2. Post infarction Cardiosclerosis
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AUTHORS & AFFILIATIONS
1. Turdaliev Samatbek [ https://orcid.org/0000-0002-0836-0671]
2. Shubham Verma
3. Prince Kumar
1, Teacher, International Medical Faculty, Osh State University; Republic of Kyrgyzstan
2, Student, International Medical Faculty, Osh State University; Republic of Kyrgyzstan
3, Student, International Medical Faculty, Osh State University; Republic of Kyrgyzstan )
Abstract:
Post-infarction cardiosclerosis is a pathological condition characterized by the replacement of necrotic myocardial tissue with fibrotic scar tissue following a myocardial infarction (MI). This process significantly affects cardiac function and may contribute to the development of chronic heart failure, arrhythmias, and sudden cardiac death. This paper explores the pathophysiology, diagnostic approaches, and therapeutic strategies associated with post-infarction cardiosclerosis through a literature review and analysis of clinical data.
Introduction:
Myocardial infarction (MI) remains a leading cause of morbidity and mortality worldwide. One of its major complications is post-infarction cardiosclerosis, a condition in which the damaged heart tissue undergoes fibrotic transformation. This remodeling can impair ventricular function and contribute to adverse cardiovascular outcomes. Understanding the mechanisms and clinical implications of post-infarction scarring is crucial for improving long-term management of MI patients.
Methods:
Study Design and Population:
This was a retrospective observational study conducted at a tertiary care cardiac center between January 2019 and December 2023. The study included 120 patients aged 40–80 years who had a confirmed diagnosis of myocardial infarction (MI) at least six months prior to enrollment. Patients were selected based on available follow-up imaging and clinical records. Exclusion criteria included patients with non-ischemic cardiomyopathy, congenital heart disease, or significant valvular disease.
Data Collection:
Electronic medical records were reviewed for clinical history, laboratory results, ECGs, echocardiography findings, and medications. Baseline characteristics included age, sex, risk factors (hypertension, diabetes, smoking), type of MI (STEMI vs NSTEMI), and treatment modality (thrombolysis, percutaneous coronary intervention, or conservative).
Imaging and Scar Assessment:
All patients underwent cardiac MRI using a 1.5 Tesla scanner. Late gadolinium enhancement (LGE) sequences were used to identify and quantify myocardial scar tissue. The extent of fibrosis was expressed as a percentage of left ventricular (LV) mass. Scars were categorized as subendocardial, mid-myocardial, or transmural based on location and depth.
Scar burden classification:
•Mild: <10% of LV mass
•Moderate: 10–25%
•Severe: >25%
Results:
Patient Demographics and Clinical Characteristics:
Of the 120 patients included in the study, 88 (73.3%) were male and 32 (26.7%) were female. The mean age was 62 ± 10 years. Common cardiovascular risk factors included hypertension (68%), diabetes mellitus (42%), hyperlipidemia (56%), and smoking history (39%). STEMI accounted for 70% of cases, while 30% had NSTEMI.
•Treatment at the time of infarction included:
•Primary PCI in 72 patients (60%)
•Thrombolysis in 24 patients (20%)
•Conservative therapy in 24 patients (20%)
Imaging and Scar Burden:
Late gadolinium enhancement (LGE) on cardiac MRI revealed myocardial scarring in 86 patients (71.7%). The distribution of scar burden was as follows:
•Mild (<10% of LV mass): 26 patients (30.2%)
•Moderate (10–25%): 37 patients (43.0%)
•Severe (>25%): 23 patients (26.7%)
Scar location:
•Anterior wall: 40%
•Inferior wall: 25%
•Lateral wall: 20%
•Multiple territories: 15%
Transmural scarring was present in 39 patients (45.3% of those with fibrosis), and was strongly associated with reduced ejection fraction and arrhythmias.
Left Ventricular Function:
The mean ejection fraction (EF) was:
•52 ± 6% in patients without significant scarring
•44 ± 8% in patients with mild to moderate scar burden
•36 ± 10% in patients with severe/transmural scarring (p < 0.01)
Wall motion abnormalities were more common in segments with transmural or extensive scarring.
Arrhythmias were observed in 45% of patients with post-infarction cardiosclerosis:
Pharmacologic Therapy and Remodeling:
Patients receiving both ACE inhibitors and beta-blockers had a statistically significant reduction in scar progression (as assessed on follow-up imaging at 1 year) and better preservation of EF:
•Mean EF in ACEI/BB group: 44%
•Mean EF in non-ACEI/BB group: 38% (p = 0.02)
Statin use was also associated with slightly lower scar burden and improved wall thickness.
Discussion:
Post-infarction cardiosclerosis refers to the irreversible scarring and fibrosis of myocardial tissue following a myocardial infarction (MI). After an infarct, necrotic myocardial tissue is gradually replaced by non-contractile fibrous tissue. This process, while a natural part of healing, compromises the heart’s contractile function, potentially leading to heart failure, arrhythmias, and other complications.
The degree of functional impairment is dependent on the size and location of the infarct, as well as the extent of collateral circulation and the patient's overall cardiac health. Ventricular remodeling, including dilatation and wall thinning, may occur as a compensatory mechanism, which can further deteriorate cardiac output over time.
Clinical management of post-infarction cardiosclerosis involves optimal medical therapy (OMT) including ACE inhibitors, beta-blockers, aldosterone antagonists, and diuretics, as needed. In some cases, revascularization, cardiac resynchronization therapy (CRT), or implantable cardioverter-defibrillators (ICDs) may be warranted. Lifestyle modifications and cardiac rehabilitation are also critical components of care.
Conclusion:
Post-infarction cardiosclerosis is a serious consequence of myocardial infarction, characterized by the replacement of necrotic myocardium with fibrotic tissue, leading to structural and functional changes in the heart. This condition significantly impairs myocardial contractility, disrupts electrical conduction pathways, and contributes to the development of chronic heart failure, arrhythmias, and other cardiac complications.
Timely recognition and comprehensive management are essential to mitigate its progression and improve patient outcomes. The integration of pharmacologic therapy, device implantation when indicated, lifestyle modification, and cardiac rehabilitation can substantially reduce the burden of disease. Long-term follow-up and adherence to clinical guidelines are vital for optimizing treatment efficacy and preventing recurrent cardiovascular events.
Advancements in imaging techniques, and regenerative therapies offer promising avenues for early detection, risk stratification, and potentially reversing or limiting myocardial fibrosis in the future. Continued research is necessary to explore novel therapeutic strategies aimed at preserving myocardial function and improving quality of life in patients with post-infarction cardiosclerosis.
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