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Biomedical subjects

H Benamer

Publications and source records attributed to H Benamer.

At least 19 recordsLinked to original sources

[Myocardial revascularization at the acute phase of myocardial infarction in the octogenarian].

Elderly patients are at high risk of complications in acute myocardial infarction (AMI). In this population, myocardial reperfusion at the acute phase improves the prognostic. The mortality rate is above 50% in the absence of reperfusion strategy, and decreases at less than 20% in case of such treatment. The thrombolytic use is limited in those patients, coronary angioplasty is taking an important place in this reperfusion therapy, but is not well evaluated in patients older than 80 years. Prospective registry of patients older than 80 years admitted in Hôpital Bichat for acute myocardial infarction within the first 6 hours (n = 92), between 1990 january to 1999 december. Eight patients (10%) received a thrombolytic therapy. Coronary angiogram was achieved in eighty patients (87%). In 58 (63%) patients a coronary angioplasty was performed. The success rate of the coronary angioplasty was 86%. In-hospital mortality rate was 26% (death in 24 patients), 20% in the absence of cardiogenic shock and 62% when this complication was noted. Two patients (2%) were treated by emergent coronary artery bypass surgery. The results comparison between the periods of 1990 to 95 and 1955 to 99 showed, a real trend of decrease mortality rate (28 to 13% in the absence of cardiogenic shock, p = 0.10), an increase of the proportion of patients treated by angioplasty. These results are more and more encouraging. Coronary reperfusion by primary angioplasty in possible in patients older than 80 years with a low rate of complications. Technical progress such as stents and GpIIb/IIIa inhibitors must be evaluated in this population.

Aged↗

A randomized double-blind trial of intravenous trimetazidine as adjunctive therapy to primary angioplasty for acute myocardial infarction.

BACKGROUND: Despite high patency rates, primary angioplasty for myocardial infarction does not necessarily result in optimal myocardial reperfusion and limitation of infarct size. Experimentally, trimetazidine limits infarct size, decreases platelet aggregation, and reduces leukocyte influx into the infarct zone. To assess trimetazidine as adjunctive therapy to primary angioplasty for acute myocardial infarction a prospective, double-blind, placebo-controlled pilot trial was performed. METHODS: 94 patients with acute myocardial infarction were randomized to receive trimetazidine (40 mg bolus followed by 60 mg/day intravenously for 48 h) (n=44) or placebo (n=50), starting before recanalization of the infarct vessel by primary angioplasty. Patients underwent continuous ST-segment monitoring to assess return of ST-segment deviation to baseline and presence of ST-segment exacerbation at the time of vessel recanalization. Infarct size was measured enzymatically from serial myoglobin measurements. Left ventricular angiography was performed before treatment and repeated at day 14. RESULTS: Blinded ST segment analysis showed that despite higher initial ST deviation from baseline in the trimetazidine group (355 (32) vs. 278 (29) microV, P=0.07), there was an earlier and more marked return towards baseline within the first 6 h than in the placebo group (P=0.014) (change: 245 (30) vs. 156 (31) microV respectively, P=0.044). There was a trend towards less frequent exacerbation of ST deviation at the time of recanalization in the trimetazidine group (23.3 vs. 42.2%, P=0.11). There was no difference in left ventricular wall motion at day 14, or in enzymatic infarct size. There was no side effect from treatment. Clinical outcomes were similar between groups. CONCLUSION: Trimetazidine was safe and led to earlier resolution of ST-segment elevation in patients treated by primary angioplasty for acute myocardial infarction.

Adolescent↗

[Revision of the "Smoker's Paradox": smoking is not a good prognostic factor immediately after myocardial infarction].

In order to determine the reasons for the low mortality after myocardial infarction in smokers compared with non-smokers (the smoker's paradox), the authors analysed the initial clinical data, the therapeutic interventions and hospital mortality in 790 consecutive patients (555 smokers, 235 non-smokers) admitted to hospital within 6 hours of the first symptoms of acute myocardial infarction and treated by intravenous thrombolytic agents and/or coronary angioplasty. Multivariate analysis with linear regression was used to identify the predictive factors of hospital mortality. The main differences between smokers and non-smokers were age (56 vs 67 years, p < 0.0001), gender (male, 90 vs 60%, p < 0.01), cardiogenic shock on admission (3 vs 8%, p < 0.01). TIMI 3 flow was obtained in the culprit artery in 84% of smokers and 79% of non-smokers (NS). Hospital mortality was 5% in the smoking population and 16% in non-smokers (p < 0.0001). In multivariate analysis, the variables of cardiogenic shock, age, gender and hypertension provided most of the prognostic information and tobacco consumption did not appear to have a protective effect. In patients admitted to hospital with acute myocardial infarction, identical incidences of early reperfusion are obtained in smokers and in non-smokers. However, mortality is higher in the non-smoking group due to more severe clinical characteristics on admission. Tobacco consumption is not a protective factor in the immediate period after acute myocardial infarction.

Aged↗

[Indications for intravenous GPIIb/IIIa receptor inhibitors in acute coronary syndrome without prolonged ST syndrome].

Platelet adhesion and aggregation play a pivotal role in the physiopathology of acute coronary syndromes. Inhibitors of the GPIIb/IIIa receptors block the final step of platelet aggregation. Clinical trials have demonstrated efficacy of these drugs to reduce ischemic complications after percutaneous coronary interventions. In the setting of acute coronary syndromes without persistent ST segment elevation, abciximab improves outcomes in case of revascularization. Tirofiban and eptifibatide limit ischemic complications in the same setting, with additional effect in patients undergoing angioplasty. Blockers of the GPIIb/IIIa receptors should be the standard of care of patients with acute coronary syndromes. The optimal therapeutic strategy should include, after proper risk stratification, an early medical approach combined with an early revascularization.

Angioplasty, Balloon, Coronary↗

Elevated levels of shed membrane microparticles with procoagulant potential in the peripheral circulating blood of patients with acute coronary syndromes.

BACKGROUND: Apoptotic microparticles are responsible for almost all tissue factor activity of the plaque lipid core. We hypothesized that elevated levels of procoagulant microparticles could also circulate in the peripheral blood of patients with recent clinical signs of plaque disruption and thrombosis. METHODS AND RESULTS: We studied 39 patients with coronary heart disease, including 12 patients with stable angina and 27 patients with acute coronary syndromes (ACS), and 12 patients with noncoronary heart disease. We isolated the circulating microparticles by capture with annexin V and determined their procoagulant potential with a prothrombinase assay. The cell origins of microparticles were determined in an additional 22 patients by antigenic capture with specific antibodies. The level of procoagulant microparticles did not differ between stable angina patients and noncoronary patients (10.1+/-1.6 nmol/L phosphatidylserine [PS] equivalent versus 9.9+/-1.6 nmol/L PS equivalent, respectively). However, procoagulant microparticles were significantly elevated in patients with ACS (22.2+/-2.7 nmol/L PS equivalent) compared with other coronary (P<0.01) or noncoronary (P<0.01) patients. Microparticles of endothelial origin were significantly elevated in patients with ACS (P<0.01), which suggests an important role for endothelial injury in inducing the procoagulant potential. CONCLUSIONS: High levels of procoagulant endothelial microparticles are present in the circulating blood of patients with ACS and may contribute to the generation and perpetuation of intracoronary thrombi.

Acute Disease↗

Reperfusion syndrome: relationship of coronary blood flow reserve to left ventricular function and infarct size.

OBJECTIVES: We tested the hypothesis that the reperfusion syndrome (RS), defined as an additional elevation of the ST segment upon reperfusion, may be a marker of microcirculatory reperfusion injury during acute myocardial infarction (AMI). BACKGROUND: The pathophysiology of the RS is unknown, and its prognostic implications are controversial. METHODS: Twenty-one patients with an anterior AMI treated < or =12 h after onset by primary coronary angioplasty (PTCA) were studied. Coronary velocity reserve (CVR), an index of microcirculatory function, was measured using a Doppler guidewire. Left ventricular (LV) ejection fraction, infarct size (percent defect) and LV end-systolic volume index (LVESVi) were evaluated by radionuclide ventriculography, 201T1 single-photon emission computed tomography and contrast ventriculography, respectively. RESULTS: Baseline ST elevation and pain-to-TIMI 3 time were similar in patients with and without RS. Patients with RS (10/21) had a lower post-PTCA CVR than patients without RS (median [95% confidence interval]: 1.2 [1-1.3] vs. 1.6 [1.5-1.7], p < 0.005). Even though predischarge CVR was similar in the two groups, infarct size at six weeks (26 [21 to 37] vs. 14 [10-17]% 201T1 defect, p = 0.001) and predischarge LVESVi (45% [40 to 52] vs. 30% [29 to 38] mL/m2, p = 0.001) were larger, and LV ejection fraction at six weeks (40% [37 to 46] vs. 55% [50 to 60], p = 0.004) was lower in patients with RS than in patients without RS. CONCLUSIONS: Patients with RS during primary PTCA for an anterior AMI have a transiently lower CVR than patients without RS, but sustained LV dysfunction and larger infarct size, suggesting that RS is a marker of microcirculatory reperfusion injury.

Aged↗

A matched comparison of the combination of prehospital thrombolysis and standby rescue angioplasty with primary angioplasty.

This study sought to assess the rate of acute Thrombolysis In Myocardial Infarction (TIMI) trial grade 3 patency that can be achieved with the combination of prehospital thrombolysis and standby rescue angioplasty in acute myocardial infarction. No large angiographic study has been performed after prehospital thrombolysis to determine the 90-minute TIMI 3 patency rate in the infarct-related artery. Hospital outcome and artery patency were compared to 170 matched patients treated with primary angioplasty. Prehospital thrombolysis was applied 151+/-61 minutes after the onset of pain in 170 patients (56+/-12 years, 86% men), using recombinant tissue-type plasminogen activator, streptokinase, or eminase. Emergency 90-minute angiography was performed in every case. All patients in whom thrombolysis failed underwent rescue angioplasty. After thrombolysis alone, TIMI grade 3 flow in the infarct-related artery was observed in 108 patients (64%), TIMI grade 2 in 12 (7%), and TIMI grade 0 or 1 in 50 (29%). Rescue angioplasty was successful in 47 of 50 attempts. Overall, TIMI 3 patency was achieved in 91%, and additionally TIMI 2 flow in 7% of patients, an average of 113+/-39 minutes after thrombolysis and 55+19 minutes after admission. Therefore, < 2 hours after thrombolysis, only 2% of patients had persistent occlusion (TIMI 0 or 1) of the infarct-related artery. In-hospital mortality was 4% overall (7 of 170), and 3% in the 155 patients in whom TIMI 3 was obtained during the acute phase. Severe hemorrhagic complications occurred in 14 patients (8%) with 2 fatal cerebral hemorrhages (7% of patients required transfusions). The matched comparison with primary PTCA showed no significant difference in hospital outcome. Combined prehospital thrombolysis, 90-minute angiography, and rescue angioplasty yield a high rate of acute TIMI 3 patency rate early after thrombolysis and hospital admission. A randomized, prospective comparison between these 2 reperfusion strategies may be now warranted.

Adult↗

Elevated cardiac troponin I predicts a high-risk angiographic anatomy of the culprit lesion in unstable angina.

BACKGROUND: This study assessed the relation between the angiographic appearance of the culprit lesion and cardiac troponin I (cTnI) or C-reactive protein (CRP) elevations within the first 24 hours in unstable angina. Intracoronary thrombus or a complex morphology, is frequently observed on angiography in patients with unstable angina and is associated with a higher rate of spontaneous or coronary angioplasty-related complications. Biochemical parameters related to myocardial injury (eg, cTnI) or to systemic inflammation (eg, CRP) are known prognostic markers for clinical outcome and may help in angiographic risk stratification to provide new adjunctive therapy. METHODS AND RESULTS: We studied 100 patients admitted for unstable angina with angiographically proven coronary artery disease (with normal creatine kinase [CK] and CK-MB mass). Serum concentrations of cTnI (N < 0.4 ng/mL) and CRP (N < 3 mg/L) were measured at admission and 12 and 24 hours later. Multivariate analysis showed that elevated cTnI (>/=0.4 ng/mL) within 24 hours (35 patients) was an independent predictor of an angiographic appearance of the culprit lesion carrying a high risk of major cardiac events in the outcome and whether angioplasty is attempted (coronary thrombus, occlusion, or type C lesions; odds ratio 4.1, 1. 6 to 10.5). cTnI levels at admission and CRP at 0, 12, and 24 hours were not predictive of high-risk angiographic anatomy. CONCLUSIONS: In patients with unstable angina and angiographically proven coronary artery disease, increased cTnI within 24 hours of admission but not increased CRP is associated with an angiographic appearance of the culprit lesion carrying a high risk of complication, especially in the event of angioplasty.

Angina, Unstable↗

Partial rupture of the tricuspid valve after extraction of permanent pacemaker leads: detection by transesophageal echocardiography.

Traumatic lesions of the tricuspid valve complicating pacemaker lead extractions appear to be rare. We report two cases of partial rupture of the tricuspid valve, following apparently uneventful extraction of permanent ventricular leads, resulting in severe regurgitation and, in one case, chronic heart failure. TEE was useful to identify the traumatic mechanism of tricuspid regurgitation (TR) and the extent of valvular lesions in these patients. Such etiology should be suspected, and TEE performed, in patients developing TR or heart failure late after lead extraction.

Aged↗

Comparison of the prognostic value of C-reactive protein and troponin I in patients with unstable angina pectoris.

This study assessed the prognostic value of cardiac troponin I (cTnI) and C-reactive protein (CRP) in unstable angina, and specifically in patients with angiographically proven coronary artery disease. These biochemical parameters, which are related to myocardial injury or to systemic inflammation, may help in short-term risk stratification of unstable angina. We prospectively studied 195 patients with unstable angina, 100 of whom had angiographically proven coronary artery disease (with normal creatine kinase [CK] and CK-MB mass). Serum concentrations of cTnI (N < 0.4 ng/ml) and CRP (N < 3 mg/L) were measured at admission, 12, and 24 hours later. The rate of in-hospital major adverse cardiac events (death, myocardial infarction, or emergency revascularization) was higher in patients with increased cTnI within the first 24 hours, regardless of the results of coronary angiography (23% vs 7%; p < 0.001). Conversely, events occurred at similar rates in patients with or without increased CRP. In patients with angiographic evidence of coronary artery disease, multivariate analysis showed that increased cTnI within 24 hours of admission (35 patients) was an independent predictor of major adverse cardiac events (odds ratio 6.7, range 1.7 to 27.3), but not cTnI levels at admission and CRP at 0, 12, and 24 hours. Thus, both in unselected patients with unstable angina and in patients with angiographically proven coronary artery disease, increased cTnI within 24 hours of admission, but not CRP, is a predictor of in-hospital clinical outcome. We also found a temporal link between cTnI increase and late elevation of CRP, suggesting that systemic inflammation may partially be a consequence of myocardial injury.

Angina, Unstable↗

Alteration of the alveolar-capillary membrane diffusing capacity in chronic left heart disease.

During left heart disease, the chronic increase in pulmonary capillary wedge pressure (PCWP) results both in vascular alterations with increased pulmonary vascular resistance (PVR), and in progressive thickening of the alveolar-capillary membrane, which diffusing capacity (Dm) is reduced. However, the total lung diffusing capacity for carbon monoxide (TLco) is inconstantly impaired, depending on the degree of pulmonary congestion. We evaluated the relation between the pulmonary hemodynamic repercussions of chronic heart disease and the 2 components of TLco, i.e., Dm and capillary blood volume. Forty-seven patients with chronic left heart disease (28 with valve disease, 19 with cardiomyopathy) underwent right heart catheterization with determination of PCWP and PVR. Pulmonary function tests, including spirometry, determination of TLco, and of its 2 components (percentage of predicted values) were performed in patients and in 15 healthy subjects. TLco and Dm, but not capillary blood volume, were significantly decreased in patients. Dm was related to PVR (p = 0.0006), and was markedly reduced in patients with high PVR (> or = 3 Wood U): 54 +/- 8% vs 80 +/- 19% in patients with normal PVR (p <0.0001). Dm < or = 66% identified all high PVR patients (sensitivity = 100%, specificity = 77%). Capillary blood volume was related to PCWP (p = 0.02), and was increased in patients with high PCWP (> 15 mm Hg): 126 +/- 30% vs 99 +/- 23% (p <0.01), but with a marked overlap. TLco values, although reduced in patients with high PVR (p <0.001), were not predictive of high PVR or high PCWP. Determination of Dm allows a more accurate detection of pulmonary hypertension complicating chronic left heart disease than the other pulmonary parameters.

Adult↗

Heterogeneity of prognosis in patient subsets treated by primary coronary angioplasty during acute myocardial infarction.

Among 377 patients consecutively treated with primary coronary angioplasty for acute myocardial infarction, in-hospital mortality was higher in patients ineligible than in patients eligible for thrombolysis (14.4% vs 7.8%, p <0.05). It remained dismal (75.9%) in patients with cardiogenic shock, but was similar in lytic-eligible patients and in those who were ineligible because of an increased bleeding risk (7.8% vs 7.2%, p = NS), and was zero in patients with nondiagnostic electrocardiograms.

Age Factors↗

Efficacy of streptokinase, but not tissue-type plasminogen activator, in achieving 90-minute patency after thrombolysis for acute myocardial infarction decreases with time to treatment. PERM Study Group. Prospective Evaluation of Reperfusion Markers.

OBJECTIVES: We sought to examine the relation between time to treatment and 90-min patency rates in patients receiving intravenous streptokinase (SK) or accelerated tissue-type plasminogen activator (t-PA). BACKGROUND: Early patency of the infarct-related artery is a major determinant of survival after thrombolysis for acute myocardial infarction. Some data suggest that time to treatment may influence the efficacy of nonfibrin-specific thrombolytic agents in restoring early patency of the infarct-related vessel. METHODS: We performed a retrospective analysis of a cohort of 481 patients receiving thrombolytic therapy for acute myocardial infarction <6 h after pain onset, all of whom underwent 90-min coronary angiography. Patency of the infarct-related artery was graded by two observers who had no knowledge of the treatment received or the time between pain and therapy. RESULTS: There was no difference in baseline clinical or angiographic characteristics according to the timing or nature of treatment. Thrombolysis in Myocardial Infarction (TIMI) flow grade 2 or 3 patency rate after SK correlated negatively with the time between onset of pain and thrombolysis (r = 0.8, p = 0.05), whereas the 90-min patency rate after t-PA appeared stable as a function of time to treatment. When patients were categorized as having received treatment <3 or > or = 3 h after pain onset, the patency rate was similar with t-PA, but significantly higher when SK was administered early rather than late, regardless of whether TIMI flow grades 2 and 3 were pooled (86.9% vs. 59.4%, p = 0.0001) or TIMI flow grade 3 alone was considered to indicate patency (81.7% vs. 53.6%, p = 0.0001). Multivariate logistic regression analysis showed a negative effect of time to treatment on the patency probability for SK (p = 0.0001) but not for t-PA. CONCLUSIONS: The efficacy of streptokinase but not t-PA in restoring early coronary patency after intravenous thrombolysis is markedly lower when patients are treated later after onset of pain.

Coronary Angiography↗

Hospital outcome after bailout coronary stenting in patients with acute myocardial infarction.

We evaluated the outcome of bailout coronary stenting in acute myocardial infarction. Fifty patients (35 men, mean age 60 plusmn; 12) with acute myocardial infarction consecutively underwent bailout stenting after primary and rescue coronary angioplasty (n=41 and 9, respectively). Cardiogenic shock was present in six patients, and 17 others had contraindications to thrombolysis. Stent implantation was successful in 49/50 patients. The antithrombotic regimen combined heparin, aspirin, and ticlopidine. One patient had symptomatic stent closure. Predischarge angiography in 41/44 survivors showed widely patent stents in 40/41 patients. Six patients (4 of whom had been admitted with cardiogenic shock) died in the hospital. During acute myocardial infarction, bailout stenting can achieve high TIMI grade 3 coronary patency (here, 92%), and low acute stent closure rates (here, 2%). However, in-hospital mortality remained high, at nearly 10%, mainly due to the severe risk profile in this patient subset.

Adult↗

Early changes in myocardial perfusion patterns after myocardial infarction: relation with contractile reserve and functional recovery.

OBJECTIVES: The purpose of this study was to assess early temporal changes in myocardial perfusion pattern by myocardial contrast echocardiography (MCE) and their relation to myocardial viability in patients with reperfused acute myocardial infarction (AMI). BACKGROUND: Myocardial contrast echocardiography no-reflow is associated with poor contractile recovery after AMI. However, little is known regarding early reversibility of microvascular dysfunction and its relation to myocardial viability. METHODS: Intracoronary MCE was performed immediately after reflow and 9 days later in 28 patients with a first AMI and successful coronary recanalization (Thrombolysis in Myocardial Infarction trial grade 3 flow). Semiquantitative contrast score and wall motion score (WMS) were assessed in each initially asynergic segment at initial and repeat MCE study. Low dose dobutamine echocardiography (DE) was performed at day 10, and follow-up (FU) rest echocardiography was performed 6 weeks later. RESULTS: Among 200 initially asynergic segments, 49% exhibited no or heterogeneous contrast enhancement at initial MCE versus 24% at restudy (p < 0.001). Three groups of segments were defined according to early changes in contrast pattern: group A, "sustained no-reflow" (n = 17); group B, improved contrast score (n = 68), and group C, "sustained reflow" (n = 112). Group A segments showed no improvement in WMS at FU. In contrast, group B segments showed significant improvement in WMS at FU (p < 0.0001), and exhibited more frequently contractile reserve at DE (36% vs. 6%, p = 0.02) and contractile recovery at FU (34% vs. 7%, p = 0.03) than group A segments. Group C segments exhibited contractile reserve and contractile recovery in 47% and 51% of segments respectively. CONCLUSIONS: Improvement in MCE perfusion pattern may occur after initial no-reflow in the days following reperfused AMI and is associated with preservation of contractile reserve and gradual regional functional recovery.

Adult↗

Conservative management of patients with acute myocardial infarction and spontaneous acute patency of the infarct-related artery.

The role of systematic emergency percutaneous transluminal coronary angioplasty (PTCA) in patients with spontaneous reperfusion during myocardial infarction is debated. We retrospectively examined the inhospital outcome of 47 consecutive patients with myocardial infarction < 6 hours and angiographically proven spontaneous patency of the infarct artery managed without initial PTCA. There was one death (2.1%) and no incidence of reinfarction. Predischarge angiography showed regression of the culprit coronary lesion to < 50% stenosis in 23% of the patients, therefore obviating the need for PTCA. However, 17% of the patients had acute recurrent ischemia, requiring emergency intervention in 10.6%. Comparison with matched patients in whom Thrombolysis in Myocardial infarction grade 3 patency was achieved by thrombolysis or by primary PTCA showed that patients with spontaneous patency tended to have smaller infarctions, as judged from a lower peak creatine kinase level (1132 +/- 1002, 2051 +/- 1536, and 2715 +/- 2146 i.u., respectively; p = 0.001) and a higher left ventricular ejection fraction (56.4%, 47.9%, and 48.7% respectively; p = 0.02). In conclusion, these patients have an excellent inhospital outcome, with evidence of less myocardial damage than in patients in whom reperfusion therapy was required to achieve TIMI 3 patency. Initial conservative treatment appears safe.

Aged↗