[False image of aortic dissection in transesophageal echography. A pitfall to be known].
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Aortic Dissection↗
Biomedical subjects
P Gibelin
Publications and source records attributed to P Gibelin.
Hemodynamic effects of prolonged enoximone infusion (7 days) in patients with severe chronic heart failure.
This study investigated the hemodynamic effects and tolerance of infusion of 10 micrograms/kg/min enoximone over 7 days in 12 patients (mean age 64.3 years) with severe chronic heart failure (10 NYHA Class III and 2 Class IV) with idiopathic dilated cardiomyopathy. Hemodynamic parameters were measured 10 minutes, 3 hours, 6 hours, 18 hours, 24 hours, and 7 days after the start of infusion. Catecholamines were assayed before the start of the infusion and on day 7. The heart rate increased on an average from 90.8 +/- 13.7 before infusion to 108.5 +/- 8.2 beats/min (p < 0.05) on day 7 (+20%). The mean arterial pressure decreased by approximately 10% (p < 0.05) between the start and end of the infusion. The pulmonary artery diastolic pressure dropped by a maximum of 30% at the 24th hour (23.1 +/- 5.1 to 16 +/- 5.4 mm Hg; p < 0.01). This decrease remained significant on day 7; the index cardiac was increased a maximum of 40% between the 18th and the 24th hour; p < 0.01). This increase was still significant on day 7 (2.35 +/- 0.44; p < 0.05; +22%). Finally, the decrease in systemic arterial resistance, which reached a maximum of 30% of the 24th hour, persisted on day 7 (-22%); 2076 +/- 451 to 1612 +/- 283 dynes/sec/cm5; p < 0.05). The norepinephrine level did not change significantly (4.5 +/- 1.2 nmol/l before infusion vs. 4.2 +/- 1.1 nmol/l on day 7). Infusion had to be stopped in one patient after 30 minutes because of prolonged severe hypotension.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
Prevalence of toxoplasma myocarditis in patients with the acquired immunodeficiency syndrome.
OBJECTIVE: To evaluate the prevalence of cardiac toxoplasmosis in a series of 182 necropsies performed between 1987 and 1991 on patients infected with the human immunodeficiency virus (HIV), to correlate this prevalence with the ante mortem diagnosis of cardiac involvement, and to assess the role of such cardiac lesions in the immediate cause of death. PATIENTS AND METHODS: Complete necropsies of 182 HIV-infected patients (48 women, 134 men) were performed consecutively between 1987 and 1991. Risk factors, identified in 174 cases, included drug abuse (111/182), homosexuality (51/182), and blood transfusions (12/182). 16 samples were systematically obtained from each heart for histological study. If trophozoites or lymphocytic myocarditis were seen, immunohistochemical investigations were carried out with polyclonal antibodies for Toxoplasma gondii. An ultrastructural study was performed in four patients with toxoplasma myocarditis. Myocardial lesions were defined by the Dallas classification. Clinical data (and information on electrocardiograms and echocardiograms) were obtained from medical records. RESULTS: Cardiac toxoplasmosis was diagnosed at necropsy in 21 (12%) patients. Cardiac lesions were associated with toxoplasmic encephalitis in 18 patients and were solitary in three patients. Acute diffuse myocarditis was present in 6/21, rare foci of myocarditis were seen in 8/21, and intramyocytic toxoplasmic cysts without any inflammatory reaction or necrosis were seen in 4/21. Anti-toxoplasma immunolabelling showed cardiac toxoplasmosis in three patients with lymphocytic myocarditis. Particles with the ultrastructural characteristics of Toxoplasma gondii trophozoites were seen in four cases. Six patients had presented with cardiac symptoms, confirmed by electrocardiographic and echocardiographic abnormalities during their disease course, and their cardiac lesions were directly responsible for the death. CONCLUSION: Cardiac toxoplasmosis was common in this necropsy series of HIV-infected patients. Cardiac toxoplasmosis had been suspected clinically in four patients. Myocardial lesions were generally asymptomatic and were not discovered until necropsy. Solitary cardiac involvement was not uncommon reflecting parasite reactivation at a myocardial site. The incidence of cardiac toxoplasmosis in this group of immunodepressed subjects from an area with a high prevalence of this parasitic disease justifies regular follow up of such patients by electrocardiography and echocardiography as well as immediate administration of anti-toxoplasma treatment should sudden heart failure occur.
Acquired Immunodeficiency Syndrome↗
[Functional classification of cardiac insufficiency].
Several systems have been proposed for assessing the degree of functional impairment of chronic cardiac failure in order to be able to compare patients and to appreciate progression of the condition in individual patients. The NYHA classification is subjective, not very reproducible, and does not provide a good prediction of exercise capacity. The Canadian classification is not much better. Feinstein's classification is too complex, impractical and has never been validated. The specific activity scale proposed by Goldman indicates the degree of functional incapacity by comparison with activities of everyday life selected for their variability and classified according to the effort required to perform them. This classification has a good reproducibility and correlates well with exercise stress testing (exercise duration, VO2 max). However, it is not particularly well suited to the French population. The examples are not very precise; in addition, contradictions are possible, making it difficult to classify some patients. The authors propose a specific activity scale adapted for French patients. This classification was studied in 45 patients with chronic primary dilated cardiomyopathy. It was reproducible and correlated well with peak VO2. The progressive design of the symptom questionnaire avoids contradiction. This classification could be useful both in everyday practice and for multicentre research studies.
Activities of Daily Living↗
[Compression of the coronary trunk by aneurysm of the antero-left Valsalva sinus associated with acute mitral insufficiency caused by rupture of the chordae following valvular prolapse. Successful triple surgical operation in a 66-year old patient].
Tearing of the chordae is a common complication of prolapse of the mitral valve; which becomes increasingly common with age. In contrast, aneurysm of the Valsalva sinus is rare in patients over 65 years of age. The antero-left sinus is an unusual location, but may be complicated by compression of the left coronary artery, which is reported in 16 cases in the literature. The case reported is unusual due to the combination in a 66-year old subject of acute mitral incompetence, due to tearing of the chordae following prolapse of the mitral valve, and an aneurysm pressing on the coronary trunk whilst remaining asymptomatic. Complete correction of the lesions was successfully achieved by surgery.
Acute Disease↗
[Treatment of chronic heart insufficiency with dobutamine. Value and limitations].
Most positively inotropic drugs are available only as intravenous injection, which restricts their use in chronic heart failure. A single and brief infusion of dobutamine--a synthetic catecholamine and potent beta 1-adrenoreceptor agonist--provides a clinical improvement which may last for several weeks. On the other hand, tachyphylaxis to dobutamine may develop after a several days' infusion, so that the drug gradually loses its effectiveness. In patients with chronic heart failure, intermittent infusions of dobutamine result in sustained clinical improvement in more than 50 percent of the cases. The relative preservation of beta-adrenoceptors seems to play a role in the beneficial effects of intermittent infusions. The most significant side-effects of dobutamine are ventricular rhythm disorders. The practical applications and supervision of repeated dobutamine infusions in chronic heart failure are detailed.
Chronic Disease↗
Influence of the rt-PA dose (1 mg/kg versus 1.5 mg/kg) and duration of administration on the patency of infarct-related coronary arteries in 81 patients.
This open study compared the efficacy and side effects of two dose regimens of intravenous rt-PA initiated before the fifth hour after the onset of myocardial infarction. The first 40 patients (group A) received 1 mg/kg of rt-PA infused over 90 minutes, including a 10-mg initial bolus. The following 41 patients (group B) received 1.5 mg/kg (20-mg initial bolus, 60% over 60 minutes and 40% over 120 minutes). Noninvasive clinical, electrocardiographic, and biochemical parameters of reperfusion were recorded systematically, along with serial measurements of fibrinogen and hemoglobin levels. Coronary arteriography and left ventriculography were performed at the 48th hour or earlier, on an emergency basis, in the absence of signs of reperfusion, or if there were clinical and ECG signs of rethrombosis. Patency of the infarct-related artery (TIMI grades 2 and 3) was achieved in 55% of the group A patients vs. 83% of the group B patients (p less than .01). Twelve emergency coronary arteriographies were performed in each group. No significant difference was observed in the ejection fraction (48% in group A vs. 52% in group B). The peak CPK level was similar in both groups, but the peak occurred earlier in group B (p less than .001). There was no statistically significant difference between the two dose regimens in terms of reduction in fibrinogen or plasminogen levels. Two deaths occurred in group A vs. one death in group B. No cerebrovascular accidents occurred in either group.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
[Acute myocardial ischemia following administration of a vasoconstrictor agent].
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Adult↗
[Cardiovascular complications of interferon].
Interferon, a fairly recent drug, is used in some cancers and other diseases. The adverse effects include cardiotoxicity which was recognized from phase-I trials. Some of these complications are very common and not serious at the dose levels administered: transient hypotension at the beginning of the treatment, atrial extrasystole. Other effects are less common and not dangerous: low-level conduction impairment or reversible hypertension as the authors recalled. There are also a much more serious forms of toxicity which may be life-threatening, one of which seems to be dose-dependent and consists of the onset of cardiomyopathy, which is usually reversible when treatment is stopped, the other is uncontrollable and usually occurs in high-risk cardiac patients from the first few injections and results in sudden death induced by acute coronary artery failure and/or serious ventricular arrhythmia. The physiopathology of this cardiotoxicity remains unknown, but as it is known to exist, rigorous cardiological monitoring of all patients receiving this treatment is necessary.
Aged↗
[Determination of the anaerobic threshold in chronic cardiac failure. Value and limitations].
Anaerobic threshold was studied in 35 patients with cardiac failure present for more than 6 months, of primary or ischemic origin and New York Heart Association Stage II or III. Each patient underwent an exercise test of ergometric bicycle (increments of 10 watts/1 minute) with analysis of expired gases respiratory cycle by respiratory cycle (oxygen consumption, carbon dioxide production, respiratory oxygen and carbon dioxide equivalent, respiratory quotient). Anaerobic threshold was determined indirectly following Wasserman's recommendations. It was possible to determine anaerobic threshold in 25 patients (83.3%). The test was well tolerated. The two best methods for detection of anaerobic threshold were divergence of the curve of production of carbon dioxide in relation to oxygen consumption and an increase in respiratory oxygen equivalent while the carbon dioxide equivalent remained constant. In addition, oxygen consumption at the anaerobic threshold was statistically correlated with functional class (p < 0.05) and with the Weber classification based upon peak oxygen consumption (p < 0.001). Finally, anaerobic threshold occurred on average at 5.4 +/- 1.8 min from the start of exercise with a heart rate of 119.7 +/- 18 bpm, an oxygen consumption of 10.5 +/- 2.3 ml/min/kg (i.e. 43.2 +/- 12.1% of maximum oxygen consumption and 70.5 +/- 19.3% of oxygen consumption limited by symptoms) and a respiratory quotient of 1.07 +/- 0.08. In conclusion, analysis of respiratory gases during exercise in cardiac failure patients enables, with sub-maximal exercise and noninvasively, the determination in the majority of cases of anaerobic threshold, which is statistically correlated with New York Heart Association stage and the Weber classification based upon oxygen consumption at peak effort.
Adult↗
[Metabolic changes in cardiac failure].
As soon as there is evidence of left ventricular dysfunction, even before clinical signs of chronic cardiac failure (CCF) have developed, intrinsic and extrinsic compensatory mechanisms are brought into play by the body. The majority of these mechanisms are under the influence of neurohumoral systems. When neurohormonal responses persist, as in CCF, they take on a beneficial nature since they participate in adaptation of the cardiovascular system as a whole, but they are also harmful since they worsen the working conditions of the myocardium by their cardiac and peripheral effects. Hyperactivity of the noradrenergic sympathetic nervous system is seen in CCF with levels 2 to 3 times higher as compared with subjects with normal left ventricular function. The circadian rhythm of catecholamines is modified. The increase in circulatory catecholamines is all the greater when cardiac failure is advanced. This release of noradrenaline (NA) is under the control of arterial baroreceptors which normally send to the central nervous system inhibitory inflow from the sympathetic nervous system. Inhibitory tone is released in case of a fall in blood pressure. Noradrenaline acts on beta-predominant myocardial receptors (inotropic and tachycardic) and alpha-predominant vascular receptors, resulting in arteriolar vasoconstriction. There is rapid onset of down regulation of myocardial beta-receptors. This fall essentially concerns beta 1, but beta 2 also, since they may be affected according to the etiology of CCF (ischemia). The Renin Angiotensin System (RAS) is also activated by the fall in systemic blood pressure. This consists of a cascade of reactions leading to the synthesis of angiotensin II responsible for powerful vasoconstriction of all arterial areas, including the coronary vessels.(ABSTRACT TRUNCATED AT 250 WORDS)
Heart Failure↗
[How to evaluate the cost/effectiveness ratio of different therapies of coronary disease].
The results of epidemiologic studies on the efficacy of different strategies of prevention or improvement of the prognosis of coronary artery disease are generally expressed in terms of percentage reduction of risk; for example, the treatment of hypercholesterolaemia reduces the risk of coronary death by 21%. In order to improve the assessment of the efficacy of these approaches the authors propose to take into account the number of subjects which needs to be treated each year to prevent one cardiovascular event more than the control group (for example, in hypercholesterolaemia, 1,736 patients). This number depends on the reduction of risk and also on the incidence of complications in the control group. Using this method, the authors classified different therapeutic strategies in order of their efficacy: thrombolytic therapy in the acute phase of myocardial infarction, then aortocoronary bypass grafting of left main coronary or triple vessel disease, secondary prevention with stopping smoking, and betablocker therapy. Finally, primary prevention with anti-smoking campaigns, treatment of hypertension and hypercholesterolemia. Based on this figure and knowing the annual cost of patient treatment, it is possible to calculate a cost-effectiveness ratio for each of these therapeutic interventions.
Adrenergic beta-Antagonists↗
[Nocturnal-diurnal changes of norepinephrine blood levels in patients with chronic cardiac insufficiency. Practical values].
The purpose of this study was to investigate circadian changes in noradrenaline (norepinephrine) levels in patients presenting with congestive heart failure. Eighteen patients were investigated with a group mean age of 66 years, 12 in NYHA class III and 6 in class IV. The cause of the heart failure was ischemia in 7 cases, valvular in 1 case and idiopathic in the other 10 cases. The mean follow-up time of the disease was 3.9 years. Six healthy volunteers were investigated following the same protocol. Blood samples were taken while the patient was lying down over a period of 24 hours, after installing a peripheral venous catheter. The assay was carried out by means of high performance liquid chromatography with electrochemical detection. In the controls, the mean noradrenaline level (norepinephrine) was 220 +/- 62 pg/ml, with daytime peaks. The heart failure patients showed a high mean level (230 +/- 404 pg/ml), with less daytime variability than the controls (92% vs 127%; p < 0.05). The 8 a.m. value was reproducible, and there was close correlation between this value and the mean value for the 24 hours (p < 0.001). Thus, the morning sample provides a good estimation of the levels over the 24 hours.
Aged↗
[Fungal myocarditis in acquired immunodeficiency syndrome].
The authors report 8 cases of fungal myocarditis discovered at autopsy of a series of 118 patients with AIDS. The cardiac disease was symptomatic and responsible for death in 2 cases. Antemortem diagnosis of fungal infection was made on examination of bronchioloalveolar lavage, the cerebrospinal fluid or gastrointestinal biopsy. The demonstration of intramyocardial pathogens was postmortem in all cases. The organism was Candida albicans in 3 cases, Cryptococcus neoformans in 3 cases, and Aspergillus fumigatus in 2 cases. The lesions were not confined to the heart; multi-visceral fungal involvement was diagnosed at autopsy in all cases. Cryptococcal and Candida myocarditis have already been described in most autopsy series in AIDS, but Aspergillus myocarditis is very rare. These fungal myocarditis are usually clinically latent or masked by neurological or respiratory symptoms.
Acquired Immunodeficiency Syndrome↗
[Cardiac toxicity of fluoro-uracil. Typical and atypical aspects. Apropos of 8 cases].
The cardiac toxicity of 5 fluoro-uracil, an antimitotic agent widely used in various protocols, has been known for 16 years. Several cases have been reported in the literature, leading to the suggestion, without formal evidence, that the chief mechanism responsible for this cardiac toxicity is "classical" coronary spasm. However, certain clinical aspects already described may shed doubt on this theory. On the basis of 8 cases, the authors report different clinical pictures all caused by cardiac toxicity of 5FU. It is of interest to note that chest pain with the classically described electrocardiographic changes did not apply in the majority of cases. The commonest pattern was asymptomatic electrocardiographic abnormalities and/or arrhythmias without angina. Among the reported cases, one patient had pain with electrocardiographic abnormalities, recurrent after the withdrawal of 5FU and resistant to maximal medical treatment, despite the absence of any coronary disease or signs of spasm. One patient had a first myocardial infarction, later rechallenge with the drug resulting in failure. In another patient, with known coronary disease, 5FU probably cause cardiogenic shock. In total, some of our cases, as well as other features described in the literature, raise questions as to the pathophysiology of the cardiac toxicity of 5FU.
Adult↗
[Atypical urinary excretion of catecholamines and their catabolites in a case of pheochromocytoma].
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Adrenal Gland Neoplasms↗
[Ischemic clinical forms of hypertrophic cardiomyopathies: differential diagnosis with myocardial infarction. Apropos of 15 cases].
This study reports 15 cases of ischaemic clinical forms of hypertrophic cardiomyopathy (HCM). In this retrospective study over a 3 year period, 15 patients with HCM presented with clinical and electrocardiographic signs simulating unstable angina (N = 5) or myocardial infarction (N = 10). All patients had chest pain lasting at least 20 minutes with pseudo-ischaemic ECG changes. Two patients were given thrombolytic therapy. The clinical and enzymatic outcome and results of complementary investigations (including coronary angiography) confirmed the absence of coronary artery disease. The diagnostic of HCM was made by echocardiography. These cases were all apparently primary forms of HCM without intraventricular pressure gradient under basal conditions. Three of the patients were known cases of HCM but the condition was diagnosed after the ischaemic presentation in the other cases. Eight of them had however been considered to have had coronary insufficiency for an average of 5 years. The clinical presentation of HCM represents a difficult differential diagnostic problem with myocardial infarction. Echocardiography is of little help in distinguishing the 2 diseases as septal hypokinesis is often observed in HCM. The clinical course usually reestablishes the diagnosis within a few hours but the delay is often too long in this situation of therapeutic emergency and the indications of thrombolysis may be wrongly posed. Although there is no available formal means of distinguishing the two conditions, this study underlines that this clinical form of HCM is not rare and that the diagnosis should be keep in mind with the other differential diagnoses of myocardial infarction.
Adult↗
[Value of the replacement of intravenous trinitrin by oral trinitrin in the acute phase of myocardial infarction complicated by regressive left ventricular insufficiency].
Left ventricular failure is a common complication of the acute phase of myocardial infarction. The most appropriate current treatment, when an increase in preload is the predominant or sole feature, involves nitroglycerin by infusion combined in varying degrees with diuretics. The aim of this study was to assess the value of maintenance treatment following intravenous nitroglycerin based upon a long acting nitrate derivative designed to achieve a hemodynamic result. Twenty patients with a mean age of 62 and with left ventricular failure during the acute phase of a myocardial infarction were studied. They were all treated with IV nitroglycerin using an automatic pump syringe. Pulmonary artery diastolic pressure, cardiac output, blood pressure and heart rate were measured hourly for six hours then every 6 hours. When PADP fell to below 18 mmHg, maintenance treatment with placebo or long acting nitroglycerin was given double-blind (10 patients were given long acting nitroglycerin and 10 patients the placebo). Pulmonary artery pressures, blood pressure and heart rate were measured every 2 hours for 8 hours, then at 12 and 24 hours. No significant difference was found in heart rate, blood pressure, cardiac output nor PADP (10 +/- 3.5 mmHg cf. 12 +/- 2.8 mmHg; NS) between the two groups. In total, maintenance treatment with long acting nitrate derivatives following IV nitroglycerin for hemodynamic purposes in patients with an acute myocardial infarction complicated by regressive cardiac failure would no appear to be necessary.
Administration, Oral↗