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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.

Purpose Downsizing pulsatile devices requires an increase of beat rate if flow capacity is to be maintained. We applied this concept to the preclinical MagScrew total artificial heart (TAH). Description The device fills passively with a stroke volume of 45 ml and beat rates up to 250 beats per minute (bpm). Evaluation Stable hemodynamics were observed during a 30-day bovine implant with a flow of 8.7 ± 1.2 L/min at beat rates of 204 ± 18 bpm. Device filling was exceptional up to 250 bpm generating flow of greater than 12 L/min. Beat rate adapted to preload in a way similar to a Frank-Starling response. Left and right atrial pressures were balanced. The aortic pulse pressure was 49–70 mm Hg, which translates to a pulsatility index of 0.49–0.77. Organ functions were preserved and blood damage did not occur. Conclusions Increasing the beat rate while downsizing the MagScrew TAH was successful with strong flow generation by passive filling. Pulsatility was maintained at high beat rates. This innovative approach may be used to develop small pulsatile pumps.

Some 10% to 15% of hypertensive patients have hyperaldosteronism, an increased ambulant aldosterone-to-renin ratio. As aldosterone reduces arterial compliance, we examined the relationship between aldosterone-to-renin ratio, aortic blood pressure (BP), arterial stiffness, and the effect of spironolactone in a hypertensive population.In 24 untreated patients (mean age 51 +/- 2 years, 10 women), we assessed arterial stiffness by augmentation index-height of the late systolic peak in the aorta, pulse pressure (Sphygmocor), and aortic pulse wave velocity (Complior).There were significant positive correlations between the aldosterone-to-renin ratio and aortic systolic pressure, aortic pulse pressure, and augmentation index and negative correlations with pulse pressure amplification, but none with brachial BP or pulse wave velocity. After randomization in a cross-over design to 50 mg of spironolactone or 2.5 mg of bendroflumetazide for 4 weeks with washout period of 1 month, both drugs significantly reduced brachial BP, but only spironolactone reduced (P.001) pulse wave velocity and augmentation index, which remained significant when corrected for its greater reduction in mean BP. There were significant (P.001) positive correlations between the ratio and decrease in aortic systolic (r = 0.78), mean (r = 0.75), diastolic BP (r = 0.66), aortic pulse pressure (r = 0.69, augmentation index (r = 0.64) and with, brachial systolic pressure (r = 0.66), brachial pulse pressure (r = 0.44, P.05) and pulse pressure amplification (r = 0.46, P.05). Such relationships were not found with pulse wave velocity.The aldosterone-to-renin ratio may have an important role in determining arterial stiffness, particularly wave reflection and aortic systolic pressure and is of predictive value for the responsiveness to spironolactone. Aldosterone antagonism has BP-independent effects on arterial stiffness.

Background In the general population, pulse pressure (PP) is a correlate of cardiovascular outcomes. Few data are available regarding the links between PP and documented coronary artery disease (CAD). Methods From July 2000 to January 2002, a total of 1337 patients referred for a first diagnostic coronary angiogram at 75 participating centers were prospectively included. Of these individuals, 280 patients receiving no hypertensive therapy constituted the study population. Pulse pressure was recorded in the aortic root before angiography, and baseline characteristics, medical history, treatment used, and data from coronary angiography were recorded. Results In the whole population, aortic PP strongly correlated with the presence and extent of CAD in univariate analyses. However, the correlation disappeared in multivariate analysis, and a strong interaction with gender was found. In women (n = 82), aortic PP was not an independent predictor of CAD. However, in men (n = 198) an independent correlation between aortic PP and CAD was found, together with age and hypercholesterolemia. In addition, PP was strongly correlated with the extent of CAD (no disease, 51 ± 16 mm Hg; one or two stenoses, 54 ± 18 mm Hg; and more than two stenoses: 64 ± 20 mm Hg). Conclusions In this multicenter study, aortic PP was significantly correlated with the presence and extent of CAD in patients without antihypertensive therapy. This correlation, however, was independent of other risk factors for CAD in men but not in women.

Objective: The aim of this study was to assess changes in early and late haemodynamic status after the Norwood procedure (NP), caused by the implementation of right ventricle-to-pulmonary artery shunt (RV-PA). Methods: A consecutive series of 68 children with hypoplastic left heart syndrome underwent NP: Group 1 (n ¼ 31) with the application of a modified Blalock-Taussig shunt and Group 2 (n ¼ 37) with RV-PA. Haemodynamic data from the early postoperative period (72 h after the operation) and cardiac catheterisation data, as well as blood tests before the hemi-Fontan procedure (HF) were analysed. Univariate (x 2 test, Mann ‐ Whitney’s and Student’s t-tests) and multiple regression analysis were carried out. Results: In Group 1, circulatory collapse requiring resuscitation occurred in 15 (48.4%) children, within 72 h after the procedure. The resuscitation was unsuccessful in nine (29%) cases. The operative mortality (30 days) was 35%. In Group 2, two (5%) children died within the early and two (5%) within the late postoperative period. The postoperative course in the remaining children from Group 2 was uneventful. In Group 2 there was a significantly higher mean diastolic pressure after NP (P , 0:05). The arterial pulse pressure after NP was significantly lower in Group 2 (P , 0:05). Before HF, the application of RV-PA was associated with a lower Qp:Qs ratio (P ¼ 0:020), lower aortic pulse pressure (P ¼ 0:004) and lower aortic oxygen saturation (P ¼ 0:039). Conclusions: A stable haemodynamic status due to independent coronary perfusion, higher diastolic and lower pulse pressure is the most advantageous effect of RV-PA, resulting in a lower mortality and morbidity after NP. A lower Qp:Qs ratio eliminates the danger of the ventricular volume overload and ensures good conditions for the development of the pulmonary circulation before HF. q 2003 Elsevier Science B.V. All rights reserved.

Background— Biventricular (BiV) and left ventricular (LV) pacing similarly augment systolic function in left bundle-branch block (LBBB)-failing hearts despite different electrical activation. We tested whether electrical synchrony is required to achieve mechanical synchronization and functional benefit from pacing. Methods and Results— Epicardial mapping, tagged MRI, and hemodynamics were obtained in dogs with LBBB-failing hearts during right atrial, LV, and BiV stimulation. BiV and LV both significantly improved chamber hemodynamics (eg, 25% increase in dP/dt max and aortic pulse pressure) compared with atrial pacing-LBBB, and this improvement correlated with mechanical resynchronization. Electrical dispersion, however, decreased 13% with BiV but increased 23% with LV pacing ( P Conclusion— Improved mechanical synchrony and function do not require electrical synchrony. Mechanical coordination plays the dominant role in global systolic improvement with either pacing approach.

ObjectivesWe characterized the relationship between systolic ventricular function and left ventricular (LV) end-diastolic pressure (LVEDP) in patients with heart failure (HF) and baseline asynchrony during ventricular stimulation.BackgroundThe role of preload in the systolic performance improvement that can be obtained in HF patients with LV stimulation is uncertain.MethodsWe measured the maximum rate of increase of LV pressure, LVEDP, aortic pulse pressure (PP) and the atrioventricular mechanical latency (AVL) between left atrial systole and LV pressure onset in 39 patients with HF. Two subgroups were identified: “responder” if PP improved, or “nonresponder.”ResultsMaximum hemodynamic improvement occurred at an atrioventricular (AV) delay that did not decrease LVEDP. Left ventricular and biventricular (BV) stimulation increased systolic hemodynamics significantly, despite no significant increase in LVEDP. All parameters decreased when the LVEDP was decreased by shorter AV delay. Left ventricular and BV stimulation provided better hemodynamics than right ventricular (RV) stimulation. For the nonresponder subgroup, systolic hemodynamics only worsened during AV delay shortening. For the responder subgroup, optimum PP was achieved when AVL was near zero.ConclusionsRestoration of optimal left atrial-ventricular mechanical timing partly contributes to the hemodynamic improvements observed in this patient subgroup. However, preload alone cannot explain the differences seen between RV and BV stimulation and the contradictory PP decreases even at maximal preload in the nonresponder subgroup. These results may be explained by a site-dependent mechanism such as the degree of ventricular synchrony. Caution should be taken in these patients when optimizing AV delays using echocardiography techniques that focus on LV inflow.

Damage of large arteries is a major factor in the high cardiovascular morbidity and mortality of patients with end-stage renal disease (ESRD). Increased aortic pulse wave velocity (PWV) and brachial pulse pressure (PP) are the principal arterial markers of cardiovascular mortality described in these patients. Whether central (carotid) PP and brachial-carotid PP amplification may predict all-cause (including cardiovascular) mortality has never been investigated. A cohort of 180 patients with ESRD who were undergoing hemodialysis was studied between January 1990 and March 2000. The mean duration of follow-up was 52±36 months (mean±SD). Mean age at entry was 51.5±16.3 years. Seventy deaths occurred, including both cardiovascular and noncardiovascular fatal events. At entry, patients underwent carotid PP measurements (pulse wave analysis), echocardiography, and aortic PWV (Doppler ultrasonography), together with standard clinical and biochemical analyses. On the basis of Cox analyses, after adjustment of age, time on dialysis before inclusion, and previous cardiovascular events, 3 factors emerged as predictors of all-cause mortality: carotid PP, brachial/carotid PP, and aortic PWV. Adjusted hazard ratios for 1-SD increments were 1.4 (1.1 to 1.8) for carotid PP, 0.5 (0.3 to 0.8) for brachial/carotid PP, and 1.3 (1.0 to 1.7) for PWV. Brachial blood pressure, including PP, had no predictive value for mortality after adjustment. These results provide the first direct evidence that in patients with ESRD, the carotid PP level and, mostly, the disappearance of PP amplification are strong independent predictors of all-cause (including cardiovascular) mortality.

quoted saying ‘‘you’re only as old as your arteries.’’ 4 At a pathobiological level, aortic wall stiffness has been associated with processes involving wall matrix, inflammation, and mechanical stress. Increased collagen content and extracellular matrix (arteriosclerosis) is commonly seen in hypertension and aging. In contrast, atherosclerosis relates to endovascular inflammation, increased cellular oxidative stress, and plaque formation; however, both processes can lead to increased vascular stiffness. 5 Patients with increased aortic stiffness have increased aortic pulse wave velocity and reduced arterial compliance. 6 The clinical implication of increased aortic stiffness results in increased afterload on the left ventricle; alteration in coronary perfusion, which affects cardiac diastolic relaxation; and increased myocardial oxygen consumption. Moreover, these surrogates have been tested in multiple trials with important CV outcomes data. Based on the studies so far, it is evident that increased aortic pulse wave velocity is a strong independent predictor of CV risk, regardless of whether it plays a causative role in CV risk or merely serves as a marker of CV disease already present. One example is found in the Strong Heart Study, 7 which evaluated 2405 patients without CV disease at entry with a 5-year follow-up. During this period, 344 patients had CV events that were significantly associated with high central pulse pressure, thus associating high central pulse pressure with increased arterial stiffness. 1 Another study, the Conduit Artery Function Evaluation (CAFE) trial 8 substudy (on behalf of the Anglo-Scandinavian Cardiac Outcomes Trial [ASCOT] Investigators), evaluated the differential impact of BPlowering drugs on central aortic pressure and clinical outcomes. The study enrolled 2073 patients from 5 ASCOT centers after being on treatment for about 1 year. A total of 19,257 patients were enrolled in the ASCOT trial. All patients had hypertension and 3 additional risk factors. They were randomized in a 2 2 factorial design to receive 1 of 2 antihypertensive regimens: amlodipine (5 ⁄10 mg) with or without perindopril (4 ⁄8 mg) or atenolol (50 ⁄100 mg) with or without a diuretic. Despite similar brachial arm systolic BPs in the two treatment arms, there was a significant decrease in both central aortic pulse pressure and central aortic systolic pressure in the angiotensin-converting enzyme (ACE) inhibitor ⁄calcium channel blocker (CCB) arm vs the b-blocker ⁄diuretic arm. This study suggested that ACE inhibitor ⁄CCB treatment was significantly better. In addition, using the Cox proportional hazards modeling, they determined that central aortic pulse pressure was significantly associated with a post hoc‐defined composite outcome of total CV events (unadjusted P

The present study tested the hypothesis that epicardial fat may be associated with augmented central aortic pressure and impaired left ventricular (LV) function. We studied 134 consecutive patients undergoing left-sided cardiac catheterization for coronary artery disease (CAD) and examined the relation of epicardial fat volume measured by multi-detector computed tomography to ascending aortic pressure and LV ejection fraction determined by cardiac catheterization as well as indices of LV diastolic function assessed by Doppler echocardiography [early diastolic mitral annular velocity (e′) and a ratio of early diastolic mitral inflow to annular velocities (E/e′)]. Epicardial fat volume indexed to body surface area correlated positively with age (r = 0.24, P

levels. The group underwent extensive hemodynamic profiling after at least 20 minutes of supine rest, including standard office brachial BP (Omron Hem-705CP) and central BP (radial tonometry with generalized transfer function, SphygmoCor). Central (heart-femoral) and peripheral (brachialankle) PWV were determined by Colin VP 2000. Strength of association was determined by Pearson correlations. Results: Means (ranges) in 78 subjects (44M, 34 F) were: age 55 (19-91) years, weight 84 (48-130) kg, height 167 (140-188) cm. Peripheral BP values (mmHg) were: systolic (S)BP 139 (100-192), diastolic (D)BP 80 (55-132), mean arterial pressure (MAP) 108 (76-162), pulse pressure (PP) 60 (35115). Corresponding central BP values were: SBP 132 (88-195), PP 52 (23-119), radial second systolic peak (P2) 131 (82-203), MAP 103 (75168). Central and peripheral PWV were: hfPWV 1182 (569-2038) and baPWV 1507 (893-3206) cm/sec. Central augmentation index values were: 139 (81-246) %. Table 1 shows correlation coefficients between BP and PWV; baPWVand hfPWV were also strongly correlated (r1⁄4.732). Conclusion: Central and peripheral PWV values are highly correlated with both central and peripheral BP values and to a lesser degree with augmentation index. There were slightly stronger associations between peripheral than central BP and PWV. These findings demonstrate the tight association between a single casual office BP and corresponding PWV values, indicating that SBP and PWV convey similar information.

levels. The group underwent extensive hemodynamic profiling after at least 20 minutes of supine rest, including standard office brachial BP (Omron Hem-705CP) and central BP (radial tonometry with generalized transfer function, SphygmoCor). Central (heart-femoral) and peripheral (brachialankle) PWV were determined by Colin VP 2000. Strength of association was determined by Pearson correlations. Results: Means (ranges) in 78 subjects (44M, 34 F) were: age 55 (19-91) years, weight 84 (48-130) kg, height 167 (140-188) cm. Peripheral BP values (mmHg) were: systolic (S)BP 139 (100-192), diastolic (D)BP 80 (55-132), mean arterial pressure (MAP) 108 (76-162), pulse pressure (PP) 60 (35115). Corresponding central BP values were: SBP 132 (88-195), PP 52 (23-119), radial second systolic peak (P2) 131 (82-203), MAP 103 (75168). Central and peripheral PWV were: hfPWV 1182 (569-2038) and baPWV 1507 (893-3206) cm/sec. Central augmentation index values were: 139 (81-246) %. Table 1 shows correlation coefficients between BP and PWV; baPWVand hfPWV were also strongly correlated (r1⁄4.732). Conclusion: Central and peripheral PWV values are highly correlated with both central and peripheral BP values and to a lesser degree with augmentation index. There were slightly stronger associations between peripheral than central BP and PWV. These findings demonstrate the tight association between a single casual office BP and corresponding PWV values, indicating that SBP and PWV convey similar information.

femoral pulse wave velocity (PWV) and carotid intimamedia thickness (IMT) evaluation. Dietary habits were evaluated through a special diet score (MedDiet score, range 0-55), which assesses adherence to the Mediterranean dietary pattern. Higher values indicate greater adherence to this pattern. Results: Based on the Med-Diet Score, three groups were formed (high 30, intermediate: 21-29 and low 20) with no significant differences in main risk factors between them. Patients with low score had significantly higher LVM, LVMI and E/E’ compared to others. Regarding vascular parameters, aortic stiffness and IMT were inversely correlated to the Med-Diet score. Associations between cardiac and vascular parameters remained significant after adjustment for age and cardiovascular risk factors. Conclusion: Low adherence to the Mediterranean type of diet is significantly associated to impaired left ventricular and vascular structure and performance. Physicians should advise for healthier dietary habits and identify those who may need more intensive follow up.

The pressure pulse does not have the same amplitude in central and peripheral arteries, but it is amplified toward the periphery; the degree of this amplification depends principally on wave reflection. Despite the conventional clinical and epidemiological focus on peripheral pressures, the most physiologically relevant pressures for both cardiac and vascular effects are central pressures. The reflected wave contributes differently in the configuration of the peripheral and central pressure waveform. Therefore, we hypothesized that agents that alter wave reflections could have an unequal effect on central and peripheral pressures in hypertensive patients. Thus, the effect of caffeine was investigated in 10 hypertensive subjects according to a randomized, placebo-controlled, double-blind, crossover design. Central aortic pressures and wave reflection were assessed with applanation tonometry and pulse wave analysis. After caffeine, augmentation index and augmented pressure increased by 4.6%, ( P P

We investigated the functional changes of the systemic vascular system due to prolonged nonpulsatile left heart bypass (NPLHB). Three adult goats underwent pulsatile left heart bypass (PLHB). Two weeks later the PLHB was changed to the NPLHB, which was conducted for 4 weeks. The aortic pulse pressure was 39 and 16 mm Hg during the PLHB and NPLHB, respectively. Systemic vascular resistance (SVR) and the plasma norepinephrine level were measured at the end of PLHB (PUL), and in the 1st, 2nd, 3rd, and 4th weeks of NPLHB (NP1w, NP2w, NP3w, and NP4w). At each point, 1 microg/kg norepinephrine was injected, and the elevation of the SVR (deltaSVR) was calculated. The SVR and the plasma norepinephrine level did not change significantly during the entire course. However, deltaSVR decreased during NPLHB and became significantly lower at NP3w and NP4w than that at PUL (NP3w: 839 +/- 164, NP4w: 746 +/- 268, and PUL: 1,239 +/- 324 dyne x s x cm(-5)). These results strongly indicated that prolonged NPLHB significantly diminished the constrictive function of the vascular system.

Background —Current definitions of hypertension are based on levels of systolic blood pressure (SBP) and diastolic blood pressure (DBP), but not on pulse pressure (PP). We examined whether PP adds useful information for predicting coronary heart disease (CHD) in the population-based Framingham Heart Study. Methods and Results —We studied 1924 men and women between 50 and 79 years of age at baseline with no clinical evidence of CHD and not taking antihypertensive drug therapy. Cox regression, adjusted for age, sex, and other risk factors, was used to assess the relations between blood pressure components and CHD risk over a 20-year follow-up. The association with CHD risk was positive for SBP, DBP, and PP, considering each pressure individually; of the 3, PP yielded the largest χ 2 statistic. When SBP and DBP were jointly entered into the multivariable model, the association with CHD risk was positive for SBP (HR, 1.22; 95% CI, 1.15 to 1.30) and negative for DBP (HR, 0.86; 95% CI, 0.75 to 0.98). Four subgroups were defined according to SBP levels ( Conclusions —In the middle-aged and elderly, CHD risk increased with lower DBP at any level of SBP≥120 mm Hg, suggesting that higher PP was an important component of risk. Neither SBP nor DBP was superior to PP in predicting CHD risk.

Arterial pulse pressure response during the strain phase of the Valsalva maneuver has been proposed as a clinical tool for the diagnosis of left heart failure, whereas responses of subjects with preserved systolic function have been poorly documented. We studied the relationship between the aortic pulse amplitude ratio (i.e., minimum/maximum pulse pressure) during the strain phase of the Valsalva maneuver and cardiac hemodynamics at baseline in 20 adults (42 ± 14 yr) undergoing routine right and left heart catheterization. They were normal subjects ( n = 5) and patients with various forms of cardiac diseases ( n = 15), and all had a left ventricular ejection fraction ≥40%. High-fidelity pressures were recorded in the right atrium and the left ventricle at baseline and at the aortic root throughout the Valsalva maneuver. Aortic pulse amplitude ratio 1) did not correlate with baseline left ventricular end-diastolic pressure, cardiac index (thermodilution), or left ventricular ejection fraction (cineangiography) and 2) was positively related to total arterial compliance (area method) ( r = 0.59) and to basal mean right atrial pressure ( r = 0.57) (each P < 0.01). Aortic pulse pressure responses to the strain were not related to heart rate responses during the maneuver. In subjects with preserved systolic function, the aortic pulse amplitude ratio during the strain phase of the Valsalva maneuver relates to baseline total arterial compliance and right heart filling pressures but not to left ventricular function.

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.

Tilmicosin(TM), a macrolide antibiotic and active ingredient in formulated Micotil 300 (Eli Lilly and Co., Indianapolis, IN, USA), is the active ingredient in a formulated animal product used for the treatment of respiratory tract infections in cattle. Owing to the concern of governmental regulatory agencies over the possibility of an accidental injection of the antibiotic to a livestock handler, the cardiovascular effects of sub lethal doses of TM were evaluated in conscious mixed-breed dogs. Left ventricular function, systemic arterial blood pressure, and heart rate (HR) responses to TM alone and in combination with propranolol(P) or dobutamine HCl(DOB) were evaluated. Dogs were instrumented with indwelling micromanometers implanted in the left ventricular chamber and in the thoracic aorta. Cardiovascular variables were recorded, and the peak value of the first derivative of left ventricular pressure (dp/dt(max)) was used as an index of left ventricular inotropic state. Six treatments were randomly assigned to each of the six dogs using a Latin square design. The six treatments were vehicle, TM alone (2.5 mg/kg of body weight), TM immediately followed by P, and TM immediately followed by 1 of 3 dosages of DOB infused for approximately 45 min. Additionally, doses of TM alone (0.25, 1.0, 2.5, and 5.0 mg/kg) were administered to complete a dose-response curve. TM caused dose dependent decreases in (dp/dt(max)) and aortic pulse pressure. HR increased dose-dependently. Left ventricular end-diastolic pressure increased at the 2.5 and 5.0 mg/kg dosages. Left ventricular systolic pressure was reduced dose-dependently at the 2.5 and 5.0 mg/kg dosages. Treatment with P exacerbated the negative inotropic effect and the decrease in left ventricular systolic pressure, but did not attenuate the tachycardia associated with TM treatment. DOB attenuated the changes in ventricular inotropic state in a dose-dependent manner. DOB infusion also restored left ventricular systolic pressure at dosages of 3 or 10 micrograms/min/kg. Our data indicate that toxic doses of TM may have a negative inotropic effect in conscious dogs. HR increased in a dose-dependent manner and was not the result of beta 1-receptor stimulation. DOB reversed some, but not all, of the effects caused by TM administration.

The aorta is a capacitance vessel that enables transformation of the “on-off” blood-flow characteristics of the left ventricle into a less pulsatile flow in more distal vessels. Thus, a smooth nonpulsatile blood-flow pattern is achieved at capillary level. Arterial wall stiffness determines the degree of energy absorbed by the elastic aorta and its recoil in diastole. Aortic pulse pressure (PP) in health is physiologically lower than peripheral PP. Reduction of elevated aortic systolic blood pressure (SBP) protects circulation from pressure-induced damage. Maintaining aortic diastolic blood pressure (DBP) ensures adequate coronary perfusion. A stiffer aorta, which can be observed with aging and in different pathological conditions such as hypertension, obesity, diabetes mellitus, and dyslipidemia, fails in both of these tasks. Numerous studies now show that PP, arterial stiffness, and early wave reflections are strong predictors of cardiovascular (CV) risk.1 The CV complications are usually located above the aortic recoil and mainly affect the heart. The downward consequences of enhanced pulsatility, particularly at the peripheral and even the microvascular levels, are less documented. The study by Mitchell et al2 in the June issue of Hypertension addresses this subject, with particular focus on a healthy elderly population. In addition to arterial stiffness, the pulse waveform characteristics are influenced by wave reflection. Energy propagated through the circulation usually meets vessel branching points, at which some of the antegrade energy is “reflected” and becomes retrograde. At some point through the aorta and its braches, the incident and reflected waves summate. Where and when this happens …

In youth, properties of the human arterial system are such that pulse pressure generated by ventricular ejection is low, and the major component of wave reflection returns to the heart after the aortic valve has shut, so making no contribution to ventricular load, but boosting pressure throughout diastole and so aiding coronary perfusion. That constitutes optimal arterial function and optimal vascular/ventricular interaction. With ageing, the aorta and elastic arteries stiffen, so that aortic pulse pressure is markedly increased. This is a consequence of a direct stiffening effect on the aorta itself, and of an indirect effect caused by early return of wave reflection consequent upon stiffening of the whole arterial system with an increase in its pulse wave velocity. There is a change in contour of the aorta pressure wave with wave generation of a late systolic peak and disappearance of the diastolic wave; the reflected wave moves from diastole and systole. Because the lowest diastolic pressure remains relatively constant [1,10], increased pulse pressure causes a substantial increase in aortic systolic pressure. Increased aortic systolic pressure is associated with increased left ventricular pressure and leads to left ventricular hypertrophy. Sustained elevation in systolic pressure and persistent left ventricular hypertrophy are associated with progressive degenerative changes in the hypertrophied myocytes such that these weaken, developing less force with each contraction. The weakened, hypertrophied fibres lengthen and the ventricle dilates, with force and cardiac output initally being maintained at greater muscle length and ventricular volume through the Frank-Starling mechanism. Ultimately compensation is lost. The hypertrophied ventricle normally functions as a flow source, which is capable of generating flow even against very high pressure. With the development of cardiac failure through muscle weakening, the ventricle comes to act as a pressure source, with ventricular output very sensitive to pressure and to changes in pressure. The normal ventricle functions in an intermediate position, even though it is closer in behaviour to a flow than to a pressure source. Wave reflection adds to pressure but subtracts from flow. In youth, wave reflection returns to the heart during diastole when the aortic valve is shut. Negative flow is not possible, so wave reflection is apparent only as a secondary pressure wave in the ascending aorta. In older subjects, when the left ventricle is beating powerfully, return of wave reflection during systole has less obvious an effect on the ascending aortic flow wave, but causes an obvious secondary boost to pressure in the ascending aorta and left ventricle. Hence, under normal circumstances, wave reflection at the heart is apparent as a positive secondary pressure wave, either because the aortic valve is shut when this wave returns, or because the ventricle possesses enough power that it virtually overcomes any negative influence on flow when reflection returns during systole. When the myocardium weakens and the heart fails, the heart starts to behave like a pressure source, and wave reflection starts to have a far greater effect on flow; wave reflection is manifested more as a negative influence on flow than as a positive influence on pressure. As heart failure develops, there is a progressive change in flow wave contour, with early deceleration of aortic flow and ultimately, abbreviation of systolic ejection duration with fall in stroke volume. Early wave reflection is the major factor in the genesis of systolic hypertension. Early wave reflection remains a major factor when heart failure develops, although its effect is apparent in reduction of late systolic flow rather than as a boost to late systolic pressure. Reduction in wave reflection through use of vasodilatory agents is a logical strategy in treatment of systolic hypertension. That type of therapy is equally logical in treatment

Background: Estimates of central aortic pulse pressure for total arterial compliance (TAC) are based on a radial-am-tic transfer function to calculate central pressure from radial applanation tonometry. However, this approach has been validated in groups with a preponderance of middle-aged men. and its validity in women and older patients has been questioned. Methods: Carotid and radial applanation tonomeby were pelformed simultaneously with pulsed wave Doppler of the LVOT using specialised software, in 96 pts (47 men: age 56+6y) with and without cardiovascular disease. TAC was calculated by the pulse-pressure method. Mean aortic pulse pressure (MAoP) was derived using a transfer function from radial tonometry, and then compared with the carotid waveform. Results: The correlation between direct carotid measurement and radial meawrement with the transfer function was good for TAC (r= .91). However, there was a significant difference in TAC in older patients (>65 years) using the two waveforms. Bland-Altman analysis of the difference (DIFF) between radial and carotid TAC showed significant differences between men and women (p=O.O06) and between younger and older patients (p=O.O5) (Table). Conclusions: Estimates of TAG calculated using the radial transfer function and direct carotid waveforms show 5.10% differences in women’and older patients. Specrfic transfer functions or use of carotid pressure waveforms should be considered in these subgroups.

BackgroundStudies showed that long-standing smokers have stiffer arteries at rest. However, the effect of smoking on the ability of the vascular system to respond to increased demands (physical stress) has not been studied. The purpose of this study was to estimate the effect of smoking on arterial stiffness and subendocardial viability ratio, at rest and after acute exercise in young healthy individuals.Methods/resultsHealthy light smokers (n = 24, pack-years = 2.9) and non-smokers (n = 53) underwent pulse wave analysis and carotid-femoral pulse wave velocity measurements at rest, and 2, 5, 10, and 15 minutes following an exercise test to exhaustion. Smokers were tested, 1) after 12h abstinence from smoking (chronic condition) and 2) immediately after smoking one cigarette (acute condition). At rest, chronic smokers had higher augmentation index and lower aortic pulse pressure than non-smokers, while subendocardial viability ratio was not significantly different. Acute smoking increased resting augmentation index and decreased subendocardial viability ratio compared with non-smokers, and decreased subendocardial viability ratio compared with the chronic condition. After exercise, subendocardial viability ratio was lower, and augmentation index and aortic pulse pressure were higher in non-smokers than smokers in the chronic and acute conditions. cfPWV rate of recovery of was greater in non-smokers than chronic smokers after exercise. Non-smokers were also able to achieve higher workloads than smokers in both conditions.ConclusionChronic and acute smoking appears to diminish the vascular response to physical stress. This can be seen as an impaired 'vascular reserve' or a blunted ability of the blood vessels to accommodate the changes required to achieve higher workloads. These changes were noted before changes in arterial stiffness or subendocardial viability ratio occurred at rest. Even light smoking in young healthy individuals appears to have harmful effects on vascular function, affecting the ability of the vascular bed to respond to increased demands.

the proportion of central aortic pulse pressure that is attributed to the reflected pulse wave. We hypothesise that in a cohort of patients, who have one or more cardiac risk factors, and suspected coronary artery disease; arterial stiffness will be elevated compared to a normal population. Methods and results: 910 patients presenting for coronary angiography at Westmead Hospital, Sydney, were recruited into the Australian Heart Eye Study (AHES). Brachial blood pressure was recorded (HEM 907, Omron). Radial arterywaveformsweremeasuredwith a tonometer and pulse wave analysis was used to derive central blood pressures, AP and AIx (SphygmoCor, AtCor Medical). The average values for each decile of age were compared against normal reference ranges derived from 4001 healthy, normotensive individuals (McEniery et al., JACC 2005). The figure shows that while AP is consistent with normal ranges, the AIx is lower than that that of normals, for both genders. mated by two techniques. First, the Pressure Equivalence (PE) technique calibrated brachial waves with brachial cuff pressure values, then the carotid wave was calibrated by assuming identical mean and diastolic pressures, with carotidSPextrapolated. Second, SphygmoCor® technique applied the Transfer Function (TF) to the radial waveform, calibrated to brachial cuff, to generate carotid SP and PP. Amplification was significant between carotid and brachial (8.0mmHg, p< 0.0001) with TF, but not with PE (1.5mmHg, p=NS). PE gave considerable amplification between brachial to radial (8.4mmHg), which was not present with the TF. Form Factors (FF= (mean pressure−diastolic pressure)/PP) for carotid and brachial waves were similar (40.2 c.f. 39.1%; p=NS), but different to the radial (34.5%; p< .0001). Amplification as brachial PP÷ carotid PP using PE was insignificant, but with TF was positive (18%, p< 0.0001). Conclusions:AIx and AP are not significantly increased in a cardiac population, contrary to expectations. doi:10.1016/j.hlc.2011.05.028

We describe a 62-year-old dilated cardiomyopathy patient in whom congestive heart failure progressed shortly after DDD mode was changed to VOO mode because of battery exhaustion. Emergency battery exchange with restoration of DDD mode improved his functional status to the previous level; pulmonary capillary wedge pressure decreased from 28 to 24 mmHg and cardiac output increased from 1.5 to 2.0 L/min associated with widening of the aortic pulse pressure. Maintenance of atrial contraction is therefore important even if left ventricular systolic function is markedly impaired and left ventricular end-diastolic pressure is increased.(Internal Medicine 32: 459-461, 1993)

To evaluate the ability of a newly designed balloon catheter with check valves to temporarily relieve hemodynamic deterioration in acute aortic regurgitation, we produced an experimental model of acute aortic regurgitation in closed-chest dogs using endomyocardial biopsy forceps. Aortic regurgitation was produced until an increase in aortic pulse pressure of over 50% was achieved. Left ventricular end-diastolic pressure rapidly increased after the production of aortic regurgitation. Immediately after the catheter began functioning, pulse pressure decreased from 133 +/- 1 to 78 +/- 5 mm Hg (mean +/- SEM) and left ventricular end-diastolic pressure also decreased from 26 +/- 1 to 13 +/- 1 mm Hg. These effects lasted as long as the catheter functioned. Although a mild (21 +/- 8 mm Hg) pressure gradient between the left ventricular peak systolic pressure and the aortic peak systolic pressure was observed when this catheter was used, forward stroke volume was no less than in the group in which the catheter had not been used. These findings suggest that the balloon catheter with check valves may effectively reduce aortic regurgitation.

We studied the aortic elastic behavior in response to vitamin D3-induced accelerated calcinosis in conscious dogs chronically instrumented with a pressure microtransducer and a pair of ultrasonic diameter dimension gauges in the upper descending thoracic aorta. The two functional phases of the elastic segmental properties of the aorta in vivo were discriminated by computation on a beat-by-beat basis from the phasic pressure-diameter (P-D) hysteresis loops in basal conditions and during the transient state of a wide range of pressures obtained mechanically (aortic occlusion) or pharmacologically (angiotensin bolus). The overall P-D curve formed by all P-D hysteresis loops was comprised of two linear relations according to a model that assumes that only elastin is stretched at lower pressures, whereas both elastin and collagen are stretched at higher pressures. The slope of the first linear portion of the P-D curve was considered as the elastin P-D elastic modulus, and the slope of the curve obtained by subtraction between the P-D curve and the extrapolation of the elastin straight line was assumed to be the collagen P-D elastic modulus. After vitamin D3-induced calcinosis, the elastin elastic modulus was unaffected, whereas the collagen elastic modulus decreased significantly during occlusion maneuvers (58.6%, p less than 0.01) and during bolus injections of angiotensin (37.2%, p less than 0.05). The collagen elastic modulus correlated with the serum calcium concentration (r = -0.65, p less than 0.001) and with the aortic pulse pressure (r = 0.51, p less than 0.01), and this relation persisted at constant heart rate. Histopathologic analysis evidenced calcium-depositing elastic lamina, focal disappearance of collagen, and rupture of elastic fibers. The present study shows that accelerated, severe, experimental calcinosis-inducing calcium deposition inside the large artery walls is accompanied by a clear-cut paradoxical reduction in arterial rigidity that is mainly due to functional and structural modification of collagen elasticity.

Summary Arterial stiffness and wave reflection are fast emerging as therapeutic targets in their own right. While thiazide diuretics have little or no effect on either arterial stiffness or wave reflection, vasodilators including nitrates and phosphodiesterase type-5 inhibitors e.g., sildenafil, reduce wave reflections and aortic pressures but not aortic stiffness. β-blockers have the opposite effect; they reduce aortic stiffness but increase aortic pulse pressure and wave reflections while calcium antagonists and α-blockers show varying effects on the vascular wall. Drugs targeting the renin–angiotensin–aldosterone system, namely angiotensin-converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARBs) and aldosterone antagonists have been shown as the most effective in reducing both arterial stiffness and wave reflection, and in some cases, to a greater extent than predicted from the extent of blood pressure (BP) reduction. Also, there is evidence of an additive effect on arterial stiffness with combined ACEI and ARBs. Exploring further the synergistic effects of anti-hypertensive drugs on arterial stiffness, a polypill containing a low-dose combination of a thiazide diuretic, calcium antagonist, β-blocker and an ACEI, decreased arterial stiffness more than the individual drugs in standard doses. However, beyond the dynamic effects of anti-hypertensive drugs, future therapies may directly target vascular structural alterations including collagen degradation, advanced glycation end-products, the matrix-metalloproteinases and vascular inflammation. Finally, one can speculate about the role of pharmacogenomics which may help tailor ‘ de-stiffening therapy ' in individuals with stiff arteries.

Radionuclide gated cardiac blood pool (GBP) imaging was used to quantitatively assess the severity of acute aortic valvular regurgitation produced experimentally in 10 anesthetized dogs. Right ventricular (RV) and left ventricular (LV) stroke counts (end-diastolic minus end-systolic counts in RV and LV regions of interest) were used as indices of the stroke volumes of the two ventricles. Regurgitant fraction (RFGBP) was derived by assuming that an excess of LV stroke counts compared to RV stroke counts was due to regurgitant flow: RFGBP = LV stroke counts - RV stroke counts/LV stroke counts X 100. Regurgitant fraction (RFEMF) was also estimated directly from an electromagnetic flowmeter (EMF) on the ascending aorta. Mean RFEMF was 55.8 +/- 17.9% (+/-SD). Close agreement was found between regurgitant fractions measured by GBP and EMF (RFGBP = 1.09, RFEMF - 4.7%, r = 0.88, p less than 0.001, SEE = 9.98%). The severity of regurgitation from blood pool images also correlated closely with aortic pulse pressure (r = 0.89) and the length of the tear in the aortic valve (r = 0.84). These results suggest that blood pool imaging may be sueful for noninvasive quantification of regurgitant flow in patients with valvular insufficiency.

Cardiovascular physiologists frequently infer directional changes in cardiac stroke volume and cardiac output from changes in aortic pulse pressure and atrial pressure. Errors are probably not infrequent. The Hamilton and Remington pressure pulse contour method can also indicate directional fluctuations in cardiac stroke volume. Comparison of the results of the two methods of analysis in situations where cardiac stroke index was changed acutely revealed good correspondence of indicated changes under conditions of simple alterations in venous return, but poor correspondence under more complex conditions such as after injections of pressor amines.

Clinical and hemodynamic data prior to and during oral guanethidine therapy in two patients with idiopathic hypertrophic subaortic stenosis are presented. In both patients the systolic intraventricular pressure gradient both at rest and during exercise was reduced following continued guanethidine administration. Concomitantly, computed values for left ventricular effective outflow tract area were significantly larger during the guanethidine studies than during the control studies. The symptomatic patient (Case 1) experienced increased work tolerance and diminished dyspnea on exertion. Guanethidine did not prevent the increased intraventricular gradient and reduction of the aortic pulse pressure which occur during isoproterenol infusion or in the contraction following a premature ventricular beat. It is suggested that chronic guanethidine administration, by reducing the systolic obstruction, may be a useful pharmacologic agent in this disorder.

Results of a study in which six supine resting subjects, wearing water-perfused suits, had body skin temperature controlled at 35 C for 30 min (control period), then rapidly increased to 40.5 C for 43 to 50 min (heating period) in a two-part experiment. In the first part of the experiment arterial mean pressure (MP) in three men was increased back to, or above control levels at the 30 to 35th min of heating by total occlusion of both legs for 8 to 10 min. Splanchnic blood flow (SBF), which had fallen from 1.4 to 0.9 L/min at occlusion, rose only 0.05 L/min during occlusion. Splanchnic vascular resistance (SVR) rose throughout heating and occlusion. In the second part of the experiment (three men) SBF fell despite a spontaneous rise in MP and aortic pulse pressure prior to leg occlusion. Cardiac output (CO) was measured just before, during and after occlusion. Occlusion raised MP 10 to 15 mm Hg and reduced CO only slightly. It is concluded that falling MP or aortic pulse pressure are not major causes of the splanchnic vasoconstriction in response to heating man.

Summary and conclusion 1. Techniques have been developed for recording of ascending aorta flow, aortic pressure, and left ventricular work in the maximally exercising animal. 2. A marked increase in cardiac output during exercise in the normal dog was accompanied by a striking heart rate increase, but little change or, even, a fall in aortic mean pressure. Aortic pulse pressure and systolic pressure invariably rose. 3. Animals with complete heart block were able to perform just as heavy an external work load at their idiopathic ventricular rates as at rapid-paced rates. 4. Cardiac output and cardiac work increased in stepwise fashion as heart rate was increased, both with and without exercise. 5. Large error is introduced by calculation of cardiac work using mean values for cardiac output and pressure compared with the results using instantaneous analog-computer techniques.

1. Cardiac inhibition follows sudden increase of pressure within the gill blood vessels of Squalus acanthias. An average increase of 10.7 mm. Hg above the average systolic pressure existing in the dorsal aorta constitutes an adequate stimulus for the inhibitory response.2. The cardio-inhibitory response is a reflex, with afferent pathways located in the branchial nerves and efferent pathways in the vagus supply to the heart. The reflex is both unilateral and crossed.3. The average ventral aortic systolic blood pressure in Squalus acanthias is found to be 28.2 mm. Hg, the average dorsal aortic systolic pressure 15.4 mm. Hg, and the average ventral aortic pulse pressure 13.3 mm. Hg. The inhibitory reflex to increased ventral aortic pressure modifies the diastolic blood pressure to a significant degree.4. The adaptive nature of the reflex is pointed out and its phylogenetic significance is discussed.

Objective: To evaluate the association of pulse pressure (PP) with mortality and major adverse cardiac events (MACE) in one-year period after anterior ST-elevation myocardial infarction (A-STEMI). Methods: A total of 261 consecutive patients whose blood pressure was measured with the aid of a catheter before primary percutaneous coronary intervention (PPCI) between August 2016 and February 2017 were included in the study. The patients were divided into three groups according to pulse pressure (PP) (Group 1, PP50 mmHg). Results: The mean age of the patients was 63.4±14.1 years, and 206 of them were male. The groups were similar in terms of age and diastolic blood pressure (DBP). The ratio of female patients in Group 1 was higher, and their systolic blood pressure (SBP) was lower than those from the other groups (P=0.005 vs. P=0.042). The rates of MACE and mortality were higher in Group 1. The predictive PP values were calculated to be 42.5 mmHg for development of MACE and 41.5 mmHg for mortality. One-year survival ratio was worse in Group 1 than in the others according to Kaplan-Meier analysis (P

The dynamic behavior of fixed LV outflow tract stenosis partly resembles that of OCM. To analyze their differences we studied basal and postextrasystolic (post-PVC) peak-to-peak LV aortic gradients, aortic systolic pressure, and pulse pressure in 14 OCM and in 36 pure VAS without two-dimensional echocardiographic findings of OCM. Fifteen mild VAS had basal gradients similar to those of OCM (39 +/- 17 mm Hg vs 24 +/- 16 mm Hg). Patients with OCM show a post-PVC gradient (109 +/- 41 mm Hg) similar to that of VAS (110 +/- 50 mm Hg). However, the latter were departing from much higher gradients (VAS 72 +/- 30 mm Hg vs OCM 24 +/- 16 mm Hg). Decrement of post-PVC aortic systolic pressure and pulse pressure were frequent in both groups, but decrement of pulse pressure greater than 5 mm Hg were more frequent in OCM. We concluded that (1) post-PVC increased aortic gradients and decreased aortic systolic pressure occurred in both VAS and OCM; (2) post-PVC decreased aortic pulse pressure might occur in VAS; and (3) association of post-PVC gradient increment greater than 75 percent and pulse pressure decrement greater than 5 mm Hg are strongly suggestive of OCM.

The effects of acute severe aortic regurgitation on the left ventricle were investigated in conscious, chronically instrumented dogs. Left ventricular dimensions and volumes were measured from biplane cineradiographs of beads positioned near the endocardium. Data were collected before and after the production of aortic regurgitation by a catheter technique. The aortic regurgitation resulted in increases in mean aortic pulse pressure from 44 to 73 mmHg (P smaller than 0.001), heart rate from 87 to 122 beats/min (P smaller than 0.02), and left ventricular end-diastolic pressure from 11 to 25 mmHg (P smaller than 0.05). Mean end-diastolic volume rose from 61 to 69 cc (P smaller than 0.001), while end-systolic volume remained unchanged at 37 cc. The end-diastolic dilatation following regurgitation was asymmetrical in that the increase in size was due principally to an increase in the septal-lateral axis. The acute volume load of aortic regurgitation was accomplished by an increase in end-diastolic volume, i.e., the Frank-Starling mechanism. The tachycardia probably reflects augmented cardiac sympathetic activity, but the constant end-systolic volume at a similar mean systolic pressure suggests that the net contractile state was unchanged.

In 14 consecutive patients with varying myocardial function, evaluation of the Valsalva maneuver was performed using aortic pulse pressure decay to investigate a possible quantitative relationship between the pattern of response and the degree of myocardial dysfunction. The aortic pulse pressure response during strain correlated with resting left ventricular end-diastolic pressure and pulmonary wedge pressure but not with resting cardiac output, cardiac index and ejection fraction. Similar results were obtained when several indices characterizing the aortic pulse pressure decay during Valsalva were used together to predict resting hemodynamic data by multiple regression analysis. In conclusion, quantitative aortic pulse pressure decay during the strain phase of the Valsalva maneuver correlated only moderately with hemodynamic indices used to identify myocardial dysfunction. These results raise doubts about the use of the Valsalva maneuver for the evaluation of myocardial dysfunction.

A formulation for determining stroke volume from arterial pressure is presented which differs from previous methods in both scope of application and theoretical basis. The formulation is specifically applicable in the presence of large successive beat-to-beat variations which occur with premature contractions and other arrhythmias. Its derivation is based upon Windkessel theory, as are most others, but special emphasis is placed upon analysis of diastolic pressure (when arterial dynamics most nearly approach characteristics assumed in Windkessel theory). The formulation contains no ad hoc parameters although mean peripheral vascular resistance must be known and redetermined when changes in resistance occur. Results from eight animal experiments are presented which indicate that this formulation predicts stroke volume to about ten-percent (10-percent) error over successive beat-to-beat changes of severalfold during episodes of mechanically induced beats and during control, isoproterenol, and angiotensin administration.

Regional vascular responses to gradual reductions in right atrial pressure and aortic pressure were investigated in nine men. In each study, lower body negative pressure was applied in a ramp of -1 mm Hg/min for 40-50 minutes. During the range from control to -20 mm Hg, right atrial pressure (4 studies) fell from 4.2 mm Hg to -0.6 mm Hg; heart rate was slightly reduced (2 beats/min), and aortic mean pressure and pulse pressure (6 studies) were unchanged. The maximal rate of rise of aortic pressure showed no consistent trends. Forearm blood flow (30 studies) fell with the onset of lower body negative pressure and reached 67% of the control value by -20 mm Hg. Splanchnic blood flow (14 studies) was significantly reduced by -7 mm Hg and fell to 89% of control by -20 mm Hg. During the range from -20 to -50 mm Hg, right atrial pressure continued to fall. Aortic mean pressure fell slightly or was unchanged in four subjects and fell dramatically at -35 mm Hg in two subjects. Aortic pulse pressure began to fall at about -20 mm Hg and fell linearly thereafter. Heart rate paralleled aortic pulse pressure ( r = -0.86 to -0.93). Forearm blood flow fell to 55% and splanchnic blood flow fell to 65% of control at -50 mm Hg. Thus, significant vasoconstriction occurred without measurable change in arterial blood pressure. We concluded that low-pressure baroreceptors, presumably in the cardiopulmonary region, initiate splanchnic and forearm vasoconstriction with more pronounced vasoconstriction occurring in the forearm.

The ear densitogram was monitored in 21 consecutive patients with various degrees of myocardial function (New York Heart Association class I to IV) during the standardized Valsalva maneuver to evaluate the quantitative relations between the pattern of response and the central circulatory pressures. The ear densitographic first derivative consistently tracked the aortic pulse pressure during the strain phase of the Valsalva maneuver (beat-to-beat correlation [r] range 0.98 to 0.72). The percent decrease of the densitographic pulse derivative during strain correlated with left ventricular end-diastolic pressure at rest (r = 0.62, p less than 0.001), but not with cardiac output, cardiac index and ejection fraction. Multiple stepwise regression was used to take into account multiple aspects (time intervals and pulse amplitudes) of the pattern of response to the Valsalva maneuver. As a result, both correlations improved substantially (r = 0.97, p less than 0.001 for left ventricular end-diastolic pressure, and r = 0.92, p less than 0.001 for pulmonary artery wedge pressure). In conclusion, the combination of several noninvasive indexes obtained by pulse amplitude and interval changes during the strain phase of the Valsalva maneuver seems to be a new and promising method for noninvasive evaluation of the status of left ventricular filling pressures.

This study was designed to evaluate separately the influence of restoration of distal pulse pressure and the influence of factors related to operation upon hemodynamic and hormonal alterations accompanying repair of canine aortic coarctation. Eight normal adult dogs underwent a sham operation and served as controls. In 10 dogs the thoracic aorta was transected and reanastomosed. In 10 dogs aortic coarctation was created within 1 week of birth by banding the aorta just proximal to the ductus ligament, thereby fixing lumenal diameter at 1 to 2 mm. Studies were performed in the latter animals 18 months after operation. These dogs were subdivided into two groups: one ( n = 6) underwent surgical repair of the coarctation; in the other ( n = 4), the coarctation was repaired and an occluder was placed on the aorta to maintain distal aortic pulse pressure at its diminished preoperative level. Normal distal pulse pressure was restored in these animals by releasing the occluder 1 week after recovery from the repair of coarctation. Each dog was studied in the conscious state before the definitive procedure and again 24 hr later. Plasma renin activity increased significantly after operation in the sham and in the transection groups. Renin activity and proximal blood pressure were significantly elevated and distal pulse pressure was diminished preoperatively in both the repair and the occluder groups. After their respective definitive procedures, the elevation in renin activity and in proximal pressure persisted in the repair group but decreased in the occluder group. This suggests that continued elevation of renin activity and blood pressure in the early postoperative period following repair of coarctation may be secondary to perioperative rather than hemodynamic factors.