In most patients with rate-responsive devices, a single sensor is sufficient to achieve a satisfactory rate response. A dual sensor combination and optimization provides an additional benefit only in a selected population with an advanced atrial chronotropic disease.

When implanted contemporarily with sacral or spinal neurostimulators, cardiac devices appear to be safe, as confirmed by the appropriate detection and interruption of arrhythmic episodes. On the other hand, neuromodulation devices could be temporarily or permanently damaged by multiple ICD discharges. It is recommended that the neurostimulator be interrogated after an ICD shock, in order to check the state of the device.

To determine the relative role of both the anatomical and dynamic components involved in the determination of systolic anterior motion (SAM) of the mitral valve, we studied 53 selected patients with hypertrophic cardiomyopathy (HCM) by M-mode and cross-sectional echocardiography (CSE). Recordings of high quality for quantitative analysis were a precondition for the inclusion in the study. Twelve of these patients had no SAM, 14 had SAM of the anterior mitral leaflet (AML), six had SAM of the posterior mitral leaflet (PML), and 21 had SAM of both the AML and PML. The length of both the AML and PML, the left ventricular outflow tract (LVOT) area and the percentage of thickening of the left ventricular posterior wall (%LVPW) were measured in 18 control subjects (group I), in patients with AML-SAM (group II), in patients with AML+ PML-SAM (Group III), in patients with PML-SAM (group IV) and in patients with HCM but without SAM (group V). The length of AML in group I (23 +/- 1.5 mm) was significantly different compared with that in groups III (28 +/- 2 mm) and IV (29 +/- 2 mm), P less than 0.001. Significant differences were present in the PML-length between group I (14 +/- 1 mm) and groups III (20 +/- 3 mm) and IV (25 +/- 4 mm), respectively (P less than 0.001), between group II (14 +/- 2 mm) and groups III and IV, respectively (P less than 0.001), and also between group V (14 +/- 1 mm) and groups III and IV (P less than 0.001). Differences were found when the %LVPW of groups II (76 +/- 17%), III (77 +/- 11%) and IV (83 +/- 19%) were compared, respectively, with groups I (42 +/- 12%) and V (54 +/- 7%), P less than 0.001; a significant difference was also found between groups I and V, P less than 0.001. The mean LVOT area was significantly reduced in groups II (3.5 +/- 1.3 cm2), III (3 +/- 1 cm2) and IV (3 +/- 1 cm2) when compared with group V (5.9 cm2), P less than 0.001. We conclude that the induction and maintenance of SAM in HCM is multifactorial, mainly depending on the length of both the AML and/or PML, the LVOT area and on the increased contractility of the LVPW.

Apical hypertrophic cardiomyopathy (AHCM) is characterized by primary hypertrophy localized exclusively in the apex of the left ventricle. Previous studies have indicated that AHCM results in a unique combination of cross-sectional echocardiographic (CSE) and ECG findings ('giant' T wave inversion and high R wave voltage in the precordial leads). The aims of this study were: (1) to assess the degree of AHCM in a quantitative fashion (2) to evaluate the possible relationship between apical hypertrophy, quantitatively determined, and ECG findings in patients with AHCM (3) to verify the changes in echocardiographic and ECG parameters over time (4) to define the relationship between the severity of AHCM and the clinical course of such patients. Eleven selected patients with AHCM were studied for an average 6 year follow-up period; there were seven men and four women (age from 18 to 62 years, mean 49). Apical hypertrophy was assessed quantitatively by determining the muscle cross-sectional area in the apical region, which was considered an index of myocardial mass. From the end-diastolic apical four chamber view, endocardial and epicardial contours were digitized in order to obtain the total muscle cross-sectional areaof the left ventricle. The walls of the left ventricle were then divided into three regions (basal, intermediate, apical). The final value of each cross-sectional muscle area was obtained from the mean measurements of four independent and blinded observers. In AHCM the apical muscle cross-sectional area (AMA) ranged from 10.3 to 17.9 cm2, mean 13.2 +/- 2.6 cm2.(ABSTRACT TRUNCATED AT 250 WORDS)

The influence of aortic regurgitation on the Doppler assessment of pressure half-time (T1/2) and on the derived calculation of the mitral-valve area has not yet been adequately evaluated in patients with mitral stenosis and associated aortic regurgitation. Therefore this study was undertaken to verify the accuracy of the T1/2 method for the noninvasive estimation of mitral-valve area in patients with mitral stenosis and associated aortic regurgitation. Data were obtained from 31 selected patients who underwent cardiac catheterization within 24 h of the noninvasive examination. From the Doppler velocity curve, T1/2 was calculated as the interval between the peak transmitral velocity and velocity/ square root of 2. Mitral-valve area was measured from the T1/2 with a computerized system using the equation: 220/T1/2, in cm2. Calculation of the mitral-valve area at catheterization was derived applying the modified Gorlin formula. Mean mitral-valve area, as determined at catheterization, ranged from 0.5 to 2.8 cm2 (1.3 +/- 0.6). Mean mitral-valve area, as calculated by continuous-wave Doppler, ranged from 0.7 to 2.7 cm2 (1.5 +/- 0.6). Linear-regression analysis of data revealed a good correlation between Gorlin and Doppler measurements of the mitral-valve area (r = 0.90, SEE = 0.28 cm2, P less than 0.001, y = 1.0x + 0.2). Doppler showed a systematic overestimate of the mitral-valve area (26%) in patients with mitral stenosis and aortic regurgitation as compared to the Gorlin formula. The overestimate of continuous-wave Doppler was even greater (39%) in a subgroup of patients with 2+ or 3+ angiographic aortic regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)