[Diagnostic and prognostic significance of CK-MB, troponins, CRP, BNP and/or NT-proBNP in coronary angioplasty. Elevation mechanisms and clinical implications]. / Intérêt diagnostique et pronostique des marqueurs biologiques dans l'angioplastie coronaire en cas d'angor stable et de syndrome coronaire aigu ST-. Quelle stratégie biologique en routine?

The recommendations from respected bodies concerning the treatment and follow up of patients undergoing coronary angioplasty for stable angina or acute coronary syndrome (ACS) are essential for reducing the risks related to the procedure, and for preventing the occurrence of long term complications. Measuring the levels of troponin and CK-MB is part of the diagnostic and prognostic strategy during the coronary angioplasty procedure. In this context, the frequent elevation of markers following uncomplicated angioplasty is a sign of minor irreversible myocardial damage, the prognostic significance of which remains under discussion. Recent data suggest that only a basal troponin elevation (more so than CK-MB) prior to angioplasty has a long term prognostic value in ACS ST- patients, and that troponin elevation occurring after the procedure in the presence of normal basal concentrations, is only associated with in-hospital complications. Determining the basal level of troponin would appear to be essential for interpreting any elevation in concentrations following angioplasty. The recommendations should integrate this fundamental point, if it is confirmed. On the other hand, the question has been raised whether other markers (CRP, BNP and/or NT-proBNP) should be systematically measured as a routine prior to angioplasty. An elevation of CRP before and/or after angioplasty is an unfavourable short and long term prognostic factor. Elevation of NT-proBNP before angioplasty is also an unfavourable long term prognostic factor. Recommending a multi-marker strategy might represent a future direction for identifying at risk patients prior to coronary angioplasty, thus enabling specific treatment to be proposed.

[Diagnostic and prognostic value of heart-type fatty acid-binding protein (H-FABP), an early biochemical marker of myocardial injury]. / Intérêt diagnostique et pronostique de H-FABP (heart-type fatty acid-binding protein ou protéine cardiaque liée aux acides gras), marqueur biochimique précoce de la souffrance myocardique.

Heart-type fatty acid-binding protein (H-FABP) is a 132 amino acids soluble protein, with general characteristics resembling myoglobin. Because of its low molecular weight (15 kd) and cytoplasmic location, it constitutes a biologic marker readily released into the circulation after myocardial injury. Despite the development of various immunoassays to measure H-FABP, few are currently easy to perform, quantitative and applicable in emergency. Most studies have shown the diagnostic sensitivity of H-FABP (i.e. its ability to detect the presence of a myocardial infarction) to be high, above that of myoglobin in patients presenting within 3 to 6 h of after the onset of chest pain. This superiority is attributable to an earlier and more rapid rise in H-FABP than in myoglobin. After thrombolysis, the serum concentrations of H-FABP peak at approximately 4 h after the onset of chest pain, and return to normal values within 24 h. Because of this rapid return of its blood concentration to baseline, H-FABP can contribute to an early biologic diagnosis of post-thrombolysis reperfusion and re-infarction. In absence of renal insufficiency, H-FABP also provides a reliable estimate of infarct size associated with ST segment elevation. When myocardial injury occurs after cardiac surgery, the second peak in H-FABP concentration precedes that of myoglobin, CK-MB or troponins. In addition, H-FABP peaks earlier and is more sensitive than troponins in the detection of subtle myocardial injury in patients presenting with acute coronary syndrome without ST segment elevation, and in patients with severe heart failure, thus offering early prognostic information. Limitations of H-FABP include a limited cardio-specificity, a narrow diagnostic window (20 to 30 h), and a nearly exclusive renal elimination.

Relation of minor cardiac troponin I elevation to late cardiac events after uncomplicated elective successful percutaneous transluminal coronary angioplasty for angina pectoris.

There is little information about the relation between mild cardiac troponin I (cTn-I) increase after coronary interventions and late outcome. We therefore focused on the long-term outcome and the clinical, morphologic, and procedural correlates of elevation of cTn-I compared with cardiac troponin T, creatine kinase (CK), CK-MB activity and mass, and myoglobin in 105 patients with successful elective percutaneous transluminal coronary angioplasty (PTCA) for stable or unstable angina. Patients with myocardial infarction and those with unstable angina who had a detectable increase in serum markers before PTCA were excluded. Markers were measured before and after the procedure and for 2 days. Patients were followed up to record recurrent angina, myocardial infarction, cardiac death, repeat PTCA, or elective coronary artery bypass graft surgery. Procedure success was achieved in all cases. Elevation in cTn-I (> or =0.1 microg/L) was observed in 23 of 105 patients (22%) (median peak: 0.25 microg/L); 18% had cardiac troponin T (cTn-T) release (> or = 0.1 microg/L, median peak 0.21); 11.4% CK-MB mass (> or =5 microg/L), and 7.6% myoglobin (> or =90 microg/L) release. Five and 2 patients had elevated CK and CK-MB activity, respectively. Fourteen of 18 patients with cTn-T elevation had a corresponding elevation in cTn-I (kappa 0.68; p = 0.001). Patients positive for cTn-I had more unstable angina (p = 0.042) and heparin before PTCA (p = 0.046), and had longest total time (p = 0.004) and single inflation (p = 0.01). By multivariate logistic regression, predictors of postprocedure cTnI elevation were maximum time of each inflation (odds ratio 9.2; p = 0.0012), type B lesions (odds ratio 6.6; p = 0.013), unstable angina (p = 0.041), and age > or =60 years (p = 0.032). Clinical follow-up was available in 103 patients (98%) (mean 19+/-10 months). Kaplan-Meier survival analysis showed that cTn-I elevation was not an important correlate of cardiac events (p = 0.34, by log-rank analysis). The incidence of recurrent angina, myocardial infarction, cardiac death, and repeat revascularization after 12 months was not different in patients positive or negative for cTn-I. We conclude that cTn-I elevation after successful PTCA is not associated with significantly worse late clinical outcome. Levels of cTn-I allow a much higher diagnostic accuracy in detecting minor myocardial injury after PTCA compared with other markers, but there is no association with periprocedural myocardial cell injury and late outcome when cTn-I and other markers are considered.

Release kinetics of serum cardiac troponin I in ischemic myocardial injury.

OBJECTIVES: The study was undertaken to evaluate the release kinetics of cardiac troponin I (cTn-I) in ischemic myocardial injury. DESIGN AND METHODS: The reference range for cTn-I was established by determination of cTn-I in sera and plasma obtained from 622 healthy volunteers (Group 1). cTn-I was compared to: (a) Creatine kinase (CK) MB mass and myoglobin in 12 patients with severe skeletal muscle damage (Group 2); (b) CK-MB activity in 48 patients with myocardial infarction (MI) receiving intravenous thrombolysis (Group 3) (in this group, an additional 43 patients with MI were analyzed separately to characterize cTn-I patterns in thrombolyzed and nonthrombolyzed populations): and in 44 patients with unstable angina (Group 4). RESULTS: In Groups 1 and 2, no positive results (> or = 0.1 microgram/L) were obtained. In Group 3, the time-courses of cTn-I were mostly monophasic in form. A pathologic increase occurred earlier in cTn-I than in CK-MB activity (p = 0.0002); the period with increased cTn-I was longer (p = 0.001), the overall sensitivity of cTn-I (93.9%) was higher than that of CK-MB activity (p = 0.00001). cTn-I was more sensitive at admission (p = 0.0004). In additional patients, the cTn-I peak occurred and cTn-I disappeared significantly later in nonthrombolyzed than in the thrombolyzed group. In Group 4, positive tests results were detected in 45% of patients for cTn-I, 16% for CK-MB activity, and 32% for CK-MB mass. CONCLUSIONS: The cTn-I assay appears to be ideally suited for the detection of ischemic myocardial injury in complex clinical situations because of its high specificity; cTn-I indicates myocardial tissue damage in patients with unstable angina and is superior to CK-MB activity and mass in this respect.

Time-course of cardiac troponin I release from isolated perfused rat hearts during hypoxia/reoxygenation and ischemia/reperfusion.

The study was designed to determine the time-course of cardiac troponin I (cTn-I) release in isolated and Langendorff-perfused rat hearts during hypoxia and reoxygenation (H/Reox), and after various durations of total ischemia and subsequent reperfusion (I/R). For this purpose, in H/Reox, cTn-I was measured with the conventional Access immunoassay (ng/ml) and a new immunoassay which operates at pg/ml, and compared with creatine kinase (CK), lactate dehydrogenase (LD) and cardiac troponin T (cTn-T). In I/R, cTn-I was compared with CK and LD. The anti-Tn-I mAbs used in cTn-I assays cross-react with cTn-I of the rat. A clear difference between time-courses and concentration levels of cTn-I in I/R and H/Reox models was found. In I/R, maximum release of cTn-I, CK and LD similarly occurred within minutes following reperfusion; however cTn-I did not return to baseline values. cTn-I levels were not linked to the duration of ischemia. In I/R, we were only able to detect small cTn-I concentrations. In H/Reox experiments, cTn-I, CK and LD increased time-dependently. We found higher cTn-I maximal peak levels detected with the Access immunoassay than with the new assay (median, 0.346 ng/ml per min/g dry wt vs 132 pg/ml per min/g dry wt). cTn-T maximal concentrations were lower than maximal cTn-I levels (median, 0.117 ng/ml per min/g dry wt). Time-courses of cTn-I release were roughly similar with both assays in the H/Reox model (r = 0.90). These data indicate that the cTn-I time-course is related to experimental model (I/R or H/Reox), but also likely depends on the sensitivity of cTn-I assays in such experimental conditions.

Comparison of the diagnostic value of cardiac troponin I and T determinations for detecting early myocardial damage and the relationship with histological findings after isoprenaline-induced cardiac injury in rats.

Cardiac troponins I (cTnI) and T (cTnT) have been shown to be highly sensitive and specific markers of myocardial cell injury. The purpose of this study was to investigate the diagnostic value of cTnI and cTnT with regard to creatine kinase (CK) and lactate dehydrogenase (LD) and to determine whether they can be used for early diagnosis of myocardial damage in rats, and to examine the relationship between cTnl and cTnT release with histological examinations, using isoprenaline-induced cardiac muscle damage as an experimental model in the rat. Eighteen Wistar rats per group were treated with a single dose of either isoprenaline (iso) or with normal saline as a control group. The anti-cTnI and cTnT monoclonal antibodies (mAbs) employed in the cTnI (Access) and cTnT (Elecsys) assays cross-react with cTnI and cTnT of the rat. A highly significant rise of cTnl or cTnT was found already 2 h after iso. The time-courses of cTnI and cTnT were monophasic in form. The highest cTnI (mean+/-S.D., 1.1+/-2.3 ng/ml) and cTnT (mean+/-S.D. 3.6+/-30 ng/ml) were found 4 h after iso. cTnI and cTnT significantly increased in iso-treated rats in comparison with controls whether the differences between 2-, 4- and 6-h levels and basal levels were considered or not. The areas under cTnl and cTnT curves (AUC) (0-6 h) and the maximal cTnI and cTnT (0-6 h) after iso were significantly different from the controls. For CK and LD, no elevation in comparison with controls could be detected (except a trend for LD whether or not the difference between 6-h levels and basal levels were considered (P=0.08) and for LD AUC (0-6 h) (P=0. 059)). Correlations between maximal cTnI and cTnT and AUC were 0.69 (P=0.0001) and 0.60 (P=0.0066), respectively. Histological examinations of iso-treated rats revealed acute focal or multifocal myofibrillar degeneration of the myocardial tissue in ten out of 14 rats and showed the earliest alterations 4 h after iso in one treated rat. Only four of the controls exhibited evidence of mild changes and slight mononuclear cell infiltration. cTnl and cTnT peak values to at least 0.35 and 1.3 ng/ml, respectively, were necessary to detect histological myocardial cell injury after iso. cTnI and cTnT were found to be early markers for diagnosing iso-induced myocardial damage in comparison with CK and LD. Elevations of cTnI and cTnT appeared to relate to the severity of histologic changes after myocardial injury. Although there was a difference in the absolute concentration of results between cTnI and cTnT assays, due to a lack of standardization and heterogeneity in the cross-reactivities of mAbs to various troponin I and T forms, cTnI and cTnT can be used as easily measurable target parameters for detection of cardiotoxic and/or cardiodegenerative effects in rats.

Evaluation of cardiac troponin I and T levels as markers of myocardial damage in doxorubicin-induced cardiomyopathy rats, and their relationship with echocardiographic and histological findings.

BACKGROUND: Cardiac troponins I (cTnI) and T (cTnT) have been shown to be highly sensitive and specific markers of myocardial cell injury. We investigated the diagnostic value of cTnI and cTnT for the diagnosis of myocardial damage in a rat model of doxorubicin (DOX)-induced cardiomyopathy, and we examined the relationship between serial cTnI and cTnT with the development of cardiac disorders monitored by echocardiography and histological examinations in this model. METHODS: Thirty-five Wistar rats were given 1.5 mg/kg DOX, i.v., weekly for up to 8 weeks for a total cumulative dose of 12 mg/kg BW. Ten rats received saline as a control group. cTnI was measured with Access(R) (ng/ml) and a research immunoassay (pg/ml), and compared with cTnT, CK-MB mass and CK. By using transthoracic echocardiography, anterior and posterior wall thickness, LV diameters and LV fractional shortening (FS) were measured in all rats before DOX or saline, and at weeks 6 and 9 after treatment in all surviving rats. Histology was performed in DOX-rats at 6 and 9 weeks after the last DOX dose and in all controls. RESULTS: Eighteen of the DOX rats died prematurely of general toxicity during the 9-week period. End-diastolic (ED) and end-systolic (ES) LV diameters/BW significantly increased, whereas LV FS was decreased after 9 weeks in the DOX group (p<0.001). These parameters remained unchanged in controls. Histological evaluation of hearts from all rats given DOX revealed significant slight degrees of perivascular and interstitial fibrosis. In 7 of the 18 rats, degeneration and myocyte vacuolisation were found. Only five of the controls exhibited evidence of very slight perivascular fibrosis. A significant rise in cTnT was found in DOX rats after cumulative doses of 7.5 and 12 mg/kg in comparison with baseline (p<0.05). cTnT found in rats after 12 mg/kg were significantly greater than that found after 7.5 mg/kg DOX. Maximal cTnI (pg/ml) and cTnT levels were significantly increased in DOX rats compared with controls (p=0.006, 0.007). cTnI (ng/ml), CK-MB mass and CK remained unchanged in DOX rats compared with controls. All markers remained stable in controls. Analysis of data revealed a significant correlation between maximal cTnT and ED and ES LV diameters/BW (r=0.81 and 0.65; p<0.0001). A significant relationship was observed between maximal cTnT and the extent of myocardial morphological changes, and between LV diameters/BW and histological findings. CONCLUSIONS: Among markers of ischemic injury after DOX in rats, cTnT showed the greatest ability to detect myocardial damage assessed by echocardiographic detection and histological changes. Although there was a discrepancy between the amount of cTnI and cTnT after DOX, probably due to heterogeneity in cross-reactivities of mAbs to various cTnI and cTnT forms, it is likely that cTnT in rats after DOX indicates cell damage determined by the magnitude of injury induced and that cTnT should be a useful marker for the prediction of experimentally induced cardiotoxicity and possibly for cardioprotective experiments.

[Brain natriuretic peptide (BNP) and N-terminal-pro BNP in chronic haemodialysed renal failure]. / BNP (brain natriuretic peptide) et N-terminal proBNP chez l'insuffisant rénal chronique hémodialysé. Mécanismes d'élévation. Implications cliniques.

Brain natiuretic peptide (BNP) and N-Terminal-pro BNP (NT-proBNP) are biological markers of left ventricular dysfunction. An increase of one of these peptides is commonly observed in patients with chronic renal failure (CRF) undergoing haemodialysis, in the absence of cardiac failure or acute myocardial ischaemia. The interpretation and clinical implications of this finding are not known. This is a problem because cardiovascular disease is the main cause of morbidity and mortality in patients undergoing haemodialysis. In these patients, left ventricular hypertrophy and left ventricular dysfunction were associated with increased mortality. A biological marker of left ventricular dysfunction enabling early identification of high risk patients would be very useful in this population. Chronic renal failure and haemodialysis do not explain increased levels of BNP and NT-proBNP. Expansion of extra-cellular volume causing myocardial stretching and increased left ventricular pressures is the principal cause of increased BNP and NT-proBNP in haemodialysis patients. The left ventricular hypertrophy and endothelial dysfunction in severe chronic renal failure, systolic and diastolic left ventricular dysfunction, the associated cardiac disease (usually ischaemic) also contribute to this increase. In view of the relationship with left ventricular hypertrophy, left ventricular dysfunction, ischaemic heart disease, BNP and NT-proBNP are predictive factors of total and/or cardiovascular mortality in asymptomatic haemodialysed patients. The BNP/NT-proBNP value should allow identification of high risk asymptomatic haemodialysed patients who would benefit from aggressive evaluation of left ventricular hypertrophy and dysfunction and appropriate, targeted therapeutic intervention.

[Troponins and chronic renal failure in dialysis patients]. / Troponines et insuffisance rénale chronique chez l'hémodialysé. Fréquence et mécanismes d'élévation. Intérêt pronostique. Implications cliniques.

Cardiovascular disease is a major cause of morbidity and mortality in dialysed patients with chronic renal failure. The diagnostic and prognostic value of cardiac troponin T (TnTc) and I (TnIc) has been questioned in this setting. Dialysed chronic renal failure patients often have raised TnTc and TnIc in the absence of acute ischaemic symptoms. This increase is the consequence of minor myocardial damage due to coronary artery disease, left ventricular hypertrophy and endothelial dysfunction. Abnormal catabolism and differences in the liberation or detection of bound or free forms of the troponins may also contribute to the finding of raised TnTc in asymptomatic chronic renal failure patients. In this population, TnTc has a better prognostic value than TnIc for the identification of patients at greater risk (mortality). Increased TnTc in asymptomatic dialysed chronic renal failure justifies a thorough cardiovascular work-up to diagnose ischaemia, left ventricular hypertrophy (which should be a target for treatment) and left ventricular dysfunction, especially in diabetic renal failure and when non-emergency surgery or renal transplantation are planned. The troponins (mainly TnTc) retain their value for stratification of risk in acute coronary syndromes of patients with renal failure. An invasive strategy and pharmacological treatment (at adapted doses), identical to those considered for patients with normal renal function, should be discussed in dialysis patients with chronic renal failure admitted for acute coronary syndromes with raised troponins.

[Troponins: new biochemical markers of myocardial damage. Structure, immunoassay and clinical application]. / Troponines: nouveaux marqueurs biochimiques de la souffrance myocardique. Structure, immunodosages et applications cliniques.

The development of immunoassay techniques has made it possible to use new biochemical markers with a high myocardial specificity. Immunoassays have been developed for two of the structural myocardial proteins: troponin I and troponin T. The authors describe the biochemical properties of the troponins and the available methods of immunoassay. The main clinical applications of troponin measurement in cardiological practice are also reported.

[Multiple congenital coronaro-left ventricular fistulas. Apropos of 7 cases]. / Les fistules congénitales multiples coronaro-ventriculaires gauches. A propos de 7 observations.

Multiple congenital coronary-left ventricular fistulae (CLVF) are rare (4.5% of all coronaro-cardiac fistulae, the same incidence as isolated CLVF); data obtained from 7 personal and 25 previously reported cases, showed that this anomaly, is diagnosed at coronary angiography performed for anginal chest pains in 2 out of 3 cases; cardiac auscultation was usually normal but the basal ECG was pathological in 3 out of 4 cases; the electrical changes suggested myocardial ischaemia in 20 out of 24 cases. However, exercise stress testing was negative in 47% of cases. Multiple CLVF usually arose from the same artery (59%); the commonest artery involved was the left anterior descending (84% of the single artery fistulae and 100% in cases of multiple CLVF arising from more than one artery). The angiographic appearances of multiple CLVF were constant: images of "intracavitary rain". Associated ventriculographic abnormalities were uncommon but coronary atherosclerosis was observed in 15% of cases. The main differential diagnosis is that of CLVF secondary to intra-left ventricular thrombosis due to the development of neovascularisation of the thrombus from the underlying endocardium. The value of non-invasive investigations (2D echocardiography alone or coupled with pulsed Doppler) has not been shown in this type of coronaro-cardiac fistulae. Surgical correction was attempted in 3 cases, 2 of which had associated cardiac pathology justifying surgery. The presence of unequivocal coronary insufficiency due to CLVF was not demonstrated despite some suggestive clinical and paraclinical indicators.

[Proximal and peripheral coronaro-pulmonary fistulae. Apropos of 10 cases]. / Fistules coronaro-pulmonaires proximales et périphériques. A propos de 10 observations.

Coronaro-pulmonary fistula (CPF) is a rare congenital malformation comprising about 17 p. 100 of coronaro-cardiac fistulae. The authors report a series of 10 cases of CPF diagnosed in over 6 000 coronary angiographic studies. This material includes 7 cases of "proximal" CPF in which the receiving vessel was the main pulmonary artery (MPA), there were two cases of fistula between the coronary and distal pulmonary arteries ("distal" fistulae), one of which had an associated proximal CPF; finally one case showed abnormal vascularisation of part of the lung by a branch of the left circumflex artery. The left coronary artery was involved in all 8 cases of proximal CPF, confirming previously published data. The communication comprised a single pedicle or a plexus arising from the initial segment of the coronary artery and draining into the MPA in all cases. Coronary angiography was performed in the 5 men and 3 women (average age 53 years) for chest pain (2 cases) acute ischaemia in the territory of the left anterior descending artery (1 case), residual post-infarction angina and assessment after infarction (2 cases), mitral valve disease (2 cases) and for a continuous murmur (1 case). The ECG was normal in 2 cases; 5 patients had ST abnormalities; left ventricular hypertrophy was observed in 2 cases but these patients had associated mitral valve disease. Radiological cardiomegaly was present in 2 cases. Finally, no significant left-to-right shunt could be detected on cardiac catheterisation. The outcome was favourable in 7 patients (resection of fistula and eventual coronary bypass surgery in 3 cases; surgical abstention in the remainder).(ABSTRACT TRUNCATED AT 250 WORDS)

[Transesophageal stimulation in the treatment of atrial flutter and tachysystole]. / La stimulation transoesophagienne dans le traitement du flutter et de la tachysystolie auriculaire.

Transoesophageal left atrial pacing was used to reduce 102 episodes of ectopic atrial rhythms (79 common flutters and 23 ectopic tachycardias) in 83 patients (64 men, 19 women) aged 33 to 85 years (average 61 years). Overdrive pacing, at a faster rate than that of the spontaneous rhythm, was delivered via a bipolar pacing catheter introduced nasally and positioned behind the atrium under fluoroscopic and/or electrocardiographic control. Long pulse durations (up to 20 ms) were used to capture the atria with intensities of less than 20 mA for better tolerance. The overall results were: a) conversion to sinus rhythm in 60.8 p. 100 of cases (47 p. 100 directly and 13.8 p. 100 after transient atrial fibrillation), b) atrial fibrillation lasting over 24 hours in 7.8 p. 100 of cases, c) failure (31.4 p. 100) due to non-capture or intolerance (20.6 p. 100) or recurrence of the arrhythmia after transient atrial fibrillation (10.8 p. 100). Atrial flutter is more accessible to pacing than tachycardia (restoration of sinus rhythm in 63.3 p. 100 and 52.2 p. 100, respectively). Arrhythmias in the postoperative period of cardiac surgery, and isolated and recent arrhythmias were more easily converted. Prior antiarrhythmic therapy did not seem to improve results. Fifty per cent of failures of oesophageal pacing were converted to sinus rhythm by endocavitary pacing. These results show that atrial flutter or tachycardia may be successfully treated by oesophageal pacing in over 50 p. 100 of cases without having to use other forms of electrotherapy (endocavitary pacing or cardioversion).

[Evaluation of the size of thrombolysed myocardial infarction by serum myosin determination]. / Evaluation de la taille de l'infarctus du myocarde thrombolysé par le dosage de la myosine sérique.

The prognosis of myocardial infarction is very dependent on the size of the infarct. The measurement of the infarct size after thrombolysis remains difficult despite the large number of methods available, all of which have drawbacks. This parameter is however essential to assess prognosis and the efficacy of thrombolytic therapy. Serum beta heavy chain myosin determination is a recently introduced method of evaluating infarct size; there are relatively few published studies, especially concerning post-thrombolytic patients. A prospective study was undertaken in 40 patients (37 men and 3 women: average age 55.6 years) with a primary myocardial infarction treated by thrombolysis. Myosin levels (peak and area under curve of 5 samples in 10 days) were compared with other methods of assessing infarct size: electrocardiogram (number of leads with Q waves, ST segment analysis), cardiac enzymes (peak and release integrals of CK abd LDH), contrast ventriculography (segmental asynergy score, ejection fraction), coronary angiography and resting MIBI myocardial scintigraphy. The peak and integral of myosin release correlated well with the other methods (p < 0.01): a correlation was particularly apparent between the integral of myosin release and MIBI scintigraphy scores (r = 0.77, p < 0.001). Complex myosin release kinetics were observed significantly more often in patients with large infarcts (p < 0.01) or in those with occlusion of the artery responsible for infarction at coronary angiography on the 6th day (p = 0.001). In conclusion, with 5 blood samples over a 10 day period, it is possible to estimate the infarct size after thrombolysis in everyday cardiological practice: this method could help identify high risk subjects (complex kinetics of myosin release and high peak myosin levels) and also could be used to assess efficacy of thrombolytic therapy in large scale trials.

[Traumatic tricuspid insufficiency. Apropos of 2 cases]. / Insuffisance tricuspide traumatique. A propos de 2 observations.

The authors report two cases of tricuspid regurgitation by a ruptured anterior papillary muscle secondary to non-penetrating thoracic trauma. In the presence of suggestive clinical and electrocardiographic abnormalities (systolic murmur, right heart failure, right bundle branch block), echocardiography confirmed the tricuspid regurgitation, showed its mechanism and excluded any other intracardiac lesions. Tricuspid annuloplasty was performed in both cases because of the persistence of failure or degradation of the patient's clinical condition. Peroperative echocardiography was used to judge the quality of the surgical repair in both cases. Traumatic tricuspid regurgitation is a rare condition and the diagnosis is often delayed. Echocardiography is the investigation of choice and guides treatment which is essentially valvular repair in symptomatic patients.

[Arteriovenous fistula caused by spontaneous rupture of an aortic or iliac aneurysm in the iliocaval venous system. Apropos of 2 cases]. / Fistule artério-veineuse par rupture spontanée d'un anévrysme aortique ou iliaque dans l'axe veineux ilio-cave. A propos de 2 observations.

The authors report two cases of arteriovenous fistula due to spontaneous rupture of an aortic or iliac aneurysm into the iliocaval venous axis. This is a rare complication of atheromatous aneurysm (less than 4% of ruptured aneurysms), often difficult to diagnose as the clinical presentation may be obscure. Although aortography is the reference diagnostic investigation, color Doppler ultrasonography enabled visualisation of the arteriovenous communication and provided an accurate diagnosis in one recent case. Treatment of these aortocaval fistulae is always surgical. The prognosis and immediate operative mortality depend mainly on the presence of an associated retroperitoneal rupture.

[Pericardial mesothelioma. Apropos of a case]. / Mésothéliome péricardique. A propos d'un cas.

A 74 year old woman without previous cardiovascular disease presented with pericardial effusion and tamponade. Two-dimensional echocardiography displayed a pericardial mass, but a diagnosis of tumour was not envisaged. Pericardiocentesis produced an exudative fluid with lymphocytes but no malignant cells. Pericardial biopsies through axillary thoracotomy indicated chronic progressive pericarditis. As the patient's haemodynamics deteriorated, sternotomy was carried out showing diffuse pericardial sclerosis corresponding, at histology, to a mixed, predominantly fibroblastic pericardial mesothelioma. The authors describe the main clinical characteristics of pericardial mesothelioma, always discovered belatedly at surgery or necropsy. They insist on the value of non-invasive methods (two-dimensional echocardiography, computed tomography) to diagnose a pericardial tumour, and on the poor prognosis of mesotheliomas, treatment still being uncertain due to the small number of cases and to the early occurrence of cardiac complications.

[Lipomatous hypertrophy of the interatrial septum. Apropos of 3 cases and review of the literature]. / Hypertrophie lipomateuse du septum interauriculaire. A propos de 3 cas et revue de la littérature.

Lipomatous hypertrophy of the interatrial septum is characterised by an accumulation of fatty tissue in the interatrial septum. The authors report three cases, one presenting with sinus tachycardia and the other two being chance findings. Echocardiography associated with cardiac computerised tomography or magnetic resonance imaging usually confirms the diagnosis. In half the cases, supraventricular arrhythmias and suggestive P wave abnormalities are observed on the electrocardiogram. The diagnostic value of transoesophageal echocardiography is emphasised; it demonstrates the massive forms which may obstruct flow from the superior vena cava into the right atrium. The authors observe a discrepancy between the prevalence of this condition in autopsy series (about 1%) and the small number of cases described at echocardiography, suggesting that the diagnosis is probably missed.

[Prognostic significance of early raised cardiac troponine I in unstable angina. Contribution to the identification of a high-risk sub-group]. / Signification pronostique de l'élévation précoce de la troponine I cardiaque chez les patients en angor instable. Contribution à l'identification d'un sous-groupe à haut-risque.

The authors compared the clinical and angiographic characteristics of 44 patients with unstable angina according to cardiac Troponine I concentrations (TnIc) during early blood sampling and then tried to determine a threshold value to predic the occurrence of cardiac events during the hospital period and after 12 months. Tnlc, creatinine-kinase (CK), CK-MB activity and CK-MB mass were sampled over 48 hours. Forty-five per cent of patients had TnIc > or = 0.1 microgram/L; CK-MB activity and CK-MB mass were detected in 16 and 32% of patients. Age, gender, classification and recurrence of angina, previous cardiac history, risk factors, coronary angiographic appearances were comparable in patients with and without raised TnIc. No major cardiac events occurred during the hospital period in either group. The number of angioplasties and coronary bypass procedures was also comparable. At one year, the incidence of myocardial infarction (N = 4) and death (N = 5) was significantly different in patients with raised Tnlc (33% versus 0% in patients without increased TnIc). However, betablocker therapy was less prescribed in the group with the poorest outcomes and left ventricular dysfunction was also significantly more common in this group. Early elevation of Tnlc could contribute to the identification of a high risk subgroup of patients with unstable angina.

[Value of human cardiac troponin I determination in the diagnosis of acute myocardial infarction]. / Intérêt du dosage de la troponine I cardiaque humaine dans le diagnostic de l'infarctus aigu du myocarde.

Immunoenzymatic assay (IEMA) of human cardiac Troponin I (TnI c) was used in patients admitted to the coronary care unit with acute myocardial infarction (AMI). TnI c was detected in all patients with AMI. The detection of TnI c was earlier after the onset of pain (4.5 +/- 2.3 hours) than that of CKMB activity (6.3 +/- 3.6 hours), p = 0.003. The kinetics of TnI c are usually monophasic and parallel to that of CKMB activity. The peak value occurs 12.2 +/- 4.6 hours and 15.8 +/- 9.0 hours after the onset of pain in patients treated by thrombolysis. The TnI c disappears from the plasma between 5 and 9 days after the onset of pain, later than CKMB activity (p = 0.0001). In 49 patients admitted for AMI treated by thrombolysis, the comparative sensitivities of TnI c (threshold: 0.1 ng/ml) and of CKMB activity (threshold: 15 IU/l; CK > or = 100 Ul/l) were, at the first sampling on admission, 61% and 22% respectively (p = 0.0002) (average interval from onset of pain to first blood sampling: 3.4 +/- 1.3 hours). TnI c was not detected in the plasma of 145 normal subjects nor in any of the 6 patients with severe muscular trauma or rhabdomyolosis (specificity: 100%). This IEMA is a specific and a sensitive method of diagnosing acute and subacute myocardial infarction. It is ideal for the detection of myocardial necrosis in complex clinical situations when the usual enzymatic markers may be ineffective.