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The most frequent manifestation of exercise deep vein thrombosis (DVT) is the one occurring in upper limbs, in some specific and stereotypic conditions, sometimes complicated by pulmonary embolisms. A few cases of lower limbs DVT are reported in athletes. Some pathophysiologic arguments (rheological modifications, parietal lesions and coagulation abnormalities) suggest a link between DVT and exertion, but the causality is sometimes difficult to establish. We report three cases of pulmonary embolism occurring after a prolonged effort of running in trained marathon athletes. To our knowledge, very few similar cases have ever been reported. The possible responsibility of such physical efforts is discussed, as well as other potential cofactors such as coagulation abnormalities and hormonal contraception.

Mitochondrial diseases may cause hypertrophic cardiomyopathy or, less commonly, dilated cardiomyopathy. The authors describe a case of a 46 year old woman with dilated cardiomyopathy associated with diabetes and deafness. This association is suggestive of the MIDD syndrome and the demonstration of metabolic abnormalities (raised serum lactic acid, abnormal lactate/pyruvate ratio) was compatible with a mitochondrial disease. This diagnosis was confirmed by finding an A3243G mutation of the mitochondrial DNA.

Background: thrombolysis (THL) and primary percutaneous coronary intervention (PCI) are therapeutic options in acute myocardial infarction (MI). These strategies have similar efficiency, particularly in the early phase. However, in these randomized studies, different times to treatment (TT) threshold are recognized as discriminant., Objectives: to validate, on a one year mortality criteria the best TT threshold in the real life., Methods: 794 patients, admitted directly in our institution with a Ml< or =12 hours; 299 were treated by THL and 495 by PCI. The primary end-point was 1-year mortality according to TT and strategy of revascularization. Three TT thresholds were tested (120, 150 and 180 min) to define the best strategy of revascularisation., Results: only the 150 min TT threshold showed a significant difference between the two strategies. If TT was less than 150 min, relative risk of 1-year mortality was 1.36 (p=0.62) for patients treated by THL compared to those treated with PCI. By contrast, the relative risk of one year mortality was 1.95 if Tr was greater than 150 min (p=0.02)., Conclusion: TT is a key factor to define the best strategy of reperfusion. The critical threshold seems to be at 150 min. THL should be considered as a therapeutic choice only if administered within the first 150 min. After this delay, primary PCI should be preferred.

The authors report the case of a 62 year old patient admitted for a tamponade, revealing a mixed lympho-epithelial thymoma with invasion of the pericardium, the aorta and of the pulmonary arteria. The histological diagnosis was confirmed by a surgical biopsy performed after emergency pericardiocentesis. A neoadjuvant chemotherapy was administered followed by incomplete surgical resection and then a post operative radiotherapy. A local relapse was diagnosed at one year follow up by CT scan and a second line chemotherapy was administered. No further relapse occurred and patient was alive at four years.

Unlabelled: The IVA/diagonal coronary bifurcation is a high risk area for atheromatous disease. Major technical and strategic risks make the treatment of these lesions a real "challenge" for the interventional cardiologist: angioplasty-stenting and surgery are in direct competition., Objectives: the aim of this study was to determine the significance of interventional techniques in treating the IVA/diagonal bifurcation, drawing on the experiences of a cardiological haemodynamic laboratory and comparing these results with those obtained with the reference technique, represented by aorto-coronary bypass with the internal mammary artery., Methods: this was a monocentric retrospective study of a series of 133 patients treated with angioplasty-stenting between January 1997 and December 2002 for a new IVA/Dg bifurcation lesion. Patients admitted for myocardial infarction were excluded., Results: no matter which angioplasty revascularisation technique was used, the angiographic success rate was 95% with 3% occlusions of the diagonal artery. At six months, 72% of patients were asymptomatic, the rate of treated lesion revascularisation (TLR) was 21.9%. At one year 68.8% of patients were asymptomatic, and the TLR was 24.2%. The technique evolved during the six years, especially with the expansion of the radial approach and increasingly frequent use of the "kissing balloon"; at one year the TLR and the rate of major cardiac events was 31% in 1997 and 15% in 2002., Conclusions: angioplasty-stenting in this at-risk region is thus favourable, and gives results comparable with those of internal mammary/IVA bypass, save on the TLR. However, the development of stents "pre-formed" for the bifurcation and especially "active" endoprostheses could represent a solution to the delicate problem of restenosis.

The aim of this study was to determine the effect of preceding unstable angina on the short-term prognosis of myocardial infarction based on early complications: cardiac failure, cardiac rupture, ventricular septal defect, sustained ventricular tachycardia ventricular fibrillation and hospital mortality. A continuous series of 1,910 patients admitted with 7 days of myocardial infarction was analysed retrospectively. The patients were divided into two groups according to their previous coronary history: Group A (myocardial infarction preceded by unstable angina) and Group B (myocardial infarction without preceding unstable angina). Group B was subdivided into Group B1 (myocardial infarction de novo) and Group B2 (myocardial infarction with previous stable angina). The results showed that patients with previous unstable angina (Group A) had a lower hospital mortality (7.9%) than those without (Group B) (13.3%) (p = 00017), fewer cardiac ruptures (1.1 versus 2.9%, p = 0.03) and less ventricular fibrillation (2.6 versus 4.5%, p = 0.053). Subgroups analysis showed that patients with de novo myocardial infarction (Group B1) had more sustained ventricular tachycardia than those with previous stable angina (Group B2) (5.3 versus 2.7%, p = 0.04). The authors conclude that pre-infarction unstable angina, possibly by ischaemic pre-conditioning, is an independent factor of a better prognosis in myocardial infarction.

Thromboembolic venous disease includes deep vein thrombosis of the lower limbs and pulmonary embolism, a common acute complication. The usual treatment is anticoagulation. Thrombolytic drugs are only used in severe cases. Of the thrombolytic agents and therapeutic protocols in use, alteplase 100 mg/2 hours seems to be the best compromise between the risk of bleeding and efficacy in reducing pulmonary resistances by 30 to 40% and relatively early pulmonary revascularisation of 40-50%. As in myocardial infarction, cerebral haemorrhage is the main complication and the risk is higher in elderly (over 70 years of age) patients who have undergone invasive procedures. Massive pulmonary embolism, defined by clinical criteria, is presently the only formal indication of thrombolysis in this context. In non-massive embolism with right ventricular dysfunction, thrombolysis could also be indicated in the absence of haemorrhagic risk. In deep vein thrombosis of the lower limbs, the role of thrombolysis is limited and controversial; in many cases, the risk of haemorrhage is greater than the potential benefits.

This study compared prospectively the diagnostic value of dobutamine echocardiography and exercise myocardial scintigraphy for restenosis at 6 months after angioplasty of the left anterior descending artery. Forty-one patients aged 58 +/- 10 years, admitted to hospital for myocardium infarction (N = 22) or unstable angina (N = 19), with single vessel disease, were treated by angioplasty of one lesion of the left anterior descending artery after initial evaluation of the left ventricular ejection fraction by echocardiography. At 6 months, left ventricular function was reassessed by echocardiography, dobutamine echocardiography and exercise myocardial scintigraphy (Thallium 201) performed without treatment. Coronary angiography was performed at the same time and showed 8 restenosis (19.5%). Overall, in this series, dobutamine echo and scintigraphy had respectively a sensitivity of 37.5% and 75%, and a specificity of 97% and 70% (p < 0.02). Nine patients had left ventricular dysfunction unchanged compared with the initial measurement without viability in the territory of the left anterior descending artery with low dose dobutamine (group 1); thirty-two patients had improved or normal left ventricular ejection fraction with myocardial viability (group 2). In group 1, no cases of restenosis were detected by dobutamine echocardiography but&#95;of them had myocardial scintigraphic evidence of ischaemia. In group 2, the sensitivity of the two techniques was comparable but dobutamine echo was more specific than scintigraphy (96 versus 75%, p = 0.03). In conclusion, dobutamine echocardiography may be indicated in the diagnosis of restenosis of the left anterior descending artery and in cases of viability in its territory. In its absence, myocardial scintigraphy seems to be preferable.

Between December 1991 and February 19999, 25 patients (56 +/- 10 years) underwent salvage angioplasty with coronary stenting after failure of thrombolysis (TIMI 2), rtPA (N = 18), n-PA (N = 4), K2-tu-PA (N = 2) and streptokinase (N = 1). All were treated by aspirin and 96% were given ticlopidine for one month. The culprit artery was the left anterior descending (48%), the left circumflex (8%) or the right coronary (44%). The average ejection fraction was 41%; 4 patients (16%) had cardiogenic shock. The stents were implanted for occlusive coronary dissection (36%), threatening dissection (40%), partial result of angioplasty (20%) or of first intention (4%). In all, 31 stents were implanted (1.2 +/- 0.57 stent/target lesion ratio with an average length of 20.9 +/- 10.2 mm). The stents were tabular in 51% of cases. The angiographic success rate (TIMI 3 and residual stenosis < 50%) was 96% with maximum inflation pressures of 13.7 +/- 2.5 atm and balloons with an average diameter of 3.3 +/- 0.5 mm. Intra-aortic balloon pumping was required in 7 patients (28%). The 30 day results included a mortality rate of 16% (4 patients), a recurrence of infarction in 4%; there were no repeat angioplasties, coronary bypass surgery or blood transfusions. The predictive factors of recurrent coronary events were: age over 60 (p = 0.04), multivessel coronary disease (p = 0.007), cardiogenic shock (p = 0.004) and left ventricular dysfunction (p = 0.015). The authors conclude that cases of failure of thrombolysis are at high risk and that salvage angioplasty with coronary stenting is associated with excellent angiographic results. Patients with cardiogenic shock, however, have a high mortality, irrespective of coronary patency and the use of intra-aortic balloon pumping.

The aim of this retrospective study was to assess pulmonary reperfusion by scintigraphy, the risks of recurrent embolism and of bleeding complications at the 7th day and 3rd month in 2 groups of patients admitted to hospital for massive pulmonary embolism without cardiogenic shock treated by intravenous thrombolysis (Group I) and by subcutaneous low molecular weight heparin (Group II) paired by Miller's index. The basal characteristics of the two groups, each comprising 31 patients, were comparable with respect to the severity of the pulmonary embolism with an average global scintigraphic defect of 40.6 +/- 13.5% in Group I and 39 +/- 13.7% in Group II. The scintigraphic changes at the 7th day were comparable with a relative improvement of 55 and 51% respectively and at 3 months of 74% in both groups. There was no significant difference in terms of recurrence of embolism (3 versus 0% at the 7th day and 3% in each group at 3 months) or of bleeding complications (13 and 10% at the 7th day and 10 and 6% at 3 months respectively). Low molecular weight heparin seems to be as effective as intravenous thrombolysis for the treatment of massive pulmonary embolism without shock. This result requires confirmation by a large scale prospective randomised trial.

The authors report a case of paradoxical embolism presenting with syncope and a transient cerebrovascular accident. A large thrombus was observed entrapped in the foramen ovale during transthoracic echocardiography and confirmed at transoesophageal echocardiography. Despite the recent cerebrovascular event surgery was successfully performed. This clinical situation, and a review of the literature illustrate the diagnostic value of transoesophageal echocardiography, the finding of an intra-atrial thrombus being a possible surgical indication when the clinical context is favourable.

The aim of this trial, undertaken with the participation of 13 centres, was to establish the minimal effective dosage of nadroparin (Fraxiparin) for the prevention of left ventricular mural thrombosis in acute anterior myocardial infarction which was not treated by thrombolysis. Patients had myocardial infarcts less than 3 days old with no previous anticoagulant therapy or for at least 24 hours without mural thrombus in the left ventricle on baseline echocardiography. The protocol consisted of an intravenous bolus of nadroparin of 3.075 IU (0.3 mL) followed by daily subcutaneous injection of either 60 IU/kg/day (group 1) or 100 IU/kg/day (group 2) for 10 days, associated with aspirin. The criterion of judgement was the number of left ventricular thrombi observed in each group: the secondary criteria were the number of deaths, haemorrhagic and thromboembolic events. One hundred and forty-eight patients were included (group 1: 79 patients, group 2: 69 patients). One hundred and nineteen were evaluated for the principal criterion including 12 were considered as failures: 9 deaths (3 in group 1 and 6 in group 2) and 1 recurrent myocardial infarction, 1 ischaemic cerebrovascular attack and 1 atrial fibrillation in group 1. One hundred and seven patients were controlled at Day 0 and Day 10. The incidence of left ventricular mural thrombi was identical in the two groups: 7/56 in group 1 (12.5%) and 9/51 in group 2 (17.6%) (NS). Analysis of secondary criteria showed no difference between the two groups: there were no major haemorrhagic complications. The authors conclude that there is no difference in efficacy between the two dosages of nadroparin. However, the incidence of left ventricular thrombi was globally low in this study (11.6%).

Between December 1991 and November 1994, a Palmaz-Schatz stent was implanted in 9 patients aged 57 +/- 14 years during the acute phase of myocardial infarction after primary angioplasty in 7 cases and salvage angioplasty in 2 cases after an interval of 175 mm +/- 62 mn from the onset of infarction, because of threatening dissection (N = 8) or a partial result (N = 1). The success rate of implantation was 100% with residual stenosis (DCI Philips system) measured at 16 +/- 8% (5 to 28%). Anticoagulant treatment comprised heparin, coumadin and aspirin in two cases, and, in the following 7 cases, low molecular weight heparin, ticlopidine and aspirin. There was one death due to cardiogenic shock on the third day despite intraaortic balloon pumping. One patient was operated for a femoral aneurysm. A prophylactic bypass procedure was performed as a semi-emergency in a stable patient. At systematic angiographic control, the residual stenosis was measured at 19 +/- 14% (10 to 43%) without reocclusion. There was no recurrence of ischaemia. The authors conclude that the encouraging results of this short series suggest that despite the highly thrombogenic situation of acute myocardial infarction and despite the context of emergency implantation of a stent. Palmaz-Schatz stent implantation gives good immediate and long-term results with respect to reocclusion and stenosis.

The indications of percutaneous transluminal coronary angioplasty (PTCA) of the proximal left anterior descending artery (LAD 1) must take into consideration the importance of the threatened myocardial territory in case of complications and the supposedly increased risk of restenosis of this arterial segment. One hundred consecutive patients (average age 59.9 +/- 11.4 years with 77% of men) outside the acute phase of myocardial infarction were included in this retrospective open study from January 1st 1988 to March 1st 1992. There were 76 cases of single vessel. The average left ventricular ejection fraction was 64.8 +/- 12%. During the hospital period, there were no deaths. 1 myocardial infarction despite emergency coronary bypass surgery, and 2 programmed coronary bypass procedures. During follow-up, "clinical restenosis" as defined by the authors was observed in 29.7% of cases; 1 patient died of cardiovascular causes, 18 had a repeat PTCA with a success rate of 100%. The clinical restenosis rate of repeat PTCA was 33%. One patient underwent a third PTCA with a successful outcome. Ten coronary bypass procedures were necessary. Restenosis was more common after PTCA of lesions situated on a bifurcation and when high inflation pressures had to be used. Restenosis was constant after repeat PTCA when the initial restenosis occurred before the 60th day.

A 32 year-old-man admitted to hospital on the third day of myocardial infarction, three months after aortic valve replacement with a mechanical Medtronic-Hall prosthesis. The embolic character of the disease was evident on coronary angiography which showed a large thrombus in the left main coronary artery. The thrombosis of the valve prosthesis was not detected by non-invasive investigations but at aortography, confirmed at surgery. Thrombolysis with rt-PA did not dissolve the clot and reoperation was necessary (valve replacement with aorto-coronary bypass grafting).

A consensus has been reached in the last few years on the validity of the indication of thrombolysis in patients with pulmonary embolism and signs of shock. In this situation, the treatment must be rapid and effective and assessed on the haemodynamic results in the initial hours. A randomised, multicentre, double-blind clinical trial has clearly shown the superiority of rtPA at the dose of 100 mg given in 2 hours over high dose prolonged urokinase, the fall in total pulmonary resistances being 36 and 18% (p = 0.0009) respectively at the second hour. With respect to the secondary effects, the risk of serious haemorrhage with rtPA does not seem to be less than that of the first generation thrombolytics, and the data of 22 published studies even shows an increased risk of cerebral haemorrhage with rtPA compared with urokinase (1.6 versus 0.5%). Recent experience has shown that bolus administration of rtPA does not improve either the efficacy or safety of this drug. Therefore rtPA (100 mg in 2 hours) is the drug of choice in patients with a low risk of haemorrhage whereas the elderly patients with low body weight and hypertensives should probably be treated with low dose urokinase given in bolus administration, the efficacy/risk ratio of which seems to be satisfactory.

Venous thrombosis and pulmonary embolism are the two faces of thromboembolic disease. In over 90% of cases, the initial treatment of the pulmonary embolism is anticoagulant therapy, the necessity and efficacy of which were demonstrated over 30 years ago with a reduction of mortality of 25 to 6%. Intravenous heparin relayed rapidly (1st to 3rd day) is still the conventional treatment protocol. Heparin therapy adapted to the result of the activated cephalin time (two to three times the control value) and oral vitamin K antagonists with a dosage adapted to keep the International Normalized Ratio between 2 and 3 is the safest and most effective treatment to date. The efficacy is shown by the low rate of recurrency, about 5% under anticoagulant therapy, lethal recurrence being very rare (less than 1%), and safety is attested by the low rate of severe bleeding complications (3 to 5%). The introduction of low molecular weight heparin and the excellent results observed in the treatment of deep vein thrombosis will probably lead to rapid extension of its indications to mild or moderate but haemodynamically well-tolerated pulmonary embolism. Hirudine and heparinoids will probably be the next step in the treatment of pulmonary embolism.

Transthoracic echocardiography rarely confirms a diagnosis of pulmonary embolism by visualizing a thrombus in the pulmonary artery or right heart chambers. However, easily observed morphological and Doppler abnormalities may result from acute pulmonary hypertension: dilatation of the right heart chambers, a very sensitive and reliable sign of severe pulmonary embolism when the ratio of the right/left ventricular dimension > 0.6: abnormal interventricular septal contraction, a very specific sign of massive pulmonary embolism, and increased systolic pulmonary artery pressure. Transthoracic echocardiography allows evaluation of the severity of pulmonary embolism but it is difficult to orientate treatment on Doppler echocardiographic data alone. Transoesophageal echocardiography is a sensitive, specific and well-tolerated investigative method for the detection of proximal emboli in patients with massive pulmonary embolism. The investigation is rapid and can be carried out at the bedside, allowing confirmation of the diagnosis in two thirds of cases and the institution of thrombolytic or surgical therapy without the need for pulmonary angiography. Doppler echocardiography is also useful for following up the haemodynamic changes and the regression of acute cor pulmonale after thrombolysis.

Myocardial infarction is a rare clinical event in young women. The usual presentation is similar to that of older adults. The authors report a case of anteroseptal infarction in a 24 year old woman presenting with paroxysmal epigastric pain without irradiation with fever, during menstruation. The electrocardiogram was compatible with acute pericarditis. The diagnosis was rectified by echocardiography which showed anteroseptal akinesia. Coronary angiography performed as an emergency showed a radiolucent mobile image in the mid segment of the left anterior descending artery with appearances of a distal embolism which were attributed to thrombosis. Intracoronary thrombolysis was associated with a good outcome.

The authors report a case of massive pulmonary embolism compromising the haemodynamic status of a 52 year old man with a formal contraindication to thrombolytic therapy. Unilateral pulmonary embolectomy was performed without cardiac pulmonary bypass, preceded by partial interruption of the inferior vena cava. Postoperative controls confirmed the success of the surgical procedure. Although the indications of surgical embolectomy are limited, especially without cardiopulmonary bypass, it may be considered for the treatment of certain cases of massive pulmonary embolism.

Between September 1992 and August 1993 transoesophageal echocardiography was undertaken in 30 patients with clinical and scintigraphic signs of pulmonary embolism. The diagnosis was confirmed by pulmonary angiography (1 patient had failure of venous puncture; 1 patient refused the investigation). The aim of this study was to assess the tolerance and to determine the diagnostic value of transoesophageal echocardiography in patients with suspected pulmonary embolism (PE). Two groups of patients were identified: Group 1: presence of thrombus in the pulmonary artery on transoesophageal echocardiography and group 2: absence of visible thrombus. The produce was well tolerated in all patients. In 21 cases (group 1) 21 thrombi were observed in the right pulmonary artery and 4 thrombi in the left pulmonary artery. The appearances were those of a mobile venous thrombosis in 20 cases (91%) and of clearcut amputation of the proximal segment of the right pulmonary artery in 1 case. No thrombus was detected in 9 patients (group 2). In group 1, the first clinical signs occurred 12 +/- 12 days and the latest signs 2 +/- 3 days before the investigation. One patient had a history of chronic bronchitis. Two patients had a history of PE but with no sign of chronic post-embolic cor pulmonale. Twenty patients underwent pulmonary angiography. Miller's index was 71 +/- 9% and obstruction of proximal pulmonary arteries was observed in 20 patients. In group 2, the PE was confirmed at angiography in 8 cases. The first clinical signs dated from 27 +/- 54 days and the latest signs were observed 6 +/- 4 days before investigation.(ABSTRACT TRUNCATED AT 250 WORDS)

Seven patients with mobile right heart thrombi, 4 floating and 3 pediculated, were recensed between 1985 and 1990. Two patients were admitted for congestive cardiac failure (Group I) and 5 patients for pulmonary embolism (Group II). Both patients in Group I were treated with heparin without complications. In one case, the size of the thrombus decreased in 10 days whereas, in the second case, it disappeared within 8 days. In Group II, the first patient underwent successful thrombectomy. The other four patients were given thrombolytic therapy (UK = 2, rt-PA = 2) associated with appropriate doses of heparin. In the two patients given UK (3M units the first day followed by 1.2 M units per day for 4 days) the thrombus disappeared in the first 48 hours of treatment. One patient had a recurrent pulmonary embolism after 2 hours' treatment; both patients had a fall in haemoglobin of 3 cg/ml at the second day. The second patient died at the 5th day. In the two patients treated by rt-PA (100 mg/7 hours) the thrombus disappeared within 4 hours of starting therapy. One patient had a probable recurrent pulmonary embolism. Both patients had a fall in haemoglobin of 3 cg/ml at the 2nd day of treatment. Right heart thrombi are rare (168 cases in the literature of which 111 were mobile). The prognosis seems to be related to echocardiographic appearances: mortality of mural thrombi is about 4% compared with 50% in mobile thrombi. Very mobile "worm-like" masses are therapeutic emergencies because of the risk of embolism (about 68%).(ABSTRACT TRUNCATED AT 250 WORDS)

After a number of disorganised trials of intravenous thrombolysis in the acute phase of myocardial infarction in the early 1970s, the idea was abandoned for nearly a decade. However, from the beginning of the 1980s a convergence of anatomical data, improved understanding of the mechanisms of thrombosis and of thrombolytic agents, and technical advances in the practice of coronary angiography led to the introduction of intracoronary thrombolysis. Analysis of the preliminary trials demonstrated the efficacy of thrombolytic therapy, first of all with Streptokinase, in recanalizing coronary arteries in the first hours of myocardial infarction. Larger series, especially one from Holland, showed a limitation of infarct size and a consequent reduction in hospital and 1 year mortality (5% versus 9.8% and 8.5% versus 16% respectively). Intravenous thrombolysis rapidly took over from intracoronary administration and the simplification of treatment facilitated the popularization of the method and the realisation of large scale clinical trials including thousands of patients. Comparisons with conventional therapy were performed in 6 large international trials ISAM, GISSI, ISIS 2, AIMS, ASSET and 5th European Cooperative Trial) using Streptokinase or second generation thrombolytics (APSAC and rt-PA). All showed a significant decrease in early mortality with thrombolytic therapy in the acute phase of myocardial infarction but with large variations (from 11% to 51%). These results helped to generalize the use of thrombolytic agents in the first hours of myocardial infarction. Advances in scientific research and methodology then allowed the last trials to be set up to compare thrombolytic agents and determine the most effective and the least dangerous.(ABSTRACT TRUNCATED AT 250 WORDS)

Partial interruption of the inferior vena cava (IVCI) by a percutaneous endovenous filter (Günther filter n = 65, LEM filter n = 36) was undertaken in 100 patients with an average of 72 +/- 11 years for recent deep vein thrombosis. The indications were: contraindications to anticoagulant therapy (36.5%); recurrent pulmonary embolism (12%); threatening venous thrombosis with a previous embolic episode (12%); caval thrombosis (15.7%); prophylactic, with no previous pulmonary embolism (23.8%). The filters were evaluated at short and mid term. There were no technical problems. The mortality rate was 17.5%, one death being probably due to recurrent pulmonary embolism. No other recurrences of pulmonary embolism were observed, indicating an efficacy of 99 per cent. The early patency rate was 96.5%, there being no difference between the two filters used, independent of the initial site of venous thrombosis, of distal migration of the filter and associated medical treatment (anticoagulation). Distal migration was observed in 76% of IVCI by the Günther filter and 48.5% by the LEM filter (p less than 0.001); tilting was observed in 7.4% of Günther and 3% of LEM filters. Five LEM filters were incompletely opened. The IVC was transfixed by 3 Günther filters. One Günther filter had fractured spokes. There were 12 recurrences of lower limb deep vein thrombosis and 16 post-deep vein thrombosis complications were recorded. These percutaneous endovenous filters are similar to the Kimray Greenfield filter with respect to efficacy and permeability although the follow-up was relatively short. The advantages of these percutaneous filters are the facility, innocuity and rapidity of their insertion with, however, a higher incidence of distal migration.

Anistreplase or APSAC (anisoylated lys-plasminogen streptokinase activator complex) is a new, third generation thrombolytic agent with a long (90 minutes) elimination half-life, so that it can be administered by bolus intravenous injection over 2 to 5 minutes. In acute myocardial infarction anistreplase in doses of 30 units gives a coronary recanalisation rate of about 65 per cent and an early coronary patency rate of about 80 per cent. It is more effective than streptokinase on coronary patency, when given within 3 hours of onset of myocardial infarction. The time required for recanalisation to occur is short (25 to 45 minutes depending on the time elapsed before administration), and the early (24 hours) coronary reocclusion rate is low (about 5%). These results, together with the ease of administration of the drug, could make anistreplase the first-choice thrombolytic agent in the treatment of recent myocardial infarction, notably in general hospitals and mobile intensive care units.

Dynamic tomographic images of the heart may be obtained by computerised treatment of a number of projections and planes recorded by a gamma camera rotating around a patient whose blood is labelled with radioactive technetium. This new technique of assessing cardiac function was tested in a group of 40 coronary patients and the results compared with standard contrast angiography. The following parameters were compared : LV volume, global and regional ejection fractions. The zones of interest were easily defined on the tomographic images and correction for background noise was negligible. Two different methods have been developed to measure volume. The first consists in counting the matrix units in three dimensions on serial planes through a given cavity. The second is based on the reconstruction of thick slices integrating all the ventricular radioactivity, the counting of which is calibrated with reference to an orthogonal plane. The correlations with angiography were excellent with both methods (R = 0,85 and 0,87 respectively). An equally good correlation was observed for ejection fraction (r = 0,85). A segmental model acceptable for both gamma line angiography, gamma tomography and contrast angiography comprises 6 segments : septal, apical, antero-lateral, postero-lateral, posterior, and inferior. The sensitivity and specificity of both isotopic methods of detection of major wall abnormalities (akinesia and dyskinesia) were assessed.(ABSTRACT TRUNCATED AT 250 WORDS)

Fibrinolysis is a physiological process which aims at dissolving intravascular thrombi and is mediated by activation of plasminogen to plasmin. Streptokinase (SK) and urokinase (UK) are non-specific plasminogen activators. They have proved effective as thrombolytic agents, but their use is limited by the risk of haemorrhages due to systemic fibrinogenolysis. More fibrin-specific drugs have recently been developed. One is a tissue plasminogen activator (t-PA), the other is a urokinase precursor (pro-UK), also called single chain urokinase plasminogen activator (scu-PA). Genetic engineering techniques have resulted in the large-scale production of a "recombinant t-PA" (rt-PA) and a "recombinant scu-PA" (r scu-PA) for therapeutic use, notably in acute myocardial infarction. In vitro, these two drugs exhibit a thrombolytic activity that is equal to, or greater than that of SK or UK. In vivo, their fibrinogenolytic effect is less pronounced, and their thrombolytic effect greater than those of SK or UK. "Acyl-enzymes" have more recently emerged. These are inactive acylated SK-plasminogen complexes which progressively become effective in plasma after deacylation. So far, the most extensively studied of these complexes is BRL 26921 (anisoylated plasminogen streptokinase activator complex, or APSAC) which is administered by bolus intravenous injection. It is more thrombolytic than SK but produces systemic fibrinogenolysis to an equivalent degree. Injected intravenously (by infusion or bolus) during the first hours of a coronary infarction these three new thrombolytic agents have proved effective in promoting coronary reperfusion, with an early coronary patency rate of 70-75%.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventriculo-atrial (VA) conduction was studied by ventricular stimulation at increasing rate and atrial mapping in 126 patients either without ventricular preexcitation (WPW) and supraventricular tachycardia (SVT) (Group I: 60 cases) or with the WPW syndrome with or without SVT (Group II: 30 cases) or with SVT without WPW (Group III: 53 cases) or with short PR intervals (Group IV: 3 cases). In Group I, 22 patients had VA block, 10 had concealed accessory pathways and 28 had nodal VA conduction. In Group II, 2 patients had VA block, 6 had nodal VA conduction and 22 had preferential retrograde conduction through the Kent bundle. In Group III, 9 patients had concealed Kent bundles and 24 had nodal retrograde conduction. In Group IV, the results were varied. The characteristics of retrograde VA conduction are therefore often different from those of anterograde conduction. 52 attacks of SVT were recorded; in the 18 cases of Group II, 5 septal, 3 right lateral, 8 left lateral Kent bundles and 2 intranodal reentries were demonstrated. In the 33 cases of SVT without overt WPW (Group III) a concealed accessory pathway was demonstrated in 9 cases. In all, approximately a half (25 out of 52) of all SVT were due to reentry involving an accessory pathway which was concealed in about one third of cases (9 out of 25) and more often situated on the left border than on the right or in the septum.

Four brothers with a maximum age difference of 20 years, the eldest of whom has been re-examined after a 10 year interval, have sinoatrial block, a supra-hisian atrioventricular block and paroxysmal atrial arrhythmias which have led to partial atrial standstill in the eldest: left anterior hemiblock is also present in the two youngest brothers. The condition is very well tolerated. This family is compared to the other 12 reported cases of familial idiopathic binodal block in the adult, an autosomal dominant condition with variable penetration. The diagnosis is reserved and justifies endocavitary investigation of the sinus node function and atrioventricular conduction in the four brothers and the most exposed members of their family. The mechanism of the condition is unknown. It seems to arise from variable degrees of nonspecific of the nodal and atrial tissues.

In a multicentre randomized open study conducted on two parallel groups the effectiveness of APSAC was compared with that of streptokinase (SK) in 116 cases of myocardial infarction treated during the first 2.75 hours. APSAC (30 IU) was administered by intravenous bolus injection over 2 to 5 minutes, and SK (1.5 million IU) by intravenous infusion over 60 minutes. The patency of the coronary artery responsible for myocardial infarction was evaluated by coronary arteriography performed 1.74 h on average after the beginning of treatment; it was 70 p. 100 in the APSAC group and 51 p. 100 in the SK group (p less than 0.05). The fall in plasma fibrinogen was similar in both groups (mean minimum level; 0.2 g/l). Haemorrhages occurred in 9/58 patients treated with APSAC (15.5 p. 100) and in 13/58 patients treated with SK (22.4 p. 100); these haemorrhages took place during the first 24 hours in 4 patients of the APSAC group and in 10 patients of the SK group. Five patients died: 2 in the APSAC group and 3 in the SK group. In a subgroup of 38 patients who underwent 3 control coronary arteriographies (at 90 min, 24 hours and 3 weeks), the patency rates were 63 p. 100, 82 p. 100 and 93 p. 100 respectively with APSAC and 44 p. 100, 86 p. 100 and 92 p. 100 respectively with SK (NS). No coronary reocclusion occurred in the APSAC group, as against 3 (1 early, 2 delayed) in the SK group. It is concluded that APSAC seems to be more effective than intravenous streptokinase; it is easier to administer (bolus injection) and does not carry a higher risk of haemorrhage.

The incidence of binodal, sinoatrial (SA) and atrioventricular (AV), block was determined in a series of 362 patients, 90 of whom had chronic sinoatrial block (group I), 162 suprahisian, infrahisian or diffuse AV block (group II), 38 with paroxysmal supraventricular tachycardia (group III), and 70 with slow atrial fibrillation, 54 of whom were studied in sinus rhythm (group IV). Electrophysiological investigation revealed: overt or latent AV block in 71% of group I, 48% of group III, and 100% of group IV; overt or latent SA block in 40 to 61% of group II, 87% of group III and 78% of group IV; paroxysmal atrial fibrillation in 61% of group I, 25% of group II and 50% of group IV; intra-atrial block in 26% of group I, 20% of group II, 16% of group III and 31% group IV. An ECG syndrome associating binodal block and disturbances or atrial conduction and excitability is suggested. The pathogenesis and anatomical basis are discussed, the prime lesion of which may be fibrosis of the atrial tissues which may ultimately result in partial or total atrial standstill.

The authors report a case of massive haemolytic anaemia with acute mitral valve regurgitation and left cardiac failure, which occurred one year after surgical reconstruction of the mitral valve for rupture of smaller leaflet chordae. Anaemia, mitral regurgitation and cardiac failure disappeared after mitral valve replacement, using a Carpentier Edwards No. 29 valve. Haemolytic anaemia following mitral valve reconstruction is exceptional. It seems to be due to the suture material lying in a turbulent regurgitation stream when mitral incompetence develops again.

18 of 39 cases of ischaemic papillary muscle dysfunction reported elsewhere underwent cardiac catheterisation and angiography. Fifteen patients had previous myocardial infarction. The average age of the patients was less than in the overall series (69 vs 73 years) but the incidence of infarction and the degree of cardiac disease were greater. The absence of catheter data in the other patients is explained by their older age (76.4 years) and the longer period of recruitment. Their results and outcome of medical or surgical treatment are reported. The pathogenesis of the syndrome is reconsidered in the perspective of paroxysmal forms. A protocol for investigation is suggested to guide the therapeutic options. Right heart catheterisation at rest (n = 16), on exercise (n = 12), under vasodilator therapy (n = 6) and during angiography (n = 2) does not show a specific profile. These investigations only provide haemodynamic data related to therapy but they are essential for the interpretation of ventriculography. Ventriculography (n = 8) demonstrated 4 cases of mitral regurgitation (2 major and 2 minor), a reduced EF (0.47 +/- 0.17), asynergy of 36.1 p. 100 of segments analysed, predominantly in the inferior and lateral zones. Coronary angiography showed triple vessel disease in 6 cases, double vessel disease in 1 case and 1 stenosis of the left main coronary artery. Stenosis was commonest on the left circumflex (87.5 p. 100) and right coronary arteries (87.5 p. 100) but also frequently involved the left anterior descending artery (75 p. 100). Of the 12 patients treated medically, 8 died (66.6 p. 100) and the survivors remain symptomatic (33.3 p. 100), half with and half without attacks. After surgery (n = 8) comprising coronary bypass surgery (n = 6) or mitral valve replacement (n = 2), patients were asymptomatic. 1 patient died of cancer. These paroxysmal forms of mitral regurgitation may be explained by the association of aggravating, reversible ischaemic or haemodynamic factors to organic mitral lesions. Mitral valve replacement is justified when dysfunction becomes permanent and coronary bypass surgery is advocated whenever possible. The indications for surgery can only be taken into account after complete haemodynamic and angiographic investigation. A protocol for the interpretation of these investigations is suggested.

The authors report a case of total anomalous pulmonary venous return (TAPVR) draining into the innominate (brachiocephalic) vein, discovered in a 40-year old male patient and successfully treated by surgery. This type of cardiopathy is usually suspected in the neonatal period, being badly tolerated, and such a prolonged survival is quite exceptional. Survival is conditioned by the site of the TAPVR, by the size of the atrial septal defect and also by the presence or absence of an obstacle to the pulmonary venous return and of pulmonary arterial hypertension. In the absence of pulmonary vascular disease, surgical correction is mandatory and results in regression of the symptoms and of the pulmonary arterial hypertension.

Sixty-seven patients with recent acute pulmonary embolism (within 5 days) and an angiographic deficit of over 30% were included in a randomised study designed to compare the efficacy of the associations of urokinase-heparin (Group I) and lysyl-plasminogen-urokinase-heparin (Group II). Plasminogen was administered as an intravenous bolus of 150 microkatal units at the beginning of the urokinase infusion, the dosage of which was set at 2 700 000 IU over 24 hours. Both groups received anticoagulant doses of heparin. The efficacy of treatment was judged by early revascularisation on pulmonary angiography performed during the 24 hours after the end of treatment and by changes in the parameters of fibrinolysis and its inhibitors. The clinical features of the two groups were comparable but the angiographic changes were more pronounced in Group I (deficit: 68.5 +/- 10.4% vs 62.3 +/- 10.9%, p less than 0.02). Treatment had to be stopped before the 24th hour in 4 cases (3 early deaths and 1 severe haemorrhage). The average revascularisation was 30.5 +/- 6.8% in Group I and 38.3 +/- 31.1% in Group II (NS). The alpha-2-antiplasmins were lower (NS) in Group II as were the fibrinogen levels (p less than 0.01 at the 12th and 24th hour) whilst the plasminogen levels and surface of fibrin plateaux were higher (p less than 0.01 at the 6th hour and p less than 0.05 at the 12th hour, respectively). These results show that moderate doses of urokinase associated with heparin are effective in the treatment of acute pulmonary embolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Experimental studies on rabbits have shown that CY 222, a low molecular weight heparin (mean: 2.500 daltons), has the anti-thrombosis properties of heparin but reduces the risk of haemorrhage in optimal doses of 1.000 AXa IC (Institut Choay) units/kg/day. The safety and effectiveness of CY 222 were tested in 47 patients presenting with a less than 5 days' old pulmonary embolism. The patients were divided into three groups according to dosage: group I (n = 16) received 500 AXa ICu/kg/day; group II (n = 17), 750 AX ICu/kg/day, and group III (n = 14), 1.000 AXa ICu/kg/day. The drug was administered by continuous intravenous infusion during 10 days. Its effectiveness was assessed from the Miller index calculated on conventional pulmonary angiograms on days 0, 5 and 10. On the 10th day of treatment, the percentage of revascularization was similar in all three groups (group I 65.9 +/- 9.9 p. 100; group II 71 +/- 6.8 p. 100; group III 68 +/- 8.5 p. 100), but the improvement was significantly more rapid in group III patients. Embolism recurred in 5 cases (2 in group I, 1 in group II, 2 in group III) and was fatal in 1 case (group I). Haemorrhagic complications were noted in 3 cases (group III patients). Except for thromboelastography, all coagulation tests were unmodified by CY 222. The anti Xa and the (very low) anti IIa activities of the drug were directly related to the doses administered.(ABSTRACT TRUNCATED AT 250 WORDS)

In a 62 years old patient suffering from stenocardia and paroxysms of atrial fibrillation, coronary angiography disclosed two coronary-pulmonary fistulas associated with a tritruncal stenotic coronary atheroma. During the operation consisting of a double aortocoronary shunt and closing the anomalous pulmonary ostium, a control coronary angiography confirmed the shunt permeability and showed the absence of opacifications at the passage of the fistulas. In the immediate postoperative period the recurrence of paroxysmal atrial fibrillation was no longer accompanied by stenocardia which did not reappear one year after operation. This observation illustrates the fact that coronary-pulmonary fistulas may aggravate a fortuitously associated coronary insufficiency.

Two cases of arteriovenous fistula arising from the internal mammary artery are described. The detection of the continuous subclavian murmur was preceded by therapeutic procedures in both cases; difficult subclavian vein catheterisation in the first; reoperation of sternotomy for postoperative haemorrhage after open heart mitral commissurotomy in the second. Oxymetry after sampling at, above and below the subclavian vein confirmed the presence of a shunt and allowed estimation of shunt flow, which was minimal in both cases, 11 and 32% of cardiac output respectively. The origin of the fistula at the internal mammary artery and the communicating vein were identified by semi-selective angiography. The latter was superior vena cava in the first case and the internal mammary vein in the second. The low shunt flow probably explains the outcome: spontaneous closure in both cases. This is exceptional in any form of arteriovenous fistula.

The authors report the case of a 49 year old woman who presented with congestive cardiac failure and hypertension. Clinical examination revealed a high output state and an abdominal mass with a continuous murmur which angiography showed to be a very vascular right renal tumour with a large and early venous return. Catheter studies confirmed the increased cardiac output (cardiac index 5.37 l/mn/m2), an increase in right heart and mean pulmonary capillary pressures (28 mmHg), decreased peripheral arterial resistances and a left-to-right shunt effect at the level of the suprarenal inferior vena cava (+ 3.8 volumes of oxygen per 100 ml). After radical right nephrectomy, the cardiac failure and hypertension regressed and the haemodynamic parameters returned to normal.

Twenty six patients with acute (less than 5 days) pulmonary embolism (PE) confirmed by bilateral pulmonary angiography with a Miller index greater than 15 were given tissue plasminogen activator (Alteplase) (rt-PA) intravenously (n = 20) or directly into the pulmonary artery (n = 6). The dosage was 100 mg/7 hours (bolus 10 mg + 40 mg/2 hours + 50 mg/5 hours). Heparin (5000 IV as a bolus and 1000 IV/hour) was associated in all cases. The Miller index decreased from 24 +/- 1 (n = 26) before treatment to 12 +/- 1 (n = 25) (p less than 0.001) after 100 mg of Alteplase, and from 25 +/- 0.4 (n = 14) to 22 +/- 0.5 (n = 14) (p less than 0.001) after 50 mg. The mean pulmonary arterial pressures fell from 30 +/- 2 mmHg to 21 +/- 2 mmHg after 50 mg (n = 26) (p less than 0.001) and to 14 +/- 1 (n = 25) (p less than 0.001) after 100 mg of Alteplase. A decrease in mean pulmonary artery pressures (-22%, p less than 0.001) and total pulmonary resistances (-29%, p less than 0.001) was obtained after one hour of thrombolysis in 12 monitored patients. There were no fatalities. Severe haemorrhage occurred in 6 cases. Therefore, Alteplase induced a rapid dissolution of recent intrapulmonary thrombi without inacceptable haemorrhagic complications. Its action could be particularly beneficial in patients with right ventricular failure due to life threatening pulmonary embolism.

A case of leiomyosarcoma of the pulmonary artery in a 64-year old man without previous cardiovascular disease is reported. The clinical picture, which comprised episodes of paroxysmal dyspnoea associated with acute cor pulmonale, suggested pulmonary embolism. Radioisotope perfusion study and pulmonary angiography seemed to confirm this diagnosis, but no improvement was obtained with a prolonged thrombolytic treatment. The presence of a median mass at CT led to exploratory thoracotomy and to the finding of a tumour in the pulmonary artery, which turned out to be a leiomyosarcoma. The disease rapidly took an unfavourable course. Comparison of this case with data from the literature showed that primary tumours of the pulmonary artery are extremely rare, that they are diagnosed with difficulty and often at a late stage and that their prognosis is usually very sombre.

Two cases of anterior transmural myocardial infarction occurring after closed chest injuries in young adults (26 and 29 years) are reported. In one case, the infarct was detected after 42 days when the patient gradually developed left ventricular failure after thoracic injury (fracture of the left 9th rib). In the other case, the diagnosis was made during the initial evaluation of a patient with multiple injuries by routine electrocardiography. Radio-isotopic investigations showed an antero-septo-apical and lateral defect with akinetic wall motion in the first case, and apical hypofixation with limited akinesis in the second one. Coronary angiography with left ventriculography was performed after 2 and 3 months respectively, and showed a prolonged non-atheromatous stenosis of the proximal left anterior descending artery with anterior wall hypokinesia, apical akinesia and mitral incompetence (Case n 1) and slight changes of the distal part of the left anterior descending artery with apical hypokinesia (Case n 2). These two cases bring the number of documented reported cases to 37 and illustrate the two possible mechanisms of myocardial infarction after closed chest trauma: direct trauma to the coronary arteries with vascular lesions and secondary myocardial infarction associated with a poor prognosis, and myocardial contusion resulting in random myocardial lesions which usually carry a better prognosis.

44 cases of paroxysmal sinoatrial tachycardia (PAT) due to reentry within the sinus node or between the sinus node and the atrium are reported; these tachycardias are usually quite well tolerated clinically as the rhythm is rarely faster than 140/min and they are often degraded by functional AV block. They can be triggered and terminated by one (or two) atrial stimuli, and reduced by carotid sinus massage but relapse in the short term. They often alternate with a disturbance of atrial excitability in patients who also have binodal disease. Their diagnosis implies endocavitary investigation showing sinusal anterograde atrial activation and atrial and ventricular stimulation to differentiate them from other types of paroxysmal tachycardia, especially those due to reentry involving concealed right sided Kent bundles. Studies of sinus node function by atrial extrastimulus techniques in 38 patients usually showed an isolated and prolonged Zone I followed, without a transitional plateau, by a Zone IV of sinus echos during which the tachycardia could be triggered. This type of tachycardia, without doubt as common as junctional tachycardia, may respond to treatment with Quinidine, Amiodarone, Verapamil, or beta-blockers, associated with permanent pacing in cases of binodal block.