Usability of myocardial work parameters to demonstrate subclinical myocardial involvement in normotensive individuals with exaggerated hypertensive response in treadmill exercise testing.

Early determination of changes in myocardial functions is essential for the protection of cardiovascular diseases. This study aimed to evaluate myocardial work parameters in healthy individuals who developed an exaggerated hypertensive response during the treadmill exercise test procedure. The study included a total of 64 patients for whom an exercise electrocardiography test was planned for functional capacity evaluation. The study population was divided according to the presence of exaggerated hypertensive response to exercise (EBPRE) (SBP/DBP ≥210/105 mmHg in males ≥190/105 mmHg in females) and normal blood pressure response to exercise (NBPRE). Patients' echocardiographic evaluations were made at rest, and myocardial work parameters were calculated. There was no statistical difference between the groups (NBPRE vs. EBPRE, respectively) in terms of left ventricular 2,3 and 4 chamber strains and global longitudinal strain (GLS) values (-20.6 ± -2.3, -19.7 ± -1.9, p:.13; -21.3 ± -2.7, -21 ± -2.4, p:.68; -21.2 ± -2.2, -21.2 ± -2.3, p:.93; and -20.8 ± -1.5, -20.4 ± -1.5, p:.23, respectively). Global constrictive work (GCW), global waste work (GWW), and global work efficiency (GWE) were not statistically different between the two groups (2374 ± 210, 2465 ± 204, p:.10; 142 ± 64, 127 ± 42, p:.31; 94.3 ± 2.5, 95.1 ± 1.5, p:.18, respectively). In contrast, global work index (GWI) parameters were different between the two groups (2036 ± 149, 2147 ± 150, p < .001). The GWI was independently associated with EBPRE (odds ratio with 95% 3.32 (1.02-11.24), p = .03). The partial effect plots were used for GWI to predict EBPRE, according to the results, an increase in GWI predicts probability of exaggerated hypertensive response. In conclusion, Myocardial work analyses might be used to identify early signs of myocardial involvement in normotensive patients with EBPRE.

A New Predictor of Mortality in ST-Elevation Myocardial Infarction: The Uric Acid Albumin Ratio.

Several studies have shown that high uric acid (UA) and low serum albumin (SA) values increase the risk of cardiovascular disease and mortality in ST-elevation myocardial infarction (STEMI). We determined whether the uric acid/albumin ratio (UAR) is a predictor of mortality in STEMI patients. All patients who presented at our center with a diagnosis of STEMI and underwent percutaneous intervention from 2015 to 2020 were screened consecutively; 4599 patients were included. A Cox proportional hazards model was used to evaluate UAR, and adjusted predictors obtained from laboratory findings and clinical characteristics contributed to mortality. Also, a regression model was presented with a directed acyclic graph (DAG). The median age of the patients was 58 years (IQR [interquartile range]: 50-67); 3581 patients (77.9%) were male. The incidence of mortality in the entire patient group was 11.9%. Median follow-up duration of all groups was 42 months. Multivariate Cox proportional regression (model-1) analysis showed age (increase 50 to 67 years; HR [hazard ratio]: 1.34, 95% CI 1.18-1.52) and UAR (increase 1.15-1.73; HR: 1.33, 95% CI 1.16-1.52) were associated with mortality. UAR may be a prognostic factor for mortality in STEMI patients and an easily accessible parameter to identify high-risk patients.

Assessment of pulmonary arterial stiffness in patients with cirrhosis: A prospective cohort study.

INTRODUCTION: In the current literature, several studies show that PAS (pulmonary artery stiffness) is associated with RV (right ventricular) dysfunction, PAH (pulmonary arterial hypertension), and disease severity in subjects with structural cardiac disease, HIV (human immunodeficiency virus), and chronic lung disease. Hence, our main aim was to use PAS to show the early changes in the pulmonary vascular region in subjects with cirrhosis. MATERIAL AND METHODS: In this prospective cross-sectional study, 39 subjects who were being followed up with cirrhosis and 41 age- and sex-matched healthy subjects were included in this study. For each case, the PAS value was obtained by dividing mean peak velocity of the pulmonary flow by the PfAT (pulmonary flow acceleration time). RESULTS: The measured PAS was 23.62 ± 5.87 (Hz/msn) in cirrhotic participants and 19.09 ± 4.16 (Hz/msn) in healthy cases (P < .001). We found a positive statistical significance between PAS and RVSP (right ventricle systolic pressure)/sPAP (systolic pulmonary arterial pressure) (r = .395; P = .013). PAS was an independent predictor that was associated with cirrhosis disease according to multivariate LR (logistic regression) analysis (OR: 1.209; 95% CI: 1.059-1.381; P = .005). CONCLUSION: Based on the study results, we consider that PAS may help in the early detection of findings in the pulmonary vascular area, even if the RV function findings or sPAP is within the normal range.

Increased circulating soluble urokinase-type plasminogen activator receptor (suPAR) levels in patients with slow coronary flow.

INTRODUCTION: Slow coronary flow (SCF) is an angiographic phenomenon characterized by delayed opacification of epicardial coronary arteries without an obstructive coronary disease. Serum soluble urokinase-type plasminogen activator receptor (suPAR) levels seem closely related to atherosclerosis due to increased inflammation and prothrombotic state. We studied whether circulating suPAR is related to SCF. MATERIAL AND METHODS: The present study was cross-sectional and observational. It included 75 individuals who underwent coronary angiography with suspected CAD and had angiographically normal coronary arteries of varying coronary flow rates. The relationship between suPAR, C-reactive protein (CRP) and SCF was investigated. Forty patients with isolated SCF (mean age: 46.0 ±4.14 years) and 35 age- and gender-matched control participants with normal coronary flow (NCF) and normal coronary arteries (NCA) (mean age: 46.0 ±5.7 years) were included in the study. We used logistic regression analysis to determine the predictors of SCF. RESULTS: The clinical characteristics were not statistically significantly different between SCF and NCA groups. Serum suPAR level was significantly higher in the SCF group than the control group (2.5-5.4 ng/ml vs. 0.1-1.4 ng/ml; p < 0.001). Also the serum CRP level was higher in the CSF group than the control group (1.57 ±0.43 mg/l vs. 0.53 ±0.23 mg/l; p < 0.001). CONCLUSIONS: This study revealed significantly increased serum suPAR levels in patients with SCF. Although we cannot draw conclusions on the underlying pathological process of SCF, we believe that these findings may be pioneering for further studies investigating the specific roles of circulating suPAR in the SCF phenomenon in the coronary vasculature.