Abstract: BACKGROUND: Diabetic cardiomyopathy has been characterized by an early impairment of left ventricular (LV) longitudinal function as opposed to preserved LV radial function. METHODS: Conventional echocardiography and longitudinal (ε(L)) and radial (ε(R)) systolic strain assessed by speckle-tracking imaging were obtained in 114 type 2 diabetic patients and 88 age-matched controls. RESULTS: LV ejection fraction was similar in diabetic patients and controls. The presence of subclinical LV systolic dysfunction in diabetic patients was demonstrated by lower values of midwall fractional shortening (18% ± 3% vs 20% ± 3%, P = .006), ε(L) (-19% ± 3% vs -22% ± 2%, P < .001), and ε(R) (50% ± 16% vs 56% ± 12%, P = .003) compared with controls. On multivariate analysis, factors predicting strain values were diabetes (P = .001) and gender (P = .001) for ε(L) and diabetes (P = .003) for ε(R). CONCLUSION: Diabetic patients without overt heart disease display subclinical alteration of both radial and longitudinal LV systolic function even after adjustment for blood pressure, age, and body mass index.
Abstract: OBJECTIVES: This study examined the effect of a single dose of cyclosporine administered at the time of reperfusion on left ventricular (LV) remodeling and function by cardiac magnetic resonance 5 days and 6 months after myocardial infarction. BACKGROUND: In a human study, administration of cyclosporine at the time of acute reperfusion was associated with a smaller infarct size. METHODS: Twenty-eight patients of the original cyclosporine study had an acute (at 5 days) and a follow-up (at 6 months) cardiac magnetic resonance study to determine LV volumes, mass, ejection fraction, myocardial wall thickness in infarcted and remote noninfarcted myocardium, and infarct size. RESULTS: There was a persistent reduction in infarct size at 6 months in the cyclosporine group compared with the control group of patients (29 +/- 15 g vs. 38 +/- 14 g; p = 0.04). There was a significant reduction of LV end-systolic volume (and a trend for LV end-diastolic volume; p = 0.07) in the cyclosporine group compared with the control group, both at 5 days and 6 months after infarction. There was no significant difference between the 2 groups in either global LV mass or regional wall thickness of the remote noninfarcted myocardium at 5 days or 6 months. Attenuation of LV dilation and improvement of LV ejection fraction by cyclosporine at 6 months were correlated with infarct size reduction. CONCLUSIONS: Cyclosporine used at the moment of acute myocardial infarction reperfusion persistently reduces infarct size and does not have a detrimental effect on LV remodeling. These results are preliminary and must be supported by further studies. (Ciclosporin A and Acute Myocardial Infarction; NCT00403728).
Abstract: BACKGROUND: Genetically modified mice offer the unique opportunity to gain insight into the pathophysiology of pulmonary arterial hypertension. In mice, right heart catheterization is the only available technique to measure right ventricular systolic pressure (RVSP). However, it is a terminal procedure and does not allow for serial measurements. Our objective was to validate a noninvasive technique to assess RVSP in mice. METHODS AND RESULTS: Right ventricle catheterization and echocardiography (30-MHz transducer) were simultaneously performed in mice with pulmonary hypertension induced acutely by infusion of a thromboxane analogue, U-46619, or chronically by lung-specific overexpression of interleukin-6. Pulmonary acceleration time (PAT) and ejection time (ET) were measured in the parasternal short-axis view by pulsed-wave Doppler of pulmonary artery flow. Infusion of U-46619 acutely increased RVSP, shortened PAT, and decreased PAT/ET. The pulmonary flow pattern changed from symmetrical at baseline to asymmetrical at higher RVSPs. In wild-type and interleukin-6-overexpressing mice, the PAT correlated linearly with RVSP (r(2)=-0.67, P<0.0001), as did PAT/ET (r(2)=-0.76, P<0.0001). Sensitivity and specificity for detecting high RVSP (>32 mm Hg) were 100% (7/7) and 86% (6/7), respectively, for both indices (cutoff values: PAT, <21 ms; PAT/ET, <39%). Intraobserver and interobserver variability of PAT and PAT/ET were <6%. CONCLUSIONS: Right ventricular systolic pressure can be estimated noninvasively in mice. Echocardiography is able to detect acute and chronic increases in RVSP with high sensitivity and specificity as well as to assess the effects of treatment on RVSP. This noninvasive technique may permit the characterization of the evolution of pulmonary arterial hypertension in genetically modified mice.
Abstract: A noninvasive assessment of infarct size and transmural extension of myocardial infarction (TEMI) is fundamental in experimental models of ischemia-reperfusion. Conventional echocardiography parameters are limited in this purpose. This study was designed to examine whether speckle tracking imaging can be used in a rat model of ischemia-reperfusion to accurately detect the reduction of infarct size and TEMI induced by erythropoietin (EPO) as early as 24 h after reperfusion. Rats were randomly assigned to one of three groups: myocardial infarction (MI)-control group, 45 min ischemia followed by 24 h of reperfusion; MI-EPO group, similar surgery with a single bolus of EPO administered at the onset of reperfusion; and sham-operated group. Short-axis two-dimensional echocardiography was performed after reperfusion. Global radial (GS(r)) and circumferential (GS(cir)) strains were compared with infarct size and TEMI assessed after triphenyltetrazolium chloride staining. As a result, ejection fraction, shortening fraction, GS(r), and GS(cir) significantly correlated to infarct size, whereas only GS(r) and GS(cir) significantly correlated to TEMI. EPO significantly decreased infarct size (30.8 + or - 3.5 vs. 56.2 + or - 5.7% in MI-control, P < 0.001) and TEMI (0.37 + or - 0.05 vs. 0.77 + or - 0.05 in MI-control, P < 0.001). None of the conventional echocardiography parameters was significantly different between the MI-EPO and MI-control groups, whereas GS(r) was significantly higher in the MI-EPO group (29.1 + or - 4.7 vs. 16.4 + or - 3.3% in MI-control; P < 0.05). Furthermore, GS(cir) and GS(r) appeared to be the best parameters to identify a TEMI >0.75 24 h after reperfusion. In conclusion, these findings demonstrate the usefulness of speckle tracking imaging in the early evaluation of a cardioprotective strategy in a rat model of ischemia-reperfusion.
Abstract: BACKGROUND: Cardiac resynchronization therapy (CRT), which improves left ventricular (LV) function and reverses LV remodeling, is an established therapy for advanced heart failure with prolonged QRS duration. The aim of this study was to examine whether CRT improves atrial function and induces atrial reverse remodeling. METHODS: A total of 46 patients with heart failure (mean age, 66.7 +/- 10.4 years) who underwent CRT were evaluated with echocardiography before and after 6 months of optimized CRT. Atrial function and LV function were assessed with M-mode, two-dimensional echocardiography, Doppler, tissue Doppler velocity, and strain (epsilon) imaging. LV reverse remodeling was defined as a reduction in LV end-systolic volume of >15%. RESULTS: In responders (n = 23), significant improvements in left atrial (LA) functional, structural, and anatomic remodeling were observed. Maximum LA area and volume decreased, the LA emptying fraction increased, A' increased, and LA epsilon increased from 25.6 +/- 11.0% to 42.6 +/- 10.4% (P < .05 overall). LA reverse remodeling was correlated with baseline LA volume (R = 0.45). Although the correlation was not significant (r = 0.24), LA reverse remodeling was also more frequent in patients with LV reverse remodeling. CONCLUSIONS: In patients with LV remodeling, significant LA reverse remodeling after CRT could be observed and detailed on transthoracic echocardiography.
Abstract: BACKGROUND: Hypoxemia is common in pulmonary hypertension (PH) and may be partly related to ventilation/perfusion mismatch, low diffusion capacity, low cardiac output, and/or right-to-left (RL) shunting. METHODS: To determine whether true RL shunting causing hypoxemia is caused by intracardiac shunting, as classically considered, a retrospective single center study was conducted in consecutive patients with precapillary PH, with hypoxemia at rest (PaO2 < 10 kPa), shunt fraction (Qs/Qt) greater than 5%, elevated alveolar-arterial difference of PO2 (AaPO2), and with transthoracic contrast echocardiography performed within 3 months. RESULTS: Among 263 patients with precapillary PH, 34 patients were included: pulmonary arterial hypertension, 21%; PH associated with lung disease, 47% (chronic obstructive pulmonary disease, 23%; interstitial lung disease, 9%; other, 15%); chronic thromboembolic PH, 26%; miscellaneous causes, 6%. Mean pulmonary artery pressure, cardiac index, and pulmonary vascular resistance were 45.8 +/- 10.8 mmHg, 2.2 +/- 0.6 L/min/m2, and 469 +/- 275 dyn.s.cm-5, respectively. PaO2 in room air was 6.8 +/- 1.3 kPa. Qs/Qt was 10.2 +/- 4.2%. AaPO2 under 100% oxygen was 32.5 +/- 12.4 kPa. Positive contrast was present at transthoracic contrast echocardiography in 6/34 (18%) of patients, including only 4/34 (12%) with intracardiac RL shunting. Qs/Qt did not correlate with hemodynamic parameters. Patients' characteristics did not differ according to the result of contrast echocardiography. CONCLUSION: When present in patients with precapillary PH, RL shunting is usually not related to reopening of patent foramen ovale, whatever the etiology of PH.
Abstract: AIMS: This study aimed to assess the influence of afterload alteration on radial (R) and longitudinal (L) left ventricular (LV) systolic regional functions. METHODS AND RESULTS: We analysed systolic myocardial function by two-dimensional strain (2D-S) and sonomicrometry (SS) in an experimental pig model of aortic banding. Both radial and longitudinal functions were analysed in six open-chest pigs under various loading conditions: baseline and graded aortic banding (subsequent increase in LV pressure of 10, 20, and 40 mmHg). Both systolic 2D-S(long) and 2D-S(rad) were significantly correlated with SS(long) and SS(rad) (r = 0.63, P < 0.001 and r = 0.65, P < 0.01, respectively). At a low increase in LV afterload, 2D-S(rad) was still preserved whereas 2D-S(long) significantly decreased. When LV afterload was subsequently increased, both 2D-S(rad) and 2D-S(long) significantly decreased. Difference in dependence to wall stress might explain these different behaviours. CONCLUSION: 2D-S shows a different response in longitudinal and radial functions to increased afterload. Longitudinal function is early impaired, whereas radial function remains preserved. This finding justifies the combined assessment of both radial and longitudinal regional myocardial functions to characterize myocardial dysfunction and might help to better identify the transition to heart failure in pressure-overload cardiomyopathy.
Abstract: The main mission statement of the European Association of Echocardiography (EAE) is 'to promote excellence in clinical diagnosis, research, technical development, and education in cardiovascular ultrasound in Europe'. As competence and quality control issues are increasingly recognized by patients, physicians, and payers, the EAE has established recommendations for training, competence, and quality improvement in echocardiography. The purpose of this document is to provide the requirements for training and competence in echocardiography, to outline the principles of quality measurement, and to recommend a set of measures for improvement, with the ultimate goal of raising the standards of echocardiographic practice in Europe.
Abstract: BACKGROUND: Cardiac magnetic resonance can detect myocardial oedema using myocardial transverse relaxation time (T2)-weighted sequences but quantitative data are lacking in patients evaluated early after acute myocardial infarction. AIM: To assess the spatial distribution of T2 in patients with recent acute myocardial infarction. METHODS: Twenty-four consecutive patients (mean age 60+/-11 years) with acute myocardial infarction (anterior, n=12; inferior, n=12) were evaluated prospectively. T2 was determined using a series of breath-hold T2-weighted segmented half-Fourier turbo-spin echo sequences. No-reflow was defined as the association of early hypoenhancement and delayed enhancement in an akinetic region after a bolus injection of DOTA-Gd (0.2 mmol/kg). RESULTS: No-reflow was present in 13 (54%) patients and absent in 11 (46%) patients. Mean T2 was increased in the infarct region (84.9+/-23.7 ms) compared with in the remote myocardium (62.8+/-10.3 ms, p=0.0001) and in control subjects (55.7+/-4.6 ms, p<0.0001), but also in the remote myocardium compared with control subjects (p<0.02). In patients with no-reflow, T2 was further increased within the infarcted subendocardium compared with in patients without no-reflow (97.9+/-24.8 ms vs 76.3+/-24.7 ms, p<0.03). Peak troponin correlated with T2 (r=0.47, p<0.02) and was higher in patients with no-reflow (297.9+/-249.7 microg/L) than in patients without no-reflow (42.4+/-43.1 microg/L, p=0.003). CONCLUSION: T2 was lengthened in both infarcted and remote myocardium and was influenced by the occurrence of no-reflow.
Abstract: BACKGROUND: Aging is accompanied by an alteration in myocardial contractility. However, its noninvasive detection is difficult. The effect of chronic exercise on this decrease is unknown. Murine models of senescence are increasingly used to test therapies in aging. We tested whether strain rate imaging detected left ventricular (LV) systolic dysfunction in aging mice and was able to assess a potential improvement after exercise. METHODS AND RESULTS: Young (3 weeks), adult (2 to 3 months), and old (6 to 18 months) C57BL6 male mice underwent echocardiograms with strain rate imaging, either in sedentary conditions or before, 2 weeks and 4 weeks after chronic swimming. Hemodynamic parameters of LV function including maximal and end-systolic elastance were obtained before euthanizing. LV fibrosis was measured using Sirius red staining. Conventional echocardiography was unable to detect LV systolic dysfunction in old mice, whereas both systolic strain rate and load-independent hemodynamic parameters such as preload recruitable stroke work and end-systolic elastance were significantly decreased. Both strain rate and load-independent hemodynamic parameters normalized after 4 weeks of exercise. Both endocardial and epicardial fibrosis were increased in the LV of aging mice. Endocardial fibrosis decreased in exercised aged mice. CONCLUSIONS: Strain rate noninvasively detects LV systolic dysfunction associated with aging in mice, whereas conventional echocardiography does not. Chronic exercise normalizes LV systolic function and decreases fibrosis in old mice. Strain rate imaging in mice may be a useful tool to monitor the effect of new therapeutic strategies preventing the myocardial dysfunction associated with aging.
