Arterial Load Research Articles

A novel echocardiographic hemodynamic index for predicting outcome of aortic stenosis patients following transcatheter aortic valve replacement.

ObjectiveTranscatheter aortic valve replacement (TAVR) reduces left ventricular (LV) afterload and improves prognosis in aortic stenosis (AS) patients. However, LV afterload consists of both valvular and arterial loads, and the benefits of TAVR may be attenuated if the arterial load dominates. We proposed a new hemodynamic index, the Relative Valve Load (RVL), a ratio of mean gradient (MG) and valvuloarterial impedance (Zva), to describe the relative contribution of the valvular load to the global LV load, and examined whether RVL predicted patient outcome following TAVR.MethodsA total of 258 patients with symptomatic severe AS (indexed aortic valve area (AVA)<0.6cm2/m2, AR≤2+) underwent successful TAVR at the University of Ottawa Heart Institute and had clinical follow-up to 1-year post-TAVR. Pre-TAVR MG, AVA, percent stroke work loss (%SWL), Zva and RVL were measured by echocardiography. The primary endpoint was all cause mortality at 1-year post TAVR.ResultsThere were 53 deaths (20.5%) at 1-year. RVL≤7.95ml/m2 had a sensitivity of 60.4% and specificity of 75.1% for identifying all cause mortality at 1-year post-TAVR and provided better specificity than MG<40 mmHg, AVA>0.75cm2, %SWL≤25% and Zva>5mmHg/ml/m2 despite equivalent or better sensitivity. In multivariable Cox analysis, RVL≤7.95ml/m2 was an independent predictor of all cause mortality (HR 3.2, CI 1.8–5.9; p<0.0001). RVL≤7.95ml/m2 was predictive of all cause mortality in both low flow and normal flow severe AS.ConclusionsRVL is a strong predictor of all-cause mortality in severe AS patients undergoing TAVR. A pre-procedural RVL≤7.95ml/m2 identifies AS patients at increased risk of death despite TAVR and may assist with decision making on the benefits of TAVR.

Severity of arterial defects in the retina correlates with the burden of intracerebral haemorrhage in COL4A1-related stroke.

Mutations in the α1 (COL4A1) or α2 (COL4A2) chains of collagen type IV, a major component of the vascular basement membrane, cause intracerebral haemorrhages with variable expressivity and reduced penetrance by mechanisms that remain poorly understood. Here we sought to investigate the cellular mechanisms of COL4A1-related intracerebral haemorrhage and identify a marker for haemorrhage risk stratification. A combination of histological, immunohistochemical, and electron microscopy analyses were used to analyse the brain parenchyma, cerebrovasculature, and retinal vessels of mice expressing the disease-causing COL4A1 p.G498V mutation. Mutant mice developed cerebral microhaemorrhages and macroscopic haemorrhages (macrohaemorrhages), the latter with reduced penetrance, mimicking the human disease. Microhaemorrhages that occurred in early postnatal life were associated with a transient, generalized increase in blood-brain barrier permeability at the level of capillaries. Macrohaemorrhages, which occurred later in life, originated from deep brain arteries with focal loss of smooth muscle cells. Similar smooth muscle cell loss was detected in retinal arteries, and a time-course analysis of arterial lesions showed that smooth muscle cells are recruited normally in arterial wall during development, but undergo progressive apoptosis-mediated degeneration. By assessing in parallel the extent of these retinal arterial lesions and the presence/absence of macrohaemorrhages, we found that the arterial lesion load in the retina is strongly correlated with the burden of macrohaemorrhages. We conclude that microhaemorrhages and macrohaemorrhages are driven by two distinct mechanisms. Moreover, smooth muscle cell degeneration is a critical factor underlying the partial penetrance of COL4A1-related macrohaemorrhages, and retinal imaging is a promising tool for identifying high-risk patients. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Safety and efficacy of ulnar artery approach for percutaneous cardiac catheterization: Systematic review and meta-analysis.

Trans-radial access has rapidly become the standard for percutaneous coronary procedures in the last decade. As proceduralists overcome the learning curve and become more competent in trans-radial access, alternative safe access sites such as the ulnar artery have been increasingly used for emergent and elective procedures. The aim of this study was to synthesize the best available evidence of the impact on major adverse cardiac events (MACE) of ulnar artery compared to radial artery cardiac catheterization. This review considered randomized controlled trials that included adult patients who had a percutaneous coronary procedure via the radial or ulnar artery. The intervention of interest was the use of ulnar compared to radial artery for cardiac catheterization. An extensive search was undertaken for published and unpublished trials up to May 2017. Methodological quality was assessed independently by two reviewers using the Joanna Briggs Institute Meta-Analysis of Statistics Assessment and Review Instrument (JBI-MAStARI) checklist. Data were analyzed using Review Manager. A total of six trials were included in the review. There was no statistically significant difference in the incidence of MACE between patients who underwent trans-ulnar or trans-radial artery catheterization (OR 0.90; 95% CI 0.65-1.25). Complications associated with access including hematoma formation, (n = 6 trials) pseudo-aneurysm, and arterio-venous fistulae formation (n = 5 trials), were investigated in a total of 5,276 patients, with no difference in these complications noted between the two groups. There were no differences in arterial access time, fluoroscopy time, and contrast load between the two groups. There is evidence to support safe use of the ulnar artery as an alternative to the radial artery for access for cardiac catheterization.

56: Evaluating cardiovascular risk 10 years after preeclampsia

Preeclampsia (PEC) is a known risk factor for future cardiovascular disease (CVD). Since overt CVD does not occur for 20-30 years after PEC exposure, it is critical to identify cardiovascular (CV) risk factors during an intermediate time period to help risk stratify women and guide early interventions. Women previously enrolled in a prospective case control study performed from 2005-2007 at our institution were contacted and offered enrollment into this cross-sectional study. The original study enrolled cases of women with MFM confirmed PEC and normotensive pregnant controls. Women with a history of chronic hypertension (CHTN) at the time of index pregnancy were excluded from this follow-up study. From Feb 2016-June 2017, study participants underwent the following detailed assessment: blood pressure (BP) evaluation, height/weight, waist circumference, fasting cholesterol and glucose, and detailed medical and CV history. Transthoracic echocardiograms (echos) were performed on all women. Clinical outcomes included: CHTN (documented history or current BP ≥140/90), dyslipidemia, and metabolic syndrome (defined by NIDDK criteria). 62 women (36 cases and 26 controls) were enrolled in this study. 83% were African American. The average age at study visit (35.8 years) and median time from PEC exposure (9 years) was not different between cases and controls. Women with a history of PEC had a significantly higher incidence of new onset CHTN compared to controls (55.6% vs. 26.9%, p=0.04). Other CV risk factors were not significantly different (Table). Although left ventricular (LV) ejection fraction was not different between the groups, longitudinal strain (a sensitive marker of systolic dysfunction), and end-systolic elastance (a marker of LV contractility), were each significantly worse in cases (p=0.008 and p=0.001, respectively). Arterial load was higher in cases compared to controls. Women with a history of PEC have a higher rate of CHTN and subclinical systolic dysfunction 8-10 years after PEC exposure. This study suggests that identifiable and easily obtained clinical risk factors and cardiac changes can be assessed and may serve to improve risk stratification for women with a history of PEC. Importantly, these findings may enable early intervention and therapeutic strategies to decrease the long term CV morbidity associated with PEC. (K12-HD001265-15)

The success of pulmonary hypertension treatment: improved cardiac function by reducing the arterial load.

The success of pulmonary hypertension treatment: improved cardiac function by reducing the arterial load.

Pharmacological heart rate lowering in patients with a preserved ejection fraction-review of a failing concept.

Epidemiological studies have demonstrated that high resting heart rates are associated with increased mortality. Clinical studies in patients with heart failure and reduced ejection fraction have shown that heart rate lowering with beta-blockers and ivabradine improves survival. It is therefore often assumed that heart rate lowering is beneficial in other patients as well. Here, we critically appraise the effects of pharmacological heart rate lowering in patients with both normal and reduced ejection fraction with an emphasis on the effects of pharmacological heart rate lowering in hypertension and heart failure. Emerging evidence from recent clinical trials and meta-analyses suggest that pharmacological heart rate lowering is not beneficial in patients with a normal or preserved ejection fraction. This has just begun to be reflected in some but not all guideline recommendations. The detrimental effects of pharmacological heart rate lowering are due to an increase in central blood pressures, higher left ventricular systolic and diastolic pressures, and increased ventricular wall stress. Therefore, we propose that heart rate lowering per se reproduces the hemodynamic effects of diastolic dysfunction and imposes an increased arterial load on the left ventricle, which combine to increase the risk of heart failure and atrial fibrillation. Pharmacologic heart rate lowering is clearly beneficial in patients with a dilated cardiomyopathy but not in patients with normal chamber dimensions and normal systolic function. These conflicting effects can be explained based on a model that considers the hemodynamic and ventricular structural effects of heart rate changes.

Influence of critical closing pressure on systemic vascular resistance and total arterial compliance: A clinical invasive study

Systemic vascular resistance (SVR) and total arterial compliance (TAC) modulate systemic arterial load, and their product is the time constant (Tau) of the Windkessel. Previous studies have assumed that aortic pressure decays towards a pressure asymptote (P∞) close to 0mmHg, as right atrial pressure is considered the outflow pressure. Using these assumptions, aortic Tau values of ∼1.5seconds have been documented. However, a zero P∞ may not be physiological because of the high critical closing pressure previously documented in vivo. To calculate precisely the Tau and P∞ of the Windkessel, and to determine the implications for the indices of systemic arterial load. Aortic pressure decay was analysed using high-fidelity recordings in 16subjects. Tau was calculated assuming P∞=0mmHg, and by two methods that make no assumptions regarding P∞ (the derivative and best-fit methods). Assuming P∞=0mmHg, we documented a Tau value of 1372±308ms, with only 29% of Windkessel function manifested by end-diastole. In contrast, Tau values of 306±109 and 353±106ms were found from the derivative and best-fit methods, with P∞ values of 75±12 and 71±12mmHg, and with ∼80% completion of Windkessel function. The "effective" resistance and compliance were ∼70% and ∼40% less than SVR and TAC (area method), respectively. We did not challenge the Windkessel model, but rather the estimation technique of model variables (Tau, SVR, TAC) that assumes P∞=0. The study favoured a shorter Tau of the Windkessel and a higher P∞ compared with previous studies. This calls for a reappraisal of the quantification of systemic arterial load.

Blood Pressure and Arterial Load After Transcatheter Aortic Valve Replacement for Aortic Stenosis

After aortic valve replacement, left ventricular afterload is often characterized by the residual valve obstruction. Our objective was to determine whether higher systemic arterial afterload-as reflected in blood pressure, pulsatile and resistive load-is associated with adverse clinical outcomes after transcatheter aortic valve replacement (TAVR). Total, pulsatile, and resistive arterial load were measured in 2141 patients with severe aortic stenosis treated with TAVR in the PARTNER I trial (Placement of Aortic Transcatheter Valve) who had systolic blood pressure (SBP) and an echocardiogram obtained 30 days after TAVR. The primary end point was 30-day to 1-year all-cause mortality. Lower SBP at 30 days after TAVR was associated with higher mortality (20.0% for SBP 100-129 mm Hg versus 12.0% for SBP 130-170 mm Hg; P<0.001). This association remained significant after adjustment, was consistent across subgroups, and confirmed in sensitivity analyses. In adjusted models that included SBP, higher total and pulsatile arterial load were associated with increased mortality (P<0.001 for all), but resistive load was not. Patients with low 30-day SBP and high pulsatile load had a 3-fold higher mortality than those with high 30-day SBP and low pulsatile load (26.1% versus 8.1%; hazard ratio, 3.62; 95% confidence interval, 2.36-5.55). Even after relief of valve obstruction in patients with aortic stenosis, there is an independent association between post-TAVR blood pressure, systemic arterial load, and mortality. Blood pressure goals in patients with a history of aortic stenosis may need to be redefined. Increased pulsatile arterial load, rather than blood pressure, may be a target for adjunctive medical therapy to improve outcomes after TAVR. URL: http://www.clinicaltrials.gov. Unique identifier: NCT00530894.

Ventricular-arterial coupling in centenarians without cardiovascular diseases.

Ventricular-arterial (VA) coupling is a central determinant of cardiovascular system performance and cardiac energetics. This index is expressed by the Ea/Ees ratio, where the effective arterial elastance (Ea) indicates the net arterial load exerted on the left ventricle and the left ventricular end-systolic elastance (Ees) is a load-independent measure of left ventricular chamber performance. Thirty-three centenarians (100.6 ± 1.2years, range 99-105years, 10M) without cardiovascular diseases underwent a complete echocardiographic evaluation and an instantaneous arterial blood pressure measurement, to characterize the Ea/Ees ratio and its two determinants indexed to body surface area. VA coupling was markedly reduced (Ea/Ees ratio 0.40 ± 0.1), reflecting a disproportionate increase in Ees index (8.5 ± 2.2mmHg/ml/m2) compared with Ea index (3.2 ± 0.8mmHg/ml/m2). Notably, the coupling ratio was significantly lower in women (0.37 ± 0.1) than in men (0.45 ± 0.1, p = 0.0003), due to an increase in Ees index significantly greater in women (9.4 ± 1.9mmHg/ml/m2) than in men (6.5 ± 1.5mmHg/ml/m2, p = 0.0002). Using multivariate regression analysis, only female gender (β coefficient -0.04, p = 0.01) and relative wall thickness (β coefficient -0.49, p < 0.0001) showed a significant inverse correlation to VA coupling. Our analysis in a population of centenarians without overt cardiovascular disease revealed very low values of VA coupling, especially in women. Both a LV structural remodeling as well as a high aortic elastance might have contributed to a secondary disproportionate increase in myocardial stiffness.

Effects of arterial load variations on dynamic arterial elastance: an experimental study

BackgroundDynamic arterial elastance (Eadyn), the relationship between pulse pressure variation (PPV) and stroke volume variation (SVV), has been suggested as a functional assessment of arterial load. The aim of this study was to evaluate the impact of arterial load changes during acute pharmacological changes, fluid administration, and haemorrhage on Eadyn. MethodsEighteen anaesthetized, mechanically ventilated New Zealand rabbits were studied. Arterial load changes were induced by phenylephrine (n=9) or nitroprusside (n=9). Thereafter, animals received a fluid bolus (10 ml kg−1), followed by stepwise bleeding (blood loss: 15 ml kg−1). The influence of arterial load and cardiac variables on PPV, SVV, and Eadyn was analysed using a linear mixed-effects model analysis. ResultsAfter phenylephrine infusion, mean (sd) Eadyn decreased from 0.89 (0.14) to 0.49 (0.12), P<0.001; whereas after administration of nitroprusside, Eadyn increased from 0.80 (0.23) to 1.28 (0.21), P<0.0001. Overall, the fluid bolus decreased Eadyn [from 0.89 (0.44) to 0.73 (0.35); P<0.01], and haemorrhage increased it [from 0.78 (0.23) to 0.95 (0.26), P=0.03]. Both PPV and SVV were associated with similar arterial factors (effective arterial elastance, arterial compliance, and resistance) and heart rate. Furthermore, PPV was also related to the acceleration and peak velocity of aortic blood flow. Both arterial and cardiac factors contributed to the evolution of Eadyn throughout the experiment. ConclusionsAcute modifications of arterial load induced significant changes on Eadyn; vasodilatation increased Eadyn, whereas vasoconstriction decreased it. The Eadyn was associated with both arterial load and cardiac factors, suggesting that Eadyn should be more properly considered as a ventriculo-arterial coupling index.

Predictors to Intravenous Fluid Responsiveness.

Management with intravenous fluids can improve cardiac output in some surgical patients. Management with static preload indicators, such as central venous pressure and pulmonary artery occlusion pressure, has not demonstrated a suitable relationship with changes in the cardiac output induced by intravenous fluid therapy. Dynamic indicators, such as the variability of arterial pulse pressure or stroke volume variation, have demonstrated a suitable relationship. Since improvement in cardiac output does not guarantee an adequate perfusion pressure, in patients with hypotension, it is also necessary to know whether arterial pressure will also increase with intravenous fluid therapy. In this regard, the functional assessment of arterial load by dynamic arterial elastance could help to determine which patients will improve not only their cardiac output but also their mean arterial pressure.

Gradual loading ameliorates maladaptation in computational simulations of vein graft growth and remodelling.

Vein graft failure is a prevalent problem in vascular surgeries, including bypass grafting and arteriovenous fistula procedures in which veins are subjected to severe changes in pressure and flow. Animal and clinical studies provide significant insight, but understanding the complex underlying coupled mechanisms can be advanced using computational models. Towards this end, we propose a new model of venous growth and remodelling (G&R) based on a constrained mixture theory. First, we identify constitutive relations and parameters that enable venous adaptations to moderate perturbations in haemodynamics. We then fix these relations and parameters, and subject the vein to a range of combined loads (pressure and flow), from moderate to severe, and identify plausible mechanisms of adaptation versus maladaptation. We also explore the beneficial effects of gradual increases in load on adaptation. A gradual change in flow over 3 days plus an initial step change in pressure results in fewer maladaptations compared with step changes in both flow and pressure, or even a gradual change in pressure and flow over 3 days. A gradual change in flow and pressure over 8 days also enabled a successful venous adaptation for loads as severe as the arterial loads. Optimization is used to accelerate parameter estimation and the proposed framework is general enough to provide a good starting point for parameter estimations in G&R simulations.

Effect of Cardiac Resynchronization Therapy on Arterial-Ventricular Coupling during Exercise in Heart Failure with Reduced Ejection Fraction

Exercise intolerance in heart failure with reduced ejection fraction (HFrEF) is mediated, in part, by an impairment in arterial-ventricular coupling. Cardiac resynchronization therapy (CRT) improves resting and paced arterial-ventricular coupling. The effect of chronic CRT on arterial-ventricular coupling during exercise in HFrEF has not been studied. PURPOSE: To study the effects of 6 months of CRT on arterial-ventricular coupling during exercise in patients with HFrEF. METHODS: Seven patients with HFrEF (59 ± 9 yrs; m/f: 5/2; NYHA III/IV = 6/1; EF = 18 ± 3%; peak VO2 = 12.5 ± 3.6 ml/kg/min) were studied pre-CRT and 6 months following (post-CRT). After resting measurements, subjects performed cycle ergometry at 22 ± 8 W (70 ± 13% of peak VO2) for 4 min. Left ventricular volumes were determined using contrast enhanced echocardiography. Blood pressure was measured manually at the brachium. End-systolic pressure (ESP) was approximated as 0.9 × systolic blood pressure. Effective arterial elastance (Ea) was calculated as ESP/stroke volume and end-systolic elastance (Ees) was calculated as ESP/end-systolic volume. Arterial-ventricular coupling was calculated as Ea/Ees. Comparisons were made with a 2 (rest, exercise) × 2 (pre-CRT, post-CRT) repeated measures factorial ANOVA and t-tests. Data are mean ± SD and P < 0.05 was significant. RESULTS: There was a main effect of CRT on Ea, where the pre-CRT Ea increased 0.28 ± 0.45 mmHg/mL during exercise and the post-CRT Ea decreased 0.12 ± 0.25 mmHg/mL (P < 0.05). There was no main effect of CRT on Ees, as both the pre-CRT (0.04 ± 0.03 mmHg/mL) and post-CRT (0.08 ± 0.04 mmHg/mL) increase in Ees from rest to exercise was not significant (P > 0.05). However, resting and exercise Ees tended to be higher post-CRT. Lastly, there was a main effect of CRT on Ea/Ees, where Ea/Ees increased 0.40 ± 1.35 mmHg/mL from rest to exercise pre-CRT and Ea/Ees decreased 0.69 ± 0.35 mmHg/mL from rest to exercise post-CRT (P < 0.05). CONCLUSION: The improvement in arterial-ventricular coupling during exercise following chronic CRT in HFrEF can be attributed to improvements in arterial loading on the left ventricle, as contractility changes related to CRT were modest.

Aortic Waveform Analysis to Individualize Treatment in Heart Failure.

Afterload reduction is a cornerstone in the management of patients with heart failure (HF) and reduced ejection fraction. However, arterial load and the effect of HF therapies on afterload might vary between individuals. Tailoring vasoactive medicines to patients with HF based upon better understanding of arterial afterload may enable better individualization of therapy. Subjects with HF and reduced ejection fraction underwent aggressive titration of vasoactive HF therapies with assessment of central aortic waveforms analyzed using pulse wave, wave separation, and arterial reservoir models. Clinical response to treatment was assessed using the 6-minute walk test distance, which increased in 25 subjects and decreased or remained unchanged in 13. Subjects with improvement on therapy displayed higher aortic pressure wave pulsatility (central pulse pressure [PP], reflected pressure wave, and reservoir pressure) at study entry compared with subjects without improvement (all P<0.05). Parameters derived by the arterial analysis methods were strongly correlated with one another and displayed similar ability to predict improvement. Aortic pressure pulsatility significantly decreased in subjects with functional improvement, whereas no change was observed in patients without functional improvement (P for interaction <0.05). These differences in arterial load at baseline and on therapy were not apparent from conventional brachial artery cuff pressure assessments. Increased aortic pressure wave pulsatility and greater decrease in pulsatility on treatment are associated with functional improvement in patients with HF and reduced ejection fraction receiving aggressive vasodilator titration. These differences are not identifiable using brachial cuff pressures. Central aortic waveform analysis may enable better individualization of vasoactive therapies in chronic HF and reduced ejection fraction. URL: http://www.clinicaltrials.gov. Unique identifier: NCT00588692.

Cardiac dysfunction in cancer survivors unmasked during exercise.

The cardiac dysfunction associated with anthracycline-based chemotherapy cancer treatment can exist subclinically for decades before overt presentation. Stress echocardiography, the measurement of left ventricular (LV) deformation and arterial haemodynamic evaluation, has separately been used to identify subclinical cardiovascular (CV) dysfunction in several patient groups including those with hypertension and diabetes. The purpose of the present cross-sectional study was to determine whether the combination of these techniques could be used to improve the characterisation of subclinical CV dysfunction in long-term cancer survivors previously treated with anthracyclines. Thirteen long-term cancer survivors (36 ± 10 years) with prior anthracycline exposure (11 ± 8 years posttreatment) and 13 age-matched controls were recruited. Left ventricular structure, function and deformation were assessed using echocardiography. Augmentation index was used to quantify arterial haemodynamic load and was measured using applanation tonometry. Measurements were taken at rest and during two stages of low-intensity incremental cycling. At rest, both groups had comparable global LV systolic, diastolic and arterial function (all P > 0·05); however, longitudinal deformation was significantly lower in cancer survivors (-18 ± 2 vs. -20 ± 2, P < 0·05). During exercise, this difference between groups persisted and further differences were uncovered with significantly lower apical circumferential deformation in the cancer survivors (-24 ± 5 vs. -29 ± 5, -29 ± 5 vs. 35 ± 8 for first and second stage of exercise respectively, both P < 0·05). In contrast to resting echocardiography, the measurement of LV deformation at rest and during exercise provides a more comprehensive characterisation of subclinical LV dysfunction. Larger studies are required to determine the clinical relevance of these preliminary findings.

Arterial-ventricular coupling and parameters of vascular stiffness in hypertensive patients: Role of gender.

ObjectiveNon-invasive estimation of arterial–ventricular coupling has been extensively used for the evaluation of cardiovascular performance, however, a relative small amount of data is available regarding arterial–ventricular coupling and its components in hypertension. The present study was designed to investigate the relationship between left ventricular elastance, arterial elastance, parameters of vascular stiffness and the influence of gender in a population of hypertensive individuals.MethodsIn 102 patients, trans-thoracic cardiac ultrasound, parameters of aortic stiffness (carotid-femoral pulse wave velocity) and wave reflection (augmentation index) were recorded. Ultrasound images of common carotid arteries were acquired for the assessment of intima-media thickness as well as carotid compliance and distensibility coefficient.ResultsMean age was 61 years, 32% diabetes, 56% dyslipidemia, 9% previous cardiovascular events; women (n = 32) and men were superimposable for cardiovascular risk factors prevalence. In the population, ventricular elastance was significantly correlated with arterial elastance (r = 0.887), age (r = 0.334), gender (r = −0.494), BMI (r = −0.313), augmentation index (r = 0.479) (all p < 0.001); and with carotid compliance and distensibility coefficient (r = 0.229 and r = − 0.250, respectively, both p < 0.05); however, only arterial elastance and gender were independently associated with ventricular elastance in multiple regression models adjusted for confounding factors. Gender-specific analysis revealed that arterial elastance and augmentation index remained statistically significant associated with ventricular elastance in men (r = 0.275, p = 0.04); instead augmentation index was no longer significant (r = 0.052, p = 0.77) in the female sex.ConclusionsIn hypertensive patients, main determinants of ventricular elastance are arterial elastance, as an integrated index of arterial vascular load, and gender; however, pressure augmentation might play an additional role in men.

Cardiac mechanics and dysfunction with anthracyclines in the community: results from the PREDICT study

BackgroundOur objective was to determine the relevance of changes in myocardial mechanics in diagnosing and predicting cancer therapeutics-related cardiac dysfunction (CTRCD) in a community-based population treated with anthracyclines.MethodsQuantitative measures of...

Ventricular-Arterial Coupling in Chronic Heart Failure.

Measures of interaction between the left ventricle (LV) and arterial system (ventricular-arterial coupling) are important but under-recognised cardiovascular phenotypes in heart failure. Ventriculo-arterial coupling is commonly assessed in the pressure-volume plane, using the ratio of effective arterial elastance (EA) to LV end-systolic elastance (EES) to provide information on ventricular-arterial system mechanical efficiency and performance when LV ejection fraction is abnormal. These analyses have significant limitations, such as neglecting systolic loading sequence, and are less informative in heart failure with preserved ejection fraction (HFpEF). EA is almost entirely dependent on vascular resistance and heart rate. Assessment of pulsatile arterial haemodynamics and time-resolved myocardial wall stress provide critical incremental physiological information and should be more widely utilised. Pulsatile arterial load represents a promising therapeutic target in HFpEF. Here, we review various approaches to assess ventricular-arterial interactions, and their pathophysiological and clinical implications in heart failure.

Association of Systemic Arterial Properties With Right Ventricular Morphology: The Multi-Ethnic Study of Atherosclerosis (MESA)-Right Ventricle Study.

BackgroundSystemic arterial stiffness is recognized as a major contributor to development of left ventricular dysfunction and failure; however, the relationship of systemic arterial properties and the right ventricle (RV) is unknown.Methods and ResultsThe associations between systemic arterial measures (total arterial compliance [TAC], systemic vascular resistance [SVR], and aortic augmentation index [AI]) and RV morphology (mass, end‐systolic [RVESV] and end‐diastolic volume [RVEDV], and ejection fraction [RVEF]) were examined using data from the Multi‐Ethnic Study of Atherosclerosis. All analyses were adjusted for anthropometric, demographic, and clinical variables and the corresponding left ventricular parameter. A total of 3842 subjects without clinical cardiovascular disease were included with a mean age of 61 years, 48% male, 39% non‐Hispanic white, 25% Chinese‐American, 23% Hispanic, and 13% black. RV measures were within normal range for age and sex. A 1‐mL/mm Hg decrease in TAC was associated with 3.9‐mL smaller RVESV, 7.6‐mL smaller RVEDV, and 2.4‐g lower RV mass. A 5‐Wood‐unit increase in SVR was associated with 0.6‐mL decrease in RVESV, 1.7‐mL decrease in RVEDV, and 0.4‐g decrease in RV mass. A 1% increase in AI was associated with 0.2‐mL decrease in RVEDV. We found significant effect modification by age, sex, and race for some of these relationships, with males, whites, and younger individuals having greater decreases in RV volumes and mass.ConclusionsMarkers of increased systemic arterial load were associated with smaller RV volumes and lower RV mass in a population of adults without clinical cardiovascular disease.

Carotid Doppler flowmetry correlates poorly with thermodilution cardiac output following cardiac surgery.

It remains unclear whether measuring carotid arterial flow by the time velocity integral using vascular Doppler ultrasound can be used to monitor cardiac output and volume responsiveness. The carotid Doppler flow (time velocity integral and peak flow velocity variation) was assessed in triplicate by an intensivist with formal vascular ultrasound training. Thirty-three patients admitted following coronary by-pass surgery were studied before and after a passive leg-raising manoeuvre to investigate volume responsiveness (more than 10% increase in cardiac output) along with indices of arterial load measuring cardiac output by thermodilution. Pearson's correlation coefficient and area under the curve (AUC) by receiver operating characteristics were calculated. A significant correlation between carotid Doppler flow and cardiac output was demonstrated in post-operative cardiac surgery patients (r = 0.80 [95%CI 0.61-0.89]), including relative changes following passive leg raising (r = 0.79 [95%CI 0.60-0.89]) that showed a mean difference of 2% with wide limits of agreements (-19% to 16%). Changes in carotid Doppler flow following passive leg raising correlated with the baseline arterial resistance but not with compliance or effective elastance. A peak flow variation > 10% before passive leg raising discriminated responders to the manoeuvre with an AUC of 0.81 [95% CI 0.55-0.95]. Weak correlations between common carotid Doppler flow and cardiac output mean that the methods cannot be used interchangeably in post-operative cardiac surgery patients.