Search

BACKGROUND Resistance, pulse wave velocity, and wave reflections have been shown to be increased in patients with essential hypertension compared with normotensive controls. These alterations are completely normalized by nitroprusside infusion but exacerbated during beta-adrenergic blockade, suggesting an enhanced smooth muscle tone that is in part modulated by adrenergically mediated vasodilation. The present study was performed to examine the extent to which this apparently enhanced smooth muscle tone is a result of alpha-adrenergically mediated vasoconstriction. METHODS AND RESULTS Age-matched normotensive and hypertensive Chinese subjects were instrumented with catheter-tipped micromanometers and an electromagnetic flow velocity sensor positioned in the ascending aorta. Aortic impedance and wave reflection properties were obtained from Fourier analysis of the pressure and flow signals during baseline conditions, after beta-blockade with propranolol (0.15 mg/kg i.v.), and after alpha-blockade with intravenous phentolamine (range, 15-80 mg) that was sufficient to either normalize blood pressure or produce a pressure that could not be further lowered. Compared with normotensives, in the baseline state, hypertensives had elevated resistance (1,962 versus 1,268 dyne.sec/cm5, p less than 0.001), total power (1,893 versus 1,568 mW, p less than 0.08), reflected pressure wave component (25.6 versus 13.5 mm Hg, p less than 0.001), ratio of reflected to forward wave (0.65 versus 0.42, p less than 0.001), and pulse wave velocity as determined from the frequency of the first zero-crossing of impedance phase angle (4.6 versus 3.5 Hz, p less than 0.03). During combined alpha- and beta-adrenergic blockade, blood pressure decreased into the normal range (from 162/103 to 131/87 mm Hg) but was still somewhat higher than that in the normotensive subjects. Resistance (1,914 dyne.sec/cm5, p less than 0.03), reflected wave (19.5 mm Hg, p less than 0.01), and ratio of reflected to forward wave (0.61, p less than 0.001) were, however, persistently elevated above normal values. CONCLUSIONS alpha-Adrenergically mediated vasoconstriction cannot account for all of the hemodynamic alterations seen in essential hypertension.

Background : Pulse pressure (PP) and systolic blood pressure (SBP), in central and peripheral arteries, may contribute differently to predictions of damage to different target organs and mortality. Method : We examined the relations of PP and SBP in central (calibrated tonometric carotid pulse) and peripheral (brachial, mercury sphygmomanometer) arteries to left ventricular mass index (LVMI), carotid intima-media thickness (IMT), glomerular filtration rate (GFR), and 10-year all-cause and cardiovascular (CV) mortality in 1272 participants (47% women, aged 30 –79 years) from a community of homogeneous Chinese. Result : LVMI was more strongly related to SBP (r = 0.420 and 0.379 for central and brachial arteries, respectively) than PP (r = 0.374 and 0.285, correspondingly). In contrast, IMT and GFR were more strongly related to central PP and SBP (r = 0.265 and 0.252 for IMT, and r = −0.256 and −0.218 for GFR, respectively) than brachial PP and SBP. A total of 130 participants died, 37 from CV causes. In univariate analysis, all four blood pressure variables significantly predicted all-cause and CV mortality. After adjustment for age, sex, current smoking, glucose, cholesterol/high-density-lipoprotein-cholesterol ratio, carotid-femoral pulse wave velocity, LVMI, IMT, and GFR, none of the blood pressure variables predicted all-cause mortality (Figure 1A ). Only central SBP independently predicted CV mortality (Hazards ratio = 1.21 per 10 mmHg) in multivariate analysis (Figure 1B ). Conclusion : PP and SBP contribute differently to damage to different target organs. Central SBP is more valuable than other blood pressure variables in predicting CV mortality.

Background Central aortic pressures and waveform convey important information about cardiovascular status, but direct measurements are invasive. Peripheral pressures can be measured noninvasively, and although they often differ substantially from central pressures, they may be mathematically transformed to approximate the latter. We tested this approach, examining intersubject and intrasubject variability and the validity of using a single averaged transformation, which would enhance its applicability. Methods and Results Invasive central aortic pressure by micromanometer and radial pressure by automated tonometry were measured in 20 patients at steady state and during hemodynamic transients (Valsalva maneuver, abdominal compression, nitroglycerin, or vena caval obstruction). For each patient, transfer functions (TFs) between aortic and radial pressures were calculated by parametric model and results averaged to yield individual TFs. A generalized TF was the average of individual functions. TFs varied among patients, with coefficients of variation for peak amplitude and frequency at peak amplitude of 24.9% and 16.9%, respectively. Intrapatient TF variance with altered loading (>20% variation in peak amplitude) was observed in 28.5% of patients. Despite this, the generalized TF estimated central arterial pressures to ≤0.2±3.8 mm Hg error, arterial compliance to 6±7% accuracy, and augmentation index to within −7% points (30±45% accuracy). Individual TFs were only marginally superior to the generalized TF for reconstructing central pressures. Conclusions Central aortic pressures can be accurately estimated from radial tonometry with the use of a generalized TF. The reconstructed waveform can provide arterial compliance estimates but may underestimate the augmentation index because the latter requires greater fidelity reproduction of the wave contour.

Aortic impedance, wave reflection magnitude, and compliance were measured in patients with Marfan's syndrome during diagnostic cardiac catheterization. Impedance and wave reflections were calculated from standard Fourier series analysis of ascending aorta micromanometer pressure and electromagnetic flow records. Compliance was estimated by a method recently proposed that uses the area under the pressure-time curve assuming a two-element Windkessel model of the circulation. Measurements were made in the baseline state, during vasodilatation with nitroprusside, after beta-adrenergic receptor blockade with intravenous propranolol, and during vasodilatation after beta-blockade. Marfan's syndrome produces alterations from normal in some hemodynamic variables: during baseline conditions, the magnitude of wave reflection was higher than in normal patients. This was normalized by vasodilatation and further increased by beta-blockade. Despite the greatly dilated aortic root, the aortic characteristic impedance was in the normal range, suggesting increased aortic wall stiffness. The baseline total arterial compliance was greatly increased with nitroprusside and was reduced by beta-blockade. beta-Blockade did not decrease the maximum acceleration of blood into the ascending aorta. These are the first detailed measurements of hemodynamic indexes in this disease. The results suggest that acute beta-blockade is not necessarily beneficial in reducing hemodynamic loading on an already dilated aortic root.

Intra-aortic balloon counterpulsation is capable of reducing afterload in patients with unstable angina. Whether it is also capable of augmenting coronary blood flow to poststenotic myocardium is controversial. We studied seven patients receiving maximal drug therapy and requiring balloon pumping for unstable angina as balloon volume and assist ratio were altered. All patients had greater than 90% stenosis of the proximal left anterior descending coronary artery. With maximal augmentation (40 cc balloon volume, 1:1 assist ratio) great cardiac vein flow, representing the efflux from the left anterior descending coronary artery bed, rose from a baseline of 52 +/- 20 to 67 +/- 25 ml/min (mean +/- SD, p = .004) and mean aortic diastolic pressure increased from 77 +/- 13 to 99 +/- 33 mm Hg (p = .004). Increased great cardiac vein flow correlated with increased mean aortic diastolic pressure across changes in balloon volumes (off, 20 cc, 30 cc, and 40 cc) and changes in assist ratio (off, 1:4, 1:2, and 1:1) (p = .02). However, the intermediate balloon volumes produced great cardiac vein flows at an intermediate level between full assist and no assist (p less than .05), whereas the intermediate assist ratios did not augment flow. Thus balloon pumping increased flow to a bed fed by collateral vessels or critical stenoses; this increased flow correlated with increased aortic diastolic pressure, indicating probable loss of autoregulatory ability.

We studied the effect of nitroprusside on the hydraulic vascular load of the right and left ventricle in seven patients with severe left ventricular failure. At doses of 0.25-0.75 micrograms/kg/min, stroke volume increased progressively from 40.1 to 48.6 ml and left ventricular end-diastolic pressure decreased from 24.5 to 11.2 mm Hg. Accompanying this improvement in left ventricular performance were dose-related decreases in mean ventricular pressures, pulmonic and systemic resistances and the lower-frequency components of input impedance moduli. Characteristic impedance and both total and oscillatory external power were decreased in the pulmonic, but not the aortic, vasculature. In this class of patients, right ventricular unloading is a striking and direct effect of nitroprusside and may account, in part, for improved left ventricular performance through ventricular interdependence.

Right ventricular loading leads to diastolic septal flattening in man without necessarily requiring right ventricular pressure to exceed left ventricular pressure. This observation suggested that the unstressed septal configuration is flat and that its normal concave shape is due to the left-to-right transseptal pressure gradient. To examine this hypothesis, we studied septal configuration by two-dimensional echocardiography in nine patients with normal global and regional left ventricular function during surgery for coronary artery disease. The transseptal pressure gradient was obtained from pulmonary capillary wedge pressure minus right atrial pressure. Measurements were obtained at control (open chest, intact pericardium [C]), with the pericardium open (OP), on cardiopulmonary bypass (CPB), and after cardiac arrest (CA). There were no changes in any measurements between C and OP or between CPB and CA. Left ventricular end-diastolic cavity area decreased from 16.5 +/- 2.1 cm2 at C to 11.1 +/- 4.5 cm2 after CPB, and further decreased to 8.9 +/- 3.5 cm2 after CA (p less than .001), yet the septum flattened, as shown by an increase in its radius of curvature from 1.7 +/- 0.5 cm during C to 2.5 +/- 0.7 cm after CPB, and to 2.9 +/- 1.0 cm after CA (p less than .001), or from 0.4 +/- 0.1 to 0.8 +/- 0.4 to 1.1 +/- 0.5 U (p less than .001) when normalized for cavity area. Diastolic transseptal pressure gradient was reduced from 4.1 +/- 2.3 mm Hg during C to 1.1 +/- 1.8 mm Hg after CPB, and to 0.5 +/- 1.4 mm Hg after CA (p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

We studied the function of right internal jugular vein valves during cardiac catheterization in 32 patients and external jugular vein valves in vitro from 13 dogs. Patients with normal central venous pressure had competent valves during cough-induced transvalvular pressure gradients of 52.4 +/- 8.6 mm Hg. Ten of 15 patients with elevated central venous pressure had either incompetent or absent internal jugular valves, the latter occurring only in patients with long-standing, severe tricuspid regurgitation. During coughing, competent valves were also demonstrated in the left internal jugular and in the right and left subclavian veins. The excised canine valves were competent at a static transvalvular pressure of 81.8 +/- 3.7 mm Hg. Five of six excised valves remained competent during pulsatile transvalvular pressure of 64.8 +/- 1.9 mm Hg. Thus, thoracic inlet venous valves are usually competent during sudden increases in intrathoracic pressure. These valves may play an important role in establishing the extrathoracic arteriovenous pressure gradient necessary for forward blood flow during cardiopulmonary resuscitation and other states with high intrathoracic pressure.

Echocardiograms were performed on 105 male participants in the National Institutes on Aging's volunteer Longitudinal Study Program. All subjects (25--84 years of age) were physically active and had no evidence of hypertension or cardiovascular disease. Measurements were made of the initial diastolic (E-F) slope of the anterior mitral valve leaflet, the aortic and left ventricular cavity dimensions, and the thickness of the posterior left ventricular wall. Fractional shortening of the minor semi-axis of the left ventricle and the velocity of circumferential fiber shortening were also determined. It was found that increasing age correlated with a decrease mitral valve E-F slope and increased aortic root diameter and left ventricular wall thickness. Aging did not affect left ventricular cavity dimension, fractional shortening of the minor semi-axis, and velocity of circumferential fiber shortening. These findings suggest that aging in the normal male is associated with altered left ventricular diastolic filling, increased aortic root diameter and left ventricle hypertrophy but little change in contractile ability in the resting state.