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This article presents a primed left ventricle heart perfusion method to generate physiologic aortic pressure (AoP) and perform functional assessment. Isolated hearts of male Yorkshire pigs were used to study the hemodynamic behaviors of AoPs generated in the primed left ventricle heart perfusion (n = 6) and conventional (zero-loaded left ventricle) Langendorff perfusion (n = 6). The measurement results show that left ventricular pressure generated in the primed left ventricle heart perfusion is a determinant of physiologic AoP (i.e. systolic and diastolic pressures within physiologic range). The aortic pulse pressure (systolic pressure = 124.5 ± 1.7 mm Hg, diastolic pressure = 87.8 ± 0.9 mm Hg, aortic pulse pressure = 36.7 ± 2.6 mm Hg) from the primed left ventricle heart perfusion represents close match with the in vivo physiologic data. The volume in the left ventricle remains constant throughout the primed left ventricle heart perfusion, which allows us to perform isovolumetric left ventricular pressure measurement in ex vivo heart perfusion (EVHP). Left ventricular contractility measurements (maximum and minimum rates of left ventricular pressure change) were derived for cardiac assessment. In summary, the proposed primed left ventricle heart perfusion method is able to create physiologic AoP and enables left ventricular functional assessment in EVHP in porcine hearts.

Introduction: Intracerebral hemorrhage (ICH) is the second most common subtype of stroke. Hypertension is a major cause of primary spontaneous ICH. However, sex difference in blood pressure (BP) and arterial stiffness among ICH patients is not well characterized. Methods: A prospective pilot study to investigate the feasibility of measuring arterial stiffness in acute primary ICH patients was approved by the institutional research board at Wake Forest Baptist Health. Eligible subjects with primary ICH were enrolled in the study within 7 days of onset. Non-invasive measurements of brachial BP, aortic BP, augmentation index at heart rate of 75 beats per minute (AIx75), and carotid-femoral pulse wave velocity (cf-PWV) were measured at the patient’s bedside, using the SphygmoCor XCEL System v1 (AtCor Medical Pty Ltd., Sydney, Australia). Results: A total of 20 patients have been enrolled in the study over 5 months. Over half the patients enrolled were female (55%, n = 11), including 82% (n = 9) White, 9% (n = 1) Asian and 9% (n = 1) Hispanic. There was increased diversity in the male patients (45%, n = 9) including 44% (n = 4) Black, 22% (n = 2) White, 22% (n = 2) Hispanic, and 11% (n = 1) Asian. Men were significantly younger than women (57 ± 5 years vs 74 ± 3 years, respectively, P = 0.009). There were no significant differences in BMI or ICH score. At the time of measurement, there were no significant sex differences in brachial or aortic blood pressures (systolic and diastolic), however, females had significantly higher AIx75 (35 ± 4 vs 20 ± 6, P = 0.036) and aortic PP (53 ± 2 mm Hg vs 42 ± 4 mm Hg, P = 0.020) than males. Sex difference in cf-PWV was not statistically significant (p = 0.054). Conclusion: In the current feasibility pilot study, preliminary data show that females had higher arterial stiffness measured as AIx75 and aortic PP than males in the acute setting of ICH. Further study will be required to ascertain whether this is related to higher age at presentation in females. Whether sex differences in arterial stiffness predict differences in the outcome among ICH patients is not well characterized; thus, assessment of 30-day functional and neurological outcomes will be performed with NIHSS and modified Rankin Scores.

OBJECTIVE We evaluated the possible correlation between pulse wave analysis (PWA) parameters measured during the first trimester of pregnancy in normotensive, low-risk women, and the development of hypertensive disorders later in pregnancy. Our hypothesis was that a still asymptomatic increase in arterial stiffness may potentially precede the onset of overt hypertension in pregnancy and that PWA could detect it. METHODS The study population (n = 1648) was recruited at the time of prenatal screening for chromosomal abnormalities (11-12 weeks of gestation). The radial pressure waveform was obtained with an applanation tonometer (Sphygmocor, Atcor Medical, West Ryde, Australia) on pregnant women in recumbent position. Arterial stiffness was evaluated using arterial PWA. The aortic systolic pressure (aSp), aortic diastolic pressure, and aortic mean pressure, the aortic pulse pressure, the augmentation pressure, and the augmentation index were calculated. The main outcome measure was the development of hypertensive disorders later in pregnancy. RESULTS The values of aSp (P

BACKGROUND Aortic knob width (AKW), which can be measured easily in simple radiography, is associated with the degree of dilatation and tortuosity of the aortic arch. Pulsatile stress influences aortic geometry. This study was carried out to investigate whether AKW can represent invasively measured aortic pulse pressure (APP). METHODS A total of 252 patients who underwent invasive coronary angiography (ICA) for the evaluation of coronary artery disease were enrolled. AKW was defined as the perpendicular length from the lateral margin of the main bronchus to the most prominent edge of the aortic knob on chest radiography. APP was measured at the ascending aorta using a pigtail catheter immediately before ICA. RESULTS When patients were divided into two groups according to the median value of APP (69 mmHg), AKW was significantly greater in patients with higher APP (≥69 mmHg) than in those with lower APP (

Introduction:A peripheral pulse pressure (PP) is larger than a central PP (PP amplification). The phenomenon has been examined in adult, but not in children.Methods:Fifty-four patients with a normal aorta were enrolled. The ascending and descending aorta pressure waveforms were recorded by a pressur

Effective treatment of systolic hypertension in elderly patients remains a major therapeutic challenge. A multicenter, double-blind, randomized controlled trial with sacubitril/valsartan (LCZ696), a first-in-class angiotensin receptor neprilysin inhibitor, was conducted to determine its effects versus olmesartan (angiotensin receptor blocker) on central aortic pressures, in elderly patients (aged ≥60 years) with systolic hypertension and pulse pressure >60 mm Hg, indicative of arterial stiffness. Patients (n=454; mean age, 67.7 years; mean seated systolic blood pressure, 158.6 mm Hg; mean seated pulse pressure, 69.7 mm Hg) were randomized to receive once-daily sacubitril/valsartan 200 mg or olmesartan 20 mg, force titrated to double the initial doses after 4 weeks, before primary assessment at 12 weeks. The study extended double-blind treatment for 12 to 52 weeks, during which amlodipine (2.5–5 mg) and subsequently hydrochlorothiazide (6.25–25 mg) were added-on for patients not achieving blood pressure target (P =0.010), further corroborated by secondary assessments at week 12 (central aortic pulse pressure, −2.4 mm Hg, P P P P

AIM To determine the degree to which an extended time to the peak of the aortic forward wave or early wave reflection time enhance associations between aortic backward wave pressure and hence central aortic pulse pressure (PPc) and left ventricular mass index (LVMI). METHODS In 701 adult participants from a community sample either receiving no antihypertensive therapy or receiving low-dose thiazide diuretic monotherapy for at least a year (the major therapy employed), we assessed aortic haemodynamics (SphygmoCor software and wave separation analysis; AtCor Medical, West Ryder, New South Wales, Australia) and LVMI (echocardiography). RESULTS An interaction between time to the peak of the aortic forward wave and aortic backward wave pressure was independently associated with aortic augmented pressure (P

Despite the well-documented value of ST2 in heart failure and myocardial infarction, the role of ST2 in vascular biology has not yet been well defined. This study was performed to investigate the association between serum soluble ST2 (sST2) and invasively measured aortic pulse pressure (APP). A total of 167 consecutive patients with suspected coronary artery disease (CAD) (65.1 ± 9.8 years; men, 65.9%) referred for invasive coronary angiography was prospectively enrolled. APP was measured at the ascending aorta with a pig-tail catheter, and arterial blood samples for the measurement of sST2 were collected before coronary angiography. Serum sST2 levels were quantified by radioimmunoassay. Most of the patients (73.9%) had significant CAD (stenosis ≥ 50%) on coronary angiography. Patients with higher APP (≥76 mmHg) showed a significantly higher sST2 level compared to those with lower APP (

OBJECTIVE: The results from the ASCOT CAFE study demonstrated the inferiority of beta blockers in reducing central aortic blood pressure. In this study, we wanted to demonstrate whether or not second-generation beta blockers with higher beta 1 selectivity, namely bisoprolol, may counterbalance the effect of bradycardia through reduced reflection wave magnitude resulting from the relative lack of increase in peripheral vascular resistance. METHOD: This was a prospective, randomized, open-label, active-controlled trial in 209 hypertensive patients to evaluate the effect of bisoprolol and atenolol on aortic pulse pressure. Patients received a once-daily 5 mg dose of bisoprolol (n = 96) or 50 mg dose of atenolol (n = 95) at baseline with titration up to bisprolol 10 mg and atenolol 100 mg allowed at the 4th week when the brachial blood pressure was above treatment goal (average dose: bisoprolol: 5.4 mg, atenolol: 52.8 mg). Central blood pressure and augmentation index were measured at baseline and 12 weeks later, by pulse wave analysis with radial artery tonometry. The primary endpoint of the study was the difference in the central pulse pressure (CPP) at 12 weeks. RESULTS: The results showed a significant reduction of CPP in both groups at week 12 of administration compared with the predose level (P < 0.05); however, there was no significant difference in terms of CPP change [bisoprolol (baseline CPP 47.49 ± 11.33, follow-up 43.09 ± 11.67) vs. atenolol (baseline CPP 45.93 ± 11.62, follow-up 42.23 ± 9.92), P = 0.594]. CONCLUSION: In this study, there was no significant difference between bisoprolol and atenolol in terms of reduction of aortic pulse pressure after 12 weeks of treatment.

Background— Different blood pressure (BP)–lowering drugs could have different effects on central aortic pressures and thus cardiovascular outcome despite similar effects on brachial BP. The Conduit Artery Function Evaluation (CAFE) study, a substudy of the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT), examined the impact of 2 different BP lowering-regimens (atenolol±thiazide-based versus amlodipine±perindopril-based therapy) on derived central aortic pressures and hemodynamics. Methods and Results— The CAFE study recruited 2199 patients in 5 ASCOT centers. Radial artery applanation tonometry and pulse wave analysis were used to derive central aortic pressures and hemodynamic indexes on repeated visits for up to 4 years. Most patients received combination therapy throughout the study. Despite similar brachial systolic BPs between treatment groups (Δ0.7 mm Hg; 95% CI, −0.4 to 1.7; P =0.2), there were substantial reductions in central aortic pressures with the amlodipine regimen (central aortic systolic BP, Δ4.3 mm Hg; 95% CI, 3.3 to 5.4; P P P P Conclusions— BP-lowering drugs can have substantially different effects on central aortic pressures and hemodynamics despite a similar impact on brachial BP. Moreover, central aortic pulse pressure may be a determinant of clinical outcomes, and differences in central aortic pressures may be a potential mechanism to explain the different clinical outcomes between the 2 BP treatment arms in ASCOT.

Specific treatment of age-related aortic wall arteriosclerosis and stiffening is lacking. Because ligands for peroxisome proliferator-activated receptor γ have beneficial effects on the arterial wall in atherosclerosis, via an antiinflammatory mechanism, we investigated whether long-term pioglitazone (Pio) treatment protects against another form of vascular wall disease, arteriosclerosis. We evaluated, in a rat model of elastocalcinotic arteriosclerosis (hypervitaminosis D and nicotine [VDN]), whether Pio (3 mg · kg −1 per day for 1.5 month PO) attenuated arteriosclerosis and its consequences: aortic wall rigidity, increased aortic pulse pressure, and left ventricular hypertrophy. In VDN rats, medial calcification was associated with monocyte/macrophage infiltration and induction of tumor necrosis factor α and interleukin 1β. Pio increased nuclear peroxisome proliferator-activated receptor γ immunostaining in the aortic wall, decreased tumor necrosis factor α ( P − ), tended to decrease interleukin 1β mRNA expression ( P =0.08 versus VDN Pio − ), blunted aortic wall calcification (271±69, P − 562±87 μmol · g −1 dry weight) and prevented fragmentation of elastic fibers (segments per 10 000 μm 2 : 8.4±0.3; P − 10.5±0.6). Pio reduced aortic wall stiffness (elastic modulus/wall stress: 4.8±0.6; P − 10.0±1.6), aortic pulse pressure (30±2 mm Hg; P − 39±4) and left ventricular hypertrophy (1.58±0.05 g · kg −1 ; P − 1.76±0.06). In conclusion, long-term Pio treatment attenuates aortic wall elastocalcinosis and, thus, lowers aortic wall stiffness, aortic pulse pressure, and left ventricular hypertrophy.

Background —Previous studies of pacing therapy for dilated congestive heart failure (CHF) have not established the relative importance of pacing site, AV delay, and patient heterogeneity on outcome. These variables were compared by a novel technique that evaluated immediate changes in hemodynamic function during brief periods of atrial-synchronous ventricular pacing. Methods and Results —Twenty-seven CHF patients with severe left ventricular (LV) systolic dysfunction and LV conduction disorder were implanted with endocardial pacing leads in the right atrium and right ventricle (RV) and an epicardial lead on the LV and instrumented with micromanometer catheters in the LV, aorta, and RV. Patients in normal sinus rhythm were stimulated in the RV, LV, or both ventricles simultaneously (BV) at preselected AV delays in a repeating 5-paced/15-nonpaced beat sequence. Maximum LV pressure derivative (LV+dP/dt) and aortic pulse pressure (PP) changed immediately at pacing onset, increasing at a patient-specific optimal AV delay in 20 patients with wide surface QRS (180±22 ms) and decreasing at short AV delays in 5 patients with narrower QRS (128±12 ms) ( P P P Conclusions —In this population, CHF patients with sufficiently wide surface QRS benefit from atrial-synchronous ventricular pacing, LV stimulation is required for maximum acute benefit, and the maximum benefit at any site occurs with a patient-specific AV delay.

Aging causes progressive changes in the structure and function of the large arteries that adversely impact the heart and vital organs. Vascular aging is a major independent risk factor for the development of cardiovascular diseases and events. Arterial stiffening is the dominant hemodynamic manifestation of vascular aging and a major independent predictor for incident hypertension. Arterial stiffening is therefore responsible for the very high residual lifetime risk for hypertension for middle-aged and elderly individuals. Asian populations may have a predisposition to increased central aortic pulse pressure because of the relatively larger diameter and thinner media at the proximal aorta that affect the interaction between ventricular ejection and arterial load. Increased arterial stiffness with aging was confirmed in several Asian populations, using either carotid-femoral pulse wave velocity (cf-PWV) or brachial-ankle pulse wave velocity (ba-PWV). Both cf-PWV and ba-PWV have been recognized as an independent predictor for cardiovascular events and all-cause mortality in Asian populations. In Asian populations, vascular aging-related medial degeneration but not atherosclerosis is the dominant factor associated with increased arterial stiffness with age. Salt intake has an independent effect on arterial wall properties contributing to increased arterial stiffness with age. Systolic hypertension is a consequence and an accelerator of the vascular aging related arterial stiffness. Asian subjects with systolic hypertension may be more prone to risks of cardiovascular disease, mortality and renal function decline than Western subjects. Strategies to prevent arterial stiffness and control systolic hypertension are urgently needed for the rapidly aging Asian populations.

BACKGROUND In large animals pulse pressure increases from central to peripheral arteries whereas mean arterial pressure decreases slightly. This haemodynamic pattern has not been verified in small animals, particularly in hypertensive rats before and after administration of antihypertensive drugs. DESIGN The intra-arterial blood pressure of normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) was determined along the aorta in anaesthetized and conscious rats. In anaesthetized rats the study was performed before and after acute intravenous nicardipine administration (30 micrograms/kg). RESULTS Mean arterial pressure was significantly higher in untreated SHR than in WKY rats, and within each strain was quite similar along the aortic tree. Pulse pressure increased significantly from the central to the terminal aorta in WKY rats, principally due to an increase in systolic blood pressure. In SHR pulse pressure did not differ along the aortic tree. Compared with in WKY rats, aortic pulse pressure in SHR was significantly elevated whereas femoral pulse pressure was quite similar. Acute nicardipine administration re-established the pulse pressure gradient in SHR, due to a significant decrease in central aortic pulse pressure with no significant change in femoral pulse pressure. CONCLUSIONS These results suggest, first, that since there are large differences in pulse pressure in the proximal aorta of SHR and WKY rats but only small or negligible differences in the distal aorta, the measurement of pulse pressure may be an available index to differentiate normotensive and hypertensive rats, and secondly, that increased aortic pulse pressure in SHR participates in the increase in cardiac afterload independently of mean arterial pressure, and may be a preferential site of action of antihypertensive agents.

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 …

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.