Background
Doppler tissue imaging (DTI) detects early signs of left ventricular (LV) dysfunction; however, the prognostic significance of DTI after ST-segment elevation myocardial infarction (STEMI) is unknown. The aim of this study was to evaluate the prognostic value of DTI after STEMI in patients treated with primary percutaneous coronary intervention.
Method
In total, 391 patients who were admitted with STEMIs and treated with primary percutaneous coronary intervention were prospectively included. All participants were examined by echocardiography 2 days (interquartile range, 1–3 days) after STEMI. Longitudinal systolic (s′), early diastolic (e′), and late diastolic (a′) myocardial velocities were measured using color DTI at six mitral annular sites and averaged to provide global estimates.
Results
The median follow-up period was 25 months (interquartile range, 19–32 months). The primary end point was a composite of death, heart failure, or a new myocardial infarction. Patients with low global systolic function (s′) or low global diastolic function (e′) had >2 times greater risk for the combined end point compared with patients with high global s′ (hazard ratio, 2.60; 95% confidence interval, 1.64–4.13; P < .001) or e′ (hazard ratio, 2.26; 95% confidence interval, 1.44–3.55; P < .001), respectively. After adjustment for age, gender, peak troponin I, previous myocardial infarction, LV ejection fraction, LV mass index, and LV dimension in a multivariate Cox model, patients with low values of both global s′ and e′ remained at significantly higher risk than patients with high s′ and/or e′ (hazard ratio, 1.69; 95% confidence interval, 1.02–2.81; P = .043).
Conclusions
A pattern of low systolic and diastolic performance as assessed by DTI is a paramount marker of adverse prognosis for patients with STEMIs independent of conventional echocardiographic parameters. DTI velocities should be evaluated together as they interact with the prognosis.
ST-segment elevation myocardial infarction (STEMI) is an acute and adverse manifestation of coronary artery disease. After STEMIs, patients are still at high risk for having major cardiovascular events. Consequently, efforts to improve risk stratification, clarify pathophysiologic mechanisms, and identify targets for therapeutic intervention are of utmost importance.
Echocardiography after a myocardial infarction (MI) is a routine procedure for risk stratification. In these patients, left ventricular (LV) systolic function has for several decades been the primary focus. However, research in diastolic function has revealed that patients with normal systolic function can display impaired diastolic function, which is an independent predictor of adverse outcomes. Consequently, we can obtain information on prognosis by adding an assessment of the diastolic function. Nevertheless, systole and diastole are interdependent and coherent, so perhaps it is possible to improve risk stratification by combining the information on systolic and diastolic performance.
Doppler tissue imaging (DTI) echocardiography is already a part of the standardized diastolic evaluation. Its ability to detect early signs of cardiac disease before it is detectable by conventional echocardiography and its strong predictive power are encouraging.
The aim of this study was to evaluate the prognostic value of systolic and diastolic DTI velocities in patients with STEMIs treated with primary percutaneous coronary intervention (pPCI).
Methods
Study Population
In the period from September 2006 to December 2008, a total of 391 patients were prospectively included in the present study and gave written informed content. Inclusion criteria were admission with STEMI and treatment with pPCI at Gentofte University Hospital (Copenhagen, Denmark). All participants underwent detailed echocardiographic examinations. Four patients were excluded because of inadequate quality of the echocardiographic examination with regard to obtaining DTI velocities and 14 because of atrial fibrillation.
The criteria for treatment with pPCI were the presence of chest pain for >30 min and <12 hours, persistent ST-segment elevation ≥ 2 mm in at least two contiguous precordial electrocardiographic leads or ≥1 mm in at least two contiguous limb electrocardiographic leads (or newly developed left bundle branch block), and subsequently, the diagnosis was confirmed by a significant troponin I (TnI) increase (>0.5 μg/L).
We collected baseline data from all patients prospectively when included in the study. Hypertension was defined as use of blood pressure–lowering drugs on admission. Diabetes was defined as fasting plasma glucose concentration ≥7 mmol/L or nonfasting plasma glucose concentration ≥11.1 mmol/L or the use of glucose-lowering drugs on admission.
TnI was measured at baseline and after 6 and 12 hours.
Echocardiography
Echocardiography was performed using Vivid 7 ultrasound systems (GE Vingmed Ultrasound AS, Horten, Norway) with a 3.5-MHz transducer by experienced sonographers. The echocardiographic examinations were performed as soon as possible after pPCI in all patients. This led to a median time span between pPCI and the echocardiographic examination of 2 days, with a 95% range of 0 to 5 days (interquartile range, 1–3 days), which mimics the average time span for echocardiographic examination for risk assessment after pPCI in eastern Denmark. All participants were examined using conventional two-dimensional echocardiography and pulsed-wave and color DTI according to standardized protocols. All echocardiograms were stored digitally and analyzed offline with commercially available software (EchoPAC; GE Vingmed Ultrasound AS) by a single investigator, who was blinded to all other patient data.
Conventional Echocardiography
LV end-diastolic dimensions (interventricular septal wall thickness, LV internal dimension, and LV posterior wall thickness) were obtained from the parasternal long-axis view at the mitral valve leaflet tips. LV mass index (LVMI) was calculated as the anatomic mass divided with body surface area. Pulsed-wave Doppler at the apical position was used to record mitral inflow between the tips of the mitral leaflets. Peak velocities of early (E) and atrial (A) diastolic filling and E-wave deceleration time (DT) were measured, and the E/A ratio was calculated. LV ejection fraction (LVEF) and LV volumes were determined using the modified biplane Simpson’s method. Left atrial volume was estimated by the area-length method in end-ventricular systole and divided by body surface area to calculate the left atrial volume index.
Two-Dimensional Strain Echocardiography
Two-dimensional strain analysis was performed from the apical four-chamber, two-chamber, and long-axis views (mean, 84 ± 23 frames/sec). Peak global longitudinal systolic strain was measured in all three apical projections and was averaged to provide global estimates.
DTI
Pulsed-wave DTI tracings were obtained with the range gate placed at the septal and lateral mitral annular segments in the four-chamber view. The averaged peak early diastolic longitudinal mitral annular velocity by pulsed-wave Doppler tissue (PW-e′) was calculated from the lateral and septal velocities and used to obtain the E/PW-e′ ratio.
Color DTI loops were obtained in the apical four-chamber, two-chamber, and long-axis views at the highest possible frame rate (mean, 169 ± 33 frames/sec). Peak longitudinal systolic (s′), early diastolic (e′), and late diastolic (a′) velocities were measured at the six mitral annular sites dividing the left ventricle into six segments of interest: septal, lateral, anterior, inferior, posterior, and anteroseptal myocardial wall. The global longitudinal performance of the left ventricle was assessed by averaging the myocardial velocities from the six mitral annular sites.
Diastolic function was assessed using mitral inflow velocity profiles and pulsed-wave DTI tracings from the septal and lateral mitral annulus according to current guidelines. It is important to note that it was PW-e′, not color DTI–obtained e′, that was used for diastolic function grading. This is essential because color DTI measures mean velocities, whereas pulsed-wave DTI measures peak velocities, such that the e′ measure would be too low and the E/e′ ratio too high compared with the guidelines if color DTI–derived e′ were used. The presence of diastolic dysfunction was identified as PW-e′ < 9 cm/sec. Grade 3 diastolic dysfunction, the restrictive pattern, was hereafter defined as an E/A ratio ≥ 2 and/or DT < 160 msec and E/e′ ratio ≥ 13. Grade 2 diastolic dysfunction, the pseudonormal pattern, was defined as an E/A ratio of 0.8 to 1.5 and/or DT of 160 to 200 ms and E/e′ ratio ≥ 9 to 12. Grade 1, the impaired relaxation pattern, was defined as an E/A ratio < 0.8 and/or DT > 200 ms and E/e′ ratio ≤ 8.
Primary PCI Procedure
pPCI was performed according to contemporary interventional guidelines using pretreatment with 300 mg acetylsalicylic acid, 600 mg clopidogrel, and 10,000 IU of unfractionated heparin. Glycoprotein IIb/IIIa inhibitors were used at the discretion of the operator. Multivessel disease was defined as two-vessel or three-vessel disease and complex lesions as type C lesions. Thrombolysis in Myocardial Infarction flow grade was rated before and after the procedure to assess the quality of the revascularization. Subsequent medical treatment included anti-ischemic, lipid-lowering, and antithrombotic drugs according to current treatment guidelines.
Follow-Up and End Points
The primary end point was the combined end point of all-cause mortality, new MI (re-MI), or admission with clinical signs of congestive heart failure (CHF) combined with a discharge diagnosis of clinical CHF. Secondary end points were all of the above analyzed separately. Follow-up was 100%. Follow-up data on re-MI and admission with CHF were obtained from the Danish National Board of Health’s National Patient Registry, using International Classification of Diseases, 10th Revision, codes and thoroughly validated using hospital source data. Follow-up data on mortality were collected from the National Person Identification Registry.
Statistical Analysis
In Tables 1 and 2 , proportions are compared using χ 2 tests, continuous Gaussian-distributed variables using Student’s t tests, and non-Gaussian-distributed variables using Mann-Whitney tests.
| Variable | No major adverse outcome ( n = 284) | Major adverse outcome ( n = 89) | P |
|---|---|---|---|
| Age (y) | 61 ± 11 | 66 ± 12 | .001 |
| Men | 76% | 73% | .61 |
| Hypertension | 32% | 33% | .88 |
| Diabetes | 8% | 10% | .55 |
| Current smoker | 53% | 48% | .46 |
| Hypercholesterolemia | 16% | 19% | .47 |
| Previous MI | 3% | 9% | .022 |
| BMI (kg/m 2 ) | 27.0 ± 4.2 | 25.9 ± 4.9 | .05 |
| Peak TnI (μg/L) | 89 (26–214) | 163 (44–308) | .004 |
| eGFR (ml/min/1.73 m 2 ) | 74 ± 21 | 74 ± 24 | .81 |
| Symptom-to-balloon time (min) | 180 (118–305) | 200 (142–328) | .12 |
| Complex lesion | 43% | 54% | .07 |
| Multivessel disease | 26% | 32% | .35 |
| LAD culprit lesion | 47% | 51% | .54 |
| RCA culprit lesion | 40% | 42% | .86 |
| Cx culprit lesion | 12% | 8% | .25 |
| Glycoprotein IIb/IIIa inhibitors | 22% | 30% | .12 |
| TIMI flow grade before pPCI | .55 | ||
| 0 | 61% | 66% | |
| 1 | 14% | 10% | |
| 2 | 10% | 12% | |
| 3 | 15% | 11% | |
| TIMI flow grade after pPCI | .40 | ||
| 0 | 4% | 3% | |
| 1 | 4% | 8% | |
| 2 | 9% | 8% | |
| 3 | 84% | 81% |
