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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 a >41-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 (p<0.001). 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 of >85 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.

We assessed the effects of left ventricular pacing on echocardiographic and clinical parameters in 13 consecutive patients with heart failure and bundle branch block by means of a controlled acute and medium-term evaluation. Left ventricular pacing induced a significant improvement in left ventricular ejection fraction, Minnesota Living with Heart Failure Questionnaire score, New York Heart Association class, and 6-minute walking test compared with sinus rhythm or right ventricular pacing.

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%; p <0.005). Embolism occurred in 12 patients (5.4%; 1 in group A [1%] vs 11% in group B [9%], p < 0.04). At multivariate analysis, thrombus morphologic changes were the most powerful predictor of embolism (p <0.001), followed by protruding shape (p <0.01) and mobility (p <0.02). In patients untreated with thrombolysis, a higher occurrence of thrombus morphologic changes (48% vs 8%, p <0.002) and protruding shape (69% vs 31%, p <0.002) 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%, p <0.002). 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.

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.

Verapamil delivered via the sinus node artery exerted a dose-related, exclusively negative chronotropic action at all concentrations studied. Perfusion through the AV node artery during AV junctional rhythm also caused a dose-related negative chronotropic response, but the concentrations required to depress this pacemaker were ten times higher than those required to depress sinus node automaticity. Verapamil administered into the AV node artery during sinus rhythm impaired AV conduction. His bundle electrograms demonstrated that depressed A-V conduction was exclusively located at the A-H level. In 5 out of 10 dogs verapamil (5 to 10 mg) delivered into the septal artery caused an abrupt onset of ventricular fibrillation without premonitory dysrhythmias. Verapamil (except at very high concentrations) did not alter the responsiveness of the sinus node and the AV junction to acetylcholine or norepinephrine, whether administered selectively into the sinus node artery or the AV node artery or released by neural stimulation. Serial injections of verapamil were associated with tachyphylaxis for the direct chronotropic and dromotropic properties of the drug.

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.