Biomedical subjects
Publications and source records attributed to P Lancellotti.
The diagnostic criteria for panic disorder include symptoms commonly experienced by patients with organic diseases. We report a case of coronary artery spasm in a patient with chest pain, exhibiting atypical characteristics, and accompanied by symptoms of nervousness. The approach and the management of anxiety disorders are discussed.
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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.
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.
OBJECTIVE: To compare the relative accuracy of dobutamine stress echocardiography (DSE) and quantitative technetium-99m sestamibi single photon emission computed tomography (mibi SPECT) for detecting infarct related artery stenosis and multivessel disease early after acute myocardial infarction. DESIGN: Prospective study. SETTING: University hospital. METHODS: 75 patients underwent simultaneous DSE and mibi SPECT at (mean (SD)) 5 (2) days after a first acute myocardial infarct. Quantitative coronary angiography was performed in all patients after imaging studies. RESULTS: Significant stenosis (> 50%) of the infarct related artery was detected in 69 patients. Residual ischaemia was identified by DSE in 55 patients and by quantitative mibi SPECT in 49. The sensitivity of DSE and mibi SPECT for detecting significant infarct related artery stenosis was 78% and 70%, respectively, with a specificity of 83% for both tests. The combination of DSE and mibi SPECT did not change the specificity (83%) but increased the sensitivity to 94%. Mibi SPECT was more sensitive than DSE for detecting mild stenosis (73% v 9%; p = 0.008). The sensitivity of DSE for detecting moderate or severe stenosis was greater than mibi SPECT (97% v 74%; p = 0.007). Wall motion abnormalities with DSE and transient perfusion defects with mibi SPECT outside the infarction zone were sensitive (80% v 67%; NS) and highly specific (95% v 93%; NS) for multivessel disease. CONCLUSIONS: DSE and mibi SPECT have equivalent accuracy for detecting residual infarct related artery stenosis of >/= 50% and multivessel disease early after acute myocardial infarction. DSE is more predictive of moderate or severe infarct related artery stenosis. Combined imaging only improves the detection of mild stenosis.
Meningitis due to Neisseria meningitidis occurred in a young man. On admission, he was in septic shock and the electrocardiogram revealed convex upwards ST-segment elevation in inferior and lateral leads. Rapid and complete normalisation of the ECG was observed and the patient had a favourable evolution with intensive therapy. The mechanisms of the ECG abnormalities in this disease are unclear. In this patient, ST-segment elevation was probably related to severe transmural ischaemia or prolonged coronary artery spasm as suggested by increase and decrease of cardiac enzymes and transient echocardiographic wall motion abnormalities without pericarditis. However, myocarditis could not be completely ruled out.
OBJECTIVE: This study sought to evaluate the safety and efficacy of arbutamine echocardiography in identifying contractile reserve and predicting functional improvement early after acute myocardial infarction (AMI). METHODS AND RESULTS: Seventeen patients with first AMI underwent arbutamine echocardiography 48 to 96 hours after AMI. Arbutamine was infused by a closed-loop delivery device. The heart rate slope was 4 beats/min and the heart rate target was 20 beats/min above baseline heart rate. A follow-up echocardiogram was obtained one month later. N-13 ammonia and F-18 FDG positron emission tomographic (PET) imaging were performed 6 +/- 2 days after AMI, before coronary angiography. Mean duration of arbutamine infusion was 6 +/- 2 min. There was no complication and there were no major side effects. Myocardial viability was identified with PET in 15 of the 17 patients. Contractile reserve was observed in 10 patients during arbutamine infusion. Functional recovery was identified in 12 patients. Sensitivity, specificity and accuracy of PET and arbutamine echocardiography for predicting functional recovery were 100%, 40%, 76% and 67%, 80%, 84%, respectively. CONCLUSIONS: Low-dose arbutamine stress testing is safe early after AMI. Contractile reserve can be rapidly identified by echocardiography and is specific, but moderately sensitive for predicting reversible dysfunction.
Shoshin is a fulminating form of cardiac beriberi developing in a few hours in a young alcoholic. Without specific treatment it evulers, toward death by cardiogenic shock and metabolic acidosis. Treatment by thiamine and alkalinisation permits a spectacular and fast recovery.
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Rupture of the interventricular septum is a classical complication of acute myocardial infarction. The diagnosis should be evoked when the patient's hemodynamic condition deteriorates in the presence of a new systolic murmur. A transthoracic or, preferably, transesophageal echocardiography confirms the diagnosis. Early surgical correction constitutes the best treatment. Despite recent progresses, mortality remains high but long term results are encouraging. The risk factors conditioning prognosis, the surgical options and the question of simultaneous coronary bypass will be discussed after a thorough review of the literature.
Acute myocardial infarction (AMI) is a serious condition which requires rapid hospital management. In this article, we review the current recommendations concerning AMI treatment, as well as our therapeutic approach, which is based on the evidence provided by several large well controlled clinical trials. Mid and long term prognosis are mainly related to the development of left ventricular dysfunction which determines heart failure, the occurrence of severe ventricular arrhythmias and the persistence of residual myocardial ischemia. Several treatments (aspirin, beta-blockade, ACE inhibitors, statins) have shown their benefit in terms of secondary prevention.
OBJECTIVES: The aims of this study were (1) to assess the relation between ST-segment elevation and wall motion response occurring during dobutamine testing and (2) to evaluate the usefulness of stress-induced ST-segment elevation for predicting functional recovery after acute myocardial infarction. BACKGROUND: Clinical significance of stress-induced ST-segment elevation after acute myocardial infarction remains controversial. According to previous studies, it may reflect a larger infarcted area, depressed left ventricular function, left ventricular aneurysm, stress-induced dyskinesia, residual myocardial ischemia, or viability in the affected region. Whether transient ST-segment elevation occurring during dobutamine testing may predict functional recovery is unknown. METHODS AND RESULTS: We studied 38 patients who underwent dobutamine stress testing early (5 +/- 2 days) after a first acute myocardial infarction. Dobutamine was infused at increasing doses from 5 to a maximum of 40 microg/kg per minute, with the addition of up to 1 mg of atropine if the target rate could not be reached by dobutamine alone. Twelve-lead electrocardiography and cross-sectional echocardiography were continuously monitored throughout the test. Dobutamine-induced ST-segment elevation was defined as a new or worsening >/=1 mm elevation, 80 ms after J point, in >/=2 infarct-related leads. Quantitative angiography was available in all patients before hospital discharge. Follow-up resting echocardiography was recorded in all patients 12 to 18 months after the acute event. ST-segment elevation was observed in 20 of the 38 patients. There were no significant differences between patients with and those without dobutamine-induced ST-segment elevation in age, site of infarction, peak level of total creatine kinase enzyme, and use of thrombolytic therapy, angioplasty, or both. Persistent akinesis without change during dobutamine stress testing was more frequently observed in patients without ST elevation (P <. 05). A biphasic response during dobutamine testing was more frequently observed in patients with ST-segment elevation (P =.01). Multivariate analysis selected 2 independent variables associated with ST-segment elevation: a biphasic response during dobutamine stress (chi-square = 7.3; P =.007) and the minimal lumen diameter of the infarct-related vessel at quantitative angiography (chi-square = 5.5; P <.02). Functional recovery was demonstrated in 26 patients. Sensitivity of ST-segment elevation for the prediction of functional recovery was 69%, specificity 83%, positive predictive value 90%, and accuracy 74%. Two independent variables predicting functional recovery were selected: dobutamine-induced ST-segment elevation (chi-square = 9.1; P =.003) and a biphasic response during stress (chi-square = 6.15; P =.013). CONCLUSIONS: Dobutamine-induced ST-segment elevation in the infarct-related leads is an ancillary sign of viable myocardium in jeopardy. It has a high specificity and an acceptable sensitivity for the prediction of functional recovery after acute myocardial infarction.
BACKGROUND: Infective endocarditis remains a life-threatening disease, and its optimal management is of paramount importance. Transesophageal echocardiography (TEE) is useful for the diagnosis of endocarditis-induced lesions, but the prognostic significance of the method remains controversial. HYPOTHESIS: The purpose of this study was to relate clinical and TEE characteristics to the occurrence of mortality and/or systemic embolization in a consecutive series of 45 patients with a diagnosis of infective endocarditis. METHODS: All patients underwent at least one monoplane TEE. Clinical data, episodes of embolization, and echocardiographic characteristics were prospectively recorded. Stepwise logistic discriminant analysis was performed to identify the independent variables that best predicted three binary outcomes: systemic embolization, death, and systemic embolization and/or death. RESULTS: Twelve of the 45 patients (27%) died from the endocarditis. Significant univariate predictors of death were the presence of paravalvular abscess (p = 0.025), number of vegetations (p = 0.021), Staphylococcus aureus isolated in blood cultures (p = 0.002), medical treatment alone (p < 0.002), and systemic embolism (p < 0.001). In multivariate analysis, systemic embolism (chi 2 = 29.3; p < 0.01), echocardiographic evidence of paravalvular abscess (chi 2 = 5.6; p = 0.018), Staphylococcus aureus endocarditis (chi 2 = 5.5; p = 0.016), and medical treatment alone (chi 2 = 5.11; p = 0.024) emerged as optimal predictors of death. Systemic embolization occurred in 12 patients. Independent variables predicting systemic embolization were a total length of vegetations > 14 mm (p = 0.01), greater age (p = 0.02), and medical treatment alone (p = 0.03). When two or more vegetations were observed, the total length is the sum of the individual sizes. Independent risk factors for the development of systemic emboli and/or death as a combined end point were total length of vegetations on TEE (chi 2 = 6.4; p = 0.003) and medical treatment alone (chi 2 = 4.1; p = 0.047). CONCLUSIONS: High-risk patients may be identified by the combination of clinical variables and TEE characteristics.
Previous studies have shown that the maintenance of cell membrane integrity and metabolism requires the persistence of residual myocardial blood flow. The purpose of this study was to assess the role of N-13 ammonia positron emission tomographic (PET) imaging performed early after an acute myocardial infarction for predicting functional recovery. Seventeen patients with an acute myocardial infarction were included in the study. Thirteen received thrombolytic therapy, 2 underwent immediate angioplasty of the infarct-related artery and 2 were treated with heparin. N-13 ammonia imaging was performed 6 +/- 2 days after the acute event and was followed by elective angioplasty in 13 patients. Using a 16-segment polar map display, regional N-13 ammonia uptake was expressed as a percentage of maximal segmental uptake and classified as normal (> 63%), moderately reduced (63-50%) and severely reduced (< 50%) based on values of tracer uptake obtained from healthy subjects. By echocardiographic assessment of regional wall thickening within 96 hours and at 1 month after the infarct, we examined the relationship between blood flow and functional outcome of myocardial segments in the infarct-related area. Regional wall thickening was graded on a 4-point scale: normal (1), hypokinesia (2), akinesia (3) and dyskinesia (4). Of 77 dyssynergic segments at baseline echocardiographic study, 43 had normal flow, 15 moderately reduced flow and 19 severely reduced flow. Segments with N-13 ammonia uptake > or = 50% demonstrated a significant improvement in wall thickening score at follow-up (p < 0.001), whereas segments with N-13 ammonia uptake < 50% showed no improvement in wall thickening scores (p < 0.001). The proportion of segments improving contractility by at least 1 score was significantly higher in the group of segments with N-13 ammonia uptake > 63%. The predictive value for defining functional recovery with segmental N-13 ammonia uptake > 63% was 86%. The predictive value for absence of recovery (uptake < 50%) was 54%. In conclusion, our data showed that early after an acute myocardial infarction N-13 ammonia imaging provides information regarding functional outcome.