Pathogenetic Link of Cardiac Rupture and Left Ventricular Thrombus Following Acute Myocardial Infarction: A Joint
Shan Ma1, Ling Bai2, Ping Liu2
1Department of Internal Medicine-Cardiovascular, Cardiovascular Hospital, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Insights
Cardiac rupture and left ventricular thrombus after myocardial infarction may be linked. Early left ventricular thrombus may result from inflammation following cardiac rupture or endocardial erosion.
Area of Science:
- Cardiology
- Pathology
Background:
- Cardiac rupture (CR) and left ventricular thrombus (LVT) are significant complications of acute myocardial infarction (MI).
- These complications are traditionally viewed as independent events following MI.
Purpose of the Study:
- To investigate the potential pathogenetic link between CR and LVT.
- To explore the relationship using a murine model of MI and human patient data.
Main Methods:
- MI was induced in mice, monitoring CR onset and performing histological examination of hearts.
- Retrospective data from 8,936 acute MI patients (2015-2022) with CR or LVT were compared to uncomplicated controls.
Main Results:
- In mice, 75% developed CR, with intramural thrombi connecting to LVT in rupture tunnels.
- In patients, CR occurred in 1.14% and LVT in 1.45%; both often within 7 days of MI.
- CR and early LVT were associated with elevated inflammatory and cardiac injury markers.
Conclusions:
- CR and LVT following MI share a potential pathogenetic link.
- Early LVT may arise from a thrombo-inflammatory response to myocardial wall rupture or erosion.
Background:
Cardiac rupture (CR) and left ventricular thrombus (LVT) remain important complications of acute myocardial infarction (MI), and they are currently regarded as independent events. We explored the pathogenetic link between CR and LVT by investigating a murine model of MI with a high frequency of CR and in patients with acute MI.
Methods:
MI was induced in mice, the onset of CR was monitored, and the hearts of mice with or without fatal CR were histologically examined. Between 2015 and 2022, from patients admitted due to acute MI, the data of patients with CR or LVT were retrospectively collected and compared to uncomplicated patients (control).
Results:
A total of 75% of mice (n = 65) with MI developed CR 2-4 days after MI. A histological examination of CR hearts revealed the existence of platelet-rich intramural thrombi in the rupture tunnel, which was connected at the endocardial site to platelet-fibrin thrombi within an LVT. In CR or non-CR mouse hearts, LV blood clots often contained a portion of platelet-fibrin thrombi that adhered to the infarct wall. In non-CR hearts, sites of incomplete CR or erosion of the infarct wall were typically coated with platelet thrombi and dense inflammatory cells. Of 8,936 patients with acute MI, CR and LVT occurred in 102 (1.14%) and 130 (1.45%) patients, respectively, with three cases having both complications. CR accounted for 32.8% of in-hospital deaths. The majority of CR (95%) or LVT (63%, early LVT) occurred within 7 days. In comparison to the control or LVT-late groups, patients with CR or early LVT reported increased levels of cellular and biochemical markers for inflammation or cardiac injury.
Conclusion:
CR and LVT after MI are potentially linked in their pathogenesis. LVT occurring early after MI may be triggered by a thrombo-inflammatory response following wall rupture or endocardial erosion.
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