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The aim of this study was to assess the long-term performance of a new dual chamber rate responsive pacing system based on the dynamic measurement of the peak endocardial acceleration (PEA) index of cardiac contractility. Seventy patients who participated in the Multicenter European Clinical Evaluation were studied 1 year after implantation by continuously recording the PEA and the heart rate (HR) during exercise stress testing and during 24 hours of usual activities. A complete examination of standard parameters was also performed to assess the pacing/sensing lead characteristics. Statistical comparisons were performed with the data recorded with the same protocol at 1 month after implant for each patient. A linear correlation coefficient was calculated between PEA and sinus rate when the patient showed predominant atrial tracked rhythm. There were no significant differences between PEA values measured at 1 month and 1 year (PEA = 0.41 +/- 0.26 g vs 0.45 +/- 0.29 g at rest and PEA = 1.63 +/- 0.77 g vs 1.72 +/- 0.83 g during peak exercise). The correlation coefficient remained stable (0.67 +/- 0.15 vs 0.65 +/- 0.14 during daily life and 0.74 +/- 0.14 vs 0.77 +/- 0.11 during exercise). The PEA signal detected by the sensor was reliable and stable. No long-term complications or adverse effects were observed, and the lead performance was comparable to that of a standard lead.

There are three fundamental mechanisms of ventricular tachycardia (VT) reentry, abnormal automaticity and triggered activity (TA) related to early or late after potentials. Reentry is certainly the mechanism of branch to branch and post-infarction VT. Early TA is responsible for Torsades de Pointes. Late TA is possibly the cause of certain verapamil-responsive VT but calcium-dependent reentry cannot be excluded. Abnormal automaticity or late TA may also play a role in catecholamine-induced VT. The development of drugs specific for the mechanism confronted with the results of programmed stimulation and mapping should improve the understanding of the mechanism of VT in each individual patient and allow more effective and better tolerated antiarrhythmic therapy.

Calculation of left ventricular mass by M mode echo is based on the assumption that the geometry of the left ventricle is an ellipsoid, the long axis of which is twice that of its short axis. The hypothesis in not always true and often leads to overestimation of the ventricular mass. The authors propose a method combining M mode data (end diastolic dimension, septal and posterior wall thickness) and 2D measurement of the left ventricular long axis: the left ventricular mass was measured by Devereux's and the authors' methods in 185 hypertensives. The 2D measurement of the long axis (mean: 84.7 mm) was much smaller than twice the short axis (mean: 52.3 mm) and the two measurements were poorly correlated. Measurement of the long axis was reproducible. The two methods of calculation were closely correlated (r = 0.95) but, on average, 23% lower with the authors' method. These results seem to be more closely related to ambulatory blood pressure than those of the classical method. The authors' combined method takes into account the true geometry of the left ventricle better than M mode method alone and avoids overestimation of left ventricular mass and the prevalence of excentric left ventricular hypertrophy in hypertensive patients.

The objective of this study was to test the influence of bisoprolol and verapamil on left ventricular filling in hypertensive patients in a 6 month randomized, double-blind trial in 54 hypertensive patients not previously treated with beta-blockers or calcium inhibitors. After administration of placebo for 14 days, an M echocardiogram of the left ventricle was recorded to determine left ventricular mass. Blood flow was evaluated by pulsed Doppler sonography. After randomization into two groups, one group received 10 mg of bisoprolol and the other 240 mg of verapamil LP in a single dose in the morning. After 2 months' treatment, the patients whose blood pressure was not well controlled were given a diuretic. Echo-Doppler was performed again by the same operator after 4-10 days on active treatment, after 6 months and after a subsequent 2 weeks of placebo for the patients treated with a single drug. The reduction in blood pressure was comparable in the two treated groups, but there was no significant decrease in left ventricular mass. Left ventricular filling was improved only in the patients receiving bisoprolol. The effect was observed immediately after the first administration and throughout the 6 months' treatment period declining slowly during the placebo wash-out. This effect appeared to be independent of any alteration in heart rate and was thought to be a specific action of this drug.

Left ventricular hypertrophy is associated with a high risk of cardiovascular complications in all the populations in which it has been studied, especially in hypertensive patients. The echocardiographic measurements of left ventricular mass provides a quantitative approach to this risk, independent of the classical cardiovascular risk factors. It is very tempting to wish to replace the measurement of risk factors which, due to their great variability, are not easy to assess (blood pressure) by a marker which integrates several of them (blood pressure, age, weight, salt intake, blood viscosity, serum cholesterol ...) and their variation with respect to time. However, it is too early to recommend this practice for routine use. M mode echocardiographic measurement of left ventricular mass is relatively difficult technique feasible only in about 80% of the population. Even in the hands of experts, its reproducibility is far from perfect. Technical developments may lead to improvement. It remains to be demonstrated that the use of these values improves the management of hypertensive patients and this will not be an easy task. However the follow-up of left ventricular mass during treatment may be an alternative to trials of morbi-mortality in hypertensive patients with the advantage of requiring a shorter follow-up period and fewer patients. It also remains to be demonstrated that regression of left ventricular hypertrophy is accompanied by a corresponding reduction in cardiovascular complications.