Raquel Yotti

A Noninvasive Method for Assessing Impaired Diastolic Suction in Patients With Dilated Cardiomyopathy

Background— Diastolic suction is a major determinant of early left ventricular filling in animal experiments. However, suction remains incompletely characterized in the clinical setting. Methods and Results— First, we validated a method for measuring the spatio-temporal distributions of diastolic intraventricular pressure gradients and differences (DIVPDs) by digital processing color Doppler M-mode recordings. In 4 pigs, the error of peak DIVPD was 0.0±0.2 mm Hg (intraclass correlation coefficient, 0.95) compared with micromanometry. Forty patients with dilated cardiomyopathy (DCM) and 20 healthy volunteers were studied at baseline and during dobutamine infusion. A positive DIVPD (toward the apex) originated during isovolumic relaxation, reaching its peak shortly after mitral valve opening. Peak DIVPD was less than half in patients with DCM than in control subjects (1.2±0.6 versus 2.5±0.8 mm Hg, P<0.001). Dobutamine increased DIVPD in control subjects by 44% (P<0.001) but only by 23% in patients with DCM (P=NS). DIVPDs were the consequence of 2 opposite forces: a driving force caused by local acceleration, and a reversed (opposed to filling) convective force that lowered the total DIVPD by more than one third. In turn, local acceleration correlated with E-wave velocity and ejection fraction, whereas convective deceleration correlated with E-wave velocity and ventriculo:annular disproportion. Convective deceleration was highest among patients showing a restrictive filling pattern. Conclusions— Patients with DCM show an abnormally low diastolic suction and a blunted capacity to recruit suction with stress. By raising the ventriculo:annular disproportion, chamber remodeling proportionally increases convective deceleration and adversely affects left ventricular filling. These previously unreported mechanisms of diastolic dysfunction can be studied by using Doppler echocardiography.

Doppler-Derived Ejection Intraventricular Pressure Gradients Provide a Reliable Assessment of Left Ventricular Systolic Chamber Function

Background—Ejection intraventricular pressure gradients are caused by the systolic force developed by the left ventricle (LV). By postprocessing color Doppler M-mode (CDMM) images, we can measure noninvasively the ejection intraventricular pressure difference (EIVPD) between the LV apex and the outflow tract. This study was designed to assess the value of Doppler-derived EIVPDs as noninvasive indices of systolic chamber function. Methods and Results—CDMM images and pressure-volume (conductance) signals were simultaneously acquired in 9 minipigs undergoing pharmacological interventions and acute ischemia. Inertial, convective, and total EIVPD curves were calculated from CDMM recordings. Peak EIVPD closely correlated with indices of systolic function based on the pressure-volume relationship: peak elastance (within-animal R=0.98; between-animals R=0.99), preload recruitable stroke work (within-animal R=0.81; between-animals R=0.86), and peak of the first derivative of pressure corrected for end-diastolic volume (within-animal R=0.88; between-animals R=0.91). The correlation of peak inertial EIVPD with these indices was also high (all R>0.75). Load dependence of EIVPDs was studied in another 5 animals in which consecutive beats obtained during load manipulation were analyzed. During caval occlusion (40% EDV reduction), dP/dtmax, ejection fraction, and stroke volume significantly changed, whereas peak EIVPD remained constant. Aortic occlusion (40% peak LV pressure increase) significantly modified dP/dtmax, ejection fraction, and stroke volume; a nearly significant trend toward decreasing peak EIVPD was observed (P=0.06), whereas inertial EIVPD was unchanged (P=0.6). EIVPD beat-to-beat and interobserver variabilities were 2±12% and 5±11%, respectively. Conclusions—Doppler-derived EIVPDs provide quantitative, reproducible, and relatively load-independent indices of global systolic chamber function that correlate closely with currently available reference methods.

Cardiac dysfunction during liver transplantation: incidence and preoperative predictors.

Background. The aim was to investigate the cardiac response during liver transplantation (LT) and analyze its relationship with clinical factors, echocardiographic, and hemodynamic findings. Methods. All patients undergoing LT for cirrhosis from 1998 to 2004 were included. Clinical data, comprehensive echocardiography, hepatic, and right heart hemodynamic measurements were analyzed. During LT patients underwent continuous right-heart pressure monitorization. Measurements 10 min after reperfusion were compared with baseline values. Abnormal cardiac response was defined as a decrease in left ventricular stroke work index despite a rise in pulmonary wedge capillary pressure. Predictors of abnormal cardiac response were investigated using logistic regression. Results. Data were available from 209 patients (mean age 52 (9) yrs; Child A 27; B 93; C 89) with a mean model for end-stage liver disease score 16.3 (4.7). Abnormal cardiac response was observed in 47 (22.5%) patients after reperfusion. Patients who developed this response had hyponatremia, lower central venous pressure, lower pulmonary artery pressure, and lower pulmonary wedged capillary pressure. Abnormal cardiac response was related to a longer postoperative intubation time. Conclusion. Abnormal cardiac response is observed during LT and may be a manifestation of occult cirrhotic cardiomyopathy. This finding is underestimated with usual diagnostic tools and could be related to indirect signs of circulatory dysfunction of advanced liver disease.

Spatio-temporal mapping of intracardiac pressure gradients. A solution to Euler's equation from digital postprocessing of color Doppler M-mode echocardiograms.

Doppler assessment of intracardiac pressure gradients using the simplified Bernoulli equation is inaccurate in the absence of a restricted orifice. The purpose of this study is to develop a new general method to map instantaneous pressure gradients inside the heart using Doppler echocardiography. Color Doppler M-mode recordings are digitally postprocessed with a software algorithm that decodes flow velocity and fits a bivariate spatio-temporal tensor-product smoothing spline. Temporal and spatial accelerations are then calculated by analytical derivation of the fitted velocity data, allowing solution of both inertial and convective terms of Eulers equation. A database of 39 transmitral inflow and transaortic outflow color Doppler M-mode recordings from 20 patients with a number of cardiac conditions was analysed, along with matched pulsed-wave spectral recordings. A close agreement was observed between the spectral and postprocessed color Doppler velocity values (error = 0.8 +/- 11.7 cm/s), validating the data decoding and fitting process. Spatio-temporal pressure-gradient maps were obtained from all studies, allowing visualisation of instantaneous pressure gradients from the atrium to the apex during left ventricular filling, and from the apex to the outflow tract during ejection. Instantaneous pressure differences between localised intracardiac sample points closely matched previously published catheterization findings, both in magnitude and waveform shape. Our method shows that intracardiac instantaneous pressure gradients can be analysed noninvasively using color Doppler M-mode echocardiography combined with image postprocessing methods.

The heart in liver transplantation

The heart and liver are organs that are closely related in both health and disease. Patients who undergo liver transplantation may suffer from heart disease that is: (a) related to the original cause of the liver disease such as hemochromatosis, (b) related to the liver disease itself, or (c) related to other associated conditions. Furthermore, liver transplantation is one of the most cardiovascular stressful events that a patient with cirrhosis may undergo. After liver transplantation, the progression of pre-existing or the development of new-onset cardiac disease may occur. This article reviews the relationship between the heart and liver transplantation in the pre-transplant, intra-operative, and post-transplant periods.

Topology of Blood Transport in the Human Left Ventricle by Novel Processing of Doppler Echocardiography

Novel processing of Doppler-echocardiography data was used to study blood transport in the left ventricle (LV) of six patients with dilated cardiomyopathy and six healthy volunteers. Bi-directional velocity field maps in the apical long axis of the LV were reconstructed from color-Doppler echocardiography. Resulting velocity field data were used to perform trajectory-based computation of Lagrangian coherent structures (LCS). LCS were shown to reveal the boundaries of blood injected and ejected from the heart over multiple beats. This enabled qualitative and quantitative assessments of blood transport patterns and residence times in the LV. Quantitative assessments of stasis in the LV are reported, as well as characterization of LV vortex formations from E-wave and A-wave filling.

Contribution of the Diastolic Vortex Ring to Left Ventricular Filling

BACKGROUND Intraventricular fluid dynamics can be assessed clinically using imaging. The contribution of vortex structures to left ventricular (LV) diastolic function has never been quantified in vivo. OBJECTIVES This study sought to understand the impact of intraventricular flow patterns on filling and to assess whether impaired fluid dynamics may be a source of diastolic dysfunction. METHODS Two-dimensional flow velocity fields from color Doppler echocardiographic sequences were obtained in 20 patients with nonischemic dilated cardiomyopathy (NIDCM), 20 patients with hypertrophic cardiomyopathy (HCM), and 20 control healthy volunteers. Using a flow decomposition method, we isolated the rotational velocity generated by the vortex ring from the surrounding flow in the left ventricle. RESULTS The vortex was responsible for entering 13 ± 6% of filling volume in the control group and 19 ± 8% in the NIDCM group (p = 0.004), but only 5 ± 5% in the HCM group (p < 0.0001 vs. controls). Favorable vortical effects on intraventricular pressure gradients were observed in the control and NIDCM groups but not in HCM patients. Differences in chamber sphericity explained variations in the vortex contribution to filling between groups (p < 0.005). CONCLUSIONS The diastolic vortex is responsible for entering a significant fraction of LV filling volume at no energetic or pressure cost. Thus, intraventricular fluid mechanics are an important determinant of global chamber LV operative stiffness. Reduced stiffness in NIDCM is partially related to enhanced vorticity. Conversely, impaired vortex generation is an unreported mechanism of diastolic dysfunction in HCM and probably other causes of concentric remodeling.

Effects of angiotensin converting enzyme inhibitors in hypertensive patients with aortic valve stenosis: a drug withdrawal study

Objective: To determine the effects of angiotensin converting enzyme (ACE) inhibitors in hypertensive patients with aortic valve stenosis (AS). Design: Observational, drug withdrawal, single blinded study, with randomisation of the order of tests. Setting: Hypertension and asymptomatic AS. Patients and interventions: 20 patients (aged 73 (9) years, valve area 0.7 (0.3) cm2, left ventricular ejection fraction ⩾ 45%) were enrolled. Each patient underwent two sets of tests (with and without taking the drug), each of which included clinical evaluation, Doppler echocardiogram, and symptom limited exercise echocardiography. Main outcome measures: Functional and haemodynamic variables while taking and not taking ACE inhibitors. Results: Drug intervention induced no change in patients’ subjective functional class. While taking ACE inhibitors, patients had a lower systolic blood pressure (140 (18) mm Hg with ACE inhibitors v 159 (12) mm Hg without ACE inhibitors, p  =  0.02), a higher mean pressure gradient (34 (15) mm Hg v 28 (18) mm Hg, p  =  0.037), and a higher left ventricular stroke work loss (19 (6)% v 14 (10)%, p  =  0.009). Other baseline functional and haemodynamic parameters were unmodified. Five patients had an abnormal blood pressure response during one of the exercise tests (two patients while taking the drug and three patients while not taking the drug). When taking ACE inhibitors, patients had a higher stroke volume at peak stress (59 (11) ml v 54 (25) ml, p  =  0.046). All other stress variables remained constant. Conclusions: In AS, the afterload relief caused by ACE inhibitors is blunted by a parallel increase in the pressure gradient. However, ACE inhibitors favourably affect stress haemodynamic function in most hypertensive patients with AS and should not be discontinued.

Systemic vascular load in calcific degenerative aortic valve stenosis: insight from percutaneous valve replacement.

BACKGROUND Systemic arterial load impacts the symptomatic status and outcome of patients with calcific degenerative aortic stenosis (AS). However, assessing vascular properties is challenging because the arterial trees behavior could be influenced by the valvular obstruction. OBJECTIVES This study sought to characterize the interaction between valvular and vascular functions in patients with AS by using transcatheter aortic valve replacement (TAVR) as a clinical model of isolated intervention. METHODS Aortic pressure and flow were measured simultaneously using high-fidelity sensors in 23 patients (mean 79 ± 7 years of age) before and after TAVR. Blood pressure and clinical response were registered at 6-month follow-up. RESULTS Systolic and pulse arterial pressures, as well as indices of vascular function (vascular resistance, aortic input impedance, compliance, and arterial elastance), were significantly modified by TAVR, exhibiting stiffer vascular behavior post-intervention (all, p < 0.05). Peak left ventricular pressure decreased after TAVR (186 ± 36 mm Hg vs. 162 ± 23 mm Hg, respectively; p = 0.003) but remained at >140 mm Hg in 70% of patients. Wave intensity analysis showed abnormally low forward and backward compression waves at baseline, increasing significantly after TAVR. Stroke volume decreased (-21 ± 19%; p < 0.001) and correlated with continuous and pulsatile indices of arterial load. In the 48 h following TAVR, a hypertensive response was observed in 12 patients (52%), and after 6-month follow-up, 5 patients required further intensification of discharge antihypertensive therapy. CONCLUSIONS Vascular function in calcific degenerative AS is conditioned by the upstream valvular obstruction that dampens forward and backward compression waves in the arterial tree. An increase in vascular load after TAVR limits the procedures acute afterload relief.

Intraventricular vortex properties in nonischemic dilated cardiomyopathy

Vortices may have a role in optimizing the mechanical efficiency and blood mixing of the left ventricle (LV). We aimed to characterize the size, position, circulation, and kinetic energy (KE) of LV main vortex cores in patients with nonischemic dilated cardiomyopathy (NIDCM) and analyze their physiological correlates. We used digital processing of color-Doppler images to study flow evolution in 61 patients with NIDCM and 61 age-matched control subjects. Vortex features showed a characteristic biphasic temporal course during diastole. Because late filling contributed significantly to flow entrainment, vortex KE reached its maximum at the time of the peak A wave, storing 26 ± 20% of total KE delivered by inflow (range: 1-74%). Patients with NIDCM showed larger and stronger vortices than control subjects (circulation: 0.008 ± 0.007 vs. 0.006 ± 0.005 m(2)/s, respectively, P = 0.02; KE: 7 ± 8 vs. 5 ± 5 mJ/m, P = 0.04), even when corrected for LV size. This helped confining the filling jet in the dilated ventricle. The vortex Reynolds number was also higher in the NIDCM group. By multivariate analysis, vortex KE was related to the KE generated by inflow and to chamber short-axis diameter. In 21 patients studied head to head, Doppler measurements of circulation and KE closely correlated with phase-contract magnetic resonance values (intraclass correlation coefficient = 0.82 and 0.76, respectively). Thus, the biphasic nature of filling determines normal vortex physiology. Vortex formation is exaggerated in patients with NIDCM due to chamber remodeling, and enlarged vortices are helpful for ameliorating convective pressure losses and facilitating transport. These findings can be accurately studied using ultrasound.