Acute effects of waterpipe smoking on blood pressure and heart rate: a real-life trial.

BACKGROUND: Waterpipe smoking is becoming a popular way of tobacco use in the world. Its acute effects on the cardiovascular system are not well investigated. MATERIALS AND METHODS: This is a trial designed to evaluate the acute effects of waterpipe smoking on blood pressure (BP) and heart rate (HR) in healthy adults. Individuals who ordered waterpipe in 6 Lebanese restaurants were enrolled (cases) and were compared to controls who consisted of subjects who were sitting at the same table of smokers but who did not smoke (passive smokers) and of subjects who were sitting in nonsmoking sections (nonsmokers). BP and HR were measured immediately before and 15 min after smoking or at baseline and 15 min later in controls. RESULTS: A total of 194 subjects were enrolled: 101 waterpipe smokers, 51 passive smokers, and 42 nonsmokers. Systolic and diastolic BP and HR significantly increased after 15 min of smoking in cases (mean 3.1 mm Hg (95% CI 0.8-5.5; p = 0.009) for systolic BP, 2.1 mm Hg (95% CI 0-4.2; p = 0.053) for diastolic BP, and 6.3 beats/minute (95% CI 4.3-8.3; p < 0.001) for HR, but did not change in controls. CONCLUSIONS: Waterpipe smoking for duration as short as 15 min has acute hemodynamic effects and significantly increases systolic BP and HR.

Association of GDF-15, hs-cTnT and NT-proBNP with coronary artery disease in patients undergoing elective angiography.

Aim: This study investigated the association between plasma levels of GDF-15, hs-cTnT and NT-proBNP and the presence of coronary artery disease (CAD) in stable patients referred for elective coronary angiography. Methods: The outcome of CAD was defined as an ordinal variable with 3 levels. The association between each biomarker and the outcome was tested using the Winell and Lindbäck method. Results: In unadjusted analysis of 252 patients, GDF-15 and hs-cTnT were associated with the presence and extent of CAD. In multivariate regression analysis including traditional risk factors, this association was no longer significant. Conclusion: NT-proBNP, GDF-15 and hs-cTnT plasma levels do not seem to improve the predictive ability of traditional risk factors for CAD in stable patients referred for coronary angiography.

This study aimed to look at a possible association between blood levels of three molecules (GDF-15, hs-cTnT and N-terminal pro B-type natriuretic peptide [NT-proBNP]) and the presence of coronary artery disease (CAD) in stable patients referred for coronary angiography. Three CAD degrees of severity were identified: no CAD, 1- or 2-vessel CAD and 3-vessel or left main CAD. The association between each of the three blood molecules and CAD was studied using a specific statistical method. In the 252 consecutive patients enrolled, the two molecules GDF-15 and hs-cTnT were significantly associated with the presence and extent of CAD, while NT-proBNP was not. However, when the statistical analysis was adjusted for the traditional risk factors of CAD (age, gender, smoking, diabetes, etc.), the association of GDF-15 and hs-cTnT with CAD was no longer significant. NT-proBNP, GDF-15 and hs-cTnT blood levels do not seem to be independent predictive tools for CAD in stable patients referred for coronary angiography.

A Practical Approach for the Use of High-Sensitivity Cardiac Troponin Assays in the Evaluation of Patients With Chest Pain.

Chest pain is a common clinical presentation, especially in the emergency department. Both rapid identification of patients with myocardial infarction as well as those with noncardiac chest pain is important in order to start therapy in the former and avoid unnecessary investigations and delay in discharge in the latter. Beside electrocardiogram, cardiac biomarkers are a key element in decision making. Conventional creatinine kinase and troponin assays are not sensitive enough and have to be repeated at least 6 to 12 hours after initial evaluation. New high-sensitivity cardiac troponin (hs-cTn) tests are currently available and if used appropriately can substantially improve management. Because of their high sensitivity and accuracy, these tests allow measurement of very low serum troponin levels, such as those present in healthy individuals and can detect small changes in troponin concentration within a short time frame. These tests are thus, very useful for the early diagnosis of myocardial infarction but can also be elevated in several other conditions that result in myocardial injury. A good understanding of the analytical characteristics of these assays is of uppermost importance for their appropriate use in clinical practice.

Antithrombotic treatment pattern in newly diagnosed atrial fibrillation patients and 2-year follow-up results for dabigatran-treated patients in the Africa/Middle-East Region: Phase II results from the GLORIA-AF registry program.

BACKGROUND: Data on the epidemiology and treatment of atrial fibrillation in the Africa/Middle East region are limited, and the use of novel oral anticoagulants and their effectiveness in real-world clinical practice has not been evaluated. METHODS AND RESULTS: This study used prospectively collected data from the Global Registry on Long-Term Oral Antithrombotic Treatment in Patients With Atrial Fibrillation (GLORIA-AF) to describe anticoagulant use and outcomes in Africa and the Middle East. Baseline characteristics of patients newly diagnosed with nonvalvular atrial fibrillation from Lebanon (242 patients, 40.3%), Saudi Arabia (236 patients, 39.3%), United Arab Emirates (87 patients, 14.5%), and South Africa (35 patients, 5.8%) were described, and clinical outcomes were investigated for all patients in this region who received dabigatran.In newly diagnosed patients (having a diagnosis within the last three months) with nonvalvular atrial fibrillation in Africa and the Middle East, the observed uptake of non-vitamin K oral anticoagulants was high in the first years following their availability; dabigatran was the most commonly used antithrombotic agent (314/600 patients), and only 1.5% of patients did not receive any antithrombotic therapy. Use of dabigatran was associated with a high persistence rate (>88% at 24 months) and low incidence rates of stroke, myocardial infarction, major bleeding, and all-cause mortality after 2 years of follow-up. CONCLUSIONS: Data from GLORIA-AF reveal a change in the landscape for stroke prevention in the AME region, and the results were consistent with those observed in the global GLORIA-AF registry, as well as those of randomized clinical trials.Clinical Trial Registration: NCT01937377 (https://clinicaltrials.gov/ct2/show/NCT01937377).

Effects of clopidogrel on soluble CD40 ligand and on high-sensitivity C-reactive protein in patients with stable coronary artery disease.

BACKGROUND: Antiplatelet therapy with clopidogrel decreases ischemic complication especially in patients with acute coronary syndromes or after percutaneous coronary interventions. Our study was designed to test the effects of clopidogrel on soluble CD40 ligand (sCD40l) and on high-sensitivity C-reactive protein (hs-CRP) in patients with stable coronary artery disease (CAD). METHODS: This is a randomized, double-blind, placebo-controlled study. A total of 73 patients with stable CAD for > 6 months were randomized to receive either clopidogrel (loading dose 300 mg followed by 75 mg/d) for 8 weeks or placebo. Soluble CD40 ligand and hs-CRP were measured at baseline and at completion of the study. RESULTS: All patients were on aspirin therapy, and 74% were on statins. Median and interquartile ranges (IQR) of sCD40l decreased from 64 pg/mL (43-99) at baseline to 53 pg/mL (35-77) at 8 weeks (P = .03) in the clopidogrel group and remained unchanged in the placebo group (59 pg/mL, IQR 35-77 vs 55 pg/mL, IQR 35-78) (P = non significant). Levels of hs-CRP were not affected by therapy and remained unchanged in both groups. CONCLUSIONS: In patients with stable CAD, clopidogrel inhibits the release of sCD40l by platelets, which may contribute to the clinical benefit provided by this drug. This, however, does not translate in a reduction of subclinical inflammation, as measured by hs-CRP.

Duration of abnormal SPECT myocardial perfusion imaging following resolution of acute ischemia: an angioplasty model.

OBJECTIVES: This study was designed to determine how long nuclear myocardial perfusion imaging (MPI) remains abnormal following transient myocardial ischemia. BACKGROUND: Acute rest MPI identifies myocardial ischemia with a high sensitivity when the radionuclide is injected during chest pain. However, the sensitivity of this technique is uncertain when the radionuclide is injected following the resolution of symptoms. METHODS: Forty patients undergoing successful coronary angioplasty were randomized into four equal groups. Tc-99m sestamibi was injected intravenously during the last balloon inflation (acute MPI) in 30 patients and then reinjected 1, 2, or 3 h later (delayed MPI). In a fourth group, the radiopharmaceutical was injected at 15 min following balloon deflation (delayed MPI). A final injection was performed at 24 to 48 h (late MPI) in 37 patients (93%). RESULTS: A perfusion defect was detected in all 30 acute MPI studies; in 7/10 patients (70%) injected at 15 min; in 11/30 patients (37%) injected at 1, 2, or 3 h; and in 7/37 patients (19%) injected at 24 to 48 h. Perfusion scores were 13.0 +/- 9.2 on acute MPI, 5.1 +/- 2.8 at 15 min (p < 0.001 vs. acute MPI); 2.6 +/- 3.0 at 1, 2, and 3 h (p < 0.001 vs. acute MPI); and 1.3 +/- 2.4 at 24 to 48 h (p < 0.001 vs. acute MPI; p < 0.03 vs. delayed MPI). CONCLUSIONS: Myocardial perfusion imaging may remain abnormal for several hours following transient myocardial ischemia even when normal flow is restored in the epicardial coronary artery.

Effects of tirofiban and statins on high-sensitivity C-reactive protein, interleukin-6, and soluble CD40 ligand following percutaneous coronary interventions in patients with stable coronary artery disease.

This study assessed the effects of tirofiban and statins on high-sensitivity C-reactive protein, interleukin-6, and soluble CD40 ligand after percutaneous coronary intervention in patients who had stable coronary artery disease. Tirofiban insignificantly limited the increase of soluble CD40 ligand after revascularization, especially in patients who had high levels of this marker at baseline (p = 0.06), whereas statins significantly inhibited increases in interleukin-6 and, to a lesser extent, high-sensitivity C-reactive protein without affecting the soluble CD40 ligand.

Pravastatin does not affect insulin sensitivity and adipocytokines levels in healthy nondiabetic patients.

BACKGROUND: The effect of statins on insulin resistance is controversial and poorly studied in nondiabetic subjects. In addition, the effect of statins on leptin and adiponectin has never been studied. METHODS: Forty healthy nondiabetic volunteers (22 men and 18 women) aged 28 to 72 were randomized either to placebo or pravastatin 40 mg daily for a 12-week period. Insulin resistance, assessed using the Quantitative Insulin Sensitivity Check Index (QUICKI), as well as serum leptin and adiponectin levels, was measured at baseline and at the end of therapy. RESULTS: Pravastatin treatment decreased total cholesterol, low-density lipoprotein cholesterol, and triglycerides levels by 24%, 32%, and 14%, respectively ( P < .05 for all), but did not affect glucose and insulin levels, the (QUICKI) index, and adiponectin and leptin levels. When stratification was performed according to QUICKI index or sex, no significant differences were observed in the prevalues and postvalues of leptin, adiponectin, or QUICKI index in the pravastatin group. Adiponectin, leptin, and QUICKI index were statistically higher in women than in men ( P < .001 for both variables). Adiponectin was negatively correlated with body mass index (BMI; r = -0.39, P < .05) and positively correlated with the QUICKI index ( r = 0.54, P < .001) and with high-density lipoprotein cholesterol ( r = 0.50, P < .01). The relation between adiponectin and QUICKI index remained significant after adjustment for sex and BMI ( P = .005 and P = .007, respectively). Leptin was only related to BMI ( r = 0.57, P < .001) and to sex ( P < .001) with no significant correlations with lipid parameters or QUICKI index. Both sex and BMI are independent predictors of leptin ( P < .001 and P < .001). CONCLUSION: A 12-week treatment with pravastatin 40 mg/d does not change the QUICKI index and leptin and adiponectin levels in healthy volunteers. In addition, our results emphasize the importance of sex and BMI in the determination of both adiponectin and leptin. Adiponectin was also related to QUICKI index, whereas this relation was not found with leptin.

Prevalence, awareness, treatment, and control of hypertension in Lebanon.

The prevalence and factors related to hypertension (HTN) treatment and control are well investigated in the Western world but remain poorly understood in the Middle East and in middle-income countries such as Lebanon. In order to measure the prevalence, awareness, treatment, and control rates of HTN in Lebanon, the authors measured blood pressure (BP) in 1697 adults. The prevalence of optimal BP (<120/80 mm Hg) was 33% and that of pre-HTN (BP ≥120/80 mm Hg but <140/90 mm Hg) was 30%. The prevalence, awareness, treatment, and control (among treated hypertensive) rates of HTN were 36.9%, 53%, 48.9%, and 54.2%, respectively. Overall, only 27% of patients with HTN had their BP under control. Awareness was the most important predictor of treatment. No predictor of control could be identified. The authors concluded that HTN is prevalent in Lebanon and its overall control is low. Improving awareness is the most important target for intervention.

Results of primary percutaneous transluminal coronary angioplasty plus abciximab with or without stenting for acute myocardial infarction complicated by cardiogenic shock.

This study examines the effects of abciximab as adjunctive therapy in primary percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction (AMI) complicated by cardiogenic shock. Abciximab improves the outcome of primary PTCA for AMI, but its efficacy in cardiogenic shock remains unknown. Case report forms were completed in-hospital and follow-up was obtained by telephone, outpatient visit, and review of hospital readmission records. A total of 113 patients with cardiogenic shock from AMI were included. All underwent emergency PTCA during which abciximab was administered to 54 patients (48%). The 2 groups of patients who received and did not receive abciximab were similar at baseline. Coronary stents were implanted slightly more often in the abciximab group (59% vs 42%; p = 0.1). A significantly improved final TIMI flow, less no-reflow, and a decrease in vessel residual diameter stenosis occurred in the abciximab group. At 30-day follow-up, the composite event rate of death, myocardial reinfarction, and target vessel revascularization was better in the abciximab group (31% vs 63%; p = 0.002). The combination of abciximab and stents was synergistic and resulted in improvement of all components of the composite end point beyond that seen with each therapy alone. Thus, abciximab therapy improves the 30-day outcome of primary PTCA in cardiogenic shock, especially when combined with coronary stenting.

Comparison of the effects of combination atorvastatin (40 mg) + ezetimibe (10 mg) versus atorvastatin (40 mg) alone on secretory phospholipase A2 activity in patients with stable coronary artery disease or coronary artery disease equivalent.

Secretory phospholipase A2 (sPLA2) is an enzyme that plays an important role in the pathogenesis of atherosclerosis and of adverse cardiovascular events. It is currently the target of emerging therapeutic agents. Our study was designed to investigate the effect of aggressive lowering of low-density lipoprotein (LDL) cholesterol with ezetimibe and atorvastatin on sPLA2 activity. We randomized 100 patients with stable coronary artery disease (CAD) or CAD equivalent (diabetes, stroke, or peripheral vascular disease) to receive ezetimibe 10 mg/day in association with atorvastatin 40 mg/day (combination therapy group) versus atorvastatin 40 mg/day and placebo (monotherapy group). Patients on statin therapy before inclusion were allowed to enter the study as long as the potency of the statin was lower than atorvastatin 40 mg/day. Lipid profile, high-sensitivity C-reactive protein (hs-CRP), and sPLA activity were measured at baseline and after 8 weeks of therapy. The decrease in LDL cholesterol was more significant in the combination therapy group, but the decrease in hs-CRP was similar. sPLA2 activity significantly decreased in the ezetimibe/atorvastatin group from 29 U/ml (interquartile range 23 to 35) to 26 U/ml (23 to 29, p = 0.001) but remained similar in the placebo/atorvastatin group (23 U/ml, 19 to 32, vs 22 U/ml, 19 to 28, p = NS). In a multivariate stepwise linear regression model, change in sPLA2 correlated with change in hs-CRP (p <0.001), baseline LDL cholesterol level (p = 0.001), body mass index (p = 0.003), diabetes mellitus (p = 0.04) and combination therapy with ezetimibe/atorvastatin (p = 0.05). In conclusion, this study demonstrates that coadministration of ezetimibe and atorvastatin decreases sPLA2 activity.

Effect of high bolus dose tirofiban on the inflammatory response following percutaneous coronary intervention.

BACKGROUND: Tirofiban at the bolus dose of 10 microg/kg does not suppress the inflammatory response following percutaneous coronary intervention (PCI). This may be due to less than optimal inhibition of platelet aggregation. High bolus dose tirofiban (25 microg/kg) allows better inhibition of platelet aggregation but its anti-inflammatory effect remains unknown. HYPOTHESIS: High bolus dose tirofiban exhibits anti-inflammatory activity. METHODS: A total of 100 patients referred for PCI were randomized to receive high bolus dose tirofiban followed by a 24-h infusion or a bolus and an infusion of saline. Patients with elevated troponin or with thrombus in the culprit lesion were excluded. Inflammatory markers were measured at baseline and at 24 h. RESULTS: Levels of soluble CD40 ligand (sCD40L) were not affected by PCI while those of interleukin-6 (IL-6) and of high sensitivity C-reactive protein (hs-CRP) significantly increased. Despite inhibiting platelet's aggregation by > 90%, tirofiban did not suppress the rise of IL-6 and hs-CRP. Median (interquartile range) elevation of IL-6 was 0.6 pg/mL (-1.5-3.6) versus 0.4 pg/mL (-0.7-1.8) and that of hs-CRP was 2.1 mg/L (0.7-5.2) versus 2.4 mg/L (1-4.7) in the tirofiban and the control groups, respectively (p = ns). However, in patients with diabetes mellitus, tirofiban significantly suppressed the rise of hs-CRP by 65% (p = 0.01), but did not significantly affect the rise of IL-6. CONCLUSION: In low-risk patients undergoing PCI, tirofiban did not attenuate the rise of inflammatory markers. However, the significant effect in diabetics suggests that tirofiban may have anti-inflammatory activity in higher risk patients.

Effect of ezetimibe/atorvastatin combination on oxidized low density lipoprotein cholesterol in patients with coronary artery disease or coronary artery disease equivalent.

Ezetimibe is effective in providing additional low-density lipoprotein (LDL) cholesterol lowering when coadministered with statins, but its effect beyond LDL cholesterol lowering is unknown. Oxidized LDL (ox-LDL) is a better predictor of adverse cardiovascular events than standard lipid parameters. The objective of this study was to investigate the effect of ezetimibe on ox-LDL. A total of 100 patients with coronary artery disease or coronary artery disease equivalent were randomized to atorvastatin 40 mg/day and ezetimibe 10 mg/day or to atorvastatin 40 mg/day and placebo. LDL cholesterol, LDL cholesterol subfractions, and ox-LDL were measured at baseline and after 8 weeks of therapy. The ezetimibe group had a larger reduction in total LDL cholesterol compared to placebo. This was due mainly to a larger reduction in large buoyant LDL (24% vs 10%, p = 0.008). Ox-LDL level did not change in the placebo group (50 +/- 13 vs 51 +/- 13 U/L), while it decreased in the ezetimibe group, from 51 +/- 13 to 46 +/- 10 U/L (p = 0.01 vs baseline and p = 0.02 vs final level in placebo). The change in ox-LDL correlated significantly with those in total LDL and in large buoyant LDL (r = 0.6 and r = 0.5, respectively, p <0.01 for both), but not with that of small dense LDL, high-density lipoprotein, or very low density lipoprotein. In conclusion, this study demonstrates that ezetimibe decreases ox-LDL cholesterol through reductions in total LDL cholesterol and in large buoyant LDL cholesterol.