Motion-Mode

Motion mode (M-mode) provides high temporal and spatial resolution of tissue motion along a single ultrasound beam. The assessment of LV mass and geometry is one of the most important clinical applications of M-mode. The prognostic role of LV mass has been shown after AMI. In 603 patients with AMI complicated by LV systolic dysfunction, heart failure (HF), or both, each 10-g/m ² increase in LV mass index and each 0.1-unit increase in relative wall thickness (RWT) were independently associated with all-cause mortality, cardiovascular (CV) death, and HF hospitalization. Among LV geometric patterns, concentric LV hypertrophy showed a stronger association with CV mortality, HF, reinfarction, stroke, and sudden cardiac death (SCD). M-mode can also provide information on LV longitudinal systolic function through the quantitation of atrioventricular plane displacement, since during cardiac systole, the atrioventricular plane moves towards the apex. In 271 patients with AMI, reduced mitral annular plane systolic excursion (MAPSE) was independently associated with all-cause mortality, HF hospitalization, reinfarction, and unstable angina; the incidence of death was 31.3% in patients with MAPSE <8 mm and 10.1% in those with MAPSE >8 mm. In addition, tricuspid annular plane systolic excursion (TAPSE) was an independent predictor of mortality after AMI, with the incidence of death being 4% in the presence of TAPSE ≥20 mm, 9% with TAPSE = 16–19 mm, and 45% with TAPSE ≤15 mm. However, M-mode has intrinsic limitations for assessing AMI patients. Mainly, the analysis of regional WMA is limited to only two walls (anterior septum and posterior wall), and no information is obtainable on evidence and magnitude of LV global systolic dysfunction. Accordingly, M-mode echo is only an adjunct to other echocardiographic techniques after AMI.

Two-Dimensional Echocardiography

The assessment of cardiac chamber size and function by 2D echocardiography provides very important prognostic information after AMI. The most used parameter is LVEF, which is obtained as the percent ratio between stroke volume and end-diastolic volume (EDV). LVEF has a very well established short-term and long-term prognostic value in this clinical setting. Worthy of note, the LVEF mortality curve after AMI exhibits a typical hyperbolic increasing with an upturn in mortality occurring at values < 40% ( Figure 1 ). In 417 patients with AMI, an LVEF < 40% was an independent predictor of the combined endpoint of death, congestive HF, and recurrent AMI (odds ratio [OR] = 3.82; 95% CI, 2.15–6.87) at 30 days after AMI. In a large prospective cohort study, 4,122 patients with AMI treated with primary percutaneous coronary intervention (PCI) underwent assessment of LVEF by invasive ventriculography, echocardiography, or radionuclide ventriculography before hospital discharge and were followed up for about 4 years. Patients with LVEF ≤30% and LVEF between >30% and ≤40% had an increased risk for SCD (hazard ratio [HR] = 5.99; 95% CI, 2.73–13.14; P < .001; HR = 3.37; 95% CI, 1.74–6.50; P < .001, respectively) and all-cause mortality (HR = 3.85; 95% CI, 2.96–5.00; P < .001; HR = 2.06; 95% CI, 1.66–2.57; P < .001, respectively) compared with patients with LVEF > 40%. Also, LV internal chamber volumes have a recognized prognostic value. In the GISSI-3 trial, predischarge LV EDV and end-systolic volume (ESV) predicted the incidence of the composite endpoint of 6-month mortality and nonfatal HF after AMI. At multivariate analysis, adjusted relative risks of the composite endpoint for an increase of 10 mL of LV EDV and ESV were, respectively, 1.16 (95% CI, 1.12–1.20) and 1.34 (95% CI, 1.28–1.41). LV regional systolic function has been also proposed for early risk stratification after AMI. Because of its recognized strong inverse relation with LVEF, it is expected that the wall motion score index (WMSI) could predict outcome after AMI. Accordingly, in 144 patients with a first AMI treated with thrombolytic therapy, a predischarge resting WMSI ≥ 1.50 was superior to LVEF ≤ 40% to identify patients who had post-AMI cardiac death, unstable angina, nonfatal reinfarction, and HF. In 767 AMI patients, WMSI was an independent predictor of death and HF hospitalization, whereas LVEF was not. This discrepancy may be explained by the fact that compensatory hyperkinesia of normal myocardial segments may mask the infarction severity and LVEF may therefore underestimate the true amount of myocardial damage after AMI. In addition, RV systolic function provides strong prognostic information in AMI patients treated with PCI. RV fractional area change (RVFAC)—but not TAPSE—independently predicted all-cause mortality, HF hospitalization, or reinfarction; the risk of adverse cardiac events was two-fold increased in patients with RVFAC < 32% compared with those with RVFAC ≥ 32%. The importance of left atrial (LA) dilation for risk stratification of AMI patients has been also investigated. It may occur after AMI in response to either volume (due to a mitral regurgitation [MR], in particular after inferior AMI) or pressure overload (increased LV filling pressures). LA dilation can be accurately detected by the LA volume index (LAVi), whose use is strongly encouraged by American Society of Echocardiography and the European Association of Cardiovascular Imaging recommendations on chamber quantification. A LAVi > 32 mL/m ² determined within 48 hours after AMI was predictor of all-cause of mortality after AMI. Conversely, in a study by Sakaguchi et al. LAVi did not show a prognostic role early after AMI (within 2 days after hospitalization), but LAVi at the time of discharge (average of 16 days after admission) and the difference in LAVi between discharge and admission were both independent predictors of the composite endpoint of cardiac death or hospitalization due to HF. The different results of these two studies can be explained by different endpoints and by the fact that patients with prior AMI, moderate/severe MR, and atrial fibrillation (AF) were excluded in Sakaguchi et al. ’s study but not in the study by Beinart et al. It makes sense that LAVi size detected several days after AMI might predict outcome better than that assessed early, LA dilation being a marker of a long time duration increase of LA pressure. Worthy of note, LA distensibility ([difference of maximal and minimal LA volume]/minimal volume × 100) was also an independent predictor of in-hospital mortality (HR = 2.37 for LA distensibility ≤ 60%; 95% CI, 1.108–5.079; P = .026) in 521 post-AMI patients. To the best of our knowledge, no information is available on the possible prognostic value of LA dilation prior to AMI, a factor that should not be underestimated in clinical practice.

Hyperbolic inverse relation between LVEF and 6-month all-cause mortality after AMI. EF values drive patient management, with those > 40% being in the ischemia domain and those < 35% in the viability domain.

(Modified from Volpi et al. ).

Standard Doppler

Standard Doppler of mitral valve, a robust and very feasible technique, provides important prognostic indexes after AMI. LV restrictive filling pattern (RFP), detected early after AMI, is a recognized predictor of adverse outcome ( Figure 2 ) regardless of LV systolic function. In a study of Temporelli et al. , the reversibility of RFP (RFP = E velocity deceleration time [DT] < 130 msec) at predischarge of 571 AMI patients not undergoing revascularization procedures was associated with a more favorable late outcome, whereas its persistence was the most powerful independent predictor of late mortality. In this study, a DT at admission < 130 msec was a strong prognosticator of LV remodeling and survival. In a meta-analysis of 12 prospective studies, including 3,396 post-AMI patients, RFP was confirmed as a predictor of all-cause mortality independently on LVEF, ESV, and Killip HF class. The detection of an LV RFP pattern and a short DT in patients with low LVEF is enough to identify high LV filling pressures and stratify prognosis after AMI, without the need of extending the diastolic evaluation to other parameters. Also, the Tei index may be useful to distinguish post-AMI high-risk patients. In 64 patients evaluated at hospital admission, a Tei index > 0.45 was an independent predictor of HF. Several studies demonstrated a significant independent association between the presence of MR and adverse events after AMI. In 1,036 STEMI patients treated by primary PCI, moderate to severe MR (graded according to initial color flow Doppler followed by quantitative parameters) was an independent predictor of death (adjusted HR = 3.1; 95% CI, 1.34–7.2) and HF (adjusted HR = 3.3; 95% CI, 1.16–9.4). In another study moderate/severe MR (graded by the effective regurgitant orifice area) independently predicted subsequent HF. Functional MR was an independent prognosticator in both ischemic and nonischemic dilated cardiomyopathy. The increase of pulmonary artery systolic pressure (PASP) may be a hemodynamic consequence of AMI by pathologic mechanisms such as ischemic MR and LV systolic and diastolic dysfunction. PASP can be determined noninvasively by adding the value of estimated right atrial pressure (size and respiratory reactivity of inferior cava) to the maximal retrograde gradient of tricuspid regurgitation. An estimated elevated PASP was found to be associated with CV morbidity and mortality in this context. Møller et al. enrolled 536 AMI patients, excluding those with significant pulmonary and mitral valve stenosis or a history of primary pulmonary hypertension, who underwent echo within 2 days after AMI. At multivariate analysis, PASP degree was correlated with age, LV diastolic function, MR, and WMSI. Each 10-mmHg increase in PASP, each grade increase of LV diastolic dysfunction, and evidence of moderate/severe RV dilatation were independent predictors of all-cause mortality. In another study, a PASP > 35 mmHg at hospital admission was predictive of a combined endpoint of all-cause death and death from HF (adjusted HR = 1.83; 95% CI, 1.31–2.57, P < .0001). All these data suggest that post-AMI consequences on pulmonary circulation may have greater prognostic implications than LV systolic dysfunction itself.

Sample of transmitral RFP in a patient after anterior AMI. Transmitral E/A ratio is 2.82, and E velocity DT is 127 msec. MV , mitral valve.

Spectral Pulse Wave Tissue Doppler Imaging

Tissue Doppler imaging (TDI) uses Doppler principles to quantify the higher-amplitude, lower-velocity signals of myocardial tissue motion along the axis of Doppler ultrasound beam. TDI has two different modalities: spectral pulse wave TDI, which can be performed during a standard echo-Doppler exam, and color TDI (CTDI), which is obtainable offline, by a post hoc elaboration. Spectral pulsed wave TDI is used to measure peak (instantaneous) myocardial velocities and is well suited to study LV longitudinal function. It has high temporal resolution but does not permit simultaneous analysis of different myocardial segments. The ratio of early transmitral flow velocity to spectral pulsed wave TDI-derived early diastolic velocity of the mitral annulus (E/e′ ratio) correlates accurately with LV filling pressures degree and has been shown to be an accurate predictor of prognosis after AMI. A post-AMI E/e′ ratio > 15 appears to be an independent predictor of all-cause mortality (relative risk = 4.8; 95% CI, 2.1-10.8, P = .0002). The E/e′ ratio is also strongly promoted by the American Society of Echocardiography and the European Association of Cardiovascular Imaging recommendations on diastolic function in relation to its high feasibility. It should therefore be used to estimate LV filling pressure degree in AMI patients with impaired or normal LVEF when the transmitral pattern is nonrestrictive and increased LV filling pressures cannot be diagnosed by the simple transmitral flow assessment. This kind of estimation can be valuable to drive therapy, in particular to administrate loop diuretics and avoid pulmonary edema.

Motion-Mode

Motion mode (M-mode) provides high temporal and spatial resolution of tissue motion along a single ultrasound beam. The assessment of LV mass and geometry is one of the most important clinical applications of M-mode. The prognostic role of LV mass has been shown after AMI. In 603 patients with AMI complicated by LV systolic dysfunction, heart failure (HF), or both, each 10-g/m ² increase in LV mass index and each 0.1-unit increase in relative wall thickness (RWT) were independently associated with all-cause mortality, cardiovascular (CV) death, and HF hospitalization. Among LV geometric patterns, concentric LV hypertrophy showed a stronger association with CV mortality, HF, reinfarction, stroke, and sudden cardiac death (SCD). M-mode can also provide information on LV longitudinal systolic function through the quantitation of atrioventricular plane displacement, since during cardiac systole, the atrioventricular plane moves towards the apex. In 271 patients with AMI, reduced mitral annular plane systolic excursion (MAPSE) was independently associated with all-cause mortality, HF hospitalization, reinfarction, and unstable angina; the incidence of death was 31.3% in patients with MAPSE <8 mm and 10.1% in those with MAPSE >8 mm. In addition, tricuspid annular plane systolic excursion (TAPSE) was an independent predictor of mortality after AMI, with the incidence of death being 4% in the presence of TAPSE ≥20 mm, 9% with TAPSE = 16–19 mm, and 45% with TAPSE ≤15 mm. However, M-mode has intrinsic limitations for assessing AMI patients. Mainly, the analysis of regional WMA is limited to only two walls (anterior septum and posterior wall), and no information is obtainable on evidence and magnitude of LV global systolic dysfunction. Accordingly, M-mode echo is only an adjunct to other echocardiographic techniques after AMI.

Two-Dimensional Echocardiography

The assessment of cardiac chamber size and function by 2D echocardiography provides very important prognostic information after AMI. The most used parameter is LVEF, which is obtained as the percent ratio between stroke volume and end-diastolic volume (EDV). LVEF has a very well established short-term and long-term prognostic value in this clinical setting. Worthy of note, the LVEF mortality curve after AMI exhibits a typical hyperbolic increasing with an upturn in mortality occurring at values < 40% ( Figure 1 ). In 417 patients with AMI, an LVEF < 40% was an independent predictor of the combined endpoint of death, congestive HF, and recurrent AMI (odds ratio [OR] = 3.82; 95% CI, 2.15–6.87) at 30 days after AMI. In a large prospective cohort study, 4,122 patients with AMI treated with primary percutaneous coronary intervention (PCI) underwent assessment of LVEF by invasive ventriculography, echocardiography, or radionuclide ventriculography before hospital discharge and were followed up for about 4 years. Patients with LVEF ≤30% and LVEF between >30% and ≤40% had an increased risk for SCD (hazard ratio [HR] = 5.99; 95% CI, 2.73–13.14; P < .001; HR = 3.37; 95% CI, 1.74–6.50; P < .001, respectively) and all-cause mortality (HR = 3.85; 95% CI, 2.96–5.00; P < .001; HR = 2.06; 95% CI, 1.66–2.57; P < .001, respectively) compared with patients with LVEF > 40%. Also, LV internal chamber volumes have a recognized prognostic value. In the GISSI-3 trial, predischarge LV EDV and end-systolic volume (ESV) predicted the incidence of the composite endpoint of 6-month mortality and nonfatal HF after AMI. At multivariate analysis, adjusted relative risks of the composite endpoint for an increase of 10 mL of LV EDV and ESV were, respectively, 1.16 (95% CI, 1.12–1.20) and 1.34 (95% CI, 1.28–1.41). LV regional systolic function has been also proposed for early risk stratification after AMI. Because of its recognized strong inverse relation with LVEF, it is expected that the wall motion score index (WMSI) could predict outcome after AMI. Accordingly, in 144 patients with a first AMI treated with thrombolytic therapy, a predischarge resting WMSI ≥ 1.50 was superior to LVEF ≤ 40% to identify patients who had post-AMI cardiac death, unstable angina, nonfatal reinfarction, and HF. In 767 AMI patients, WMSI was an independent predictor of death and HF hospitalization, whereas LVEF was not. This discrepancy may be explained by the fact that compensatory hyperkinesia of normal myocardial segments may mask the infarction severity and LVEF may therefore underestimate the true amount of myocardial damage after AMI. In addition, RV systolic function provides strong prognostic information in AMI patients treated with PCI. RV fractional area change (RVFAC)—but not TAPSE—independently predicted all-cause mortality, HF hospitalization, or reinfarction; the risk of adverse cardiac events was two-fold increased in patients with RVFAC < 32% compared with those with RVFAC ≥ 32%. The importance of left atrial (LA) dilation for risk stratification of AMI patients has been also investigated. It may occur after AMI in response to either volume (due to a mitral regurgitation [MR], in particular after inferior AMI) or pressure overload (increased LV filling pressures). LA dilation can be accurately detected by the LA volume index (LAVi), whose use is strongly encouraged by American Society of Echocardiography and the European Association of Cardiovascular Imaging recommendations on chamber quantification. A LAVi > 32 mL/m ² determined within 48 hours after AMI was predictor of all-cause of mortality after AMI. Conversely, in a study by Sakaguchi et al. LAVi did not show a prognostic role early after AMI (within 2 days after hospitalization), but LAVi at the time of discharge (average of 16 days after admission) and the difference in LAVi between discharge and admission were both independent predictors of the composite endpoint of cardiac death or hospitalization due to HF. The different results of these two studies can be explained by different endpoints and by the fact that patients with prior AMI, moderate/severe MR, and atrial fibrillation (AF) were excluded in Sakaguchi et al. ’s study but not in the study by Beinart et al. It makes sense that LAVi size detected several days after AMI might predict outcome better than that assessed early, LA dilation being a marker of a long time duration increase of LA pressure. Worthy of note, LA distensibility ([difference of maximal and minimal LA volume]/minimal volume × 100) was also an independent predictor of in-hospital mortality (HR = 2.37 for LA distensibility ≤ 60%; 95% CI, 1.108–5.079; P = .026) in 521 post-AMI patients. To the best of our knowledge, no information is available on the possible prognostic value of LA dilation prior to AMI, a factor that should not be underestimated in clinical practice.

Hyperbolic inverse relation between LVEF and 6-month all-cause mortality after AMI. EF values drive patient management, with those > 40% being in the ischemia domain and those < 35% in the viability domain.

(Modified from Volpi et al. ).

Standard Doppler

Standard Doppler of mitral valve, a robust and very feasible technique, provides important prognostic indexes after AMI. LV restrictive filling pattern (RFP), detected early after AMI, is a recognized predictor of adverse outcome ( Figure 2 ) regardless of LV systolic function. In a study of Temporelli et al. , the reversibility of RFP (RFP = E velocity deceleration time [DT] < 130 msec) at predischarge of 571 AMI patients not undergoing revascularization procedures was associated with a more favorable late outcome, whereas its persistence was the most powerful independent predictor of late mortality. In this study, a DT at admission < 130 msec was a strong prognosticator of LV remodeling and survival. In a meta-analysis of 12 prospective studies, including 3,396 post-AMI patients, RFP was confirmed as a predictor of all-cause mortality independently on LVEF, ESV, and Killip HF class. The detection of an LV RFP pattern and a short DT in patients with low LVEF is enough to identify high LV filling pressures and stratify prognosis after AMI, without the need of extending the diastolic evaluation to other parameters. Also, the Tei index may be useful to distinguish post-AMI high-risk patients. In 64 patients evaluated at hospital admission, a Tei index > 0.45 was an independent predictor of HF. Several studies demonstrated a significant independent association between the presence of MR and adverse events after AMI. In 1,036 STEMI patients treated by primary PCI, moderate to severe MR (graded according to initial color flow Doppler followed by quantitative parameters) was an independent predictor of death (adjusted HR = 3.1; 95% CI, 1.34–7.2) and HF (adjusted HR = 3.3; 95% CI, 1.16–9.4). In another study moderate/severe MR (graded by the effective regurgitant orifice area) independently predicted subsequent HF. Functional MR was an independent prognosticator in both ischemic and nonischemic dilated cardiomyopathy. The increase of pulmonary artery systolic pressure (PASP) may be a hemodynamic consequence of AMI by pathologic mechanisms such as ischemic MR and LV systolic and diastolic dysfunction. PASP can be determined noninvasively by adding the value of estimated right atrial pressure (size and respiratory reactivity of inferior cava) to the maximal retrograde gradient of tricuspid regurgitation. An estimated elevated PASP was found to be associated with CV morbidity and mortality in this context. Møller et al. enrolled 536 AMI patients, excluding those with significant pulmonary and mitral valve stenosis or a history of primary pulmonary hypertension, who underwent echo within 2 days after AMI. At multivariate analysis, PASP degree was correlated with age, LV diastolic function, MR, and WMSI. Each 10-mmHg increase in PASP, each grade increase of LV diastolic dysfunction, and evidence of moderate/severe RV dilatation were independent predictors of all-cause mortality. In another study, a PASP > 35 mmHg at hospital admission was predictive of a combined endpoint of all-cause death and death from HF (adjusted HR = 1.83; 95% CI, 1.31–2.57, P < .0001). All these data suggest that post-AMI consequences on pulmonary circulation may have greater prognostic implications than LV systolic dysfunction itself.

Sample of transmitral RFP in a patient after anterior AMI. Transmitral E/A ratio is 2.82, and E velocity DT is 127 msec. MV , mitral valve.

Spectral Pulse Wave Tissue Doppler Imaging

Tissue Doppler imaging (TDI) uses Doppler principles to quantify the higher-amplitude, lower-velocity signals of myocardial tissue motion along the axis of Doppler ultrasound beam. TDI has two different modalities: spectral pulse wave TDI, which can be performed during a standard echo-Doppler exam, and color TDI (CTDI), which is obtainable offline, by a post hoc elaboration. Spectral pulsed wave TDI is used to measure peak (instantaneous) myocardial velocities and is well suited to study LV longitudinal function. It has high temporal resolution but does not permit simultaneous analysis of different myocardial segments. The ratio of early transmitral flow velocity to spectral pulsed wave TDI-derived early diastolic velocity of the mitral annulus (E/e′ ratio) correlates accurately with LV filling pressures degree and has been shown to be an accurate predictor of prognosis after AMI. A post-AMI E/e′ ratio > 15 appears to be an independent predictor of all-cause mortality (relative risk = 4.8; 95% CI, 2.1-10.8, P = .0002). The E/e′ ratio is also strongly promoted by the American Society of Echocardiography and the European Association of Cardiovascular Imaging recommendations on diastolic function in relation to its high feasibility. It should therefore be used to estimate LV filling pressure degree in AMI patients with impaired or normal LVEF when the transmitral pattern is nonrestrictive and increased LV filling pressures cannot be diagnosed by the simple transmitral flow assessment. This kind of estimation can be valuable to drive therapy, in particular to administrate loop diuretics and avoid pulmonary edema.

Color Tissue Doppler Imaging

CTDI quantifies mean velocities (cm/sec) of a given myocardial segment with the possibility of evaluating multiple structures and segments in a single view. The prognostic value of CTDI has been demonstrated after AMI. In 391 STEMI patients treated with primary PCI, CTDI-derived longitudinal systolic (s′), early diastolic (e′), and late diastolic (a′) myocardial velocities were measured at six mitral annular sites and averaged to provide global estimates. At multivariate analysis, the sum of global s′, e′, and a′ velocities (optimal cutoff point = 17.2 cm/sec) was independently associated with the composite endpoint of all-cause mortality, new AMI, and HF hospitalization. In another study, myocardial performance index assessed by CTDI through the mitral leaflet was an independent predictor of a combined outcome including death, HF hospitalization, or new AMI (optimal cutoff point = 0.52). The major weakness of both spectral pulse wave TDI and CTDI is represented by their angle dependency, common to all Doppler-based technologies. Moreover, TDI is not independent on heart translational motion and is influenced from tethering of adjacent segments. This limitation may be overcome by TDI-derived strain imaging that provides quantitative information on deformation (strain) and rate of deformation (strain rate) of a given myocardial segment or overall myocardium (=global strain). In a study of Sjøli et al. , TDI-derived global longitudinal strain (GLS) < −15.6% and LVEF <44% were both independent predictors of cardiac death, reinfarction, HF hospitalization, unstable angina, or life-threatening arrhythmia after AMI. Nevertheless, Doppler-derived strain is strongly limited by technical problems, mainly the need of a high frame rate during images acquisition, vulnerability to signal noise, poor spatial resolution, and angle dependence. These limitations reduce the feasibility and reproducibility of this technique, which has never been introduced in routine clinical practice.

Speckle-Tracking Echocardiography

Two-dimensional STE is based on the quantitative analysis of spatial dislocation (tracking) of acoustic markers (“speckles”) generated by the interaction between the ultrasound beam and myocardial fibers during the cardiac cycle. Two-dimensional STE overcomes both the angle dependency and signal-to-noise ratio of CTDI-derived strain imaging. It has a recognized better reproducibility than TDI-derived strain. Two-dimensional STE allows a functional evaluation of all myocardial deformations, longitudinal strain (LS) being a marker of subendocardial longitudinal shortening (expressed in negative value), midwall circumferential strain (again negative values), and radial strain (positive values). Notably, subendocardial fibers are more prone to ischemic damage and early altered during acute ischemia, a characteristic that can be efficiently utilized in acute coronary syndromes. Two-dimensional STE is also very feasible, relatively operator independent, and much more reproducible than 2D LVEF, another point of strength in this clinical setting. The prognostic value of 2D STE-derived longitudinal function after AMI has been described in recent studies. In 50 anterior AMI patients treated with PCI, systolic LS derived from seven segments of left anterior descending artery territory was an independent predictor of death and HF. In 659 AMI patients treated by primary PCI, systolic GLS and LS rate of the infarct zone were independently associated with all-cause mortality. In particular, at univariate analysis, patients with systolic GLS > −15.1% and systolic GLS rate (GLSr) > −1.06 sec ⁻¹ showed HRs of 4.5 (95% CI, 2.1–9.7) and 4.4 (95% CI, 2.0–9.5), respectively, for all-cause mortality. In another study, a reduced systolic GLS predicted HF during hospitalization for AMI also in the presence of normal LVEF. These data suggest that we should pay particular attention to HF symptoms in the first phases of AMI in patients when GLS is impaired. GLS has shown an incremental value beyond traditional echo parameters for risk stratification after AMI. Ersbøll et al. found that impaired systolic GLS—but not reduced LVEF (<40%)—was a powerful independent predictor of a composite endpoint of all-cause of mortality and HF hospitalization and cardiac death. A systolic GLS ≥ −14% was associated with a three-fold increase in risk for the combined endpoint of all-cause mortality and HF hospitalization (HR = 3.21; 95% CI, 1.82–5.67; P < .001). In a study of 576 AMI patients treated by primary PCI, systolic GLS and WMSI were independently associated with the composite endpoint of all-cause mortality, reinfarction, hospitalization, HF, or stroke within 1 year, whereas LVEF and ESV did not enter the model. In particular, patients with systolic GLS ≥ −10% experienced more adverse events than patients with systolic GLS ≤ −15% (HR = 4.6; 95% CI, 2.8–7.7; P < .001). The latest American guidelines suggest administering angiotensin-converting enzyme inhibitors (ACEi) within the first 24 hours in patients with anterior STEMI, HF, or LVEF ≤40% and with NSTEMI and LVEF ≤40%, hypertension, diabetes, or stable chronic kidney disease. Aldosterone antagonist should be given to patients with STEMI or NSTEMI who are already receiving ACEi and beta blockers and who have LVEF ≤40% and either HF symptoms or diabetes. On the basis of the above-mentioned evidence, GLS can identify patients who might benefit from antiremodeling therapy independently on LVEF and even represent a selection criterion for future clinical trials. In another study of Ersbøll et al. on 988 AMI patients, systolic GLS (HR = 1.24; 95% CI, 1.10–1.40; P = .0004) and mechanical dispersion (=SD of average time from ECG-derived peak R to peak systolic LS [HR = 10 msec = 1.15; 95% CI, 1.01–1.31; P = .03]) were both associated with risk of ventricular arrhythmias and SCD after AMI at multivariate analysis; these associations remained significant in subgroups of patients with LVEF < 35% and > 35%. The impact of mechanical dispersion on risk prediction on ventricular arrhythmias after AMI has been confirmed by Haugaa and coworkers. Prediction and prevention of SCD early after AMI represent a clinical challenge, and the Defibrillator IN Acute Myocardial Infarction Trial failed to demonstrate an overall survival advantage of implantable cardioverter defibrillator (ICD) implantation within 40 days in AMI patients with in-hospital LVEF ≤35%. Accordingly, both European and American guidelines for management of ventricular arrhythmias suggest reevaluating LVEF (6–12 weeks and 40 days or more after AMI, respectively) to identify candidates for ICD. In this clinical contest, the study of Ersbøll et al. suggests possible additional information on LS to LVEF in the early AMI phase for identifying more accurately patients to be referred to ICD. On the grounds of all these studies, in the setting of AMI patients, systolic GLS ( Figure 3 ) should be integrated into the assessment of LVEF and WMSI, which are operator dependent and poorly reproducible.

Global and regional LS assessed by 2D STE after anterior AMI. The bull’s-eye representation ( right bottom ) depicts a clear involvement of anterior septum and anterior and lateral walls, and the systolic GLS average is −9.1%, a cutoff point value prognostically validated in this clinical setting. In the left section of each view (apical long axis and four chamber on the top and two chamber at the left bottom ) is shown the color representation of STE on 2D imaging and quantitation of peak regional strain values (normally negative) referring to six myocardial regions. In the right upper section of each view regional color systolic curves of systolic strain are marked, while the dotted white line corresponds to average strain (GS). In the right lower section , qualitative color M-mode strain representation referring to the six consecutive myocardial segments is shown: at the bottom , LV basal right segments; in the central part , LV apex; at the top , LV basal segments ( yellow color ); dark red indicates normal strain; light red , reduced strain; and pink color, strongly impaired or even absent systolic strain. ANT , anterior; AVC , atrioventricular contraction; GLPS , global lateral pulse strain; GS , global strain; INF , inferior; LAT , lateral; SEPT , septum.

Recently, regional diastolic strain rate has been proposed as a further marker of elevated LV filling pressure degree. In a total of 1,048 post-AMI patients, after a median follow-up of 29 months, the ratio of transmitral E velocity to global diastolic strain rate (E/e′sr, optimal cutoff value >1.25) was superior to E/e′ ratio and independently associated with the composite endpoint of all-cause mortality, HF hospitalization, stroke, and new onset AF, and the prognostic value of E/e′ was driven by mortality (HR per 1-unit change, 2.52; 95% CI, 2.09–3.04; P < .0001) and HF admission (HR per 1-unit change, 2.79; 95% CI, 2.23–3.48; P < .0001).

In addition, the assessment of RV myocardial function by 2D STE has shown a prognostic value after AMI. In 621 AMI patients treated with primary PCI, RV LS and RVFAC—but not TAPSE—independently predicted a composite endpoint including all-cause mortality, HF hospitalization, or reinfarction; in particular, the risk of adverse outcomes was increased three-fold in patients with RV LS ≥ −22.1% compared with patients with RV LS < −22.1%. Two-dimensional STE can also provide a comprehensive LA assessment. LA function can be divided into three phases: in the first phase, as a reservoir, the LA stores pulmonary venous return during systole and isovolumic relaxation; in the second one, as conduit, the LA transfers blood passively into LV; in the third, as booster pump, it actively contracts during end diastole. During the reservoir phase, LA LS increases as a consequence of atrial filling, achieving a positive peak just before mitral valve opening, the so-called peak atrial LS. LA strain has been explored in 843 patients with AMI: at univariate analysis, peak atrial strain predicted HF hospitalization, but at multivariate analysis, LV systolic GLS and maximal LA volume removed this effect. Accordingly, further experience is needed to eventually promote LA strain in this clinical setting.

Recently, a layer-specific analysis of myocardial deformation has allowed accurate discrimination of transmurality of myocardial infarction and prediction of functional recovery after AMI. However, further studies are needed to clarify the prognostic role of layer-specific strain analysis in patients with AMI.

Coronary Flow Velocity Pattern and Reserve

Doppler-derived coronary flow velocity reserve (CFVR) has also been proposed for early risk stratification in patients after AMI. Iwakura et al. first demonstrated that coronary flow assessed by invasive Doppler guide wire allows the identification of the presence of coronary microvascular dysfunction after AMI. In particular, the coronary flow pattern in patients with no reflow was characterized by the appearance of systolic retrograde flow, diminished systolic anterograde flow, and rapid deceleration of diastolic flow after coronary intervention. CFVR can also be obtained noninvasively by transthoracic Doppler echo, which is easily available at bedside and not expensive. In a small prospective study, a DT of diastolic coronary flow velocity ≤600 msec, assessed by this technique 12–48 hours after PCI, was an independent predictor of subsequent HF (OR = 11.04; 95% CI, 1.43–85.11; P = .021). In 55 patients with first anterior STEMI successfully treated with primary PCI (thrombolysis in myocardial infarction flow grade 3), a CFVR < 1.7 determined <12 hours after symptoms onset independently predicted in-hospital cardiac events (in particular, HF [OR = 12; 95% CI, 1.4–93; P < .02]) as well as global and regional LV function recovery (OR = 23; 95% CI, 5–98; P < .01; and OR = 58; 95% CI, 2–73; P = .01, respectively). This finding was interpreted by the authors as due to coronary microvascular dysfunction because of the documented patency of the epicardial coronary vessel. On the basis of these results, noninvasive detection of impaired coronary microcirculation, despite successful percutaneous treatment of the culprit lesion, could drive management of patients with low LVEF to prevent in-hospital HF: patients with CFVR > 1.7 should not be referred for prophylactic ICD implantation because of a high probability of LV function recovery.

Myocardial Contrast Echocardiography

MCE is a bedside technique that assesses myocardial perfusion using microbubbles and can be used to determine infarct size and hence myocardial viability; it is a powerful predictor of hard cardiac events after AMI. In a study by Lepper et al. , the size of persistent MCE perfusion defect after revascularization for AMI had a high predictive value for LV remodeling during a 4-week follow-up period. In a study of Dwivedi et al. , 95 patients underwent MCE within 7 ± 2 days after AMI, and residual myocardial viability was assessed through contrast defect index (CDI): this was calculated as the sum of the contrast scores (1 = homogeneous opacification; 2 = heterogeneous opacification; 3 = minimal/absent contrast opacification) of all LV interpretable segments divided by the number of LV segments analyzed. At multivariable analysis, elevated CDI, as a marker of lower residual myocardial viability, was a predictor of the composite endpoint of cardiac death and nonfatal AMI and of cardiac death, whereas LVEF and ESV did not achieve statistical significance. The optimal cutoff of CDI was 1.86 for the composite endpoint of cardiac death and nonfatal AMI (sensitivity, 62%; specificity, 84%) and for cardiac death (sensitivity, 87%; specificity, 84%). In addition, the extent of microvascular damage, quantified by CDI, was the most important predictor of LV remodeling among patients with first successfully reperfused STEMI (thrombolysis in myocardial infarction flow grade 3). It is conceivable that LV function assessed early after AMI could overestimate the extent of irreversible infarct area because of myocardial stunning, while MCE—by assessing the infarct area through the absence/reduction of tissue-level perfusion—could provide a more realistic picture and stronger prognostic information, especially in patients with impaired LVEF.

Figure 4 shows a typical example of incremental usefulness of downstream tissue-level perfusion assessment compared with angiographic data. Real-time MCE clearly shows the absence of myocardial perfusion a few hours after primary PCI. MCE is able to detect the relevant percentage of patients (1/4 to 1/3) with a no-reflow phenomenon after AMI, similar to cardiac magnetic resonance, but with lower cost and easy performance at the bedside in a coronary care unit. The application of MCE molecular imaging in acute coronary syndromes can be of potential interest. This technology is based on the use of microbubbles functionalized with ligand molecules that bind to molecular markers of disease. Since during acute myocardial ischemia/reperfusion an endothelial up-regulation of leukocyte adhesion molecules occurs and persists even after ischemia resolution (ischemic memory), microbubbles adhering to endothelial selectins might permit echo identification of recently ischemic myocardial territories and facilitate the diagnostic approach in patients with chest pain of undetermined origin. Future investigations are needed to clarify the role of MCE molecular imaging in this clinical context.

MCE performed after successful percutaneous transluminal coronary angioplasty. At the top left , the coronary angiography shows the total proximal left anterior descending (LAD) coronary artery occlusion before performing primary PCI. The top right shows the open artery after thromboaspiration and primary PCI with good final result (thrombolysis in myocardial infarction 3 flow). The bottom left shows an echocardiographic four-chamber view obtained soon after primary angioplasty with infusion of a 0.5-mL bolus of microbubble contrast media (SonoVue), using contrast-specific very-low mechanical index real-time imaging. It shows almost complete absence of tissue-level perfusion (black myocardium) in the apical and midapical segments (which were also akinetic) compared with normally perfused basal and non-LAD segments. The bottom right similarly shows the echocardiographic two-chamber view, which confirms the absence of myocardial perfusion in the mid and apical anterior segments.

Three-Dimensional Echocardiography

RT3DE imaging is a major innovation of cardiac ultrasound. It can provide accurate and reliable measurements of chamber size, mass, geometry, and function. It also offers a comprehensive anatomic characterization of valvular abnormalities, improving diagnosis and preoperative planning. RT3DE overcomes several limitations of 2D echo because it is more accurate for evaluating LV volumes and LVEF without the need of a geometric assumption and errors caused by possible foreshortened views. To date, no clinical study has demonstrated any kind of association of RT3DE parameters with major adverse CV events after AMI. However, some data have shown the usefulness of an RT3DE-derived sphericity index calculated 6 days after the acute events in predicting subsequent LV remodeling. In a recent study of 100 patients with successfully reperfused first AMI, 3D STE discriminated transmural from nontransmural extent of scar and predicted microvascular obstruction, using cardiac magnetic resonance as the gold standard. The best 3D strain component for detecting nonviable segments with microvascular obstruction was global area strain (area under the curve = 0.867), a parameter that encompasses longitudinal and circumferential strain. In another study including 160 patients with first AMI treated by primary PCI, global 3D LS provided incremental value over clinical and conventional echo variables in predicting global LV function recovery (the c-statistic improved from 0.64 to 0.71 to 0.84).

Stress Echocardiography

SE performed early after AMI has been demonstrated to predict subsequent recovery of global and regional systolic function. The viability of two or more contiguous to infarct regions, by low-dose dobutamine SE—performed 3 days after AMI—was an independent predictor of 3-month LVEF improvement. The viability of two or more contiguous to infarct segments at low-level exercise SE and at low-dose dobutamine—5 ± 2 days after AMI—predicted myocardial recovery at rest 1 month later. Even 2D STE applied to low-dose dobutamine SE appears to be promising for determining the probability of LV functional recovery after AMI. In particular, LS < −14.92% and LS rate < −1.30 sec ⁻¹ at low dobutamine predicted LV regional recovery with sensitivity of 86.0%, 87.0%, and 86.1% and specificity of 87.6%, 83.3%, and 86.1%, respectively. SE also identifies AMI patients at increased risk of subsequent adverse events. In a large-scale multicenter prospective study, 755 in-hospital patients underwent pharmacological SE with either dipyridamole or dobutamine and an exercise ECG 10 days from AMI. At multivariate analysis, peak stress WMSI was an independent predictor of all-cause mortality; WMSI difference between rest and peak stress was the most important predictor of the composite endpoint of death, nonfatal AMI, and rehospitalization for unstable angina. In the Cost of Strategies after Myocardial Infarction (COSTAMI) trial, a pharmacological SE performed early after uncomplicated AMI followed by early discharge in case of negative test provided a similar clinical outcome but lower costs than delayed discharge followed by exercise ECG. In the COSTAMI II trial, exercise SE early after AMI allowed risk stratification with similar costs to predischarge exercise ECG. The Viability-Guided Angioplasty after Acute Myocardial Infarction trial demonstrated that in patients with sub-AMI, not treated by primary or rescue PCI, the detection of myocardial viability at low-dose dobutamine identified a subgroup to be referred to viability-guided PCI of infarct-related coronary artery.

A Comprehensive Echocardiographic Prognosticator

In the last 20 years, several studies have addressed the importance of transthoracic echocardiography for the prediction of risk for subsequent adverse events after AMI. Supplemental Tables 1 and 2 summarize the characteristics of the study populations of studies using conventional echo indexes and advanced ultrasound technologies, respectively. Populations were similar for age, gender, and CV risk factors, but the therapeutic strategies for AMI were different. Obviously, in most studies dealing with advanced imaging, AMI patients were treated by myocardial revascularization, a setting where the degree of LV dysfunction is generally mild. Conversely, in historical studies using conventional echo, several patients followed a conservative strategy, with a consequent higher rate of LV dysfunction and HF. LVEF, LAVi, RVFAC, MR degree, PASP, and E/e′ ratio emerge as the main conventional parameters in AMI patients treated by PCI. According to the scientific literature, morphologic and functional data can be very useful to predict complications during AMI hospitalization and more delayed post-AMI CV events and mortality. Table 1 reports independent associations (by multiple linear regression analyses) of echo indexes with clinical outcomes, specifying the timing of echo and follow-up duration. In all of the studies, it was not possible to distinguish echo abnormalities preceding AMI from those caused by AMI because preacute event data were not available. In relation to the need for an early risk stratification for patients experiencing AMI, we propose an echo-based algorithm for AMI patients ( Figure 5 ). Of interest, in studies showing incremental value of GLS and RV strain over conventional echo parameters (LVEF or RVFAC and TAPSE), the majority of patients enrolled were treated with PCI (79.1% and 100%, respectively) and had normal or mildly reduced LVEF. The strength of this approach is consistent with the possibility of identifying post-AMI patients with LVEF > 40%—who are not particularly considered by actual guidelines for more aggressive treatment (antiremodeling, antiarrhythmic therapy, etc.)—but who could nevertheless have an adverse prognosis. The main weakness of this approach corresponds to the limited availability of advanced echo and the need for physicians with advanced ultrasound competencies in coronary care units, the lack of well-defined prognostic cutoff points of novel echo parameters in relation to specific endpoints, and the absence of information on optimal timing of echo exam during and after hospitalization.

Table 1

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