Search

Some patients with right ventricular (RV) apical pacing show contractile asynchrony of the left ventricle. Whether the asynchrony is due to RV pacing or was a preexistimg condition remains unknown. The aim of this study was to evaluate how much pacing from the RV apex affects left ventricular (LV) electromechanical activation and to assess whether the extent of LV asynchrony during RV pacing can be predicted by clinical, electrocardiographic, or echocardiographic findings obtained during spontaneous rhythm. We evaluated 56 patients with narrow QRS and preserved atrioventricular conduction who received permanent backup RV pacing. Intra-LV electromechanical activation was assessed during spontaneous rhythm and during pacing using tissue Doppler echocardiography. An abnormal intra-LV electromechanical delay (EMD) (defined as a41-ms difference between the faster and slower activated LV wall) was found in 15 patients (27%) during spontaneous rhythm and 28 patients (50%) during RV pacing (p0.001). Of the 9 baseline variables (age, gender, history of heart failure, QRS duration in spontaneous rhythm and during pacing, LV end-diastolic and end-systolic diameters, LV ejection fraction, and intra-LV EMD in spontaneous rhythm), an abnormal baseline intra-LV EMD and QRS duration of85 ms were independent predictors of an abnormal intra-LV delay during RV pacing. RV apical pacing induces asynchrony of LV contractions in a substantial percentage of patients but not in all. Although normal baseline intra-LV electromechanical activation cannot exclude the development of significant asynchrony during RV pacing, the presence of preimplant LV asynchrony predicts for a worsening of this detrimental effect.

Previous hemodynamic studies have shown that both left ventricular (LV) and biventricular pacing results in similar and significant improvement of LV function in a selected population of patients with depressed systolic function and left bundle branch block (LBBB).1‐5 According to the actual understanding of mechanism of pacing in heart failure, pacing resynchronizes the delayed portion of the ventricle, bypassing the site of block. We performed a controlled evaluation of the acute and medium-term effects of this new pacing modality on cardiac performance and quality of life. ••• We evaluated 13 consecutive patients (mean age 68 6 19 years, 9 men) who underwent LV pacing for treatment of drug refractory heart failure. Their mean ejection fraction was 28 6 14. All were in stable clinical condition under optimized pharmacologic therapy (digoxin, diuretics, angiotensin-converting enzyme inhibitors in all, carvedilol in 3) for $1 month before the study, but all patients complained of severe symptoms that impaired their quality of life. The mean score of the Minnesota Living with Heart Failure Questionnaire (LHFQ) was 57 6 20 (i.e., a value comparable to that observed in patients with severe heart failure). 6 Six patients were in sinus rhythm; all of them had a LBBB with a mean QRS duration of 162 6 10 ms and their mean PR interval was 236 6 85 ms. Seven patients had permanent atrial fibrillation and underwent ablation of the atrioventricular junction in conjunction with pacemaker implantation. An electrocardiogram showed LBBB in 6 of these patients with a QRS mean duration of 160 6 35 ms. LV stimulation was obtained through insertion of a lead into the coronary sinus vein in 11 cases and by an epicardial lead in 2 patients. The chosen site of stimulation was the lateral wall of the left ventricle, approximatively between the apex and the base. In 2 patients, this position could not be obtained and the lead was left in the greater cardiac vein. Ten patients received a conventional dual-chamber pacemaker (rate responsive for those patients in atrial fibrillation); 3 patients with associated ventricular tachyarrhythmias received a dual-chamber pacemaker with defibrillator back-up. In the 6 patients with sinus rhythm, the atrial port of pacemaker and/or defibrillator was connected to the lead positioned in the right atrium and the ventricular port was connected to the lead positioned in the coronary sinus vein; thus, the mode of pacing was atrial synchronous LV pacing. In the 7 patients with atrial fibrillation and induced atrioventricular block, the atrial port of the pacemaker was connected to the lead inserted into the coronary sinus vein and the ventricular port was connected to the lead inserted into the right ventricle apex. The atrioventricular interval of the pacemaker (the actual LV-right ventricular interval in these cases) was programmed to .200 ms to avoid right ventricular pacing unless failure of LV pacing occurred. Thus, the mode of pacing was rate responsive LV pacing with back-up right ventricular pacing for safety reasons. The study was designed to compare the LV pacing with the native sinus rhythm or right ventricular pacing (for those patients in atrial fibrillation plus atrioventricular junction ablation). To do this in patients with sinus rhythm, the pacemaker was programmed alternatively on (pacing) or off (native sinus rhythm); the atrioventricular interval was adjusted to obtain the best hemodynamic benefit as evaluated by echocardiographic measurements. In patients with atrial fibrillation, the pacemaker was programmed to alternative atrial pacing (LV pacing) or ventricular pacing (right

We investigated left atrial appendage function by transesophageal echocardiography, on the day after external electrical cardioversion to sinus rhythm, in 41 patients with nonvalvular atrial fibrillation. After cardioversion, appendage contraction synchronized with the electrical and mechanical activity of the atrium, which was restored in about 70% of the patients.

To prospectively assess the predictive value of left ventricular (LV) thrombus anatomy for defining the embolic risk after acute myocardial infarction (AMI), 2 comparable groups of patients with a first anterior AMI (group A, 97 thrombolysed patients; group B, 125 patients untreated with antithrombotic drugs [total 222]) underwent prospective serial echocardiography (follow-up 39 +/- 13 months) at different time periods. LV thrombi were detected in 26 patients in group A (27%) and in 71 in group B (57%; p0.005). Embolism occurred in 12 patients (5.4%; 1 in group A [1%] vs 11% in group B [9%], p0.04). At multivariate analysis, thrombus morphologic changes were the most powerful predictor of embolism (p0.001), followed by protruding shape (p0.01) and mobility (p0.02). In patients untreated with thrombolysis, a higher occurrence of thrombus morphologic changes (48% vs 8%, p0.002) and protruding shape (69% vs 31%, p0.002) were observed, whereas thrombus mobility was similar in the 2 groups (18% vs 8%, p = NS). Thrombus resolution occurred more frequently in thrombolysed patients (85% vs 56%, p0.002). Thus, after anterior AMI, changes in LV thrombus anatomy frequently occur and appear the most powerful predictor of embolization. A minor prevalence of thrombus, a more favorable thrombus anatomy, and a higher resolution rate may contribute to reduce embolic risk after thrombolysis.

Most cases of cardiac contusion due to blunt chest trauma are frequently seen after motor vehicle accidents, and only rarely during sport practice. Therefore, there are only few reports of such injuries occurring during competitive sport activities.1–3 We describe the first case of cardiac trauma occasionally observed in a professional boxer after a world championship boxing match.

This study evaluated the influence of thrombolysis followed by full anticoagulation on the frequency of left ventricular (LV) thrombi after acute myocardial infarction (AMI). Nineteen consecutive patients with a first anterior wall AMI who received 1,500,000 IU of streptokinase within 3 hours of symptom onset, followed by full anticoagulation, underwent echocardiographic studies within 24 hours of symptoms, and then on days 2, 3, 5, 7, 12, 30 and 90. Forty-four patients, with comparable clinical features and echocardiographic protocol but without antithrombotic therapy, served as the control group. LV thrombi developed in 4 of 19 (21%) treated patients and in 23 of 44 (52%) control subjects (p = 0.02). LV aneurysm or major wall motion abnormalities were noted in 8 of 19 (42%) treated patients and in 30 of 44 (68%) control subjects (p less than 0.05). No significant difference was found between treated and untreated patients when comparing the incidence of thrombi in the subgroups of patients with aneurysm or major wall motion abnormalities (3 of 8 vs 21 of 30) and in the subgroups with less extensive LV dysfunction. Thrombi disappeared during hospitalization in 3 of 4 treated patients, but in none of the controls. Fewer patients treated with intravenous streptokinase followed by full anticoagulation developed LV thrombi compared to patients treated with conventional therapy. This difference may be related to a reduced occurrence of major LV wall motion abnormalities. Resolution of thrombi frequently occurs in the hospital phase of AMI; therefore, only frequent echocardiographic examinations can assess the true frequency of LV thrombi.