Evaluation of aortic distensibility with transesophageal echocardiography.

Distensibility of the descending aorta was evaluated during routine transesophageal echocardiography (TEE) in 50 subjects (16 to 80 years, average age 53). M-mode measurements of aortic systolic (SD) and diastolic diameter (DD) were taken distal to the left subclavian artery. Simultaneously, cuff brachial artery systolic (SBP) and diastolic (DBP) pressures were measured. Aortic pressure strain modulus (Ep), calculated as brachial artery pulse pressure/aortic strain, averaged 1.19 +/- 0.95 10(6) dynes/cm2. Elasticity index beta, defined as 1n (SBP/DBP)/aortic strain, averaged 3.77 +/- 2.12. Both Ep and beta were correlated with age (r = 0.65, p less than 0.001; and r = 0.70, p less than 0.0001). In 20 subjects aortic pulse wave velocity was assessed at the same time using simultaneous high fidelity recordings of carotid and femoral artery pressure waveforms. Aortic pulse wave velocity averaged 818 +/- 231 cm/sec and was correlated with Ep (r = 0.60, p less than 0.01) and with age (r = 0.55, p less than 0.05). Intraobserver and interobserver variability for aortic diameter measurement ranged from 0.2 to 0.5 mm.     

Pulse pressure and echocardiographic findings in essential hypertension

Blood pressure, carotid-femoral pulse wave velocity and cardiac mass as judged on echocardiography were evaluated in 11 normal subjects and 36 patients with sustained essential hypertension of similar age. The hypertensive patients were divided into two groups of similar age, weight, height and mean arterial pressure: patients in the first group (Group I) had a pulse pressure inferior to 60 mmHg and in the second group (Group II) had a pulse pressure equal or superior to this value. Group II patients had significant higher values for cardiac mass (148.8 +/- 44.3 vs 116.3 +/- 19.8 g/m2; P less than 0.01) (+/- 1 s.d.) than Group I, while mean arterial pressure and pulse wave velocity were similar in the two groups. Stroke volume was significantly higher in Group II than in normal subjects (99.5 +/- 17.1 versus 82.7 +/- 16.9 ml; P less than 0.05). The study findings suggested that the increased pulse pressure in hypertensive patients might influence the development of cardiac hypertrophy independently of mean arterial pressure and aortic distensibility. The increased pulse pressure could reflect a disturbance between ventricular ejection and impedance affecting the ventricle with a resulting increase in pulsatile energy losses and further increase in cardiac mass.     

Index of arterial and venous compliance and echocardiographic parameters in essential permanent arterial hypertension

Forearm venous tone (FVT), carotido-femoral pulse wave velocity (PWV), and left ventricular end diastolic diameter (LVD), left ventricular posterior wall thickness (LVPWT), myocardiac mass (MM), measured by echography were evaluated on 25 subjects with sustained essential hypertension and 30 normotensive subjects with same age and same sex. For the overall population, FVT is positively correlated with LVD (r = 0.45, p less than 0.001), with LVPWT (r = 0.37, p less than 0.01) and with MM (r = 0.55, p less than 0.001). PWV is not correlated with LVD but is positively correlated with LVPWT (r = 0.48, p less than 0.001) and with MM (r = 0.40, p less than 0.01). Stroke volume is positively correlated with FVT (r = 0.42, p less than 0.01), but not with PWV. This study shows that in a population of normals and sustained essential hypertensive subjects: i) indexes of venous compliance are correlated with myocardial thickness, myocardiac mass, left ventricular diameter and stroke volume, while ii) indexes of arterial compliance are only correlated with myocardial thickness. Thus, the modifications of arterial and venous compliance observed in sustained essential hypertension influence cardiac structure and function.     

The Marfan syndrome: abnormal aortic elastic properties

Aortic distensibility and aortic stiffness index were measured at the ascending aorta (3 cm above the aortic valve) and the mid-portion of the abdominal aorta from the changes in echocardiographic diameters and pulse pressure in 14 patients with the Marfan syndrome and 15 age- and gender-matched normal control subjects. The following formulas were used: 1) Aortic distensibility = 2(Changes in aortic diameter)/(Diastolic aortic diameter) (Pulse pressure); and 2) Aortic stiffness index = ln(Systolic blood pressure)/(Diastolic blood pressure)(Changes in aortic diameter)/Diastolic aortic diameter. Pulse wave velocity was also measured. Compared with normal subjects, patients with the Marfan syndrome had decreased aortic distensibility in the ascending and the abdominal aorta (2.9 +/- 1.3 vs. 5.6 +/- 1.4 cm2 dynes-1, p less than 0.001 and 4.5 +/- 2.1, vs. 7.7 +/- 2.5, cm2 dynes-1, p less than 0.001, respectively) and had an increased aortic stiffness index in the ascending and the abdominal aorta (10.9 +/- 5.6 vs. 5.9 +/- 2.2, p less than 0.005 and 7.1 +/- 3.1 vs. 3.9 +/- 1.2, p less than 0.005, respectively). Aortic diameters in the ascending aorta were larger in these patients than in normal subjects, but those in the abdominal aorta were similar in the two groups. Linear correlations for both aortic distensibility and stiffness index were found between the ascending and the abdominal aorta (r = 0.85 and 0.71, respectively). Pulse wave velocity was more rapid in the patients than in the normal subjects (11.6 +/- 2.5 vs. 9.5 +/- 1.4 m/s, respectively, p less than 0.01). Thus, aortic elastic properties are abnormal in patients with the Marfan syndrome irrespective of the aortic diameter, which suggests an intrinsic abnormality of the aortic arterial wall.     

Gender differences in the timing of arterial wave reflection beyond differences in body height.

OBJECTIVES: The timing of arterial wave reflection affects the shape of the arterial waveform and thus is a major determinant of pulse pressure. This study assessed differences in wave reflection between genders beyond the effect of body height. METHODS: From 1123 elderly (aged 71 +/- 5 years) currently untreated hypertensives, we selected 104 pairs of men and women with identical body height (average 164 +/- 4 cm). All subjects underwent echocardiography, including measurement of aortic arch expansion, automated blood pressure measurements, measurement of ascending aortic blood flow and simultaneous carotid artery tonometry. RESULTS: Women had higher pulse (80 +/- 17 versus 74 +/- 17 mmHg, P < 0.05) and lower diastolic pressure (79 +/- 11 versus 82 +/- 10 mmHg, P < 0.05). Whilst heart rate was similar, women had a longer time to the systolic peak (210 +/- 28 versus 199 +/- 34 ms, P < 0.01) and a longer ejection time (304 +/- 21 versus 299 +/- 25 ms, P < 0.001). Wave reflection occurred earlier in women (time between maxima 116 +/- 55 versus 132 +/- 47 ms, P < 0.05) and augmentation index was higher (36 +/- 11 versus 28 +/- 12%, P < 0.001). Aortic diameter was smaller in women and the aortic arch was stiffer (median Ep 386 versus 302 kN/m2, P < 0.05). Hence, systemic arterial compliance was less in women (0.8 +/- 0.2 versus 1.0 +/- 0.3 ml/mmHg). CONCLUSIONS: We conclude that elderly hypertensive men and women have a different timing of both left ventricular ejection and arterial wave reflection when both genders are matched for body height. Women have smaller and stiffer blood vessels resulting in an earlier return of the reflected wave, which is likely due to an increased pulse wave velocity in women.     

Noninvasive determination of aortic input impedance and external left ventricular power output: a validation and repeatability study of a new technique.

OBJECTIVE. The study was designed to test whether aortic input impedance and left ventricular power output can be accurately assessed noninvasively. BACKGROUND. Aortic input impedance describes both the pulsatile and nonpulsatile artery load encountered by the left ventricle. Until now, this measure of afterload has only been determined by invasive techniques. METHODS. The aortic pressure wave was estimated by recording the calibrated carotid artery pressure wave noninvasively with use of a micromanometer-tipped probe by the technique of applanation tonometry. Flow was determined with pulsed wave Doppler measurement of ascending aortic velocity profile and aortic diameter. In 18 subjects undergoing cardiac catheterization, invasive measurements were taken to assess the accuracy of noninvasive data. In 17 other subjects noninvasive measurements were taken on different days to assess the reproducibility of results. RESULTS. Noninvasive pressure measurements correlated well with invasive data: systolic pressure (mm Hg), noninvasive 126 +/- 28 versus invasive 127 +/- 28, r = 0.96, p less than 0.001; diastolic pressure (mm Hg), noninvasive 71 +/- 10 versus invasive 66 +/- 7, r = 0.60, p less than 0.02; augmentation index (%), noninvasive 23.9 +/- 9.3 versus invasive 30.7 +/- 11.9, r = 0.87, p less than 0.001. Doppler-measured cardiac output was closely correlated with invasively measured flow (liters/min): Doppler, 5.3 +/- 1.2 versus invasive, 5.5 +/- 1.3, r = 0.98, p less than 0.001. Impedance and left ventricular power variables calculated from noninvasive and invasive techniques were also closely related: systemic vascular resistance (dynes.s.cm-5), noninvasive 1,479 +/- 488 versus invasive 1,502 +/- 498, r = 0.91, p less than 0.001; characteristic impedance (dynes.s.cm-5), noninvasive 137 +/- 52 versus invasive 136 +/- 79, r = 0.92, p less than 0.001; pulsatile power (mW), noninvasive 249 +/- 94 versus invasive 291 +/- 103, r = 0.91, p less than 0.001; mean power (mW), noninvasive 1,107 +/- 319 versus invasive 1,144 +/- 266, r = 0.93, p less than 0.001. Repeated measures of impedance variables and power output showed coefficients of variation of less than 9%. CONCLUSIONS. Measurement of noninvasive impedance by this technique provides an accurate and repeatable assessment of mean and pulsatile cardiac load.     

Ascending aorta distensibility abnormalities in hypertensive patients and response to nifedipine administration.

PURPOSE: The purpose of the present investigation was to study the distensibility of the ascending aorta in patients with arterial hypertension and normal subjects before and after administration of a calcium antagonist, nifedipine. PATIENTS AND METHODS: The distensibility of the ascending aorta was measured before and after nifedipine administration in 22 male hypertensive patients and 12 age-matched male normotensive subjects. Aortic distensibility was calculated as a function of changes in aortic diameter and pulse pressure, using the formula: 2 x (pulsatile change in aortic diameter)/[(diastolic aortic diameter) x (aortic pulse pressure)]. Aortic diameters were measured by echocardiography and aortic pressures were obtained by catheterization of the ascending aorta. RESULTS: In the basal state, the distensibility of the ascending aorta and aortic strain were lower in hypertensive patients than in normotensive subjects (p < 0.001); the lower aortic distensibility, however, was associated with a greater distending pressure. A good inverse correlation (r = -0.81) was found between mean aortic pressure and aortic distensibility. The aortic distensibility was increased after nifedipine administration in both groups; this increase in aortic distensibility, however, was lower in the patients with hypertension compared with normotensive subjects (p < 0.001). CONCLUSIONS: Aortic distensibility is decreased in patients with arterial hypertension. Nifedipine administration increased the distensibility of the ascending aorta both in patients with arterial hypertension and in normotensive subjects. The increase of aortic distensibility after nifedipine administration was lower in hypertensive patients.     

Importance of aortic baroreflex in regulation of sympathetic responses during hypotension. Evidence from direct sympathetic nerve recordings in humans

Arterial baroreceptors in the carotid sinus and aortic arch regions reflexly regulate heart rate and peripheral vascular responses during changes in arterial pressure. The relative influence of these two arterial baroreflex pathways on the control of these autonomic responses is debatable. Recent studies in our laboratory demonstrate that the aortic baroreflex produces substantial and sustained inhibition of efferent sympathetic nerve activity to muscle (MSNA) during increases in arterial pressure. The regulation of MSNA by these two baroreflexes in humans during hypotension, and particularly the role of the aortic baroreflex, remains undefined. We therefore performed a new series of studies to assess the relative influence of the aortic and carotid baroreflexes on MSNA responses during sustained decreases in arterial pressure. In eight normal male subjects, aged 23 +/- 1 years (mean +/- SEM), we directly measured mean arterial pressure, heart rate, central venous pressure, and MSNA (microneurography) during hypotension (combined aortic and carotid baroreceptor deactivation) produced by intravenous infusion of sodium nitroprusside and during nitroprusside infusion with superimposed application of external neck suction. Neck suction was applied at levels sufficient to maintain transmural carotid sinus pressure above control levels (carotid baroreceptor activation) while the aortic baroreflexes remained deactivated. Central venous pressure was maintained constant with volume infusion. We also studied responses of these same subjects to direct carotid baroreceptor deactivation with the application of external neck pressure. During neck pressure alone, there was a reflex increase in mean arterial pressure; thus, during this portion of the protocol, we achieved carotid baroreceptor deactivation with some aortic baroreceptor activation. Nitroprusside infusion (combined aortic and carotid deactivation) decreased mean arterial pressure from 90.8 +/- 3.1 to 77.8 +/- 1.1 mm Hg (p less than 0.01) with concomitant increases in heart rate from 62.6 +/- 3.0 to 89.7 +/- 6.1 beats/min (p less than 0.001) and in MSNA from 273.8 +/- 43.0 to 950.6 +/- 133.5 units (p less than 0.001). During continued nitroprusside infusion with superimposed neck suction (aortic baroreceptor deactivation and carotid baroreceptor activation), mean arterial pressure decreased to 70.3 +/- 1.9 mm Hg (p less than 0.001 vs. control), heart rate decreased to 82.5 +/- 6.5 beats/min (p less than 0.01 vs. control or vs. nitroprusside alone), but MSNA remained markedly increased at 889.7 +/- 105.1 units (p less than 0.001 vs. control; p = NS vs. nitroprusside alone).(ABSTRACT TRUNCATED AT 400 WORDS)     

Changes in left ventricular diastolic performance after aortic balloon valvuloplasty: acute and late effects

To evaluate acute and follow-up changes in left ventricular diastolic performance, simultaneous digital left ventriculography and micromanometry were performed in 49 patients undergoing aortic balloon valvuloplasty. All patients improved symptomatically after valvuloplasty, and 26 returned 6.3 +/- 1.5 months later for follow-up catheterization. Immediately after valvuloplasty, aortic valve area increased (before 0.5 +/- 0.2 versus after 0.8 +/- 0.2 cm2, p less than 0.01), cardiac output (before 4.3 +/- 1.2 versus after 4.4 +/- 1.3 liters/min) and ejection fraction (before 51 +/- 18% versus after 52 +/- 17%) did not change and diastolic indexes worsened, signified by a decrease in peak filling rate (before 247 +/- 80 versus after 226 +/- 78 ml/s, p less than 0.01) and increase in the time constant of isovolumetric relaxation (tau) (before 78 +/- 29 versus after 96 +/- 40 ms, p less than 0.01) and the modulus of chamber stiffness (before 0.107 +/- 0.071 versus after 0.141 +/- 0.083, p less than 0.01). At follow-up catheterization, 16 patients continued to have symptomatic improvement (group 1) and 10 had recurrence of symptoms (group 2). Aortic valve area, cardiac output and ejection fraction at follow-up catheterization in both groups were similar and unchanged from values before valvuloplasty.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pathophysiology of isolated systolic hypertension in elderly patients: Doppler echocardiographic insights

Systemic hemodynamics were evaluated with aortic pulsed wave Doppler echocardiography in 79 elderly subjects with isolated systolic hypertension participating in the Systolic Hypertension in the Elderly Program (SHEP) and were compared with the values in 39 normal age-matched subjects. Cardiac output was elevated (4.50 +/- 1.13 L/min versus 3.94 +/- 1.12 L/min, p less than 0.05) in patients with isolated systolic hypertension in comparison with values in normal elderly subjects. Systemic vascular resistance did not differ between both groups (2140 +/- 536 dyn.sec/cm-5 versus 2011 +/- 553 dyn.sec/cm-5, p = NS). The mean acceleration of blood during left ventricular ejection was similar in patients with isolated systolic hypertension in comparison with normals (12.6 +/- 5.6 m/sec2 versus 11.5 +/- 3.5 m/sec2, p = NS). Patients with isolated systolic hypertension had significantly decreased arterial compliance, as measured by the stroke volume-to-pulse pressure ratio (0.77 +/- 0.26 cm3/mm Hg versus 1.11 +/- 0.30 cm3/mm Hg, p less than 0.0001). The prevalence of aortic and mitral regurgitation as well as valvular and annular calcification did not differ between analyzed groups. Isolated systolic hypertension in elderly patients appears to be multifactorial, with reduced arterial compliance and increased cardiac output both playing a role.     

Hemodynamics of the Mueller maneuver in man: right and left heart micromanometry and Doppler echocardiography

Ten subjects with normal hemodynamics were studied during elective cardiac catheterization with right and left heart multisensor micromanometry to assess hemodynamic responses to the Mueller maneuver. Simultaneous right and left circulatory hemodynamics and left ventricular, pulmonary arterial, and aortic pressures were recorded, in addition to pulmonary arterial and aortic flow velocities. Steady-state cardiac outputs were determined by thermal dilution. Aortic systolic and mean pressures were not significantly changed during the Mueller maneuver, in contrast to a lower diastolic (p = .019) and higher pulse pressure (p = .016). Mean right atrial pressure (+/- SE) decreased from 7 +/- 1 to -17 +/- 4 mm Hg (p = .0002) and the right atrial "x" descent was markedly accentuated. Left ventricular end-diastolic pressure decreased from 12 +/- 4 to -3 +/- 13 mm Hg (p = .0025). Systemic vascular resistance and left ventricular peak positive dP/dt were increased during the Mueller maneuver (p less than .02), cardiac output and stroke volume were reduced (p less than .05), and there was no significant change in heart rate. Right and left peak flow velocities showed a trend toward a bilateral decrease (right, p = .054; left, p greater than .1), and times to peak flow velocity were increased in the pulmonary artery (p = .007) and reduced in the aortic root (p = .03). Normal subjects were studied separately by pulsed Doppler echocardiography. During the sustained Mueller maneuver, the internal jugular and right ventricular dimensions decreased, and superior vena cava Doppler flow was reduced.(ABSTRACT TRUNCATED AT 250 WORDS)     

Arterial baroreflex control of sympathetic nerve activity during elevation of blood pressure in normal man: dominance of aortic baroreflexes

Arterial baroreceptors in the carotid sinus (CBR) and aortic arch (ABR) regions exert important control over heart rate and peripheral vascular responses to changes in arterial pressure. The relative roles of these two baroreflex pathways on control of sympathetic nerve activity during sustained elevation of arterial pressure in man is unknown. We therefore studied the relative contributions of the carotid versus the aortic baroreflexes on the control of muscle sympathetic nerve activity (MSNA) during elevation of arterial pressure in normal human subjects. In eight normal men (group I), we measured MSNA (microneurography) during sustained elevation of arterial pressure produced by intravenous infusion of phenylephrine (PE) alone (combined ABR and CBR activation) versus during PE infusion with superimposed application of sustained external neck pressure (NP). NP was applied during sustained PE infusion to eliminate the increase in transmural carotid sinus pressure and thus remove CBR activation, thereby causing ABR stimulation alone. Mean arterial pressure was measured directly, central venous pressure was held constant during PE infusion, and MSNA was measured as total activity (burst frequency X amplitude) and expressed as units. Infusion of PE (ABR and CBR activation) increased mean arterial pressure from 87.2 +/- 2.8 to 94.9 +/- 2.9 mm Hg (+/- SE, p less than .001). This was accompanied by a decrease in heart rate from 65.8 +/- 3.4 to 56.1 +/- 3.3 beats/min (p less than .001) and a decrease in MSNA from 236.2 +/- 47.5 to 84.5 +/- 19.3 units (p less than .001). During infusion of PE with superimposed NP (ABR activation alone), mean arterial pressure increased further to 101.2 +/- 2.9 mm Hg (p less than .001 versus control or PE alone), and heart rate returned to control levels of 62.9 +/- 2.0 beats/min (p = NS vs control; p less than .01 PE vs PE plus NP), but MSNA remained reduced at 48.6 +/- 9.2 units (p less than .01 vs control; p = NS vs PE alone). Thus, combined activation of ABR and CBR resulted in a 65 +/- 5% attenution of MSNA, while activation of ABR alone resulted in a 73 +/- 7% attenuation of MSNA. In a separate series of experiments in seven subjects (group II) we used sustained external neck suction alone to activate the CBR (leaving the ABR either unchanged or minimally deactivated) and studied the MSNA responses to this CBR activation.(ABSTRACT TRUNCATED AT 400 WORDS)     

Aorta-left ventricle coupling in permanent arterial hypertension using Doppler echocardiography

We have studied 12 sustained hypertensive patients (H) (9 men and 3 women) untreated and without other heart disease than a left ventricular hypertrophy, 37 to 70 years of age (mean 56 +/- 12) and 12 normotensive subjects (N) of the same sex and 35 to 77 years of age (mean 52 +/- 16 ans). We have measured 1) arterial pressure (AP) by a standard mercury sphygmomanometer, 2) diameter of ascending aorta (AD), end diastolic left ventricular radius (r) and thickness (Th) by M mode echocardiography with 2D echo control., 3) isthmus-diaphragm pulse wave delay (PWD) from aortic velocity curves recorded in the isthmus and diaphragm aortic crossing by pulsed doppler. We derived 1) the pulse wave velocity (PWV) as PW = SL/PWD where SL is the sternal length, 2) PWV/AD ratio as an indirect index of characteristic impedance, 3) Th/r and LV mass (m) according to Teichholz formula: (table; see text) In both groups 1) m is significantly correlated with SAP (r = 0.67 p less than 0.001), PP (r = 0.61 p less than 0.001), PWV (r = 0.52 p less than 0.01) but not with PWV/AD; 2) Th/r ratio is significantly correlated with SAP (r = 0.64 p less than 0.001), PP (r = 0.63 p less than 0.001), PWV (r = 0.53 p less than 0.001) and PWV/AD (r = 0.41 p less than 0.05). Relationship between PWV and age of H is linear (r = 0.75 p less than 0.001) and shifted at left of that of N which is also linear (r = 0.061 p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Ventricular/vascular interaction in patients with mild systemic hypertension and normal peripheral resistance

Total left ventricular external power and aortic input impedance spectra were calculated from recordings of pulsatile pressure and flow in the ascending aorta of 22 human subjects undergoing cardiac catheterization. Eleven subjects had increased aortic pressure (systolic 153 +/- 3.8[SEM] mm Hg, p less than .001; diastolic 91 +/- 2.4 mm Hg, p less than .03; mean 118 +/- 2.4 mm Hg, p less than .001) and constituted the group with mild hypertension (average age 50 +/- 1.9 years). The other 11 (age-matched) subjects had normal arterial pressures and constituted the control group. Cardiac output in the hypertensive group was abnormally high (6.9 +/- 0.3 liters/min, p less than .04) compared with that in control subjects (6.1 +/- 0.2 liters/min), so that peripheral resistance was similar. Characteristic aortic impedance (index of aortic elastance) was increased in the hypertensive group (142 +/- 19 vs 72 +/- 4.5 dyne-sec-cm-5, p less than .002), as was the fluctuation of impedance moduli and phase. These elevated pulsatile components of arterial load were associated with a significant (p less than .002) increase in pulsatile left ventricular external power (89%), and the increased cardiac output was associated with a significant (p less than .001) increase in steady flow power (31%). The ratio of pulsatile to total power was also increased (38%) in the hypertensive group (p less than .001). Increased characteristic aortic impedance in the hypertensive group suggests that the human aorta is stiffer, and fluctuations in the impedance spectra suggest increased or less dispersed wave reflections.(ABSTRACT TRUNCATED AT 250 WORDS)     

Assessment of arterial distensibility in patients with cardiac syndrome X

This study aims to investigate arterial distensibility by using carotid-femoral (aortic) pulse wave velocity measurements in patients with cardiac syndrome X. The authors studied 10 patients with cardiac syndrome X (mean age 49.4 +/-7.5, 39 to 67 years old, 3 men) and 10 healthy subjects (mean age 50.0 +/-10.5, 38 to 70 years old, 3 men). Carotid-femoral pulse wave velocity measured by a Complior Colson device was calculated for each patient. The carotid-femoral pulse wave velocity was increased in patients with cardiac syndrome X as compared with age-matched control subjects (10.25 +/-1.28 vs 8.95 +/-0.89 m/s, p = 0.01). In contrast, there were no significant differences in the age, weight, height, body mass index, waist/hip ratio, systolic blood pressure, diastolic blood pressure, mean blood pressure, pulse pressure, and heart rate (p=0.76,p=0.17,p=0.36,p=0.08, p=0.21,p=0.14,p=0.89,p=0.30,p=0.10, p = 0.36, respectively). No significant correlation was found between pulse wave velocity and age, sex, height, weight, heart rate, systolic blood pressure, diastolic blood pressure, mean blood pressure, and pulse pressure in the studied groups (p>0.05). The arterial distensibility was decreased in patients with cardiac syndrome X. The deterioration in these patients showed that this disease might be a more generalized disturbance of the vasculature. Measurements of carotid-femoral pulse wave velocity may provide a simple and noninvasive technique to identify patients at increased risk of vascular disease.     

Effects of sublingual nitrate in patients receiving sustained therapy of isosorbide dinitrate for coronary artery disease

To examine the effects of sublingual isosorbide dinitrate (ISDN) in patients receiving sustained ISDN therapy, 24 patients with coronary artery disease were divided into 2 groups. Group C comprised 12 patients without sustained ISDN therapy and group N included 12 patients with sustained ISDN therapy. Before and during administration of sublingual ISDN in both groups, aortic systolic pressure, left ventricular end-diastolic pressure and coronary artery diameter were examined at cardiac catheterization. During sublingual ISDN, the aortic systolic pressure decreased by 20 +/- 6% (138 +/- 26 to 112 +/- 27 mm Hg, p less than 0.01) in group C and 10 +/- 6% (127 +/- 26 to 113 +/- 23 mm Hg, p less than 0.01) in group N (p less than 0.01, group C vs group N). The left ventricular end-diastolic pressure decreased by 65 +/- 16% (11 +/- 5 to 4 +/- 3 mm Hg, p less than 0.01) in group C and 43 +/- 14% (12 +/- 5 to 7 +/- 3 mm Hg, p less than 0.01) in group N (p less than 0.01, group C vs group N). During sublingual ISDN, the diameters of the proximal and distal segments of the left anterior descending and circumflex coronary arteries increased more significantly in group C than in group N (p less than 0.01, group C vs group N). Thus, sublingual ISDN produced less reduction of aortic systolic pressure and left ventricular end-diastolic pressure, and less dilation of coronary artery diameter in patients receiving sustained therapy with ISDN than in those without sustained therapy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Attenuation of the microcirculation in young patients with high-output borderline hypertension

Previous studies have shown abnormalities of the microvasculature in the spontaneously hypertensive rat and human subjects with established hypertension. We have studied the conjunctival microvasculature in relation to systemic and forearm hemodynamics in 24 normal subjects (NL) and 10 subjects with intermittent elevation of blood pressure (BHT). Macrophotographs of the conjunctival circulation were measured for arteriolar diameter and density of arterioles, capillaries, and venules. Blood pressure was measured by Arteriosonde, cardiac index by echocardiography, and forearm hemodynamics by mercury-filled strain-gauge venous occlusion plethysmography. Average diastolic blood pressure in the NL group was 74 +/- 1.7 mm Hg, while that of the BHT subjects was 89 +/- 3.1 mm Hg (p less than 0.005). Capillary density, venous density, and total vascular density were significantly lower in the BHT than NL group, while arteriolar density did not differ significantly. Cardiac index was significantly higher, and peripheral vascular resistance significantly lower, in the BHT as compared to the NL subjects. Forearm blood flow was higher in the NL subjects. The diameter of the preterminal arterioles of the BHT subjects was 27% greater than NL (p less than 0.02). The capillary density was inversely related to the cardiac index (r = -0.482, p less than 0.01), but was not related to blood pressure (r = -0.207). We conclude that the high cardiac output phase of early essential hypertension in humans is accompanied by a reduction in the number of filtering capillaries, and that the rarefaction of capillaries is more closely related to the elevation of cardiac output than to raised blood pressure.     

Aortic diameter and pressure-flow sequence identify mechanism of blood flow during external chest compression in dogs

Aortic flow and pressure relations and aortic diameter were examined during sinus rhythm, internal cardiac massage, vest cardiopulmonary resuscitation, conventional manual cardiopulmonary resuscitation and high impulse manual cardiopulmonary resuscitation in 14 anesthetized large dogs. During sinus rhythm and during internal cardiac massage, ascending aortic flow and pressure increased simultaneously and the rise in ascending aorta pressure preceded the rise in descending aortic pressure by (mean +/- SEM) 28 +/- 4 and 30 +/- 1 ms, respectively. In contrast, during vest, conventional and high impulse cardiopulmonary resuscitation, ascending aortic flow lagged behind the initial rise in aortic pressure by 40 +/- 4 to 46 +/- 4 ms and ascending and descending aortic pressure increased simultaneously (p less than 0.001 for each external compression mode versus sinus rhythm and internal massage). The ratio of pulse pressure to stroke volume increased by an order of magnitude during all modes of external chest compression (p less than 0.001 versus sinus rhythm and internal massage) and aortic diameter decreased during vest and high impulse cardiopulmonary resuscitation (p less than 0.05 versus sinus rhythm and internal massage). The hemodynamics of external chest compression depart from the normal physiologic sequence of stroke volume-induced increase in aortic pressure and diameter. The rise in aortic pressure precedes flow into the aorta, stroke volume does not fully account for pulse pressure, and aortic diameter decreases during chest compression. These data support the hypothesis that blood flow is due to fluctuations in intrathoracic pressure for high impulse as well as vest and conventional cardiopulmonary resuscitation.     

Preload, adrenergic activity, and aortic compliance in normal and hypertensive patients

Aortic compliance is a major determinant of systolic blood pressure and of impedance to left ventricular ejection. However, little is known about its regulating factors. To assess the effects of preload and adrenergic activity on aortic compliance, we studied 10 normal subjects and nine untreated hypertensive patients at rest and during lower body negative pressure. Aortic compliance was measured invasively from the diastolic decay of the aortic pressure tracing and systemic vascular resistance. Preload was decreased stepwise by lower body negative pressure (-5 to -40 mm Hg) while adrenergic activity was assessed by the change in plasma norepinephrine at a maximum level of negative pressure suction. At rest, aortic compliance was lower in hypertensive subjects compared with its value in normal individuals (0.048 +/- 0.012 [SD] versus 0.071 +/- 0.009 units, p less than 0.001) but correlated inversely with systolic blood pressure in both groups (r = -0.64 in normotensive individuals, r = -0.83 in hypertensive subjects, r = -0.88 for the whole group, p less than 0.001 for all). Whereas resting pulmonary wedge pressure was higher in hypertensive subjects compared with normal individuals (16 +/- 4 [SD] versus 11 +/- 3 mm Hg, p less than 0.05), resting plasma norepinephrine levels were not different between the two groups (261 +/- 139 versus 251 +/- 103 pg/ml). Neither of these two resting indices correlated with baseline aortic compliance in both normotensive individuals and hypertensive patients. During lower body negative pressure (LBNP), cardiac filling pressure (right atrial pressure and pulmonary wedge pressure) as well as cardiac output decreased in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of age and end-stage renal disease on the stiffness of carotid wall material in hypertension

BACKGROUND: Incremental elastic modulus, which is the slope of the relationship between stress and strain of arterial vessels, is a marker of wall material stiffness. The radial artery incremental elastic modulus, which is not influenced by age, is normal or reduced in patients with essential hypertension but increased in patients with end-stage renal disease. Authors of studies on hypertension largely ignore the question of whether the incremental elastic modulus, measured in the common carotid artery as typical of a central artery site, differs according to age or to the presence of end-stage renal disease or both. SUBJECTS AND METHODS: The carotid incremental elastic modulus was measured in 208 hypertensive patients divided into four groups according to age (< or = or > 55 years) and the presence or absence of end-stage renal disease. The incremental elastic modulus was calculated from transcutaneous measurements of arterial internal diameter and wall thickness (echo-tracking device) and carotid pulse pressure (tonometry). Because the four groups of subjects had the same mean arterial pressure, the static incremental elastic modulus was calculated both in isobaric conditions and for the same wall stress. RESULTS: In nonuremic subjects, lumen diameter, wall thickness and the incremental elastic modulus were significantly (P < 0.001) increased in older subjects whereas compliance and distensibility were decreased. The mean (+/- SD) elastic modulus was 0.41 +/- 0.14 x 10(3) kPa in younger and 0.71 +/- 0.28 x 10(3) kPa in older subjects. In uremic subjects, the corresponding values were 0.48 +/- 0.30 and 0.90 +/- 0.49 x 10(3) kPa, and therefore higher than in nonuremic subjects, irrespective of age. Multiple regression analysis showed that age, mean arterial pressure and the presence of end-stage renal disease independently influenced carotid diameter, distensibility and the incremental elastic modulus. CONCLUSIONS: In hypertensive patients, the carotid incremental elastic modulus is increased independently in aging men and women and in the presence of uremia. This increase is not dependent on mechanical factors such as the level of mean blood pressure.