Maria Chiara Cavallini

Is the absence of a normal nocturnal fall in blood pressure (nondipping) associated with cardiovascular target organ damage

Objective To determine whether the failure to decrease blood pressure normally during sleep is associated with more prominent target organ damage. Methods Cardiac and vascular structure and function were characterized in 183 asymptomatic, unmedicated hypertensive patients and compared with their ambulatory blood pressures. Results The 104 patients with a normal (> 10%) nocturnal fall in systolic blood pressure (dippers) were similar to the 79 patients with an abnormal fall (nondippers) in sex, race, body size, smoking history, and average awake ambulatory blood pressure. Nondippers tended to be older (57 versus 54 years, P = 0.06). The supine blood pressure upon completion of the ultrasound studies was higher in the nondippers (156/93 versus 146/89 mmHg, P < 0.005) as was the variability of the awake diastolic blood pressure. There were no differences between dippers and nondippers in left ventricular mass (170 versus 172 g), mass index (90 versus 91 gm/m2), prevalence of abnormal ventricular geometry, common carotid artery diameter (5.74 versus 5.75 mm), and vascular strain. Although nondippers were more likely to have carotid artery plaque (41 versus 27%, P = 0.053) and an increased intimal–medial thickness (0.84 versus 0.79 mm, P < 0.05), adjustment for age rendered the differences insignificant. There were no differences in the relation of awake and sleeping systolic pressures to the left ventricular mass (r = 0.36 and 0.35, respectively, both P < 0.005) or to the carotid wall thickness (r = 0.28 and 0.29, respectively, both P < 0.005). When the 114 men and 69 women were considered separately, similar findings were obtained. When the 109 whites and 56 blacks (African-Americans and Afro-Caribbeans) were considered separately, there were no differences in left ventricular structure in either group, and differences in vascular structure were confined to the white subgroup. Conclusion The lack of a normal nocturnal fall in blood pressure is not associated with an increase in left ventricular mass or in arterial disease independently of age. Age-related changes in carotid artery wall thickness and plaque among nondippers may reflect a contribution of an altered baroreceptor function to the lack of normal nocturnal and supine blood pressure decreases.

Efficacy of physiotherapy interventions late after stroke: a meta-analysis

Objective Physiotherapy is usually provided only in the first few months after stroke, while its effectiveness and appropriateness in the chronic phase are uncertain. The authors conducted a systematic review and meta-analysis of randomised clinical trials (RCT) to evaluate the efficacy of physiotherapy interventions on motor and functional outcomes late after stroke. Methods The authors searched published studies where participants were randomised to an active physiotherapy intervention, compared with placebo or no intervention, at least 6 months after stroke. The outcome was a change in mobility and activities of daily living (ADL) independence. The quality of the trials was evaluated using the PEDro scale. Findings were summarised across studies as effect size (ES) or, whenever possible, weighted mean difference (WMD) with 95% CI in random effects models. Results Fifteen RCT were included, enrolling 700 participants with follow-up data. The meta-analysis of primary outcomes from the original studies showed a significant effect of the intervention (ES 0.29, 95% CI 0.14 to 0.45). The efficacy of the intervention was particularly evident when short- and long-distance walking were considered as separate outcomes, with WMD of 0.05 m/s (95% CI 0.008 to 0.088) and 20 m (95% CI 3.6 to 36.0), respectively. Also, ADL improvement was greater, though non-significantly, in the intervention group. No significant heterogeneity was found. Interpretation A variety of physiotherapy interventions improve functional outcomes, even when applied late after stroke. These findings challenge the concept of a plateau in functional recovery of patients who had experienced stroke and should be valued in planning community rehabilitation services.

Association of the Auscultatory Gap with Vascular Disease in Hypertensive Patients

The loss and reappearance of Korotkoff sounds during cuff deflation done to measure auscultatory blood pressure are a common finding in clinical practice. This auscultatory gap can cause underestimation of systolic blood pressure and, less commonly, overestimation of diastolic blood pressure. Although the auscultatory gap was first described by Krylov in 1906 [1] and its potential clinical relevance was suggested by Cook and Taussig in 1917 [2], the mechanism underlying the formation of the gap has rarely been studied. Neither the relation of the auscultatory gap to cardiovascular structure and function nor the prognostic importance of the gap has been assessed. Our goals were to 1) determine the prevalence of the auscultatory gap in a large cohort of asymptomatic patients with hypertension who were not receiving medication and 2) evaluate the relation between the auscultatory gap and cardiac and vascular structure and function, with special attention to findings that have been related to prognosis in previous studies [3]. Methods Study Sample One hundred sixty-eight patients with hypertension who were referred from the Hypertension Center of The New York Hospital were studied between December 1990 and November 1993. All patients were studied after they had not received medications for at least 3 weeks; 65 patients (39%) had never received antihypertensive medications. Essential hypertension was diagnosed by the presence of a sustained increase in blood pressure ( 140 mm Hg systolic pressure or more than equals 90 mm Hg diastolic pressure, or both, on three determinations done at least 2 weeks apart). Patients with diagnoses of secondary hypertension or diabetes mellitus and patients with clinical evidence of coronary artery disease (typical angina or echocardiographic evidence of myocardial infarction) or cerebrovascular disease (transient ischemic attack or stroke) were excluded. Isolated systolic hypertension (systolic pressure more than equals 160 mm Hg and diastolic pressure less than 90 mm Hg) was present in 25 patients (15%). Valvular heart disease was excluded by Doppler echocardiography. Standard blood laboratory analyses were done for all patients. The study was done in accordance with protocols approved by the Committee on Human Rights in Research of Cornell University Medical College. Wideband External Pulse Recording The presence of auscultatory gaps was evaluated using wideband external pulse recording in addition to standard auscultation. Wideband external pulses represent vibrations on the body surface that are caused by pulsatile blood flow, and they are detected using a wideband pressure sensor that includes frequencies below the audible range. We recorded wideband external pulses from the left arm while the cuff pressure was deflated from greater than systolic pressure to less than diastolic pressure while the patient was in the supine position. This was done using a specially designed foil electret sensor (AT&T Bell Laboratories, Murray Hill, New Jersey) positioned over the brachial artery under the distal portion of the blood pressure cuff. This equipment has been described in detail [4-7]. Simultaneous traditional auscultation was done by a trained observer who used a switch to mark the onset and disappearance of Korotkoff sounds. In the right arm, a Finapres noninvasive finger pulse recording device (model 2300, Ohmeda, Englewood, Colorado), which has been shown to accurately reflect changes in intra-arterial pressure [8], provided a beat-to-beat representation of arterial pressure. The wideband external pulse recorded during cuff deflation was previously reported [7] to be composed of 1) a low-frequency signal [K1] that appears when the cuff pressure is greater than systolic pressure and disappears when the cuff pressure is less than diastolic pressure; 2) a high-frequency signal [K2] that is related to the Korotkoff sound and appears when the cuff pressure is at systolic pressure and disappears when the cuff pressure is at diastolic pressure; and 3) a large-amplitude, low-frequency signal (K3) that appears when the cuff pressure is between systolic and diastolic pressure and that is still present when the cuff pressure decreases to less than diastolic pressure. Auscultatory gaps were characterized by comparing the auscultatory markers or stethoscope signals with the corresponding wideband external pulse. Three types of auscultatory gaps, which have been described previously [6], were identified. The nature and relative frequency of each type of gap were determined on the basis of each patients normal breathing pattern and a cuff pressure deflation rate of 2 to 4 mm Hg per second. A gap characterized by the intermittent disappearance of Korotkoff sounds when the cuff pressure is slightly less than systolic pressure (G1 gap) is associated with the intermittent disappearance of the K2 signal when the sound disappears and with the presence of the K1 and K2 signals when the sound is heard. The G1 gap is caused by a phasic decrease in systolic pressure to less than the cuff pressure during inspiration. A gap that occurs when the cuff pressure is slightly greater than diastolic pressure (G2 gap) is characterized by the intermittent disappearance of the K2 signal when the sound disappears and the presence of the K1, K2, and K3 signals when the sound is heard. The G2 gap results from a phasic increase of arterial diastolic pressure during expiration. The classic auscultatory gap (G3 gap; Figure 1) occurs when the cuff pressure is between the systolic and diastolic pressures, independent of respiratory variations in arterial pressure; it is characterized by a loss of audible sound but the presence of an under-developed K2 signal [6]. Although wideband external pulse recording is the definitive method for evaluating and identifying auscultatory gaps [6], the three types of gaps may be easily detected and classified at the bedside using standard sphygmomanometry to detect the loss and reappearance of Korotkoff sounds in relation to the respiratory cycle and systolic and diastolic blood pressures. Figure 1. Recording of classic auscultatory gap (G3). Echocardiography Standard M-mode and two-dimensional echocardiography were done in all patients by a highly skilled research technician using commercially available equipment. Left ventricular dimensions were measured according to the recommendations of the American Society of Echocardiography [9, 10]. A blinded investigator did M-mode measurements of tracings on several cycles using a digitizing tablet, and the measurements were averaged. Left ventricular mass was calculated using the Penn convention and was adjusted for body surface area [11]. Left ventricular volumes were obtained using the correction of Teichholz and colleagues [12]. Fractional shortening, ejection fraction, relative wall thickness, stroke volume, cardiac output, and total peripheral resistance were calculated using standard formulas. Carotid Ultrasonography We did carotid ultrasonography as previously described [13]. Extracranial carotid arteries on both sides were scanned with a 7.5-MHz imaging transducer using multiple projections to detect the presence of discrete carotid atherosclerosis [14]. A two-dimensionally guided M-mode tracing of the distal common carotid artery, about 1 cm proximal to the carotid bulb, was obtained with simultaneous electrocardiography and carotid pressure waveform (see below) and recorded on a 0.5-inch Super VHS videotape. Suitable frames for measurements were digitized using a frame-grabber (Imaging Technology, Inc., Woburn, Massachusetts) interfaced with a high-resolution (640 480 pixel) video monitor and stored on diskettes. The axial resolution of the M-mode system is 0.2 mm. A blinded investigator measured carotid tracings on the stored images using a mouse-driven computer program after calibration for depth and time. The simultaneous carotid pressure tracing was used to ensure that measurement of the carotid artery was done at end-diastolic and peak-systolic pressures. Measurements included that of the intima-media thickness of the far wall of the distal common carotid artery at end diastole (as has been validated in anatomic correlation studies [15, 16]) and the internal dimensions of the carotid artery at end diastole and peak systole, which were determined by continuous tracing of the intimalumen interface of the near and far walls. The relative wall thickness of the artery was also calculated [13]. All measurements were obtained on several cycles and were averaged. Standard measurements of wall thickness were never obtained at the level of a discrete plaque. Arterial Pressure Waveform and Arterial Stiffness Carotid pressure waveforms were obtained using a high-fidelity external pressure transducer functioning as an applanation tonometer (model SPT-301, Millar Instruments, Inc., Houston, Texas) that was applied to the cutaneous surface corresponding to a common carotid artery. Waveforms and modulus and phase of harmonic components obtained with this transducer closely resemble those derived from intra-arterial recordings [17]. The correlation between the tonometer and the simultaneous intra-arterial recordings has been validated [17-20]. The transducer registers absolute changes in blood pressure over a range of 300 mm Hg, but it requires external calibration to obtain actual carotid blood pressure values. Because mean arterial blood pressure does not vary substantially in the capacitance vessels [21, 22], we measured brachial arterial blood pressure using cuff and mercury sphygmomanometry while each patient was supine, and we assigned mean blood pressure (diastolic pressure + [1/3 pulse pressure]) to the computer-derived mean blood pressure of the carotid waveforms. After calibration, carotid peak-systolic and end-diastolic pressures were calculated by computer. Carotid arterial stiffness was evaluated by the following three methods [23].

Day Care for older dementia patients: favorable effects on behavioral and psychological symptoms and caregiver stress

To assess the effects of Day Care (DC) on older subjects with dementia and their caregivers.

Tools for Observational Gait Analysis in Patients With Stroke: A Systematic Review

Background Stroke severely affects walking ability, and assessment of gait kinematics is important in defining diagnosis, planning treatment, and evaluating interventions in stroke rehabilitation. Although observational gait analysis is the most common approach to evaluate gait kinematics, tools useful for this purpose have received little attention in the scientific literature and have not been thoroughly reviewed. Objectives The aims of this systematic review were to identify tools proposed to conduct observational gait analysis in adults with a stroke, to summarize evidence concerning their quality, and to assess their implementation in rehabilitation research and clinical practice. Methods An extensive search was performed of original articles reporting on visual/observational tools developed to investigate gait kinematics in adults with a stroke. Two reviewers independently selected studies, extracted data, assessed quality of the included studies, and scored the metric properties and clinical utility of each tool. Rigor in reporting metric properties and dissemination of the tools also was evaluated. Results Five tools were identified, not all of which had been tested adequately for their metric properties. Evaluation of content validity was partially satisfactory. Reliability was poorly investigated in all but one tool. Concurrent validity and sensitivity to change were shown for 3 and 2 tools, respectively. Overall, adequate levels of quality were rarely reached. The dissemination of the tools was poor. Conclusions Based on critical appraisal, the Gait Assessment and Intervention Tool shows a good level of quality, and its use in stroke rehabilitation is recommended. Rigorous studies are needed for the other tools in order to establish their usefulness.

Is Antidepressant Treatment Associated with Reduced Cognitive Decline in Alzheimer's Disease?

Background: Although antidepressant drugs (ATD) are frequently prescribed to patients with Alzheimer’s disease (AD), their effect on cognitive status has been only rarely assessed. Methods: The impact of depressive symptoms and ATD on cognitive status was retrospectively assessed in 72 older AD outpatients with mild-to-moderate cognitive impairment, treated with cholinesterase inhibitors, over a 9-month follow-up. Results: Compared to subjects without baseline depressive symptoms, those with symptoms who were continuously treated with ATD had less cognitive decline; those never treated, or not continuously treated despite baseline symptoms, had an intermediate trend. Such a protective action of ATD was, at least in part, independent of their action on depressive symptoms. Conclusion: These observations suggest that ATD may reduce cognitive decline in depressed older AD patients.

[OP.3C.02] LOOKING FOR THE OPTIMAL BLOOD PRESSURE VALUES IN OLD PEOPLE WITH COGNITIVE DECLINE: A LONGITUDINAL STUDY BASED ON 24-HOUR AMBULATORY BLOOD PRESSURE MONITORING

Objective: Available data on the prognostic role of blood pressure in older subjects with cognitive impairment are still scarce. We recently showed that tight control of blood pressure may be associated with a greater progression of cognitive impairment in the short term. Aim of this study is to evaluate the long term association of clinical and ambulatory blood pressure (BP) and antihypertensive drugs (AHD) with survival and desease progression in older subjects with cognitive impairment. Design and method: We enrolled 198 subjects (average age 79, 72% with high BP) with Mild Cognitive Impairment (39%) or dementia (61%) referred to the memory clinic. Each patient underwent cognitive assessment with Mini Mental State Examination (MMSE) and 24-hour blood pressure monitoring (ABPM). Subjects were divided into tertiles according to the values of systolic (SBP) and diastolic (DBP) blood pressure, assessed both clinically and by ABPM (mean daytime and night-time). Results: After a mean 3-year follow-up, an independent association was observed between higher night-time SBP (> 135 mmHg) and mortality (p < 0,001), after adjustment for age, vascular comorbidity and functional status. A similar, although weaker association was observed for higher night-time DBP and daytime SBP. Conversely, MMSE decline was greater in patients with lower daytime SBP (< 128 mmHg) (p = 0.029), but limited to the subgroup of subjects receiving AHD (p = 0.002), independently of age, vascular comorbidity and baseline MMSE score. No significant association was observed for clinical SBP. Conclusions: In this study higher mean SBP, especially at night, was predictive of mortality at 3 years, while lower average daytime SBP in subjects receiving AHD was associated with progression of cognitive impairment. High-normal SBP values (130–145 mmHg) seem to be the optimal target to reduce the risk of mortality and the progression of cognitive decline among cognitively impaired older subjects. ABPM is needed for BP assessment in this vulnerable population.

Pulsology Reloaded: Commentary on Similar Effects of Treatment on Central and Brachial Blood Pressure in Older Hypertensive Subjects

The Losartan Intervention For Endpoint reduction in hypertension (LIFE) Study,1 the Second Australian National Blood Pressure Trial (ANBP2),2 and the Anglo-Scandinavian Cardiovascular Outcome Trials3 have shown that different antihypertensive treatments may have different impacts on the rate of events in hypertension while achieving comparable brachial blood pressure (BP) reduction. Thus, although brachial BP estimation by classic Riva–Rocci cuff sphygmomanometer and the Korotkoff auscultatory technique have provided almost all of our knowledge on epidemiology, prognosis, and treatment of hypertension,4,5 recent trials1–3 are revealing intrinsic limitations of the conventional approach, because the real goal of treatment in hypertension is the reduction in the number and the rate of untoward events. More recently, the Conduit Artery Function Evaluation (CAFE) Study6 described higher central BP as a key factor explaining the greater number and rate of events with atenolol than with amlodipine plus perindopril. Central pressure waveform and BP values can be estimated by applanation tonometry, a method supported by solid theoretical principles and modeling studies in experimental settings.7 Analysis of the systolic portion of the carotid pressure waveform allows for obtaining indices of the arterial viscous-elastic properties that correlate with end-organ damage and clinical outcomes in hypertension.8 Therefore, the indices of arterial waveform reflection and mechanics and central BP assessed by applanation tonometry have the potential to add significant information for risk stratification beyond and above brachial BP. In fact, the conclusions of the CAFE Study were well received.9 In addition, applanation tonometry has also been associated with 2D-guided M-mode vascular ultrasonography to assess simultaneously the viscous-elastic properties of the carotid artery, the intima–media thickness, and quantification of atherosclerosis.8 Assessment of cardiovascular target organ damage is curial for a global risk assessment …