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G Helft

Publications and source records attributed to G Helft.

At least 19 recordsLinked to original sources
PubMed2006

[The best of thrombosis in 2005].

The year 2005 was rich in new information. Many articles were published on antithrombotic therapy, the key stone in the management of several cardiovascular diseases which are the cardiologists' "daily bread". Antithrombotic treatment is essential in the treatment of patients undergoing interventional coronary procedures. The loading dose of 300 mg clopidogrel has been questioned. The ARMYDA-2 trial showed that a loading dose of 600 mg of clopidogrel administered 4 to 8 hours before coronary angioplasty significantly reduced the number of peri-procedural myocardial infarctions without increasing the risk of bleeding complications. Other molecules such as prasugrel could provide an alternative to treatment with clopidogrel. The results of a phase 2 trial (JUMBO-TIMI 26) comparing clopidogrel and prasugrel have opened the way for a large scale phase 3 trial which is currently under way. In myocardial infarction, the CLARITY-TIMI 28 trial showed that patients under 75 years of age with acute myocardial infarction of less than 12 hours duration treated with aspirin and thrombolytic therapy had better results with respect to the combined criteria of patency of the culprit artery and ischaemic complications with the addition of clopidogrel. In the CREATE trial, patients with acute myocardial infarction had a lower mortality and recurrence of infarction without significantly increasing the risk of stroke with reviparin. The development of ximelagatran has been held up by a potentially serious hepato-toxicity. Two large-scale trials were published this year, one in atrial fibrillation and the other in venous thrombosis. In the former, the hypothesis of non-inferiority compared with well conducted oral anticoagulation with coumadine was supported and, in the latter, the hypothesis of non-inferiority compared with treatment with enoxaparin followed by warfarin was also confirmed despite a higher number of coronary events in the xinelagatran group. Another study which merits a citation showed that in patients with a previous history of aspirin-induced bleeding ulcers, the association of low dose aspirin and a proton pump inhibitor was superior to the prescription of clopidogrel in the prevention of recurrent bleeding. A study of the pharmacogenetics of coumadine and the variability of its dosage was also a valuable contribution. In the field of management of bleeding, a study demonstrated the potential benefits of treatment with VIIa recombinant factor.

Angioplasty, Balloon, Coronary↗
PubMed2006

[The value of active stents for coronary angioplasty in patients with chronic renal failure].

UNLABELLED: The risk of intra-stent restenosis has diminished considerably with the advent of endoprostheses which actively release sirolimus or paclitaxel. Patients with chronic renal failure constitute a high cardiovascular risk population, in whom the incidence of coronary heart disease is particularly high, representing one of the principal causes of death. The aim of this study, which included 152 patients, was to quantify the value of active stents for coronary angioplasty in patients with chronic renal failure. Thirty eight patients with chronic renal failure who underwent angioplasty with active stents were matched for age, sex and the presence of diabetes with 3 other groups of patients: one group with active stents but without renal failure, one group with inactive stents and no renal failure, and one group with inactive stents and chronic renal failure. The average follow up was 16 +/- 5 months. The acute stent thrombosis rate (2%) was not elevated in cases of renal failure nor after active stent implantation. Chronic renal failure significantly increased the mortality rate 16 months after angioplasty, whichever type of stent was used: 8 versus 2% deaths in patients with an inactive stent (p = 0.001). In renal failure, the risk of death was lower with an active stent (8 vs 26% with an inactive stent, p<0.05). Similarly, there was a non-significant trend towards a lower risk of death and/or infarction in renal failure after active stents (8 vs 21% with an inactive stent, NS). CONCLUSIONS: In this study, coronary angioplasty with an active stent in patients with chronic renal failure was associated with a lower mortality rate compared with inactive stents, with no increase in the risk of acute thrombosis.

Angioplasty, Balloon, Coronary↗
PubMed2005

[The best of thrombosis in 2004].

The optimal pharmacological antithrombotic treatment for interventional coronary procedures is a controversial subject. The ISAR-REACT trial investigated the necessity of a IIb/IIIa glycoprotein inhibitor in procedures not considered at high risk, that is to say excluding acute coronary syndromes, and concluded that there was no additional gain with this treatment compared with placebo when the patient was pre-treated with 600 mg of clopidogrel. The REPLACE-2 trial proposed an alternative to a treatment with NFH and IIb/IIIa glycoprotein inhibitor with the use of a direct antithrombin, bivalirudine. Heparin therapy of acute coronary syndromes and the eventual ensuing interventional coronary procedure may employ NFH or LMWH. New large scale trials (SYNERGY and phase A of the so-called A to Z trial) compared the two approaches and are reported later on. If facilitated angioplasty is a seductive concept, the best antithrombotic association remains to be determined (BRAVE trial). Bitherapy with a platelet inhibitor and an antithrombotic, ximegalatran, was tested in the ESTEEM trial and in the post-infarct period. Bitherapy with platelet inhibitors clopidogrel and aspirin versus clopidogrel alone was tested in patients with "ischaemic" stroke but does not seem to be more effective than monotherapy. In pulmonary embolism, the fondaparinux seems to be an alternative to NFH. Finally, the concept of resistance to platelet inhibitors is in vogue and is the subject of some interesting trials.

Angioplasty↗
PubMed2004

Cumulative adverse effects of diabetes mellitus and hypertension on coronary flow velocity reserve.

BACKGROUND: this study aimed to assess the hypothesis that essential hypertension (EH) may increase coronary microcirculation dysfunction in patients with type 2 diabetes mellitus (DM). Microvascular dysfunction has been reported in patients with DM or EH. Discordant results have been reported on cumulative adverse effects of the simultaneous presence of DM and EH on coronary flow velocity reserve (CFR). METHODS: CFR were compared in 13 hypertensive diabetics (group 1), 12 normotensive diabetics (group 2), 11 hypertensive non diabetics (group 3) and 29 normotensive non diabetic patients (group 4). CFR was calculated using an intracoronary Doppler-tipped flow wire. RESULTS: CFR was significantly lower in patients with both DM and EH (2.2 +/- 0.4 in group 1 vs 2.8 +/- 0.5, 2.8 +/- 0.6 and 2.9 +/- 0.7 in groups 2, 3 and 4 respectively, p<0.01). The presence of hypertension reduced CFR in diabetic patients with angiographically abnormal but unobstructed coronary arteries (2.1 +/- 0.3 in hypertensive vs 3.1 +/- 0.2 in normotensive diabetic patients, p<0.02). No cumulative adverse effect was observed in diabetics with angiographically normal coronary arteries (2.3 +/- 0.6 in hypertensive vs 2.6 +/- 0.5 in normotensive diabetic patients, NS). Multivariate analysis revealed that combination of DM and EH (p<0.007) was independently related to CFR. CONCLUSIONS: the presence of hypertension appears to worsen coronary microangiopathy in diabetic patients with unobstructed coronary artery disease. The cumulative effect of EH and DM on CFR impairment has consequences for decision-making during coronary angioplasty and could identify patients at risk for cardiomyopathy.

Blood Flow Velocity↗
PubMed2003

[Clopidogrel and thrombopenia. A case report].

We report our experience with a case of isolated profound thrombocytopenia after clopidogrel (thienopyridine) administration. No adverse event such as bleeding or thrombotic event had occurred, although clopidogrel has been discontinued two weeks after the coronary artery stenting. Despite the safety of clopidogrel, this case demonstrates that clopidogrel can be associated not only with thrombotic thrombocytopenic purpura but also with isolated thrombocytopenia.

Angioplasty, Balloon, Coronary↗
PubMed2003

Antistreptokinase platelet-activating antibodies are common and heterogeneous.

BACKGROUND: Platelet activation by antistreptokinase (SK) antibodies could impair the clinical effect of SK administration. OBJECTIVE: To better describe anti-SK antibodies with particular emphasis on procoagulant activities as a result of platelet activation. PATIENTS AND METHODS: Sera were collected from 146 patients with coronary artery disease: non-SK-treated, 95 from mainland France, 31 from French Polynesia; 20 patients from mainland in year 2 after SK treatment. Serum-induced SK-dependent platelet activation resulting in procoagulant activities was assessed with washed platelets from five donors representative of the known patterns of reactivities to IgG. RESULTS: Concentrations (2-5252 microg mL(-1)) and fibrinolytic neutralization titres (< 10 to > 1280) were found in the expected wide range and correlated (rho = 0.66, P < 0.0001). Platelet activation was detected with 145 samples, but varied in intensity and pattern (depending on the donors), although there was no systematic hierarchy; it was presumably due to IgG (inhibited by an IgG Fc receptor-blocking antibody and recovered in the IgG fraction) and only partially affected by aspirin. Marked platelet activation could be detected in samples with concentration as low as 2 microg mL(-1), and/or no detectable neutralizing titers. The way of immunization to SK was not found to influence the functional profile of antibodies. CONCLUSION: Anti-SK platelet-activating antibodies are widespread, heterogeneous, poorly predictable on the basis of their antifibrinolytic effect and strong enough to trigger procoagulant activities. Their clinical relevance should be formally assessed, using patients' own platelets for detection owing to the variation of platelet reactivity.

Adult↗
PubMed2003

Myocardial viability, coronary flow reserve, and in-hospital predictors of late recovery of contractility following successful primary stenting for acute myocardial infarction.

OBJECTIVE: To assess the relation between myocardial viability, coronary flow reserve, and recovery of myocardial contractility after stenting for acute myocardial infarction. DESIGN: Consecutive sample prospective study. SETTING: University hospital. PATIENTS: 41 patients with single vessel disease and successful primary stenting for a first acute myocardial infarction. INTERVENTIONS: (201)Tl single photon emission computed tomography, contrast ventriculography, and intracoronary Doppler performed 7 (1) days after primary stenting. MAIN OUTCOME MEASURES: Regional contractility recovery assessed by contrast ventriculography at 6 (1) months' follow up. RESULTS: On univariate analysis, contractility recovery was correlated to prereperfusion anterograde and collateral flow grades (r = 0.41, p = 0.03 and r = 0.55, p = 0.0004), viability index (r = 0.55, p = 0.04), peak creatine kinase concentrations (r = -0.55, p = 0.0005), left ventricular ejection fraction (r = 0.45, p = 0.005), end diastolic pressure (r = -0.62, p < 0.0001), end systolic volume index (r = -0.47, p = 0.01), and the extent of hypokinetic area (r = -0.48, p = 0.003), but not the coronary flow reserve. On multivariate analysis, independent predictors of late contractility recovery were prereperfusion anterograde and collateral flow grades and viability index. Relative coronary flow reserve, reflecting the culprit vessel's microvascular function, was correlated only to the extent of the infarct risk area (r = -0.45, p = 0.003). CONCLUSIONS: Independent predictors of contractility recovery between the seventh day and the sixth month after successful stenting for acute myocardial infarction are prereperfusion anterograde and collateral flows and myocardial viability. The culprit vessel's microvascular dysfunction is independent of myocardial viability and contractility and correlated to the extent of "jeopardised microvasculature".

Catheterization↗
PubMed2003

[Absence of nephro-protective effect of acetylcysteine in patients with chronic renal failure investigated by coronary angiography].

Recent studies have suggested that an oral dose of acetylcysteine could play a prophylactic role in the prevention of nephrotoxicity from iodine contrast media in patients affected by chronic renal failure. Between June 2001 and September 2002 we selected 120 patients with a basal plasma creatinine level greater than 1.36 mg/dl investigated by coronary angiography. The treatment group included 60 patients who received 600 mg of acetylcysteine in the morning and evening before the day of the examination together with intravenous saline hydration. The control group patients received hydration alone. The clinical characteristics of the groups were comparable as well as the basal plasma creatinine level: 2.01+/-1.1 mg/dl in the acetylcysteine group and 1.81+/-0.69 in the control group. The plasma creatinine level was measured 24 and 48 hours after coronary angiography. The respective changes in plasma creatinine level at 24 and 48 hours were 0.12+/-0.29 and 0.02+/-0.29 mg/dl in the acetylcysteine group and 0.06+/-0.29 and 0.07+/-0.43 mg/dl in the control group (NS). Acute renal failure caused by the contrast medium, defined by an increase of 25% in the plasma creatinine level compared to the basal value, occurred in 3 patients from the acetylcysteine group and 2 patients from the control group. The only predictive factor for acute renal failure was the quantity of contrast medium (316+/-141 vs 173+/-115 ml, p<0.05). In conclusion, acute renal failure caused by contrast medium is rare in sufficiently hydrated patients with moderate chronic renal failure when a low dose of contrast medium is used. Our study does not confirm a prophylactic effect of acetylcysteine in the prevention of nephrotoxicity from contrast media following coronary angiography in patients with moderate chronic renal failure.

Acetylcysteine↗
PubMed2002

[Value of combined coronary angioplasty and coronary angiography].

Combined coronary angioplasty and coronary angiography is performed in most catheter laboratories and has become a routine procedure. The aim of this study was to assess its clinical results and economic value. This was a retrospective monocenter study performed over an 11 year period (1990-2000) which included 2,727 patients requiring coronary angioplasty after coronary angiography. The angioplasty procedure was performed at the same time as angiography (combined, n = 1,809) or after angiography (deferred, n = 631). Patients admitted for acute coronary syndromes not stabilised by pharmacological interventions were excluded from the study. The comparison of these two modes of angioplasty was based on primary success rates, complications, duration of hospital stay and hospital costs. The combined procedure was used progressively more frequently over the study period, increasing from 54% to 88% in 2000. The hospital clinical results (Success and complication rates) were comparable in the two groups. The predictive factors of failure were the year of the angioplasty procedure and occlusive lesions on multivariate analysis. The combined procedure was associated with a shorter hospital stay than deferred angioplasty (8.2 +/- 6.1 days versus 15.0 +/- 8.0 days, p = 0.0001) and with lower costs. The authors conclude that combined coronary angiography-angioplasty is as effective and as safe as deferred angioplasty. It is associated with a shorter hospital stay and lower hospital costs.

Aged↗
PubMed2002

[Mediastinal tumor revealed by myocardial infarction].

We report the case of a patient with a past history of coronary atherosclerosis treated with primary angioplasty 5 hours following an inferior myocardial infarction. Echocardiography performed during the procedure revealed a mediastinal tumour invading the tricuspid, responsible for the occlusion of the right coronary. Infarction due to tumour compression is a rare presentation of mediastinal tumour. Diagnosis relies on echocardiographic, CT or magnetic resonance imaging. The prognosis is linked to the tumour pathology.

Coronary Artery Disease↗
PubMed2001

Effects of lipid-lowering by simvastatin on human atherosclerotic lesions: a longitudinal study by high-resolution, noninvasive magnetic resonance imaging.

BACKGROUND: This study was designed to investigate the effects of lipid-lowering by simvastatin on human atherosclerotic lesions. METHODS AND RESULTS: Eighteen asymptomatic hypercholesterolemic patients with documented aortic and/or carotid atherosclerotic plaques were selected for the study. A total of 35 aortic and 25 carotid artery plaques were detected. Serial black-blood MRI of the aorta and carotid artery of the patients was performed at baseline and 6 and 12 months after lipid-lowering therapy with simvastatin. The effects of the treatment on atherosclerotic lesions were measured as changes in lumen area, vessel wall thickness, and vessel wall area, a surrogate of atherosclerotic burden. Simvastatin induced a significant (P<0.01) reduction in total and LDL cholesterol levels at 6 weeks that was maintained thereafter. At 6 months, no changes in lumen area, vessel wall thickness, or vessel wall area were observed. However, at 12 months, significant reductions in vessel wall thickness and vessel wall area, without changes in lumen area, were observed in both aortic and carotid arteries (P<0.001). CONCLUSIONS: This in vivo human study demonstrates that effective and maintained lipid-lowering therapy by simvastatin is associated with a significant regression of atherosclerotic lesions. Our observation suggests that statins induce vascular remodeling, as manifested by reduced atherosclerotic burden without changes in the lumen.

Aorta↗
PubMed2001

Atherosclerotic aortic component quantification by noninvasive magnetic resonance imaging: an in vivo study in rabbits.

OBJECTIVES: We sought to demonstrate the ability that noninvasive in vivo magnetic resonance imaging (MRI) has to quantify the different components within atherosclerotic plaque. BACKGROUND: Atherosclerotic plaque composition plays a critical role in both lesion stability and subsequent thrombogenicity. Noninvasive MRI is a promising tool for the characterization of plaque composition. METHOD: Thoracic and abdominal aortic atherosclerotic lesions were induced in rabbits (n = 5). Nine months later, MRI was performed in a 1.5T system. Fast spin-echo sequences (proton density-weighted and T2-weighted [T2W] images) were obtained (in-plane resolution: 350 x 350 microns, slice thickness: 3 mm). Magnetic resonance images were correlated with matched histopathological sections (n = 108). RESULTS: A significant correlation (p < 0.001) was observed for mean wall thickness and vessel wall area between MRI and histopathology (r = 0.87 and r = 0.85, respectively). The correlation was also present on subanalysis of the thoracic and upper part of the abdominal aorta, susceptible to respiratory motion artifacts. There was a significant correlation for plaque composition (p < 0.05) between MRI and histopathology for the analysis of lipidic (low signal on T2W, r = 0.81) and fibrous (high signal on T2W, r = 0.86) areas with Oil Red O staining. T2-weighted images showed greater contrast than proton density-weighted between these different components of the plaques as assessed by signal intensity ratio analysis with the mean difference in signal ratios of 0.47 (S.E. 0.012, adjusted for clustering of observations within lesions) being significantly different from 0 (t1 = 39.1, p = 0.016). CONCLUSIONS: In vivo noninvasive high resolution MRI accurately quantifies fibrotic and lipidic components of atherosclerosis in this model. This may permit the serial analysis of therapeutic strategies on atherosclerotic plaque stabilization.

Animals↗
PubMed2001

Cardiac gated breath-hold black blood MRI of the coronary artery wall: an in vivo and ex vivo comparison.

BACKGROUND: High resolution magnetic resonance (MR) imaging of the coronary artery wall in vivo has been limited by the cardiac and respiratory motion, flow artifacts as well as the relatively small size of the coronary arteries. We sought to validate in vivo black blood MR imaging of the coronary artery wall using a double inversion recovery fast spin echo MR imaging sequence with limited breath-holding and cardiac gating for suppression of motion artifacts by comparison with ex vivo MR imaging. METHODS: Yorkshire albino swine (n = 6) were used in this study and coronary lesions were induced with balloon angioplasty. Four weeks after balloon injury of the coronary arteries MR imaging of the coronary artery lesions was performed. High resolution in vivo and ex vivo images of the coronary artery wall and lesions were obtained using a double inversion recovery fast spin echo sequence in a 1.5 T MR system. There was a statistically significant agreement (p < 0.0001) between measurements of vessel wall area (r = 0.87, slope = 0.87) and maximal wall thickness (r = 0.84, slope = 0.88) from in vivo and ex vivo MR images of the coronary arteries. The mean differences between in vivo and ex vivo measurements were 0.56 +/- 1.98 mm2 for vessel wall area and 0.02 +/- 0.36 mm for maximal wall thickness. CONCLUSIONS: Using breathholding and cardiac gating, it is possible to perform high resolution MR imaging of the coronary artery wall in vivo with good suppression of motion artifacts with a double inversion recovery fast spin echo black blood imaging sequence.

Animals↗
PubMed2001

Anti-thrombotic, anti-platelet and fibrinolytic therapy: current management of acute myocardial infarction.

Significant advances in the treatment of patients with acute myocardial infarction (MI) have been obtained in recent times. In particular, thrombolytic therapy has been shown to preserve ventricular function and improve survival in patients with acute MI. Therapies now include third-generation thrombolytic agents, percutaneous transluminal coronary angioplasty (PTCA) and intracoronary stenting, and new anti-thrombotic therapies including anti-platelet treatment with glycoprotein (GP) IIb/IIIa inhibition and direct anti-thrombin agents. This review will focus on the use of GP IIb/IIIa antagonists and thrombin inhibitors as adjunctive therapies to thrombolytic treatment of patients with acute MI.

Journal Article↗
PubMed2001

Clinical outcome following coronary angioplasty in dialysis patients: a case-control study in the era of coronary stenting.

BACKGROUND: Balloon coronary angioplasty has been reported to be ineffective in patients treated for end stage renal disease because of a high restenosis rate. OBJECTIVE: To compare the clinical outcome following coronary angioplasty with provisional stenting in dialysis versus non-dialysis patients. DESIGN: A case-control study. PATIENTS: Of 1428 consecutive patients who underwent coronary angioplasty, 100 (7%) were being treated for end stage renal disease. These were compared with 100 control patients matched for age, sex, coronary lesions, presence of diabetes mellitus, and rate of coronary stenting (40%). MAIN OUTCOME MEASURES: In-hospital and one year clinical outcome. RESULTS: The rates of procedural success (90% v 93%), in-hospital mortality (1% v 0%), stent thrombosis (0% v 0%), and Q wave myocardial infarction (0% v 1%) were similar in dialysis and non-dialysis patients. One year clinical outcome after coronary angioplasty was similar in the two groups in terms of clinical restenosis (31% v 28%) and myocardial infarction (6% v 2%), but cardiac death was more common in dialysed patients (11% v 2%, p < 0.03). CONCLUSIONS: Dialysis does not increase the risk of clinical restenosis after coronary angioplasty with provisional stenting. Coronary angioplasty is a safe and effective therapeutic procedure in selected dialysis patients with culprit lesions accessible to stenting. However, the one year survival is reduced in this high risk population.

Adult↗
PubMed2001

Coronary artery disease: pathogenesis and acute coronary syndromes.

Atherosclerotic diseases and their thrombotic complications remain the leading causes of mortality and morbidity in Western society. In the United States, cardiovascular disease is responsible for one in every 2.4 (41.4%) deaths and is the leading single cause of mortality. Furthermore, the presence of atherosclerotic disease (defined as thickening of the arterial wall through the accumulation of lipids, macrophages, T-lymphocytes, smooth muscle cells, extracellular matrix, calcium and necrotic debris) is more prevalent, but by itself rarely fatal. The crucial, final common process for the conversion of a nonocclusive, often clinically silent atherosclerotic lesion to a potentially fatal condition is often plaque disruption. The mortality associated with atherosclerotic disease relates to the acute coronary syndromes, including acute myocardial infarction, unstable angina pectoris and sudden cardiac death. Substantial clinical, experimental and postmortem evidence demonstrates the central role that a superimposed acute thrombosis on a disrupted atherosclerotic plaque plays in the onset of acute coronary syndromes. Therefore, therapeutic approaches to date have focused on reducing such thrombotic complications of atherosclerotic plaques (i.e., antiplatelet, anticoagulant and thrombolytic therapies) to reduce the resulting morbidity and mortality. In this review, we will focus on the current theories of atherogenesis and how they impact on our understanding of acute coronary syndromes.

Chemokines↗