Can we predict cardiac rupture in patients with ST-segment elevation myocardial infarction?

Cardiac rupture (CR) is a rare complication of acute myocardial infarction (AMI), especially ST-segment elevation myocardial infarction (STEMI) (1) and is a catastrophic event with mortality up to 92.5% (2-5). Early studies reported 4–24% (average 8%) incidence of CR following AMI (6). Improvements in revascularization techniques such as thrombolytics and primary percutaneous coronary intervention (PCI) decreased the incidence of CR from ~8% to 0.14–0.96% over the last decades (7,8). Delays in hospital admission and myocardial revascularization have been associated with higher incidence of AMI complications (8). Delays in AMI care during the coronavirus disease 2019 (COVID-19) pandemic led to late presentation and increased rates of catastrophic AMI complications such as CR (9,10).

Several studies have examined variables associated with CR in AMI patients. In one study, STEMI had four to five times higher risk compared with non-STEMI and unstable angina (1), and CR was independently associated with ST-segment elevation/left bundle branch block, female sex, previous stroke, older age, higher heart rate, and 30-mm drop in systolic blood pressure. Low-molecular weight heparin use and beta-blockers during the first 24-hour period were associated with lower risk of CR (1). Older age (11), first AMI (12), peak creatine kinase-MB >150 IU/L, anterior location, lateral location (12), transmural infarction, pericardial effusion of 10 mm or more (13), lower body mass index (BMI) (7), longer time to revascularization (7), have been associated with higher risk of CR. In contrast, left ventricular hypertrophy, congestive heart failure, history of previous infarcts (11), early use of beta-blockers, and timely intervention were associated with lower incidence of CR (7,14). One autopsy study reported that CR patients had heavier hearts than would be expected based on body weight; BMI was significantly associated with CR only in men, and most CR cases occurred in the anterior wall (45%), followed by the posterior (38%) and lateral (9%) wall (15).

In this issue of the Journal of Thoracic Disease, Xu et al. (16) examined various clinical and angiographic variables associated with CR in a retrospective analysis of 22,016 STEMI patients admitted to two hospitals in China between 2013 and 2021. CR occurred in 195 patients (0.9%) who were compared with 390 controls. Compared with non-CR patients, CR patients were older, more likely to be women, to have acute heart failure and cardiogenic shock, and less likely to have single lesions. They were also more likely to have lateral wall AMI as identified by the electrocardiogram (23.6% vs. 8.2%, P<0.001). Door to balloon time was 63 minutes in both groups and vessel distribution of culprit lesions were similar. However, the thrombolysis in myocardial infraction (TIMI) grade was lower in the CR group compared with non-CR group both before (0.20±0.40 vs. 0.45±0.76, P=0.003) and after (2.55±0.92 vs. 2.96±0.23, P=0.001) primary PCI.

On multivariable analysis female sex, older age, smoking, total chest pain time, recurrent acute chest pain, high lateral wall infarct (identified by the electrocardiogram), acute heart failure, and N-terminal prohormone brain natriuretic peptide were independently associated with CR. In a subsequent analysis of patients who agreed to undergo primary PCI, having a single lesion and higher TIMI grade pre- or post-PCI were associated with lower risk of CR.

The authors are to be congratulated for enhancing our understanding of which AMI patients might be at increased risk for CR. However, there are certain limitations in this study. First, the derivation of the control group was not specified. Second, the sensitivity or specificity of the reported risk factors for CR was not reported. Given the low prevalence of CR (0.9%) the positive predictive value of any parameter or combination is likely to be low.

In summary, CR is an infrequent but often catastrophic complication of AMI. Although several parameters have been associated with higher CR risk, our ability of identify patients who will develop CR remains limited. Even if we could accurately identify patients who will eventually develop CR, treatment would be challenging, as preemptive cardiac surgery is not a good option. Therefore, prevention of CR remains key: achieving prompt reperfusion with primary PCI remains our best tool at hand. If CR occurs, emergent surgical repair of the ruptured myocardium offers the best chance for survival.

Acknowledgments

Funding: None.

Footnote

Provenance and Peer Review: This article was commissioned by the editorial office, Journal of Thoracic Disease. The article did not undergo external peer review.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jtd.amegroups.com/article/view/10.21037/jtd-22-655/coif). ESB reports consulting/speaker honoraria from Abbott Vascular, American Heart Association (associate editor Circulation), Amgen, Asahi Intecc, Biotronik, Boston Scientific, Cardiovascular Innovations Foundation (Board of Directors), ControlRad, CSI, Elsevier, GE Healthcare, IMDS, InfraRedx, Medicure, Medtronic, Opsens, Siemens, and Teleflex; and research support from Boston Scientific, GE Healthcare; owner, Hippocrates LLC; shareholder: MHI Ventures, Cleerly Health, Stallion Medical. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. López-Sendón J, Gurfinkel EP, Lopez de Sa E, et al. Factors related to heart rupture in acute coronary syndromes in the Global Registry of Acute Coronary Events. Eur Heart J 2010;31:1449-56. [Crossref] [PubMed]
2. Kageyama S, Nakanishi Y, Murata K, et al. Mortality and predictors of survival in patients with recent ventricular septal rupture. Heart Vessels 2020;35:1672-80. [Crossref] [PubMed]
3. Formica F, Mariani S, Ferro O, et al. Fatal huge left free wall ventricular rupture after acute posterior myocardial infarction. Case Rep Cardiol 2013;2013:691971. [Crossref] [PubMed]
4. Qian G, Jin RJ, Fu ZH, et al. Development and validation of clinical risk score to predict the cardiac rupture in patients with STEMI. Am J Emerg Med 2017;35:589-93. [Crossref] [PubMed]
5. Fu Y, Li KB, Yang XC. A risk score model for predicting cardiac rupture after acute myocardial infarction. Chin Med J (Engl) 2019;132:1037-44. [Crossref] [PubMed]
6. Reddy SG, Roberts WC. Frequency of rupture of the left ventricular free wall or ventricular septum among necropsy cases of fatal acute myocardial infarction since introduction of coronary care units. Am J Cardiol 1989;63:906-11. [Crossref] [PubMed]
7. Yip HK, Wu CJ, Chang HW, et al. Cardiac rupture complicating acute myocardial infarction in the direct percutaneous coronary intervention reperfusion era. Chest 2003;124:565-71. [Crossref] [PubMed]
8. Varghese S, Ohlow MA. Left ventricular free wall rupture in myocardial infarction: A retrospective analysis from a single tertiary center. JRSM Cardiovasc Dis 2019;8:2048004019896692. [Crossref] [PubMed]
9. Garcia S, Albaghdadi MS, Meraj PM, et al. Reduction in ST-Segment Elevation Cardiac Catheterization Laboratory Activations in the United States During COVID-19 Pandemic. J Am Coll Cardiol 2020;75:2871-2. [Crossref] [PubMed]
10. Garcia S, Dehghani P, Grines C, et al. Initial Findings From the North American COVID-19 Myocardial Infarction Registry. J Am Coll Cardiol 2021;77:1994-2003. [Crossref] [PubMed]
11. Becker RC, Hochman JS, Cannon CP, et al. Fatal cardiac rupture among patients treated with thrombolytic agents and adjunctive thrombin antagonists: observations from the Thrombolysis and Thrombin Inhibition in Myocardial Infarction 9 Study. J Am Coll Cardiol 1999;33:479-87. [Crossref] [PubMed]
12. Mann JM, Roberts WC. Rupture of the left ventricular free wall during acute myocardial infarction: analysis of 138 necropsy patients and comparison with 50 necropsy patients with acute myocardial infarction without rupture. Am J Cardiol 1988;62:847-59. [Crossref] [PubMed]
13. Doi K, Yaku H. Ventricular Free Wall Rupture. Kyobu Geka 2015;68:616-9. [PubMed]
14. Pujari SH, Agasthi P. Left Ventricular Rupture. StatPearls 2022. Available online: https://www.ncbi.nlm.nih.gov/books/NBK559271/
15. Hutchins KD, Skurnick J, Lavenhar M, et al. Cardiac rupture in acute myocardial infarction: a reassessment. Am J Forensic Med Pathol 2002;23:78-82. [Crossref] [PubMed]
16. Xu Z, Li Y, Zhang R, et al. Risk factors for cardiac rupture after acute ST-segment elevation myocardial infarction during the percutaneous coronary intervention era: a retrospective case-control study. J Thorac Dis 2022;14:1256-66. [Crossref] [PubMed]