The Correlation between Elevated HDL-Cholesterol, Body Mass Index, and Presence of Thyroid Nodules: A Retrospective Analysis.

BACKGROUND: Elevated high-density lipoprotein-cholesterol (HDL-cholesterol) levels have been linked to unfavorable outcomes in various clinical settings, but the association with thyroid nodules remains unclear. We aimed to analyze the correlation between elevated HDL-cholesterol and the presence of thyroid nodules along with certain demographic and clinical findings. METHODS: In this retrospective study, the patients were divided into three groups based on their body mass index (BMI): <25, 25-29, and >30 and evaluated. Data of 677 patients aged between 15 and 95 years (52.6 ± 15.6) were evaluated. The entire study population comprised 516 females (76.2%). RESULTS: Thyroid nodules (67.1%) and left ventricle diastolic dysfunction (LVDD) (58.1%) were the two most frequent findings in the overall cohort. In the multivariate regression model, BMI, heart rate, and HDL-cholesterol values were significant and independent predictors (p = 0.000 for all) of the presence of thyroid nodules. The presence of thyroid nodules is higher in females, particularly within the higher BMI groups [odds ratio (OR) = 1.048 (CI = 1.02-1.08) for BMI < 25, p = 0.003; OR = 1.094 (CI = 1.05-1.14) for BMI 25-29, p = 0.000; OR = 1.115 (CI = 1.05-1.19) for BMI ≥ 30]. This higher incidence is not observed in males. CONCLUSION: While the precise mechanisms underlying this association are yet to be fully elucidated, elevated HDL-cholesterol may serve as an indicator of thyroid nodules rather than a marker of cardiovascular protection.

Can high-sensitive troponin levels within the normal range predict positivity in treadmill test?

BACKGROUND: This study aimed to determine whether a high level of high-sensitivity troponin T (hsTnT) predicts a positive treadmill test in patients with suspected stable ischemic heart disease (SIHD). METHODS: In all, 366 patients with suspected SIHD were included in the study. We measured the serum hsTnT levels before the treadmill test. The treadmill test was performed according to the Bruce protocol. RESULTS: Of the 366 patients, 97 had positive treadmill tests. The hsTnT levels were significantly higher in the positive group than in the negative group. In the binary logistic regression analysis, hsTnT, pretest probability, metabolic equivalents (METs), target heart rate (THR) percentage, and Duke treadmill score (DTS) were independent predictors of a positive treadmill test [hsTnT odds ratio (OR): 2.178, P < 0.001; pretest probability OR: 1.036, P = 0.007; METs OR: 0.755, P = 0.008; THR OR: 0.773, P < 0.001; DTS OR: 2.661, P = 0.012]. In the receiver operating characteristic (ROC) curve analysis, the area under the curve (AUC) value of the model with the combined parameters of hsTnT, pretest probability, METs, THR, and DTS was statistically significant in predicting a positive treadmill test [combined model AUC: 0.945 (0.922-0.968), P < 0.001]. CONCLUSIONS: In sum, high pretest hsTnT levels predicted a positive treadmill test in patients with suspected SIHD. Analysis of the hsTnT levels before the treadmill test can increase the sensitivity and specificity of the treadmill test. The methods for measuring hsTnT levels are cheap and easily accessible and can be used before the treadmill test in patients with suspected SIHD.

Blood pressure, autonomic stress, and inflammatory markers during sleep deprivation and recovery in healthy men.

OBJECTIVE: Recent community-based studies have identified sleep deprivation (SD) as an important modifiable risk factor for hypertension However, the underlying mechanisms linking SD to hypertension remain elusive. Thus, this study investigates blood pressure (BP) responses to cardiac autonomic stress tests in the presence of SD. Furthermore, we analyzed vascular inflammatory biomarkers as a possible underlying factor linking SD to increased BP. METHODS: Ten healthy male volunteers (age, 21.6±1.2 years) underwent repeated autonomic stress tests for three consecutive days (baseline, SD, and recovery). The autonomic stress tests included the Valsalva maneuver, mental arithmetic, isometric handgrip, and cold pressor tests. Each day, resting BPs were measured, venous blood samples were collected for intercellular adhesion molecule 1, vascular cell adhesion molecule 1, and E-selectin measurements, and stress tests were performed between 0900 and 1100. Ambulatory BP was recorded during the entire SD period (24 h). RESULTS: One-night SD abolished BP reactivity to the Valsalva maneuver, isometric hand grip, and cold pressor tests, which returned after recovery sleep. Ambulatory BP monitoring showed that the mean systolic and diastolic BPs were 121.1±8.5 mm Hg and 72.8±6.3 mm Hg, respectively, between 0700 and 2300 and 120.3±9.6 mm Hg and 74.1±6.1 mm Hg, respectively, between 2300 and 0700 during the SD day (p>0.05 for both). Vascular inflammatory markers seemed unrelated to BP changes. CONCLUSION: Acute SD altered BP responses to cardiac autonomic stress tests in healthy men without affecting resting BP levels. SD led to a non-dipping pattern in BP oscillation. Collectively, these findings highlight the importance of sleep in regulating BP.

Relationship between the infarct localization and left ventricular rotation parameters following acute ST-segment elevation myocardial infarction.

OBJECTIVE: This study was an investigation of the role of left ventricular (LV) apical rotation seen in the early period after myocardial infarction (MI) in predicting infarct localization. METHODS: A total of 124 patients with a ST-Segment elevation myocardial infarction (STEMI) diagnosis who underwent primary percutaneous coronary intervention (PCI) and 50 healthy volunteers with similar demographic characteristics were included in the study. The relationship between 2-dimenstional speckle tracking echocardiography (STE)-guided LV apical rotation angle measurements and technetium-99m sestamibi-single-photon emission computed tomography (SPECT)-guided infarct localization was evaluated. Conventional echocardiography and STE were performed on average 2 days after PCI, and gated SPECT myocardial perfusion imaging (MPI) was performed within an average of 60 days. RESULTS: The apical rotation angle was lower in patients with an anterior MI compared with those who had an inferior MI and the control group (AntMI-InfMI: 6.51±2.4°, AntMI-Control: 13.20±2.5°, InfMI-Control: 14.3±2.1°; p value: 0.00, 0.00, 0.15, respectively). SPECT MPI analysis revealed the presence of an LV apical scar in all patients with acute anterior MI, but only 14 of those with inferior MI group (usually the inferoapical wall). The apical rotation angle recorded in patients with apical scar was lower than that of the patients without apical scar (7.6±2.8° and 14.5±2°, respectively; p=0.00). Receiver operating characteristic curve analysis yielded an area under the curve for apical rotation of 0.799 (p<0.01). The optimal cutoff value of 12.1° had a sensitivity of 78.3% and a specificity of 68.2% for predicting LV apical scar following STEMI. CONCLUSION: Detection of apical rotation angle decrease in the early period after STEMI may be useful in predicting extension of infarct scarring to the LV apex.

Late Versus Early Myocardial Remodeling After Acute Myocardial Infarction: A Comparative Review on Mechanistic Insights and Clinical Implications.

In the setting of acute myocardial infarction (AMI), adverse myocardial remodeling (AMR) has been universally regarded as an early-onset phenomenon generally arising within the first few weeks (usually within days in the infarct zone) following myocardial injury. On the other hand, onset of cardiac morphological changes in this setting may potentially extend far beyond this time frame (usually beyond several months after the index AMI), suggesting a prolonged latent period in certain cases. In clinical practice, this delayed form of post-AMI remodeling, namely late AMR, has emerged as an interesting and underrecognized phenomenon with poorly understood mechanisms. Notably, systemic inflammation and associated growth factors seem to play a pivotal role in this setting. Accordingly, the present article primarily aims to discuss potential mechanisms and clinical implications of late AMR (in a comparative manner with its classical early counterpart) among AMI survivors along with a particular emphasis on potential benefits of certain anti-inflammatory strategies in this setting.

Natriuretic Peptides in Clinical Practice.

Natriuretic peptides have long been introduced into clinical practice. These biomarkers have certainly been shown to provide useful information in the diagnosis, prognosis and risk stratification in heart failure and also may have a role in the guidance of heart failure therapy. Although, there are some limitations in using of these markers such as lack of specificity, aging, renal dysfunction or obesity, among the huge number of candidates for heart failure biomarkers, only natriuretic peptides are currently widely used in daily clinical practice in heart failure. Recent heart failure guidelines recognize natriuretic peptides as an essential tool in the new diagnostic and therapeutic algorithms. Furthermore, natriuretic peptides are not only used in the diagnosis or prognosis of heart failure, but also these biomarkers are referred to have some potential role in primary prevention, cardio-oncology, advanced heart failure, assessment of response to cardiac resynchronization therapy, pulmonary arterial hypertension, acute coronary syndromes, atrial fibrillation and valvular heart disease. In this article, natriuretic peptides have been reviewed for their updated information and new recommendations in heart failure and also potential role of these biomarkers in the management of various clinical conditions have been addressed in the form of expert opinion based on the available data in the literature.

Late coronary ischemic syndromes associated with transcatheter aortic valve implantation: A review of mechanistic and clinical aspects.

In the past years, transcatheter aortic valve implantation (TAVI) has emerged as a promising option for the treatment of aortic valve pathologies particularly in the the presence of surgically high-risk situations. Importantly, a variety of specific procedural complications including acute coronary osteal occlusion, though very rare, has been reported in major clinical studies. However, little is known about the late impact of TAVI on coronary system at the macro and microvascular levels. On the other hand, clinical studies as well as real life experiences have shown variable rates of acute coronary syndrome (ACS) readmissions among TAVI recipients in the short and long terms. Within this context, it may be suggested that even though late coronary ischemic events arising after TAVI, to some extent, appears to be spontaneous or attributable to certain stressors, TAVI may also have the potential to directly account for, accelerate or contribute to the evolution of these ischemic events on follow-up. Accordingly, the present review primarily focuses on potential association of TAVI with late coronary ischemic syndromes along with a particular emphasis on its mechanistic basis and clinical implications among TAVI recipients.

Left Ventricular Dysfunction in the Setting of Takotsubo Cardiomyopathy: A Review of Clinical Patterns and Practical Implications.

Takotsubo cardiomyopathy (TTC) is primarily regarded as a form of acute and transient myocardial disease with a variety of characteristic wall-motion abnormalities. Importantly, a significant portion of TTC cases generally present with variable degrees of acute left ventricular (LV) dysfunction with or without clinical HF. On the other hand, LV dysfunction in the setting of TTC has been universally and exclusively considered as a synonym for systolic dysfunction, potentially overlooking other forms of myocardial pathologies, including transient diastolic dysfunction, in this setting. More interestingly, recent observations suggest that TTC, despite its macroscopic recovery, may not always manifest as a fully reversible phenomenon, suggesting persistence of microscopic changes at the cellular level to some degree. In clinical practice, these residual changes might largely account for the evolution of certain pathologies, including persistent diastolic dysfunction and subclinical LV dysfunction with variable symptomatology (particularly those arising during high levels of myocardial workload, including exercise, etc.) among TTC survivors. Within this context, the present review aims to highlight various clinical patterns and implications of LV dysfunction in the setting of TTC, and to provide basic information regarding morphological and mechanistic characteristics of wall-motion abnormalities in this setting.

Speckle-tracking strain assessment of left ventricular dysfunction in synthetic cannabinoid and heroin users.

OBJECTIVE: There is growing evidence regarding the numerous adverse effects of synthetic cannabinoids (SCBs) on the cardiovascular system; however, no studies have shown the cardiovascular effects of opioids using strain echocardiography. This study examines the cardiac structure and function using echocardiographic strain imaging in heroin and synthetic cannabinoid users. METHODS: This double-blind study included patients who were admitted or referred to a rehabilitation center for heroin (n=31) and synthetic cannabinoid users (n=30). Heroin users and synthetic cannabinoid users were compared with healthy volunteers (n=32) using two-dimensional (2D) speckle-tracking (ST) echocardiography. RESULTS: No differences were found in the baseline characteristics and 2D echocardiography values. The mean global longitudinal strain value was -20.5%±2.4% for SCB users, -22.3%±2.4% for opioid users, and -22.5%±2.2% for healthy volunteers (p=0.024). The mean apical 2-chamber (AP2C) L-strain values were -20.1%±3.1%, -22.4%±3.0%, and -22.3%±2.8% for SCB users, opioid users, and healthy volunteers, respectively (p=0.032). The mean apical 4-chamber (AP4C) L-strain values were -20.7%±2.5% for SCB users, -23.2%±3.2% for opioid users, and -23.8%±3.1% for healthy volunteers (p<0.001). CONCLUSION: SCBs are potential causes of subclinical left ventricular dysfunction.

Patient characteristics and statin discontinuation-related factors during treatment of hypercholesterolemia: an observational non-interventional study in patients with statin discontinuation (STAY study).

OBJECTIVE: The purpose of this study was to identify patient characteristics and statin discontinuation-related factors in patients with hypercholesterolemia. METHODS: A total of 532 patients (age mean±SD: 57.4±11.5 years; 52.4% women, 47.6% men) with hypercholesterolemia and statin discontinuation were included in this national cross-sectional non-interventional observational study. Data on socio-demographic characteristics of patients, cardiovascular risk factors, past treatment with and discontinuation of statin treatment were collected in one visit. RESULTS: Mean±SD duration of hypercholesterolemia was 4.9±4.2 years at time of discontinuation of statin treatment. Statin treatment was initiated by cardiologists in the majority of cases (55.8%), whereas discontinuation of statin treatment was decided by patients in the majority of cases (73.7%), with patients with higher (at least secondary education, 80.4%) more likely than those with lower (only primary education, 69.7%) to decide to discontinue treatment (p=0.022). Negative information about statin treatment disseminated by TV programs-mostly regarding coverage of hepatic (38.0%), renal (33.8%), and muscular (32.9%) side effects (32.9%)-was the most common reason for treatment discontinuation. CONCLUSION: The decision to discontinue statin treatment was made at the patient's discretion in 74% of cases, with higher likelihood of patients with higher educational status deciding to discontinue treatment and switch to non-drug lipid-lowering alternatives. Cardiologists were the physicians most frequently responsible for the initiation of the statin treatment; coverage of several non-life-threatening statin side effects by TV programs and patients' lack of information regarding high cholesterol and related risks were the leading factors predisposing to treatment discontinuation.

Angiographic outcomes with early eptifibatide therapy in non-ST-segment elevation acute coronary syndrome (from the EARLY ACS Trial).

Early administration of glycoprotein IIbIIIa inhibitors results in improved angiographic parameters, including thrombolysis in myocardial infarction (TIMI) flow grade, corrected TIMI frame count, and TIMI myocardial perfusion grade (TMPG) among patients with ST-segment elevation myocardial infarction. Whether the same is true in the setting of non-ST-segment elevation acute coronary syndrome is unknown. The goal of the early glycoprotein IIbIIIa inhibition in non-ST-segment elevation acute coronary syndrome (EARLY ACS) angiographic substudy was to compare angiographic outcomes among patients with non-ST-segment elevation acute coronary syndrome who were administered early routine versus delayed provisional eptifibatide. Of 9,406 patients in the EARLY ACS trial, 2,066 patients were included in the angiographic substudy (early routine eptifibatide [n=1,042] or early placebo [n=1,024] with delayed provisional eptifibatide after angiography and before percutaneous coronary intervention [PCI]). The angiographic substudy primary end point was the incidence of TMPG 3 before and after PCI. TMPG 3 before (43.7% vs 44.9%, p=0.58) and after PCI (52.4% vs 50.1%, p=0.73) was similar for early routine versus delayed provisional eptifibatide, respectively. Angiographic procedural complications consisting of a composite of loss of side branch, abrupt vessel closure, distal embolization, and no reflow occurred less frequently in early routine group versus delayed provisional group (9.3% vs 13.6%, respectively, p=0.01). In the EARLY ACS angiographic substudy, the use of early routine eptifibatide resulted in fewer angiographic procedural complications. These data provide support for the use of eptifibatide in the catheterization laboratory during high-risk cases merely to prevent angiographic procedural complications.

Coronary slow flow phenomenon associated with high serum levels of soluble CD40 ligand and urotensin II: a multi-marker approach.

BACKGROUND: The aim of this study was to evaluate the serum soluble CD40 ligand (sCD40L) levels, serum uroten- sin II levels, and serum leptin levels as an indirect indicator of endothelial dysfunction, inflammation, and atherosclerosis at the microvascular level, and the comparison of those values with those of the control group with a nor- mal coronary flow pattern. METHODS: The study included 35 consecutive patients (17 women, 18 men; average age: 51.20 ± 10.93 years) in our hospital who underwent coronary angiography due to objective myocardial ischemia and in whom slow coronary flow was detected. The control group included 34 consecutive patients with normal coronary flow pattern (18 women, 16 men; average age: 54.59 ± 12.40 years). The coronary flow rates of all patients and control subjects were documented by the thrombolysis in myocardial infarction (TIMI) frame count. Serum sCD40L concentrations, serum urotensin II concentrations and serum leptin concentrations were measured by an enzyme-linked immunosorbent assay method using commercially available kits. RESULTS: The corrected TIMI frame count for LAD, Cx, RCA, and mean TIMI frame count were significantly higher in patients with slow coronary flow (SCF), compared to subjects with normal coronary flow (43.8 ± 1.7 vs. 17.7 ± 4.7, p < 0.001; 27.9 ± 6.9 vs. 11.9 ± 4.8, p < 0.001; 25.4 ± 8.4 vs. 11.1 ± 3.1, p < 0.001; and 32.3 ± 6.4 vs. 13.7 ± 5, p < 0.001, respectively). The serum soluble CD40 ligand and serum urotensin II levels were significantly higher in the slow coronary flow group compared to the control group (12.00 ± 5.43 ng/mL--6.49 ± 5.03 ng/mL, p < 0.001; and 50.94 ± 34.28 pg/mL--26.91 ± 11.52 pg/mL, p < 0.001, respectively). In addition, there was no statistically significant difference between the slow coronary flow group and the control group with regard to serum leptin levels and hs-CRP levels (both p > 0.05). CONCLUSIONS: This study suggests that soluble CD40 ligand and urotensin II likely play a role in the pathogenesis of slow coronary flow.