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Biomedical subjects

J C Potier

Publications and source records attributed to J C Potier.

At least 19 recordsLinked to original sources

[Lyme's disease, a possible cause of isolated acute myocarditis].

The frequency of cardiac lesion in patients with other signs of Lyme disease has been estimated at 8 percent. The usual manifestation of myocardial involvement is a varying degree of atrioventricular block or more diffuse signs of myocarditis. Autopsy or intramyocardial biopsy provides a histological diagnosis of myocarditis. Microscopy shows a diffuse lympho-plasmocytic infiltrate with presence of macrophages in the myocardium, associated with a varying number of necrotic myocytes. Structures resembling spirochetes have been found in some cases. Exceptionally, the cardiac lesion may be isolated, presenting as an acute atrioventricular block and/or an acute myocarditis; in such cases the diagnosis of cardiac lesion caused by Lyme disease is made on serological grounds. We report the case of a 30-year old man admitted for acute myocarditis which turned out to be totally regressive. Intramyocardial biopsy showed interstitial congestion associated with inflammatory lympho-histiocytic infiltrates and eosinophilic polymorphonuclears; the myocardial fibres in contact with these infiltrates appeared to be altered. The diagnosis of Lyme disease was subsequently confirmed by serological tests. Patients with myocarditis caused by Lyme disease must be treated with antibiotics. Recent reports have demonstrated the presence of spirochetes in the myocardium of patients with dilated cardiomyopathy, suggesting that the spirochete Borrelia burgdorferi might be associated with, or play a part in, the subsequent occurrence of dilated cardiomyopathy.

Acute Disease

[Isolated right ventricular infarction of coronary origin. Three cases].

In a series of more than 700 patients admitted over a 2-year period to an intensive care unit, 3 patients with isolated right ventricular infarction were observed. At electrocardiography the condition was characterized by isolated ST elevation in the anterior precordial leads. Infarction was due to obstruction of a right marginal coronary artery in 2 cases and of a small right coronary artery feeding only the right ventricle in one case. In the absence of electrocardiographic signs in the inferior territory, this ST elevation is suggestive of an anterior infarction in constitution, but the characteristic "dome-like" shape of the elevation, its decrease from V2 or V3 to V4 or V5 and the progressive regression of repolarization disorders without occurrence of Q wave suggest a diagnosis of right ventricular infarction. This diagnosis can rapidly be confirmed by a normal left ventricular function at echocardiography.

Adult

[Correlations between the different criteria of late potentials and results of programmed ventricular stimulation after myocardial infarction].

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)

Action Potentials

[ST segment elevation in anterior precordial leads and right ventricular infarction. Apropos of 6 cases].

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.

Adult

[Myocardial infarction complicating exercise test performed 72 hours after coronary 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.

Aged

[Left coronaro-ventricular fistula after myocardial infarction. Apropos of a case].

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.

Angioplasty, Balloon, Coronary

[Myocardial dissection in infarction of the right ventricle. Clinical echocardiographic and pathological aspects].

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.

Aged

Serum digoxin levels related to plasma propafenone levels during concomitant treatment.

Nine patients with supraventricular rhythm disorders were treated during 5-day periods with different oral doses (300, 450, 600, and 900 mg daily) of propafenone concomitantly to long-term digoxin treatment. A poor correlation (r = .398; P less than .05) was obtained when the difference between the mean digoxin serum level (calculated with the Cmin data determined each of the 5 days) observed during a given propafenone dose and the mean digoxin serum level observed before propafenone treatment, was correlated with the dose of propafenone; but an evident correlation (r = .778; P less than .01) was found when the difference in digoxin level was correlated with the plasma propafenone concentration. The propafenone effect of increasing digoxin blood levels was thus concluded to be poorly dose dependent but strongly concentration dependent. The association of propafenone to a long-term digoxin treatment can be considered with a low risk of toxicity when plasma propafenone concentration does not exceed about 1000 ng/mL. Propafenone plasma levels are unpredictable in view of their wide interindividual variation for a given dose, so their measurement is advised to detect high levels and consequently to prevent a rise in digoxin serum concentrations with the possibility of toxicity. In clinical practice, when propafenone concentration determinations are not readily available, digoxin serum levels at least have to be carefully monitored.

Administration, Oral

Malignant ventricular tachycardia during propafenone treatment in a child with junctional automatic tachycardia: effectiveness of intravenous molar sodium lactate.

Propafenone may aggravate the preexisting arrhythmia or induce another one. Usually, such proarrhythmic effects occur in patients with spontaneous ventricular arrhythmias and/or coronary heart disease with poor left ventricular function. We report the case of a 5-year-old girl with junctional automatic tachycardia and no structural heart disease, in whom malignant ventricular tachycardia occurring during propafenone treatment could be terminated by molar sodium lactate (MSL) infusion. The serum propafenone level obtained before MSL infusion was within the therapeutic range. Two hypothesis could explain the beneficial effects of MSL in our patient: (1) alkalinization facilitates the cell membrane hyperpolarization and thus can decrease the voltage-dependent effect of Class Ic drugs, (2) alkalinization could displace propafenone from its tissue receptor sites by an increase in the nonionized fraction.

Atrioventricular Node

[Initial primary sarcoma of the pulmonary valve and trunk of the pulmonary artery].

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.

Adult

[Myocardial involvement in AIDS. Echographic study in 85 human immunodeficiency virus infected patients].

Histological and echographic studies of HIV-seropositive patients demonstrated the reality of myocardial involvement during the acquired immunodeficiency syndrome. Eight-five seropositive, asymptomatic patients, 55 of them classified as group IV (CDC criteria), were subjected to echocardiography and measurement of the reduction of the left ventricle fraction. An echographic anomaly was found in 8/85 seropositive patients and in 7/55 group IV patients. This affect on left ventricular contractility seems to occur in patients with a low number of CD4+ lymphocytes (p = NS) and is statistically significantly associated with the level of anti-P24 antibodies/antigenemia (absence of antibodies and positive antigenemia) (p less than 0.05).

Acquired Immunodeficiency Syndrome

[Dissection of aorta after aortic valve replacement].

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.

Aortic Dissection

[Echocardiographic aspects of multiple myxoma in Carney's syndrome].

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.

Adult

[Cardiac involvement in malignant non-Hodgkin's lymphoma].

Selective cardiac involvement by a malignant non-Hodgkin's lymphoma (primary lymphoma of the heart) is extremely rare. Cardiac lesions occurring in the course of a malignant non-Hodgkin's lymphoma (secondary lymphoma of the heart) are found at autopsy in about 10 per cent of the cases. Secondary lymphoma of the heart may involve all cardiac structures, but lesions of the right heart, and particularly the right atrium, are predominant. Clinical manifestations are usually non-specific and appear at a late stage, reflecting diffuse involvement. When the malignant non-Hodgkin's lymphoma is known, systematic two-dimensional echocardiography should easily detect the lymphomatous cardiac infiltration, irrespective of the presence or absence of symptoms. When the malignant non-Hodgkin's lymphoma is unknown, only histology can show that the heart tumour is a lymphoma, evaluate its extension and confirm that it is limited to the cardiac walls, provided the disease is treated at an early stage, prolonged complete remissions are observed after chemotherapy and/or radiotherapy.

Echocardiography

[Comparison of the efficacy of verapamil and diltiazem in stable exercise angina. A double-blind and crossover study].

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)

Aged

[So-called uremic heart diseases].

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)

Cardiomyopathies

[Cardiac sarcoidosis responsible for localized left ventricular ectasia and refractory ventricular tachycardia. Anatomoclinical study].

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.

Cardiomyopathies

[Transient reduction of ventricular tachycardia with adenosine-5'-triphosphate. A possible action of ATP on purinergic receptors].

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.

Adenosine Triphosphate