Evaluation of urinary na levels as a risk factor in patients with coronary artery disease.

INTRODUCTION: Restriction of salt intake is advised in the general population to reduce cardiovascular risk. Daily higher salt intake may contribute to high coronary artery disease (CAD) prevalence in the Turkish population, although there is limited data regarding salt intake and urinary sodium (Na) extraction in patients with CAD. In this study, we aimed to assess the relationship between urine Na, potassium (K), protein and creatine levels in patients with CAD. METHODS: One hundred participants, aged 30-65, who underwent coronary angiography under elective conditions were enrolled in this study between May 2019 and August 2019. Patients who had known CAD before, acute coronary syndrome, hypertension, congestive heart failure, diabetes mellitus (DM), structural heart disease, malignancy, renal failure, and severe comorbid states were excluded from the study. Coronary angiograpy revealed CAD in 61 patients and normal coronary arteries in 39 patients who were classified as the control group. Morning urine samples were collected for analysis. The 24-hour urine sodium was calculated using the KAWASAKI method. RESULTS: Spot urinary protein extraction and spot urinary micro-protein/creatinine ratio were significantly higher in the CAD group than in the control group (p=0.035, p=0.031, respectively). Also, serum creatinine (Cr) was found to be higher while glomerular filtration rate (GFR) and Na levels were found to be lower in the CAD group than in the control group (p=0.014, p=0.012, p=0.016 respectively). The logistic regression model was statistically significant, χ2(25)=41.45, p=0.021 and GFR, Na levels, spot urinary micro-protein/creatinine, and HDL levels were assessed as predictive factors for CAD.CONCLUSION: Urinary Na and K extraction is not affected by the presence of CAD. Also, spot urinary Na/ K ratio and 24-hour sodium extraction were similar between patients with and without CAD. However, decreased GFR and increased urinary micro-protein/creatinine ratio could be risk factors for CAD. Furter studies with large samples are needed to assess this relationship (Tab. 6, Ref. 16).

Could serum ACE2 levels predict infarct size in acute phase of ST-segment elevation myocardial infarction: a comparative study with classical biomarkers.

OBJECTIVE: Serum ACE2 level in the acute phase of ST-segment elevation myocardial infarction may be an indicator of heart failure, however, limited studies have reported conflicting results. Therefore, in our study, we aimed to evaluate the relationship between serum ACE2 level and infarct size in the acute phase of ST-segment elevation myocardial infarction and compare the predictive value of ACE2 level with classical biomarkers. PATIENTS AND METHODS: Sixty-six patients after the primary percutaneous coronary intervention were included in the study. For the measurement of serum ACE2 levels, blood samples were taken twice from the patients: in the first 24 hours and on the 5th day of the infarction, and once from 30 healthy volunteers. hs-cTnT, BNP, and CRP levels were measured daily, and their peak values were taken. On the 7th day of ST-segment elevation myocardial infarction, gSPECT was used with the 99mTc-MIBI method for assessment of infarct size. RESULTS: Baseline ACE2 values were found to be higher in patients compared to controls, and ACE2 values obtained on the 5th day were found to be higher than the baseline values in the patients. There was no significant correlation between serum ACE2 levels and the RSS (%), while peak levels of hs-cTnT, BNP, and CRP were assessed as predictive factors for the RSS (%). CONCLUSIONS: Although serum ACE2 levels increased in the acute phase of ST-segment elevation myocardial infarction, this increase was not associated with infarct size. Serum ACE2 level did not provide additional benefit to classical biomarkers for infarct size-related prognosis prediction.

Evaluation of long-term pituitary functions in patients with severe ventricular arrhythmia: a pilot study.

INTRODUCTION: Traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), stroke and cerebrovascular disease (CVD) are identified as risk factors for hypopituitarism. Pituitary dysfunction after TBI, SAH, and CVD may present in the acute phase or later in the course of the event. Chronic hypopituitarism, particularly growth hormone (GH) deficiency is related to the increased cardiovascular morbidity and mortality. In patients with serious ventricular arrhythmias, who need cardiopulmonary resuscitation, brain tissue is exposed to short-term severe ischemia and hypoxia. However, there are no data in the literature regarding pituitary dysfunction after ventricular arrhythmias. PATIENTS AND METHODS: Forty-four patients with ventricular arrhythmias [ventricular tachycardia (VT), ventricular fibrillation (VF)] (mean age, 55.6 ± 1.8 years; 37 men, 7 women) were included in the study. The patients were evaluated after mean period of 21.2 ± 0.8 months from VT-VF. Basal hormone levels, including serum free triiodothyronine (fT3), free thyroxine (fT4), TSH, ACTH, prolactin, FSH, LH, total testosterone, estradiol, IGF-1, and cortisol levels were measured in all patients. To assess (GH)-insulin like growth factor-1 (IGF-1) axis, glucagon stimulation test was performed and 1 µg ACTH stimulation test was used for assessing hypothalamic-pituitary-adrenal (HPA) axis. RESULTS: The frequencies of GH, gonadotropin and TSH deficiency were 27.2, 9.0, 2.2%, respectively. Mean IGF-1 levels were lower in GH deficiency group, but it was not statistically significant. CONCLUSION: The present preliminary study showed that ventricular arrhythmias may result in hypopituitarism, particularly in growth hormone deficiency. Unrecognized hypopituitarism may be responsible for some of the cardiovascular problems at least in some patients.