(1/884) QT dispersion in patients with chronic heart failure: beta blockers are associated with a reduction in QT dispersion.
OBJECTIVE: To compare QT dispersion in patients with impaired left ventricular systolic function and in matched control patients with normal left ventricular systolic function. DESIGN: A retrospective, case-control study with controls matched 4:1 for age, sex, previous myocardial infarction, and diuretic and beta blocker treatment. SETTING: A regional cardiology centre and a university teaching hospital. PATIENTS: 25 patients with impaired left ventricular systolic function and 100 patients with normal left ventricular systolic function. MAIN OUTCOME MEASURES: QT and QTc dispersion measured by three methods: the difference between maximum and minimum QT and QTc intervals, the standard deviation of QT and QTc intervals, and the "lead adjusted" QT and QTc dispersion. RESULTS: All measures of QT/QTc dispersion were closely interrelated (r values 0.86 to 0.99; all p < 0.001). All measures of QT and QTc dispersion were significantly increased in the patients with impaired left ventricular systolic function v controls (p < 0.001): 71.9 (6.5) (mean (SEM)) v 46.9 (1.7) ms for QT dispersion, and 83.6 (7.6) v 54.3 (2.1) ms(-1-2) for QTc dispersion. All six dispersion parameters were reduced in patients taking beta blockers (p < 0.05), regardless of whether left ventricular function was normal or impaired-by 9.4 (4.6) ms for QT dispersion (p < 0.05) and by 13.8 (6. 5) ms(-1-2) for QTc dispersion (p = 0.01). CONCLUSIONS: QT and QTc dispersion are increased in patients with systolic heart failure in comparison with matched controls, regardless of the method of measurement and independently of possible confounding factors. beta Blockers are associated with a reduction in both QT and QTc dispersion, raising the possibility that a reduction in dispersion of ventricular repolarisation may be an important antiarrhythmic mechanism of beta blockade. (+info)
(2/884) Three-dimensional reconstruction of the color Doppler-imaged vena contracta for quantifying aortic regurgitation: studies in a chronic animal model.
BACKGROUND: The purpose of this study was to investigate the use of 3-dimensional (3D) reconstruction of color Doppler flow maps to image and extract the vena contracta cross-sectional area to determine the severity of aortic regurgitation (AR) in an animal model. Evaluation of the vena contracta with 2-dimensional imaging systems may not be sufficiently robust to fully characterize this region, which may be asymmetrically shaped. METHODS AND RESULTS: In 6 sheep with surgically induced chronic AR, 18 hemodynamically different states were studied. Instantaneous regurgitant flow rates were obtained by aortic and pulmonary electromagnetic flowmeters (EMFs) as reference standards, and aortic regurgitant effective orifice areas (EOAs) were determined from EMF regurgitant flow rates divided by continuous-wave (CW) Doppler velocities. Composite video data for color Doppler imaging of the aortic regurgitant flows were transferred into a TomTec computer after computer-controlled 180 degrees rotational acquisition. After the 3D data transverse to the flow jet were sectioned, the smallest proximal jet cross section was identified for direct measurement of the vena contracta area. Peak regurgitant flow rates and regurgitant stroke volumes were calculated as the product of these areas and the CW Doppler peak velocities and velocity-time integrals, respectively. There was an excellent correlation between the 3D-derived vena contracta areas and reference EOAs (r=0.99, SEE=0.01 cm2) and between 3D and reference peak regurgitant flow rates and regurgitant stroke volumes (r=0.99, difference=0.11 L/min; r=0.99, difference=1.5 mL/beat, respectively). CONCLUSIONS: 3D-based determination of the vena contracta cross-sectional area can provide accurate quantification of the severity of AR. (+info)
(3/884) Transcatheter closure of muscular ventricular septal defects with the amplatzer ventricular septal defect occluder: initial clinical applications in children.
OBJECTIVES: The aim of this study was to close muscular ventricular septal defects (MVSDs) in children, with a new device, the Amplatzer ventricular septal defect occluder (AVSDO). BACKGROUND: The design of previously used devices for transcatheter closure of MVSDs is not ideal for this purpose and their use has been limited by several drawbacks. METHODS: Six patients, aged 3 to 10 years, with MVSDs underwent transcatheter closure using the AVSDO. The device is a modified self-centering and repositionable Amplatzer device that consists of two low profile disks made of Nitinol wire mesh with a 7-mm connecting waist. The prosthesis size (connecting waist diameter) was chosen according to the measured balloon stretched VSD diameters. A 6-F or 7-F sheath was used for the delivery of the AVSDO. Fluoroscopy and transesophageal echocardiography were utilized for optimal guidance. RESULTS: The location of the defect was midmuscular in five patients and beneath the pulmonary valve in one. The balloon stretched MVSD diameter ranged from 6 to 11 mm. Device placement was successful in all patients, and complete occlusion occurred in all six patients (95% confidence interval 54.06% to 100%). Two patients developed transient complete left bundle branch block. No other complications were observed. CONCLUSIONS: This encouraging initial clinical success indicates that the AVSDO is a promising device for transcatheter closure of MVSDs in children. Further clinical trials and longer follow-up are needed before the widespread use of this technique can be recommended. (+info)
(4/884) Mechanisms of retarded apical filling in acute ischemic left ventricular failure.
BACKGROUND: We examined the hypothesis that retardation of apical filling as measured by color M-mode Doppler echocardiography in the diseased left ventricle (LV) reflects a decrease in the intraventricular mitral-to-apical pressure gradient. METHODS AND RESULTS: In 9 open-chest anesthetized dogs, micromanometers were placed near the mitral tip and in the apical region. From the color M-mode Doppler images, the time delay (TD) between peak velocity at the mitral tip and the apical region was determined as an index of LV flow propagation. Acute ischemic LV failure was induced by coronary microembolization. Induction of ischemia caused a marked increase in LV end-diastolic pressure and a decrease in LV ejection fraction. The time constant of LV isovolumic apical pressure decay (tau) increased from 31+/-8 to 49+/-16 ms (P<0.001). The peak early diastolic mitral-to-apical pressure gradient (DeltaPLVmitral-apex) decreased from 1.9+/-0.9 to 0.7+/-0.5 mm Hg (P<0.01), and TD increased from 5+/-3 to 57+/-26 ms (P<0.001). The slowing of flow propagation was limited to the apical portion of the LV cavity. The TD correlated with DeltaPLVmitral-apex (r=-0.94, P<0.01) and with tau (r=0.92, P<0.01). Before ischemia, the mitral-to-apical flow propagation velocity far exceeded the velocity of the individual blood cells, whereas during ischemia, flow propagation velocity approximated the blood velocity. CONCLUSIONS: Retardation of apical filling in acute ischemic failure was attributed to a decrease in the mitral-to-apical driving pressure, reflecting slowing of LV relaxation. The slowing of flow propagation appeared to represent a shift in apical filling from a pattern of column motion to a pattern dominated by convection. (+info)
(5/884) Primary right atrial angiosarcoma mimicking acute pericarditis, pulmonary embolism, and tricuspid stenosis.
A 29 year old white man presented to the emergency room with new onset pleuritic chest pain and shortness of breath. He was initially diagnosed as having viral pericarditis and was treated with non-steroidal anti-inflammatory drugs. A few weeks later he developed recurrent chest pain with cough and haemoptysis. Chest radiography, cardiac examination, transthoracic and transoesophageal echocardiography pointed to a mass that arose from the posterior wall of the right atrium, not attached to the interatrial septum, which protruded into the lumen of the right atrium causing intermittent obstruction of inflow across the tricuspid valve. Contrast computed tomography of the chest showed a right atrial mass extending to the anterior chest wall. The lung fields were studded with numerous pulmonary nodules suggestive of metastases. A fine needle aspiration of the pulmonary nodule revealed histopathology consistent with spindle cell sarcoma thought to originate in the right atrium. Immunohistochemical stains confirmed that this was an angiosarcoma. There was no evidence of extracardiac origin of the tumour. The patient was treated with chemotherapy and radiation. This case highlights the clinical presentation, rapid and aggressive course of cardiac angiosarcomas, and the diagnostic modalities available for accurate diagnosis. (+info)
(6/884) Combined aortic and mitral stenosis in mucopolysaccharidosis type I-S (Ullrich-Scheie syndrome).
The genetic mucopolysaccharidosis syndromes (MPS) are autosomal recessive inborn errors of metabolism. Heart valve involvement in MPS is not uncommon but only a few case reports of successful cardiac surgery are available. In particular, reports of combined aortic and mitral stenosis associated with MPS type I-S are very rare. Both type I and type VI MPS are associated with significant left sided valvar heart disease that requires surgical valve replacement because of irregular valve thickening, fibrosis, and calcification. A 35 year old man had severe mitral valve stenosis after successful surgical replacement of a stenotic aortic valve. Valvar heart disease was investigated by cardiac ultrasound and left heart catheterisation. Histomorphological characterisation of the affected mitral valve was performed. The case illustrates typically associated clinical features of cardiac and extracardiac abnormalities found in MPS type I-S. (+info)
(7/884) Clinical manifestation and survival of patients with idiopathic bilateral atrial dilatation.
We studied the histories of eight patients who lacked clear evidence of cardiac abnormalities other than marked bilateral atrial dilatation and atrial fibrillation, which have rarely been discussed in the literature. From the time of their first visit to our hospital, the patients' chest radiographs and electrocardiograms showed markedly enlarged cardiac silhouettes and atrial fibrillation, respectively. Each patient's echocardiogram showed a marked bilateral atrial dilatation with almost normal wall motion of both ventricles. In one patient, inflammatory change was demonstrated by cardiac catheterization and endomyocardial biopsy from the right ventricle. Seven of our eight cases were elderly women. Over a long period after the diagnosis of cardiomegaly or arrhythmia, diuretics or digitalis offered good results in the treatment of edema and congestion in these patients. In view of the clinical courses included in the present study, we conclude that this disorder has a good prognosis. (+info)
(8/884) Quantitative systolic and diastolic transmyocardial velocity gradients assessed by M-mode colour Doppler tissue imaging as reliable indicators of regional left ventricular function after acute myocardial infarction.
AIMS: The aim of this study was to determine whether myocardial velocity gradients assessed by M-mode colour Doppler tissue imaging could be of clinical relevance and represent reliable indicators of regional left ventricular function after acute myocardial infarction. METHODS AND RESULTS: Among 64 consecutive patients with a first acute myocardial infarction, in 50 who had a marked asynergy in the parasternal short-axis view at the mid-papillary muscle level, myocardial velocities and velocity gradients were assessed in the anteroseptum and posterior wall by M-mode Doppler tissue imaging. Similar measurements were obtained in 11 matched healthy volunteers who served as a control group. In patients with anterior myocardial infarction, the peak myocardial velocity gradient in the anteroseptum was significantly lower when compared with controls (mean +/- [SD] 0.0 +/- 0.5 vs 1.1 +/- 0.7 s-1 during systole, P < 0.01; and 0.3 +/- 0.6 vs 2.0 +/- 0.5 s-1 during diastole, P < 0.01). Conversely, the peak systolic myocardial velocity gradient in the posterior wall was significantly higher than in controls (2.6 +/- 1.2 vs 1.8 +/- 1.2 s-1, P < 0.05). In patients with inferior myocardial infarction, the peak velocity gradient in the posterior wall was significantly lower when compared with healthy subjects (0.9 +/- 0.6 vs 1.8 +/- 1.2 s-1 during systole and 1.4 +/- 1.4 vs 4.9 +/- 1.2 s-1 during diastole, both P < 0.01). The peak systolic tissue velocity gradient in the anteroseptum was significantly higher than in controls (2.1 +/- 1.0 vs 1.1 +/- 0.7 s-1, P < 0.01). CONCLUSION: The present study indicates that myocardial velocity gradients assessed by M-mode Doppler tissue imaging are of clinical relevance for the characterization of ischaemic myocardial dysfunction after infarction and may provide quantitative assessment of segmental left ventricular function in this clinical setting. (+info)