Abstract-Hypercholesterolemia and hypertension are frequently associated with elevated sympathetic activity. Both are independent cardiovascular risk factors and both affect endothelium-mediated vasodilation. To identify the effects of cholesterol-lowering and antihypertensive treatments on vascular reactivity and vasodilative capacity, we studied 30 hypercholesterolemic hypertensive subjects. They received placebo for 4 weeks, either enalapril or simvastatin for 14 weeks, and, finally, both medications for an additional 14 weeks. Postischemic forearm blood flow (MFBF) and minimal vascular resistance (mFVR) were used as indices of vasodilative capacity and structural vascular damage, respectively. Key Words: hypertension Ⅲ hypercholesterolemia Ⅲ cardiovascular reactivity Ⅲ plethysmography Ⅲ vascular damage B oth hypertension and hypercholesterolemia, which frequently occur together, 1,2 are independent risk factors for cardiovascular events, 3 induce vascular damage, 4 and affect coronary flow by impairing endothelium-mediated vasodilation. 5 Moreover, borderline-to-mild hypertensive subjects, in whom sympathetic overdrive and exaggerated cardiovascular stress reactivity have been shown, 6 tend frequently to have high total (TOT-C) and LDL cholesterol (LDL-C) levels. 7,8 Several studies have shown also that patients characterized by emotional alertness often present dyslipidemia, exaggerated cardiovascular reactivity, and hypertension. 9,10 In hemodynamic terms, borderline hypertensive subjects in the resting state fail to accommodate to increased cardiac output with appropriate vasodilation 11 and, during laboratory mental stress, do not proportionally adjust forearm blood flow (FBF) while their blood pressure (BP) significantly increases. 12 Sympathetic overactivity emanating from the central nervous system 11 also enhances the effects of local factors that are conducive to vascular damage, including shear stress and turbulence, endothelial dysfunction, and atherosclerotic lesions. 13 Therefore, hypertension and hypercholesterolemia, though independent cardiovascular risk factors, may share physiopathological features that can be related to vascular sympathetic overactivity.In clinical studies, antihypertensive treatment with angiotensin-converting enzyme inhibitors (ACEIs) 14,15 as well as cholesterol-lowering therapy with statins 16,17 were found to improve vasodilating properties and to reduce vascular damage. Nevertheless, to the best of our acknowledge, no study has investigated their effect on regional vascular stress response and vascular structure in hypercholesterolemic hypertensive subjects. The current study analyzed forearm vascular response to psychophysiological tasks in hypercho-

Many biological and psychological factors induce haemodynamic and extra-cardiovascular functional changes mediated by the autonomic nervous system. Pharmacological blood pressure reduction, as a neurovegetative stimulus, can change the arousal of the sympathetic nervous system. We evaluated the effects of two calcium channel blockers, verapamil and amlodipine, both administered as monotherapies, upon the sympathetic stress response in 23 randomized mild-to-moderate essential hypertensives (161 +/- 2/98 +/- 1 mmHg). Patients performed four stress tests (mental arithmetic, colour word Stroop, cold pressor and handgrip) while extracardiovascular and haemodynamic functions were assessed non-invasively at every heart beat, during baseline, stress and recovery phases. The sympathetic response was evaluated by computing the 'area-under-the-curve' (value x time) measured during the psychophysiological session. The session was repeated at run-in, after placebo and during treatment. After one month's treatment, baseline blood pressure was significantly reduced in patients treated with amlodipine (139 +/- 1/84 +/- 1 mmHg; P < 0.001) and verapamil (140 +/- 2/85 +/- 1 mmHg; P < 0.001). The emotional arousal (frontalis muscular contraction, skin conductance) was unchanged, but the cutaneous vascular response was reduced (P < 0.05) in patients treated with verapamil. No changes in systolic or diastolic blood pressure were detectable, but amlodipine increased the heart rate response (P < 0.05). In contrast, verapamil reduced the heart rate (P < 0.05) without depressing the cardiac output response, which was increased with amlodipine (P < 0.05). Total vascular resistance was significantly (P < 0.001) reduced with both the treatments. Consequently, functional cardiac load, expressed by pressure-rate product and cardiac power, was significantly enhanced with amlodipine and reduced with verapamil. In conclusion, the abnormal sympathetic stress response, which characterizes the hypertensive patient, might be affected by the choice of medication. Verapamil in particular, moderated emotional arousal, the vasoconstrictive response and reduced cardiac load without lowering cardiac output demands. In contrast, in patients treated with amlodipine, in whom the cardiac output response was increased, the pattern was reversed and the functional cardiac load was also increased.

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Background: In patients (pts) with sick sinus syndrome (SSS), right ventricular apical (RVA) pacing increased the risk of developing atrial fibrillation (AF). However, the mechanism of proarrhythmic effect of RVA pacing remains unclear. Methods: We performed detailed echocardiograhic examination with Tissue Doppler Imaging in 60 pts with SSS (mean age 73A9 years, 42 F) who implanted with DDD pacemakers during atrial and ventricular pacing with atrioventricular interval programmed at 120-150 mesc (ApVp mode) and AAI mode with (ApVs mode) at 70 bpm. Echo measurements were taken after 15 mins of pacing in each mode. The myocardial atrial contraction velocity was measured at annulus of right free wall (Ra), septal (Sa) and lateral free wall (La) respectively. Results: As expected, the AV interval was significantly shorter (118A25 vs.163A45 ms, P=0.002), and QRS duration was longer (146A33 vs.97A26 ms, P,0.001) during ApVp mode as compared with ApVs mode. Although there was no significant difference in left ventricular ejection fraction, left atrial (LA) ejection fraction (50A14 vs.55A14%, P=0.005), LA active emptying fraction (32A17 vs.37A16%, P=0.018) and LA filling fraction (43A13 vs. 48A13%, P=0.007) were all significant improved by 18%, 54% and 18%, respectively during ApVs mode as compared with ApVp mode. Furthermore, atrial myocardial contraction velocities among Ra (14.0A3.8 vs.15.2A4.6cm/s, P=0.026), Sa (7.8A2.6 vs. 8.8A2.8cm/s, P=0.001), and La (8.9A3.2 vs.9.7A2.7cm/s, P=0.020) were also significantly increased during ApVs mode by 12%, 19% and 21%, respectively as compared with ApVp mode (Figure). Conclusions: In pts with SSS, avoidance of RVA pacing during ApVs mode improves LA haemodynamic and mechanical function, which might contribute to a lower risk of development of AF after pacemaker implantation. P773Qualitative and quantitative assessment of 3 novel post-processing methods for enhancing echocardiographic images. Echocardiography, while a prevalent tool for assessing cardiac morphology and function, suffers from a range of artefacts that reduce its diagnostic value. This work qualitatively and quantitatively evaluates 3 novel post-processing methods for enhancing echocardiographic images. Data enhancement is achieved by utilising multiple partially decorrelated instances of a cardiac cycle acquired through a single acoustic window. Such information has until now been largely disregarded during data post-processing. Moreover, unlike past approaches, data enhancement is achieved without filtering out information based on static or adaptive selection criteria. Qualitative assessment using 32 clinical datasets demonstrated (i) suppression of cavity noise, (ii) increase in tissue/cavity contrast, and (iii) visual enhancement of tissue structures previously masked-out by various artefacts (Figure 1). The effect of each post-processing method on the diagnostic value of cardiac ultrasound data was quantitatively assessed by examining the repeatability coefficient variations (via Bland-Altman plots) in clini...

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