Left ventricle remodeling after aortic valve replacement with a stentless bioprosthesis.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to F Rigo.
Explore the source record for details and available documents.
BACKGROUND: In the stress imaging era, ECG positivity is regarded as a frequent source of false-positive responses. However, it is known that normal coronary arteries frequently coexist with abnormal endothelial function in patients with chest pain. AIM: To evaluate the anatomical coronary epicardial, and functional systemic endothelial determinants of wall motion and electrocardiographic responses during stress testing. METHOD: Sixty-eight in-hospital patients with chest pain syndrome, no previous myocardial infarction, and off nitrate therapy at the time of testing underwent, on different days, in random order and within 1 month: (1) stress ECG echo testing (with dipyridamole in 43, dobutamine in 3, and exercise in 22 patients); (2) coronary angiography; (3) endothelium-dependent, flow-mediated dilation of the brachial artery during reactive hyperaemia using high-resolution ultrasound. Criteria of positivity were: ST segment depression >0.1mm in the stress ECG; regional dysfunction >2 segments demonstrated by stress-echo; diameter reduction >50% on coronary angiography; and <5% flow-mediated dilation as revealed by endothelial function. RESULTS: Significant coronary artery disease was present in 39 patients, and was predicted on multivariate analysis by stress-induced wall motion abnormalities (OR=108.8; 95% CI=8.5-1,389.4, P=0.0003), but not by either ST segment depression (P=0.13; OR=0.47; 95% CI=0.7-1.3) or reduced flow-mediated dilation (P=0.81; OR=0.87; 95% CI=0.27-2.8). Abnormal flow-mediated dilation was present in 53 patients (78%), and was predicted by stress-induced ST segment depression (P=0.023; OR=6.2; 95% CI=1.3-30.5), but not by either stress echo positivity (P=0.66; OR=0.77; 95% CI=0.23 to 2.5) or angiographically assessed coronary artery disease. There was no correlation between flow-mediated dilation and extent of coronary artery disease as assessed by the angiographic Duke score (from 0=normal to 100=most severe disease): r=-0.13, P=0.91. CONCLUSION: Epicardial coronary artery anatomy affects wall motion abnormalities, and systemic endothelial dysfunction affects ST segment depression during stress. However, echocardiographic positivity is unrelated to endothelial dysfunction, and electrocardiographic positivity is an inaccurate predictor of coronary stenosis. An integration of ECG and functional markers is warranted in the stress testing lab.
BACKGROUND: Up to 57% of atrial fibrillation (AF) recurrences after cardioversion take place during the first 30 days following direct current shock (DCS) delivery. Previous echocardiographic studies on sinus rhythm (SR) maintenance after cardioversion have focused mainly on parameters recorded before DCS, while other studies have reported on the indices recorded soon after delivery of the shock. METHODS: Therefore, we investigated 18 patients with nonrheumatic AF, selected to undergo DCS, by both transthoracic (TTE) and transesophageal (TEE) echocardiography performed within 10 minutes before and after the electrical shock delivery. TTE was utilized for the evaluation of left atrium and left ventricle shape as well as for mitral Doppler flow sampling, while TEE was used to evaluate left atrial appendage (LAA) morphology and function, to score the LAA spontaneous echo contrast, and to evaluate the flow of left superior pulmonary vein; the transesophageal probe was left in situ during the electrical procedure. Thirty days after cardioversion, 10 (55%) patients maintained SR (Group 1) while 8 (45%) reverted to AF (Group 2). We compared the mean values of the parameters recorded in the two groups both before and after DCS. RESULTS: Although many parameters of pre- and postcardioversion analysis proved to be significantly different between the two groups, the most marked differences were exhibited by the following postcardioversion indices: Peak Doppler flow velocity of the end-diastolic mitral flow (30.10 +/- 5.24 vs. 20.50 +/- 6.32 cm/sec, P = 0.003); sum of peak velocities of the end-diastolic contraction (A) and relaxation (A(1)) of LAA (A + A(1) = 58.20 +/- 17.02 vs. 31.25 +/- 9.27 cm/sec, P = 0.001); duration of A + A(1) (162.70 +/- 27.01 vs. 133.75 +/- 5.31 msec, P = 0.002); and sum of durations of the early diastolic forward (E) and reverse (E(1)) flow of LAA (101.90 +/- 35.15 vs. 53.33 +/- 16.33 msec, P = 0.006). CONCLUSIONS: Using a single echocardiographic examination during DCS and after induction of anesthesia, without further discomfort to patients, we were able to identify useful parameters for the prediction of future electrical activity of the heart before as well as soon after DCS. Postcardioversion indices, derived by both TTE and TEE, were even more predictive of SR maintenance after 1 month than precardioversion parameters.
BACKGROUND AND AIM OF THE STUDY: Intraoperative transesophageal echocardiography (TEE) is commonly used during aortic valve surgery. In aortic valve replacement (AVR), this permits measurement of the aortic annulus, study of the anatomy of aortic valve components, and prediction of prosthesis valve size. After cardiopulmonary bypass (CPB), echocardiography is valuable in checking prosthesis function. In this study, we evaluated the impact of intraoperative TEE on the decision-making process of aortic Toronto stentless prosthetic valve (TSPV) implantation. METHODS: Fifty-two consecutive patients undergoing elective AVR were collected prospectively. Multiplane TEE was performed before CPB to determine diameters of the aortic valve annulus and sinotubular junction. This was to evaluate the feasibility of TSPV implantation in the aortic position and to predict prosthesis size. Further TEE evaluation was carried out after CPB to assess prosthetic valve function. RESULTS: TEE allowed measurement of the aortic annulus and sinotubular junction, and enabled correct prediction of prosthesis size. Ultrasonic evaluation also revealed contraindications to TSPV implantation in five patients. In one case, color-Doppler examination led to immediate successful surgical correction of prosthetic incompetence. CONCLUSION: Intraoperative multiplane TEE examination is useful in the decision-making process in AVR with the TSPV by selecting patients suitable for the stentless valve, predicting prosthesis size, and checking prosthesis function.
Cataract extraction performed under local anesthesia is not so safe. During a 2 years period, 8 patients have presented a complication: 3 patients are presented with diplopia, 4 patients are presented with eyeball perforation and 1 patient developed a central complication. All those complications are caused by the superior peribulbar injections of anesthetics. A survey of the different etiologies of the superior rectus muscle blow and of eyeball perforation is given.
The remarkable hemodynamic features of the aortic Toronto SPV prosthesis have been reported. To assess the efficacy of these characteristics to produce a favorable left ventricular remodeling and to test the limits of the dobutamine stress test to check these results, 25 consecutive patients, who had undergone aortic valve replacement with Toronto SPV, were monitored with dobutamine and exercise stress tests for 1 year. Among the prosthetic and left ventricular morphological and functional parameters evaluated, dobutamine infusion produced an overestimation of prosthetic and left ventricular outflow tract gradients, effective orifice area, and prosthetic resistance compared with the more physiological exercise test (P<.01). These misleading results were probably due to the inotropic and unloading effects of dobutamine in still hypertrophied hearts. Indexed myocardial mass and wall thickness decreased significantly during the follow-up period (P<.01), whereas left ventricular diastolic diameter and ejection fraction showed no significant variations. These data show that the positive left ventricular remodeling is due only to the regression of the hypertrophy and not to the reduction of left ventricular diameters. Based on results from this study, the dobutamine stress test should be avoided to evaluate patients with aortic valve prostheses and still present left ventricular hypertrophy. The Toronto SPV produces a favorable left ventricular remodeling during the first year of follow-up, and is likely to improve.
Cat-scratch disease is a subacute, regional lymphadenitis syndrome that occurs mainly in children. The causative agent is Bartonella henselae. After an incubation period ranging usually between 1 and 2 weeks, red papules develop at the site of cutaneous inoculation and persist until the development of lymphadenopathy with some malaise. Cases with complications have been observed including Parinaud oculoglandular syndrome, encephalopathy, a variety of exanthems and granumatous hepatitis. Diagnosis is based on serologic tests and, when necessary, antimicrobial treatment can be considered. Incision and drainage should not be done.
OBJECTIVES: The aim of this study was to evaluate the usefulness of transesophageal echocardiography (TEE) for the diagnosis of arrhythmogenic right ventricle cardiomyopathy (ARVC). PATIENTS: Using TEE and the standard transthoracic echocardiography (TTE), we studied 19 patients affected with hyperkinetic ventricular arrhythmias with a LBBB pattern, as well as 10 normal control subjects (C). METHODS: We calculated the following parameters: the fractional area change (FAC) of the end-diastolic right ventricule (RV) area; the global wall motion score (WMS) by the algebraic sum of the score of each of the 9 wall segments including the inflow, outflow and apex of RV; the asynergy index (AI) by the percentage of the 9 segments with a score > or = 2; the average thickness of moderator band and papillar muscles (ATMP); the echo reflectivity score (ERS) and the structural abnormalities score (SAS) of RV. The diagnosis of ARVC was proposed when RV segmental wall motion abnormalities were visualized, or when a decrease of the ventricular FAC and dysmorphic aspects were contemporaneously present. The results of the two echocardiographic approaches were compared, and in arrhythmic patients (A) echocardiographic results were compared with those obtained by cineventriculography (CVG), which we had adopted as the reference diagnostic method. RESULTS: The comparison between A and C showed significant differences for all parameters if calculated by the TEE (p < 0.003-0.0001), except for ATMP if calculated by TTE (p < 0.003-0.0001). The comparison between TEE and TTE approaches did not show any difference in the C group while in the A group only FAC and ERS resulted similar; the values of the remaining parameters were significantly greater if calculated by TEE than by TTE (WMS = 7.3 +/- 4.1 vs 4.3 +/- 2.3: p < 0.01; AI = 22.6 +/- 18.5 vs 11.6 +/- 10.3: p < 0.05; ATMP = 6.1 +/- 0.9 vs 5 +/- 1.2 mm: p < 0.04; SAS = 2.2 +/- 0.8 vs 1.4 +/- 0.7: p < 0.002). In 17 of the 19 patients who were clinically suspected to be affected with ARVC the diagnosis was confirmed by CVG; 12 of them (70%) were correctly identified by TTE and 17 (100%) by TEE. One of the two negative patients was erroneously considered positive both by TTE and TEE. CONCLUSIONS: TEE is a usefull diagnostic tool for ARVC and is more accurate than TTE for the identification of the concealed or dubitative forms of the disease.
BACKGROUND: We studied 105 patients (pts) in order to help clarify the pathogenetic mechanisms of idiopathic atrial fibrillation (AF). Eighty of these pts (Group I) had experienced paroxysmal AF, and 25 were normal control subjects (Group II). Twenty-two pts out of Group I had idiopathic paroxysmal AF (Group IA), while the remaining 58 (Group IB) presented with a heart disease or a WPW pattern. METHODS: All pts underwent endocavitary (EEPS) (69) or transesophageal (TEPS) (36) electrophysiologic study. In all pts the inducibility of a sustained AF (greater than 1 min) was tested by aggressive stimulation protocols including high frequency atrial bursts. RESULTS: In Group I a sustained AF was induced in 82% of cases vs 4% of Group II cases (p less than 0.001). In Group I there was no difference between pts with or without idiopathic AF (IA 73% vs IB 86%, NS). In two pts with idiopathic AF a concealed Kent bundle was identified and a reciprocating atrioventricular tachycardia was induced, which in one case spontaneously degenerated into AF. Four athletes with idiopathic AF were studied before and after autonomic blockade. AF was induced in all during the basal state, lasting several hours, and after autonomic blockade in 3 pts, lasting again for several hours. In 1 patient (pt) the arrhythmia spontaneously resolved within 50 sec. CONCLUSIONS: 1) The induction of a sustained AF by EEPS or TEPS is a pathologic phenomenon which is frequently observed in pts with clinical episodes of paroxysmal AF, while it is very rare in normal control subjects. 2) Pts with idiopathic AF have an electrophysiologic behaviour similar to pts with non-idiopathic AF. This fact suggests that among the former, most cases probably have a concealed atrial anomaly. In some cases this atrial anomaly can be related to the existence of a Kent bundle. 3) In athletes with paroxysmal AF the inducibility of a sustained AF both in the basal state and after autonomic blockade suggests that the vagal prevalence typical of such subjects probably plays a secondary role.
Explore the source record for details and available documents.
UNLABELLED: Atrial fibrillation or flutter is frequently inducible during endocavitary or transesophageal electrophysiologic study. However, its clinic and prognostic significance has not yet been clarified. We studied 443 patients: 276 underwent endocavitary electrophysiologic study, 228 underwent transesophageal electrophysiologic study and 61 underwent both methods. In 343 of them a satisfactory echocardiogram was obtained. Patients were divided in three groups: gr. I, 93 patients with documented episodes of paroxysmal atrial fibrillation or flutter; gr. II, 257 patients with or without heart disease without clinical atrial fibrillation or flutter; gr. III, 93 symptomatic or asymptomatic Wolff-Parkinson-White patients without clinical atrial fibrillation or flutter. Gr. I included patients without overt heart disease (20), with WPW (11), mitral valve prolapse (4), and miscellaneous (58). Gr. II included patients without overt heart disease (49), with concealed Kent bundles (7), Mahaim (1) or James fibers (1) mitral valve prolapse (6), sick sinus syndrome (40), miscellaneous (91), or syncope of an unknown origin (62). Atrial vulnerability was evaluated both by endocavitary and transesophageal electrophysiologic study using two different protocols; the first protocol was moderately aggressive (prot. A), while the second was aggressive (prot. B). Endocavitary electrophysiologic study. Prot. A: single and double extrastimuli at the three heart rates (sinus, 100 and 150/m'), 10/m' incremental atrial pacing from 160 to 250/m; prot. B: prot. A + incremental atrial pacing from 260/m' up to 2:1 St-A block. Transesophageal electrophysiologic study. Prot. A: 10" atrial burst at 100-600/m' prot. B: prot. A + 6-9" increasing rate bursts from 200 to 800/m'. End point of all protocols: initiation of greater than 1' atrial fibrillation or atrial flutter. RESULTS: Endocavitary electrophysiologic study. A greater than 1' atrial fibrillation or atrial flutter was induced with the two protocols respectively in 67% (52/78) and 85% (51/60) of gr. I, in 17% (26/150) and 36% (38/105) of gr. II and in 35% (17/48) and 44% (21/48) of gr. III (gr. I vs gr. II p less than 0.001 for prot. A and p less than 0.01 for prot. B; gr. II vs gr. III p less than 0.001 for prot. A and NS for prot. B). Induced atrial fibrillation or atrial flutter using the two protocols had a greater than 5' duration respectively in 83 and 78% of gr. I, 62 and 42% of gr. II and in 41 and 38% of gr. III.(ABSTRACT TRUNCATED AT 400 WORDS)
Left ventricular (LV) function in 45 patients with native aortic valve infective endocarditis was studied in order to identify high surgical risk patients and the pattern of irreversible myocardial damage. LV function was studied by M-mode and 2D-echocardiography (LV volumes; ejection fraction, EF; peak systolic pressure to end-systolic volume ratio (PAP/ESV) as an index of myocardial contractility; LV mean systolic wall stress as an index of LV afterload and the radius to thickness ratio (R/Th). Thirteen patients underwent aortic valve replacement with an overall operative mortality of 15%. The cause of death was intractable heart failure. Different EF vs stress relationships could be described for different level of myocardial contractility: patients with intractable heart failure had a severely depressed myocardial contractility so that for a given level of LV stress, EF was significantly lower. High operative risk patients were identified by the PAP/ESV vs R/Th relation. All surgical deaths occurred in patients with a severely depressed myocardial contractility (PAP/ESV less than 2) and inadequate hypertrophy (R/Th greater than 4). Reversal of LV dysfunction in patients with moderately depressed myocardial contractility depended on the pattern of LV hypertrophy; a normal post-operative EF was achieved only in patients with adequate hypertrophy (R/Th less than 4).
Explore the source record for details and available documents.
To analyze cardiac motion during ventricular fibrillation (VF), we used transesophageal echocardiography to study nine male subjects, aged 44 +/- 7 years, affected by heart disease who have poor left ventricular function, during implantation of an Implantable Cardioverter Defibrillator, when VF is induced several times to determine the defibrillation threshold. Wall and valvular motion, transmitral and transaortic blood flow, and blood echoreflectivity were evaluated in all patients. Moreover, in basal conditions, during VF, 1 and 5 minutes after restoration of basal rhythm, we calculated the left ventricular end-diastolic volume (EDLVV) and area (EDLVA), the left ventricular end-systolic volume and area, the ejection fraction, and the fractional area change with a four-chamber echocardiographic view. At the onset of VF, the myocardium and valves exhibited a chaotic motion. About 10 seconds later the oscillatory movement of the heart walls became more ample and regular; the mitral valve showed a cyclic closure and opening with a forward flow, and the aortic valve exhibited similar behavior, although at a lower intensity. A spontaneous echo contrast appeared inside the atrial and ventricular cavities, gradually becoming an incrt homogeneous mass that was completely flushed away with the restoration of the basal rhythm. When VF started, EDLVV (286 +/- 98 ml) and EDLVA (50 +/- 16.5 cm2) decreased abruptly (EDLVV = 182 +/- 65 ml, p < 0.02; EDLVA = 38 +/- 9.2 cm2,p < 0.05); so did ejection fraction (31.8% +/- 15% versus 11% +/- 5%; p < 0.003) and fractional area change (25.8% +/- 6.5% versus 7% +/- 3.4%; p < 0.001). When the basal rhythm was restored, the heart extended again and EDLVV, EDLVA, ejection fraction, and fractional area change after 1 and 5 minutes were similar to those calculated before induction of VF. This behavior was observed during both the first and last induced VF. Thus during VF, great variations of heart morphology and dynamics, as well as blood echoreflectivity, occur; the heart seems to make attempts to organize its dynamics during the arrhythmia. Repeated episodes of VF and defibrillation with low energies do not seem to worsen left ventricular dynamics even in impaired hearts.