Determinants/Predictors of QT Abnormalities in Patients on Psychotropic Medications in a Nigerian Tertiary Hospital.

Cardiovascular disease is a major global burden and a leading cause of premature death among patients with severe mental illness. Over time, research and clinical practice have paid increased attention to the impact of psychiatric medications on cardiac repolarization. In a resource-limited setting, it is common for psychotropic medications to be initiated and maintained in an outpatient setting without baseline or follow up ECG. This study evaluated the determinants and predictors of QT abnormalities among patient taking psychotropic drugs. We conducted a cross-sectional study in a population of 150 psychiatric patients on psychotropics and 75 controls. We studied the effects of various psychotropic drugs on QT dispersion (QTd) and corrected QT interval (QTc) as well as correlation with the types and dosages of psychotropic drugs used. All the subjects had detailed clinical examination and resting electrocardiogram (ECG) at 25 mm/sec done. QTc was determined using Bazett formula and QTd was determined by subtracting shortest from longest QT in 12-lead ECG. The prevalence of prolonged QTc and QTd as well as the mean QTc and QTd were significantly higher in patients than the control group. The mean QTc was significantly higher in patient on typical antipsychotics compared to those on atypical antipsychotics. Age, heart rate and antipsychotic dose in chlorpromazine equivalent were predictors of QTc with the heart rate being the most powerful predictor among them. Psychotropic drugs use is associated with QTc and QTd prolongation with age, heart rate and antipsychotic dose as predictors of QTc.

Permanent standard time is the optimal choice for health and safety: an American Academy of Sleep Medicine position statement.

The period of the year from spring to fall, when clocks in most parts of the United States are set one hour ahead of standard time, is called daylight saving time, and its beginning and ending dates and times are set by federal law. The human biological clock is regulated by the timing of light and darkness, which then dictates sleep and wake rhythms. In daily life, the timing of exposure to light is generally linked to the social clock. When the solar clock is misaligned with the social clock, desynchronization occurs between the internal circadian rhythm and the social clock. The yearly change between standard time and daylight saving time introduces this misalignment, which has been associated with risks to physical and mental health and safety, as well as risks to public health. In 2020, the American Academy of Sleep Medicine (AASM) published a position statement advocating for the elimination of seasonal time changes, suggesting that evidence best supports the adoption of year-round standard time. This updated statement cites new evidence and support for permanent standard time. It is the position of the AASM that the United States should eliminate seasonal time changes in favor of permanent standard time, which aligns best with human circadian biology. Evidence supports the distinct benefits of standard time for health and safety, while also underscoring the potential harms that result from seasonal time changes to and from daylight saving time. CITATION: Rishi MA, Cheng JY, Strang AR, et al. Permanent standard time is the optimal choice for health and safety: an American Academy of Sleep Medicine position statement. J Clin Sleep Med. 2024;20(1):121-125.

Serum uric acid and left ventricular hypertrophy in hypertensive patients in Ado-Ekiti.

INTRODUCTION: systemic hypertension is a foremost risk factor for cardiovascular morbidity and mortality. Its actions are manifested on organs like the brain, heart and kidneys. High serum uric acid (SUA) escalates cardiovascular vulnerability in patients with systemic hypertension. METHODS: a cross-sectional study was performed in 271 (178 females, 93 males) patients with systemic hypertension. Two hundred and seventy one healthy age and sex matched non-hypertensive persons obliged as controls. Left ventricular hypertrophy (LVH) was estimated by echocardiography. Blood samples were collected for measuring uric acid levels. RESULTS: mean SUA was significantly higher among the hypertensive patients (371±125µmol/L) than in the controls (269 ± 101.4µmol/L; p < 0.001), and the prevalence of hyperuricemia was 46.9% among the hypertensives and 11.1% among the controls (P < 0.001). Independent predictors of SUA were class of systemic hypertension, left ventricular mass index (LVMI), body mass index (BMI) and age. However, class of hypertension was the best independent predictor of SUA levels in the multivariate regression model (ß = 0.597). Linear regression revealed SUA levels ≥ 430µmols/l as a predictor of stage 2 hypertension (F = 26.620, p = < 0.001). Among the hypertensive patients, LVH was present in 39.3% of those with hyperuricemia and in 28.0% of those with normal SUA levels (p = 0.003). CONCLUSION: results indicate serum uric acid is positively correlated with hypertension and a reliable indicator of LVH in study population.