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Reciprocal ST segment changes are frequent during acute inferior myocardial infarction, yet their significance remains controversial. In order to investigate the implications of these changes, the ECG obtained on admission for 83 patients with acute inferior myocardial infarction was compared with the clinical course and the results of angiographic and coronary arteriographic studies performed an average of 3 weeks after the onset of symptoms. Group 1 consisted of 59 patients with at least 1 mm of horizontal on downsloping ST segment depression in at least 1 of leads V to V. Group 2 consisted of 24 patients without precordial ST depression in this area. Group 1 patients were generally older than group 2 patients (59.6 ± 6.4 versus 54 ± 5.3 yr, P<0.01) had higher total creatine kinase (CK) levels and MB fractions (1835 ± 940 versus 875 ± 305, P < 001, 269 ± 102 versus 95 ± 35 for MB fraction) and more complications during the hospital course (80% versus 38% P<0.01) and greater left ventricular dysfunction (ejection fraction 52.2 ± 6% for group I versus 59.2±7% for group 2; cardiac index 2.75±0.41min m for group 1 versus 3.25 ± 0.3 lmin m for group 2 P<0.005). No difference was observed on biplane angiography as far as left ventricular wall kinesis was concerned. By contrast, coronary arteriography revealed more frequent left coronary artery disease in group 1 patients (84%) than in group 2 patients (37%) P<0.005, the left anterior descending and circumflex arteries being equally often affected. Finally, the persistence of ST segment depression for more than 48 hours was associated with a more severe depression of the ejection fraction than transient depression (less than 48 hours). In summary, the presence of ST segment depression in the precordial leads during the acute phase of inferior myocardial infarction was associated with greater myocardial necrosis and more frequent left coronary artery disease, thus identifying a subset of high risk patients. [ABSTRACT FROM PUBLISHER]

Objective Between July 1992 and December 1994, 16 French hospital centres, mainly cardiological, participated in a non-controlled observational study on venous thromboembolic disease. The objective of this survey was to collect data concerning the current status of pulmonary embolism and deep venous thrombosis. Patients During this period, 547 patients were included: 446 with deep venous thrombosis and 387 with pulmonary embolisms. Results Mean age of patients was 63±21 years. There were no significant differences between the sexes. Pulmonary embolism and deep venous thrombosis tended to occur more frequently during the autumn and winter. In 30% of cases, prior deep venous thrombosis or pulmonary embolism was noted. No cause was found for the condition in 47% of cases. Ultrasound (echocardiography and/or venous ultrasound) was the most frequently requested investigation. Intravenous heparin remains the most widely used treatment (76%). Oral anticoagulation was begun before day 3 in less than 31% of cases. Thrombolytic treatment was used in 20% of pulmonary embolism cases, but was rarely prescribed for deep venous thrombosis (2·2%). The hospital recurrence rate (12/547 cases) was fairly low. The search for occult malignancy, performed in 48% of cases, seems to remain one of the major concerns of physicians. The combined pulmonary embolism and deep venous thrombosis mortality rate was 4·4%, while the death rate for pulmonary embolism alone was 6·2%. [ABSTRACT FROM PUBLISHER]

Background and Objective: In patients presenting with pulmonary embolism (PE), echocardiography, in some cases, reveals mobile clots in right heart (RH) cavities. How these clots evolve after treatment, in particular after thrombolytic treatment (TT), is unknown. We sought to determine the outcome of these mobile clots in the RH during TT. Methods and Results: Of a series of 343 patients who had been hospitalized for PE in our department, echocardiography performed on hospital admittance showed a mobile clot in the RH in 18 patients (mobile clot incidence, 5.2%). This subgroup of 18 patients presented with a more severe form of PE than the 325 patients without mobile clots in the RH. In our series, 16 patients were treated with thrombolytic agents. Close echocardiography monitoring showed the outcomes of these mobile clots during and after TT. In 50% of cases, the clot disappeared rapidly in < 2 h after the end of TT. In 50% of the remaining cases, the clot disappeared later, half within 12 h following the completion of TT, and the other half within 24 h. All patients were alive on day 30 without any clinical sequellae. Conclusion: In these particular forms of PE with mobile clots in the RH, the short time lag required to disperse the clot after TT makes it imperative to delay any decision about new aggressive therapy. [ABSTRACT FROM AUTHOR]

In 20 patients who had recently had an acute myocardial infarction, we compared endocoronary electrocardiographic modifications recorded during angioplasty with thallium-201 for the detection of myocardial viability. Our data demonstrate that endocoronary electrocardiography can be an easy and reliable tool to assess viability, with sensitivity, specificity, and positive and negative predictive values of 100%, 80%, 94%, 100%, respectively. [ABSTRACT FROM AUTHOR]

Background: Elevated plasma homocysteine levels are associated with increased risk of vascular disease and of congestive heart failure (CHF), with a relationship between homocysteine values and disease severity. Hyperhomocysteinemia is a risk factor for cardiac dysfunction. In this study, the predictive value of elevated homocysteine levels was investigated in the prognosis of ischemic and non-ischemic CHF., Methods: A total of 159 patients with CHF, 89 with non-ischemic and 70 with ischemic CHF (83% males, mean age 62 years, mean ejection fraction 27%), and 119 controls (79% males, mean age 59.8 years) had fasting blood samples taken to measure plasma homocysteine, vitamin B(12) and folate levels. Coronary angiography was performed for all patients. The mean duration of follow-up was 49.6+/-36.7 months., Results: As in other studies, the mean level of homocysteinemia was significantly higher in the CHF group (15.80 micromol/L) than in the control group (10.90 micromol/L) (p=0.001) whatever the etiology (non-ischemic, 16.11+/-6.84 micromol/L; ischemic, 15.41+/-6.45 micromol/L). This result was observed without vitamin deficiency, but in patients, the mean creatinine value was moderately higher than in controls. We found a positive correlation between plasma homocysteine levels and New York Heart Association (NYHA) classification, creatinine and age. Moreover, hyperhomocysteinemia appears to be a powerful predictive factor of mortality in CHF patients (relative risk of death, 4.23; p=0.0003). In the follow-up of this study, 41.5% of patients with homocysteinemia >17 micromol/L died vs. 21.3% of patients with levels <17 micromol/L. In multivariate analysis, when homocysteine levels were adjusted for a second parameter (age, NYHA, creatinine, diabetes), the risk of death remained significant after each adjustment., Conclusions: Elevated homocysteine levels observed in CHF patients, whatever the etiology of their heart disease (ischemic or non-ischemic), were correlated with the severity of the disease. Hyperhomocysteinemia appears to be a predictive factor of mortality in CHF patients.

Traumatic aortic valve regurgitation is a rare complication of non-penetrating thoracic trauma. The most frequent lesion is the isolated injury of the non-coronary cusp. Actually, the transoesophageal echocardiography is the procedure of choice to confirm the diagnosis and to reveal the associated cardiovascular lesions. Surgical management with early operation is the best policy, however this surgery can be delayed for treatment of other life-threatening injuries. Up today, aortic valve replacement (AVR) was recommended to repair traumatic aortic valve regurgitation; nevertheless, in the recent international literature, the number of cases reports with conservative surgery (CS) is increasing: 10 AVR (group I) and 10 CS (group II). Analysis of the post-operative and long term periods shows good results: it confirms the excellent clinical evolution in the group I (mean time of follow-up: 18.2 +/- 16.3 months), and reveals satisfactory results in the group II for patients with isolated lesion (mean time of follow-up: 29.1 +/- 30.7 months). In conclusion, each time the traumatic aortic regurgitation is due to an isolated lesion, the conservative surgery should be performed in order to avoid aortic valve replacement and its potential complications especially in young patients with healthy valves. However, the aortic valve replacement is the safest technique for complex or multiple injuries of the aortic valve.

Anticancer chemotherapy continues to advance. One of the new therapeutic orientations is the targeting of receptors which regulate the tumoral activity of the malignant cells. Trastuzumab is the prototype of these new chemotherapeutic agents. It is a monoclonal antibody directed against a tyrosine kinase receptor related to the EGF (Epidermal Growth Factor): the HER receptor. This receptor is also present in myocardial cells. Blockade of this myocardial receptor could cause severe cardiotoxicity about which some information is available but which continues to pose many problems. This data should be known as cardiologists will be consulted before the prescription of Trastuzumab and could also be confronted by these cardiotoxic effects. Precise physiopathological explanations have already been published from experimental studies which show the deleterious effects of the suppression of certain HER receptors on the heart. These studies not only explain all the clinical signs of Trastuzumab's cardiotoxicity but also suggest ways of preventing and treating some of these cases of cardiac failure.

Can the biochemical evidence for "new thrombophilic factors" influence the duration of AVK treatment following the occurrence of a first pulmonary embolus? Certainly for the classic but very rare antithrombin defects as well as for the existence of circulating anticoagulant. Possibly for protein C and S defects. On the other hand, the existence of a heterozygotic "Leiden" mutation of factor V, or factor II, and an increase of factors VIII, IX, or XI, do not at present warrant a change in AVK prescription. In effect, in the case where the existence of a thrombogenic state implies a prolongation of AVK treatment with its significant potential complications, it is indispensable that the risk/benefit ratio is well founded, which is not the case for these "new" thrombophilic states. The coexistence of several of these new biochemical anomalies (for example the association of a factor V and factor II mutation) probably represents an excess risk of thrombosis, but in this situation the reasoning remains the same. On the other hand, faced with a confirmed recurrence, the studies in the literature tell us that very long term treatment should be debated independently from the biochemical results. It is conceivable that there are biochemical anomalies (sometimes quite frequent which should be viewed as "normal variants") which, although they have great significance for improving the understanding of venous thrombo-embolic disease, do not at present warrant a change in our therapeutic protocols. Another facet of the problem concerns the use of D-dimers following the first months of AVK treatment in order to possibly distinguish patients at low risk of recurrence. The first results of this approach are interesting, but require confirmation before they can be used in practice.

An atrial arrhythmia could be encountered during the atrial lead implantation. The lead placement must subsequently be delayed after restitution of the sinus rhythm or completely abandoned. The authors investigate the atrial lead placement during atrial arrhythmia and the lead performance at 6-month follow-up. The study population was 65 patients aged 78.5 years, 42 males and 28 structural heart diseases. They were implanted for sick sinus syndrome (n=14), atrioventricular block (n=44), infra-hisian conduction abnormality (n=7) in association with an atrial fibrillation (63.1%), an atrial flutter (24.6%) or an atrial tachycardia (12.3%). The onset of the arrhythmia was < or = 7 days (47.7%) or > 7 days (52.3%). An atrial lead was placed in the right atrial appendage under fluoroscopic control. If the sinus rhythm was not restored at 1 month, an electrical cardioversion was performed. The per-implantation atrial signal amplitude was 2.2+/-1.5 mV (range 0.5 mV to 7 mV). Sinus rhythm was restored in 54 patients. At 1 month, one patient was in an incessant atrial fibrillation. The 53 patients in sinus rhythm had a good atrial lead performance. Out of 46 patients who completed the 6-month follow-up, 4 had an arrhythmia recurrence. The 42 patients in sinus rhythm had a good atrial lead performance. At 1 and 6-month follow-up, the atrial pacing threshold (1.1+/-0.7 V vs 1.2+/-1.0 V, ns) and the atrial signal amplitude (2.1+/-1.0 mV and 2.1+/-0.9 mV, ns) were stable. Comparing the patients with a recent or a chronic arrhythmia, the pacing thresholds (1.2+/-1.1 V vs 1.14+/-0.8 V, ns), the atrial signal amplitudes (2.17+/-0.9 mV vs 2.05+/-0.9 mV, ns) and the proportion of satisfactory pacemaker performance in DDD(R) mode for the patients in sinus rhythm (100% vs 100%, ns) did not statistically differ between the two groups at 6 months. In conclusion, the placement of an atrial lead in the right atrial appendage during an atrial arrhythmia is feasible with a good lead performance at 6 months in sinus rhythm regardless the onset time of the arrhythmia and provides a satisfactory atrial-based pacing with the preservation of the atrioventricular synchrony.

Malignant disease predisposes to deep venous thrombosis (DVT) or pulmonary embolism (PE) in several ways. One classical situation is that of DVT or PE with no apparent cause which may be the first sign of an occult cancer. In this domain, although the epidemiological data is well known, it is important to recognise the limitations of "blind" investigations. Another situation is more common. The patients have a diagnosed malignancy and thromboembolic disease is the main extra-cancer complication. The approach to this problem is changing, both in primary prevention where many trials have already reported encouraging results, and in the treatment after the event where classical therapeutic protocols are not always well adapted. Ancestral fears of the prescription of anticoagulants in cancer patients must cede to a more objective benefit/risk analysis which seems to be very favourable in some situations. Moreover, some publications have demonstrated a chance finding of a possible anticancer effect of antithrombotic agents.

The necessity of anticoagulant treatment after a pulmonary embolus or a deep venous thrombosis has been demonstrated. The modalities of this treatment have been well established, especially the usefulness of initial heparin therapy followed by a period of antivitamin K treatment with an "ideal target INR" between 2 and 3. One of the last questions in this therapeutic protocol is the duration of antivitamin K treatment. The choice of duration of treatment must be made on numerous criteria. It is necessary to distinguish the circumstances of the occurrence of the DVT or the PE and the context. It is thus possible for less than 3 months treatment in secondary venous thrombo-embolic disease, which occurs in precise, recognised circumstances for which the cause will have been controlled. Otherwise, in so-called idiopathic venous thrombo-embolic disease, which is distinguished by a higher prevalence of recurrences, it is known that long-term antivitamin K treatment is effective for the thrombo-embolic recurrences but at the price of a risk of haemorrhage. Finally thrombo-embolic recurrences also benefit from a long treatment. These circumstances of occurrence are thus important in order to decide the choice of treatment duration. But, in our opinion, the compliance to antivitamin K treatment remains the primary criterion to consider. The dilemma facing the prescriber is to evaluate the risk-benefit ratio of each patient, asking especially if the antivitamin K treatment surveillance of a particular patient will be done as well as in the randomised studies. For the future, long-term antivitamin K does not perhaps represent the only therapeutic option. The results of studies evaluating the durations of long-term treatment with less intense levels of anticoagulation (INR < 2) as well as therapeutic alternatives to antivitamin K (antiaggregants or other antithrombins) are awaited.

In the cardiac patient, there are clinical situations where antivitamin K is indicated more by the co-existing pathological associations or by a particular thrombogenic situation than by the cardiac disease itself. The presence of an embologenic abnormal rhythm, an apical thrombus or a large anterior akinesis are recognised as situations where antivitamin K must be discussed and, except for absolute contraindication, initiated. The studies undertaken for several decades are highly instructive and their contributions are considerable in the different questions which could be asked regarding the efficacy of antivitamin K. In particular they have the merit of signalling the correct directions to take and the errors to avoid. Concerning the evolution of cardiac disease, it must be admitted that the very good results of antivitamin K treatment alone at high dose are to be balanced against their haemorrhagic risk. The studies testing the association of low-dose aspirin with moderate-dose antivitamin K (INR 2 to 2.5) are to date very promising. The evaluation of the understanding of the treatment by patient education remains a major stage when initiating antivitamin K treatment in the cardiac patient.

Unlabelled: It has been shown in clinical studies that for subjects with a low likelihood of coronary artery disease (CAD), attenuation correction (AC) improves the specificity of defect detection in the inferior wall (right coronary artery [RCA] region). The aim of this study was to investigate the effect of AC on the visual interpretation of the RCA and anteroseptal (corresponding to the left anterior descending artery [LAD]) regions in CAD patients., Methods: Fifty-six patients with suspected CAD underwent 20Tl stress/4 h-delayed imaging SPECT using a simultaneous 201Tl emission/99mTc transmission imaging protocol. Images were reconstructed using the maximum likelihood-expectation maximum algorithm without and with AC. The stress/4 h-delayed images were interpreted blindly for reversible or fixed defects in the RCA and LAD regions by three experienced physicians. Coronary angiography, electrocardiography and enzyme findings were used to establish diagnoses of ischemia or infarction, and receiver operating characteristic (ROC) analyses were performed., Results: Statistical testing of ROC curve areas showed that defect detection performance improved with AC when compared with performance without AC in the RCA region. This was mainly the result of a systematic increase in specificity of 12% or more (for any observer and any type of defect) for a similar sensitivity (no definite change in sensitivity values). However, defect detection performance significantly decreased in the LAD territory with AC images (P < 0.05) because of a systematic decrease in sensitivity of 20% or more, with no consistent change in specificity. Similar trends were observed when reversible and fixed defects were considered separately., Conclusion: AC significantly affects the visual interpretation of 201Tl stress/4 h-delayed SPECT images. This study confirmed the increase in specificity obtained with AC in the RCA territory. However, in the population considered, the studied AC was deleterious for the LAD territory assessment.

Objectives: Our aim was to confirm the poor prognosis related to thoracic aortic plaques, in particular aortic debris, diagnosed by transesophageal echocardiography (TEE) and to evaluate patients' prognosis as a function of the antithrombotic treatment., Background: Aortic atheroma (AA) has been widely studied. However, it is still not known which antithrombotic treatment should be adopted in this disease., Methods: Patients referred for TEE and diagnosed with AA were followed. All thromboembolic events and deaths were recorded during a follow-up of 22+/-10 months. The antithrombotic treatment to be adopted was left to the discretion of the practitioner in charge of the patient., Results: Aortic atheroma was found in 12% of all TEE performed and in 27.5% of TEE performed for stroke. This prevalence was higher when no other etiology existed to explain the stroke (p < 0.001). During follow-up, an end point occurred in 22.5% of patients. The more severe the AA the greater the incidence of events (p = 0.007). A higher mortality rate is shown in patients with aortic debris (p = 0.049). Compared with those treated with oral anticoagulants, patients with aortic plaques >4 mm thick treated with antiplatelets had more embolic events and combined events (p = 0.01 and p = 0.007, relative risk [RR] = 5.9, 95% confidence interval [CI] = 1.4 to 15, respectively); patients with aortic debris had more combined events and a higher mortality rate (p = 0.001, RR = 7.1, 95% CI = 1.2 to 19 and p = 0.019, RR = 9.1, 95% CI = 1.2 to 25, respectively)., Conclusions: We confirm the high incidence of vascular events and deaths in patients with AA. We have demonstrated, for the first time in this condition, a better outcome among patients treated with oral anticoagulants versus antiplatelets.

Background: The link between travel and the risk of venous thromboembolic disease (VTED) has been widely suspected. However, only cases or series of cases have been reported in the literature., Study Objectives: By means of a case-control study, we sought to confirm this relationship and to determine the main features, if any, of these posttravel VTEDs., Design: The history, in particular the history of recent travel, of 160 patients presenting in our department with VTED was scrupulously investigated. All journeys undertaken during the preceding 4 weeks and lasting > 4 h by whatever means of transport were considered. The same questionnaire was submitted to a control group., Results: When the two groups of patients are compared, a history of recent travel is found almost four times more frequently in the VTED group (p < 0.0001). The odds ratio for having a VTED in patients who traveled was 3.98 (95% confidence interval, 1.9 to 8.4). Means of travel used included the train in 2 cases, airplane in 9, and car in 28. Mean duration of travel was 5.4+/-2.1 h. These posttravel VTEDs are not confined to a specific location, seem to involve no particular predisposition, and are more often "idiopathic." This fact supports the hypothesis that travel alone can produce vein clot formation., Conclusions: A history of recent travel is a risk factor for VTED. Posttravel venous thrombotic events can occur after short journeys in patients with no other risk factors or concomitant disease

Masquerading bundle branch block associates left bundle branch block in the standard lead and right bundle branch block in the precordial leads. Mr R., 67 year old, was referred for investigation of syncope. He had a history of idiopathic dilated cardiomyopathy (normal coronary arteries; EF: 14%, CI: 2.2 l/min/m2 at later investigations). The ECG showed LBBB with left axis deviation, a PR interval at the upper limits of normal and ventricular premature beats. During observation, he had another syncopal episode and the ECG showed wide complex tachycardia (160 bpm) reduced by external cardioversion. Electrophysiological investigations showed inducible VT due to bundle branch reentry. The HV interval in sinus rhythm was 80 ms. Radiofrequency ablation of the right bundle led to first degree AVB with masquerading bundle branch block with an increased HV interval of 120 ms. The usual facility of ablation of the right bundle branch block is an argument in favour of the hypothesis whereby masquerading bundle branch block is a variety of RBBB with severe conduction defects of the two branches.

Circulating endothelin-1, a very strong peptide vasoconstrictor first discovered in 1988, is raised in cardiac failure. This increase contributes to the deleterious effects of cardiac failure. Although specific anti-endothelin drugs are under development in this condition, the effects of more commonly used drugs on circulating endothelin-1 levels are not well known. The aim of this study was to evaluate the effects of ACE inhibitor therapy on plasma endothelin-1 levels in cardiac failure. The plasma endothelin-1 levels were measured in 24 patients (stages III and IV of the NYHA classification), before and after treatment with angiotensin converting enzyme inhibitor (Captopril: test doses, then 75 mg/day). A control group of 10 paired patients was used to shake off the effects of bed rest and hospital salt-free diet. The initial endothelin-1 levels were high but equivalent in the control and study groups: 9.13 +/- 1.87 fmol/mL vs 8.98 +/- 1.92 fmol/mL. Plasma endothelin-1 decreased significantly in the study group 72 hours after beginning ACE inhibitor therapy (7.44 +/- 1.95, p < 0.02) but remained higher than normal (p < 0.01), whereas the values in the control group remained the same. This study demonstrates a decreases in plasma endothelin-1 levels 72 hours after onset of ACE inhibitor therapy in patients with stable severe cardiac failure. This results, already suggested by many experimental studies and certain ancillary clinical trials, could explain some of the beneficial effects of ACE inhibitors in this condition.

Objectives: High blood levels of homocysteine have been recently described as a risk factor for thromboembolic events and early development of atherosclerosis. The aim of this work was to study homocysteine blood levels in patients under 55 years of age with acute coronary artery disease., Patients and Methods: The study included 110 patients (98 men, 12 women) with poorly controlled angina pectoris (n = 35) or in the acute phase of myocardial infarction (n = 65). Homocysteine was assayed by liquid chromatography in all patients on the day of the acute episode and 24 hours later. Homocysteine levels were also determined in 40 controls under 55 years of age with no history of coronary artery disease., Results: Blood level of homocysteine was 10.6 +/- 6.2 mumol/l in the patients and 7.7 +/- 2.5 mumol/l in the controls (p < 0.01). The difference was greater in the 30-40 year age rang with 14.4 +/- 2 mumol/l in patients versus 6.4 +/- 1.5 mumol/l in controls (p < 0.001). The assays were reproducible at 24 hours (difference less than 10%). The levels were significantly higher in patients with several diseased arteries than those with single-artery disease. The difference between patients and controls was especially remarkable for non-smokers and those with high cholesterol levels., Conclusion: Hyperhomocysteinemia would be a factor favoring early development of coronary atherosclerosis.

Background and Study Objective: The value of the ECG for the diagnosis of pulmonary embolism (PE) is debatable. Once the diagnosis of PE has been established, however, the ECG could allow the massive forms to be distinguished. The purpose of our study was to analyze the ECG signs in patients hospitalized for PE in a cardiology unit., Design: Taking a series of 80 consecutive patients hospitalized for PE, we analyzed the ECGs on admission and then during hospitalization. We sought to evaluate changes in ECG signs compared with angiographic and hemodynamic changes in PE., Results: T-wave inversion in the precordial leads is the most common abnormality (68%), and represents the ECG sign best correlated to the severity of the PE. Among those patients with anterior T-wave inversion, 90% had a Miller index over 50% (mean, 60 +/- 8%). Eighty-one percent had a mean pulmonary arterial pressure (PAP) over 30 mm Hg (mean, 37 +/- 8%). This subepicardial ischemic pattern is an even stronger marker of severity when it appears as early as the first day (p < 0.01). Its reversibility is correlated to the changes in PE. After thrombolysis in particular, normalization of repolarization systematically indicates mean Miller and PAP indexes of < 20% and < 20 mm Hg, respectively., Conclusions: The anterior subepicardial ischemic pattern is the most frequent ECG sign of massive PE. This parameter is easy to obtain and reflects the severity of PE. Its reversibility before the sixth day points to a good outcome or high level of therapeutic efficacy.

The tilt test is a widely used diagnostic tool for the investigation of syncope of suspected vasovagal origin. Some workers suggest that the sensitivity should be increased at the price of the loss of some specificity. Passive (non-sensitised) or isoproterenol (sensitised) protocols have not been widely studied on a large scale. The authors report the respective results of two protocols (passive and sensitised with isoproterenol proposed by Benditt et al.) applied to the same subject at 24 hours' interval in a random order in a series of 108 patients (age 56 +/- 19.3 years, 72 men) with unexplained syncope or malaise. After 30 minutes in decubitus, an 80 degrees tilt was maintained for 45 minutes for the passive test and for 25 minutes for the sensitised test, followed by a continuous infusion of isoproterenol in 10 minutes intervals of decubitus and inclination at successive doses of 1.3 and 5 micrograms/min. One or both tests were positive in 62 patients (57.4%). The overall concordance of the two tests (both positive or both negative) was 53.7%. In a subgroup of 60 subjects with clinically suggestive vasovagal attacks, the sensitivity of the passive test was 25% compared with 73.3% with the isoproterenol test (p < 0.001). Based on this difference of sensitivity between the two protocols, and knowing the good specificity of the isoproterenol test, the authors recommended the isoproterenol test as being of great practical value.

The authors report the case of a non-Hodgkin malignant lymphoma (NHL) of the heart presenting with syncope. The diagnosis of a cardiac tumours was made by echocardiography. Myocardial biopsy enabled diagnosis of a highly malignant NHL in a patient with a history of low grade NHL. Chemotherapy with CNOP (Cyclophosphamide, Novantrone, Oncovin, Prednisone) induced total regression of the tumour. The patient is in total remission 23 months later. The authors emphasise the value of echocardiography in the diagnosis and follow-up of this pathology. The case is also noteworthy because of the unusual transformation of a low grade to a high grade cardiac NHL.

Cerebral emboli, regardless of their nature, can be detected by transcranial Doppler by performing long-term recordings of the middle cerebral artery. The signals detected, called HITS (high intensity transient signals) described in vitro and in vivo have particular physical characteristics. These embolic signals have been identified in patients with prosthetic heart valves, in patients with atrial fibrillation, following myocardial infarction, following cerebrovascular accident, in patients with carotid stenosis or aortic plaques, during cardiac and carotid surgery and during carotid angiography. During assessment of a cerebrovascular accident, the discovery of HITS could be an argument in favour of an embolic origin. This new technique raises great hopes for establishing the relationship between the discovery of emboligenic heart disease and their neurological clinical manifestations. This new technique has many fields of application: investigation of asymptomatic emboli in patients with emboligenic heart disease, efficacy of antiaggregant, anticoagulant or surgical treatments.

The necessity for anticoagulant treatment after pulmonary embolism or deep vein thrombosis has been demonstrated. The modalities of this treatment have been established, especially the value of initial heparin relayed by oral antivitamin K therapy with a target INR value between 2 and 3. The last question remaining in this protocol is that of the duration of anticoagulant treatment. The choice of duration of anticoagulation should take into consideration two potential complications: haemorrhage due to over-anticoagulation and excessive duration of therapy, and recurrent thromboembolism which could result from an inadequate duration of therapy. Several trials have addressed this question and have led to a consensus of opinion: therefore, secondary venous thrombo-embolic disease, occurring under known, special circumstances, the cause of which has been treated, should be given 4 to 6 weeks anticoagulant therapy. In the other cases, so-called idiopathic venous thromboembolism (the proportion of which is on the increase), recent studies are inadequate to reach a consensus. These "idiopathic" forms are characterised by a higher incidence of recurrent thromboembolism of "secondary" cancer and coagulation abnormalities. The search for the optimal duration of anticoagulant therapy in these forms requires prospective trials taking their features into account and should lead to further therapeutic options. The evaluation of longer treatment protocols with less intensive degrees of anticoagulation and of alternatives to oral vitamin K antagonists is justified.

There are few conditions in medicine as difficult to diagnose as pulmonary embolism. This is certainly not due to the rarity of the disease which is probably as common as myocardial infarction in France. The circumstances surrounding pulmonary embolism and the risk factors of deep venous thrombosis have been well identified. The risk of thromboembolic venous disease has been assessed for each type of surgery. The methods of treatment and prevention have progressed over a number of years. However, in practice, these advances have not "transformed" the frequency of the disease or reduced its mortality. Further progress could come from improved identification of patients at risk, especially by biological tests and new abnormalities of blood coagulation.

We evaluated the hemodynamic impact of right ventricular pacing at different stimulation frequencies. Fourteen patients with a right ventricular pacemaker (VVI pacing with retrograde P wave) but without clinical and electrocardiographic evidence of coronary artery disease underwent two equilibrium radionuclide angiographies: one under low heart rate (50/60 beats per minute) and the other under fast heart rate (90/100 beats per minute). Left ventricular global and sectorial ejection fractions, amplitude and phase images of first harmonic, and sectorial phases of left ventricle were analyzed. In twelve patients (84.7%), sectorial ejection fraction abnormalities in the left ventricular apicoseptal and inferoapical regions were observed under low heart rate, and worsened under fast heart rate, while new onset sectorial ejection fraction abnormalities under fast heart rate were observed in the other two patients with normal sectorial ejection fraction under low heart rate. Sectorial ejection fractions of left ventricular apicoseptal and inferoapical regions significantly changed between low and high heart rate (- 14.1 +/- 3.8%, p < 0.005; - 7.5 +/- 2.4%, p < 0.01 respectively). Left ventricular sectorial phases were abnormal in only two patients (14.3%) under low heart rate, and in twelve patients (84.7%) under fast heart rate. Our study confirms that left ventricular regional wall motion abnormalities during VVI pacing significantly worsen under fast heart rate in comparison to those under low heart rate.

The authors describe a case of sinus tachycardia, an unusual cardiac complication of mediastinal radiotherapy; occurring in two patients by the first days of treatment and persisting for several years. No other cause for this tachycardia could be detected in either case. Electrophysiological investigation of one of the two patients was normal. Despite the risk of a high-degree conduction disorder, "symptomatic" beta-blocker treatment was prescribed, but only induced a limited effect.

Interatrial conduction time (IACT) and left atrial dimension (LAD) were determined in 75 patients (41 males, 34 females, mean age 78.2 +/- 7.9 years) undergoing atrioventricular (AV) stimulation. The LAD was measured by M mode echocardiography as the distance between the posterior aortic wall and the posterior left atrial wall. The IACT was determined during a transvenous dual chamber pacemaker implant done under local anesthesia (lidocaine). The spontaneous interatrial conduction time (SIACT) was measured from the intrinsic deflection (ID) of the right atrium recorded in a unipolar mode (unipolar J-shaped lead positioned in the right appendage) to the ID of the left atrium (bipolar esophageal lead, left atrial positive deflection equal to the negative one) during sinus rhythm. The right atrium then was paced at a rate slightly greater than the spontaneous one. The paced interatrial conduction time (PIACT) was measured from the stimulus artifact to the left atrial ID. The PIACT was also measured during incremental right atrial pacing (10 beats/min step increase to 180 beats/min) and, from these measurements, the maximum increase of PIACT (MIPIACT) was deduced. The LAD was measured at 39.5 +/- 8.7 mm, SIACT at 70.3 +/- 24.8 msec, PIACT at 118.8 +/- 27.9 msec, and MIPIACT at 16.5 +/- 16.4 msec. We found highly significant relationships between SIACT and LAD (P = 0.0006, r = 0.39), PIACT and LAD (P = 0.0001, r = 0.45), and MIPIACT and LAD (P = 0.0006, r = 0.38). We also noted that the LAD was greater in patients in whom MIPIACT was > 10 msec than in patients in whom the MIPIACT was negligible (P < 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)

The lack of knowledge of the origin of venous thrombosis (VT) causes frustration and distress to the clinician. Some results published in the literature suggest a lot of potential aetiologies. Anyhow, we are far from getting a proof that a systematic and exhaustive search for a potential cause, for instance impairment of blood coagulation or infraclinical cancer, could be of benefit for the patient and could present a good cost/efficacy ratio. Consensus recommendations limit the extent of blood coagulation studies only to some precise clinical situations. New biological data evidencing a resistance to activated C protein in 20 to 50 per cent of VT cases, will likely bring new rules. As far as infraclinical cancers are concerned and whether their relationship to idiopathic VT is well-established, it is still doubtful that such systematic heavy and expensive checking up could be of any benefit.