43 ES and 40 other PAH aetiologies patients) and 37 controls between March 2011 and June 2015. Patients with complex congenital heart disease were excluded. Fifty-three patients (63.9%) were in NYHA functional class ≥III at baseline and 60 (72.3%) were on advanced therapies. Mean RV peak longitudinal strain was -16.3 ± 7% in ES, lower compared with healthy controls (P < 0.001) but similar to other PAH aetiologies (P = 0.6). Mean RV peak transverse strain was +26.1 ± 17% in ES, lower than in controls (P < 0.001) but higher than in other PAH aetiologies (P < 0.001). No difference was observed between ES and other PAH in LV circumferential and longitudinal strain. Over a median follow-up of 22.6 months (3.3-32.2), 22 (26.5%) patients died all from cardio-pulmonary causes. ES and RV peak transverse strain were independent predictors of survival. RV peak transverse strain ≤22% identified patients with a 14-fold increased risk of death. CONCLUSION: Right ventricular remodelling differs between adults with ES and other PAH aetiologies. ES and increased RV free wall transverse strain are associated with better survival.

Early detection of cardiac involvement in sarcoidosis with 2-dimensional speckle-tracking echocardiography.

BACKGROUND/OBJECTIVES: Cardiac sarcoidosis (CS) is associated with high morbidity and sudden death. The absence of specific symptoms and lack of diagnostic gold standard technique is challenging. New imaging methods could improve the diagnosis of CS. The aim of our study was to assess the role of left ventricular (LV) longitudinal and circumferential strain as estimated by 2D speckle-tracking imaging in patients with diagnosed sarcoidosis without cardiac involvement according to the current guidelines. We investigated the prevalence of LV strain impairment in this population and assessed its relationship with clinical outcomes, composite of mortality, heart failure, arrhythmia and/or secondarily development of CS and cardiac device implantation. METHODS AND RESULTS: We performed a prospective case-control longitudinal study including 35 patients with diagnosed sarcoidosis and normal cardiac function as assessed by standard transthoracic echocardiography and 35 healthy age- and gender-matched controls. All patients underwent a comprehensive echocardiographic study. Mean age of patients was 47.9±14.8years old (22 women). Compared with controls, global LV longitudinal strain (LV GLS) was reduced in sarcoidosis patients: (-17.2±3.1 vs -21.3±1.5%, p<0.0001). Circumferential LV strain was preserved in patients compared to controls (-19.9±-4.3% vs -21.3±1.5%, p=0.12). Impaired LV GLS was significantly associated with clinical outcomes (HR 1.56; [1.16-2.11], p<0.01) on univariate analysis. CONCLUSION: Speckle-tracking echocardiography revealed decreased longitudinal LV strain in sarcoidosis patients that was associated with outcomes. LV GLS may represent an early marker of myocardial involvement in sarcoidosis patients that needs to be studied further.

Speckle-tracking imaging in patients with Eisenmenger syndrome.

BACKGROUND: Adults with Eisenmenger syndrome have a survival advantage over those with idiopathic pulmonary arterial hypertension. Improved survival may result from preservation of right ventricular (RV) function. AIMS: To assess left ventricular (LV) and RV remodelling in patients with Eisenmenger syndrome compared to a control population, using speckle-tracking imaging. METHODS: Adults with Eisenmenger syndrome and healthy controls were enrolled into this prospective two-centre study. Patients with Eisenmenger syndrome with low acoustic windows, irregular heart rhythm or complex congenital heart disease were excluded. Clinical assessment, B-type natriuretic peptide (BNP), 6-minute walk test and echocardiography (including dedicated views to perform offline two-dimensional-speckle-tracking analysis) were performed on inclusion. RESULTS: Our patient population (n=37; mean age 42.3 ± 17 years) was mostly composed of patients with ventricular septal defect (37.8%) or atrial septal defect (35.1%). Compared with the control population (n=30), patients with Eisenmenger syndrome had reduced global LV longitudinal strain (-17.4 ± 3.5 vs. -22.4 ± 2.3; P<0.001), RV free-wall longitudinal strain (-15.0 ± 4.7 vs. -29.9 ± 6.8; P<0.001) and RV transverse strain (25.8 ± 25.0 vs. 44.5 ± 15.1; P<0.001). Patients with Eisenmenger syndrome also more frequently presented a predominant apical longitudinal and transverse strain profile. Among patients with Eisenmenger syndrome, those with a post-tricuspid shunt presented with reduced global LV longitudinal strain but increased RV transverse strain, compared to patients with pre-tricuspid shunt. CONCLUSION: Patients with Eisenmenger syndrome had impaired longitudinal RV and LV strain, but present a relatively important apical deformation. RV and LV remodelling, as assessed by speckle-tracking imaging, differ between patients with pre- and post-tricuspid shunt.

[Do weather and seasons influence our heart?]. / Météo et saisons influencent-elles notre cœur?

There are numerous publications about impact of meteo, seasons and pollution on cardiovascular diseases. Cardiovascular diseases, in particular myocardial infarction and heart failure, have been consistently more frequent during winter in the northern and southern hemisphere. Chronic exposure to air pollution influences the development of atherosclerosis and increases the risk for coronary artery disease. There is a positive association between short-term increase in gaseous components with the risk of hospitalization or death from congestive heart failure. The considerable impact on health care service warrants a comprehensive approach to cardiovascular disease management.

B blood group: A strong risk factor for venous thromboembolism recurrence.

BACKGROUND: Non-O blood group patients are at higher risk of first episode of venous thromboembolism (VTE). However, only little is known about the risk of recurrence according to the blood group. In this study, we aimed to determine the impact of ABO blood group on VTE recurrence. METHODS: We prospectively recruited 106 consecutive patients with a first documented episode of pulmonary embolism (PE). Patients were followed at least 12months after anticoagulation discontinuation. The main endpoint was recurrence of symptomatic VTE. RESULTS: Data from 100 patients were analyzed. Median follow-up was 28months [24-34.8]. PE was unprovoked in 48 patients. Mean anticoagulation duration was 5.3±2.2months. The rate of VTE recurrence was 12.7 per 100 patient-years (30 recurrences). B blood group patients had a 2.7-fold increased risk of VTE recurrence (95%CI 1.1-6.2, p=0.03). On multivariate analysis, B blood group was the strongest independent predictor of VTE recurrence (Hazard Ratio (HR) 2.6, 95%CI 1.1-6.1, p=0.04). In contrast, A and AB blood groups were not associated with VTE recurrence. VTE recurrences were less frequent in O blood group compared to non-O patients (HR 0.5, 95%CI 0.2-1.1, p=0.09). O blood group women had a 5-fold decreased risk of VTE recurrence (HR 0.2, 95%CI 0.1-0.8, p=0.01). CONCLUSIONS: Non-O blood groups, beyond being involved in the occurrence of a first VTE event, also contribute to VTE recurrence. B blood group is strongly associated with VTE recurrence, thus high-risk B blood group patients could benefit from long-term anticoagulation therapy after a first VTE event.

The So-Called 'Eclipsed' Mitral Regurgitation.

An 89-year-old female was referred to the authors' institution for repeating pulmonary edema. Recent transthoracic echocardiography (TTE) showed only a mild mitral regurgitation (MR), but a transient severe reversible functional MR was observed during an episode of respiratory distress. TTE demonstrated the functional nature of the regurgitation with a transient tenting of the mitral leaflets, resulting in a total absence of coaptation.

Real time three-dimensional echocardiographic assessment of left ventricular function in heart failure patients: underestimation of left ventricular volume increases with the degree of dilatation.

BACKGROUND: Accurate quantification of left ventricular (LV) volumes and ejection fraction (EF) is of critical importance. Cardiac magnetic resonance (CMR) is considered as the reference and three-dimensional echocardiography (3DE) is an accurate method, but only few data are available in heart failure patients. We therefore sought to compare the accuracy of real time three-dimensional echocardiography (RT3DE) and two-dimensional echocardiography (2DE) for quantification of LV volumes and EF, relative to CMR imaging in an unselected population of heart failure patients. METHODS AND RESULTS: We studied 24 patients (17 men, age 58 ± 15 years) with history of heart failure who underwent echocardiographic assessment of LV function (2DE, RT3DE) and CMR within a period of 24 hours. Mean LV end-diastolic volume (LVEDV) was 208 ± 109 mL (121 ± 64 mL/m(2) ) and mean LVEF was 31 ± 12.8%. 3DE data sets correlate well with CMR, particularly with respect to the EF (r: 0.8, 0.86, and 0.95; P < 0.0001 for LVEDV, LVESV, and EF, respectively) with small biases (-55 mL, -44 mL, 1.1%) and acceptable limits of agreement. RT3DE provides more accurate measurements of LVEF than 2DE (z= 2.1, P = 0.037) and lower variability. However, 3DE-derived LV volumes are significantly underestimated in patients with severe LV dilatation. In patients with LVEDV below 120 mL/m(2) , RT3DE is more accurate for volumes and EF evaluation. CONCLUSION: Compared with CMR, RT3DE is accurate for evaluation of EF and feasible in all our heart failure patients, at the expense of a significant underestimation of LV volumes, particularly when LVEDV is above 120 mL/m(2) .

Insuficiencia cardiaca en el infarto agudo de miocardio: comparación de pacientes con o sin criterios de insuficiencia cardiaca del registro FAST-MI / Heart failure in acute myocardial infarction: a comparison between patients with or without heart failure criteria from the FAST-MI registry

Introducción y objetivos. El papel las lipoproteínas de alta densidad en la estratificación de riesgo en pacientes con dolor torácico no está bien definido. El objetivo de este estudio es conocer la contribución relativa del perfil lipídico al riesgo de padecer síndrome coronario agudo de los pacientes ingresados por dolor torácico en una planta de cardiología. Métodos. Incluimos todos los ingresos consecutivos no programados en planta de cardiología durante 15 meses y realizamos seguimiento al año. Resultados. Se incluyó a 959 pacientes, 457 (47,7%) diagnosticados de dolor torácico no isquémico, 355 (37%) de síndrome coronario agudo sin elevación del ST y 147 (15,3%) de síndrome coronario agudo con elevación del ST. El 54,6% de los pacientes presentaron cifras de lipoproteínas de alta densidad < 40mg/dl y la prevalencia fue más elevada entre los pacientes con síndrome coronario agudo (el 69,4 frente al 30,6%; p<0,01). Se observó mayor presencia de síndrome coronario agudo a menores cifras medias de lipoproteínas de alta densidad. Edad, tabaquismo activo, diabetes mellitus, glucemia basal > 100mg/dl y concentraciones de lipoproteínas de alta densidad < 40mg/dl se asociaron independientemente a la presencia de síndrome coronario agudo, el factor con mayor asociación (odds ratio=4,11; intervalo de confianza del 95%, 2,87-5,96). El análisis de supervivencia determinó que los pacientes con síndrome coronario agudo, frente a dolor torácico no isquémico, asociaron un riesgo significativamente superior de mortalidad por cualquier causa, así como por causa cardiovascular. Conclusiones. Las concentraciones bajas de colesterol unido a las lipoproteínas de alta densidad (≤ 40mg/dl) se asociaron de manera independiente a diagnóstico de síndrome coronario agudo en pacientes ingresados por dolor torácico, con una relación inversa significativa entre los valores más bajos de lipoproteínas de alta densidad y el diagnóstico de síndrome coronario agudo (AU)

Introduction and objectives. To compare acute myocardial infarction patients with or without congestive heart failure in the French FAST-MI registry. Methods. The French FAST-MI registry included 374 centers and 3059 patients over a 1-month period at the end of 2005, with 1-year follow-up. Among this population, patients with at least one congestive heart failure criterion constituted group 1 (n=1149; 37.5%) and were compared to patients without congestive heart failure (group 2, n=1910; 62.5%). The congestive heart failure patients were further divided according to presence of both beta-blockers and antagonists of the renin-angiotensin-aldosterone system at hospital discharge (n=511) or not (n=498), in order to assess the real-world clinical importance of recommended medications. Results. Overall in-hospital and 1-year mortality rates were 3.4% and 13.2%, respectively. In hospital survivors, presence of congestive heart failure was associated with increased mortality (adjusted hazard ratio=1.55; 95% confidence interval, 1.10-2.17; P=.01). Survival was higher in patients without congestive heart failure, compared with congestive heart failure patients receiving or not recommended medications (P<.001). Congestive heart failure patients receiving neither renin-angiotensin-aldosterone system blockers nor beta-blockers (adjusted hazard ratio=1.66; 95% confidence interval, 1.08-2.55; P=.02) had a significantly higher risk of death than patients receiving both classes of medications (adjusted hazard ratio=1.16; 95% confidence interval, 0.82-1.64; not statistically significant). Patients receiving only one of the recommended classes had an intermediate risk (adjusted hazard ratio=1.47; 95% confidence interval, 1.04-2.07; P=.03). Conclusions. Patients admitted for acute myocardial infarction with congestive heart failure criteria are still at very high risk of mortality. When receiving major recommended medications, they presented with significantly reduced mortality rates. Additional efforts should therefore be made to encourage the prescription of recommended medications in acute myocardial infarction patients with congestive heart failure (AU)

Heart failure in acute myocardial infarction: a comparison between patients with or without heart failure criteria from the FAST-MI registry.

INTRODUCTION AND OBJECTIVES: To compare acute myocardial infarction patients with or without congestive heart failure in the French FAST-MI registry. METHODS: The French FAST-MI registry included 374 centers and 3059 patients over a 1-month period at the end of 2005, with 1-year follow-up. Among this population, patients with at least one congestive heart failure criterion constituted group 1 (n=1149; 37.5%) and were compared to patients without congestive heart failure (group 2, n=1910; 62.5%). The congestive heart failure patients were further divided according to presence of both beta-blockers and antagonists of the renin-angiotensin-aldosterone system at hospital discharge (n=511) or not (n=498), in order to assess the real-world clinical importance of recommended medications. RESULTS: Overall in-hospital and 1-year mortality rates were 3.4% and 13.2%, respectively. In hospital survivors, presence of congestive heart failure was associated with increased mortality (adjusted hazard ratio: 1.55; 95% confidence interval, 1.10-2.17; P=.01). Survival was higher in patients without congestive heart failure, compared with congestive heart failure patients receiving or not recommended medications (P<.001). Congestive heart failure patients receiving neither renin-angiotensin-aldosterone system blockers nor beta-blockers (adjusted hazard ratio: 1.66; 95% confidence interval, 1.08-2.55; P=.02) had a significantly higher risk of death than patients receiving both classes of medications (adjusted hazard ratio: 1.16; 95% confidence interval, 0.82-1.64; not statistically significant). Patients receiving only one of the recommended classes had an intermediate risk (adjusted hazard ratio: 1.47; 95% confidence interval, 1.04-2.07; P=.03). CONCLUSIONS: Patients admitted for acute myocardial infarction with congestive heart failure criteria are still at very high risk of mortality. When receiving major recommended medications, they presented with significantly reduced mortality rates. Additional efforts should therefore be made to encourage the prescription of recommended medications in acute myocardial infarction patients with congestive heart failure.

A genome-wide association study identifies two loci associated with heart failure due to dilated cardiomyopathy.

AIMS: Dilated cardiomyopathy (DCM) is a major cause of heart failure with a high familial recurrence risk. So far, the genetics of DCM remains largely unresolved. We conducted the first genome-wide association study (GWAS) to identify loci contributing to sporadic DCM. METHODS AND RESULTS: One thousand one hundred and seventy-nine DCM patients and 1108 controls contributed to the discovery phase. Pools of DNA stratified on disease status, population, age, and gender were constituted and used for testing association of DCM with 517 382 single nucleotide polymorphisms (SNPs). Three DCM-associated SNPs were confirmed by individual genotyping (P < 5.0 10(-7)), and two of them, rs10927875 and rs2234962, were replicated in independent samples (1165 DCM patients and 1302 controls), with P-values of 0.002 and 0.009, respectively. rs10927875 maps to a region on chromosome 1p36.13 which encompasses several genes among which HSPB7 has been formerly suggested to be implicated in DCM. The second identified locus involves rs2234962, a non-synonymous SNP (c.T757C, p. C151R) located within the sequence of BAG3 on chromosome 10q26. To assess whether coding mutations of BAG3 might cause monogenic forms of the disease, we sequenced BAG3 exons in 168 independent index cases diagnosed with familial DCM and identified four truncating and two missense mutations. Each mutation was heterozygous, present in all genotyped relatives affected by the disease and absent in a control group of 347 healthy individuals, strongly suggesting that these mutations are causing the disease. CONCLUSION: This GWAS identified two loci involved in sporadic DCM, one of them probably implicates BAG3. Our results show that rare mutations in BAG3 contribute to monogenic forms of the disease, while common variant(s) in the same gene are implicated in sporadic DCM.

[Drug treatment for hypertrophic cardiomyopathy]. / Traitements médicamenteux de la cardiomyopathie hypertrophique.

Drug treatment of hypertrophic cardiomyopathy is the first-line treatment, at the onset of clinical signs and symptoms. Beta-blockers are proposed for symptomatic patients with no gradient or with a gradient that appears only on exertion. Verapamil is the standard second-line drug,when the beta-blockers are insufficient or ineffective but must be avoided when there is blockage at rest with severe symptoms. Disopyramide is indicated for patients with obstruction who do not respond to beta blockers and/or verapamil. Treatment with anticoagulants is widely prescribed because this disease is highly emboligenic.

Prognostic value of homocysteinemia in patients with congestive heart failure.

BACKGROUND: Elevated plasma homocysteine levels are associated with increased risk of vascular disease and of congestive heart failure (CHF), with a relationship between homocysteine values and disease severity. Hyperhomocysteinemia is a risk factor for cardiac dysfunction. In this study, the predictive value of elevated homocysteine levels was investigated in the prognosis of ischemic and non-ischemic CHF. METHODS: A total of 159 patients with CHF, 89 with non-ischemic and 70 with ischemic CHF (83% males, mean age 62 years, mean ejection fraction 27%), and 119 controls (79% males, mean age 59.8 years) had fasting blood samples taken to measure plasma homocysteine, vitamin B(12) and folate levels. Coronary angiography was performed for all patients. The mean duration of follow-up was 49.6+/-36.7 months. RESULTS: As in other studies, the mean level of homocysteinemia was significantly higher in the CHF group (15.80 micromol/L) than in the control group (10.90 micromol/L) (p=0.001) whatever the etiology (non-ischemic, 16.11+/-6.84 micromol/L; ischemic, 15.41+/-6.45 micromol/L). This result was observed without vitamin deficiency, but in patients, the mean creatinine value was moderately higher than in controls. We found a positive correlation between plasma homocysteine levels and New York Heart Association (NYHA) classification, creatinine and age. Moreover, hyperhomocysteinemia appears to be a powerful predictive factor of mortality in CHF patients (relative risk of death, 4.23; p=0.0003). In the follow-up of this study, 41.5% of patients with homocysteinemia >17 micromol/L died vs. 21.3% of patients with levels <17 micromol/L. In multivariate analysis, when homocysteine levels were adjusted for a second parameter (age, NYHA, creatinine, diabetes), the risk of death remained significant after each adjustment. CONCLUSIONS: Elevated homocysteine levels observed in CHF patients, whatever the etiology of their heart disease (ischemic or non-ischemic), were correlated with the severity of the disease. Hyperhomocysteinemia appears to be a predictive factor of mortality in CHF patients.

Association of MTRRA66G polymorphism (but not of MTHFR C677T and A1298C, MTRA2756G, TCN C776G) with homocysteine and coronary artery disease in the French population.

Methylenetetrahydrofolate reductase polymorphism (MTHFR C677T) is an established determinant of homocysteine plasma level (t-Hcys) while its association with coronary artery disease (CAD) seems to be more limited. In contrast, the association of the substitutions A2756G of methionine synthase (MTR), A66G of methionine synthase reductase (MTRR) and C776G of transcobalamin (TCN) to both t-Hcys and CAD needs to be evaluated further. The objective was to evaluate the association of these polymorphisms with t-Hcys and CAD in a French population. We investigated the individual and combined effects of these polymorphisms and of vitamin B12 and folates with t-Hcys in 530 CAD patients and 248 matched healthy controls. t-Hcys was higher in the CAD group than in controls (11.8 vs 10.4 microM, P < 0.0001) and in carriers of MTRRAA and MTHFR 677TT than in those carrying the most frequent allele of both polymorphisms (13.8 vs 11.4 microM, P = 0.0102 and 12.5 vs 11.0 mM, P = 0.0065 respectively). The frequency of MTRR A allele was higher in CAD patients than in controls (0.48 [95% CI: 0.44-0.52] vs 0.38 [95% CI: 0.32-0.44], P = 0.0081) while no difference was observed for MTHFR 677T frequency. In multivariate analysis, t-Hcys > median and MTRRAA genotype were two significant independent predictors of CAD with respective odds ratios of 3.1 (95 % CI: 1.8-5.1, P < 0.0001) and 4.5 (95% CI: 1.5-13.1, P = 0.0051). In conclusion, in contrast to North Europe studies, MTRRAA genotype is a genetic determinant of moderate hyperhomocysteinemia associated with CAD in a French population without vitamin fortification.

[Acute cardiogenic pulmonary edema and its treatment]. / Oedème aigu pulmonaire cardiogénique et son traitement.

Acute cardiogenic pulmonary oedema is a medical emergency. Most episodes occur in the morning or at night. Pulmonary oedema occurs more frequently in the colder months. It generally results from an acute left ventricular insufficiency, itself resulting from systolic or diastolic dysfunction, myocardial infarction is the main etiology. Clinical presentation may be atypical. Treatment is based on oxygen, diuretics and nitrates. In severe cases, mechanical ventilation may be necessary.