Subclinical left ventricular systolic dysfunction in patients with mild-to-moderate rheumatic mitral stenosis and normal left ventricular ejection fraction: an observational study

2013 ◽  
Author(s):  
Ozlem Yildirimturk ◽  
Fatma Funda Helvacioglu ◽  
Yelda Teyyareci ◽  
Selen Yurdakul ◽  
Saide Aytekin
Keyword(s):  
Left Ventricular Ejection Fraction ◽  
Observational Study ◽  
Ejection Fraction ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Systolic Dysfunction ◽  
Ventricular Ejection Fraction ◽  
Normal Left Ventricular

scholarly journals Systolic left ventricular dysfunction in patients with clinically suspected myocarditis

2020 ◽  
Vol 17 (4) ◽  
pp. 452-460
Author(s):  
N. P. Mitkovskaya ◽  
E. M. Balysh ◽  
T. V. Statkevich ◽  
N. A. Ladygina ◽  
E. B. Petrova ◽  
...  
Keyword(s):  
Heart Rate ◽  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Ventricular Ejection ◽  
Left Ventricular Ejection ◽  
Ventricular Systolic Dysfunction ◽  
Ventricular Ejection Fraction

The aim of the study was to investigate the features of clinically suspected myocarditis complicated by the left ventricular systolic dysfunction development. 93 patients with clinically suspected myocarditis were examined. The average age was 36.63 ± 1.15 years. In 43.01 % of patients the disease was accompanied by a decrease in left ventricular systolic function. In the group of patients with left ventricular systolic dysfunction in comparison with those with preserved left ventricular ejection fraction, a significantly lower proportion of men (75 % versus 81 %, respectively, χ2 = 9.3, p < 0,01) and a higher average group age (40.7 ± 1.87 versus 33.6 ± 1.3 years, respectively, p <  0,01) were revealed. The course of the disease in patients with left ventricular systolic dysfunction was characterized by a more frequent development of rhythm disturbances (65 % versus 43.3 %, respectively, χ2  = 4.3, p  < 0,05) and a higher heart rate at admission (94.5 (75‒100) and 85 (70‒89) beats per minute, respectively, p = 0.006). The structural and functional state of the heart according to echocardiography in patients with a reduced left ventricular ejection fraction versus comparison group was characterized by larger heart chambers sizes, more pronounced violations of local left ventricular contractility, more frequent involvement of the right ventricle in the pathological process (56.3  % versus 22.2  %, respectively, χ2   =  6.4, p  < 0,05). The relationships between the left ventricular ejection fraction Весці Нацыянальнай акадэміі навук Беларусі. Серыя медыцынскіх навук. 2020. Т. 17, № 4. C. 452–460 453 and the patient’s age (r = ‒0.36), the value of the heart rate at admission (r = ‒0.32), the severity of heart failure at admission, the degree of impaired local contractility of the left ventricle, the degree of right ventricular function (TAPSE, r  =  0.58), the severity of myocardial fibrosis according to cardiovascular magnetic resonance imaging (r = ‒0.32) were revealed.

scholarly journals THE EXTRACELLULAR MATRIX DEGRADATION MARKERS AS PREDICTORS OF LEFT VENTRICULAR SYSTOLIC DYSFUNCTION AMONG PATIENTS WITH STEMI

2021 ◽  
Vol 48 (1) ◽  
Author(s):  
I. M. Fushtey ◽  
E. V. Sid
Keyword(s):  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Matrix Metalloproteinase ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Ventricular Ejection ◽  
Left Ventricular Ejection ◽  
Ventricular Systolic Dysfunction ◽  
Ventricular Ejection Fraction

Abstract The purpose of the study. To determine predictor value of the extracellular matrix degradation markers relative to the occurrence of left ventricular systolic dysfunction among patients with STEMI determined. Materials and methods. The results of the study are based on data obtained from a comprehensive survey of 162 patients with STEMI. The first group consisted of 145 patients with STEMI and left ventricular ejection fraction > 45% (median age – 59 (52–64) years); the second group consisted of 17 patients with STEMI and left ventricular ejection fraction < 45% (median age 61 (55–63) years). All persons were comparable in age, social status, and gender. The sample of patients was carried out in the period from 2015 to January 2018 on the basis of the MI «Regional medical center of cardiovascular diseases» of the Zaporizhzhia regional Council. Results. Significantly, the level of 5816,3 (5487,7–6538,6) PG/ml of matrix metalloproteinase-9 was higher in the left ventricular ejection fraction group < 45% compared to 5129,6 (3984,6–5975,8) PG/ml in the left ventricular ejection fraction group > 45%, (p < 0,05). The level of tissue inhibitor of matrix metalloproteinase-2 among patients with left ventricular ejection fraction < 45% was 524,8 (484,6–648,7) PG/ml and was considerably higher compared to 459,7 (368,3–549,2) PG/ml in the left ventricular ejection fraction group > 45%, (p < 0,05). The largest area under the ROC curve (AUC = 0,694, 95% CI 0,617 to 0,764) among the analyzed markers of extracellular matrix degradation was tissue inhibitor of matrix metalloproteinase-2. At the distribution point > 483,7 PG/ml, the sensitivity was 76,47% and the specificity was 62,07% for left ventricular systolic dysfunction among patients with STEMI. The calculated relative risk was for matrix metalloproteinase-9 > 5247,9 PG/ml for the development of left ventricular systolic dysfunction was 7,139, 95% CI 1,686–30,218. For the level of tissue inhibitor of matrix metalloproteinase-2 > 483,7 PG/ml, the relative risk was 4,271, 95% CI 1,455–12,536 for the development of left ventricular systolic dysfunction. Conclusions. Patients having STEMI with left ventricular ejection fraction < 45% had essentially higher levels of matrix metalloproteinase-9 and tissue inhibitor of matrix metalloproteinase-2. At matrix metalloproteinase-9 > 5247.9 PG/ml level relative risk of the developing left ventricular systolic dysfunction in patients with STEMI increases by 7.139 times. Keywords: acute myocardial infarction, matrix metalloproteinase-9, tissue inhibitor of matrix metalloproteinase-2, left ventricular systolic dysfunction.

scholarly journals Hypertrophic Cardiomyopathy With Left Ventricular Systolic Dysfunction

Circulation ◽  
2020 ◽  
Vol 141 (17) ◽  
pp. 1371-1383 ◽  
Author(s):  
Peter Marstrand ◽  
Larry Han ◽  
Sharlene M. Day ◽  
Iacopo Olivotto ◽  
Euan A. Ashley ◽  
...  
Keyword(s):  
Left Ventricular Ejection Fraction ◽  
Natural History ◽  
Ejection Fraction ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Ventricular Ejection ◽  
Left Ventricular Ejection ◽  
Composite Outcome ◽  
Ventricular Ejection Fraction

Background: The term “end stage” has been used to describe hypertrophic cardiomyopathy (HCM) with left ventricular systolic dysfunction (LVSD), defined as occurring when left ventricular ejection fraction is <50%. The prognosis of HCM-LVSD has reportedly been poor, but because of its relative rarity, the natural history remains incompletely characterized. Methods: Data from 11 high-volume HCM specialty centers making up the international SHaRe Registry (Sarcomeric Human Cardiomyopathy Registry) were used to describe the natural history of patients with HCM-LVSD. Cox proportional hazards models were used to identify predictors of prognosis and incident development. Results: From a cohort of 6793 patients with HCM, 553 (8%) met the criteria for HCM-LVSD. Overall, 75% of patients with HCM-LVSD experienced clinically relevant events, and 35% met the composite outcome (all-cause death [n=128], cardiac transplantation [n=55], or left ventricular assist device implantation [n=9]). After recognition of HCM-LVSD, the median time to composite outcome was 8.4 years. However, there was substantial individual variation in natural history. Significant predictors of the composite outcome included the presence of multiple pathogenic/likely pathogenic sarcomeric variants (hazard ratio [HR], 5.6 [95% CI, 2.3–13.5]), atrial fibrillation (HR, 2.6 [95% CI, 1.7–3.5]), and left ventricular ejection fraction <35% (HR, 2.0 [95% CI, 1.3–2.8]). The incidence of new HCM-LVSD was ≈7.5% over 15 years. Significant predictors of developing incident HCM-LVSD included greater left ventricular cavity size (HR, 1.1 [95% CI, 1.0–1.3] and wall thickness (HR, 1.3 [95% CI, 1.1–1.4]), left ventricular ejection fraction of 50% to 60% (HR, 1.8 [95% CI, 1.2, 2.8]–2.8 [95% CI, 1.8–4.2]) at baseline evaluation, the presence of late gadolinium enhancement on cardiac magnetic resonance imaging (HR, 2.3 [95% CI, 1.0–4.9]), and the presence of a pathogenic/likely pathogenic sarcomeric variant, particularly in thin filament genes (HR, 1.5 [95% CI, 1.0–2.1] and 2.5 [95% CI, 1.2–5.1], respectively). Conclusions: HCM-LVSD affects ≈8% of patients with HCM. Although the natural history of HCM-LVSD was variable, 75% of patients experienced adverse events, including 35% experiencing a death equivalent an estimated median time of 8.4 years after developing systolic dysfunction. In addition to clinical features, genetic substrate appears to play a role in both prognosis (multiple sarcomeric variants) and the risk for incident development of HCM-LVSD (thin filament variants).

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