Objective: This was an investigation of the relationship between the N-terminal pro-brain natriuretic peptide (NT-proBNP) level and mortality in patients with stage 3-4 chronic kidney disease (CKD).
Methods: This study was designed as a subgroup analysis of the Heart Failure Prevalence and Predictors in Turkey (HAPPY) study. The HAPPY study included 4650 randomly selected individuals from the 7 geographical regions of Turkey. A total of 191 subjects from the original cohort with an estimated glomerular filtration rate (eGFR) <60 mL/min/1.1.73 m² were enrolled in this study and the relationship between NT-proBNP and mortality was investigated. Prognostic variables for total and cardiovascular mortality were also examined using Cox regression analysis.
Results: The mean length of follow-up was 76.12±22.45 months. The mean NT-proBNP level was 423.54±955.88 pg/mL. During follow-up, 51 subjects (26.7%) died from any cause and 36 subjects (18.8%) died from a cardiovascular cause. The presence of hypertension (hazard ratio [HR]: 1.89; 95% confidence interval [CI]: 1.01–3.50; p=0.048), anemia (HR: 2.49; 95% CI: 1.20–5.15; p=0.014), male gender (HR: 2.64; 95% CI: 1.44–4.86; p=0.002) and log NT-proBNP (HR: 4.93; 95% CI: 2.83-8.58; p<0.001) were independent variables for total mortality. The presence of hypertension (HR: 2.47; 95% CI: 1.09–5.56; p=0.029), male gender (HR: 2.79; 95% CI: 1.38–5.62; p=0.004), eGFR (HR: 0.94; 95% CI: 0.91–0.98; p=0.005) and log NT-proBNP (HR: 6.31; 95% CI: 3.11–12.81; p<0.001) were independent predictors of cardiovascular mortality.
Conclusion: NT-proBNP was found to be an independent prognostic marker in patients with stage 3–4 CKD.

Objective: Genetic risk factors that cause coronary artery disease (CAD) demonstrate variations in different populations. In this study, a single nucleotide polymorphism in the APOA5 gene was targeted to determine genetic contributors to atherosclerotic CAD. The effects of this polymorphism on the development of CAD and known risk factors of the disease were examined.
Methods: A total of 448 patients with angina or acute myocardial infarction who underwent coronary angiography were grouped as individuals with normal coronary arteries (≤30% stenosis) and critical disease (≥50% stenosis). The angiographic severity and the extent of atherosclerotic CAD were assessed using the Gensini and SYNTAX scores. Individuals were genotyped for the APOA5−1131T>C polymorphism using hydrolysis probes and the results were evaluated.
Results: The APOA5−1131T>C polymorphism was associated with the serum lipid levels in the non-CAD group (p<0.05). In addition, the effect of APOA5 gene polymorphism on clinical status and other parameters was determined to vary depending on gender. A borderline association was found between APOA5 −1131T>C and type 2 diabetes mellitus (p=0.055). This polymorphism was found to be associated with obesity and it was observed that the APOA5 -1131C allele carriers had a reduced risk for obesity (p<0.05). Logistic regression analysis adjusted for age and gender indicated that APOA5 -1131C allele carriage had a protective effect against obesity in the study group (odds ratio: 0.48, 95% confidence interval: 0.29-0.78; p=0.003).
Conclusion: In this study, the APOA5 gene polymorphism, one of the genetic factors that may lead to atherosclerotic CAD, was found to be associated with obesity. The APOA5 −1131T>C polymorphism was associated with important risk factors for CAD, obesity and serum lipid levels.

Objective: The aim of the present study was to examine the association between 2 polymorphisms of the endothelial nitric oxide (eNOS) gene (-786T>C and +894G>T) and the no-reflow/slow-flow phenomenon in post-primary percutaneous coronary intervention (PPCI) patients.
Methods: A total of 103 post-PPCI patients were enrolled. Coronary no-reflow phenomenon was defined as a Thrombolysis in Myocardial Infarction (TIMI) flow grade 0–1 and coronary slow-flow phenomenon (CSFP) was defined as a TIMI flow grade ≤2.
Results: Due to the small number of post-PPCI patients with the no-reflow phenomenon (n=4), the primary comparison was made between CSFP (n=20) and normal flow (n=83) groups. There was a greater frequency of CSFP among carriers of the –786C allele of the eNOS –786T>C polymorphism (odds ratio [OR]: 3.90; 95% confidence interval [CI]: 0.87–17.45; p=0.07). However, no such association was detected between the +894T allele of the eNOS +894G>T and CSFP (OR: 0.92; 95% CI: 0.21–3.98; p=0.91). In the adjusted analysis, the -786T>C polymorphism did not reach statistical significance.
Conclusion: There was no significant association between CSFP and 2 of the most common polymorphisms of the eNOS gene in post-PPCI patients.

Objective: Peripheral artery disease (PAD) is a condition caused by the narrowing of limb arteries due to atherosclerosis. In recent years, polymorphisms in a number of genes have been shown to contribute to the risk of PAD development. However, whether the contribution of these inheritable factors is independent of traditional cardiovascular risk factors remains unclear. This study was an investigation of the effects of diabetes mellitus (DM) and genetic background, examined singly and together, on the pathogenesis of PAD.
Methods: The effects of the factor V Leiden (G1691A), factor V H1299R, prothrombin G20210A, factor XIII V34L, B-fibrinogen -455 G>A, PAI-1 4G/5G, HPA1, MTHFR C677T, MTHFR A1298C, ACE I/D, APO B R3500Q, and APOE polymorphisms were evaluated using a cardiovascular disease strip assay (CVD StripAssay). Two groups were created: 100 patients with PAD (50 with DM, 50 without DM) and 60 controls without PAD (30 with DM, 30 without DM).
Results: There was a significantly greater presence of the MTHFR A1298C and PAI 4G/5G homozygous polymorphisms in the PAD patients compared with the control group (p=0.035, p=0.004, respectively). There were no significant associations between the other genotypes and polymorphism frequencies. In the presence of DM, the PAI-1 4G/5G homozygous polymorphism was linked to the formation of PAD (p=0.021). Regression analysis indicated that the PAI-1 4G/5G gene homozygous polymorphism demonstrated a 17.1 times greater risk for DM with PAD [95% confidence interval (CI): 2.113-138.660; p=0.008] and the MTHFR A1298C homozygous polymorphism demonstrated a 316.6 times greater risk (95% CI: 10.763-9315.342; p<0.001) for the possibility of DM with PAD.
Conclusion: The MTHFR A1298C and PAI 4G/5G homozygous polymorphisms may be associated with the development of PAD. The presence of the PAI 4G/5G homozygous polymorphism with DM was a powerful predictor for the development of PAD.

Objective: Stress is known to be a significant risk factor for coronary atherosclerosis and adverse cardiovascular events; however, the stress-related coronary atherosclerotic burden has not yet been investigated. The aim of this study was to investigate the relationship between the Perceived Stress Scale (PSS) and the SYNTAX scores in patients with ST-segment elevation myocardial infarction (STEMI).
Methods: A total of 440 patients with STEMI were prospectively enrolled and divided into 2 groups according to the PSS score with a ROC curve analysis cut-off value of 17.5. In all, 361 patients with a low PSS score were categorized as Group 1 and 79 patients with a high PSS score were categorized as Group 2.
Results: The SYNTAX score [Group 1, 16.0 (10.0–22.5); Group 2, 22.5 (15.0–25.5); p<0.001] and the SYNTAX score II were significantly higher in Group 2 [Group 1, 24.8 (19.0–32.6); Group 2, 30.9 (22.3–38.9); p<0.001]. Spearman analysis demonstrated that the PSS score was associated with the SYNTAX score (r=0.153; p=0.001) and the SYNTAX score II (r=0.216; p<0.001). Additionally, the PSS (odds ratio: 2.434, confidence interval: 1.446-4.096; p=0.001) was determined to be an independent predictor of a moderate-to-high SYNTAX score. The PSS score of patients with in-hospital mortality was also higher than those who survived [15 (10–20); 9 (4–16), respectively; p=0.007].
Conclusion: Stress appears to accelerate the coronary atherosclerotic process and the associated burden. An increased stress level was found to be an independent predictor of a high SYNTAX score.

Objective: There is no clear consensus regarding the definition of low cardiac output syndrome (LCOS) or the follow-up of this patient group. Given this lack of a clinical definition, the aim of this study was to use a LCOS score (LCOSs) similar to the low cardiac output score previously presented in the literature and evaluate the relationship between a high LCOSs and poor clinical outcome.
Methods: A total of 54 patients were prospectively evaluated after cardiac surgery. The LCOSs was used to evaluate the deve-lopment of low cardiac output. Each parameter was scored as 1 point. The score was calculated every hour for 24 hours postoperatively and the highest score was recorded as the peak score (pLOCSs). The LOCSs at the time of admission to the pediatric intensive care unit, at the 4th, 8th, and 16th hour were recorded and a cumulative score (cLOCSs) score was calculated.
Results: The mean age of the patients was 49.40±53.15 months and 24.07% had LOCS. In the group with LCOS, the cLOCSs, vasoactive-ınotropic score (VIS), lactate mean, aortic clamp time, and the total cardiopulmonary bypass time were significantly higher. In this study, a significant and positive correlation was found between the cLOCSs and pLOCSs and the length of hospital stay, length of stay in the pediatric intensive care unit, VIS, lactate mean, and aortic clamp duration.
Conclusion: The objective of this study was to draw attention to the potential use of a common language in the care of critical pediatric patients undergoing cardiac surgery with a previously defined scoring method that includes parameters indicating poor perfusion in the patient.

Cardiac amyloidosis (CA) is a progressive infiltrative cardiomyopathy. Amyloid fibrils in the form of misfolded endogenous proteins accumulate in the heart, as well as the kidneys, liver, and gastrointestinal tract. The most common forms of CA are transthyretin (TTR) and immunoglobulin light chain amyloidosis (AL). CA has long been thought to be a rare disease. However, recent reports have suggested that 13% of heart failure patients with a preserved ejection fraction and 16% of advanced-age patients with severe aortic stenosis have TTR-CA. Patients with TTR-CA have a poor prognosis, with a median survival of 2–4 years; however, early diagnosis and novel therapeutic options have been shown to significantly improve the prognosis. Scintigraphy using bone isotopes is considered a highly reliable and easy-to-use method in the diagnosis of TTR-CA. This is a review of the role of scintigraphic imaging with technetium-99m- labeled bisphosphonates in the diagnostic work-up process of TTR-CA and the applicable protocols.

Homozygous familial hypercholesterolemia (HoFH) is a rare, autosomal dominant disease that leads to premature cardiovascular disease (CVD). Since monozygotic twins share the intrauterine environment and have the same age and gene profile, they could represent a very special resource for the investigation of the causes and the natural course of FH. This report is a description of 36-year-old monozygotic twin brothers with almost identical early coronary artery involvement due to FH concomitant with high lipoprotein(a) (Lpa) levels and a review of the literature. Sequence analysis revealed that the twins were homozygous for the LDLR c.1060+10G>A (rs12710260) mutation and heterozygous for the LDLR c.542C>T (rs557344672) mutations. Both were also homozygous for the c.1060+7T>C (rs2738442) and c.1586+53A>G (rs1569372) mutations in the LDLR gene as well as c.4265A>T (rs568413) mutations in the APOB gene. In the literature, there are 7 twin cases with reported FH, but none with high Lpa levels. The HoFH twins in this case report had lower low-density lipoprotein (LDL) cholesterol levels than expected (before treatment 204 and 223 mg/dL), with almost identical coronary involvement. Both had an extremely high Lpa level (308 and 272 nmol/L) with a very low coronary calcium score (16 AU) and a good response to statins (>60%). There was a history of the first CVD event occurring at nearly the same age (32–34 years) in the family. This could be an important aspect of FH families as a result of the similar timing of cumulative LDL exposure exceeding the threshold of CVD events. In conclusion, this first report of monozygotic HoFH twins with elevated Lpa levels and almost identical early coronary artery involvement at the same age provides evidence to substantiate the hypothesis of lifetime cholesterol burden/exposure.

Prosthetic valve thrombosis (PVT) is a life-threatening valve dysfunction. In asymptomatic cases, as well as certain symptomatic patients with PVT, the results of the first-line imaging tool, transthoracic echocardiography, may be inconclusive in terms of illustrating the thrombus, which is necessary in order to select the proper treatment option. Hence, a differential diagnosis based on clinical presentation may be challenging, and multimodality imaging, including echocardiography, cine fluoroscopy, and cardiac computed tomography, is usually required to distinguish between PVT and other prosthesis-related pathologies, such as pannus, vegetation, and prosthesis-patient mismatch.

A 58-year-old man with a left ventricular assist device (LVAD), which had been implanted 1 year earlier, presented with rest dyspnea. Moderate to severe aortic regurgitation (AR), pre-postcapillary pulmonary hypertension, modarete right ventricular (RV) failure, and low cardiac output were observed at presentation. Transcatheter aortic valve implantation (TAVI) was performed to treat the AR and a self-expandable aortic valve was implanted. Within minutes, hypotension, RV and inferior vena cava dilatation, and left atrial (LA) and left ventricular (LV) collapse occurred and persisted despite LVAD speed reduction. It was observed that severe RV failure had developed and venoarterial extracorporeal membrane oxygenation (VA-ECMO) was applied. Following VA-ECMO treatment, the RV dimensions decreased, and the LA and LV dimensions began to increase, as well as the LVAD flow. Weaning from VA-ECMO was unsuccessful and exitus occurred on the fifth day after TAVI secondary to RV failure. It was surmised that the decrease in blood circulation from the aorta to the LV after treatment of severe AR with TAVI caused an acute increase in the cardiac output and the RV preload. The acute increase in the RV preload led to acute severe right heart failure. It is necessary to prepare the RV to compete with an acute increase in preload before TAVI even when there is only modarete RV failure.