Methods

We performed a retrospective, single-center observational study at the Tel-Aviv Sourasky Medical Center, a tertiary referral hospital with a 24/7 primary PCI service.

Included were 340 patients admitted between June 2011 and December 2013 to the cardiac intensive care unit with the diagnosis of first acute STEMI and treated with primary PCI. Of these patients, 52 attended follow-up at our institution, which included an echocardiographic examination with full diastolic function assessment. Baseline demographics, cardiovascular history, clinical risk factors, treatment characteristics, and laboratory results were all retrieved from the hospital electronic medical records. Diagnosis of STEMI was established in accordance to published guidelines, including a typical chest pain history, diagnostic electrocardiographic changes, and serial elevation of cardiac biomarkers. The study protocol was approved by the local institutional ethics committee. Primary PCI was performed on patients with symptoms ≤12 hours in duration as well as in patients with symptoms lasting 12 to 24 hours in duration if the symptoms persisted at the time of admission. All patients received optimal medical therapy in accordance with current recommendations for patients with STEMIs. Heart failure was defined as clinical or radiographic evidence of pulmonary congestion.

All patients underwent screening echocardiographic examinations within 3 days of admission. Follow-up echocardiography was performed within 178 ± 62 days. Echocardiography was performed with a Philips iE33 machine equipped with S5-1 transducers (Philips Medical Systems, Andover, MA). The echocardiograms were interpreted by Y.T. and S.K. LV diameters and septal and posterior wall width were measured from the parasternal long axis by means of a two-dimensional or two-dimensionally guided M-mode echocardiogram, perpendicular to the LV long axis at or immediately below the level of the mitral valve leaflet tips. LV ejection fraction was calculated using the biplane method of disks (modified Simpson rule). The 16-segment model was used for scoring the severity of segmental wall motion abnormalities according to the American Society of Echocardiography. Early transmitral flow velocity (E) and late atrial contraction (A) velocity were measured in the apical four-chamber view to provide an estimate of LV diastolic function. Early diastolic mitral annular velocity (e′) was measured using spectral tissue Doppler imaging in both septal and lateral positions. The ratio of peak E to peak e′ was calculated (mitral E/e′ ratio) from the average of at least three cardiac cycles, and the deceleration time of the E wave was also measured. Left atrial volume was calculated using the biplane area-length method at the end of LV systole. LV end-diastolic volume (LVEDV) and LV end-systolic volume were measured using the modified Simpson rule, on the basis of tracings of the interface between the compacted myocardium and the LV cavity in the apical four- and two-chamber views. Volumes of the left atrium and left ventricle were indexed using the patient’s body surface area. Right atrial (RA) pressure was estimated by the inferior vena cava (IVC) diameter as well as its response to inspiration, as previously described. Briefly, expiratory and inspiratory IVC diameters and percentage collapse were measured in subcostal views within 2 cm of the right atrium. IVC diameter < 2.1 cm that collapsed >50% with a sniff suggested normal RA pressure (assigned as 5 mm Hg), whereas IVC diameter > 2.1 cm that collapsed <50% with a sniff suggested high RA pressure (15 mm Hg). In patients with IVC diameters > 2.1 cm and no collapse (<50%) with a sniff, RA pressure was upgraded to 20 mm Hg. In indeterminate cases in which the IVC diameter and collapse did not fit this paradigm, secondary indices of elevated RA pressure were integrated. If uncertainty remained, RA pressure was left at an intermediate value of 10 mm Hg. Peak systolic pulmonary artery pressure was estimated using the modified Bernoulli formula (4 × [peak systolic tricuspid regurgitation velocity at end-expiration] ² ) + RA pressure. Prior data have demonstrated that E/septal e′ ratio > 15 was associated with adverse outcomes and LV remodeling after acute MI. In addition, this is the site least affected by the location of infarction, so velocity changes in this region are relatively similar in patients with inferior and anterior infarcts. For these reasons, the cohort was dichotomized on the basis of E/septal e′ value. A pooled analysis was performed for patients with E/septal e′ ratios >15 and ≤15 in the second echocardiographic examination.

All data were summarized and displayed as mean ± SD for continuous variables and as number (percentage) of patients in each group for categorical variables. Because of the small number of patients evaluated, we did not assume a normal distribution and performed nonparametric tests only. Categorical data were compared using χ ² and Fisher exact tests. Continuous variables were compared using the Mann-Whitney U test or the Kruskal-Wallis test. Correlations were evaluated using the Pearson test. Interobserver variability was determined by a second independent blinded observer who measured the echocardiographic variables in 10 randomly selected patients. Interobserver variability was assessed using the within-subject coefficient of variation. The within-subject coefficient of variation (calculated as the ratio of the SD of the measurement difference to the mean value of all measurements) provides a scale-free, unitless estimate of variation expressed as a percentage. We measured interobserver reproducibility for E/e′ ratio and LVEDV and expressed it using the coefficient of variation. All analyses were considered significant at a two-tailed P value < .05. SPSS was used to perform all statistical evaluations (SSPS, Chicago, IL).

Results

A total of 52 patients underwent two echocardiographic examinations and were recruited for the study. Their mean age was 61 ± 10 years, and 39 (75%) were men. The mean E/e′ ratio on the first echocardiographic examination was 13.2 ± 4.8 (range, 5.3–27.2). Patients were divided into two groups according to their admission E/septal e′ ratio: group 1 ( n = 33) with E/septal e′ ratio ≤ 15 and group 2 ( n = 19) with E/septal e′ ratio > 15. Baseline characteristics for each group are shown in Table 1 . Patients with E/septal e′ ratios > 15 were more likely to be older and female and to have a more severe extent of coronary artery disease, a longer time to culprit vessel reperfusion, a higher prevalence of heart failure, and higher admission C-reactive protein levels. There was no difference in optimal medical therapy applied between the groups, but patients with E/septal e′ ratios > 15 were more likely to receive diuretics upon hospital discharge.

Echocardiography

The first echocardiographic examination was performed within 1.4 ± 0.3 days for both groups. Table 2 presents the echocardiographic findings according to E/septal e′ ratio in the first echocardiographic examination. Although LV ejection fraction was comparable between the groups (43.7 ± 8.4% vs 45.9 ± 7.0%, P = .408), patients with E/septal e′ ratios > 15 had higher E-wave velocities ( P = .008), lower e′ septal velocities ( P < .001), and higher pulmonary artery pressures (37 ± 16 vs 28 ± 6 mm Hg, P = .05). No significant changes were observed in left atrial volume indexes (34.4 ± 12.4 vs 30.3 ± 7.2 mL/m ² , P = .124). Follow-up echocardiography was performed within 178 ± 62 days. Of the 19 patients with E/septal e′ ratios > 15 on the first echocardiographic examination, 11 demonstrated E/septal e′ ratios > 15 in the second examination. Of 33 patients with E/septal e′ ratios ≤ 15 on the first examination, five shared an increase in E/septal e′ > 15 on the second examination. We therefore performed a pulled analysis of patients with E/septal e′ >15 and ≤15 in the second echocardiographic examination ( Table 3 ). Patients with E/septal e′ ratios > 15 had lower LV ejection fractions (45 ± 12% vs 52 ± 8%, P = .03), higher indexed LVEDVs (81.3 ± 22.9 vs 69.2 ± 13.4 mL/m ² , P = .01) and indexed LV end-systolic volumes (33.0 ± 12.2 vs 23.7 ± 13.4 mL/m ² , P = .02), as well as higher peak systolic pulmonary pressure (34 ± 9 mm Hg vs 26 ± 6 mm Hg, P < .001). Moreover, patients with E/septal e′ > 15 demonstrated a significant increase in indexed LVEDV (15.7 ± 15.3 vs 0.54 ± 18.6 mL/m ² , P = .006), representing LV remodeling. Among these patients, a positive correlation was found between the change in E/septal e′ ratio and the change in indexed LVEDV (linear R ² = 0.344, P = .03; Figure 1 ).

Table 2

Characteristics of first echocardiographic examination stratified by E/septal e′ ratio

Variable	E/septal e′ ratio		P
	≤15 ( n = 33)	>15 ( n = 19)
Biplane LV ejection fraction (%)	45.9 ± 7.0	43.7 ± 8.4	.408
Wall motion index	1.56 ± 0.40	1.89 ± 0.44	.105
Heart rate (beats/min)	75 ± 12	74 ± 14	.764
Systolic blood pressure (mm Hg)	136 ± 19	133 ± 28	.204
Diastolic blood pressure (mm Hg)	81 ± 13	79 ± 14	.596
Left atrial volume (mL 3 )	58.1 ± 13.9	62.8 ± 23.0	.479
Left atrial volume index (mL/m 2 )	30.3 ± 7.2	34.4 ± 12.4	.124
Mitral inflow E wave (cm/sec)	66 ± 21	82 ± 14	.008
Mitral inflow E/A ratio	1.07 ± 0.47	1.08 ± 0.38	.608
Septal e′ (cm/sec)	6.61 ± 1.38	4.55 ± 1.06	<.001
Lateral e′ (cm/sec)	8.77 ± 3.71	7.66 ± 2.95	.228
Mitral E deceleration time (msec)	186 ± 59	180 ± 55	.909
Indexed LVEDV (mL/m 2 )	60.3 ± 13.4	62.3 ± 13.4	.565
Indexed LVESV (mL/m 2 )	26.5 ± 14.1	28.7 ± 16.9	.307
Ventricular septal thickness (cm)	1.1 ± 0.14	1.1 ± 0.2	.491
Posterior LV wall thickness (cm)	1.0 ± 0.17	9 ± 4	.757
Peak systolic PA pressure (mm Hg)	28 ± 6	37 ± 16	.05
RA pressure (mm Hg)	6 ± 2	7 ± 5	.533

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