Biomedical subjects
Publications and source records attributed to L A Piérard.
Severe electrolyte imbalance is rarely the cause of cardiac decompensation. We report the case of a young patient with acute left ventricular failure due to severe hypocalcaemia secondary to the intestinal malabsorption of calcium with inflammatory bowel disease. The interesting feature of this case was the rapid haemodynamic deterioration and the total reversal within one week following correction of the hypocalcaemia.
The effect of calcium antagonist on clinical outcome is controversial. A recent study investigated the safety and efficacy of the calcium antagonist nifedipine GITS (gastro-intestinal therapeutic system) in patients with stable, but symptomatic coronary disease. ACTION randomised 7.665 patients to double-blind addition of nifedipine 60 mg once daily or placebo during a mean follow-up of 4.9 years. Most patients were already treated by a beta-blocker, a statine, or aspirine. The addition of nifedipine was well tolerated with a low incidence of side effects. With nifedipine, the development of heart failure was reduced by 29 %. There was also a reduction in the need for coronary angiography and bypass grafting (reduction of 18 and 21%, respectively). The primary efficacy and safety outcomes were not different between nifedipine GITS and placebo. The rate of total mortality and cardiovascular death were not significantly different. The addition of nifedipine GITS to convential treatment of stable angina is safe, has no effect on major cardiovascular event free survival, but reduces the need for coronary angiography and interventions.
Tachycardias arise from an arrhythmogenic substrate triggered by a random factor (generally an extrasystole) and modulated by the autonomic nervous system. The three components are interactive, but their intensity and conjunction vary continuously. During the last decade, major achievements have been made to clarify definition and classification of data reported in the literature, helping our understanding of the mechanisms of ventricular arrhythmias. Nowadays, the pathophysiology of cardiac arrhythmias is well-known at the cellular and molecular ion channel activity. The progress of epidemiology and molecular genetics have allowed a better knowledge of the genotype-phenotype correlation in young patients presenting syncopes due to torsades de pointes or polymorphic ventricular tachychardia episodes which may degenerate into ventricular fibrillation and cause sudden death. The data of numerous large prospective randomised studies have led to more rational treatments with the progressive withdrawal of class I antiarrhythmics and their replacement by betablocking agents. The surgical approach of ventricular tachycardia has been overcome by the automatic implantable defibrillator and in some well-defined clinical situations, catheter ablation is used.
Paroxysmal atrial fibrillation is one of the most common disorders of cardiac rhythm. It is often a step toward permanent arhythmia, specially if associated with cardiac disease. The management objectives of intermittent arhythmia may be different, as maintenance of sinus rhythm. However, risks of stroke and thrombo-embolism are similar to those for sustained atrial fibrillation and must be carefully assessed. In this article we review the epidemiology, pathophysiology, clinical aspects and current guidelines for treatment and management of paroxysmal atrial fibrillation.
Paroxysmal supraventricular tachycardias are often encountered in young and otherwise healthy patients. They are rarely life threatening even though they may alter the quality of life. In this article, we review the acute treatment of an episod of tachycardia and the prevention of recurrences.
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AIMS: To develop optimal methods for the objective non-invasive diagnosis of coronary artery disease, using myocardial Doppler velocities during dobutamine stress echocardiography. METHODS AND RESULTS: We acquired tissue Doppler digital data during dobutamine stress in 289 subjects, and measured myocardial responses by off-line analysis of 11 left ventricular segments. Diagnostic criteria developed by comparing 92 normal subjects with 48 patients with coronary disease were refined in a prospective series of 149 patients referred with chest pain. Optimal diagnostic accuracy was achieved by logistic regression models, using systolic velocities at maximal stress in 7 myocardial segments, adjusting for independent correlations directly with heart rate and inversely with age and female gender (all p<0.001). Best cut-points from receiver-operator curves diagnosed left anterior descending, circumflex and right coronary disease with sensitivities and specificities of 80% and 80%, 91% and 80%, and 93% and 82%, respectively. All models performed better than velocity cut-offs alone (p<0.001). CONCLUSION: Non-invasive diagnosis of coronary artery disease by quantitative stress echocardiography is best performed using diagnostic models based on segmental velocities at peak stress and adjusting for heart rate, and gender or age.
The aging of the cardiovascular system leads to an increased incidence of hypertension, coronary artery disease and ischemic stroke. Since cardiovascular disease is the leading cause of morbidity and mortality in patients > or = 70 years old, prevention seems crucial for improving quality of life and reducing medical costs. In this article we present some aspects of cardiovascular prevention in elderly patients.
Cardiac transplantation is the treatment of choice for refractory heart failure. An immunosuppressive therapy must be given in the perioperative course to avoid graft rejection. In this article, we review the main classes of immunosuppressive agents (calcineurin inhibitors, anti-metabolities, corticoïds) and their side effects. The general preventive measures and the different kinds of rejection (hyperacute, acute vascular, acute cellular and chronical) are discussed. The current bacterial, protozoarian, mycotic and viral infections are described. We finish with the risk of cancer, mainly skin tumours and non-Hodgkinian lymphomas.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Mitral insufficiency can have a dynamic character, correlating to an intermittent increase in the area of the regurgitant orifice and the regurgitant volume. Among the various stress methods, echocardiography during effort on a bicycle in the semisitting position appears to be the technique of choice for evaluating this dynamic character. Thanks to the improvement of the Doppler signal quality, quantification of the regurgitant volume variations can be obtained in a reproducible manner at rest and during effort by applying the "PISA" method.
OBJECTIVES: We sought to examine the feasibility and reliability of quantifying mitral regurgitation (MR) during exercise by Doppler echocardiography in patients with heart failure and to assess the relationship between dynamic MR and systolic pulmonary artery pressure changes. BACKGROUND: The severity of MR can be quantified by using several echocardiographic methods. Quantitation of MR during dynamic exercise has not yet been performed. METHODS: Symptom-limited, semi-supine two-dimensional and Doppler echocardiograms during bicycle exercise were obtained in 27 consecutive patients with heart failure and functional MR. Regurgitant volume was measured at rest and during exercise by the proximal isovelocity surface area (PISA) method and by quantitative Doppler echocardiography. Exercise-induced changes in regurgitant volume were compared with changes in the regurgitant jet area to left atrial area ratio, vena contracta width and trans-tricuspid pressure gradient. RESULTS: The regurgitant volume measured by the PISA method increased from 21 +/- 12 ml (range 5 to 55) at rest to 39 +/- 23 ml (range 8 to 85) during exercise (p < 0.0001). The difference between two observers was low for both rest (2.0 +/- 2.7 ml) and exercise measurements (3.5 +/- 6.2 ml). The regurgitant volume measured by quantitative Doppler echocardiography increased from 29 +/- 13 to 49 +/- 24 ml (p = 0.0001). Excellent correlation between the two methods was obtained with exercise (r = 0.92). Exercise-induced changes in regurgitant volume, as measured by the PISA method, correlated well with regurgitant volume changes measured by quantitative Doppler echocardiography (r = 0.88), changes in vena contracta width (r = 0.82) and changes in trans-tricuspid pressure gradient (r = 0.73), but not with changes in regurgitant jet area to left atrial area ratio (r = 0.29). Seventeen patients stopped exercise because of fatigue and 10 because of dyspnea. These 10 patients exhibited greater increases in regurgitant volume (34 +/- 6 vs. 11 +/- 8 ml), corresponding to a significant elevation of the trans-tricuspid gradient (48 +/- 14 vs. 20 +/- 14 mm Hg). CONCLUSIONS: Quantitation of functional MR during exercise is feasible in patients with heart failure. There is a good correlation between regurgitant volume measured during exercise by the PISA method and that obtained by quantitative Doppler echocardiography, suggesting that the technique is reliable. An increase in mitral regurgitant volume during dynamic exercise correlates well with elevation of systolic pulmonary artery pressure.
This study sought to examine the effects of graded dobutamine infusion on QT dispersion early after acute myocardial infarction (AMI) and to investigate the relation of dobutamine-induced changes in QT dispersion to wall motion responses. Seventy-eight patients with a first AMI underwent dobutamine-atropine stress echocardiography 5 +/- 2 days after admission. Contractile reserve was identified in 45 patients and ischemic myocardium in 40. Sixteen patients had persistent akinesia. The best cut-off value of QT dispersion on the baseline electrocardiogram for predicting myocardial viability was 65 ms (sensitivity and specificity of 68%). Dobutamine infusion increased QT dispersion only in patients with viable myocardium (61 +/- 18 to 83 +/- 19 ms, p = 0.003) and/or ischemia (72 +/- 16 to 112 +/- 25 ms, p < 0.0001). No change was observed in patients with persistent akinesia (84 +/- 10 to 87 +/- 15 ms, p = NS). QT dispersion increased by 22 +/- 12 ms with administration of low-dose dobutamine in patients who had viable myocardium and by 47 +/- 21 ms with administration of low- to high-dose dobutamine in patients with ischemic myocardium. An increase in QT dispersion of > or = 20 ms from at rest to low-dose dobutamine infusion was associated with myocardial viability with a sensitivity of 78% and a specificity of 79%, whereas an increase in QT dispersion of > or = 10 ms from low- to high-dose dobutamine infusion predicted ischemic myocardium with a sensitivity of 85% and a specificity of 82%. In conclusion, (1) low QT dispersion on the baseline electrocardiogram is determined by the presence of viable myocardium, (2) a dobutamine-induced increase in QT dispersion is associated with viable and jeopardized myocardium, and (3) unchanged QT dispersion during dobutamine stress is a simple marker of extensive necrosis.
BACKGROUND: The clinical significance of stress-induced ST elevation early after acute myocardial infarction and its relation to functional recovery remain controversial. The aims of this study were (1) to determine the incidence of ST elevation during dobutamine and exercise tests and (2) to assess the relative accuracy of exercise and dobutamine ST elevation for predicting functional recovery after acute myocardial infarction. METHODS AND RESULTS: We investigated 52 patients who underwent supine exercise (from 25 W to maximal charge) and dobutamine (from 5 to 40 microg/kg per minute and up to 1 mg atropine) stress electrocardiography in the same position. ST elevation was defined as new or worsening at >1 mm, 80 ms after J point. Echocardiography and quantitative angiography were available in all patients before hospital discharge. The follow-up resting echocardiogram was recorded 30 +/- 6 days after the acute event. ST elevation developed during 30 (58%) dobutamine and 24 (46%) exercise tests. The sum of ST elevation was higher during dobutamine testing (7.7 +/- 3.8 mm) than during exercise (5.5 +/- 2.5 mm) (P =.03). A low peak creatine kinase level was the single independent predictor of dobutamine-induced ST elevation. Functional improvement occurred in 35 patients. Two independent predictors of functional recovery were selected from multivariate analysis: dobutamine ST elevation (chi(2) = 9.1; P =.0026) and low peak creatine kinase level (chi(2) = 5.1; P =.025). When dobutamine ST elevation was not included in multivariate analysis, exercise-induced ST elevation emerged as an independent predictor of functional recovery (chi(2) = 5.0; P =.023). Significant linear correlation was found between the sum of ST elevation at peak dobutamine stress and the extent of functional recovery (r = 0.87; P <.0001). In contrast, no correlation was observed with exercise ST elevation (r = 0.06; P = not significant). CONCLUSIONS: Stress-induced ST elevation is an ancillary sign of viable myocardium that can recover. The sum of ST elevation at peak dobutamine stress correlates with the extent of functional recovery.
We studied the relation between the ischemic threshold at the onset of wall motion abnormality on exercise echocardiography (EE) and the severity of coronary stenosis in patients with 1-vessel coronary artery disease (CAD). We screened 216 consecutive patients who underwent coronary angiography and EE for suspected CAD. Ninety-five (74 men; age, 56 +/- 12 years) satisfied the study criteria, that is, the presence of 1-vessel disease or no evidence of CAD on angiography and a normal baseline echocardiogram. Eighty-seven patients had 1-vessel CAD on angiography, and exercise-induced wall motion abnormality occurred in 73 (77%). Optimal cutoff values of percent diameter stenosis and minimal lumen diameter for predicting a positive EE were 61% (sensitivity and specificity of 76%) and 1.12 mm (sensitivity and specificity of 74%). Among patients with positive EE, heart rate-blood pressure product at ischemic threshold was correlated with quantitative coronary stenosis (r = -0.72, P <.001). The ischemic threshold from continuous monitoring of left ventricular function during semisupine EE is correlated with the severity of coronary stenosis among patients with 1-vessel disease and a normal resting echocardiogram.
OBJECTIVES: To assess the relative value of electrocardiographic, echocardiographic, angiographic, and in-hospital therapeutic indices for predicting late functional recovery after acute myocardial infarction, and to determine the variables associated with absence of recovery, partial recovery, and full recovery. DESIGN: Prospective observational follow up study. SETTING: Teaching hospital. PATIENTS: 74 consecutive patients with a first uncomplicated acute myocardial infarct. INTERVENTIONS: Dobutamine-atropine stress echocardiography was performed mean (SD) 5 (2) days after the acute event. Quantitative angiography was available in all patients before hospital discharge. A follow up resting echocardiogram was obtained 12 (2) months later. RESULTS: Functional recovery (partial, n = 18; full, n = 27) was observed in 45 of the 74 patients. Recovery was associated with earlier thrombolytic treatment (p = 0.008), earlier peak concentration of creatine kinase (p = 0.009), greater contractile reserve (p = 0.0001), non-Q wave acute myocardial infarction (p = 0.002), and more frequent elective angioplasty of the infarct related vessel (p = 0.0004). Three independent variables were selected stepwise from multivariate analysis for predicting late recovery: contractile reserve (chi(2) = 24.2, p < 0.0001); non-Q wave infarction (chi(2) = 15.7, p = 0.0001); and the time from symptom onset to thrombolysis (chi(2) = 4.94, p = 0.026). Three independent variables predicted full recovery: contractile reserve (chi(2) = 17.2, p = 0.0001); non-Q wave infarction (chi(2) = 10.1, p = 0.0016); and elective angioplasty of the infarct related artery (chi(2) = 4.53, p = 0.033). Only contractile reserve (chi(2) = 17.0, p < 0.001) was selected from the multivariate analysis for its ability to distinguish between partial recovery and absence of recovery. CONCLUSIONS: Late recovery of contraction relates to earlier treatment, which is associated with lower infarct size unmasked by a non-Q wave event and the presence of contractile reserve. Elective coronary angioplasty of the infarct related artery before hospital discharge is associated with full recovery.