Pheochromocytoma with catecholamine-induced impairment of cardiac neuronal function.
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Adolescent↗
Biomedical subjects
J C Potier
Publications and source records attributed to J C Potier.
[Proarrhythmic effects of anti-arrhythmia agents].
Antiarrhythmic medications are widely used either at the ventricular or supraventricular level. However, those drugs can induce severe side effects. Actually, antiarrhythmic drugs are paradoxically able to favour the occurrence of new arrhythmias or aggravate the preexisting arrhythmia for which they were indicated. These proarrhythmic effects have been found in 10 to 20% of patients, as evidenced by literature. Moreover, the CAST study showed a significant increase in mortality in patients with non sustained ventricular arrhythmias after myocardial infarction who were treated with either flecainide or encainide, compared to the placebo group. This overmortality seems to be due, in large, to the proarrhythmic effects of antiarrhythmic drugs. Several mechanisms have been evoked, related to the type of antiarrhythmic drug and to the presenting arrhythmia: early post-depolarization due to slow calcium and sodium inward currents in the case of torsades de pointes, facilitation of intraventricular reentries in the case of class 1c antiarrhythmic drugs, facilitation of the ventricular response of atrial arrhythmias. These deleterious effects, that can be very serious, are unpredictable, not toxicity-related and all antiarrhythmic drugs are involved. Their detection appears to be difficult and is based upon ECG, Holter monitoring, treadmill test and possibly electrophysiologic study. The use of antiarrhythmic drugs requires the knowledge of their proarrhythmic effects, the analysis of the benefit-risk ratio--particularly if left ventricular function is impaired--and careful monitoring.
Anti-Arrhythmia Agents↗
[Myocardial infarction and revascularization. Current indications].
The physiopathologic role of thrombosis in the genesis of myocardial infarction, began to be suspected early in the 20th century but its logical treatment, thrombolysis, was first used on a large scale only ten years ago. Today, it is well established that short, middle and long-term mortality is correlated to coronary permeability, the delay in the revascularization treatment start-up, its efficacy, its swiftness of action, and to the maintaining of permeability following reperfusion. The importance of time elapse before reperfusion is obtained was demonstrated as early as 1986 by the GISSI study. According to this study, the administration of streptokinase (compared to a conventional treatment) reduced mortality at 21 days respectively by 47%, 23%, and 17%, depending on whether patients were treated within one hour, three hours, or between 3 and 6 hours following the onset of the painful symptoms. One of the major teachings of the GUSTO study, reported at the end of 1993, was the confirmation of the so-called "open artery" theory: mortality at 30 days was of 4.5% among patients whose coronary circulation was restored at the 90th minute, whatever thrombolytic treatment was used, compared to 8.9% when the coronary artery remained occluded. The value of aspirin in preserving coronary permeability following thrombolysis was demonstrated by the ISIS-2 study: mortality at 5 weeks was reduced by 23% in the group of patients randomised to receive only aspirin, while it was reduced by 25% in the group of patients randomised to be treated with streptokinase, and by 42% in the group randomised to receive both aspirin and streptokinase, compared to the group who received neither aspirin nor streptokinase. However, mortality during the first days following randomisation was identical among the groups, with or without aspirin, which suggested its action was rather one of prevention against reocclusion than one of accelerating dissolution of the thrombus. However, in spite of improved therapeutical protocols, a normal flow, which is the major criteria for a reduced mortality, is only obtained at the 90th minute in 54% of the patients who were administered the up-to-date treatment ie aspirin-accelerated t-PA-heparin in combination.(ABSTRACT TRUNCATED AT 400 WORDS)
Angioplasty, Balloon, Coronary↗
[Endocarditis caused by Cardiobacterium hominis].
The incidence of endocarditis due to Cardiobacterium hominis is probably underestimated because clinical presentations vary greatly and culture of this Gram negative germ is difficult. A 48-year-old man with a past history of post-streptococcic aortic regurgitation was hospitalized twice within 1 week for fever (38 degrees C) and junctional tachycardia which responded to amiodarone. Subsequently, infero-apical necrosis was documented. Based on the result of the laboratory tests, coronary embolism was suspected although 12 blood cultures were negative. The patient recovered well with a standard antibiotic treatment. Fifteen days later, the blood cultures revealed Cardiobacterium hominis. Antibiotic therapy was adapted and aortic valve replacement was programmed. Two months later the patient died from uncontrollable left heart failure. A 63-year-old man who had had mitral valve replacement 10 years earlier for Streptococcus mitis endocarditis was hospitalized for fever (38 degrees C) and a painful left calf. Phlebocavography eliminated deep vein thrombosis and a complete cardiac work-up was inconclusive. Endocarditis was suspected although blood cultures were negative. The patient was given oral penicillin and discharged after one week. Three months later, the patient was again febrile (38 degrees C) and suffered a cerebral vascular event. Fourteen days after blood sampling, cultures revealed Cardiobacterium hominis. The patient's haemodynamic status worsened and valve replacement with atrioplasty was performed. Outcome after 4 years follow-up has been favourable. Endocarditis due to Cardiobacterium hominis, a saprophitic germ of the upper airway and the female genital tract, has been reported in 64 cases in the literature. The clinical picture is often limited to fever and a heart murmur and laboratory tests show an accelerated erythrocyte sedimentation rate and hyperleukocytosis. Inflammatory type anaemia is often found due to the latency of the endocarditis. Complications are frequent and can be fatal due to massive pulmonary emboli, cerebral vascular events or irreversible heart failure. C. hominis is sensitive to amoxycillin and netilmicin. Surgical treatment of the valvulopathy is indicated.
Anti-Bacterial Agents↗
[Subacute rupture of the free wall of the heart. Clinical echocardiographic and pathological aspects apropos of 10 cases].
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.
Aged↗
[Myoglobin and CPK-MM isoforms during the acute phase of myocardial infarction].
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.
Aged↗
[Early clinical, electrocardiographic and biological criteria of reperfusion after intravenous fibrinolysis during the acute phase of myocardial infarction].
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)
Accelerated Idioventricular Rhythm↗
[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↗