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Despite significant advances in therapeutic methods over the decades, Heart Failure (HF) remains today a major public health problem with a significant economic burden. HF is currently the leading cause of hospitalization in people older than 65 years with still high early post-discharge readmission rates. The present thesis was conducted to develop new management strategies to improve HF prognosis and reduce its economic burden. In a first step, we built a new individualized dynamic non-invasive automated and autonomous alert triggering system for early detection and early preventive therapeutic intervention of HF deterioration which performed better than the previous systems. In a second step, we showed that traditional health status measures of morbidity and mortality and quality-of-life health status measures provide additive information in defining HF prognosis. Both health instruments should now be used together to assess health in a global perspective for HF patients., (MED - Sciences médicales) -- UCL, 2018

Purpose: Heart failure (HF) is a complex syndrome. Its appropriate management should combine several health measurements. We assessed the relationship between the Kansas City Cardiomyopathy Questionnaire (KCCQ) and the Pocock’s clinical score. // Methods: We conducted a prospective registry of HF outpatients. The main outcome was occurrence of death or hospitalization during a 6-month follow-up. A multivariate logistic regression was performed, including the KCCQ overall summary score, the Pocock’s clinical score and their interaction in the model. // Results : From January 2008 to December 2010, 143 patients were involved. Mean age of patients was 68 years, and 74 % were men. KCCQ’s overall summary score and Pocock’s clinical score were inversely correlated (r = −0.24, p = 0.026). A total of 61 (42.7 %) events occurred. There was a high proportion of events (77.8 %) in patients with a Pocock’s clinical score >50 %, whatever the KCCQ score value. When the KCCQ score was ≤50 %, there was a low increase in risk as the Pocock’s clinical score increased (OR 2.0 [0.6; 6.6]). However, when the KCCQ score was between 50 and 75 or ≥75 %, there was a high increase in risk as the Pocock’s clinical score increased (OR 6.9 [1.2; 38.9] and OR 7.4 [0.8; 69.7], respectively). // Conclusions : Patients with a high Pocock’s clinical score are at a high risk of death or hospitalization. For patients with a low Pocock’s clinical score, the KCCQ score can identify those at risk of these events.

Background-In the Superior Yield of the New Strategy of Enoxaparin, Revascularization, and Glycoprotein IIb/IIIa Inhibitors (SYNERGY) study, patients assigned enoxaparin or unfractionated heparin (UFH) were treated with alternative anticoagulant therapy after randomization at physician discretion, a practice made possible because the trial was open label. Using SYNERGY as an example, we demonstrate the difficulty of evaluating the effect of postrandomization events in clinical trials and discuss possible methodology. Methods and Results-Patients with and without postrandomization crossovers were characterized and event rates analyzed. Statistical modeling was performed using inverse probability weighting and landmark analyses to evaluate the potential impact of postrandomization crossovers on event rates and treatment effect. Of 9978 SYNERGY patients, 9613 (96.3%) received at least 1 dose of randomized therapy and are included in these analyses. Of these, 740 (7.7%; 554 enoxaparin; 186 UFH) had postrandomization crossover. Crossover patients had higher unadjusted rates of 30-day death/myocardial infarction (MI) (18.9% versus 14.0%), thrombolysis in MI (TIMI) bleeding (16.9% versus 7.6%), Global Use of Strategies to Open Occluded Coronary Arteries bleeding (4.5% versus 2.3%), and transfusions (32.3% versus 15.2%). Adjustment for timing of crossover relative to the events attenuated the difference noted in death/MI but accentuated the association with TIMI bleeding. After adjustment using the inverse probability weighting technique, only a modest difference in the absolute treatment effect was observed between enoxaparin and UFH on death/MI (0.6% [unadjusted] versus 0.8% [adjusted]) and TIMI major bleeding (1.5% [unadjusted] versus 1.0% [adjusted]). The landmark analysis indicated a significant association between crossover from enoxaparin to UFH and TIMI bleeding but not in the other direction, and no crossover association was found in death/MI. Conclusions-Postrando

Background: Obese patients are at increased risk of acute coronary syndromes (ACS). We evaluated the prevalence of obesity in a large ACS population, as well as the relationship between body mass index (BMI) and the use of cardiac medications and procedures, clinical outcomes, and treatment effects between enoxaparin and unfractionated heparin (UFH). Methods: Using the database of the SYNERGY trial, we identified 9978 patients in 12 countries who were randomly assigned to receive enoxaparin or UFH. Patient weight at baseline and 30-day follow-up was recorded. BMI information was available on 9837 patients. BMI was analyzed in clinically meaningful categories (<20, 20-25, 30-35, >= 35 kg/m(2)) and as a continuous variable. Results: Thirty-two percent of patients were obese ( BMI >= 30), with a greater proportion of patients with obesity from North America (36%) compared with other regions. Enoxaparin was dosed as 1 mg/kg regardless of body weight without maximum. The first dose of enoxaparin was underdosed in 15% of patients assigned enoxaparin, and obese patients were more likely to be underdosed than non-obese patients. Obese patients were younger, less often white, had more diabetes, hypertension, hyperlipidemia, family history of coronary artery disease, and congestive heart failure but fewer strokes, less peripheral vascular disease, and less often smoked. After adjustment, increased BMI was not an independent predictor of bleeding outcomes or 30-day death/myocardial infarction (MI), but increased BMI was predictive of lower 1-year mortality in the subgroup of patients with BMI at baseline below approximately 30 kg/m(2). No statistical interaction term was observed between obesity and randomized therapy for the outcomes of death/MI at 30 days and 6 months; death at 30 days, 6 months, and 1 year; and GUSTO or TIMI bleeding. Conclusions: Nearly one third of patients in SYNERGY were obese. Despite multiple comorbidities, obese patients had better unadjusted short

Background: Chronic kidney disease (CKD) is a risk factor for coronary heart disease and bleeding with antithrombotic therapy in patients with acute coronary syndromes (ACS). We evaluated the effect of renal function on efficacy and outcomes in high-risk patients with NSTE ACS in the SYNERGY trial. Methods: Creatinine clearance (CrCl) at the time of randomization was analyzed as a continuous variable added to multivariable logistic regression models for 30-day death or MI, non-CABG-associated TIMI major bleeding, GUSTO severe bleeding, and transfusion in the overall study population, patients undergoing coronary angiography, and patients undergoing PCI. Results: Of 9838 patients with a CrCl value, 70.6% (N = 6950) had CrCl >= 60 mL/min, 27.8% (N = 2732) had CrCl 30-59 mL/min, and 1.6% (N = 156) had CrCl<30 mL/min. No randomized treatment by CrCl interaction test was found to be statistically significant, suggesting renal insufficiency affected enoxaparin and unfractionated heparin outcomes similarly. After adjustment, CrCl was an independent predictor of 30-day death or MI (OR 1.06, 95% CI 1.03-1.09), TIMI major bleeding (OR 1.06, 95% CI 1.02-1.10), GUSTO severe bleeding (OR 1.10, 95% CI 1.03-1.17), and transfusion (OR 1.07, 95% CI 1.04-1.11). Conclusions: Patients with CKD had higher rates of 30-day death or MI and bleeding than those without CKD, regardless of randomized antithrombin therapy. While this analysis suggests that there is a rise in bleeding events as CrCl falls for patients in either treatment group, it is unknown whether a reduction in dose would decrease bleeding risk. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

Myocardial infarction often develops when thrombosis occurs at lesions that have not previously been flow limiting. However, the development of cardiogenic shock complicating acute myocardial infarction in such circumstances has received little attention. The characteristics of 15 patients with cardiogenic shock who had no flow-limiting angiographic stenoses were compared with those of 767 patients with >= 1 stenosis who were enrolled in the Should We Emergently Revascularize Occluded Coronary Arteries for Cardiogenic Shock (SHOCK) trial and registry. Compared with patients with 1 flow-limiting stenosis, patients with no flow-limiting stenoses were less likely to have pulmonary edema on chest x-ray (29% vs 62%, p = 0.008) and to be white (53% vs 82%, p = 0.011), and they had lower median highest creatine kinase levels (702 vs 2,731 U/L, p = 0.018). For SHOCK trial patients, 1-year survival was 49% for patients with >= 1 flow-limiting stenosis and 71% for those with no flow-limiting stenoses (p = 0.268). In conclusion, patients with cardiogenic shock without flow-limiting stenosis have different characteristics, and potentially disease mechanisms, and they do not require revascularization. (c) 2009 Elsevier Inc. (Am J Cardiol 2009;104:24-28)

Background Non-steroidal anti-inflammatory drugs (NSAIDs) may be prothrombotic, may worsen hypertension or congestive heart failure and obstruct access to the binding site of aspirin to cyclooxygenase-1 and thereby interfere with aspirin's mechanism of action in reducing death and recurrent myocardial infarction (MI). We hypothesized that treatment with NSAIDs prior to an index MI would be associated with an increase in the risk of death, heart failure and recurrent MI among patients with ST-segment elevation MI (STEMI) treated with fibrinolytic therapy. Methods In ExTRACT-TIMI 25, patients with STEMI were treated with aspirin and fibrinolytic therapy and randomized to either enoxaparin or unfractionated heparin. We included patients who had received NSAIDs within 7 days of enrollment and evaluated the incidence of MI, the composite of death and MI and the composite of death, MI, severe heart failure and shock through 30 days. Results Of 20,479 patients enrolled, 572 (2.8%) received an NSAID within 7 days of enrollment. NSAID treatment prior to entry was associated with a higher incidence of 30-day death or nonfatal recurrent MI (15.9% vs. 10.8%, univariate P < 0.001). In multivariable models adjusting for randomization group and differences in baseline characteristics, NSAID use was associated with higher odds of MI (adjusted odds ratio [ORadj] 1.44, 95% confidence interval [CI] 1.01-2.07, P = 0.047), the composite of death and MI (ORadj 1.29, 95% CI 1.00-1.66, P = 0.051), and the composite of death, MI, severe heart failure and shock (ORadj 1.29, 95% CI 1.02-1.65, P = 0.037). Conclusions Among STEMI patients treated with a fibrinolytic agent and aspirin, use of NSAIDs in the week preceding the incident event was associated with a higher incidence of MI, the composite of death and MI as well as the composite of death, MI, severe heart failure and shock at 30 days.

Aims Elderly patients are at high risk from non-ST-segment elevation acute coronary syndromes (NSTE ACS) as well as from treatment-related complications. Age-associated changes in physiology may alter the risk and benefit expected from therapy. The SYNERGY database was used to study the influence of age on treatment outcomes with enoxaparin vs. unfractionated heparin (UFH) in patients with high-risk NSTE ACS. Methods and results Age was analysed as a continuous and categorical variable (< 65, 65-74, and >= 75 years, and < 75 and >= 75 years) for descriptive purposes. Logistic regression was used to adjust the outcomes of 30-day death, death or myocardial infarction (MI), and major bleeding for baseline characteristics. Odds ratios compared outcomes by age and by treatment within age groups. Model interaction terms were used to test for statistically different outcomes by treatment and age. Overall, 9977 randomized patients had age information, of whom 25.5% (2540) were >= 75 years of age. Elderly patients (>= 75 years) had more cardiovascular risk factors, prior cardiac disease, and higher acuity at presentation. After adjustment, advanced age (per 10 years) was associated with 30-day death or MI [risk odds ratios (ROR): 1.14, P = 0.002], 30-day death (ROR: 1.54, P < 0.0001), and 1-year death (ROR: 1.47, P < 0.0001), as well with TIMI major bleeding (ROR: 1.21, P = 0.001), GUSTO severe bleeding (ROR: 1.20, P = 0.047), and transfusion (ROR: 1.04, P = 0.324). Although there was a higher rate of GUSTO severe bleeding noted with enoxaparin in elderly patients, the overall relationships between treatment (UFH or enoxaparin) and outcomes did not vary significantly as a function of the patient's age. Conclusion Although higher rates of adverse events are seen in the oldest subgroup (age >= 75 years) treated with enoxaparin, statistical comparisons confirm similar efficacy and safety of enoxaparin and UFH across age subgroups as was demonstrated overall in SYNERGY.

BACKGROUND: Despite advances in pharmacologic therapy and invasive management strategies for patients with non-ST-segment elevation acute coronary syndromes (NSTE ACS), these patients still suffer substantial morbidity and mortality. OBJECTIVE: The objective of this study was to analyze independent predictors of 1-year mortality in patients with high-risk NSTE ACS. DESIGN AND PARTICIPANTS: A total of 9,978 patients were assigned to receive enoxaparin or unfractionated heparin (UFH) in this prospective, randomized, open-label, international trial. MEASUREMENTS: Vital status at 1 year was collected. Univariable and multivariable predictors of 1-year mortality were identified. Three different multivariable regression models were constructed to identify: (1) predictors of 30-day mortality; (2) predictors of 1-year mortality; (3) predictors of 1-year mortality in 30-day survivors. The last model is the focus of this paper. RESULTS: Overall, 9,922 (99.4%) of patients had 1-year follow-up. Of the 56 patients (37 UFH-assigned and 19 enoxaparin-assigned) without 1-year data, 11 patients were excluded because of withdrawal of consent, and 45 could not be located. One-year mortality was 7.5% (7.7% enoxaparin-assigned patients; 7.3% UFH-assigned patients; P=0.4). In patients surviving 30 days after enrollment, independent predictors of 1-year mortality included factors known at baseline such as increased age, male sex, decreased weight, having ever smoked, decreased creatinine clearance, ST-segment depression, history of diabetes, history of angina, congestive heart failure, coronary artery bypass grafting, increased heart rate, rales, increased hematocrit, lowered hemoglobin, and higher platelet count. Factors predictive of mortality during the hospitalization and 30-day follow-up period were decreased weight at 30 days from baseline, atrial fibrillation, decreased nadir platelet, no use of beta-blockers and statins up to 30 days, and not receiving an intervention (c-index=0.8

OBJECTIVES The purpose of this study was to compare the effect of receiving pretreatment with antithrombin before randomization as well as overall efficacy and safety of enoxaparin versus unfractionated heparin (UFH) in the SYNERGY (Superior Yield of the New Strategy of Enoxaparin, Revascularization, and Glycoprotein IIb/IIIa Inhibitors) trial. BACKGROUND The SYNERGY trial results demonstrated noninferiority in outcomes with enoxaparin compared with UFH. Randomized treatment was independent of prerandornization treatment. METHODS Analyses were first performed on the 4 prerandomization subgroups: patients who received no antithrombin therapy and those who were treated with enoxaparin or UFH or both. Then, we focused on the subgroup of patients who received no pretreatment or were pretreated with and randomized to the same drug. Of the 9,978 patients, 2,440 did not receive prerandomization therapy and 6,138 received consistent therapy through randomization. The primary end point was the composite of death and nonfatal myocardial infarction (MI) at 30 days. RESULTS After adjustment for differences among the subgroups, no significant difference in the association between the 4 pretreatment groups and death or MI remained (p = 0.171). The randomized treatment effect on 30-day death or MI tended to vary with pretreatment (p = 0.055 for interaction test after adjustment). Patients who received consistent therapy with enoxaparin had significantly less death or MI than patients randomized to UFH (adjusted p = 0.041) with a trend toward increased bleeding. CONCLUSIONS Treatment with antithrombin therapy before randomization had potential impact on comparison of study drug effects. After adjustment for differences in baseline characteristics between subgroups, consistent therapy with enoxaparin might be superior to UFH in reducing death or nonfatal MI, with a modest excess in bleeding.

Context Cardiogenic shock remains the major cause of death for patients hospitalized with acute myocardial infarction (MI). Although survival in patients with cardiogenic shock complicating acute MI has been shown to be significantly higher at 1 year in those receiving early revascularization vs initial medical stabilization, data demonstrating long-term survival are lacking. Objective To determine if early revascularization affects long-term survival of patients with cardiogenic shock complicating acute MI. Design, Setting, and Patients The Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock ( SHOCK) trial, an international randomized clinical trial enrolling 302 patients from April 1993 through November 1998 with acute myocardial infarction complicated by cardiogenic shock ( mean [SD] age at randomization, 66 [ 11] years); long-term follow-up of vital status, conducted annually until 2005, ranged from 1 to 11 years ( median for survivors, 6 years). Main Outcome Measures All-cause mortality during long-term follow-up. Results The group difference in survival of 13 absolute percentage points at 1 year favoring those assigned to early revascularization remained stable at 3 and 6 years (13.1% and 13.2%, respectively; hazard ratio [HR], 0.74; 95% confidence interval [CI], 0.57-0.97; log-rank P=. 03). At 6 years, overall survival rates were 32.8% and 19.6% in the early revascularization and initial medical stabilization groups, respectively. Among the 143 hospital survivors, a group difference in survival also was observed ( HR, 0.59; 95% CI, 0.36-0.95; P=. 03). The 6-year survival rates for the hospital survivors were 62.4% vs 44.4% for the early revascularization and initial medical stabilization groups, respectively, with annualized death rates of 8.3% vs 14.3% and, for the 1-year survivors, 8.0% vs 10.7%. There was no significant interaction between any subgroup and treatment effect. Conclusions In this randomized trial, almost two thirds of

OBJECTIVE: To describe the use of volumetric capnography, a plot of expired CO(2) concentration against expired volume, in monitoring fibrinolytic treatment of major pulmonary embolism. DESIGN AND SETTING: Two case reports in the emergency department of a teaching hospital. PATIENTS: Two conscious and spontaneously breathing patients (69- and 31-year-old women) with major pulmonary embolism requiring thrombolysis. Decision for thrombolysis was based on the association of right ventricular afterload on echocardiography, with respiratory failure and hypotension in the first patient, and dyspnea and hemodynamically stable parameters in the second one. INTERVENTIONS: Successive capnographic measurements were performed before, during, and after thrombolysis. Curves of volumetric capnography were obtained from a sidestream gas monitor with flow sensor and an arterial blood gas analysis for CO(2) partial pressure. MEASUREMENTS AND RESULTS: We calculated late deadspace fraction, previously suggested as the most effective capnographic parameter in the diagnosis of pulmonary embolism. Late deadspace fraction decreased in the two patients, respectively, from 64.4% to 1.1% and from 25.6% to 5.7% after thrombolysis, with a concomitant disappearance of right heart dysfunction signs on echocardiography. CONCLUSIONS: Volumetric capnography can monitor thrombolysis in major pulmonary embolism. Differences between volumetric capnography technology and the more traditional arterial to end-tidal CO(2) gradient are important to take into account for clinical application.

Enoxaparin has demonstrated advantages over unfractionated heparin in low- to moderate-risk patients with non-ST-segment elevation acute coronary syndromes (ACS) treated with a conservative strategy. To compare the outcomes of patients treated with enoxaparin vs unfractionated heparin and to define the role of enoxaparin in patients with non-ST-segment elevation ACS at high risk for ischemic cardiac complications managed with an early invasive approach. The Superior Yield of the New Strategy of Enoxaparin, Revascularization and Glycoprotein IIb/IIIa Inhibitors (SYNERGY) trial was a prospective, randomized, open-label, multicenter, international trial conducted between August 2001 and December 2003. A total of 10 027 high-risk patients with non-ST-segment elevation ACS to be treated with an intended early invasive strategy were recruited. Subcutaneous enoxaparin (n = 4993) or intravenous unfractionated heparin (n = 4985) was to be administered immediately after enrollment and continued until the patient required no further anticoagulation, as judged by the treating physician. The primary efficacy outcome was the composite clinical end point of all-cause death or nonfatal myocardial infarction during the first 30 days after randomization. The primary safety outcome was major bleeding or stroke. The primary end point occurred in 14.0% (696/4993) of patients assigned to enoxaparin and 14.5% (722/4985) of patients assigned to unfractionated heparin (odds ratio [OR], 0.96; 95% confidence interval [CI], 0.86-1.06). No differences in ischemic events during percutaneous coronary intervention (PCI) were observed between enoxaparin and unfractionated heparin groups, respectively, including similar rates of abrupt closure (31/2321 [1.3%] vs 40/2364 [1.7%]), threatened abrupt closure (25/2321 [1.1%] vs 24/2363 [1.0%]), unsuccessful PCI (81/2281 [3.6%] vs 79/2328 [3.4%]), or emergency coronary artery bypass graft surgery (6/2323 [0.3%] vs 8/2363 [0.3%]). More bleeding was observe

BACKGROUND: Quantification of fibrinolytic activity (FAct) in clinical practice has been abandoned because of the complexity of existing assays. The relationship between thrombolytic drug concentration and FAct is complex. FAct profiles of currently used thrombolytic drugs were not characterized. METHODS: By use of a system that quantifies FAct by shortening of clot lysis onset time (LOT), we measured LOT in vitro with incremented concentrations of alteplase (t-PA) and tenecteplase (TNK-tPA) and ex vivo in patients with acute myocardial infarction who were receiving front-loaded t-PA (n = 31), 30 to 40 mg TNK-tPA (n = 19), and 120 kU/kg lanoteplase ([n-PA] n = 23). RESULTS: In vitro, FAct depended on drug concentration by means of a double exponential model revealing 2 distinct activity zones (weak/strong). Ex vivo, no FAct was detected before agent administration (LOT > 1200 seconds). Ten minutes after a bolus was given, FAct was sharply increased in all patients, but it increased more with TNK-tPA than with t-PA or n-PA (mean LOT of 109, 125, and 130 seconds, respectively, P <.05). At 90 minutes, accelerated infusion of t-PA resulted in FAct that remained stronger than that observed for TNK-tPA (P <.0001) or n-PA (P =.011). At 180-minutes, significant FAct (LOT <600 seconds) was only observed in patients who received n-PA. CONCLUSION: This study provides the first direct comparison of FAct between t-PA, TNK-tPA, and n-PA by use of the LOT test, the results of which are reliably related to drug concentration. The ideal FAct profile would combine an immediate strong FAct of relatively short duration, as seen with TNK-tPA, that may contribute to its better efficacy/safety profile in the Assessment of Safety and Efficacy of a New Thrombolytic Agent-2 (ASSENT-2) trial. Prolonged FAct after n-PA may contribute to increased hemorrhagic complications, as seen in the Intravenous n-PA for Treatment of Infarcting Myocardium Early-2 (InTIME-2) trial. Thus, characterizing FAct

A new bedside lytic assay using dry reagent technology for rapid (3-5 min) detection of streptokinase resistance (SKR) was recently introduced, which measures lysis onset time (LOT) of whole blood clot in response to high and low streptokinase (SK) concentrations: 100 U/ml (SK100) and 10 U/ml (SK10). SKR was defined by prolongation of LOT, previously correlated with the standard SK Reactivity Test and with clinical outcome of acute myocardial infarction (AMI) SK-treated patients, high SKR when SK100>50 seconds and SK10>120 seconds; partial SKR when SK10>120 seconds. Five prospective clinical groups (325 patients) were screened in cardiac units of four university hospitals, In patients previously treated with SK, the prevalence of SKR was 87% (70% high, 17% partial); in those who had documented streptococcal infection, 92% (75% high, 17% partial); and in patients with rheumatic heart disease, 76% (all high). SKR prevalence was 55% (33% high, 22% partial) in those with recent respiratory tract infection. In 225 acute coronary patients, SKR was 28% (21% high, 7% partial), and was identical by gender, but was 36% (32% high, 4% partial) in patients greater than or equal to 65 years Versus 19% (9% high, 10% partial) in those < 65 years (P < 0.0001). In conclusion, we demonstrated (with a rapid functional assay) the consistence of our results with the expected prevalence of SKR in the groups studied, this points out to the feasibility of pre-therapeutic detection of SKR and choice between t-PA and SK made at bedside without delaying the onset of treatment. As SKR is common among candidates for thrombolysis, pre-therapeutic detection of SKR merits further investigation. (C) 2000 Harcourt Publishers Ltd.

OBJECTIVES We sought to compare the characteristics and outcomes of patients with acute myocardial infarction (MI) and cardiogenic shock (CS) caused by rupture of the ventricular free wall or tamponade versus shock from other causes. BACKGROUND Free-wall rupture is a recognized cause of mortality in patients with acute MI. Some of these patients present subacutely, which provides an opportunity for intervention. Recognition of factors that distinguish them from the overall shock cohort would be beneficial. METHODS The international SHOCK Trial Registry enrolled patients concurrently with the randomized SHOCK Trial. Thirty-six centers consecutively enrolled all patients with suspected CS after MI, regardless of trial eligibility. RESULTS Of the 1,048 patients studied, 28 (2.7%) had free-wall rupture or tamponade. These patients had less pulmonary edema, less diabetes, less prior MI, and less prior congestive heart failure (all p < 0.05). They more often had new Q waves in two or more leads (51.9% vs. 31.5%, p < 0.04), but MI location and time to shock onset after MI did not differ. Of patients with rupture or tamponade, 75% had pericardial effusions. No hemodynamic characteristics identified patients with rupture/tamponade. Most patients with rupture/tamponade had surgery and/or pericardiocentesis (27/28); their in-hospital survival rate was identical to that of the group overall (39.3%). Women and older patients with rupture/tamponade tended to survive intervention less often. CONCLUSIONS Free-wall rupture and tamponade may present as CS after MI, and survival after intervention is similar to that of the overall shock cohort. AU patients with CS after MI should have echocardiography in order to detect subacute rupture or tamponade and initiate appropriate interventions. (J Am Coll Cardiol 2000;36:1117-22) (C) 2000 by the American College of Cardiology.

Background Diltiazem reduces non-fatal reinfarction and refractory ischaemia after non-Q-wave myocardial infarction, an acute coronary syndrome similar to the incomplete infarction that occurs after successful reperfusion. We postulated that this agent would reduce cardiac events in patients after acute myocardial infarction treated initially with thrombolytic agents-a clinical application previously unexplored with heart-rate-lowering calcium antagonists. Methods A prospective, randomised, double-blind, sequential trial was done in 874 patients with acute myocardial infarction, but without congestive heart failure, who first received thrombolytic agents. Patients received either 300 mg oral diltiazem once daily, or placebo, initiated within 36-96 h of infarct onset, and given for up to 6 months. The trial primary endpoint was the cumulative first event rate of cardiac death, non-fatal reinfarction, or refractory ischaemia. Additional prespecified endpoints included several composites of non-fatal cardiac events (non-fatal reinfarction combined with refractory ischaemia, all recurrent ischaemia, or the need for myocardial revascularisation). The diagnosis of ischaemia, whether refractory or recurrent, and the need for myocardial revascularisation, was always based on objective electrocardiographical evidence of ischaemia, either at rest or on exertion. Results For the trial primary endpoint, 131 events occurred in the 444 placebo patients and 97 events in the 430 diltiazem patients (hazard ratio 0.79; 95% CI, 0.61-1.02; p=0.07). For non-fatal cardiac events, diltiazem treatment was associated with a relative decrease (0.76; 0.58-1.00) in the combined event rate of non-fatal reinfarction and refractory ischaemia. There was a similar decrease in the composite non-fatal endpoints of non-fatal reinfarction combined with all recurrent ischaemia (0.80; 0.64-1.00) and non-fatal reinfarction combined with the need for myocardial revascularisation (0.67; 0.46-0.96). The need

Background The leading cause of death in patients hospitalized for acute myocardial infarction is cardiogenic shock. We conducted a randomized trial to evaluate early revascularization in patients with cardiogenic shock. Methods Patients with shock due to left ventricular failure complicating myocardial infarction were randomly assigned to emergency revascularization (152 patients) or initial medical stabilization (150 patients). Revascularization was accomplished by either coronary-artery bypass grafting or angioplasty. Intraaortic balloon counterpulsation was performed in 86 percent of the patients in both groups. The primary end point was mortality from all causes at 30 days. Six-month survival was a secondary end point. Results The mean (+/-SD) age of the patients was 66+/-10 years, 32 percent were women, and 55 percent had been transferred from other hospitals. The median time to the onset of shock was 5.6 hours after infarction, and most infarcts were anterior in location. Ninety-seven percent of the patients assigned to revascularization underwent early coronary angiography, and 87 percent underwent revascularization; only 2.7 percent of the patients assigned to medical therapy crossed over to early revascularization without clinical indication. Overall mortality at 30 days did not differ significantly between the revascularization and medical-therapy groups (46.7 percent and 56.0 percent, respectively; difference, -9.3 percent; 95 percent confidence interval for the difference, -20.5 to 1.9 percent; P = 0.11). Six-month mortality was lower in the revascularization group than in the medical-therapy group (50.3 percent vs. 63.1 percent, P=0.027). Conclusions In patients with cardiogenic shock, emergency revascularization did not significantly reduce overall mortality at 30 days. However, after six months there was a significant survival benefit. Early revascularization should be strongly considered for patients with acute myocardial infarction complicated by c

Background Cardiogenic shock (CS) is the leading cause of death in patients hospitalized with acute myocardial infarction (MI). Nonrandomized studies suggest reduced mortality rate with revascularization. Trial design The SHOCK trial is a multicenter, randomized, and unblinded study with a Registry for trial-eligible and ineligible nonrandomized patients. The trial is testing the hypothesis that a direct invasive strategy of emergency revascularization for patients with cardiogenic shock complicating acute MI will reduce 30-day all-cause mortality rate by 20 absolute percentage points compared with initial medical stabilization. Eligibility criteria include development of CS within 36 hours of an acute transmural MI as evidenced by ST elevation or new left bundle branch block MI; clinical criteria for CS with hemodynamic confirmation; absence of a mechanical, iatrogenic, or other cause of shock; and enrollment within 12 hours of CS diagnosis. Patients randomly assigned to emergency revascularization immediately undergo coronary angiography, with percutaneous transluminal coronary angioplasty or coronary artery bypass grafting depending on the coronary anatomy Patients assigned to initial medical stabilization may undergo revascularization greater than or equal to 54 hours after randomization. End points The primary end point is all-cause 30-day mortality after randomization. Secondary end points include death at trial termination, changes in left ventricular dimensions and function measured by echocardiography at randomization and 2 weeks later, and changes in quality of rife and physical functioning from 2 weeks after discharge to 6 months after MI.

D’après la littérature, l’évolution postopératoire habituelle après chirurgie de pontage coronaire serait caractérisée par une diminution significative du débit cardiaque associée à une élévation des résistances vasculaires systémiques. Cette description ne nous semble pas correspondre à la réalité actuelle et ce travail a été entrepris pour décrire et analyser l’évolution que nous observerons réellement à l’heure actuelle. La première partie du travail concerne, tout d’abord, une analyse des méthodes dont nous disposons pour évaluer et surveiller l’évolution hémodynamique au lit du patient. En effet, le cathéter d’artère pulmonaire (Swan-Ganz) habituellement utilisé dans ce but présente certaines limitations bien connues et décrites. Nous avons évalués l’utilité clinique et la fiabilité de certaines techniques qui pourraient pallier certains de ces défauts. En munissant le cathéter d’artère pulmonaire d’une thermistance à réponse rapide, il est possible de mesurer la fraction d’éjection du ventricule droit de même que les volumes ventriculaires droit, données d’interprétation délicate. La technique de double dilution permet également de mesurer les volumes ventriculaires droits et permettrait de mesurer le débit cardiaque sans cathéter d’artère pulmonaire ; le coût de la technique et la difficulté de placer correctement le cathéter à fibres optiques nécessaire en limitant cependant l’utilité. Le cathéter de Swan-Ganz à débit continue s’est, quant à lui, révélé fiable en pratique clinique, d’utilisation aisée et est appelé à remplacer le cathéter d’artère pulmonaire conventionnelle qui reste, malgré tout, à l’heure actuelle la meilleure technique de surveillance utilisable sur une grande échelle. Dans la deuxième partie, l’évolution hémodynamique postopératoire a été analysée chez 200 patients opérés de pontage coronaire. Ces 200 patients ont té randomisés en fonction de la technique de cardioplégie utilisée : dans le 1er groupe la protection myocardique é, After leaving the operating room, patients undergoing cardiac surgery are closely monitored in the intensive care unit. Their hemodynamic profile, describing blood flow characteristics in the organism, is indeed particularly prone to profound alterations during and after surgical procedures on the heart. The three main factors regulating blood flow in the human body are cardiac function, circulating blood volume and vasomotor tone (Little, 1997). As depicted figure 1, these regulating factors have strong interactions and are also, at various degrees, modulated by external influences. If we keep in mind how much one of these factors is submitted to alterations during cardiac surgery (cardiac arrest, extra-corporeal circulation, bleeding …) and how much the external influences are modified by anaesthesia and surgery, we can easily understand that postoperative hemodynamic stability is far from being guaranteed and requires close monitoring. The techniques used for hemodynamic monitoring in the intensive care unit have to fulfil some criteria. Among these, safety for the patients, cost and possibility of implementing the technique on a large scale are of major concern (Polk, 1990 – Nelson, 1993). The tools that are conventionally used for bedside monitoring, especially the pulmonary artery catheter, have inherent limitations so that newer techniques are proposed to improve our practice. The first part of this work is devoted to the clinical evaluation of some of these newer techniques and, particularly, their validity and usefulness in the postoperative care after cardiac surgery. The hemodynamic evolution following coronary surgery is usually reported to be characterized by a typical pattern of myocardial depression associated with increased systemic vascular resistances (Breisblatt, 1991 – Bojar, 1999). Unlike this description, the clinical picture we observed in our daily practice appeared quite different, especially since the progressive introduction, Thèse de doctorat en sciences médicales (soins intensifs cardio-vasculaires) -- UCL, 1999