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Biomedical subjects

J M Juliard

Publications and source records attributed to J M Juliard.

At least 19 recordsLinked to original sources

[Myocardial infarction and disseminated lupus erythematosus].

Myocardial infarction is an underestimated complication of disseminated lupus erythematosus (DLE). Its features, treatment and prognosis are poorly understood. From June 1988 to December 2002, out of 1572 consecutive patients admitted during the first hours of acute myocardial infarction with ST elevation, 7 (5 women, aged 38 +/- 7 years) had DLE. The commonest risk factor was smoking (N = 4). There was a higher incidence of anterior infarction (N = 5). The infarct occurred 7 +/- 5 years after diagnosis of DLE. There were other complications of DLE in all cases. Three patients had antiphospholipid syndromes. The culprit artery was usually the left anterior descending (N = 5). The lesions included stenosing atheroma (N = 5) and extensive thrombosis (N = 5). The coronary disease was usually limited to a single vessel (N = 5). Revascularisation procedures include pre-hospital thrombolysis (N = 3) followed by immediate angioplasty (N = 2) or primary angioplasty (N = 4). TIMI grade 3 flow was obtained in all cases, 278 +/- 162 min after the onset of symptoms. The clinical course was characterised by acute reocclusion in 3 patients, recurrent in 2 patients with an antiphospholipid syndrome, and death in 1 case. Acute myocardial infarction occurs in already complicated cases of DLE, in young patients, associating atherosclerosis and extensive thrombosis. The risk of early reocclusion after reperfusion is high, especially in cases with the antiphospholipid syndrome.

Adult↗

[Angioplasty of saphenous vein grafts in the acute phase of myocardial infarction. Short and mid-term results].

The impact of the progress of interventional cardiology on the improved prognosis of myocardial infarction due to occlusion of a saphenous vein bypass graft is not well known. The aim of this study was to report the modalities and results at short and medium term of revascularisation by angioplasty of venous grafts in the acute phase of myocardial infarction. Out of a total of 870 consecutive patients treated by angioplasty in the first 6 hours of myocardial infarction with persistent ST elevation between 1990 and 2002, 16 (2%) had acute occlusion of a saphenous vein graft. Twelve of the 16 patients had previous myocardial infarction; perfusion was obtained in 7 patients. The attempt failed in 9 patients because of "no-reflow" (n=5), the extensive nature of the thrombosis (n=2) and technical failure (n=2). Three patients died in hospital, all after failed angioplasty. At 6 months, of the 13 survivors of the hospital period, 2 had been readmitted for a revascularisation procedure. At 2 years, 3 patients had died, 2 were readmitted for recurrent myocardial infarction and 8 patients remained free of a major cardiovascular event. Reperfusion by angioplasty of an occluded saphenous vein graft in the acute phase of myocardial infarction remains imperfect and the prognosis at short and medium term is poor.

Aged↗

[Femoral artery hemostasis after coronary angioplasty with moderate dose of heparin].

UNLABELLED: Early retraction of the arterial introducer facilitates patient management after coronary angioplasty. Closure systems permit rapid haemostasis, but are costly and do not avoid all serious vascular complications. Moderate doses of heparin, used often at the moment, could allow immediate retraction of the introducer with rapid and safe haemostasis by manual compression. METHODS: We evaluated prospectively in 350 consecutive patients the safety and efficacy of immediate retraction of the 6F introducer after coronary angioplasty performed by the femoral route with a moderate dose of heparin (70 IU. kg-1). Only procedures during acute infarction or using abciximab electively were excluded. RESULTS: Retraction of the introducer was immediate in 340 patients (97%). The dose of heparin administered was 5300 +/- 800 IU and the compression time was 11 +/- 4 minutes. The activated clotting time at retraction of the introducer was 254 +/- 46 s. Six (1.7%) serious vascular complications (4 significant haematomas and 2 false aneurysms) were noted during the hospital phase. A single patient (0.6%) was transfused and no vascular surgical procedure was necessary. The average duration of stay after angioplasty was 2.6 +/- 2.2 days and 73% of patients left before 48 hours. CONCLUSION: Immediate retraction of the arterial introducer is possible with simple manual compression, after coronary angioplasty performed with a moderate dose of heparin.

Angioplasty↗

[Changes in reperfusion strategies in the acute phase of myocardial infarction from 1988 to 2001].

The objective of this study was to evaluate the evolution of therapeutic strategies in the course of myocardial infarction. Two successive periods were studied: 1988/96 (700 patients) and 1996/2001 (700 patients). The following parameters were compared: patient characteristics, management methods, and results on the hospital morbidity and mortality. The patient characteristics were little changed, in terms of age and sex, with a drop in the frequency of anterior infarcts during the second period (46 vs 51%, p = 0.0001). The average delay to admission remained stable over both periods, 186 vs 189 min. During the second period, primary angioplasty was favoured (66 versus 44%, p = 0.0001), associated with a wider use of stents (47 against 4%, p = 0.0001) and anti GP IIb/IIIa (24 against 0.5%, p = 0.0001). In the acute phase, TIMI3 reperfusion was obtained in 81% of cases (88/96 period) against 88% during the second period (p = 0.02). The hospital mortality was reduced by 1.2% (8.9 against 7.7%, NS). Without cardiogenic shock, the mortality was comparable between the two groups (5%), whereas it diminished in the small group of patients (5%) in cardiogenic shock, from 76 to 66% (NS). Haemorrhagic complications were reduced, but the rate of symptomatic reocclusion remained stable (2.5%). With multivariate analysis, the independent predictive mortality factors were identical in the two groups: age and cardiogenic shock on admission. Currently, TIMI3 reperfusion is possible in close to 90% of patients in the acute phase of infarction. Our efforts should focus on earlier management, especially for older patients, too often excluded without reason, and for those in cardiogenic shock, which constitutes a therapeutic quest for the future. The theory of angioplasty facilitated by anti GP IIb/IIIa and/or prehospital thrombolysis must be evaluated scientifically with the goal of early and efficient reperfusion for the greatest number of patients.

Aged↗

[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↗

[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↗

[Resistance to ACE inhibitors. Myth or reality?].

Angiotensin Converting Enzyme (ACE) inhibitors represent a major advance in the treatment of: hypertension, and generally speaking, in cardiovascular prevention; myocardial infarction; cardiac failure. They have a cardio and vascular protective action by tending to correct hypertension, left ventricular hypertrophy and remodelling, endothelial dysfunction, arterial smooth muscle proliferation and thrombotic phenomena. However, besides the cough that this therapeutic class engenders, a major question remains unanswered: is there resistance to this family of drugs? In other words, does left ventricular remodelling and arterial smooth muscle proliferation continue with regular treatment at the prescribed dosages? The synthesis of angiotensin II does not only depend on the angiotensin converting enzyme but also on the quality of angiotensin I and the presence of other enzymes such as chymase. A secondary increase of angiotensin II with ACE inhibitor therapy may reflect insufficient blockade of the renin-angiotensin system or a synthesis of angiotensin II by an alternative pathway to the converting enzyme. In vivo measurement of ACE inhibition shows that blockade of the renin-angiotensin system is automatically limited due to the very accurate regulation of angiotensin II concentrations.

Angiotensin II↗

[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↗

[Acute myocardial infarction: prehospital phase and first hospital days].

During acute myocardial infarction, pre-hospital stage and the first hours after admission are crucial for initiating reperfusion therapy, which is determinant for short- and mid-term survival. Within 12 hours after onset of chest pain, either thrombolysis or primary angioplasty contribute to reduce mortality rate, the earlier being the better. Therapeutic advances, regarding either thrombolysis or angioplasty, are directed towards an earlier, more efficient and stable (without reocclusion) patency of the infarct-related artery. Most promising results so far have been obtained with platelet glycoprotein (GP) IIb/IIIa receptor blockers, in combination with thrombolysis or angioplasty.

Angioplasty↗

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↗

Decreased no-reflow in patients with anterior myocardial infarction and pre-infarction angina.

AIMS: Pre-infarction angina is associated with better outcome after myocardial infarction. The aim of this study was to assess whether pre-infarction angina is associated with decreased no-reflow after coronary recanalization. METHODS AND RESULTS: Twenty-three patients underwent intracoronary myocardial contrast echocardiography during the acute phase of anterior myocardial infarction after successful recanalization, and before hospital discharge. Myocardial perfusion was graded semi-quantitatively in the area at risk (dyssynergic segments). Global left ventricular function was assessed by radionuclide angiography on days 8 and 42 and regional wall motion was assessed by 2D echocardiography on days 0 and 42. Fourteen patients had pre-infarction angina (angina less than 7 days before myocardial infarction) and nine did not. Baseline characteristics were similar in the two groups. The myocardial contrast echocardiography perfusion score in the area at risk after recanalization was higher in the patients with pre-infarction angina than in those without (0.72 +/- 0.19 vs 0.53 +/- 0.22, P=0.04), and the incidence of no-reflow (myocardial contrast echocardiography perfusion score < or =0.5) was lower (14% vs 56%, P=0.04). This difference persisted 8 +/- 2 days after myocardial infarction (0. 87 +/- 0.11 vs 0.69 +/- 0.26, P=0.04), and was associated with greater mid-term (day 42) improvement in left ventricular function in patients with pre-infarction angina than in those without, as assessed by changes in radionuclide left ventricular ejection fraction (+5.8 +/- 8.1% vs -3.3 +/- 4.6%, respectively;P=0.01) and by changes in regional wall motion score on 2D echocardiography (-0. 61 +/- 0.39 vs -0.24 +/- 0.17, respectively;P=0.04). CONCLUSION: Pre-infarction angina is associated with preservation of the microvasculature, reflected by reduced no-reflow. This may be a mechanism underlying greater recovery of left ventricular function in patients with pre-infarction angina.

Adult↗

Acute assessment of microvascular perfusion patterns by myocardial contrast echocardiography during myocardial infarction: relation to timing and extent of functional recovery.

OBJECTIVE: To examine the relation between the initial microvascular perfusion pattern, as assessed by intracoronary myocardial contrast echocardiography (MCE), immediately after restoration of TIMI (thrombolysis in myocardial infarction) (TIMI) grade 3 flow during acute myocardial infarction, and the extent and timing of functional recovery in the area at risk. SETTING: Referral centre for interventional cardiology. METHODS: Intracoronary MCE was performed 15 minutes after TIMI grade 3 recanalisation of the infarct artery in 25 patients. Segmental myocardial contrast patterns were graded semiquantitatively (0, none; 0.5, heterogeneous; 1, homogeneous). Functional recovery was assessed by echocardiography on days 9 and 42. RESULTS: Among 174 myocardial segments in the area at risk, wall motion recovery on day 9 was observed in 40% of MCE grade 1 segments but there was no significant recovery in grade 0 or 0.5 segments. On day 42, recovery had occurred in 56% of MCE grade 1 segments (p < 0. 0001 v MCE grade 0 and 0.5; p = 0.0001 v MCE grade 1 on day 9), and 22% of MCE grade 0.5 segments (p = 0.02 v MCE grade 0; p = 0.0005 v MCE grade 0.5 on day 9); MCE grade 0 segments did not recover. Negative predictive value in predicting recovery by contrast enhancement was 95% and 89% by days 9 and 42, respectively. CONCLUSIONS: Contractile recovery occurs earliest in well reperfused segments. Up to one quarter of segments with heterogeneous contrast enhancement show wall motion recovery within the first six weeks. Myocardial perfusion after recanalisation in acute myocardial infarction, even if heterogeneous, is a prerequisite for postischaemic functional recovery. Thus preservation of acute myocardial perfusion is associated with more complete and early functional recovery.

Adult↗

[Angioplasty in acute myocardial infarction].

Primary PTCA has become a common method for achieving recanalization of the infarct vessel in acute myocardial infarction. The excellent results of large randomised trials comparing it to intravenous thrombolysis however have not been consistently duplicated in large registries reflecting clinical practice in the real world. Therefore, there is a need for critical and careful assessment of angioplasty performance, specifically criteria related to operator and center volume as well as the ability to implement angioplasty rapidly after diagnosis. It has been specifically established that intra-hospital delays in the time to balloon angioplasty are associated with clear increases in mortality rates. It is therefore necessary to implement quality insurance programs to continuously monitor centers using primary PTCA as their reperfusion method of choice. Recent studies have demonstrated that stents and adjuvant pharmacological therapies, specially GpIIb/IIIa antagonists are associated with improved results. Despite the high patency rates achieved with angioplasty, a consistent series of experimental and clinical observations indicate that the quality of myocardial reperfusion downstream of the epicardial coronary vessel is a critical determinant of prognosis. Specifically, no-reflow, which can be ascertained using perfusion imaging techniques, but also indirectly, using the electrocardiogram, is an ominous element. The challenge of the coming years will be to test effective preventive or curative treatments for no-reflow.

Angioplasty, Balloon, Coronary↗

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↗