An exploratory assessment of stretch-induced transmural myocardial fiber kinematics in right ventricular pressure overload.

Right ventricular (RV) remodeling and longitudinal fiber reorientation in the setting of pulmonary hypertension (PH) affects ventricular structure and function, eventually leading to RV failure. Characterizing the kinematics of myocardial fibers helps better understanding the underlying mechanisms of fiber realignment in PH. In the current work, high-frequency ultrasound imaging and structurally-informed finite element (FE) models were employed for an exploratory evaluation of the stretch-induced kinematics of RV fibers. Image-based experimental evaluation of fiber kinematics in porcine myocardium revealed the capability of affine assumptions to effectively approximate myofiber realignment in the RV free wall. The developed imaging framework provides a noninvasive modality to quantify transmural RV myofiber kinematics in large animal models. FE modeling results demonstrated that chronic pressure overload, but not solely an acute rise in pressures, results in kinematic shift of RV fibers towards the longitudinal direction. Additionally, FE simulations suggest a potential protective role for concentric hypertrophy (increased wall thickness) against fiber reorientation, while eccentric hypertrophy (RV dilation) resulted in longitudinal fiber realignment. Our study improves the current understanding of the role of different remodeling events involved in transmural myofiber reorientation in PH. Future experimentations are warranted to test the model-generated hypotheses.

Utility of the amplitude of RV1+SV5/6 in assessment of pulmonary hypertension.

Electrocardiogram (ECG) has been widely used for assessment of right ventricular (RV) hypertrophy (RVH) in patients with pulmonary hypertension (PH). However, it still remains unclear which ECG criteria of RVH are useful to predict for the severity of PH. The aim of our study was to examine the utility of ECG findings of RVH in assessment of PH. A total of 53 patients (42 women, mean age; 57.6 ± 16.4 years) with pre-capillary PH, who were diagnosed by right heart catheterization, underwent blood sampling, ECG, and cardiac magnetic resonance within a week before the right heart catheterization. We assessed the traditional ECG criteria of RVH in PH patients, and compared to age- and gender-matched control subjects without PH confirmed by 2-dimensional echocardiography (n = 42, mean age 55.3 ± 15.9 years). We also analyzed the clinical variables associated with ECG findings in patients with PH. Mean pulmonary arterial pressure (mPAP), cardiac index, and pulmonary vascular resistance (PVR) in PH patients were 35.3 ± 11.9 mmHg, 2.82 (2.09-3.45) L/min/m2, and 576 ± 376 dyne·sec·cm-5, respectively. The prevalence of right axis deviation (43.4%), R:S ratio V1 > 1 (32.1%), and RV1+SV5/6 > 10.5 mm (69.8%) in PH patients was greater than those in control subjects (p < 0.001). In univariate analysis, mPAP, PVR, RV wall thickness, RV mass index, RV volume, and RV ejection fraction (EF) (inversely) were significantly correlated with the amplitude of RV1+SV5/6. Multiple regression analysis revealed that mPAP and RVEF (inversely) were independently associated with the amplitude of RV1+SV5/6 (R2 = 0.282). Also, we performed the survival analysis among pre-capillary PH patients. During a mean follow-up of 3.7 years, patients with ≥ 16.4 mm of RV1+SV5/6 had worse prognosis than those with < 16.4 mm (Log rank p = 0.015). In conclusion, the amplitude of SV1+RV5/6 could be the most useful factor reflected for RV remodeling, hemodynamics and survival in patients with pre-capillary PH.

Eisenmenger syndrome - an electrocardiographic and echocardiographic assessment of the right ventricle.

BACKGROUND: Eisenmenger syndrome represents severe, irreversible, and end-stage pulmonary arterial hypertension (PAH) associated with congenital heart defects. For long-term outcome optimal right ventricular (RV) adaptation is crucial with precise assessment of its hypertrophy, dilatation and function. OBJECTIVES: Associations of electrocardiographic (ECG) and echocardiographic (ECHO) RV characteristics were analyzed. METHODS: Included were 52 patients (39F/13M), median age 45 years (24-78). Following ECG parameters were analyzed: Butler-Leggett formula (B-L), Sokolow-Lyon criterion (S-L), QRS duration (QRS), maximum spatial QRS vector magnitude (QRS max); and ECHO parameters: RV diameter (RVd), RV wall thickness (RVAW), RV/LV function. RESULTS: Following significant ECG-ECHO associations were demonstrated: S-L criterion and B-L formula with RVAW (p 120 ms only with severely dilated RV (RVd > 45 mm), while QRS max 33 mm); A new combined scoring system was introduced. CONCLUSIONS: In Eisenmenger syndrome RV hypertrophy is compensatory; diagnosis of prognostically unfavorable RV dilatation is therefore important. Combined ECG-ECHO analysis enables more accurate risk stratification. QRS duration > 120 ms seems to be a late marker; QRS max together with ECHO parameters may help to distinguish patients at higher risk for clinical deterioration (Tab. 3, Fig. 8, Ref. 53).

Sequential Right and Left Ventricular Assessment in Posttetralogy of Fallot Patients with Significant Pulmonary Regurgitation.

BACKGROUND: The natural history of right ventricular (RV) and left ventricular (LV) size and function among adults with tetralogy of Fallot (TOF) repair and hemodynamically significant pulmonary regurgitation (PR) is not known. The main aim of this study was to determine changes in RV and LV size and function over time in an adult population with TOF repair and hemodynamically significant pulmonary regurgitation. METHODS: Forty patients with repaired TOF and hemodynamically significant PR were included. These patients were identified on the basis of having more than one CMR between January 2008 and 2015. Patients with a prosthetic pulmonary valve or any cardiac intervention between CMR studies were excluded. Rate of progression (ROP) of RV dilation was determined for both indexed right ventricular end-systolic volume (RVESVi) and indexed right ventricular end-diastolic volume (RVEDVi), and calculated as the difference between the last and first volumes divided by the number of years between CMR#1 and CMR#2. Subjects were also divided into two groups based on the distribution of the ROP of RV dilation: Group I-rapid ROP (>50th percentile) and Group II-slower ROP (≤50th percentile). RESULTS: The interval between CMR#1 and CMR#2 was 3.9 ± 1.7 years (range 1-8 years). We did find a significant change in RVEDVi and RVESVi over this time period, although the magnitude of change was small. Nine patients (23%) had a reduction in right ventricular ejection fraction (RVEF) by greater than 5%, 13 patients (33%) had an increase in RVEDVi by greater than 10 mL/m2 and seven patients (18%) had an increase in RVESVi by greater than 10 mL/m2 . Median ROP for RVEDVi was 1.8 (range -10.4 to 21.8) mL/(m2 year); RVESVi 1.1 (range -5.8 to 24.5) mL/(m2 year) and RVEF -0.5 (range -8 to 4)%/year. Patients with a rapid ROP had significantly larger RV volumes at the time of CMR#1 and lower RVEF as compared to the slow ROP group. There was no overall significant change in LVEDVi, LVESVi, or LVEF over this time period. CONCLUSIONS: We have demonstrated, in a small population of patients with hemodynamically significant PR, that there is a small increase in RV volumes and decrease in RVEF over a mean 4-year period. We believe it to be reasonable practice to perform CMR at least every 4 years in asymptomatic patients with repaired TOF and hemodynamically significant PR. We found that LV volumes and function remained stable during the study period, suggesting that significant progressive LV changes are less likely to occur over a shorter time period. Our results inform a safe standardized approach to monitoring adults with hemodynamically significant PR post TOF repair and assist in planning allocation of this expensive and limited resource.

Novel assessment of haemodynamic kinetics with acute exercise in a rat model of pulmonary arterial hypertension.

NEW FINDINGS: What is the central question of this study? The acute effect of exercise at moderately high intensity on already-elevated pulmonary arterial pressures and right ventricular wall stress in a rat model of pulmonary arterial hypertension (PAH) is unknown. What is the main finding and its importance? We show, for the first time, that in a rat model of PAH, exercise induces an acute reduction in pulmonary artery pressure associated with lung endothelial nitric oxide synthase activation, without evidence of acute right ventricular inflammation or myocyte apoptosis. Haemodynamic measures obtained with traditional invasive methodology as well as novel implantable telemetry reveal an exercise-induced 'window' of pulmonary hypertension alleviation, supporting future investigations of individualized exercise as therapy in PAH. Exercise improves outcomes of multiple chronic conditions, but controversial results, including increased pulmonary artery (PA) pressure, have prevented its routine implementation in pulmonary arterial hypertension (PAH), an incurable disease that drastically reduces exercise tolerance. Individualized, optimized exercise prescription for PAH requires a better understanding of disease-specific exercise responses. We investigated the acute impact of exercise on already-elevated PA pressure and right ventricular (RV) wall stress and inflammation in a rat model of PAH (PAH group, n = 12) induced once by monocrotaline (50 mg kg(-1) , i.p.; 2 weeks), compared with healthy control animals (n = 8). Single bouts of exercise consisted of a 45 min treadmill run at 75% of individually determined aerobic capacity (V̇O2max). Immediately after exercise, measurements of RV systolic pressure and systemic pressure were made via jugular and carotid cannulation, and were followed by tissue collection. Monocrotaline induced moderate PAH, evidenced by RV hypertrophy, decreased V̇O2max, PA muscularization, and RV and skeletal muscle cytoplasmic glycolysis detected by increased expression of glucose transporter-1. Acute exercise normalized the monocrotaline-induced elevation in RV systolic pressure and augmented pulmonary endothelial nitric oxide synthase activation, without evidence of increased RV inflammation or apoptosis. Real-time recordings of pulmonary and systemic pressures during and after single bouts of exercise made using novel implantable telemetry in the same animal for up to 11 weeks after monocrotaline (40 mg kg(-1) ) corroborated the finding of acute PA pressure decreases with exercise in PAH. The PA pressure-lowering effects of individualized exercise associated with RV-neutral effects and increases in vasorelaxor signalling encourage further development of optimized exercise regimens as adjunctive PAH therapy.

Assessment of right ventricular geometry and mechanics in chronic obstructive pulmonary disease patients living at high altitude.

Degree of increase in pulmonary artery pressure (PAP) and adaptive responses in right ventricular morphology and mechanics play an important role in the prognosis of chronic obstructive pulmonary disease (COPD) patients. Three dimensional echocardiography and deformation imaging are recent advancements in echocardiography that allow more through assessment of right ventricle. We aimed to investigate right ventricular geometry and mechanics in a stable COPD population living at moderately high altitude. A total of 26 stable COPD patients with variable disease severity were included to this study. Pulmonary function tests, six minutes walking test (6MWT) and two- and three-dimensional echocardiography were performed for evaluation and data collection. Both systolic (43.06 ± 11.79 mmHg) and mean (33.38 ± 9.75 mmHg) PAPs were significantly higher in COPD patients compared to controls (p < 0.05, p < 0.001; respectively). Right ventricular volumes were similar between groups, although right ventricular free wall thickness was significantly increased in COPD group. The number of subjects with a sub-normal (<40 %) right ventricular ejection fraction was significantly higher in COPD group (45.8 vs. 17.4 %, p < 0.05), and the mean right ventricular strain was significantly lower (-21.05 ± 3.80 vs. -24.14 ± 5.37; p < 0.05). Only mean PAP and body surface area were found as independent predictors for 6MWT distance. Increased PAP and reduced right ventricular contractility were found in COPD patients living at moderately high altitude, although right ventricular volumes were normal. Similar findings can be expected in other COPD patients with high PAP, since these findings probably represents the effect of increased PAP on right ventricular mechanics.

Right and left ventricular function and myocardial scarring in adult patients with sickle cell disease: a comprehensive magnetic resonance assessment of hepatic and myocardial iron overload.

BACKGROUND: Patients with Sickle cell disease (SCD) who receive regular transfusions are at risk for developing cardiac toxicity from iron overload. The aim of this study was to assess right and left cardiac volumes and function, late gadolinium enhancement (LGE) and iron deposits in patients with SCD using CMR, correlating these values with transfusion burden, ferritin and hemoglobin levels. METHODS: Thirty patients with SCD older than 20 years of age were studied in a 1.5 T scanner and compared to age- and sex-matched normal controls. Patients underwent analysis of biventricular volumes and function, LGE and T2* assessment of the liver and heart. RESULTS: When compared to controls, patients with SCD presented higher left ventricular (LV) volumes with decreased ejection fraction (EF) with an increase in stroke volume (SV) and LV hypertrophy. The right ventricle (RV) also presented with a decreased EF and hypertrophy, with an increased end-systolic volume. Although twenty-six patients had increased liver iron concentrations (median liver iron concentration value was 11.83 ± 9.66 mg/g), only one patient demonstrated an abnormal heart T2* < 20 msec. Only four patients (13%) LGE, with only one patient with an ischemic pattern. CONCLUSIONS: Abnormal heart iron levels and myocardial scars are not a common finding in SCD despite increased liver iron overload. The significantly different ventricular function seen in SCD compared to normal suggests the changes in RV and LV function may not be due to the anemia alone. Future studies are necessary to confirm this association.

Application of 3-dimensional speckle tracking imaging to the assessment of right ventricular regional deformation.

BACKGROUND: The aim of this study was to carry out 3-dimensional speckle tracking imaging (3DSTI) of the right ventricle (RV) and evaluate RV regional wall deformation. METHODS AND RESULTS: 3DSTI of the RV was performed in 35 normal subjects, 8 patients with arrhythmogenic right ventricular cardiomyopathy, and 8 patients with pulmonary arterial hypertension. Peak systolic area change ratio and regional contraction timing relative to global systolic time (time to peak strain/time to end-systole×100) were measured in each segment. Good-quality images were acquired of the inflow segment in 87%, apex in 87%, outflow in 57%, and septum in 94% of the 35 normal subjects. In normal subjects, peak systolic area change ratio of the inflow anterior wall was -41±14%; inflow inferior wall, -35±9%; apical anterior wall, -41±10%; apical inferior wall, -31±11%; outflow, -31±9%; and septum wall, -36±11%. Contraction timing of the apical anterior wall and septum wall were earlier than those of other segments. In patients with RV dysfunction, 3DSTI indicated low peak systolic area change ratio in the damaged area. CONCLUSIONS: RV 3DSTI indicated segmental heterogeneity in magnitude and timing of RV contraction. 3DSTI may be a promising modality for providing precise quantitative information on complex RV wall motion.

Reversible pulmonary trunk banding: VII. Stress echocardiographic assessment of rapid ventricular hypertrophy in young goats.

BACKGROUND: Ventricle retraining with abrupt systolic overload can cause myocardial edema and necrosis, followed by late ventricular failure. Intermittent systolic overload could minimize the inadequacy of conventional pulmonary artery banding. The present study compared ventricle function under dobutamine stress in 2 protocols of systolic overload in young goats. METHODS: Nineteen young goats were divided into 3 groups: sham (n = 7; no systolic pressure overload), continuous (n = 6; systolic overload maintained for 96 hours), and intermittent (n = 6; 4 periods of 12-hour systolic overload, paired with a 12-hour resting period). Echocardiographic and hemodynamic evaluations were performed daily. The myocardial performance index and ejection fraction were evaluated at rest and during dobutamine stress. The goats were then killed for morphologic evaluation. RESULTS: The intermittent group underwent less systolic overload than the continuous group (P < .05). Nevertheless, both groups had increased right ventricular and septal masses compared with the sham group (P < .0002). Echocardiography revealed a major increase in right ventricular wall thickness in the intermittent group (+64.8% ± 23.37%) compared with the continuous group (+43.9% ± 19.26%; P = .015). Only the continuous group remained with significant right ventricular dilation throughout the protocol (P < .001). The intermittent group had a significantly better myocardial performance index at the end of the protocol, under resting and dobutamine infusion, compared with the continuous group (P < .012). CONCLUSIONS: Both systolic overload protocols have induced rapid right ventricular hypertrophy. However, only the intermittent group had better preservation of right ventricular function at the end of the protocol, both at rest and during dobutamine infusion.

Assessment of ventricular functions by tissue Doppler echocardiography in children with asthma.

Patients with asthma develop pulmonary hypertension due to recurrent hypoxia and chronic inflammation, leading to right heart enlargement with ventricular hypertrophy. Patients with severe asthma can experience cor pulmonale later in life, but little is known about ventricular function during the early stages of the disease. This study aimed to investigate ventricular functions in asymptomatic children with asthma as detected by conventional echocardiography and tissue Doppler echocardiography (TDE). Fifty-one pediatric patients (mean age 10.4 ± 2.2 years) with asthma and 46 age- and sex-matched healthy children (mean age 10.9 ± 2.4 years) were studied. All subjects were examined by conventional echocardiography and TDE, and they had pulmonary function tests on spirometry. The right-ventricular (RV) wall was statistically (p = 0.01) thicker among asthmatic patients (4.7 ± 1.5 mm) compared with healthy children (3.6 ± 0.4 mm). However, conventional pulsed-Doppler indices of both ventricles did not differ significantly between asthmatic patients and healthy children (p > 0.05). The results of TDE examining RV diastolic function showed that annular peak velocity during early diastole (E'), annular peak velocity during late diastole (A') (16.4 ± 1.8 and 5.1 ± 1.4 cm/s, respectively), E'/A' ratio (3.2 ± 0.7), isovolumetric relaxation time (67.7 ± 10.2 ms) and myocardial performance index (48.1 % ± 7.0 %) of the lateral tricuspid annulus among asthmatic patients differed significantly (p = 0.01) from those of healthy children (13.2 ± 2.3, 8.2 ± 2.0 cm/s, 1.6 ± 0.5, 46.2 ± 8.7 ms, and 42.0 % ± 5.7 %, respectively). Only peak expiratory flow (PEF) rate from the pulmonary function tests was negatively correlated with the E'/A' ratio of the tricuspid annulus (r = -0.38, p = 0.01). This study showed that although the findings of clinical and conventional echocardiography were apparently normal in children with asthma, TDE showed subclinical dysfunction of the right ventricle, which is negatively correlated with PEF. These findings signify the diagnostic value of TDE in the early detection and monitoring of such deleterious effects among asthmatic patients.

Cardiac magnetic resonance imaging for the assessment of the heart and pulmonary circulation in pulmonary hypertension.

Pulmonary hypertension is a disease of the pulmonary arteries resulting in a progressive increase in pulmonary vascular resistance, ultimately leading to right ventricular failure and death. The functional capacity of the right ventricle is a major prognostic determinant. Our understanding of right ventricle performance in pulmonary hypertension has been hindered by the lack of techniques that give a reliable picture of right ventricle morphology and function. Cardiac magnetic resonance (CMR) imaging enables a unique combination of morphological and functional assessment of the right ventricle and pulmonary circulation. In this review article, we introduce the technique of CMR imaging, review its use in imaging of the heart and pulmonary circulation and discuss its current and future application to the management of patients with pulmonary hypertension. There have been recent major advances in our understanding of the mechanism of disease development, in the diagnostic process, and in the treatment of pulmonary hypertension. Therapeutic advances in the management have reinforced the requirement for noninvasive, accurate and reproducible methods of assessment to act as "end-points" to measure the effects of treatment. We anticipate CMR imaging will increasingly be utilised as the primary modality for combined anatomic and functional assessments that enable more complete and efficient evaluation of pulmonary hypertension patients.

Doppler echocardiographic assessment of left ventricular diastolic function in chronic hypoxic rats.

Little information is available on the mechanism of diastolic left ventricular (LV) dysfunction in patients with chronic respiratory disease complicated by hypoxia. The purpose of this study was to investigate how chronic hypoxia impairs LV diastolic function in an hypoxic animal model. Thirty-six male Wistar rats 8 weeks old were assigned to normoxia (N), chronic hypoxia (CH), and re-normoxia (RN) groups, 12 rats per group. The N group rats were kept in ambient air for 8 weeks, while the CH group was kept hypoxic for 8 weeks. After 8 weeks of hypoxia the RN group rats were kept for a further 8 weeks in ambient air. LV systolic and diastolic functions, as well as right ventricular (RV) function, were analyzed using Doppler echocardiography;we also measured the hematocrit, and weighed the LV and RV. Hematocrit, RV weight/body weight, and RV weight/LV weight were higher in the CH group than in the other 2 groups. However, most of these parameters returned to normoxia levels after re-normoxia. In the CH group, LV dimension and area were smaller than in the other 2 groups. LV systolic function was preserved in all groups;however, in the CH group, mitral flow showed a restrictive pattern, while pulmonary flow demonstrated a pulmonary hypertensive pattern with prolonged RV ejection time. In conclusion, chronic hypoxia induced pulmonary hypertension and RV hypertrophy. Although LV systolic function was preserved, diastolic function was impaired in hypoxia. Ventricular interaction may impair LV diastolic function.

Genomic assessment of a multikinase inhibitor, sorafenib, in a rodent model of pulmonary hypertension.

Pulmonary hypertension (PH) and cancer pathology share growth factor- and MAPK stress-mediated signaling pathways resulting in endothelial and smooth muscle cell dysfunction and angioproliferative vasculopathy. In this study, we assessed sorafenib, an antineoplastic agent and inhibitor of multiple kinases important in angiogenesis [VEGF receptor (VEGFR)-1-3, PDGF receptor (PDGFR)-beta, Raf-1 kinase] as a potential PH therapy. Two PH rat models were used: a conventional hypoxia-induced PH model and an augmented PH model combining dual VEGFR-1 and -2 inhibition (SU-5416, single 20 mg/kg injection) with hypoxia. In addition to normoxia-exposed control animals, four groups were maintained at 10% inspired O(2) fraction for 3.5 wk (hypoxia/vehicle, hypoxia/SU-5416, hypoxia/sorafenib, and hypoxia/SU-5416/sorafenib). Compared with normoxic control animals, rats exposed to hypoxia/SU-5416 developed hemodynamic and histological evidence of severe PH while rats exposed to hypoxia alone displayed only mild elevations in hemodynamic values (pulmonary vascular and right ventricular pressures). Sorafenib treatment (daily gavage, 2.5 mg/kg) prevented hemodynamic changes and demonstrated dramatic attenuation of PH-associated vascular remodeling. Compared with normoxic control rats, expression profiling (Affymetrix platform) of lung RNA obtained from hypoxia [false discovery rate (FDR) 6.5%]- and hypoxia/SU-5416 (FDR 1.6%)-challenged rats yielded 1,019 and 465 differentially regulated genes (fold change >1.4), respectively. A novel molecular signature consisting of 38 differentially expressed genes between hypoxia/SU-5416 and hypoxia/SU-5416/sorafenib (FDR 6.7%) was validated by either real-time RT-PCR or immunoblotting. Finally, immunoblotting studies confirmed the upregulation of the MAPK cascade in both PH models, which was abolished by sorafenib. In summary, sorafenib represents a novel potential treatment for severe PH with the MAPK cascade a potential canonical target.

Noninvasive assessment of pulmonary arterial capacitance by echocardiography.

BACKGROUND: Pulmonary arterial capacitance (PAC) has been associated with right ventricular (RV) workload and mortality in pulmonary hypertension, but is not routinely evaluated in children. We investigated whether PAC can be estimated noninvasively by echocardiography. METHODS: We retrospectively determined PAC in 31 children with pulmonary hypertension, using echocardiography, and compared the results with those obtained at cardiac catheterization. RESULTS: PAC derived from echocardiography was similar to that derived from catheterization (mean +/- SD 1.16 +/- 1.0 vs 1.10 +/- 0.95 mL(3) x mm Hg(-1), P = not significant) and the two correlated well (r = 0.74, P < .0001). There was a highly significant polynomial relationship between PAC and RV anterior wall thickness indexed to body surface area (R(2) = 0.54, P < .0001), but not between pulmonary vascular resistance and RV wall thickness. Pulmonary vascular resistance and PAC did not correlate. CONCLUSIONS: Echocardiography can reliably estimate PAC, which strongly correlates with RV hypertrophy, a surrogate for RV work.

Live three-dimensional transthoracic echocardiographic assessment of anomalous origin of left coronary artery from the pulmonary artery.

We describe live three-dimensional transthoracic echocardiographic (3DTTE) findings in a 52-year-old female who had previously undergone an aortopulmonary tunnel operation for anomalous origin of the left coronary artery (ACA) from the pulmonary artery. Three-dimensional transthoracic echocardiography clearly delineated the origin of the ACA from the posterolateral aspect of the main pulmonary artery just above the pulmonary valve, the surgically created tunnel, as well as a small defect in the tunnel near the aortic end communicating with the pulmonary artery.

Quantitative assessment of regional right ventricular function with color kinesis.

We used color kinesis, a recent echocardiographic technique that provides regional information on the magnitude and timing of endocardial wall motion, to quantitatively assess regional right ventricular (RV) systolic and diastolic properties in 76 subjects who were divided into five groups, as follows: normal (n = 20), heart failure (n = 15), pressure/volume overload (n = 14), pressure overload (n = 12), and RV hypertrophy (n = 15). Quantitative segmental analysis of color kinesis images was used to obtain regional fractional area change (RFAC), which was displayed in the form of stacked histograms to determine patterns of endocardial wall motion. Time curves of integrated RFAC were used to objectively identify asynchrony of diastolic endocardial motion. When compared with normal subjects, patients with pressure overload or heart failure exhibited significantly decreased endocardial motion along the RV free wall. In the presence of mixed pressure/volume overload, the markedly increased ventricular septal motion compensated for decreased RV free wall motion. Diastolic endocardial wall motion was delayed in 17 of 72 segments (24%) in patients with RV pressure overload, and in 31 of 90 segments (34%) in patients with RV hypertrophy. Asynchrony of diastolic endocardial wall motion was greater in the latter group than in normal subjects (16% versus 10%: p < 0.01). Segmental analysis of color kinesis images allows quantitative assessment of regional RV systolic and diastolic properties.