Cardiology Research, ISSN 1923-2829 print, 1923-2837 online, Open Access
Article copyright, the authors; Journal compilation copyright, Cardiol Res and Elmer Press Inc
Journal website https://www.cardiologyres.org

Original Article

Volume 14, Number 2, April 2023, pages 123-132

Immobilizing Interstitial Cardiac Fibrosis

Figures

Figure 1.
Figure 1. Echocardiography of a 67-year-old male patient showing immobilizing interstitial cardiac fibrosis. Diffuse decrease in LV myocardial contractility was noted. LV contractility was reduced. Total LVEF was 41%. LVEF: left ventricular ejection fraction.
Figure 2.
Figure 2. 99mTc scintigraphy of the myocardium (a: LV myocardial perfusion; b: LV myocardial function) of a 49-year-old male patient showing immobilizing interstitial cardiac fibrosis. Diffuse decrease in perfusion and diffuse decrease in regional systolic wall thickening in the entire LV myocardium without a clear differentiation between the areas of local hypoperfusion and local hypokinesia were noted. LV contractility was significantly decreased. Total LVEF was 37%. LVEF: left ventricular ejection fraction.
Figure 3.
Figure 3. Diffuse spread of induced immobilizing interstitial cardiac fibrosis in a 68-year-old male patient. (a-c) Early stages (approximately 1 month). (d) Extravascular compression of coronary arterioles, areas of scarring (hematoxylin and eosin stain, a: × 100, b: × 80, c, d: × 40).
Figure 4.
Figure 4. Histological preparations of the myocardium showing a significant increase in the volume of connective tissue in group I patients. (a) Weigert’s stain, × 100. (b) Masson’s stain, × 200. (c) Van Gieson’s stain, × 200.
Figure 5.
Figure 5. The stage of coronary angiopathy (in group I) is an extremely severe degree of fibrosis with constriction of the peripheral coronary bed (hematoxylin and eosin stain, a-c: × 200, d: × 400).
Figure 6.
Figure 6. (a) Type I collagen fibers in group I chaotic intersection of bundles forming closed spaces around individual cardiomyocytes; in group II ordered arrangement of collagen fibers. (b) Type III collagen fibers in group I disordered arrangement, without clearly distinguishable spatial structures; in group II rare bundles of collagen fibers (Weigert’s stain, × 400).
Figure 7.
Figure 7. Metalloproteinase expression: (a) MMP-2 (immunohistochemical study, × 200 increase); (b) MMP-9 (immunohistochemical stain, × 200). MMP: matrix metalloproteinase.

Tables

Table 1. Clinical and Demographic Characteristics of Patients
 
IndicatorGroup I (n = 32)Group II (n = 37)P
SD: standard deviation.
Sex, n (%)
  Male22 (69%)26 (70%)0.89
  Female10 (31%)11 (30%)0.78
Age, years (mean ± SD)60.25 ± 7.969.5 ± 5.40.62
Body mass index, kg/m2 (mean ± SD)28.5 ± 6.827.3 ± 5.40.75
Heart weight, g (mean ± SD)479 ± 152319 ± 540.069
Heart failure, n (%)32 (100%)16 (43%)< 0.001
Hypertension, n (%)20 (62.5%)21 (56.7%)0.63
Dyslipidemia, n (%)15 (46.8%)11 (29.7%)0.14
Smoking, n (%)7 (21.9%)10 (27%)0.78
Ejection fraction (echocardiography), % (mean ± SD)40.3±4.5%60.7±5.1%< 0.001

 

Table 2. Concomitant Diseases in Patients
 
Concomitant diseasesGroup I (n = 32), n (%)Group II (n = 37), n (%)OR (95% CI)P
CI: confidence interval; OR: odds ratio; SARS-CoV-2: severe acute respiratory syndrome coronavirus 2.
Type 2 diabetes mellitus15 (47%)3 (8%)10.0 (2.54 - 39.34)< 0.001
Myocardial infarction5 (16%)4 (11%)1.53 (0.37 - 6.26)0.723
Systemic connective tissue diseases25 (78%)2 (5%)62.5 (11.9 - 326.5)< 0.001
Viral pneumonia (SARS-CoV-2) within 12 months17 (53%)7 (19%)4.86 (1.66 - 14.25)0.003
Tuberculosis3 (9%)0 (0%)-0.095
Bacterial infections within 12 months10 (31%)4 (11%)3.75 (1.04 - 13.47)0.069
Oncological diseases (radiation therapy)6 (19%)0 (0%)-0.008
Heart rhythm disturbances28 (88%)7 (19%)30.0 (7.918 - 113.7)< 0.001
Chronic kidney disease8 (25%)3 (8%)3.8 (0.9 - 15.7)0.097
Chronic obstructive pulmonary disease2 (6%)3 (8%)0.76 (0.12 - 4.83)1.0