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The aim of the present study was to evaluate the mechanism of cerebrovascular autoregulation in patients with neurocardiogenic syncope using bilateral transcranial Doppler (TCD) monitoring during head upright tilt table testing (HUT). Two hundred and six patients were prospectively studied. One hundred and fifty-nine subjects (77%) had a prior history of syncope and 47 (23%) had presyncope. Ninety-nine patients (48%) had syncope or presyncope during HUT with a 76% fall in diastolic middle cerebral artery blood flow velocity (D-MCA-BFV). Systolic MCA-BFV (S-MCA-BFV) fell by 33%. Deepening of the dicrotic notch in the Doppler waveform always preceded the fall in D-MCA-BFV. Patients without syncope or presyncope (n=96) had smaller changes in cerebral blood flow velocities during HUT and only twenty-two subjects had transient deepening of the dicrotic notch. Eleven subjects had presyncope during HUT due to an exaggerated response to nitrates with progressive arterial hypotension without bradycardia and changes during TCD monitoring that were intermediate between positive and negative HUT. In conclusion, patients with neurocardiogenic syncope have changes in cerebral blood flow during the event. TCD monitoring during HUT helps to assess these alterations.

DDD and AAI pacemakers are considered physiological, since they preserve atrioventricular (AV) synchrony. Artificial pacing, however, is performed largely from right heart chambers, causing aberrant depolarization pathways. Pacing at the right atrial appendage (RAP) is known to delay left atrial contraction due to interatrial conduction time (IACT), and right ventricular (RV) apical pacing (RVP) delays left ventricular (LV) contraction due to interventricular conduction time (IVCT). These delays may render the left heart AV intervals (LAV) either too short or too long, thus affecting LV systolic function. The purpose of this study was to evaluate the actual LAV intervals during conventional, right heart AAI and DDD pacing. Resulting LAV intervals were compared to programmed AV values during all DDD pacing modalities. Ten patients with DDD and six patients with AAI pacemakers were studied. IACT was measured from the atrial spike to the onset of left P wave, as recorded by an esophageal lead. Systolic time intervals were measured using either a carotid pulse tracing or a densitogram (photoplethysmography). LV function was appraised by measuring rate-corrected LV ejection time (LVETc). IVCT was measured indirectly as the lengthening of LV preejection period (PEP) caused by RV pacing, as compared to normal depolarization pathway. Intrinsic IACT and IVCT were considered zero. Right heart AV intervals (RAV) were measured from surface ECG and LAVs were calculated according to the following equations: Sinus Rhythm: LAV = RAV; Atrial Pace + Ventricular Sense: LAV = RAV - IACT; Atrial Sense + Ventricular Pace: LAV = RAV + IVCT; Sequential AV Pace: LAV = RAV - IACT + IVCT.(ABSTRACT TRUNCATED AT 250 WORDS)

Ejection fraction (EF), the ratio between stroke volume (SV) and end-diastolic volume (EDV), is a valuable contractility indicator. Unlike SV, the Frank-Starling effect is automatically compensated in the calculation of EF. It was the aim of this study to evaluate the physiological behavior of impedance derived measurements of relative right ventricular (RV) volumes and EF, obtained with standard pacing leads. Seven patients were evaluated at the time of pacemaker implant or replacement. Since no absolute standard of comparison was available for RV volumes, the value of the measurements was assessed by observing their behavior under cardio-circulatory challenges. A 2.5-kHz carrier was fed to the ring and tip electrodes of standard bipolar pacing leads and the resulting voltage was digitized and stored. The peak-to-peak voltage (PPV) of the carrier at the time of QRS was used as EDV, and the largest PPV as end-systolic volume (ESV). Relative SV was the difference between EDV and ESV, and EF = SV/EDV x 100. Pacing was used to reduce EDV, and the effect of contractility was tested with isometric hand grip, recumbent leg exercise, or isoproterenol drip. Only minimal changes in EF were noted during incremental pacing; relative SV and EDV decreased as expected; and EF increased significantly during contractility challenges. A high correlation coefficient was observed between EDV and SV changes induced by incremental pacing at rest (r values from 0.62 to 0.98, P from < 0.01 to 0.001). The study revealed that impedance volumetry, utilizing conventional bipolar pacing leads, yields useful hemodynamic data related to EDV, ESV, and EF. Given the simplicity of the method, it is reasonable to conclude on the feasibility of using said impedance derived hemodynamic parameters in implantable rhythm control devices.

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AF-nHB corrected bundle branch blocks in patients with severe conduction disturbances, even in those with dilated cardiomiopathy, outstanding from RVA. Also, the occurrence of cardiac memory during AF-nHB turned up as an observational finding of this study.