Prevalence, Correlates, and Prognostic Significance of In-Hospital Transthoracic Echocardiography Use in Stable Acute Myocardial Infarction
by
, and
Alon Shechter
1,2, 
Arthur Shiyovich
3,4
,
Robert J. Siegel
5,6, 
Olga Morelli
1,2,
Harel Gilutz
7 and
Ygal Plakht
8,9,* 1
Department of Cardiology, Rabin Medical Center, Petach Tikva 4910000, Israel
2
Gray Faculty of Medical and Health Sciences, Tel Aviv University, Tel Aviv 6997801, Israel
3
Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women’s Hospital, Boston, MA 02115, USA
4
Cardiovascular Division, Department of Medicine, Harvard Medical School, Boston, MA 02115, USA
5
Department of Cardiology, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA
6
David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA 90095, USA
7
Goldman Medical School, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheva 8410501, Israel
8
Department of Nursing, Recanati School for Community Health Professions, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheva 8410501, Israel
9
Department of Emergency Medicine, Soroka University Medical Center, Beer Sheva 8410101, Israel
*
Author to whom correspondence should be addressed.
J. Cardiovasc. Dev. Dis. 2026, 13(7), 322; https://doi.org/10.3390/jcdd13070322
Submission received: 24 May 2026
/
Revised: 6 July 2026
/
Accepted: 9 July 2026
/
Published: 10 July 2026
(This article belongs to the Section Imaging)
Abstract
Little is known regarding in-hospital transthoracic echocardiography (TTE) utilization and its prognostic implications among stable patients with acute myocardial infarction (AMI). We aimed to explore patient and disease characteristics, treatment strategies, and mid-term outcome following uncomplicated AMI according to TTE use during the hospitalization phase. A single-center, retrospective analysis was conducted that included consecutive adult individuals admitted for AMI who did not develop cardiogenic shock and who survived the index hospitalization. Stratified by in-hospital TTE administration status, the cohort was evaluated for all-cause mortality at 1-year post-discharge. Overall, 15,971 subjects (mean age 66 ± 14 years, 69.8% males, 46.1% with ST-elevation myocardial infarction) were analyzed, of whom 12,610 (79.0%) underwent TTE. TTE use correlated with younger age, fewer comorbidities, greater odds of invasive revascularization and intensive coronary care unit management, and lengthier hospital stay. Ultimately, it was associated with a lower rate, cumulative incidence, and—independent of accompanying prognostic markers—risk of all-cause mortality (n = 1032/12,619, 8.2% vs. n = 804/3361, 23.9%, p < 0.001; Log-Rank p < 0.001; adjusted hazard ratio 0.75, 95% confidence interval 0.67–0.83, p < 0.001). Similar results were observed within a 6270-patient, 1-1 propensity score-matched sub-cohort. To conclude, in our experience, in-hospital TTE administered for stable AMI patients was associated with improved mid-term survival. Further research is needed to re-evaluate the present-day recommendation’s Level of Evidence C for its routine use.
1. Introduction
A simple, readily available, bedside non-invasive imaging modality, transthoracic echocardiography (TTE), is potentially advantageous in subjects with acute coronary syndromes, as it allows for the appreciation of cardiac structure and function as well as hemodynamic status, thus assisting treating teams in recognizing therapeutic targets, formulating management strategies and, ultimately, enhancing downstream patient course [1]. Nevertheless, currently there are only limited data to support the theoretical prognostic benefit associated with routinely performing TTE in stable acute myocardial infarction (AMI) patients during hospitalization, as reflected by a Level of Evidence C recommendation for such practice in the most recent European [2] and American [3] guidelines. To address this knowledge gap, and specifically test the hypothesis linking TTE administration with improved survival following uncomplicated AMI, we analyzed a large, contemporary database according to TTE use during the index admission.
2. Materials and Methods
2.1. Study Population and Outcome
Our study represents a sub-analysis of the previously described [4,5] Soroka Acute Myocardial Infarction (SAMI) registry. Included in the present, retrospective study were adult (i.e., ≥18-year-old) Israeli citizens admitted for AMI at Soroka University Medical Center, Israel, between 2002 and 2017 who did not develop cardiogenic shock and who survived the acute hospitalization phase. For subjects with multiple hospitalizations, we considered only the initial one. The study outcome was all-cause mortality during the first year after discharge.
Conforming to the Declaration of Helsinki, the project was approved by Soroka’s Institutional Review Board (approval number SOR-0319-16), and the need for informed consent was waived.
2.2. Data Collection and Definitions
Clinical data were retrieved from a web-based medical chart, in which baseline comorbidities were identified by International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) [6] codes, as documented in real-time by the treating physicians and according to accepted diagnostic criteria. Deaths were confirmed using the Israeli Ministry of the Interior Population Registry.
AMI diagnosis was based upon the constellation of ischemic signs and/or symptoms coupled with an abrupt rise and fall in cardiac biomarker levels consistent with acute myocardial injury, as dictated by the Universal Definition of Myocardial Infarction at the time [7]. Diagnosis of obstructive coronary artery disease required angiographic evidence of a ≥70% vessel diameter narrowing.
Echocardiographic diagnoses aligned with the American Society of Echocardiography guidelines. Accordingly, severe left ventricular dysfunction was defined by an ejection fraction of <30%, and pulmonary hypertension as an estimated pulmonary arterial systolic pressure of ≥37 mmHg.
2.3. Statistical Analysis
Both the entire cohort and a propensity score (PS)-matched sub-cohort were analyzed according to the administration of in-hospital TTE. Within the latter, pairing was dictated by the probability of undergoing TTE, using a nearest neighbor, 1-to-1 matching method, and a tolerance of ≤0.2. Included in the binary logistic regression model used for predicting this probability were baseline/presenting characteristics of known or perceived prognostic significance, all selected prior to the execution of descriptive analyses: increasing age, male sex, atherosclerotic risk factors, chronic obstructive pulmonary disease, chronic kidney disease, pre-existent chronic coronary syndrome, clinical heart failure, right heart failure, atrial fibrillation/flutter, and more recent year of event. Between-group balance for each of PS variable was assessed using absolute standardized differences, as depicted by a Love plot (Figure S1). In addition, discriminative ability of the score was checked using Harrell’s C-statistic, which proved acceptable (0.72, 95% CI 0.71–0.73, p < 0.001).
At all stages, variables were reported as frequencies and percentages or means and standard deviations and compared using Pearson’s Chi-Square or Student’s t tests, as appropriate.
The time-dependent probability and cumulative incidence of mortality as a function of TTE performance were assessed by the Kaplan–Meier method and compared using the Log-Rank test. Independent associations with the risk for all-cause death were evaluated by a Cox proportional hazard multivariable analysis and expressed using each’s unadjusted hazard ratio (HR)/adjusted HR (AdjHR) and the latter’s 95% confidence interval (CI). The model incorporated covariates exhibiting a p-value of <0.1 on the univariable stage. The proportional hazards assumption was evaluated qualitatively by checking for parallel orientation of the log-minus-log survival plots for all covariates. Model fit was assessed using the −2 log likelihood and likelihood ratio test.
Statistical significance required a two-sided p-value of <0.05. All analyses were performed using Statistical Package for the Social Sciences (SPSS), version 31 (IBM Corporation, Armonk, NY, USA).
3. Results
3.1. Baseline Characteristics of the Study Population
A total of 15,971 individuals qualified for analysis (Figure 1). Of them, 12,610 (79.0%) underwent TTE during their hospital stay. Notably, TTE utilization rose during the study recruitment period, from 74.2% in 2002 to 86.6% in 2017 (p for trend <0.001).
Compared to patients who were not scanned, those within the TTE group were recruited to the study at a later calendar year and were younger and more likely to be males of a non-Jewish minority background (Table 1). They also exhibited an overall higher burden of atherosclerotic cardiovascular risk factors but fewer comorbidities including overt heart failure. Echocardiograms demonstrated severe left ventricular dysfunction in 1316 (8.2%) out of the 12,610 cases referred for TTE, right ventricular dysfunction in 971 (7.7%), moderate and above mitral regurgitation in 670 (4.2%), moderate and above tricuspid regurgitation in 426 (2.7%), and pulmonary hypertension in 913 (5.7%).
3.2. Acute Event Aspects
Subjects who underwent TTE presented more commonly with ST elevation myocardial infarction (STEMI) (n = 6356, 50.4% vs. n = 1005, 29.9%, p < 0.001) and with a similarly low rate (0.3%) of cardiac arrest compared to those who did not undergo TTE (Table 2). The former were more likely to be assessed angiographically and to obtain definitive revascularization, leading to more intensive coronary care unit admissions/transfers and longer hospital stays. Also, their hospitalization courses were characterized by more frequent arrhythmic sequelae and fewer bleeding complications and sepsis. Specifically among patients who underwent both TTE and invasive revascularization and for whom data regarding respective timings were available (n = 10,356), TTE preceded revascularization by more than a day in 1129 (10.9%) cases, took place within a day of revascularization in 7238 (70.0%), or was performed more than a day after revascularization in 1989 (19.2%).
3.3. Outcome
By 1 year after discharge, 1836 (11.5%) patients died. TTE performance was associated with a lower rate, cumulative incidence, and—independent of accompanying prognostic markers at baseline and during hospitalization—risk of all-cause mortality (n = 1032/12,619, 8.2% vs. n = 804/3361, 23.9%, p < 0.001; Log-Rank p < 0.001; unadjusted HR 0.31, 95% CI 0.28–0.34, p < 0.001; AdjHR 0.75, 95% CI 0.67–0.83, p < 0.001) (Figure 2 and Table 3).
Of note, within the TTE/invasive revascularization subgroup, death rate was highest among patients scanned after revascularization (n = 187/1989, 9.4%), intermediate among those scanned before revascularization (n = 48/1129, 4.3%), and lowest among those scanned surrounding revascularization (n = 284/7238, 3.9%) (p < 0.001).
Per exploratory analysis, the significant association between TTE performance and reduced mortality risk was confined to patients presenting with non-ST elevation MI (NSTEMI) (AdjHR 0.71, 95% CI 0.63–0.80, p < 0.001) and those managed non-invasively (AdjHR 0.72, 95% CI 0.64–0.81, p < 0.001), as opposed to patients with STEMI (AdjHR 0.92, 95% CI 0.74–1.13, p = 0.417) and those referred to invasive revascularization (AdjHR 0.88, 95% CI 0.69–1.13, p = 0.328).
3.4. Propensity Score Matching Analysis
Within a 6270-case PS-matched sub-cohort, composed of 3135 patients who underwent TTE and 3135 matched controls who did not, most differences in baseline characteristics and acute event aspects became neutralized (Table 4 and Table 5). Still, ST elevation, angiographic assessment, invasive revascularization, and intensive care unit management were more common in the TTE group. Similar to the total unmatched cohort, patients who underwent TTE experienced fewer, more distant death events (n = 471, 15.0% vs. n = 690, 22.0%, p < 0.001; Log-Rank p < 0.001), and TTE utilization conferred a lower death risk (unadjusted HR 0.65, 95% CI 0.58–0.73, p < 0.001; AdjHR 0.77, 95% CI 0.68–0.88, p < 0.001) (Figure 3 and Table 6). Likewise, the prognostic significance of TTE administration was only observed among NSTEMI cases (AdjHR 0.75, 95% CI 0.65–0.86, p < 0.001) and non-invasively managed patients (AdjHR 0.75, 95% CI 0.65–0.86, p < 0.001), as opposed to STEMI scenarios (AdjHR 0.89, 95% CI 0.68–1.16, p = 0.369) and invasively treated subjects (AdjHR 0.90, 95% CI 0.67–1.21, p = 0.492).
4. Discussion
In this single-center, retrospective study, we examined the utilization of in-hospital TTE among 15,971 real-world patients admitted for non-fatal, stable AMI over a period of 15 years. Its results revealed the following: 1. TTE was performed more frequently in later years and in almost 80% of subjects overall. 2. Compared to patients who did not undergo TTE during the index hospitalization, those who did presented at a younger age and with fewer comorbidities, were more often managed invasively and within the intensive coronary care unit, and exhibited a lengthier hospital stay. 3. TTE performance was associated with improved 1-year survival, independently conferring a mortality risk that was 1.3 times lower than that observed within the no-TTE group.
The current literature concerning the prevalence, correlates, and prognostic significance of in-hospital TTE administration in AMI is limited. In the largest report prior to ours, covering almost 100,000 admissions across nearly 400 centers in the United States, TTE was performed in 74% of cases and a more liberal use of TTE correlated with higher costs and longer hospitalizations without affecting inpatient mortality nor 3-month readmissions [8]. Importantly, the authors relied on an administrative, billing code-focused database that spanned merely one year of practice (2014) and which included a highly heterogenous population treated in centers of varying capabilities (with some not offering percutaneous coronary intervention services at all). Moreover, the study’s analyses revolved around inter-center comparisons rather than patient-level, actual administration of TTE per se, all while considering stable/unstable patients and first-time/repeat hospitalizations as one. An earlier study (2001–2011) examining the use of echocardiography in various medical conditions identified enhanced in-hospital survival among AMI patients who underwent TTE [9]. However, echocardiography was performed in only 7% of cases and no adjustment was made for deaths occurring prior to the performance of TTE. Bearing in mind these previous works’ setbacks, we designed the present study which focused on mid-term survival post-AMI, presumably providing a more accurate reflection of TTE utilization.
Our observations have two clinically relevant implications. The first is that performing TTE during hospitalization for AMI was linked to better prognosis following discharge. It could be that earlier detection of actionable conditions known to affect survival, such as systolic dysfunction, diastolic impairment, valvular disorders, and structural/thrombotic complications allowed for a more comprehensive management (that is, beyond mere revascularization) within the TTE group that in turn led to improved outcomes. Consistent with this assumption were: a. the lower death rates reported among revascularized patients who underwent TTE at an earlier stage; and b. the confinement of the reduced death hazard associated with TTE use to patients presenting with NSTEMI or who were managed non-invasively, both of whom are traditionally less exposed to prognostically meaningful interventions and may thus derive added benefit from TTE. Alternatively, the administration of TTE may have simply served as a surrogate of stricter guideline-directed therapy adherence and hence higher standards of care. This hypothesis fits well with the observation linking TTE performance with greater utilization of invasive revascularization and intensive care environment and more advanced year of event, although the latter did not alter the independent prognostic value of TTE use (and, furthermore, intensive care unit stay and event year were not associated with survival on their own). As our registry lacked information regarding full TTE reports, their impact on management strategy, death causes, and clinical pathways leading to TTE use in the first place, the exact mechanism(s) underlying our findings remain speculative. Accordingly, and as much as the study’s extensive multivariable analyses implied the independent predictive role of TTE use, further, preferentially prospective validation is needed.
The second message offered by our study is that TTE was relatively underutilized during the hospitalization phase surrounding AMI diagnosis, much in the same manner reported by prior publications [10]. In light of the observed intergroup differences in patient characteristics and revascularization approach, it could be that TTE was perceived as lower-yield in those subjects who were deemed too high risk or unfit for interventional therapies a priori. Technical obstacles, too, may have contributed to the low usage of TTE in persons presenting with numerous comorbidities, in whom hand-held echocardiography could constitute a similarly accurate and more feasible alternative [11]. Once again, we were unable to identify causality, thus we are leaving it for future studies to better define barriers for the implementation of TTE in this setting.
Limitations
First, our study stemmed from a single-center, retrospective analysis that did not employ randomization nor external adjudication, potentially leading to selection bias and hampering the generalizability of the results. However, we relied on a large cohort that represented a population of close to 1 million and whose baseline characteristics resembled those of prior registries. Also, randomized-controlled trials of TTE utilization among stable AMI patients are hardly pragmatic, arguably making real-world exploration as our the next best alternative. Secondly, and again reflecting the study’s retrospective design, statistical precision and associated clinical relevance of our findings may be questionable. Yet, based on the sample size, exposure (i.e., TTE use) distribution, event rate, and Cox model utilized, and assuming a two-sided α of 0.05 and 80% power, we estimated the minimum detectable effect size as HR for all-cause mortality of approximately 0.90, a figure which is generally considered clinically meaningful in cardiovascular outcome research, particularly in settings where imaging may influence downstream decision-making rather than exert direct therapeutic effects. Thirdly, aiming to focus on patients for whom current practice guidelines provide expert opinion-based recommendation only, and in view of the study’s objective to explore the 1-year trajectory of these individuals, we deliberately excluded in-hospital fatalities, hence introducing survivor bias. This could also mitigate the possibility of immortal time bias and in essence led to a modest 7.8% exclusion rate (Figure 1). Fourthly, the protracted timeframe of enrollment may have led to inconsistencies in medical definitions and treatment approaches, which also could have affected the interpretation of the findings. Nevertheless, both study groups were exposed to similarly evolving diagnostic criteria and practices, and admission year did not possess an independent prognostic capacity nor did it undermine the significant association demonstrated between TTE performance and 1-year mortality. Fifthly, in addition to death causes, we were also unaware of the exact TTE scope (complete vs. focused), and—in some patients—timing, as well as MI types (e.g., type 2) and extent (e.g., Killip class, serum biomarker levels), medical therapies other than blood transfusion, and reason for re-admissions. Consequently, we could not comment on the pathophysiologic basis accounting for our observations nor rule out confounding by non-coronary-related phenomena. Lastly, and in view of the evaluation of multiple covariates by a Cox regression model, chance findings could not be entirely excluded, necessitating cautious interpretation which takes into consideration effect size (and the possibility of smaller effect sizes than the one estimated above), confidence intervals, and their clinical plausibility.
5. Conclusions
In our large, single-center experience, in-hospital TTE was utilized in close to 80% of subjects with stable, non-fatal AMI and was associated with a lower-risk patient profile, a higher rate of invasive coronary interventions and intensive care management, and a more favorable 1-year survival. These findings call for further assessment of the routine use of TTE in such scenarios.
Supplementary Materials
The following supporting information can be downloaded at https://www.mdpi.com/article/10.3390/jcdd13070322/s1. Figure S1: Love plot for balance in propensity score variables.
Author Contributions
Conceptualization, A.S. (Alon Shechter); methodology, A.S. (Alon Shechter) and Y.P.; formal analysis, Y.P.; data curation, H.G. and Y.P.; writing—original draft preparation, A.S. (Alon Shechter); writing—review and editing, A.S. (Alon Shechter), A.S. (Arthur Shiyovich), R.J.S., O.M., H.G. and Y.P. All authors have read and agreed to the published version of the manuscript.
Funding
This research received no external funding.
Institutional Review Board Statement
The study was conducted in accordance with the Declaration of Helsinki and approved by the Soroka Medical Center Institutional Review Board (initial approval SOR-0319-16, granted 19 September 2016, extended up to 13 December 2022).
Informed Consent Statement
Patient consent was waived due the study’s retrospective nature.
Data Availability Statement
The data underlying this article will be shared upon reasonable request to the corresponding author.
Conflicts of Interest
The authors declare no conflicts of interest.
Abbreviations
The following abbreviations are used in this manuscript:
| AMI | Acute myocardial infarction |
| TTE | Transthoracic echocardiography |
References
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Figure 1.
Study flow chart. SUMC = Soroka University Medical Center; TTE = transthoracic echocardiography.
Figure 1.
Study flow chart. SUMC = Soroka University Medical Center; TTE = transthoracic echocardiography.
Figure 2.
Cumulative survival according to transthoracic echocardiography use. TTE = transthoracic echocardiography.
Figure 2.
Cumulative survival according to transthoracic echocardiography use. TTE = transthoracic echocardiography.
Figure 3.
Cumulative survival according to transthoracic echocardiography use within the propensity score-matched sub-cohort. TTE = transthoracic echocardiography.
Figure 3.
Cumulative survival according to transthoracic echocardiography use within the propensity score-matched sub-cohort. TTE = transthoracic echocardiography.
Table 1.
Baseline clinical characteristics.
| Total Cohort (N = 15,971) | Transthoracic Echocardiography Use | p-Value | ||
|---|---|---|---|---|
| Yes (n = 12,610) | No (n = 3361) | |||
| Demographic details | ||||
| Age | <0.001 | |||
| Continuous (years) | 66 ± 14 | 64 ± 13 | 72 ± 14 | |
| <65 years | 7926 (49.6) | 6959 (55.2) | 967 (28.8) | |
| 65–74 years | 3623 (22.7) | 2836 (22.5) | 787 (23.4) | |
| ≥75 years | 4422 (27.7) | 2815 (22.3) | 1607 (47.8) | |
| Sex male | 11,152 (69.8) | 9165 (72.7) | 1987 (59.1) | <0.001 |
| Non-Jewish minority | 2651 (16.6) | 2213 (17.5) | 438 (13.0) | <0.001 |
| Atherosclerotic cardiovascular risk factors | ||||
| Diabetes mellitus | 6444 (40.3) | 4912 (39.0) | 1532 (45.6) | <0.001 |
| Dyslipidemia | 12,975 (81.2) | 10,556 (83.7) | 2419 (72.0) | <0.001 |
| Hypertension | 8280 (51.8) | 6438 (51.1) | 1842 (54.8) | <0.001 |
| Obesity | 3579 (22.4) | 3033 (24.1) | 546 (16.2) | <0.001 |
| Smoking history | 6743 (42.2) | 5879 (46.6) | 864 (25.7) | <0.001 |
| Family history of ischemic heart disease | 1494 (9.4) | 1360 (10.8) | 134 (4.0) | <0.001 |
| Cardiovascular comorbidities | ||||
| Chronic coronary syndrome | 12,496 (78.2) | 10,473 (83.1) | 2023 (60.2) | <0.001 |
| History of myocardial infarction | 1786 (11.2) | 1320 (10.5) | 466 (13.9) | <0.001 |
| Prior revascularization | ||||
| Percutaneous coronary intervention | 1907 (11.9) | 1493 (11.8) | 414 (12.3) | 0.448 |
| Coronary artery bypass grafting | 1243 (7.8) | 889 (7.0) | 354 (10.5) | <0.001 |
| Peripheral arterial disease | 1799 (11.3) | 1337 (10.6) | 462 (13.7) | 0.266 |
| Atrial fibrillation/flutter | 2447 (15.3) | 1738 (13.8) | 709 (21.1) | <0.001 |
| Atrioventricular block | 592 (3.7) | 470 (3.7) | 122 (3.6) | 0.791 |
| Clinical heart failure | 2556 (16.0) | 1870 (14.8) | 686 (20.4) | <0.001 |
| Non-cardiovascular comorbidities | ||||
| Chronic obstructive pulmonary disease | 1232 (7.7) | 880 (7.0) | 352 (10.5) | <0.001 |
| Stage ≥III chronic kidney disease | 5157 (32.3) | 3749 (29.7) | 1408 (41.9) | <0.001 |
| Anemia | 8498 (53.2) | 6437 (51.0) | 2061 (61.3) | <0.001 |
| Neurological disorders | 2567 (16.1) | 1710 (13.6) | 857 (25.5) | <0.001 |
| Malignancy | 612 (3.8) | 422 (3.3) | 190 (5.7) | <0.001 |
| Substance use disorder | 340 (2.1) | 284 (2.3) | 56 (1.7) | 0.036 |
| Psychotic disorders | 258 (1.6) | 177 (1.4) | 81 (2.4) | <0.001 |
Data are presented as number (percent) or mean ± standard deviation. Figures in bold denote statistical significance.
Table 2.
Acute event aspects.
| Total Cohort (N = 15,971) | Transthoracic Echocardiography Use | p-Value | ||
|---|---|---|---|---|
| Yes (n = 12,610) | No (n = 3361) | |||
| Clinical presentation | ||||
| ST elevation myocardial infarction | 7361 (46.1) | 6356 (50.4) | 1005 (29.9) | <0.001 |
| Cardiac arrest | 52 (0.3) | 43 (0.3) | 9 (0.3) | 0.508 |
| Right heart failure | 1251 (7.8) | 971 (7.7) | 280 (8.3) | 0.227 |
| Angiographic parameters | ||||
| Angiogram performed | 11,038 (69.1) | 10,356 (82.1) | 682 (20.3) | <0.001 |
| Vessels significantly involved | <0.001 | |||
| 0 | 507 (4.6) | 446 (4.3) | 61 (8.9) | |
| 1 | 3076 (27.9) | 2913 (28.1) | 163 (23.9) | |
| 2 | 3092 (28.0) | 2913 (28.1) | 179 (26.2) | |
| 3/Left main | 4363 (39.5) | 4084 (39.4) | 279 (40.9) | |
| Hospital course | ||||
| Revascularization approach | <0.001 | |||
| None/ conservative treatment | 4207 (26.3) | 2087 (16.6) | 2120 (63.1) | |
| Percutaneous coronary intervention | 9720 (60.9) | 8753 (69.4) | 967 (28.8) | |
| Coronary artery bypass grafting | 2044 (12.8) | 1770 (14.0) | 274 (8.2) | |
| Intensive coronary care unit stay | 11,029 (69.1) | 10,119 (80.2) | 910 (27.1) | <0.001 |
| Ventricular tachycardia | 378 (2.4) | 332 (2.6) | 46 (1.4) | <0.001 |
| Any form of pacing | 284 (1.8) | 269 (2.1) | 15 (0.4) | <0.001 |
| Mechanical ventilation | 548 (3.4) | 438 (3.5) | 110 (3.3) | 0.570 |
| Gastrointestinal bleeding | 320 (2.0) | 242 (1.9) | 78 (2.3) | 0.140 |
| Blood transfusion | 1887 (11.8) | 1449 (11.5) | 438 (13.0) | 0.014 |
| Sepsis | 124 (0.8) | 85 (0.7) | 39 (1.2) | 0.004 |
| Hospitalization length | ||||
| Continuous (days) | 10.0 ± 9.0 | 10.3 ± 9.2 | 8.8 ± 8.1 | <0.001 |
| ≥7 days | 7538 (47.2) | 6207 (49.2) | 1331 (39.6) | <0.001 |
Data are presented as number (percent) or mean ± standard deviation. Figures in bold denote statistical significance.
Table 3.
Multivariable Cox proportional hazard model for the outcome of all-cause mortality at 1 year.
Table 3.
Multivariable Cox proportional hazard model for the outcome of all-cause mortality at 1 year.
| Univariable | Multivariable | |||
|---|---|---|---|---|
| HR (95% CI) | p-Value | AdjHR (95% CI) | p-Value | |
| Year of admission (continuous, per 1-year increase) | 0.97 (0.96–0.98) | <0.001 | 1.00 (0.99–1.02) | 0.456 |
| Demographic details | ||||
| Age ≥ 65 vs. <65 years | 4.42 (3.78–5.18) | <0.001 | 2.26 (1.91–2.66) | <0.001 |
| Sex male | 0.52 (0.47–0.57) | <0.001 | 0.92 (0.83–1.02) | 0.102 |
| Atherosclerotic cardiovascular risk factors | ||||
| Dyslipidemia | 0.46 (0.41–0.50) | <0.001 | 0.75 (0.68–0.83) | <0.001 |
| Obesity | 0.49 (0.42–0.56) | <0.001 | 0.77 (0.67–0.88) | <0.001 |
| Diabetes mellitus | 1.51 (1.42–1.70) | <0.001 | 1.18 (1.07–1.30) | <0.001 |
| Cardiovascular comorbidities | ||||
| Chronic coronary syndrome | 0.30 (0.27–0.33) | <0.001 | 0.81 (0.73–0.91) | <0.001 |
| Peripheral arterial disease | 2.35 (2.10–2.62) | <0.001 | 1.49 (1.32–1.67) | <0.001 |
| Atrial fibrillation/flutter | 2.62 (2.38–2.90) | <0.001 | 1.28 (1.16–1.42) | <0.001 |
| Clinical heart failure | 2.75 (2.49–3.03) | <0.001 | 1.31 (1.18–1.46) | <0.001 |
| Non-cardiovascular comorbidities | ||||
| Chronic obstructive pulmonary disease | 2.55 (2.25–2.88) | <0.001 | 1.59 (1.40–1.81) | <0.001 |
| Stage ≥ III chronic kidney disease | 3.36 (3.06–3.69) | <0.001 | 1.42 (1.28–1.58) | <0.001 |
| Anemia | 3.13 (2.81–3.49) | <0.001 | 1.56 (1.39–1.75) | <0.001 |
| Neurological disorders | 3.22 (2.93–3.54) | <0.001 | 1.57 (1.42–1.74) | <0.001 |
| Malignancy | 3.88 (3.37–4.47) | <0.001 | 2.32 (2.00–2.68) | <0.001 |
| Substance use disorder | 2.19 (1.69–2.83) | <0.001 | 1.83 (1.37–2.46) | <0.001 |
| Psychotic disorders | 2.55 (2.25–2.88) | <0.001 | 1.46 (1.12–1.88) | 0.004 |
| Clinical presentation | ||||
| ST elevation (vs. non-ST elevation) myocardial infarction | 0.46 (0.42–0.51) | <0.001 | 1.01 (0.90–1.13) | 0.880 |
| Right heart failure | 2.64 (2.34–2.98) | <0.001 | 1.39 (1.23–1.58) | <0.001 |
| Hospital course | ||||
| Invasive revascularization vs. conservative approach | 0.15 (0.14–0.17) | <0.001 | 0.45 (0.39–0.52) | <0.001 |
| Mechanical ventilation | 2.50 (2.10–2.98) | <0.001 | 1.34 (1.12–1.61) | 0.001 |
| Transthoracic echocardiography use | 0.31 (0.28–0.34) | <0.001 | 0.75 (0.67–0.83) | <0.001 |
Figures in bold denote statistical significance. AdjHR = adjusted hazard ratio; CI = confidence interval; HR = hazard ratio.
Table 4.
Baseline clinical characteristics of the propensity score-matched sub-cohort.
| Propensity Score-Matched Sub-Cohort (N = 6270) | Transthoracic Echocardiography Use | p-Value | ||
|---|---|---|---|---|
| Yes (n = 3135) | No (n = 3135) | |||
| Demographic details | ||||
| Age | ||||
| Continuous (years) | 71.42 ± 13.04 | 71.4 ± 12.59 | 71.41 ± 13.48 | 0.938 |
| <65 years | 1953 (31.1) | 986 (31.5) | 967 (30.8) | 0.711 |
| 65–74 years | 1533 (24.4) | 753 (24.0) | 780 (24.9) | |
| ≥75 years | 2784 (44.4) | 1396 (44.5) | 1388 (44.3) | |
| Sex male | 3833 (61.1) | 1921 (61.3) | 1912 (61.0) | 0.816 |
| Non-Jewish minority | 455 (7.3) | 31 (1.0) | 424 (13.5) | <0.001 |
| Atherosclerotic cardiovascular risk factors | ||||
| Diabetes mellitus | 2808 (44.8) | 1379 (44.0) | 1429 (45.6) | 0.204 |
| Dyslipidemia | 4736 (75.5) | 2380 (75.9) | 2356 (75.2) | 0.481 |
| Hypertension | 3448 (55.0) | 1720 (54.9) | 1728 (55.1) | 0.839 |
| Obesity | 1098 (17.5) | 557 (17.8) | 541 (17.3) | 0.595 |
| Smoking history | 1696 (27.0) | 837 (26.7) | 859 (27.4) | 0.532 |
| Family history of ischemic heart disease | 323 (5.2) | 189 (6.0) | 134 (4.3) | 0.002 |
| Cardiovascular comorbidities | ||||
| Chronic coronary syndrome | 4020 (64.1) | 2000 (63.8) | 2020 (64.4) | 0.598 |
| History of myocardial infarction | 732 (11.7) | 270 (8.6) | 462 (14.7) | <0.001 |
| Prior revascularization | ||||
| Percutaneous coronary intervention | 716 (11.4) | 303 (9.7) | 413 (13.2) | <0.001 |
| Coronary artery bypass grafting | 588 (9.4) | 235 (7.5) | 353 (11.3) | <0.001 |
| Peripheral arterial disease | 801 (12.8) | 369 (11.8) | 432 (13.8) | 0.017 |
| Atrial fibrillation/flutter | 1304 (20.8) | 658 (21.0) | 646 (20.6) | 0.709 |
| Atrioventricular block | 281 (4.5) | 163 (5.2) | 118 (3.8) | 0.006 |
| Clinical heart failure | 1253 (20.0) | 631 (20.1) | 622 (19.8) | 0.776 |
| Non-cardiovascular comorbidities | ||||
| Chronic obstructive pulmonary disease | 589 (9.4) | 263 (8.4) | 326 (10.4) | 0.006 |
| Stage ≥ III chronic kidney disease | 2556 (40.8) | 1266 (40.4) | 1290 (41.1) | 0.537 |
| Anemia | 3741 (59.7) | 1848 (58.9) | 1893 (60.4) | 0.247 |
| Neurological disorders | 1432 (22.8) | 716 (22.8) | 716 (22.8) | 1.000 |
| Malignancy | 320 (5.1) | 149 (4.8) | 171 (5.5) | 0.207 |
| Substance use disorder | 108 (1.7) | 54 (1.7) | 54 (1.7) | 1.000 |
| Psychotic disorders | 149 (2.4) | 70 (2.2) | 79 (2.5) | 0.456 |
Data are presented as number (percent) or mean ± standard deviation. Figures in bold denote statistical significance.
Table 5.
Acute event aspects within the propensity score-matched sub-cohort.
| Propensity Score-Matched Sub-Cohort (N = 6270) | Transthoracic Echocardiography Use | p-Value | ||
|---|---|---|---|---|
| Yes (n = 3135) | No (n = 3135) | |||
| Clinical presentation | ||||
| ST elevation myocardial infarction | 2327 (37.1) | 1363 (43.5) | 964 (30.7) | <0.001 |
| Cardiac arrest | 17 (0.3) | 10 (0.3) | 7 (0.2) | 0.466 |
| Right heart failure | 569 (9.1) | 291 (9.3) | 278 (8.9) | 0.568 |
| Angiographic parameters | ||||
| Angiogram performed | 2723 (43.4) | 2042 (65.1) | 681 (21.7) | <0.001 |
| Vessels significantly involved | 0.198 | |||
| 0 | 197 (7.2) | 136 (6.7) | 61 (9.0) | |
| 1 | 640 (23.5) | 477 (23.4) | 163 (23.9) | |
| 2 | 758 (27.8) | 579 (28.4) | 179 (26.3) | |
| 3/Left main | 1128 (41.4) | 850 (41.6) | 278 (40.8) | |
| Hospital course | ||||
| Revascularization approach | <0.001 | |||
| None/ conservative treatment | 2948 (47.0) | 1052 (33.6) | 1896 (60.5) | |
| Percutaneous coronary intervention | 2699 (43.0) | 1734 (55.3) | 965 (30.8) | |
| Coronary artery bypass grafting | 623 (9.9) | 349 (11.1) | 274 (8.7) | |
| Intensive coronary care unit stay | 2969 (47.4) | 2062 (65.8) | 907 (28.9) | <0.001 |
| Ventricular tachycardia | 107 (1.7) | 61 (1.9) | 46 (1.5) | 0.144 |
| Any form of pacing | 103 (1.6) | 88 (2.8) | 15 (0.5) | <0.001 |
| Mechanical ventilation | 227 (3.6) | 124 (4.0) | 103 (3.3) | 0.156 |
| Gastrointestinal bleeding | 149 (2.4) | 80 (2.6) | 69 (2.2) | 0.362 |
| Blood transfusion | 823 (13.1) | 416 (13.3) | 407 (13.0) | 0.736 |
| Sepsis | 57 (0.9) | 23 (0.7) | 34 (1.1) | 0.143 |
| Hospitalization length | ||||
| Continuous (days) | 9.93 ± 9.10 | 11.03 ± 9.68 | 8.82 ± 8.32 | <0.001 |
| ≥7 days | 2973 (47.4) | 1724 (55.0) | 1249 (39.8) | <0.001 |
Data are presented as number (percent) or mean ± standard deviation. Figures in bold denote statistical significance.
Table 6.
Multivariable Cox proportional hazard model for the outcome of all-cause mortality at 1 year within the propensity score-matched sub-cohort.
Table 6.
Multivariable Cox proportional hazard model for the outcome of all-cause mortality at 1 year within the propensity score-matched sub-cohort.
| Univariable | Multivariable | |||
|---|---|---|---|---|
| HR (95% CI) | p-Value | AdjHR (95% CI) | p-Value | |
| Year of admission (continuous, per 1-year increase) | 0.98 (0.97–0.99) | <0.001 | 1.01 (1.00–1.02) | 0.214 |
| Demographic details | ||||
| Age ≥ 65 vs. <65 years | 3.83 (3.01–4.87) | <0.001 | 2.27 (1.78–2.90) | <0.001 |
| Sex male | 0.68 (0.61–0.77) | <0.001 | 0.97 (0.86–1.10) | 0.633 |
| Atherosclerotic cardiovascular risk factors | ||||
| Diabetes mellitus | 1.21 (1.08–1.36) | 0.001 | 1.05 (0.93–1.19) | 0.408 |
| Dyslipidemia | 0.58 (0.51–0.65) | <0.001 | 0.76 (0.67–0.86) | <0.001 |
| Obesity | 0.53 (0.44–0.64) | <0.001 | 0.78 (0.64–0.94) | 0.010 |
| Cardiovascular comorbidities | ||||
| Chronic coronary syndrome | 0.44 (0.39–0.49) | <0.001 | 0.84 (0.73–0.96) | 0.009 |
| Peripheral arterial disease | 1.96 (1.70–2.26) | <0.001 | 1.45 (1.25–1.68) | <0.001 |
| Atrial fibrillation/flutter | 1.86 (1.64–2.10) | <0.001 | 1.20 (1.06–1.37) | 0.005 |
| Clinical heart failure | 2.06 (1.83–2.34) | <0.001 | 1.28 (1.13–1.46) | <0.001 |
| Non-cardiovascular comorbidities | ||||
| Chronic obstructive pulmonary disease | 2.14 (1.84–2.5) | <0.001 | 1.57 (1.34–1.85) | <0.001 |
| Stage ≥ III chronic kidney disease | 2.37 (2.11–2.67) | <0.001 | 1.33 (1.17–1.51) | <0.001 |
| Anemia | 2.40 (2.09–2.75) | <0.001 | 1.46 (1.27–1.68) | <0.001 |
| Neurological disorders | 2.39 (2.12–2.69) | <0.001 | 1.62 (1.44–1.83) | <0.001 |
| Malignancy | 3.04 (2.54–3.63) | <0.001 | 2.19 (1.83–2.62) | <0.001 |
| Psychotic disorders | 1.72 (1.27–2.32) | <0.001 | 1.39 (1.03–1.88) | 0.033 |
| Clinical presentation | ||||
| ST elevation (vs. non-ST elevation) myocardial infarction | 0.57 (0.50–0.65) | <0.001 | 1.04 (0.90–1.20) | 0.619 |
| Right heart failure | 2.08 (1.78–2.44) | <0.001 | 1.35 (1.15–1.60) | <0.001 |
| Hospital course | ||||
| Invasive revascularization vs. conservative approach | 0.21 (0.18–0.24) | <0.001 | 0.42 (0.35–0.51) | <0.001 |
| Mechanical ventilation | 2.34 (1.87–2.93) | <0.001 | 1.44 (1.14–1.82) | 0.002 |
| Transthoracic echocardiography use | 0.65 (0.58–0.73) | <0.001 | 0.77 (0.68–0.88) | <0.001 |
Figures in bold denote statistical significance. AdjHR = adjusted hazard ratio; CI = confidence interval; HR = hazard ratio.
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MDPI and ACS Style
Shechter, A.; Shiyovich, A.; Siegel, R.J.; Morelli, O.; Gilutz, H.; Plakht, Y. Prevalence, Correlates, and Prognostic Significance of In-Hospital Transthoracic Echocardiography Use in Stable Acute Myocardial Infarction. J. Cardiovasc. Dev. Dis. 2026, 13, 322. https://doi.org/10.3390/jcdd13070322
AMA Style
Shechter A, Shiyovich A, Siegel RJ, Morelli O, Gilutz H, Plakht Y. Prevalence, Correlates, and Prognostic Significance of In-Hospital Transthoracic Echocardiography Use in Stable Acute Myocardial Infarction. Journal of Cardiovascular Development and Disease. 2026; 13(7):322. https://doi.org/10.3390/jcdd13070322
Chicago/Turabian StyleShechter, Alon, Arthur Shiyovich, Robert J. Siegel, Olga Morelli, Harel Gilutz, and Ygal Plakht. 2026. "Prevalence, Correlates, and Prognostic Significance of In-Hospital Transthoracic Echocardiography Use in Stable Acute Myocardial Infarction" Journal of Cardiovascular Development and Disease 13, no. 7: 322. https://doi.org/10.3390/jcdd13070322
APA StyleShechter, A., Shiyovich, A., Siegel, R. J., Morelli, O., Gilutz, H., & Plakht, Y. (2026). Prevalence, Correlates, and Prognostic Significance of In-Hospital Transthoracic Echocardiography Use in Stable Acute Myocardial Infarction. Journal of Cardiovascular Development and Disease, 13(7), 322. https://doi.org/10.3390/jcdd13070322
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