Noninvasive estimation of central blood pressure and the augmentation index in the seated position: a validation study of two commercially available methods.

OBJECTIVES: The aim of this study was to examine the utility of the generalized transfer function (GTF) and the late systolic shoulder of the radial pressure waveform (SBP2) for estimating seated central systolic blood pressure (c-SBP) and seated c-augmentation index (c-AIx). METHODS: In 199 participants (182 cardiovascular disease patients and 17 normal individuals; mean age: 65.7 ±â€Š10.6 years), c-SBP and c-AIx were estimated using the SphygmoCor and Omron HEM-9000AI systems. Both estimates were compared with carotid SBP and augmentation index (AIx). All measurements were performed with the participants in the seated position. RESULTS: Mean c-SBP was 121.7 ±â€Š18.6 mmHg and 122.6 ±â€Š19.8 mmHg according to the GTF and SBP2 methods, respectively, and carotid SBP was 124.4 ±â€Š19.2 mmHg. There were close correlations between the three values (GTF vs. carotid SBP: r = 0.986, SBP2 vs. carotid SBP: r = 0.975, GTF vs. SBP2: r = 0.989, all P < 0.0001), all of which met the AAMI SP10 criteria and the grade A British Society of Hypertension criteria. The relationship between c-AIx estimated using the GTF method and carotid AIx was comparable to that reported previously for supine individuals (r = 0.703, P < 0.0001). The seated carotid-radial artery amplifications of the first and second harmonics were identical to those reported in previous supine studies. Both methods produced reproducible estimates of c-SBP and c-AIx (r = 0.997-0.910, all P < 0.0001). CONCLUSION: The present study indicates that the GTF and SBP2 methods can be used to estimate c-SBP and c-AIx in seated individuals.

Noninvasive pulse waveform analysis in clinical trials: similarity of two methods for calculating aortic systolic pressure.

BACKGROUND: Concerns persist about the validity of generalized transfer function-derived, aortic blood-pressure measurements during the administration of vasoactive agents in clinical trials. Hence, we compared this transfer-function method with another, which estimates aortic systolic pressure directly from the late systolic shoulder of the radial pressure wave, after administration of placebo, ramipril, or atenolol. METHODS: We recorded radial pressure pulse waveforms, using a commercially available system, in 30 subjects with >or=1 coronary risk factor in an acute study of ramipril at 10 mg and atenolol at 100 mg. Directly recorded radial and derived aortic pressure pulse waveforms were examined individually and were ensemble-averaged, and the difference between radial and aortic pressure responses was examined. RESULTS: The late systolic shoulder response from radial waveforms was reduced by 15.8 mm Hg (SD, 12.2 mm Hg) more with ramipril than with atenolol. This was similar to a difference of 14.6 mm Hg (SD, 11.2 mm Hg) calculated for the aortic systolic pressure response using the transfer-function technique. Ramipril caused a greater reduction in the aortic systolic pressure response (22.2 mm Hg), whereas with atenolol, there was a modest decrease (7.6 mm Hg). The mean difference between aortic systolic pressures measured from direct radial waveforms and from derived aortic pressure between 3 and 5 h after dosing under all circumstances was 1.6 mm Hg (SD, 8.9 mm Hg). CONCLUSIONS: Central pressure derived from radial pressure waveforms using a generalized transfer function gave similar results for central pressure measured directly from radial waveforms. The hemodynamic benefits of angiotensin-converting enzyme inhibitor, angiotensin receptor blocker, and calcium channel blocker over beta-blocker antihypertensive therapy in recent trials were confirmed by this study.

Pulse wave analysis and pulse wave velocity: a review of blood pressure interpretation 100 years after Korotkov.

The pulsatile component of blood pressure (ie, pulse pressure) has received considerable attention as an important risk factor for cardiovascular disease. In particular, central blood pressure measurements in the ascending aorta or in the carotid artery are expected to be more useful than conventional brachial pressure measurements for predicting cardiovascular events because central pressure, not the brachial pressure, is the pressure that target organs encounter. Due to wave reflection, the blood pressure in the upper limb does not represent the central blood pressure; therefore, leading researchers have enthusiastically promoted a noninvasive method of measuring central blood pressure and the resulting aortic stiffness. Until now, there has been an increasing body of evidence to support the accuracy and superiority of central blood pressure measurements as well as the assessment of aortic properties over classical brachial pressure measurements. In this review, the information regarding these "central" indices derived from 2 main methods, namely "pulse wave analysis" and "pulse wave velocity", for the application of central blood pressure measurements and arterial stiffness to clinical study and practice, has been summarized.

Age-related changes in carotid artery flow and pressure pulses: possible implications for cerebral microvascular disease.

BACKGROUND AND PURPOSE: We sought to establish the relation between the pulsatile components of pressure and flow waveforms in the carotid artery and their change with age. METHODS: Distention (pressure) and axial flow velocity waveforms were recorded noninvasively and simultaneously from the common carotid artery of 56 healthy subjects aged 20 to 72 years. RESULTS: There was a close relation between the time intervals of pressure and flow waves: from foot to first shoulder or peak, to second shoulder or peak, and to incisura (r=0.97, P<0.0001 for each), which approximated the line of identity. The peak and nadir of flow velocity decreased with age, but late systolic flow augmentation increased substantially (1.6 times in the older group); this can be attributed to earlier wave reflection from the lower body. Pressure augmentation index (PAI) and flow augmentation index (FAI) increased similarly with age (PAI (%) = 0.84 x age - 26.6; FAI (%) = 0.75 x age + 11.9; both P<0.0001). CONCLUSIONS: Arterial stiffening with aging increases carotid flow augmentation and can explain the increasing flow fluctuations in cerebral blood vessels. Measurement of carotid FAI may provide a gauge for risk of cerebral microvascular damage, just as PAI provides a gauge for risk of left ventricular hypertrophy and failure.

Clinical use of indices determined non-invasively from the radial and carotid pressure waveforms.

OBJECTIVE: To evaluate the clinical use of radial and carotid artery applanation tonometry as an independent supplement to cuff sphygmomanometry. METHODS: In 44 patients, radial and carotid tonometric pressure recordings were taken at short intervals apart by two persons who had prolonged experience with both. Comparisons were made between directly recorded radial and carotid waveforms and between aortic waves synthesized from both, using SphygmoCor. Focus was on waveform features: time intervals between wavefoot and incisura, denoting ejection duration, between wavefoot and first systolic peak or shoulder T1, and augmentation index - the rise in pressure from this point to systolic peak divided by pulse pressure. RESULTS: No patient had discomfort with radial tonometry, whereas many found carotid tonometry uncomfortable. Beat-to-beat variability was lower for the radial than carotid site. The device's operator "quality index" was achieved for 78% of radial waveforms but just 20% of carotid waveforms (P<0.05). Interobserver variability was lower for all indices derived from radial, cf. carotid, waveforms. For the two observers combined, there was no difference between aortic indices determined from carotid and radial sites except for T1 (radial-derived 117+ or -17 ms, cf. carotid-derived 103+ or -17 ms, P<0.05), but this did not influence the value of augmentation index (radial-derived 26+ or -13%, cf. carotid-derived 28+ or -14%, P=NS). CONCLUSION: The present study conforms with most published results, and indicates superiority of radial to carotid tonometry in clinical practice.

Effect of sildenafil on cardiac performance in patients with heart failure.

Sildenafil is rarely used in patients with heart failure despite a high prevalence of erectile dysfunction, and the theoretic possibility that by increasing nitric oxide availability, it may improve left ventricular (LV) load and performance. This study aimed to determine the peak effects of sildenafil on LV load and performance in patients with heart failure caused by systolic LV dysfunction. Twenty patients with controlled LV failure and ejection fractions <35% received sildenafil 50 mg or a matching placebo when not receiving regular medication for > or =12 hours, in a randomized, placebo-controlled, double-blind, 2-way crossover fashion. Cardiac output was measured by Doppler echocardiography. The aortic pressure waveform was determined using generalized transfer function from radial artery applanation tonometry. Aortic and femoral arterial stiffness was determined as carotid-femoral and femoral-pedal pulse-wave velocity (PWV); wave reflection was measured as an augmentation index (AIx). Cardiac index increased significantly (by 0.37 L/min.m(2), p <0.0001), with the peak effect 60 minutes after sildenafil administration. Compared with the baseline value, total systemic resistance showed a reduction of 479 dynes.s.cm(-5) (p <0.0001). Aortic and lower limb PWV decreased significantly (by 0.89 and 1.14 m/s, respectively, p <0.0001 for both), as did AIx (by 3.6% absolute, p <0.0001); these remained significant after adjustment for mean pressure and heart rate changes. In conclusion, sildenafil improves cardiac performance because of a decrease in LV load, which is caused by decreases in peripheral resistance, in aortic and large artery stiffness, and in wave reflection from peripheral sites. This can explain the increase in cardiac output and in exercise capacity with sildenafil in patients with heart failure.

Benefits from angiotensin-converting enzyme inhibitor 'beyond blood pressure lowering': beyond blood pressure or beyond the brachial artery?

OBJECTIVE: The substantial benefits of ramipril over conventional therapy in high-risk patients are not always associated with clinically significant differences in brachial arterial pressure, and largely remain unexplained. We undertook this acute study to establish the magnitude of and reason for different acute effects of ramipril and atenolol on arterial pressure. METHODS: We enrolled 30 patients, who took 10 mg ramipril, 100 mg atenolol, and placebo at intervals of > or = 7 days, in a randomized, double-blind, placebo-controlled trial. After baseline, measurements were taken at 30-60 min intervals for 5 h, and comprised cuff brachial pressure, radial artery tonometry with generation of central aortic pressure, and pulse wave velocity for aorta, upper limb and lower limb arteries. RESULTS: Both ramipril and atenolol reduced arterial pressure, and the diastolic pressure fall was similar in the aorta and brachial artery, but the systolic pressure fall for ramipril was greater than for atenolol (by 5.2 mmHg, P < 0.0001) in the aorta compared with the brachial artery. The aortic systolic pressure difference with ramipril in comparison with atenolol was accompanied by an absolute difference of 10.7% (P < 0.0001) in the augmentation index, denoting a reduction in peripheral wave reflection by ramipril. The aortic pulse wave velocity fell to a similar degree with ramipril in comparison with atenolol, but fell to a greater degree (1.35 and 0.44 m/s, respectively, P < 0.0001 for both) in muscular arteries of the lower and upper limbs. CONCLUSION: A greater (average, 5.2 mmHg) decrease in aortic systolic pressure caused by ramipril may explain the greater benefit of ramipril over atenolol. The difference is attributable to decreased stiffness of peripheral arteries and a reduction in wave reflection.

Effect of caffeine on aortic elastic properties and wave reflection.

OBJECTIVE: Caffeine is the most widely used pharmacologically active substance. Aortic elastic properties and arterial wave reflection are important factors for the efficient performance of the cardiovascular system, as well as prognosticators of cardiovascular risk. We investigated the effect of caffeine on aortic elastic properties and wave reflection. DESIGN: We studied the effect of caffeine (250 mg) in 20 healthy subjects according to a randomized, placebo-controlled, double-blind, cross-over design. METHODS: Aortic stiffness was evaluated with carotid-femoral pulse wave velocity and wave reflection with augmentation index of the aortic pressure waveform. RESULTS: Pulse wave velocity increased (by 0.51 m/s, 0.001) denoting an increase in aortic stiffness. Augmentation index and augmented pressure increased (by 6.8%, and by 4.4 mmHg, respectively, P <0.001 for both) denoting increased wave reflections. Concurrently, both radial and aortic systolic, diastolic and pulse pressure increased significantly. However, this increase was 20 and 9% larger for aortic systolic pressure (at 30 and 60 min, P <0.001 and P <0.05, respectively) and 56% larger for aortic pulse pressure (at 30 min, P <0.001) compared with the corresponding upper limb values. This indicates that peripheral pressure measurements are not an accurate guide for the pressor effect of caffeine in central arteries. CONCLUSIONS: Caffeine affects unfavorably aortic stiffness and enhances wave reflections. This finding has implications for the impact of caffeine consumption on cardiovascular risk.

Caffeine increases aortic stiffness in hypertensive patients.

BACKGROUND: Caffeine is the most widely used pharmacologic substance. Aortic stiffness is an important factor for cardiovascular system performance and a prognosticator of cardiovascular risk. We investigated the effect of caffeine on aortic stiffness in treated hypertensive patients. METHODS: We studied the effect of caffeine (250 mg) in 12 treated hypertensive patients according to a randomized, placebo-controlled, double-blind, cross-over design during a 3-h period. Aortic stiffness was evaluated by carotid-femoral pulse wave velocity. RESULTS: Systolic blood pressure (BP) and pulse pressure increased significantly throughout the study (by 12.3 and 7.4 mm Hg, P =.005 and P <.01, respectively), whereas diastolic BP did not change. Pulse wave velocity increased (by 0.57 m/sec, P <.05) denoting an increase in aortic stiffness. This effect of caffeine lasted throughout the study (3 h), peaking at 60 min and decreasing progressively thereafter. CONCLUSIONS: These results demonstrate, for the first time, that caffeine exerts an acute unfavorable effect on aortic stiffness in treated hypertensive patients. This finding has important implications for the impact of caffeine consumption on cardiovascular risk in hypertension.

Effect of sildenafil on arterial stiffness and wave reflection.

While sildenafil (Viagra) is widely prescribed for erectile dysfunction, its effect on arterial function is not established. The elastic properties of the aorta, as well as the magnitude and timing of wave reflection, are important factors for efficient performance of the cardiovascular system and have been identified as prognosticators of cardiovascular risk. A total of 24 subjects with coronary artery disease, of whom 14 were hypertensives, aged 69 +/- 8 years, were studied in a randomized, placebo-controlled, double-blind, cross-over design. Measurements lasted for 3 h after the sildenafil intake (50 mg, p.o.) or placebo. Aortic elastic properties were evaluated with carotid-femoral pulse wave velocity; wave reflection was evaluated with augmentation index and augmented pressure of the aortic pressure waveform. Pulse wave velocity decreased significantly (by 0.65 m/s, p = 0.005), denoting a decrease in aortic stiffness. Augmentation index and augmented pressure decreased significantly (by 4.47% absolute and by 4.01 mmHg; p < 0.001 and p = 0.001, respectively), denoting a decreased effect of wave reflection from the periphery. Aortic pulse pressure decreased significantly (by 6.74 mmHg, p < 0.05). An active effect of the drug on aortic wall appears to contribute to the decrease in pulse wave velocity, although other mechanisms such as a decrease of blood pressure and autonomic reflexes could also have contributed. The effect of sildenafil lasted throughout the study (3 h), being evident 30 min after drug intake. In conclusion, this study shows, for the first time, that sildenafil has a favorable effect on aortic stiffness and wave reflection in patients with coronary artery disease. This finding may have important implications for cardiovascular performance and exercise capacity during intercourse.