Association of hypokalemia with severe arrhythmias in patients with acute myocardial infarction

Clinical and animal studies suggest that the ischemic heart can be particularly vulnerable to hypokalemia leading to the cardiac arrhythmia. To evaluate the association of severe arrhythmia with hypokalemia in patients with acute myocardial infarction [AMI]. Retrospective study. Coronary Care Unit, Salmaniya Medical Complex. Two hundred and seventy-four patients with AMI had serum potassium levels measured on admission along with other cardiovascular risk factors. Serum potassium concentrations were significantly decreased with the severity of arrhythmias [no arrhythmias; 4.2 +/- 0.80 mmol/l, supra-ventricular; 3.8 +/- 0.9 mmol/l, and ventricular arrhythmias; 3.3 +/- 0.5 mmol/l, p=0.0001]. The risks of supra-ventricular and ventricular arrhythmias were significantly increased by 2.4 and 8.3 fold, respectively in patients with serum potassium levels at the lowest quartile [<3.5 mmol/l] compared with the highest quartile of serum potassium when adjusted for other risk factors. The results of this study suggest that hypokalemia is independently associated with the severity of arrhythmias in patients with AMI

predictive value of admission serum glucose and glycosylated haemoglobin [HbA1C] in patients presenting with acute myocardial infarction [AMI]: short term outcome

Recent data indicated a high prevalence of abnormal glucose metabolism in patients with no history of diabetes mellitus [DM] at the time of acute myocardial infarction [AMI]. The aim of this retrospective study was to assess the predictive value for clinical outcome for admission hyperglycemia in patients presenting with acute ST-elevation myocardial infarction [STEMI]. Other risk factors such as history of DM, hypertension, Body Mass Index [BMI], smoking, serum level of glycosylated haemoglobin [HbA1c] and low density lipoprotein [LDL] were evaluated. The data of two hundred and eighty five [285] patients with STEMI was extracted and evaluated retrospectively. Patients were classified according to admission serum glucose [AG] into three groups: Group 1 with AG level of <=7 mmol/L and group 2 with AG level between >7 and <15 mmol/Land group 3 of AG >/= 15 mmol/L. In the study group the mean age was 59.7 +/- 14 years, range [24-88] and 180 [63%] were male. 173 [60%] patients with STEMI had hyperglycemic with glucose of more than 7 mmol/L with or without history of DM, eighty four [29%] patients had hyperglycemia and history of DM,89 [31%] patients had hyperglycemia [stress] without DM. Thirty two percent had history of hypertension and 26% had history of smoking. The frequency of more than two Major Acute Cardiac Events [MACE] such as pulmonary odema, significant arrhythmias, or cardiogenic shock were at frequency of 70% in group 3.19% in group 2, and 11% in group 1. Thirty patients died during the study [10.5%]: twelve patients [4.2%] were in group 3, eleven patients [3.9%] in group 2 and seven [2.4%] in group 1. The odds ratio of stress hyperglycemia in group 3 compared with group 1 after adjustment for age and sex as predictor of mortality was 3.3 [Cl 0.99-10.98, P=0.032, like wise, the odds ratio in group 2 compared with group 1 after adjustment was 2.4 [Cl: 0.75- 8.07, P=0.065].The history of DM, high serum level of LDL and the level of HBA1 c and Anterior AMI were significant predictors of adverse outcome while other risk factors such as BMI, history of hypertension and smoking were of no significance. These data indicate that hyperglycemia of more than 15 mmol/L on admission without history of DM is powerful predictor of adverse clinical outcome in the setting of acute myocardial infarction. Other useful predictors are history of DM, and high serum level of glycosylated hemoglobin, LDL and the site of anterior MI on ECG. The BMI, history of hypertension and smoking are not useful predictors of adverse mortality

Cardiovascular responses to tonic pain in REM sleep-deprived rats. Role of melatonin and beta endorphin

Chronic pain is associated with increased incidence of hypertension. Sleep deprivation, common in patients with chronic pain, is associated with increased blood pressure and heart rate. This study was designed to determine whether sleep deprivation induces increased cardiovascular responses to pain. In addition; we examined the role of melatonin and endorphins in mediating these responses. The study was conducted in Sprague-Dawely rats divided into a control group [n=8] and Rapid Eye Moment sleep deprived [REMSD] group [n=8]. REM sleep deprivation was done for three days using the inverted flowerpot technique. Systolic BP and HR were recorded at baseline as well as 5, 10 and 30 minutes after intra-plantar formalin injection. In addition, serum melatonin and endorphin levels were determined. Under basal conditions, BP and HR and following acute pain [1[st] phase of formalin injection] were comparable with non-sleep deprived [non-SD] state. In contrast, the REMSD rats showed significantly greater increases in HR and BP during the 2[nd] phase of formalin pain as compared to non-SD state. These changes were associated with significant reductions in serum melatonin and endorphin levels in REMSD rats. These data indicate that exaggerated blood pressure and HR responsiveness to pain in sleep deprivation could be mediated through reductions in melatonin and endorphin

Interactions between leptin, neuropeptide-Y and insulin with chronic diurnal fasting during Ramadan

Background: Fasting during the month of Ramadan for Muslims is a unique metabolic model that includes abstinence from food and fluid intake during the period from dawn to sunset as well as a reduction in meal frequency and alterations in the sleep-wakefulness cycle. Leptin, neuropeptide-Y and insulin are thought to play an important role in long-term regulation of caloric intake and energy expenditure. However, the long-term changes and interactions between these factors during this pattern of fasting are not known

Subjects and Methods: The study was conducted on 46 healthy female volunteers [age, 22 +/- 2 years; BMI, 25.3 +/- 0.7 kg/m2]. Anthropometrical measurements, estimation of body fat and fasting serum levels of neuropeptide Y, leptin, insulin and glucose were estimated at baseline [day 1], days 14 and 28 of the month of Ramadan and 2 weeks after Ramadan

Results: Baseline serum levels of leptin correlated positively with body fat [r=0.87, P=0.0002]. Serum leptin levels exhibited a significant increase by approximately 41% and neuropeptide-Y levels were decreased by 30.4% throughout the month of Ramadan. In addition, a significant correlation [r=0.63, P=0.0001] was found between changes in serum leptin and serum insulin. However, changes in serum neuropeptide-Y levels did not correlate with those of leptin or insulin

Conclusion: Long-term fasting with interrupted nocturnal eating is associated with significant elevations in serum leptin and insulin and reduction in serum neuropeptide-Y. The changes in serum leptin are likely mediated through insulin. However, changes in neuropeptide-Y appears to be mediated independently of leptin or insulin during this type of fasting