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Despite improved management of myocardial infarction, the incidence of cardiogenic shock remains constant at about 7.5% of cases. Patients who develop cardiogenic shock are older and much more often women. The site of infarction is usually anterior, transmural with greater left ventricular systolic dysfunction and a higher increase in cardiac enzymes. Diastolic intra-aortic balloon pumping is the usual treatment but survival only seems to be increased in patients undergoing revascularisation. Surgical revascularisation and circulatory assist devices have been proposed but patient selection in these studies was biased and optimised the results. The effect of thrombolysis was analysed in a subgroup of patients in the GISSI study. The 30 day mortality was 69.9% in 146 patients treated by streptokinase and 70.1% in patients given placebo. Thrombolysis only benefitted patients with an anterior myocardial infarction aged less than 65 and treated within 6 hours of the onset of pain. Although there are no randomised studies of the value of angioplasty in patients in cardiogenic shock. Several uncontrolled series suggest that this type of procedure reduces short and long-term mortality. However, the prognosis is not as good when unselected consecutive groups of patients are studied in whom infarction is complicated by cardiogenic shock immediately and who undergo "aggressive" revascularisation: 72% of patients die in hospital and there are few long-term survivors. The prognosis appears to be particularly poor in patients over 70 years of age with a previous history of myocardial infarction or who undergo prolonged pre-hospital cardiopulmonary resuscitation. However, the implantation of coronary stents associated with circulatory assist devices seems to improve the prognosis of infarction complicated by cardiogenic shock by ensuring adequate coronary flow and reducing the risk of reocclusion.

Dissection of the aorta is a serious condition but rare in young women, and occurring during the 3rd trimester of pregnancy. The main risk factors are hypertension and diseases of the connective tissue or of collagen (Marfan's syndrome and Ehlers-Danlos disease). The authors report a case of dissection of the aorta managed in a pluridisciplinary manner by the anaesthetists, cardiologists, obstetricians and cardiothoracic surgeons, which resulted in a favourable outcome for both mother and baby. The diagnosis of Ehlers-Danlos disease was made from the onset and, over a period of 10 years with CT scan and annual echocardiographic follow-up, total replacement of the supra-coronary aorta was performed in several stages.

The authors studied 18 patients (15 men, 3 women) with an average age of 67 +/- 8 years with refractory cardiac failure. In order to determine the potential of pacing to raise cardiac output in severe cardiac failure. The average ejection fraction was 26 +/- 6.5%. All patients were in sinus rhythm:resting cardiac output was 3.35 l/min. Two temporary pacing catheters were positioned in the right atrium and at the apex of the right ventricle for dual-chamber mode pacing triggered by the spontaneous P waves. Changes in cardiac output were measured by Doppler echocardiography at different values of atrioventricular delay. Patients were considered to be responders if their cardiac outputs rose by 15%. In 7 patients meeting this criterion, the average increase in cardiac output was 27% (2.99 +/- 0.7 to 3.81 +/- 0.86 l/mn; p < 0.01); all had dilated cardiomyopathies with left bundle branch block and the optimal AV delay was 103 +/- 21 ms (80-140 ms); the duration of diastolic filling increased from 212 +/- 98 to 292 +/- 116 ms (p = 0.02). In the non-responding group (11 patients with an increase of cardiac output of only 3.6 +/- 0.09 to 3.9 +/- 0.92 l/mn; p < 0.01), the underlying disease process was mainly ischaemic. Two predictive factors of efficacy of dual-chamber pacing were identified: a short ventricular filling period (29 +/- 8% of the RR interval in the responders vs 44 +/- 9% in the non-responders; p < 0.01) and the presence of 1st degree atrioventricular block. Dual-chamber pacing could be a valuable method of increasing resting cardiac outputs in a selected group of patients with severe, refractory, cardiac failure.

Three distinct forms of rupture of the heart may be identified after myocardial infarction: sudden rupture with massive intrapericardial haemorrhage, and sudden death with clinical signs of electromechanical dissociation; rupture into the pericardium resulting in a false aneurysm, the treatment of which is surgical; subacute rupture which accounts for 30% of cases in which bleeding into the pericardium is slow and/or repeated. Over an 8 year period and in a series of 2,400 consecutive infarcts admitted to the intensive care unit, 10 cases of subacute rupture of the heart were diagnosed. They were 6 men and 4 women, with a mean age of 73.6 years. The clinical presentation was isolated chest pain in 5 cases, syncope alone in 2 cases and the association of pain and syncope in 3 cases. Six patients were in shock on admission. In two cases, shock developed after admission. The infarction was confirmed biologically by a significant elevation of creatinine kinase in 9 out of 10 cases. Transmural infarction was observed in 9 cases: the infarct was electrocardiographically non-transmural in 1 case. Emergency echocardiography showed pericardial effusion in all cases, usually moderate, but sometimes compressive with an intrapericardial echogenic mass suggesting a thrombus. Haemodynamic improvement was obtained by medication allowing cardiac catheterisation which showed adiastole in 3 cases. Coronary angiography was performed in 7 cases. In 5 of the 7 cases, apart from occlusion of the artery presumed to be responsible for the infarct, the coronary vessels were diffusely infiltrated without significant stenosis. Left ventriculography was performed in 7 cases. In 6 of the 7 cases regional akinesis was demonstrated: the 7th case showed dyskinesia of the anterior wall. In two cases, contrast medium was observed to fill the pericardium during ventriculography, indicating myocardial rupture. The diagnosis of subacute rupture, suggested by clinical and paraclinical (particularly echocardiography), was confirmed in 9 cases at surgery and in the 10th case at autopsy. Surgery consisted of repairing the rupture. In the last two cases, biological glue was used to reinforce the surgical repair. The clinical outcome was good after surgery in 6 cases with a follow-up of 5 months to 8 years. The diagnosis of subacute rupture should therefore be made on clinical and echocardiographic criteria, as these results suggest that surgery is often possible, with a good prognosis.

The biological diagnosis is usually late with respect to clinical and electrocardiographic signs of acute myocardial infarction. Recent laboratory methods have stimulated renewed interest in very early marker of infarction: myoglobin and CPK isoforms. The authors undertook a prospective study of the diagnostic sensitivity of myoglobin (MG), CPK and CPK-MM isoforms in 30 consecutive patients undergoing intravenous thrombolytic therapy in the acute phase of myocardial infarction. Blood samples were obtained on admission and every 30 minutes for 1 h 30. The Mb contributed to diagnosis of infarction on admission in 89% of patients. This percentage fell to 44% for the ratio MM3/MM1 > 0.5 to 27% for the CPK and to 24% for the ratio MM3/MM1 > 1. The sensitivity of all tests increased in the later blood samples but it remained low in the CPK and MM3/MM1 > 1 criteria. The diagnostic sensitivity of the first sample was also better in patients admitted after the 3rd hour (Mb = 100%; MM3/MM1 > 0.5: 58%; CPK: 41%) compared with those admitted before the 3rd hour (Mb = 82%; MM3/MM1 > 0.5: 35%; CPK: 17%). These results show that the diagnostic sensitivity of biological markers of myocardial infarction is very different. The serum myoglobin is an earlier and more sensitive marker than the CPK or CPK-MM isoforms.

Between May 1991 and February 1992, 31 consecutive patients were included in a prospective study, the aims of which were to determine the criteria of early coronary revascularisation after intravenous thrombolysis in the acute phase of myocardial infarction. The rise in serum myoglobin, the ST segment elevation, accelerated idioventricular rhythm and the evolution of chest pain were analysed. All patients underwent coronary angiography. Twenty-six were revascularized and 5 remained with coronary occlusion. Two types of serum myoglobin curves were demonstrated. Those with a sudden , decrease and a well defined peak in the first 4 hours were specific for revascularisation and easily identified (Group A: 16 patients). The graphs with a progressively rising slope to a peak after the 4th hour were observed in patients with coronary occlusion, but also in 10 patients with recanalized arteries (Group B). No significant difference was demonstrated with regards to the clinical and coronary angiographic parameters between patients in Group A and Group B. On the other hand, the time between the onset of chest pain and peak myoglobin was shorter in Group A (298 +/- 81 min) than in recanalised patients in Group B (380 +/- 54 min) (p < 0.05). The difference in the profile of the serum myoglobin could therefore reflect restoration of arterial flow in myocardial cells which had not suffered the same period of ischemia. ST segment elevation may increase, decrease of remain stable at 120 minutes in patients revascularised and those remaining occluded. In 9 patients, the ST elevation increased compared with the initial electrocardiogram .(ABSTRACT TRUNCATED AT 250 WORDS)

Five to ten per cent of survivors of acute myocardial infarction die within two years. The majority of these deaths are sudden and are attributed to a lethal ventricular arrhythmia. This is usually ventricular tachycardia degenerating to ventricular fibrillation. These post-infarction tachycardias are generally due to reentry. They require an anatomic arrhythmogenic substrate, a zone of delayed conduction. This can be detected as late potentials on signal averaged ECG. The triggering of a significant ventricular arrhythmia by ventricular stimulation is closely correlated to the occurrence of a severe ventricular arrhythmia in the months following infarction. Programmed ventricular stimulation could, therefore, help to identify patients requiring close follow-up and/or preventive antiarrhythmic therapy, but cannot be offered to all patients because of its invasive nature. Seventy nine post-infarction patients were studied prospectively. All underwent coronary angiography, signal averaging electrocardiography, and programmed ventricular stimulation at least 15 days after infarction. Fifty five patients had at least one criterion of late potentials (QRS duration > or = 110 ms and/or amplitude of the last 40 ms < 27 microV and/or duration of potentials of under 40 microV > 37 ms). Twenty four patients had no late potentials. The results of programmed stimulation were estimated to be positive when sustained or unsustained monomorphic ventricular tachycardia was triggered, and negative when ventricular fibrillation, ventricular flutter unsustained polymorphic ventricular tachycardia or no arrhythmia could be induced. Programmed ventricular pacing triggered 15 significant events, 17 unsustained polymorphic ventricular tachycardias, 13 ventricular flutters and 11 ventricular fibrillations. The exploration was negative in 23 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Dissection of the inferior wall of the right ventricle during the acute phase of myocardial infarction with right ventricular involvement is a mechanical complication which has been recently identified, the diagnosis being almost exclusively post-mortem. The authors report the clinical, echocardiographic and pathological features of myocardial dissection in four patients. Between 1985 and 1988, the diagnosis of myocardial dissection was made by echocardiography in 4 patients aged 77 to 80 years, admitted to hospital for an acute inferior wall myocardial infarction. All 4 patients had signs of acute right ventricular failure indicating right ventricular necrosis and a loud systolic murmur at the left sternal border; 2 patients were in shock. The ECG showed signs of inferior wall infarction with, in 2 patients, electrical changes suggestive of right ventricular involvement. Echocardiography showed dissection of the inferior wall of the right ventricle as a pulsatile, echo-free space in the diaphragmatic wall of the right ventricle which appeared to obstruct right ventricular ejection in end systole to a variable degree. The outcome was fatal in all cases with death resulting from refractory myocardial failure. Pathological analysis confirmed biventricular inferior wall infarction also involving the posterior part of the interventricular system, the site of a small tear on the left side which communicated with a neo-cavity dissecting the RV posterior wall. The right coronary artery was totally occluded in all cases. The anatomical lesions were fully concordant with the echocardiographic data: the dissection filled with blood from the left ventricle at each systole creating a pulsatile space in the diaphragmatic wall of the ventricle obstructing ejection.

Coronary artery-cardiac fistulae are uncommon and usually congenital abnormalities. The majority of these fistulae communicate with the right heart chambers. Acquired coronary-left heart fistulae are very rare: secondary to trauma, cardiac surgery, angioplasty or endomyocardial biopsy. Fistulae secondary to myocardial infarction are rare but have been described. The authors report the case of a man with anterior wall infarction treated by fibrinolysis and by angioplasty of the left anterior descending artery (LAD) 48 hours later. This dilatation was complicated by repeated occlusion but a good result was obtained after in situ and then systemic fibrinolysis. Control coronary angiography after angioplasty performed 6 months later showed the presence of micro-fistulae between the distal part of the LAD, the left diagonal entry and the left ventricular chamber which were not present on the coronary angiogram before the angioplasty. The fistulae appeared to be secondary to a localised infarct which occurred after distal thrombosis of the LAD during angioplasty.

The authors report a case of myocardial infarction complicating an exercise stress test performed 48 hours after successful angioplasty of a stenosed left anterior descending artery in a patient with unstable angina. Three similar cases have been previously reported. The probable mechanisms of coronary obstruction in this context are rupture of an atheromatous plaque, thrombosis and coronary spasm.

ST segment elevation in the anterior precordial chest leads may be observed in some cases of right ventricular infarction alone or associated with left ventricular inferior wall infarction. Six out of 700 patients admitted to our Coronary Care Unit over a 2 year period had right ventricular infarction with these electrocardiographic changes. In three cases, isolated right ventricular infarction was due to occlusion of a right marginal artery (N = 2) or of a small right coronary artery (N = 1) which only vascularised the right ventricle. In 2 cases, right ventricular infarction was associated with a recent or chronic left ventricular inferior wall infarct. This type of ST segment elevation may suggest a left ventricular anterior wall infarct especially when there are no changes in the inferior leads, as was the case in our first patient. However, the dome-like appearance of the ST segment, the reduction in amplitude of ST elevation from V2 to V5, the progressive regression of the ST changes without the appearance of Q waves, are more suggestive of the diagnosis of right ventricular infarction. In addition, normal left ventricular dilatation on echocardiographic examination rapidly confirms the diagnosis.

Primary sarcomas arising from the trunk or branches of the pulmonary artery are exceedingly rare and usually diagnosed at autopsy. The authors report the case of a 31 year old man referred for investigation of recurrent syncope. Echocardiography, right ventriculography and the thoracic computed tomography led to early diagnosis of a pulmonary artery tumour and surgical resection. Histology revealed a primary sarcoma. The early postoperative course was uncomplicated but one month after surgery a local recurrence was diagnosed at routine echocardiographic examination. The syncopal symptoms recurred seven months after surgery and echocardiography showed tumour recurrence on the interventricular septum and in the pulmonary artery. A second palliative operation was attempted but was unsuccessful because of the size of the tumour.

In Carney's syndrome, the association of cardiac myxomas, spotty pigmentation and endocrine over activity, the myxomas are usually multiple and have atypical locations. The authors report a case in which an accurate diagnosis of these multiple myxomas was made by transoesophageal echocardiography, although transthoracic echocardiography had missed the diagnosis.

The authors report 4 cases of aortic dissection after aortic valve replacement. The aorta was dilated in all four cases before surgery. Two patients died within hours of the dissection, illustrating the poor prognosis of this complication and the difficulties of surgical management. The features of these four cases were compared to those of 29 other cases reported in the last ten years. The initial surgical indication for valve replacement was equally divided between aortic stenosis and regurgitation. The onset of dissection after surgery was very variable, ranging from a few hours to several years after valve replacement. Abnormalities of the aortic wall and peroperative trauma play an important role in the pathogenesis of this complication. The prognosis is very poor, which underlines the importance of preventive measures and regular follow-up of these patients.

A 70 year old woman was admitted for right ventricular failure and cyanosis of recent onset. Echocardiography showed a very large, homogenous, immobile, smooth-contoured mass filling the right atrium. Right atrial pressures were raised but the other intracardiac pressures were normal at catheterisation. Right heart angiography confirmed the voluminous right atrial mass and dilatation of the hepatic veins and showed early opacification of the left heart chambers. A right-to-left shunt was confirmed by oximetry which showed significant desaturation of the blood in the left atrium and ventricle (saturation 78% in the left ventricle). The tumour was also documented by a thoracic CT scan. At surgery, a very large, malignant right atrial tumour was resected which histological examination showed to be an angiosarcoma. The interatrial septum seemed to be intact: there was no true atrial septal defect but a persistent foramen ovale was found. After resection of the tumour the right atrium was reconstructed. The initial postoperative period was uncomplicated but the patient died nine months later of metastatic disease particularly affecting the liver and brain. The clinical presentation of malignant cardiac tumour is very variable but a right-to-left interatrial shunt through a patent foramen ovale has only been reported previously in 2 cases of primary malignant tumours (a rhabdomyosarcoma and an angiosarcoma) and in 1 case of a secondary cardiac metastasis.

The authors report the case of a 63 year old woman admitted to hospital for recurrent refractory ventricular tachycardia. Echocardiography and cardiac scintigraphy showed global left ventricular function. Ventriculography confirmed the left ventricular dysfunction and also showed a localised aneurysm of the anterior left ventricular wall. Surgical resection of the aneurysm and an encircling endocardial ventriculotomy were performed but the patient died of a low output syndrome. Pathological examination of the excised tissue showed granulomatous lesions associated with fibrosis interrupting the striated myocardial bundles. The granulomata consisted in a large number of epithelioid histiocytes and very large giant cells with many nuclei. The diagnosis made retrospectively was that of cardiac sarcoidosis causing a ventricular aneurysm and global left ventricular dysfunction. The diagnosis of cardiac sarcoidosis is difficult in the absence of systemic extracardiac involvement because the clinical manifestations and complementary investigations are non specific. The diagnosis may be made by endomyocardial biopsy in 25 per cent of cases, thereby leading to specific treatment with steroids which is sometimes effective.

The authors report the case of a 46 year old man in whom a regular, wide complex tachycardia was terminated temporarily by the injection of adenosine-5'-triphosphate (ATP:Striadyne); endocavitary electrophysiological studies showed the tachycardia to be of ventricular origin. After aminophylline, an inhibitor of certain purinergic receptors, the tachycardia could be reproduced at will and was sustained whereas only short runs of tachycardia could be induced under basal conditions. The mode of action of the ATP on this type of tachycardia could be a direct effect of the molecule on the purinergic receptors specifically inhibited by aminophylline.

Calcium channel blockers are now recommended for the treatment of stable angina but few studies have been carried out comparing the efficacy of verapamil and diltiazem in this indication. The short-term efficacy of these two drugs was compared in a double-blind crossover trial in 12 patients. The following protocol was used, 24 hour selection period followed by two crossover treatment periods versus double placebo. Exercise stress tests were performed 2 hours after the last dose at the end of each treatment period. Each patient underwent 3 stress tests: the first during the selection period whilst taking verapamil and diltiazem placebo (ET0), the second after the first treatment period at day 7 (ET1) and the third after the second treatment period at day 14 (ET2). A comparison of exercise capacity (ET0 to ET1 and ET2) showed improved effort tolerance and an increase in the ischaemic threshold with calcium blocker therapy. The duration of effort, the maximum sustained load, the rate-pressure product and the time to ST depression were all significantly increased. On the other hand, there were no significant changes in the percentage theoretical maximum heart rate attained, the heart rate at which ST depression occurred, the maximum ST depression and the incidence of angina. A comparison between ET1 and ET2 did not show any difference in the parameters of maximum effort or of the appearance of myocardial ischaemia. The comparison of exercise stress tests performed after treatment with verapamil and after diltiazem showed that the total duration of exercise, the maximum sustained load (in watts) and the rate-pressure product were identical.(ABSTRACT TRUNCATED AT 250 WORDS)

The overall cardiovascular mortality in patients with chronic renal failure is about 30 per cent of which 10 per cent is attributed to myocardial infarction. This prevalence led some workers to propose a hypothesis of "accelerated atherosclerosis" due to the hyperlipidaemia observed in 30 to 70 per cent of patients. However, the concept of accelerated atherosclerosis, which was based essentially on clinical studies, has been questioned. Pericardial effusion is a common complication of chronic renal failure and has been reported in over 62 per cent of patients in echocardiographic studies. There are many causes and symptoms are often mild; systematic echocardiographic examination of patients with renal failure undergoing haemodialysis has shown 32 per cent of pericardial effusions to be asymptomatic. There are two potential complications: cardiac tamponade and, lesser frequently, constrictive pericarditis. Cardiac failure is a common cause of death in patients undergoing long-term dialysis. The myocardial histological appearances are those of fibrosis, the etiology of which is not fully understood although the dialysis membranes and hypotensive episodes occurring during haemodialysis have been thought to play a role. Left ventricular hypertrophy and fibrosis may give rise to ventricular arrhythmias which could explain some of the cases of sudden death observed in patients with renal failure and often wrongly attributed to ischemic heart disease. Another form of myocardial disease which is observed later is characterised by an alteration of systolic function with left ventricular dilatation and hypokinesia and increased end diastolic pressures without an increase in left ventricular wall thickness. Valvular heart disease may also result from renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)

The authors report the case of a cardiac tumour documented by 2 D echocardiography, presenting in the newborn with cardiac arrest. The echocardiographic features of multiple nodules disseminated in the ventricular walls suggested a diagnosis of rhabdomyoma. The initial course was complicated by poorly tolerated attacks of tachycardia which were rapidly brought under control with amiodarone. The long term outcome was clinically favourable with a rapid regression of the number and size of the tumours on echocardiography, and a tendency to normalisation of the electrocardiogramme. The possibility of regression, which has already been reported by many investigators, suggests that these cardiac tumours may have a better prognosis than previously thought.

Numerous studies have been devoted to the effect of slow calcium channel inhibitors on plasma digoxin concentrations. The principal drugs tested, verapamil and nifedipine, were found to increase significantly plasma digoxin levels mainly by reducing digoxin total clearance. Very few studies on the nicardipine-digoxin interaction have been reported. The dual purpose of the present study was to evaluate the influence of orally administered nicardipine on plasma digoxin concentrations over 24 hours and to measure possible variations in the pharmacodynamic effects of digoxin in 9 patients with chronic congestive heart failure. The pharmacodynamic assessment involved simple and cross-sectional echocardiography, systolic time interval measurements and cardiac catheterization. In these patients under chronic digoxin treatment, oral nicardipine had little effect on plasma digoxin concentrations which increased but not significantly; no sign of digitalis toxicity was observed. Nicardipine improved left ventricular function and myocardial contractility by reducing after-load, the nicardipine-induced peripheral vasodilatation tending to counteract the digoxin-induced vasoconstriction.

The authors report a case of an anomalous left coronary artery discovered by chance in a totally asymptomatic 39 year old man. Appearances of anterior myocardial infarction were observed on routine preoperative ECG in a man with multiple injuries. Coronary angiography showed an anomalous left coronary artery arising from the main pulmonary artery. Left ventricular function was poor with associated mitral regurgitation. Surgical correction consisted in an end-to-end venous graft between the ostium of the coronary artery detached from the pulmonary artery and the right anterior border of the ascending aorta. Left ventricular function did not improve four months after surgical correction. The irreversibility of the myocardial lesions argues in favour of an early correction of this malformation.

The authors report two new cases of cardiac disease associated with distomatosis: one case of biventricular fibroblastic parietal endocarditis affecting mainly the left side in a young female of 26 years, and one case of cardiomyopathy with atrial endocardial fibrosis, affecting especially the left ventricle in a man of 47. Bearing in mind the five cases reported in the literature, the authors propose a classification of cardiac disorders supposed to be due to distomatosis using three groups (endocardial fibrosis, cardiomyopathy, myocarditis) and relate them to a common pathogenesis based on immuno-allergic theory.

The authors report the case of a patient with coronary spasm characterised on exercise stress testing by an initial depression of the ST segment followed by ST elevation at the 3rd minute of recovery. Coronary angiography showed an important, transient collateral system arising from the left coronary artery, probably minimising the effects of complete occlusion of a dominant right coronary artery. The authors discuss effort-induced spasm and collateral circulation.

Two rare mechanical complications of right ventricular infarction are reported: myocardial dissection and rupture of the RV free wall. The diagnosis was made by 2D echocardiography in both cases. Myocardial dissection resulted in the formation of an oblong, expansive, intraparietal space. The rupture of the RV free wall was visualised as a breach of the continuity of the ventricular wall. These cases underline the importance of 2D echocardiography in the acute phase of myocardial infarction for the diagnosis of these complications.

The authors report the results of 8 cases of percutaneous transluminal coronary angioplasty of occluded arteries: the artery concerned was the proximal segment of the left anterior descending artery in 5 cases and the proximal segment of the right coronary artery in 3 cases. All patients had unstable angina with a very positive exercise stress test. The conservation of viable myocardium was the result of an excellent collateral circulation from the controlateral vessel in all patients. In 7 out of the 8 cases, the guide wire and dilating balloon were correctly positioned by opacifying the distal segments of the occluded artery by injection of contrast into the controlateral artery. Almost simultaneous injection of the occluded and controlateral vessels allowed evaluation of the length of the occlusion. Controlateral opacification disappeared immediately after adequate recanalisation to reappear during inflation of the balloon. These cases show that in patients with chronic coronary occlusion, opacification of its distal segments by injection of contrast into the controlateral vessel seems to be helpful and without risk to the patient.

A 67 year old woman was admitted for assessment of asymptomatic aortic stenosis. A large left atrial myxoma was demonstrated by 2D and M mode echocardiography. Coronary angiography was performed as part of the investigation of the aortic stenosis and showed that the tumour depended on the right coronary artery for its blood supply. Careful frame-by-frame study showed the presence of a true right coronary-left coronary fistula through the tumour. The authors discuss the different clinical presentations of left atrial myxomas and their vascularisation in the rare cases in which it has been described.

The authors report the occurrence of a transient Q wave in a case of adrenergic myocarditis consecutive to a hypersecretory phaeochromocytoma. There was no biochemical evidence of anatomical infarction. During a hyperadrenergic clinical attack, electrocardiography displayed a pattern of incipient anteroseptal infarction with a Q wave of necrosis, while echocardiography recorded a very low and paradoxical septal contraction together with marked abnormalities of mitral valve kinetics. Under medical treatment the Q wave totally regressed within a few hours, without rise in enzyme levels. The echocardiographic abnormalities gradually disappeared over a few days. After surgical excision of the phaeochromocytoma, both electrocardiography and echocardiography were perfectly normal. In such cases the Q wave is most probably due to a direct impact of catecholamines of the myocardium, with deep but reversible alterations of cellular metabolism. The echocardiographic abnormalities reflect an acute disorder of ventricular filling responsible for delay in mitral valve opening and disappearance of the E wave. The paradoxical septal kinetics are more difficult to explain; they seem to be related to adrenergic hyperactivity.

A new case of assumed parasitic cardiac disease is reported once more; a 67 year old woman with a trematode injection presenting with mitral incompetence and left ventricular failure. Biventricular endomyocardial fibrosis predominating at the apex was diagnosed at angiography and confirmed at surgery. Mitral incompetence was related to retraction of the papillary muscles which were surrounded by fibrosis, the rest of the mitral apparatus being normal. There was no indication for endocardectomy and so, mitral valve replacement alone was performed. There are few previous reports of parasitic cardiac disease: one case of left ventricular endomyocardial fibrosis, one case of biventricular fibroplastic parietal endocarditis and one case of cardiomyopathy. This report emphasises the need for cardiac examination in patients with parasitic diseases.

We report 5 cases of isolated ostial stenosis of the left main coronary vessel. Isolated ostial stenosis occurs preferentially in young or middle aged women for whom coronary insufficiency is usually not a serious threat. Patients with this type of lesion have characteristically severe angina of relatively recent onset. The condition may be difficult to diagnose at angiography, but a fall in pressure when the tip of the catheter enters the coronary lumen beyond the stenosis, a lack of reflux of the contrast medium into the sinus of Valsalva during intracoronary injection and its persistence in the coronary vessel should alert the investigator. A pathological study of 3 cases revealed typical atheromatous lesions in 2 patients (with extension of an aortic plaque to the left coronary ostium in one, and atheroma localized on the ostium in the other) and a purely fibrous lesions in a patient who had undergone thoracic radiotherapy 5 years previously. Although relatively rare, stenosis must be diagnosed in view of its sombre spontaneous prognosis (one patient died 3 days after coronary arteriography), of the risk of underestimating its frequency, and of the hazards of selective coronary catheterization in such patients (one of our patients died 15 minutes after coronary exploration).

The authors report the case of a double rupture of the heart (septal and parietal intrapericardial) on the 5th day of primary transmural anterior myocardial infarction in a 73 year old women. The diagnosis of septal rupture was made after cardiac arrest and the findings of a systolic murmur, and by echocardiography. Intrapericardial free wall rupture was diagnosed at surgery. The incidence, predisposing factors, gravity, prognostic factors and different medico-surgical therapeutic approaches to septoparietal complications of acute myocardial infarction are reviewed.

The authors report the case of a 53 year old patient who had undergone triple coronary bypass surgery for unstable angina. Recurrence of chest pain 4 months after surgery led to control coronary angiography which showed severe stenosis of the proximal and distal parts of the aorto-right coronary graft. Endoluminal dilatation was performed a few days later but, during angiography, complete occlusion of the graft was observed. This was repermeabilised without difficulty and a "remodelling" of the graft was carried out. The outcome was favourable with the complete regression of symptoms. The following alternatives to surgery are discussed: in cases of thrombosis which usually occur in the month following surgery, fibrinolysis may be attempted with a high success rate but a significant risk of haemo-pericardium: in cases of fibrous proliferation of the intima leading to stenosis or occlusion, endoluminal dilatation seems to be the procedure of choice, but this must always be carried out under surgical cover.