Diagnosis and management of heart failure from hospital admission to discharge: A practical expert guidance.

Heart failure (HF) has high event rates, mortality, and is challenging to manage in clinical practice. Clinical management is complicated by complex therapeutic strategies in a population with a high prevalence of comorbidity and general frailty. In the last four years, an abundance of research has become available to support multidisciplinary management of heart failure from within the hospital through to discharge and primary care as well as supporting diagnosis and comorbidity management. Within the hospital setting, recent evidence supports sacubitril-valsartan combination in frail, deteriorating or de novo patients with LVEF≤40%. Furthermore, new strategies such as SGLT2 inhibitors and vericiguat provide further benefit for patients with decompensating HF. Studies with tafamidis report major clinical benefits specifically for patients with ATTR cardiac amyloidosis, a remaining underdiagnosed and undertreated disease. New evidence for medical interventions supports his bundle pacing to reduce QRS width and improve haemodynamics as well as ICD defibrillation for non-ischemic cardiomyopathy. The Mitraclip reduces hospitalisations and mortality in patients with symptomatic, secondary mitral regurgitation and ablation reduces mortality and hospitalisations in patients with paroxysmal and persistent atrial fibrillation. In end-stage HF, the 2018 French Heart Allocation policy should improve access to heart transplants for stable, ambulatory patients and, mechanical circulatory support should be considered to avoid deteriorating on the waiting list. In the community, new evidence supports that improving discharge education, treatment and patient support improves outcomes. The authors believe that this review fills the gap between the guidelines and clinical practice and provides practical recommendations to improve HF management.

[ST elevation myocardial infarction in young adults: Is there an interest for thrombophilia screening?] / Syndrome coronarien aigu avec sus-décalage du segment ST chez les jeunes adultes : le bilan de thrombophilie a-t-il un intérêt ?

BACKGROUND: Coronary lesions characteristics as well as patient thrombogenicity can explain coronary events manifestation. In young patient, local conditions are usually less important and thrombogenicity could play a significant role. Assessing thrombophilia could be justified in young patients and may induce an adapted therapeutic management. PURPOSE: We aimed to assess the prevalence of thrombophilia and therapeutic modification in young adults aged≤55 years admitted in our department for ST elevation myocardial infarction (STEMI). METHODS: From January 2013 to January 2017, data on all patients aged≤55 years with STEMI admitted in emergency were retrospectively retrieved from our database. Thrombophilia investigation was made regarding clinical (with or without cardiovascular risk factors [CVRF]), biological and/or angiographic evaluation. RESULTS: A total of 133 patients aged≤55 years with STEMI were included. Cardiac arrest occurred in 15 patients (11%). One or less CVRF were found in 47 patients (35%). Smoking was reported in 93 patients (70%) and drug addiction (cannabis, cocaine) in 19 patients (14%). A subset of 51 patients (38%) were screened for thrombophilia. Patients with thrombophilia assessment were younger, less active smokers and presented less CVRF than patients without investigation (P<0.001). Single vessel diseased was found in 88 patients (66%). No differences regarding coronary procedural characteristic were found between the two groups. The most frequently encountered aetiology, found in 122 patients (92%), was de novo intra-arterial thrombosis related to atherosclerosis. In patients with thrombophilia assessment (n=51), one or more abnormal biological results was found in 22 patients (43%) and a therapeutic adjustment was made in 6 patients (12%). CONCLUSION: Thrombophilia screening in young STEMI adults showed an abnormality in 43% of cases. Antithrombotic treatment can be modified after its demonstration.

[Diabetes and heart failure, a fatal association]. / Diabète et insuffisance cardiaque, une association morbide.

The prevalence of heart failure and diabetes are both increasing: 25 to 30% of patients with heart failure suffer from diabetes, and the latter aggravates heart failure. The presence of macro- or micro-angiopathy, cardiac neuropathy or renal failure worsens the clinical pattern and disturbs treatment strategies. Doppler-echocardiography and the dosage of BNP can probably help to detect and consequently to treat prematurely heart failure in the diabetic patient. The usual treatments in heart failure have similar or lower efficacy in the diabetic patient, and treatment intolerance is frequent. Treatments used for diabetes can be handled with difficulty in case of heart failure (metformin, glitazones). In the future, it is therefore extremely important: 1--to prevent the occurrence of diabetes in patients with glucose intolerance; 2--in diabetic patients, to prematurely detect cardiac dysfunction and optimally control diabetes, in order to avoid its occurrence; 3--and finally, in diabetic patients with heart failure, to optimize the medical treatment, in order that these patients have similar benefits compared to non-diabetic patients with heart failure. The ACE-inhibitors and angiotensin-2 antagonists seem to have an important role. Treatments breaking the glycation bridges, as well as statins, appear as interesting therapeutic options. Finally, the exact role of myocardial revascularization, either by angioplasty or surgery, might probably be important.

[Rotational coronary angiography]. / Angiographie coronaire rotationnelle.

CONTEXT: Rotational angiography (RA) is a radiological technique that provides multiple views of a vessel for a single injection of contrast. Its significance in the field of coronary angiography is poorly known at present. This study aimed to compare the radiation dose as well as the volume of contrast used during RA compared to standard angiography (SA), and to evaluate its diagnostic precision. METHOD: 78 patients sent for diagnostic coronary angiography were explored using the radial approach. The patients were randomised between RA (3 acquisitions for the left coronary and 1 for the right coronary) or SA. Once a decision to undertake angioplasty had been made following the angiography (RA or SA), the initial study was complemented using the alternative technique (SA or RA) before the angioplasty procedure was performed at a later stage. The severity of the lesions as shown by RA and SA was compared by four experienced coronary angiography operators. RESULTS: 65 patients (mean age 61+/-10 years--mean BMI 26+/-4 Kg/m2) underwent complete RA+SA investigation. The total x-ray dose used during ciné-angiography, the dose received by the patient, and the volume of contrast were significantly reduced in the RA group compared to the SA group (-25%; -36%; -33% respectively). An evaluation of the severity of the stenoses was performed on 168 arterial segments. There was a significant correlation between the two techniques (R=0.95--p<0.001) and the intra-observer variability was non significant (3.7+/-6.8%--p=NS). CONCLUSIONS: Rotational angiography allows the radiation dose and the volume of contrast to be reduced, while retaining a diagnostic precision similar to that of standard angiography.

Inflammation versus mechanical stretch biomarkers over time in acutely decompensated heart failure with reduced ejection fraction.

Heart failure can be associated with inflammation but it is unclear if inflammation is directly related to hemodynamic worsening or is an independent pathway. Our aim was to investigate inflammation and mechanical stress using serial measurements of biomarkers in acute and chronic heart failure with reduced ejection fraction (AHF and CHF). METHOD: The following biomarkers were measured on admission, at discharge and one month after discharge: B-type natriuretic peptide (BNP), high-sensitivity C-Reactive protein (hsCRP), Tumour Necrosis Factor alpha (TNFα), interleukin 6 (IL6), myeloperoxidase (MPO), suppression of tumorigenicity 2 (ST2), mid-regional pro-adrenomedullin (MR-proADM), galectin 3 (Gal3), Growth differentiating factor 15 (GDF15) and procalcitonin (PCT). RESULTS: In control CHF group (n=20, 69±11y, NYHA 1-2), most biomarker levels were low and stable over time. In AHF (n=55, 71±14y), BNP, ST2 and GDF15 levels were highly increased on admission and then decreased rapidly with clinical improvement; BNP, ST2 and GDF15 levels were statistically correlated (r=0.64, 0.46 and 0.39; p<0.001 for both). Both hsCRP, MPO, TNFα and Gal3 levels were increased in most AHF patients (70, 56, 83 and 98% respectively) with poor change over time. HsCRP, MPO and TNFα levels were correlated. IL6, MR-proADM and PCT levels were slightly increased, without change over time. Highest quartiles of BNP and ST2 were associated with death or readmission at one year (HR 2.33 [95CI 1.13-4.80] and 2.42 [1.27-4.60]). CONCLUSION: AHF is associated with systemic inflammation. This inflammatory response continued up to one month after discharge despite normalisation of mechanical stress-related markers.

Interaction between pulse wave velocity, augmentation index, pulse pressure and left ventricular function in chronic heart failure.

Pulse wave velocity (PWV), the carotid augmentation index (AIx), and pulse pressure (PP) may be prognostic factors in heart failure, but the possible influence of the ejection fraction (EF) and other simple haemodynamic variables on them has not been investigated in this setting. Noninvasive methods were used to measure carotid-radial (CR), carotid-femoral (CF) PWV and AIx, and brachial PP, in 135 consecutive patients with stable symptomatic chronic heart failure. The patients were divided into two groups, with preserved (>or=40%) or reduced (<40%) EF. CF-PWV, AIx and PP were lower in the decreased EF group (8.85+/-2.77 versus 10.60+/-2.75 m/s, P<0.001; 121+/-21 versus 132+/-24, P=0.009 and 41+/-19 versus 67+/-17 mmHg, P<0.001), but CR-PWV values were similar regardless of the EF status. These results were not modified after adjustment for age and sex. Multiple regression analysis showed that AIx and PP were systematically related to time domain parameters (heart rate or ejection duration) and EF, whatever the group. CF-PWV was weakly related to time domain values and unrelated to mean blood pressure (BP) or EF in the preserved EF group, whereas it was related to both mean BP and EF in the low EF group. In conclusion, whatever the EF level, PP and AIx were strongly modulated in the time domain, by pressure and by the EF level. The same relationships were found with CF-PWV, but only in the reduced EF group. Whether CF-PWV is the best prognostic factor in patients with 'diastolic' heart failure must be confirmed in a prospective study.

[Heart failure and cachexia]. / Insuffisance cardiaque et cachexie.

Cachexia is related to a malnutrition state related to hypercatabolism. Initially described in cancer, it is also related to several chronic diseases including heart failure. Defined by an unintentional weight loss exceeding 7.5% of body mass during more than 6 months, it is presented by the association of nutritional deficiencies, digestive and/or urinary losses as well as metabolic abnormalities causing fat and lean mass loss and is associated to a poor prognosis. The pathophysiology of cachexia and heart failure presented some similarities associating especially neuro-hormonal activation, a cortisol/DHEA ratio imbalance, as well as pro-inflammatory cytokines activation. Currently the treatment of cachexia is mainly preventive, based on ACE-inhibitors and beta-blockers therapy and physical reconditioning. The benefits of hormonal and nutritional substitutes remains to be evidenced.

[Massive pulmonary embolism and stroke due to thrombus across the foramen ovale]. / Thrombus enclavé dans le foramen ovale responsable d'embolie pulmonaire et d'accident vasculaire cérébral.

We report the case of a man admitted for massive pulmonary embolism. Transthoracic echocardiography showed a serpentine thrombus in the right atrium across the foramen oval. Because of an acute worsening of the circulatory insufficiency, an intravenous thrombolysis was prescribed and the patient recovered progressively. An early control echocardiography showed the disappearing of the intracardiac thrombus and no evidence of abnormality of interatrial septum. While there was no evidence of venous thrombosis in legs, a renal cancer was diagnosed by echography. Silent stroke were highlighted at the scanner. This clinical case leads to discuss the origin of thrombus (in situ formation or thrombus migration) as well as the treatment (heparinotherapy, thrombolysis, surgical embolectomy, definitive closure of the foramen oval).

Cardiac metaiodobenzylguanidine uptake in patients with moderate chronic heart failure: relationship with peak oxygen uptake and prognosis.

OBJECTIVES: This prospective study was undertaken to correlate early and late metaiodobenzylguanidine (MIBG) cardiac uptake with cardiac hemodynamics and exercise capacity in patients with heart failure and to compare their prognostic values with that of peak oxygen uptake (VO2). BACKGROUND: The cardiac fixation of MIBG reflects presynaptic uptake and is reduced in heart failure. Whether it is related to exercise capacity and has better prognostic value than peak VO2 is unknown. METHODS: Ninety-three patients with heart failure (ejection fraction <45%) were studied with planar MIBG imaging, cardiopulmonary exercise tests and hemodynamics (n = 44). Early (20 min) and late (4 h) MIBG acquisition, as well as their ratio (washout, WO) were determined. Prognostic value was assessed by survival curves (Kaplan-Meier method) and uni- and multivariate Cox analyses. RESULTS: Late cardiac MIBG uptake was reduced (131+/-20%, normal values 192+/-42%) and correlated with ejection fraction (r = 0.49), cardiac index (r = 0.40) and pulmonary wedge pressure (r = -0.35). There was a significant correlation between peak VO2 and MIBG uptake (r = 0.41, p < 0.0001). With a mean follow-up of 10+/-8 months, both late MIBG uptake (p = 0.04) and peak VO2 (p < 0.0001) were predictive of death or heart transplantation, but only peak VO2 emerged by multivariate analysis. Neither early MIBG uptake nor WO yielded significant insights beyond those provided by late MIBG uptake. CONCLUSIONS: Metaiodobenzylguanidine uptake has prognostic value in patients with wide ranges of heart failure, but peak VO2 remains the most powerful prognostic index.

Adenoviral SERCA1a gene transfer to adult rat ventricular myocytes induces physiological changes in calcium handling.

OBJECTIVE: We examined the functional consequences of expressing adult rabbit fast skeletal sarcoplasmic reticulum (SR) Ca(2+)-ATPase (SERCA1a) in isolated adult rat ventricular myocytes. METHODS: Myocytes were infected with a recombinant adenovirus harboring SERCA1a. Then 2 days after myocyte infection, protein expression was estimated using Western blot and SDS-PAGE analysis. We also measured the ATP-dependent oxalate-facilitated Ca(2+) uptake of myocyte homogenates and monitored Ca(2+) transient in myocytes loaded with the Ca(2+) dye, indo-1. RESULTS: SERCA1a gene expression resulted in a 36% increase in the total SERCA protein level in infected myocytes compared to controls (P<0.01), while SERCA2 and phospholamban levels did not change. This increase was associated with a 42% rise in SR Ca(2+) uptake (P<0.01), while tau (the time constant of Ca(2+) transient decay), and the time to peak fell by 32% (P<0.01) and 38% (P<0.001), respectively. Increasing the frequency of stimulation from 0.2 to 2 Hz decreased tau in both cell types (P<0.01). However, the decrease was much smaller in infected (P<0.01) than in uninfected cells (P<0.001). Isoproterenol (1 microM) further decreased tau in infected myocytes by 23% (P<0.05). In these cells, the diastolic [Ca(2+)](i) decreased by 50% (P<0.05) while the systolic [Ca(2+)](i) increased by 19% (P<0.05). No difference was found in the speed of SR Ca(2+) reloading after caffeine washout between the two cell types. CONCLUSION: Adenovirus-mediated SERCA1a gene transfer to adult rat ventricular myocytes enhances SR Ca(2+) handling to a degree similar to that observed following physiological stimulation.

How to optimize in vivo gene transfer to cardiac myocytes: mechanical or pharmacological procedures?

An efficient gene delivery system is a prerequisite for myocardial gene therapy. Among the various procedures studied so far, catheter-based percutaneous gene delivery to the myocardium through the coronary vessels seems the most relevant to routine clinical practice; however, the optimal conditions remain to be determined. We selectively infused adenoviral vectors encoding luciferase (1 x 10(9) PFU) or beta-galactosidase (1 x 10(10) PFU) into coronary arteries of adult rabbits in various experimental conditions. Coronary artery occlusion for 30 sec, during and after adenovirus delivery, was required to observe luciferase activity in the target area of the circumflex artery (4.0 +/- 1.0 x 10(5) vs. 1.1 +/- 0.2 x 10(4) RLU/mg with and without coronary occlusion, respectively, p < 0.01, and 1.0 +/- 0.1 x 10(3) RLU/mg using nonselective infusion). When adenoviruses were delivered using high-pressure infusion (82 +/- 12 vs. 415 +/- 25 mmHg before and during infusion, respectively, p < 0.01), luciferase activity increased to 8.5 +/- 2.5 x 10(5) RLU/mg (p < 0.05 vs coronary occlusion alone). Coronary venous sinus occlusion with saline buffer retroinfusion starting before and during anterograde adenovirus delivery resulted in a further 4.7-fold increase in luciferase activity (4.4 +/- 0.8 x 10(6) RLU/mg, p < 0.01) with 5-25% blue-stained myocytes in the target area, compared with 0-5% with the other procedures. Histamine or VEGF-A(165) pretreatment, used to increase vascular permeability, slightly increased gene transfer efficiency (8.5 +/- 2.0 x 10(5) and 9.0 +/- 2.5 x 10(5) RLU/mg respectively, p < 0.05 vs. coronary occlusion alone). We conclude that catheter-mediated adenoviral gene transfer to cardiac myocytes through coronary vessels can be a very efficient procedure for myocardial gene therapy, particularly when the vector residence time and perfusion pressure in the vessels are increased.

Highly efficient adenovirus-mediated gene transfer to cardiac myocytes after single-pass coronary delivery.

Efficient and homogeneous gene transfer to cardiac myocytes is a major target in myocardial gene therapy. The aim of this study was to determine the conditions permitting efficient, homogeneous, adenovirus-mediated gene transfer to cardiac myocytes, with a view to application during coronary artery catheterization. Gene transfer to adult rat ventricular myocytes was conducted using type 5 adenoviruses carrying the lacZ reporter gene. Adenovirus delivery via coronary arteries was performed on isolated perfused rat hearts, and gene transfer efficiency was analyzed on whole ventricles, freshly isolated myocytes, and cultured myocytes. Single-pass delivery of 1 X 10(9) PFU associated with 1 min of no-flow yielded only 1 +/- 0.5% of positive myocytes. Pretreatment by histamine perfusion (10(-5) M final concentration) increased this value to 30 +/- 9% (p < 0.001), and pretreatment by Ca2+-free buffer perfusion increased it to 67 +/- 8% (p < 0.001). Combination of the two pretreatments had no additional effect. Increasing the viral dose to 3 X 10(9) PFU increased transfection efficiency only in permeabilized vessels. The 1-min no-flow period after adenovirus delivery was crucial for efficient gene transfer: despite histamine pretreatment, only 2 +/- 1% positive myocytes were observed without flow interruption (p < 0.05 versus 1 min of no-flow). Gene transfer was shown to occur in situ during cardiac perfusion, rather than during heart digestion or myocyte isolation. This study shows that highly efficient adenovirus-mediated gene transfer to cardiac myocytes in situ can be achieved by single-pass intracoronary vector delivery, provided that vascular permeability is first increased and coronary flow is briefly interrupted.

Fucans, sulfated polysaccharides extracted from brown seaweeds, inhibit vascular smooth muscle cell proliferation. I. Comparison with heparin for antiproliferative activity, binding and internalization.

Smooth muscle cell (SMC) proliferation is inhibited both in vivo and in vitro by heparin. However, the precise mechanisms of action are still not understood. The analogy between two sulfated polysaccharides, heparin and fucan, has led us to compare in detail their effects on SMC growth. We have prepared and characterized a 19 kDa fucan fraction from brown seaweed, Ascophyllum nodosum. Fucan affects the growth of SMCs in a time- and dose-dependent, reversible and non-toxic fashion. As determined by cell counting, [3H]thymidine incorporation, and microcytofluorimetry analysis, heparin was less active than fucan in inhibiting SMC growth. Fucan and heparin act by preferential blocking of G0/G1, thus decreasing the G0/S transition. Binding experiments with [125I]fucan indicated saturable, unlabeled-fucan displaceable binding sites with an apparent Kd of 30 nM. Moreover, displacement experiments performed with various polysaccharides revealed that antiproliferative compounds interacted with these membrane sites, but non-antiproliferative polysaccharides (dextran, chondroitin sulfate) did not, providing evidence of a correlation between binding to SMCs and their antiproliferative activity. When cells were exposed at 37 degrees C to a fluorescent 5-([4,6-dichlorotriazin-2-yl]-amino)fluorescein (DTAF)-fucan, internalization occurred and punctate vesicles were observed which accumulated rapidly in the perinuclear region as previously reported for heparin. Nuclear preparations (membranes + contents) of cultured SMCs previously incubated with radiolabeled heparin or fucan indicated the presence of radioactivity, suggesting an antiproliferative action of both polysaccharides at the nuclear level. Collectively, these observations indicated that fucan and heparin share some similar mechanisms of action, such as SMC growth inhibition, binding, and internalization. In the accompanying paper (Logeart et al., Eur. J. Cell Biol. 74, 1997, this issue), we describe the effect of fucans of different molecular weights and conclude that there is no direct link between polysaccharide degradation and the antiproliferative effect on SMCs.

Fucans, sulfated polysaccharides extracted from brown seaweeds, inhibit vascular smooth muscle cell proliferation. II. Degradation and molecular weight effect.

Fucan, a sulfated polysaccharide extracted from brown seaweeds, inhibits smooth muscle cell (SMC) proliferation with a higher antiproliferative activity than heparin (Logeart et al., Eur. J. Cell Biol. 74, 1997, this issue). In order to investigate the structure-activity relationship of fucan on SMC growth, we have prepared by size exclusion chromatography fucan fractions of various molecular masses ranging from 5.5 to 556 kDa. Our experiments showed that the antiproliferative activity is dependent on the molecular weight of the polysaccharide. The molecular weight threshold indicated that about 30 saccharidic units on fucan were necessary to give the antiproliferative activity on SMCs. A kinetics study of DNA synthesis using tritiated thymidine uptake was also performed with different molecular weight fucan fractions. Although all tested fractions acted as soon as the cells enter the first cell cycle, the duration and potency of action varied. Moreover, displacement experiments of iodinated fucan revealed that the low molecular fucan fraction interacted weakly with the binding sites. Finally, gel permeation chromatography of internalized radiolabeled heparin and fucans was performed with SMCs. A rapid degradation of internalized heparin was observed, whereas only low molecular weight fucan fractions were partially degraded by SMCs. Together, these results indicate the significance of molecular weight on the antiproliferative activity of fucans on SMCs, and might help to understand their mechanism of action. In addition, the degradation experiments with internalized heparin and fucans ruled out a direct link between polysaccharide degradation and the antiproliferative effect on SMCs.

Hemodynamic criteria for diagnosis of right ventricular ischemia associated with inferior wall left ventricular acute myocardial infarction.

To test the diagnostic value of different hemodynamic indexes for the diagnosis of acute right ventricular (RV) ischemic dysfunction, we studied 2 groups of consecutive patients admitted for an acute left ventricular inferior wall myocardial infarction: 51 patients with (group 1) and 32 patients without (group 2) RV ischemia as determined by coronary angiography. In both groups, we analyzed by right-sided cardiac catheterization right-sided heart pressures, pulmonary capillary wedge pressure, and cardiac index. We also calculated pressure ratios (mean right atrial pressure or RV end-diastolic over pulmonary capillary wedge pressures), pulmonary vascular resistance, and RV stroke work index. We found significant differences (p < 0.01) between the 2 groups when comparing mean right atrial pressure, RV end-diastolic pressure, ratio of these 2 pressures over pulmonary capillary wedge pressure, RV stroke work index, and right atrial and RV pressure waveforms. The best combined sensitivity, specificity, positive predictive value, negative predictive value, and diagnostic accuracy were found for the right atrial M or W waveform pattern, isolated or combined with a disproportionate elevation of RV end-diastolic over pulmonary capillary wedge pressures (respectively, 92%, 94%, 90%, 87%, and 89%). Volume loading was performed in 27 patients (18 with and 9 without RV ischemia). Right heart pressures and RV stroke work index increased significantly and similarly in both groups. Cardiac index increased significantly only in patients without RV ischemia (p = 0.02). However, volume loading did not significantly modify the diagnostic value of the different hemodynamic criteria studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Usefulness of pulmonary regurgitation Doppler tracings in predicting in-hospital and long-term outcome in patients with inferior wall acute myocardial infarction.

Right ventricular (RV) involvement is frequent during inferior wall acute myocardial infarction (AMI) and has been reported as a risk factor for in-hospital morbidity and mortality. The objectives of the present study were: (1) to evaluate in-hospital events in patients with and without RV involvement as diagnosed by abnormal flow characteristics derived from pulmonary regurgitation (PR) analysis (pressure half-time of PR, PHT(PR) < or = 150 ms and the lowest mid-diastolic to peak early diastolic velocity ratio, Vmin/Vmax < or = 0.5); and (2) to determine the influence of RV involvement in complications at long-term follow-up. Among 126 consecutively admitted patients with inferior wall AMI (mean age, 58 +/- 13 years), 101 had PR. We determined the prognostic significance of in-hospital and long-term events for the following variables: age > or = 65 years, ST-segment elevation > or = 1 mm in lead V4R, RV dilation, PHT of PR < or = 150 ms and Vmin/Vmax < or = 0.5, thrombolytic therapy, 3-vessel disease, and diabetes mellitus. We found that the PR derived Doppler index (PHT of PR < or = 150 ms and Vmin/Vmax < or = 0.5) was the only predictor of overall in-hospital clinical events (hazards ratio, 2.7, 95% confidence interval, 1.2 to 6.1, p = 0.016). At long-term follow-up (mean: 20 +/- 12 months, range 12 to 69), event-free survival analysis showed that age > or = 65 years was the only predictor of any event (relative risk, 3.7, 95% confidence interval, 2.1 to 6.3, p < 0.0001). Thus, RV involvement diagnosed with the use of PR flow-derived variables is an accurate and independent predictor of in-hospital complications. However, RV involvement does not influence long-term prognosis.

Derivatized dextrans modulate collagen synthesis in aortic smooth muscle cells.

The effect of specifically derivatized dextrans, with or without antiproliferative activity on smooth muscle cells (SMC), was investigated on type I and type III collagen biosynthesis and mRNA levels in post-confluent SMC cultures. Our results indicate that dextran derivatives decreased total protein and collagen synthesis independently of their antiproliferative activities. However, the most substituted dextran, the one exhibiting the strongest antiproliferative activity towards SMC, was the most active in modulating type III collagen expression. In addition, only the two dextran derivatives bearing benzylamide groups inhibited collagen excretion.

ST-segment elevation in precordial leads: anterior or right ventricular myocardial infarction?

Isolated acute right ventricular (RV) infarction is rare, and ECG diagnosis may be difficult. We report two cases of acute myocardial infarction with ST-segment elevation in anterior precordial leads caused by such an RV involvement. Potential mechanisms for the relationship are given.