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To examine the ability of myocardial contractile reserve (MCR) assessment to predict the improvement of left ventricular ejection fraction with treatment by carvedilol, a prospective study was undertaken in 85 patients with chronic heart failure and left ventricular ejection fraction

Objective: A relative hyperadrenergic tone related to abnormalities of the autonomic nervous system is suspected in the mechanisms of sudden death. Therefore, we assessed the role of an elevated basal heart rate in the occurrence of sudden death in a long-term cohort study. Methods: 7746 subjects aged 42–53 years, underwent ECG and physical examination conducted by a physician under standardized conditions, provided blood samples for laboratory tests, and answered questionnaires administered by trained interviewers. The vital status was obtained from specific inquiries up to the time of retirement and then by death certificates. Men with known ischemic heart disease were further excluded from analysis which was conducted on the 7079 remaining subjects. Results: After an average follow-up period of 23 years, there were 2083 deaths, among which were 603 cardiovascular deaths including 118 sudden deaths and 192 following myocardial infarction. The crude risk of sudden death increased linearly with the level of resting heart rate and the risk in men in the highest quintile of heart rate was 3.8 fold than in those in the lowest quintile, whereas rates were approximatively twice higher for fatal myocardial infarction, cardiovascular and total mortality (all P

Exercise testing is widely used in the diagnosis of coronary artery disease, but the long-term outcome for asymptomatic persons with exercise-induced premature ventricular depolarizations remains unclear. We used data from the Paris Prospective Study I to assess the long-term outcome for such persons.A total of 6101 asymptomatic French men (42 to 53 years of age) who were free of clinically detectable cardiovascular disease underwent a standardized graded exercise test between 1967 and 1972. Subjects were prospectively classified as having or not having frequent premature ventricular depolarizations (a run of two or more consecutive premature ventricular depolarizations or premature ventricular depolarizations constituting more than 10 percent of all ventricular depolarizations during any of the 30-second electrocardiographic recordings).During exercise, 138 subjects had frequent premature ventricular depolarizations. After 23 years of follow-up, these subjects had a higher risk of death from cardiovascular causes than the men without frequent premature ventricular depolarizations during exercise (relative risk, 2.67; 95 percent confidence interval, 1.76 to 4.07). In a multivariate model, with adjustment for age, body-mass index, heart rate at rest, systolic blood pressure, tobacco use, level of physical activity, presence or absence of diabetes, total cholesterol level, and the presence or absence of premature ventricular depolarizations before exercise and during recovery from exercise, both an exercise test that was positive for ischemia and the occurrence of frequent premature ventricular depolarizations during exercise remained independently associated with an increased risk of death from cardiovascular causes, with similar relative risks (2.63 [95 percent confidence interval, 1.93 to 3.59] and 2.53 [95 percent confidence interval, 1.65 to 3.88], respectively).The occurrence of frequent premature ventricular depolarizations during exercise in asymptomatic middle-aged men is associated with a long-term increase in the risk of death from cardiovascular causes.

Familial Hypertrophic Cardiomyopathy (FHC) is an autosomal dominant disease characterised by ventricular hypertrophy, with predominant involvement of the interventricular septum. It is a monogenic disease with a high level of genetic heterogeneity (nine genes and more than 110 mutations reported so far). We describe a family with a new R869G mutation in the β -myosin heavy chain gene ( MYH7 ). This mutation was found in the heterozygous status in both parents and in the homozygous status in the two children. A haplotype analysis on the MYH7 locus with microsatellite markers showed that the same haplotype is transmitted within the family, suggesting a founder effect. Clinically, the father was asymptomatic with mild left ventricular hypertrophy on echocardiography. The mother had a mild form of hypertrophic cardiomyopathy and remained asymptomatic until 60 years old when an atrial fibrillation occurred. For the two children, clinical diagnosis was performed at 12 and 8 years and atrial fibrillation occurred at 17 years. For both children, the evolution was characterized by left ventricle (LV) systolic dysfunction and a severe dilatation of the left atrium before 40 years of age. Conclusions: In this family, a new R869G mutation in the MYH7 gene was found. Interestingly, a mutation was found at the homozygous status for the first time in FHC. This finding suggests that this particular mutation is compatible with life, but for homozygous subjects, age at onset of symptoms was earlier and the disease much more severe than in the heterozygous subjects, suggesting a gene-dose effect.

Background —Constrictive remodeling plays a prominent role in restenosis after balloon angioplasty, but its regulation remains unclear. Because endothelial dysfunction and changes in extracellular matrix have been reported after angioplasty, this study was designed to simultaneously evaluate endothelial function and collagen and elastin changes after restenosis and arterial remodeling. Methods and Results —Atherosclerosis was induced in femoral arteries of 22 New Zealand White rabbits by air-desiccation and a high-cholesterol diet. One month later, angioplasty was performed. Histomorphometry and in vitro assessment of endothelial function were performed 4 weeks after angioplasty. Restenosis correlated with constrictive remodeling ( r =0.60, P =0.01) but not with neointimal growth ( r =−0.06, P =0.79). Restenosis correlated with an impaired relaxation to acetylcholine (ACh; r =0.61, P =0.02) but not with the response to the endothelium-independent vasodilator sodium nitroprusside ( r =−0.25, P =0.40). Restenosis correlated positively with collagen accumulation ( r =0.69, P =0.004) and inversely with elastin density ( r =−0.48, P =0.05). Relaxations to ACh were significantly more decreased in arteries with constrictive remodeling than in those with enlargement remodeling (3.7±7.9% versus 35.5±15.0%, P =0.04). Neointimal collagen density was significantly higher in arteries with constrictive remodeling than in those with enlargement remodeling (34.5±4.5% versus 18.2±4.7%, P =0.03). Endothelial function and collagen and elastin density were independent predictors of restenosis in the study. Conclusions —These results demonstrate that the severity of restenosis after angioplasty correlated with both defective endothelium-dependent relaxation and increased collagen density.

Background —Sudden death was found to share the same set of usual risk factors as coronary events and therefore could not be specifically predicted in the population. It appears, however, that parental history of sudden death has not been investigated yet as a risk factor for sudden death. Therefore, we assessed risk factors, including parental sudden death, associated with the occurrence of sudden death in a long-term cohort study. Methods and Results —We included 7746 men employed by the city of Paris who were 43 to 52 years of age in 1967 to 1972 in the Paris Prospective Study I. Each subject underwent a physical examination and an ECG, provided blood for laboratory tests, and answered questionnaires administered by trained interviewers who paid particular attention to family medical history. Men with known ischemic cardiac disease were further excluded from analysis. For 95.5% of the men, vital status was obtained from specific inquiries until retirement, then by death certificates. Resting heart rate, systolic or diastolic blood pressure, tobacco consumption, body mass index, diabetes status, serum cholesterol, and parental history of sudden death were independent factors associated with sudden death during follow-up (23 years on average). When adjusted for confounding variables, including parental history of myocardial infarction, relative risk of sudden death associated with parental sudden death was 1.80 (95% CI, 1.11 to 2.88). Conclusions —Parental sudden death is an independent risk factor for sudden death in middle-aged men. The existence of familial risk factors for sudden death may help provide better identification of subjects at high risk of and early prevention of sudden death.

Cardiac myosin binding protein C (MyBP-C) is a sarcomeric protein belonging to the intracellular immunoglobulin superfamily. Its function is uncertain, but for a decade evidence has existed for both structural and regulatory roles. The gene encoding cardiac MyBP-C (MYBPC3) in humans is located on chromosome 11p11.2, and mutations have been identified in this gene in unrelated families with familial hypertrophic cardiomyopathy (FHC). Detailed characterization of the MYBPC3 gene is essential for studies on gene regulation, analysis of the role of MyBP-C in cardiac contraction through the use of recombinant DNA technology, and mutational analyses of FHC. The organization of human MYBPC3 and screening for mutations in a panel of French families with FHC were established using polymerase chain reaction, single-strand conformation polymorphism, and sequencing. The MYBPC3 gene comprises >21 000 base pairs and contains 35 exons. Two exons are unusually small in size, 3 bp each. We found six new mutations associated with FHC in seven unrelated French families. Four of these mutations are predicted to produce truncated cardiac MyBP-C polypeptides. The two others should each produce two aberrant proteins, one truncated and one mutated. The present study provides the first organization and sequence for an MyBP-C gene. The mutations reported here and previously in MYBPC3 result in aberrant transcripts that are predicted to encode significantly truncated cardiac MyBP-C polypeptides. This spectrum of mutations differs from the ones previously observed in other disease genes causing FHC. Our data strengthen the functional importance of MyBP-C in the regulation of cardiac work and provide the basis for further studies.

AimTo assess the value of velocity and flow rate-related parameters obtained by cardiac magnetic resonance (CMR) for evaluation of left ventricular (LV) diastolic function (DF) in patients (pts) with hypertrophic cardiomyopathy (HCM).MethodsCMR was performed in 26 HCM pts and 24 healthy volunteers (HV) matched for age, gender, body surface area (BSA) and blood pressure. DF parameters were obtained using a semi-automated software enabling extraction of transmitral flow, including transmitral Ef and Af flow rate peaks, isovolumetric relaxation time (IVRT) and early peak diastolic longitudinal myocardial velocity E’ obtained using 2D phase contrast-CMR. LV mass and volumes and left atrial (LA) volumes were measured from cine CMR images.ResultsMean age was 47.0±20.2 years in HCM pts and 47.5±16.1 in HV (p=NS). LV mass, mass/end-diastolic volume and LA volumes were increased in HCM pts (table). Late gadolinium enhancement was found in 20 HCM pts. While there was no significant difference in Ef/Af, myocardial longitudinal velocity E’ and LA emptying fraction were markedly lower in HCM pts. Furthermore, E/E’ ratio and E wave deceleration time (DT) were higher in HCM pts. There was a linear relationship between increased LV mass and increased LA volumes (p

Background Beneficial hemodynamic effects after dynamic cardiomyoplasty have been inconsistently demonstrated, and the effects seen may be due to the wrap itself, to flap stimulation, or both. The aim of this study was to determine whether flap stimulation per se acts as a systolic active process after cardiomyoplasty. Methods and Results Catheterizations were performed in 13 patients 14.4±7 months after cardiomyoplasty. New York Heart Association functional class decreased from 3.3 to 2.1 after the procedure ( P =.0005). Hemodynamic evaluations were first performed with the stimulator on in the 2:1 mode and then after the stimulator had been off for at least 24 hours. Left ventricular (LV) ejection fraction increased from 25.1±6% before surgery to 28.2±6.7% with the stimulator on after cardiomyoplasty ( P =.04). When stimulation was stopped, there was no change ( P >.05) in indexes of systolic or diastolic LV function (peak systolic LV pressure, LV ejection fraction, peak positive dP/dt, peak negative dP/dt, or τ). Pulmonary capillary wedge pressure and cardiac index were unchanged when stimulated and nonstimulated settings were compared ( P >.05). However, a remarkable heterogeneity of individual responses was observed. Ejection fraction and cardiac index decreased with the stimulator off in 3 patients, but peak positive dP/dt decreased in 6 patients; diastolic function deteriorated in 2 patients, but a slight improvement was noted in 3 patients. Cardiothoracic ratio, echocardiographic LV end-diastolic dimension, and fractional shortening remained unchanged between immediate ( Conclusions In the majority of our patients, there was no short-term hemodynamic benefit of flap stimulation; therefore, we conclude that the efficacy of cardiomyoplasty may be a consequence of a passive “girdling effect,” which limits the progression of ventricular enlargement and further deterioration of ejection fraction.

UNLABELLED Familial hypertrophic cardiomyopathy (HCM) has been poorly studied, although it may represent 50% of all HCM. We studied 346 subjects belonging to 20 unrelated families. Patients were considered affected in view of left ventricular (LV) wall thickness. One hundred twenty-seven adults were considered affected, id est. had a left ventricular wall thickness (LVWT) > 13 mm, whereas 123 had a LVWT > 15 mm, suggesting that the cut-off value is usually not critical. Within affected patients, 95% had an asymmetrical HCM (interventricular septum/left posterior wall thickness > 1.3 mm), whereas 84% had a ratio > 1.5. Distribution of the affected patients according with Maron's classification are in keeping with published studies about sporadic forms. Doppler derived isovolumetric relaxation time was prolonged in HCM (105 +/- 23 vs 88 +/- 16 msec, P < 0.001), and the ratio peak velocity of A wave over peak velocity of E wave was significantly lower in affected individuals (0.99 +/- 0.56 vs 0.83 +/- 0.46, P < 0.05). None of the 24 children studied (10 +/- 3 years) were considered affected according to echocardiographic criteria. CONCLUSION Echocardiography is the obligatory first step during genetic study for recognizing familial HCM. It allows classification in adults but not in children. Doppler estimate of diastolic function may be helpful in the future to recognize genetically affected subjects with normal or subnormal echocardiographic examination.

Autologous skeletal myoblast transplantation might improve postinfarction ventricular function, but graft viability and differentiation (ie, proof of concept) has not been shown. A 72-year-old man had autologous cultured myoblasts from his vastus lateralis injected to an area of transmural inferior myocardial infarction in non-reperfused scar tissue. He showed improvement in symptoms and left-ventricular ejection fraction. When he died 17.5 months after the procedure, the grafted post-infarction scar showed well developed skeletal myotubes with a preserved contractile apparatus. 65% of myotubes expressed the slow myosin isoform and 33% coexpressed the slow and fast isoforms (vs 44% and 0.6%, respectively, in skeletal muscle). Myoblast grafts can survive and show a switch to slow-twitch fibres, which might allow sustained improvement in cardiac function.

BackgroundData from several previous studies examining heart-rate and cardiovascular risk have hinted at a possible relationship between heart-rate and non-cardiac mortality. We thus systematically examined the predictive value of heart-rate variables on the subsequent risk of death from cancer.MethodsIn the Paris Prospective Study I, 6101 asymptomatic French working men aged 42 to 53 years, free of clinically detectable cardiovascular disease and cancer, underwent a standardized graded exercise test between 1967 and 1972. Resting heart-rate, heart-rate increase during exercise, and decrease during recovery were measured. Change in resting heart-rate over 5 years was also available in 5139 men. Mortality including 758 cancer deaths was assessed over the 25 years of follow-up.FindingsThere were strong, graded and significant relationships between all heart-rate parameters and subsequent cancer deaths. After adjustment for age and tobacco consumption and, compared with the lowest quartile, those with the highest quartile for resting heart-rate had a relative risk of 2.4 for cancer deaths (95% confidence interval: 1.9-2.9, pInterpretationResting and exercise heart rate had consistent, graded and highly significant associations with subsequent cancer mortality in men.

The hereditary haemochromatosis gene (HFE) has recently been proposed as a disease modifying gene.1 The rationale is that two common mutations of the HFE gene (C282Y and H63D) are found in a majority of patients with genetic haemochromatosis who are either homozygotes (C282Y/C282Y) or compound heterozygotes (C282Y/H63D). These mutations have been shown to contribute to more subtle modifications of iron homeostasis at the heterozygous state.2 In turn, iron may predispose to myocardial damage through the production of activated oxygen species. Recently, Mahon and colleagues have reported an association between the H63D mutation and idiopathic dilated cardiomyopathy (IDCM).3 In this study, 207 unrelated white patients with dilated cardiomyopathy and 200 controls were tested for HFE C282Y and H63D mutations. An increased proportion of H63D heterozygotes was found among patients (36%) as compared to the control group (27%). No association was found with C282Y mutation and as the H63D mutation had a relatively minor effect on iron status, these authors proposed that this association may be …

Intramyocardial skeletal muscle transplantation has been shown experimentally to improve heart function after infarction. We report success with this procedure in a patient with severe ischaemic heart failure. We implanted autologous skeletal myoblasts into the postinfarction scar during coronary artery bypass grafting of remote myocardial areas. 5 months later, there was evidence of contraction and viability in the grafted scar on echocardiography and positron emission tomography. Although this result is encouraging, it requires validation by additional studies.

BackgroundIn ischemic mitral regurgitation (IMR), leaflet tethering is caused by post-MI LV and annular remodeling. Severing second-order mitral chordae significantly decreases tethering and MR. We tested whether undersized ring annuloplasty can improve chordal cutting efficacy by reducing annulus-related tethering.MethodsPosterolateral MI created chronic remodeling and MR in 28 sheep. At 3 months, sheep were randomized to sham surgery vs isolated annuloplasty undersized by 2 sizes vs isolated bileaflet chordal cutting vs at the combined therapy (n=7 each). At baseline, chronic MI (3 months) and sacrifice (6.6 months) we measured LV volumes and ejection fraction (EF), wall motion score index (WMSi), MR Regurgitation fraction (MRRF) and vena contracta (VC), Mitral annulus area (MAA) and posterior leaflet (PL) restriction angle (PL to MAA) by 2D and 3D echo.ResultsAll groups were comparable at baseline and chronic MI, with mild- moderate MR (MRVC 4.6±1.0mm, MRRF 24±2.6%) and MA dilatation (p

Five patients were studied 5-13 months after dynamic cardiomyoplasty for refractory heart failure. In two, muscle flap stimulation caused a pronounced increase in cardiac index (mean 55%) and ejection fraction (mean 75%); no patient showed improvement in cardiac filling pressure. 2 years after surgery, one of the patients with haemodynamic improvement died from ventricular fibrillation, and histochemistry of the stimulated muscle flap revealed predominantly fatigue-resistant type I fibres, without evidence of fibrosis. In selected cases, dynamic cardiomyopathy could be of long-term benefit.

Alcohol septal ablation appears to be a successful strategy for severe obstructive cardiomyopathy, resulting in reductions in clinical symptoms and left ventricular outflow tract gradient (LVOTG). However, rates of mortality (1–4%) and permanent complete atrioventricular (AV) blockage (15–30%) associated with …

Background To investigate the adverse effects of anticoagulant therapy during pregnancy in a tertiary care center. Material and methods A prospective study was carried out between 1 January 1977 and 31 December 1994 and included 54 pregnancies in 50 women treated with anticoagulants. In Group I (n=43) oral anticoagulants were replaced for heparin from the sixth until the end of the twelfth week of gestation. In Group II (n= 11) the pregnancy was diagnosed after the ninth week of gestation and acenocoumarol was not substituted. All patients received vitamine K antagonists during the second and third trimesters. Heparin was given after 36 weeks of pregnancy until the tenth day in the postpartum period. Statistical comparisons used Chi square test (with the Yates correction when appropriate) and Student t test. Results. Mechanical heart valve prosthesis was the most frequent indication (68%). There was one artificial heart valve thrombosis during first trimester in Group I and none in Group II (p=0.45). One spontaneous abortion occurred in each group (p=0.86). Seven cardiac complications (13.7%) occurred during the second and third trimesters. We recorded no thrombotic episode of an artificial heart valve after the first trimester of pregnancy. Hemorrhagic complications occurred in mid pregnancy (one case=2%) and during peripartum (eight cases=16%). Two maternal deaths occurred in the postpartum period, both were linked with the anticoagulant therapy. There was one coumarin embryopathy (Group II: 9%), but no neonatal mortality. Conclusions (1) Hemorrhagic complications occur among 16% of patients receiving anticoagulant therapy during pregnancy. (2) Delivery and postpartum are the most critical periods.

A rapid up and down motion (“crochetage”) of the R ware in at least one inferior lead — involving the initial 30 to 70 msec of the QRS - is usually observed in pts with ostium secundum (OS) ASD, but its diagnostic value was not previously studied. Thus, we retrospectively tested the presence of a “crochetage” in 2 groups (Gr) of pts: Gr 1 (568 pts with OS ASD and QRS duration lesser than 120 msec); Gr 2 (459 pts with normal heart, matched for age with Gr 1). In Gr 1, an incomplete right bundle branch block (RBBB) was present in 522 pts, mean pulmonary artery pressure (PAP) and shunt severity (Qp/Qs) were assessed in all pts, and surgery was performed in 484 pts.Results(1) In Gr 1, a “crochetage” was absent in 143 pts (Gr A, 27%), present in one inferior lead in 80 pts (Gr B, 15%) and in 2 to 3 leads in 309 pts (Gr C, 58%); (2) Sensitivity, specificity, accuracy and positive predictive value (PPV) of a “crochetage” pattern for an OS ASO reached 73%, 93%, 92% and 94%; comparatively, they reached 98%, 89%, 94% and 91% for a RBBB pattern; when associated to an incomplete RBBB, the PPV of a “crochetage” pattern reaches 96% if limited to one lead and 99.5% if present in 2 to 3 inferior leads; (2) In Gr 1, age and PAP were not different between Gr A, B or C; means Qp/Qs were 2.8 in Gr A, 3.6 in Gr Band 3.8 in Gr C (p 30mmHgl. this pattern was present in 213 leads in 29% of cases if Qp/Qs < 1.5 vs 67% if Qp/Qs > 1.5 (p

Objectives. This study sought to determine the clinical significance of a “crochetage” pattern—a notch near the apex of the R wave in electrocardiographic (ECG) inferior limb leads—in secundum atrial septal defect.Background. Atrial septal defect is often overdiagnosed on the basis of classical clinical features. Thus, more specific signs on the ECG for screening are needed.Methods. We searched for a crochetage pattern in 1,560 older children and adults: 532 with secundum atrial septal defect, 266 with ventricular septal defect, 146 with pulmonary stenosis, 110 with mitral stenosis, 47 with cor pulmonale and 459 normal subjects.Results. This pattern was observed respectively in 73.1%, 35.7%, 23.3%, 6.4%, 10.6% and 7.4% of these groups (p < 0.001). In atrial septal defect, its incidence increased with larger anatomic defect (p < 0.0001) or greater left-to-right shunt (p < 0.0001), even in the presence of pulmonary hypertension. By multiple regression analysis, only shunt size (p < 0.0006) and defect location (p < 0.0001) were the determinants of its presence. In all groups, the specificity of this sign for the diagnosis was remarkably high when present in all three inferior limb leads (≥92%), even when comparison was limited to patients with an incomplete right bundle branch block (≥95.2%). Early disappearance of this pattern was observed in 35.1% of the operated-on patients although the right bundle branch block pattern persisted.Conclusions. A crochetage pattern of the R wave in inferior limb leads is frequent in patients with atrial septal defect, correlates with shunt severity and is independent of the right bundle branch block pattern. Sensitivity and specificity of this sign are remarkably high when it is associated with an incomplete right bundle branch block or present in all inferior limb leads.

SummaryHeart failure constitutes an important medical, social and economic problem. The prevalence of heart failure is estimated as 2–3% of the adult population and increases with age, despite the scientific progress of the past decade, especially the emergence of natriuretic peptides, which have been widely used as reliable markers for diagnostic and prognostic evaluation. Identification of new reliable markers for diagnosis, analysis, prognosis of mortality and prevention of hospitalization is still necessary. Galectin-3 is a soluble β-galactoside-binding protein secreted by activated macrophages. Its main action is to bind to and activate the fibroblasts that form collagen and scar tissue, leading to progressive cardiac fibrosis. Numerous experimental studies have shown the important role of galectin-3 in cardiac remodelling due to fibrosis, independent of the fibrosis aetiology. Galectin-3 is significantly increased in chronic heart failure (acute or non-acute onset), independent of aetiology. Some clinical studies have confirmed the predictive value of galectin-3 in all-cause mortality in patients with heart failure. In our review, we aim to analyse the role of galectin-3 in the development of heart failure, its value in screening and clinical decision making and its possible predictive application in follow-up as a “routine” test in an addition to established biomarkers, such as B-type natriuretic peptide and N-terminal prohormone of B-type natriuretic peptide.

background Changes in heart rate during exercise and recovery from exercise are mediated by the balance between sympathetic and vagal activity. Since alterations in the neural control of cardiac function contribute to the risk of sudden death, we tested the hypothesis that among apparently healthy persons, sudden death is more likely to occur in the presence of abnormal heart-rate profiles during exercise and recovery. methods A total of 5713 asymptomatic working men (between the ages of 42 and 53 years), none of whom had clinically detectable cardiovascular disease, underwent standardized graded exercise testing between 1967 and 1972. We examined data on the subjects’ resting heart rates, the increase in rate from the resting level to the peak exercise level, and the decrease in rate from the peak exercise level to the level one minute after the termination of exercise. results During a 23-year follow-up period, 81 subjects died suddenly. The risk of sudden death from myocardial infarction was increased in subjects with a resting heart rate that was more than 75 beats per minute (relative risk, 3.92; 95 percent confidence interval, 1.91 to 8.00); in subjects with an increase in heart rate during exercise that was less than 89 beats per minute (relative risk, 6.18; 95 percent confidence interval, 2.37 to 16.11); and in subjects with a decrease in heart rate of less than 25 beats per minute after the termination of exercise (relative risk, 2.20; 95 percent confidence interval, 1.02 to 4.74). After adjustment for potential confounding variables, these three factors remained strongly associated with an increased risk of sudden death, with a moderate but significantly increased risk of death from any cause but not of nonsudden death from myocardial infarction. conclusions The heart-rate profile during exercise and recovery is a predictor of sudden death.

A cardiac event in the course of echinococcosis is uncommon (0.5 to 2%), but when it does occur it is associated with an increased risk of potentially lethal complications (such as fissures, rupture with embolic complications and anaphylactic shock). 1 The techniques of cardiac imaging, notably 2-dimensional (2-D) echocardiography, have greatly facilitated the detection of cardiac involvement in echinococcosis. The place of this examination, as well as that of computed tomography (CT) and nuclear magnetic resonance (NMR) imaging, is discussed in connection with a case of cardiac hydatic cyst associated with polyvisceral infection. 2,3

Electrical therapies by defibrillators (ICD) and resynchronization devices (CRT-D – CRT-P), have demonstrated their benefits on symptoms, morbidity and mortality in selected heart failure patients (HF). The ITHAQUE survey aims to describe the different supports of patients in HF patients with impaired left ventricular (LV) function (LV ejection fraction < 45%)Methods927 patients treated for HF were seen in outpatient visit with a general cardiologist (75%) or in a tertiary center (25%). A survey of treatments and follow-ups was completed by the physician. 3 groups under optimal treatment, defined by the French Society of Cardiology (SFC) guidelines, have been analyzed:Gr1 – Class 1B (patients with ischemic cardiomyopathy and coronary revascularization, NYHA II and III, LVEF 120 ms)ResultsOf the total patients, 79 received an ICD (8.5%), 22 a CRT-D (2.4%) and 76 a CRT-P (8.2%). On the other side, 279 patients eligible according to the recommendations of the SFC did not receive additional treatment with ICD or CRT (30%). Pharmacological treatment associated is mainly composed of IEC (76.5%), Beta-blockers (76.6%), Diuretics (90%), anticoagulants (80%) and Anti-arrhythmic (31%). Rules lifestyle modifications (77.8%) and practice of physical activity (31.2%) are also prescribed, associated or not.ConclusionAlthough the specific conditions of therapeutic patient must be taken into account, the ITHAQUE survey did show that the electrical therapies recommended by the SFC for heart failure patients with systolic dysfunction are underused.