3D and 4D Ultrasound: Current Progress and Future Perspectives.

PURPOSE OF REVIEW: Three-dimensional (3D) echocardiography (3DE) and 4-dimensional echocardiography (4DE), also known as real-time (RT) 3DE (RT3DE), are rapidly emerging technologies which have made significant impact in the clinical arena over the years. This review will discuss the recent applications of 3DE in diagnosing and treating different types of cardiovascular disease. RECENT FINDINGS: Recent studies using 3DE expanded on prior findings and introduced additional applications to different cardiac conditions. Some studies have used 3D parameters to prognosticate long-term outcomes. Numerous innovative software designs including fully automated algorithms have been introduced to better evaluate valvular heart disease and cardiac function. SUMMARY: With further evolution of 3DE technologies, this imaging modality will emerge as a powerful tool and likely become the imaging modality of choice in the diagnosis and management of various cardiac disorders.

Right ventricular function in heart failure with preserved ejection fraction: a community-based study.

BACKGROUND: The prevalence and clinical significance of right ventricular (RV) systolic dysfunction (RVD) in patients with heart failure and preserved ejection fraction (HFpEF) are not well characterized. METHODS AND RESULTS: Consecutive, prospectively identified HFpEF (Framingham HF criteria, ejection fraction ≥50%) patients (n=562) from Olmsted County, Minnesota, underwent echocardiography at HF diagnosis and follow-up for cause-specific mortality and HF hospitalization. RV function was categorized by tertiles of tricuspid annular plane systolic excursion and by semiquantitative (normal, mild RVD, or moderate to severe RVD) 2-dimensional assessment. Whether RVD was defined by semiquantitative assessment or tricuspid annular plane systolic excursion ≤15 mm, HFpEF patients with RVD were more likely to have atrial fibrillation, pacemakers, and chronic diuretic therapy. At echocardiography, patients with RVD had slightly lower left ventricular ejection fraction, worse diastolic dysfunction, lower blood pressure and cardiac output, higher pulmonary artery systolic pressure, and more severe RV enlargement and tricuspid valve regurgitation. After adjustment for age, sex, pulmonary artery systolic pressure, and comorbidities, the presence of any RVD by semiquantitative assessment was associated with higher all-cause (hazard ratio=1.35; 95% confidence interval, 1.03-1.77; P=0.03) and cardiovascular (hazard ratio=1.85; 95% confidence interval, 1.20-2.80; P=0.006) mortality and higher first (hazard ratio=1.99; 95% confidence interval, 1.35-2.90; P=0.0006) and multiple (hazard ratio=1.81; 95% confidence interval, 1.18-2.78; P=0.007) HF hospitalization rates. RVD defined by tricuspid annular plane systolic excursion values showed similar but weaker associations with mortality and HF hospitalizations. CONCLUSIONS: In the community, RVD is common in HFpEF patients, is associated with clinical and echocardiographic evidence of more advanced HF, and is predictive of poorer outcomes.

Three-dimensional color Doppler echocardiographic quantification of tricuspid regurgitation orifice area: comparison with conventional two-dimensional measures.

BACKGROUND: Three-dimensional (3D) color Doppler echocardiography (CDE) provides directly measured vena contracta area (VCA). However, a large comprehensive 3D color Doppler echocardiographic study with sufficiently severe tricuspid regurgitation (TR) to verify its value in determining TR severity in comparison with conventional quantitative and semiquantitative two-dimensional (2D) parameters has not been previously conducted. The aim of this study was to examine the utility and feasibility of directly measured VCA by 3D transthoracic CDE, its correlation with 2D echocardiographic measurements of TR, and its ability to determine severe TR. METHODS: Ninety-two patients with mild or greater TR prospectively underwent 2D and 3D transthoracic echocardiography. Two-dimensional evaluation of TR severity included the ratio of jet area to right atrial area, vena contracta width, and quantification of effective regurgitant orifice area using the flow convergence method. Full-volume breath-hold 3D color data sets of TR were obtained using a real-time 3D echocardiography system. VCA was directly measured by 3D-guided direct planimetry of the color jet. Subgroup analysis included the presence of a pacemaker, eccentricity of the TR jet, ellipticity of the orifice shape, underlying TR mechanism, and baseline rhythm. RESULTS: Three-dimensional VCA correlated well with effective regurgitant orifice area (r = 0.62, P < .0001), moderately with vena contracta width (r = 0.42, P < .0001), and weakly with jet area/right atrial area ratio. Subgroup analysis comparing 3D VCA with 2D effective regurgitant orifice area demonstrated excellent correlation for organic TR (r = 0.86, P < .0001), regular rhythm (r = 0.78, P < .0001), and circular orifice (r = 0.72, P < .0001) but poor correlation in atrial fibrillation rhythm (r = 0.23, P = .0033). Receiver operating characteristic curve analysis for 3D VCA demonstrated good accuracy for severe TR determination. CONCLUSIONS: Three-dimensional VCA measurement is feasible and obtainable in the majority of patients with mild or greater TR. Three-dimensional VCA measurement is also feasible in patients with atrial fibrillation but performed poorly even with <20% cycle length variation. Three-dimensional VCA has good cutoff accuracy in determining severe TR. This simple, straightforward 3D color Doppler measurement shows promise as an alternative for the quantification of TR.

Comparative study of high-resolution microimaging with 30-MHz scanner for evaluating cardiac function in mice.

BACKGROUND: The accurate assessment of cardiac function in mice is challenging because of their small heart size and rapid heart rate. METHODS: We examined the usefulness of novel high-resolution echocardiography (HRE) with a 30-MHz transducer in evaluating cardiac function in 20 mice compared with conventional echocardiography (CE) with a 13-MHz transducer. The left ventricular (LV) regional wall motion (RWM), LV end-diastolic dimension, fractional shortening, anterior LV wall thickness, E/A, and myocardial performance index were assessed. RESULTS: RWM analysis was more feasible by HRE than by CE (P < .05). Interobserver agreement in RWM analysis and correlation in LV end-diastolic dimension, fractional shortening, anterior LV wall thickness, E/A, and myocardial performance index were all better with HRE than CE. CONCLUSIONS: HRE is superior to CE in assessing LV function in mice. HRE is potentially a useful method for accurate assessment of cardiac function in various mice models.

H(2)O(2) regulates cardiac myocyte phenotype via concentration-dependent activation of distinct kinase pathways.

Reactive oxygen species (ROS) can act as signaling molecules to stimulate either hypertrophy or apoptosis in cardiac myocytes. We tested the hypothesis that the phenotypic effects of ROS are due to differential, concentration-dependent activation of specific kinase signaling pathways. Adult rat ventricular myocytes were exposed to H(2)O(2) over a broad concentration range (10-1000 microM). Low concentrations of H(2)O(2) (10-30 microM) increased protein synthesis without affecting survival. Higher concentrations of H(2)O(2) (100-200 microM) increased apoptosis (assessed by TUNEL). Still higher concentrations of H(2)O(2) (300-1000 microM) caused both apoptosis and necrosis. A hypertrophic concentration of H(2)O(2) (10 microM) increased the activity of ERK1/2, but not that of JNK, p38 kinase or Akt. An apoptotic concentration of H(2)O(2) (100 microM) activated JNK, p38 kinase and Akt, and further activated ERK1/2. The MEK1/2 inhibitor U0126 prevented the hypertrophic effect of 10 microM H(2)O(2). The apoptotic effect of 100 microM H(2)O(2) was inhibited bya dominant-negative JNK adenovirus, and was potentiated by U0126 or an Akt inhibitor. Thus, the concentration-dependent effects of ROS on myocyte hypertrophy and growth are due, at least in part, to the differential activation of specific kinase signaling pathways that regulate hypertrophy and apoptosis.

Beta-adrenergic receptor-stimulated apoptosis in cardiac myocytes is mediated by reactive oxygen species/c-Jun NH2-terminal kinase-dependent activation of the mitochondrial pathway.

Stimulation of beta-adrenergic receptors (betaARs) causes apoptosis in adult rat ventricular myocytes (ARVMs). The role of reactive oxygen species (ROS) in mediating betaAR-stimulated apoptosis is not known. Stimulation of betaARs with norepinephrine (10 micromol/L) in the presence of prazosin (100 nmol/L) for 24 hours increased the number of apoptotic myocytes as determined by TUNEL staining by 3.6- fold. The superoxide dismutase/catalase mimetics Mn(III)tetrakis(1-methyl-4-pyridyl)porphyrin pentachloride (MnTMPyP; 10 micromol/L) and Euk-134 decreased betaAR-stimulated apoptosis by 89+/-6% and 76+/-10%, respectively. Infection with an adenovirus expressing catalase decreased betaAR-stimulated apoptosis by 82+/-15%. The mitochondrial permeability transition pore inhibitor bongkrekic acid (50 micromol/L) decreased betaAR-stimulated apoptosis by 76+/-8%, and the caspase inhibitor zVAD-fmk (25 micromol/L) decreased betaAR-stimulated apoptosis by 62+/-11%. betaAR-stimulated cytochrome c release was inhibited by MnTMPyP. betaAR stimulation caused c-Jun NH2-terminal kinase (JNK) activation, which was abolished by MnTMPyP. Transfection with an adenovirus expressing dominant-negative JNK inhibited betaAR-stimulated apoptosis by 81+/-12%, and the JNK inhibitor SP600125 inhibited both betaAR-stimulated apoptosis and cytochrome c release. Thus, betaAR-stimulated apoptosis in ARVMs involves ROS/JNK-dependent activation of the mitochondrial death pathway.