Electrocardiographic alterations in patients consuming synthetic cannabinoids.

INTRODUCTION: The aim of this study was to investigate the electrocardiographic parameters in patients consuming synthetic cannabinoids. METHODS: Thirty-five patients who were consuming synthetic cannabinoids were enrolled to the study, prospectively. The control group included 35 healthy age and sex-matched volunteers. The standard 12-lead surface electrocardiograms of the study population were recorded. P maximum (Pmax), P minimum (Pmin), P wave dispersion, interatrial duration, P wave area in D2 derivation, abnormal P terminal force in V1 derivation, heart rate, QT interval, corrected QT, QT dispersion, PR interval duration and macrovolt T-wave alternans were evaluated by two experienced cardiologists. The intra-observer and inter-observer variations for all measurements were non-significant. RESULTS: Pmax and Pmin duration was not different between the groups ( p=0.96, p=0.15, respectively). However, P wave dispersion was higher in the patient group compared to control group (34±9.4, 29.5±6.6, p=0.02, respectively). QT interval was significantly higher in the patient group than the control group (380.3±25, 365.6±22.8, p=0.01, respectively). Besides, corrected QT was higher in the patient group compared to control group (415±36.8, 392±15.5, p=0.001, respectively). QT dispersion was also higher in the patient group than the control group (39.8±10.0, 29.2±5.4, p<0.001, respectively). CONCLUSION: Altered electrocardiography parameters linked with atrial and ventricular arrhythmia development may be observed in patients consuming synthetic cannabinoids. These patients should be evaluated regularly for cardiovascular disease and arrhythmia development. The electrocardiogram, which is a cheap and easy test to apply, can be used to determine the pro-arrythmic risk in patients consuming synthetic cannabinoids.

The association of serum procalcitonin level with the no-reflow phenomenon after a primary percutaneous coronary intervention in patients with ST-elevation myocardial infarction.

OBJECTIVE: The no-reflow phenomenon is associated with adverse outcomes in patients with acute ST-elevation myocardial infarction (STEMI) treated by a primary percutaneous coronary intervention (PPCI). Procalcitonin (PCT) is a marker of systemic inflammatory states and an elevated serum PCT concentration is related to an increased risk of cardiovascular events. We aimed to assess whether serum PCT level at admission is an independent predictor of no-reflow in patients with STEMI treated with PPCI. PATIENTS AND METHODS: Between November 2012 and December 2014, 501 consecutive patients with STEMI who underwent PPCI within the first 12 h following the onset of symptoms were enrolled. Serum PCT levels were measured on admission. Patients (age: 59±13 years, 73.5% men) were divided into the two groups: no-reflow and reflow. The no-reflow phenomenon was defined as final Thrombolysis In Myocardial Infarction flow grade less than 3 after PPCI. RESULTS: No-reflow was diagnosed in 91 (18.2%) patients. PCT levels were significantly higher in patients who developed no-reflow than in those who did not [0.102 (0.063-0.247) vs. 0.042 (0.020-0.076) µg/l, P<0.001]. In receiver operating characteristics curve analysis, the cut-off value of PCT was 0.066 µg/l for the prediction of no-reflow (area under the curve: 0.776, 95% confidence interval: 0.720-0.831, P<0.001, sensitivity: 73%, specificity: 70%). On multivariate analysis, serum PCT (>0.066 µg/l) value was an independent predictor of no-reflow (odds ratio: 3.377, 95% confidence interval: 1.572-7.255, P=0.002), together with early patency of culprit artery (P=0.046), Killip class more than or equal to 2 at presentation (P=0.028), and total stent length (P=0.004). CONCLUSION: Increased admission PCT level is associated independently with no-reflow after PPCI in STEMI patients.

Elevated serum fibrinogen levels and risk of contrast-induced acute kidney injury in patients undergoing a percutaneous coronary intervention for the treatment of acute coronary syndrome.

OBJECTIVES: Contrast-induced acute kidney injury (CI-AKI) is a common complication of diagnostic and therapeutic catheterizations, especially in the setting of acute coronary syndrome (ACS). Fibrinogen is a well-known cardiovascular risk factor. We evaluated whether serum fibrinogen level is associated independently with CI-AKI in patients with ACS who underwent a percutaneous coronary intervention (PCI). METHODS: Patients (n=710, aged 61 ± 13, 69% men) were classified into two groups: CI-AKI and non-CI-AKI. CI-AKI was defined as an increase of at least 0.5 mg/dl or at least 25% in the serum creatinine level within 72 h following PCI. RESULTS: CI-AKI occurred in 75 (10.6%) patients. We found significantly higher serum fibrinogen levels in patients who developed CI-AKI than in those who did not (498 ± 152 vs. 386 ± 96 mg/dl, P<0.001). Multivariate logistic regression analysis showed that serum fibrinogen level (odds ratio 1.006, 95% confidence interval 1.003-1.009, P<0.001), age, glomerular filtration rate, female sex, and white blood cell count were correlated with the development of CI-AKI. CONCLUSION: Serum fibrinogen level is associated independently with a higher risk of CI-AKI in patients with ACS undergoing PCI.

Increased apolipoprotein A-I levels mediate the development of prehypertension among Turks.

OBJECTIVE: We aimed to assess whether apolipoprotein (apo) A-I levels that generated type-2 diabetes and coronary disease among Turks contribute to prehypertension and hypertension. METHODS: A population-based sample of 2207 adults (mean age 53±11 years) was studied prospectively over a 6.5 years' follow-up. Individuals with hypertension and/or prehypertension were excluded at baseline. RESULTS: At baseline, levels of apoA-I increased in each sex, from the normotensive to prehypertensive and hypertensive group (by mean 7.6 mg/dL, p<0.001) concomitantly with age, waist circumference, fasting triglycerides, apoB, C-reactive protein (CRP) and homeostasis model assessment. In logistic regression models, adjusted for confounders comprising waist circumference or triglycerides, prehypertension was predicted independently by apoA-I at RRs of 1.23 (95%CI 0.97; 1.52)] or 1.32 (95%CI 1.04; 1.74), respectively. Despite showing a positive association, apoA-I did not independently predict in similar models the development of hypertension; the determinants were rather waist circumference, or fasting triglycerides or CRP [RR 1.16 (95%CI 1.05; 1.28)] and, in women, diabetes. In a linear regression analysis for circulating apoA-I including 10 variables, apoB and in men systolic blood pressure were positively associated. CONCLUSION: In contributing to prehypertension, the pro-inflammatory apoA-I, mediated by apoB, is independent of triglyceridemia. Other inflammatory processes conjointly are likely mechanistically involved in the development of hypertension in a population with prevalent metabolic syndrome.

High serum apolipoprotein E determines hypertriglyceridemic dyslipidemias, coronary disease and apoA-I dysfunctionality.

The relevance of serum apolipoprotein E (apoE) levels to two hypertriglyceridemic dyslipidemias has not been clarified. We explored, in a cross-sectional (and short-term prospective) evaluation, the independent relationship of serum apoE to the atherogenic dyslipidemia, hypertriglyceridemia with elevated apoB (HtgB) and to apoA-I dysfunctionality, previously shown in Turkish adults to be independent of apoE genotype. Serum apoE concentrations were measured by immunonephelometry in 1,127 middle-aged adults. In multivariable regression analysis, apoE concentrations showed log-linear associations with apoB and apoA-I levels, waist circumference, independent of C-reactive protein (CRP), homeostatic model assessment (HOMA) index and other confounders. The likelihood of atherogenic dyslipidemia and of HtgB roughly tripled per 1-SD increment in apoE concentrations, additively to apoE genotype, HOMA, apoA-I, CRP concentrations and waist circumference; yet apoA-I, protective against atherogenic dyslipidemia, appeared to promote HtgB, a finding consistent with apoA-I dysfunctionality in this setting. Each 1-SD increment in the apoE level was moreover, associated in both genders with MetS (at OR 1.5), after adjustment for sex, age, apoB, apoA-I and CRP, or for apoE genotypes. Circulating apoE predicted in both genders age-adjusted prevalent and incident coronary heart disease (CHD), independent of apoE genotype and CRP (OR 1.32 [95 % CI 1.11; 1.58]). To conclude, in a general population prone to MetS, elevated apoE concentrations are strongly linked to HtgB and atherogenic dyslipidemia, irrespective of apoE genotype, are associated with MetS and CHD. Excess apoE reflects pro-inflammatory state and likely autoimmune activation.

High levels of serum uric acid impair development of coronary collaterals in patients with acute coronary syndrome.

We evaluated the association of serum uric acid (SUA) level and development of coronary collateral vessels (CCVs) in patients with acute coronary syndrome (ACS). Patients (n = 224) with ACS were included in the study. Coronary collateral vessels were graded according to the Rentrop scoring system. Rentrop grade 0 was accepted as absence of CCV (group 1; n = 117) and Rentrop grade ≥1 was accepted as presence of CCV (group 2; n = 107). Rentrop 0-1 (poor CCV) were determined in 167 patients and Rentrop 2-3 (good CCV) were determined in 57 patients. Both presence of CCV (P < .001) and development of good CCV (P = .003) were significantly associated with low levels of SUA. We suggest that high levels of SUA affect the CCV development negatively in nondiabetic and nonhypertensive patients with ACS.

Arrhythmic effects of ivabradine in patients with coronary artery disease.

OBJECTIVES: Ivabradine is the first specific heart rate-lowering agent that has completed clinical development for stable angina pectoris. The aim of the present study was to investigate the effects of ivabradine therapy on P-wave duration, dispersion and QT duration, dispersion in coronary artery disease patients. METHODS AND RESULTS: The study population consisted of 21 patients with CAD who have confirmed by coronary angiography previously. Written informed consent was obtained in all patients. Twelve-lead electrocardiogram was recorded for each subject at a rate of 50mm/s on admission and repeated after 1 month ivabradine therapy. QT duration, QT dispertion, maximum and minimum QT duration calculated. Maximum and minimum P wave and P wave dispersion has been calculated. Heart rate was decreased after ivabradine therapy. (75+/-15 and 63+/-10, P=0.02).There was no difference between Pmax, Pmin and Pdis values before and after treatment. QTmax value was prolonged after treatment. (410+/-43 and 431+/-14, P=0,005) but there was no difference between cQTmax value.(455+/-38 and 439+/-21) There was no difference between QTdis and cQTdis values before and after treatment. (44+/-18 & 49+/-14; and 49+/-22 & 48+/-15). QTmax was prolonged after ivabradine therapy but cQTmax, Pdis, QTdis and cQTdis were not prolonged. CONCLUSION: There is no relationship between ivabradine therapy and increased risk of ventricular and atrial arrhythmia in coronary artery disease patient.