Short-term prognosis of patients with acute coronary syndromes through the evaluation of physical activity status, the adoption of Mediterranean diet and smoking habits: the Greek Acute Coronary Syndromes (GREECS) study.

PURPOSE: Our aim was to evaluate whether healthy dietary habits, physical activity and non-smoking are associated with less severe acute coronary syndromes and better short-term prognosis. SUBJECTS AND METHODS: From October 2003 to September 2004, 2172 patients (1649 males), hospitalized for severe acute coronary syndromes in six major hospitals in Greece were included in the study. The severity of severe acute coronary syndromes was assessed through troponin-I and maximum creatinine kinase MB levels, while 30-day recurrent event rate (death or rehospitalization for cardiovascular disease, angioplasty or coronary artery bypass surgery) was used to evaluate the prognosis of the patients. A 'healthy index' that assessed adherence to the Mediterranean diet, moderate alcohol intake, physical activity and abstinence from smoking was developed (range 0-4). RESULTS: One unit increment in the healthy index was associated with -12.4+/-2.4 ng/ml decrease in troponin I levels (P=0.001) and -9.7+/-2.5 ng/ml decrease in maximum creatinine kinase MB levels (P=0.001). The in-hospital mortality rate was 3.2% in males and 5.7% in females (i.e. overall 82 deaths, P=0.009); during the first 30 days following hospitalization the event rate was 15.7% in males and 16.3% in females (P=0.001). Values of the healthy index above one (i.e. presence of two or more protective factors) seemed to be associated with 44-84% lower risk of having recurrent events (P<0.001), even after various adjustments were made. CONCLUSION: Among patients who had had severe acute coronary syndromes, a healthy lifestyle seemed to be associated with less severe cardiac events and lower risk of death or rehospitalization 30 days after the event.     

Impact of type 2 diabetes mellitus on diffuse inflammatory activation of de novo atheromatous lesions: Implications for systemic inflammation

AimsLocal coronary and systemic inflammation is pronounced in patients with diabetes mellitus (DM). Intracoronary thermography detects local inflammation and C-reactive protein (CRP) is a marker of systemic inflammation. We investigated whether or not, in patients with DM, thermal heterogeneity of culprit lesions (CLs) correlates with that of non-culprit lesions (NCLs) and with systemic inflammation.MethodsWe included DM patients who had two angiographically significant lesions and were undergoing percutaneous coronary intervention. We measured the temperature difference (ΔT) between the lesion and proximal vessel wall.ResultsWe included 104 (n = 208 lesions) patients: 32 (n = 64 lesions) had DM and 72 (n = 144 lesions) were non-DM (control group). ΔT was increased in DM in both CLs and NCLs (CLs: DM = 0.12 ± 0.06 °C; no DM = 0.06 ± 0.04 °C; P < 0.01 versus NCLs: DM = 0.13 ± 0.08 °C versus no DM = 0.06 ± 0.05 °C; P < 0.01). Patients with DM had similar ΔT in CLs and NCLs (P = 0.49). A linear correlation was detected between heat production in all lesions and CRP (R = 0.45; P < 0.01), which was attributed to the correlation of ΔT in lesions of patients with DM and CRP (R = 0.32; P < 0.01). In lesions of patients with low CRP, a greater rate of discrepancy was found, as 100% of lesions in patients with DM versus 66.1% of lesions of patients without DM had a high ΔT in one or both lesions (P < 0.01).ConclusionIn patients with DM, local inflammatory activation is diffuse and correlates with systemic inflammation. However, low systemic inflammatory activation does not always predict an increase in local thermal heterogeneity.     

α<Subscript>2β</Subscript> adrenoreceptor 301–303 deletion polymorphism in polycystic ovary syndrome

α_2β adrenoreceptor 301–303 deletion polymorphism does not influence basal metabolic rate, insulin resistance or weight gain in Greek women with polycystic ovary syndrome.     

Vascular endothelium and inflammatory process, in patients with combined Type 2 diabetes mellitus and coronary atherosclerosis: the effects of vitamin C.

AIMS: Type 2 diabetes mellitus (DM) and coronary artery disease (CAD) are both associated with endothelial dysfunction and elevated oxidative and inflammatory state. We examined the effect of vitamin C on endothelial function and levels of soluble vascular cell adhesion molecule (sVCAM-1), interleukin-6 (IL-6) and tumour necrosis factor (TNF-alpha), in DM patients with or without CAD and in non-diabetic subjects. METHODS: Thirty-seven patients with DM + CAD, 17 patients with DM without CAD and 21 non-diabetic subjects were divided into groups receiving vitamin C 2 g/day or no anti-oxidant for 4 weeks. Forearm blood flow was determined using venous occlusion gauge-strain plethysmography. Forearm vasodilatory response to reactive hyperemia was considered as index of endothelium-dependent dilation. RESULTS: Baseline levels of IL-6 and TNF-alpha were significantly higher in patients with DM + CAD compared with patients with DM (P < 0.01) or non-diabetic subjects (P < 0.01). IL-6 and TNF-alpha levels were also higher in DM compared with non-diabetic subjects (P < 0.05). sVCAM-1 levels were lower in non-diabetic controls compared with DM + CAD (P < 0.05) or DM (P < 0.05). Reactive hyperaemia was higher in non-diabetic controls compared with DM + CAD (P < 0.001) or DM (P < 0.001). Vitamin C significantly increased reactive hyperaemia only in the DM + CAD group, while it had no effect on serum levels of sVCAM-1, TNF-alpha and IL-6 in any of the groups. CONCLUSIONS: Type 2 diabetes mellitus is associated with impaired endothelial function and increased levels of TNF-alpha, IL-6 and sVCAM-1, especially in patients with DM and CAD. Vitamin C significantly increased forearm vasodilatory response to reactive hyperaemia only in patients with combined DM and CAD.     

Apolipoprotein E polymorphism is not associated with lipid levels and coronary artery disease in Greek patients with familial hypercholesterolaemia

Abstract Familial hypercholesterolaemia is a genetic disorder characterised by high low-density lipoprotein (LDL) cholesterol concentrations, which frequently gives rise to premature coronary artery disease (CAD). The clinical expression of familial hypercholesterolaemia is highly variable even in patients carrying the same LDL receptor gene mutation. This variability may be due to environmental and other genetic factors. Apolipoprotein E (Apo-E) has been extensively studied for its effects on the phenotype of familial hypercholesterolaemia. In this study we examined the influence of Apo-E genotype on lipid parameters and the incidence of CAD in 93 Greek patients with familial hypercholesterolaemia. Apo-E E2, E3 and E4 allele frequencies were 0.06, 0.86 and 0.09 respectively. The levels of total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides, apolipoproteins A and B and lipoprotein α did not differ significantly among carriers and non-carriers of the E4 allele. The prevalence of CAD and hypertension did not differ either. Our results suggest that the E4 allele is not associated with lipid levels or with the prevalence of CAD among familial hypercholesterolaemia patients of the Greek population. *The two authors were equally involved in the work     

Climatological variations in daily hospital admissions for acute coronary syndromes

OBJECTIVE: We examined the association between climatologic parameters and daily admissions for non-fatal acute coronary syndromes (ACS) to emergency units of hospitals in the greater Athens area, from January 2001 to August 2002. METHODS: Daily mean, maximum and minimum temperatures, relative humidity, wind speed, barometric pressure and a thermo-hydrological index (T.H.I.) were measured at the meteorological station of the Laboratory of Climatology of the Geology Department of the University of Athens. In addition, the daily number of admissions for acute myocardial infarction or unstable angina in the five major general hospitals in the greater Athens area was recorded. Generalized additive models (GAM) were applied to regress-time-series of daily numbers of outpatients with acute cardiac events against climatological variations, after controlling for possible confounders and adjustment for over dispersion and serial correlation. RESULTS: Five thousand four hundred fifty-eight Athenians with non-fatal acute cardiac events were admitted to the selected hospitals during the period of the study, 4093 (75%) males and 1365 (25%) females. There was a negative correlation between hospital admissions and mean daily temperature (MDT) with a 1 degrees C decrease in mean air temperature yielding a 5% increase in hospital admissions (P<0.05). This association was stronger in females and the elderly (P<0.01). Relative humidity was positively correlated with hospital admissions (P<0.05). CONCLUSION: Despite the relatively short study period (<2 years), these findings suggest a significant association between cold weather and increased coronary heart disease incidence, especially in the elderly and females.     

Cardiovascular efficacy and safety of dipeptidyl peptidase-4 inhibitors: A meta-analysis of cardiovascular outcome trials

BACKGROUND Dipeptidyl peptidase-4(DPP-4) inhibitors are a generally safe and well tolerated antidiabetic drug class with proven efficacy in type 2 diabetes mellitus(T2 DM). Recently, a series of large, randomized controlled trials(RCTs) addressing cardiovascular outcomes with DPP-4 inhibitors have been published.AIM To pool data from the aforementioned trials concerning the impact of DPP-4 inhibitors on surrogate cardiovascular efficacy outcomes and on major cardiac arrhythmias.METHODS We searched PubMed and grey literature sources for all published RCTs assessing cardiovascular outcomes with DPP-4 inhibitors compared to placebo until October 2020. We extracted data concerning the following "hard" efficacy outcomes: fatal and non-fatal myocardial infarction, fatal and non-fatal stroke, hospitalization for heart failure, hospitalization for unstable angina, hospitalization for coronary revascularization and cardiovascular death. We also extracted data regarding the risk for major cardiac arrhythmias, such as atrial fibrillation, atrial flutter, ventricular fibrillation and ventricular tachycardia.RESULTS We pooled data from 6 trials in a total of 52520 patients with T2 DM assigned either to DPP-4 inhibitor or placebo. DPP-4 inhibitors compared to placebo led to a non-significant increase in the risk for fatal and non-fatal myocardial infarction [risk ratio(RR) = 1.02, 95%CI: 0.94-1.11, I2 = 0%], hospitalization for heart failure(RR = 1.09, 95%CI: 0.92-1.29, I2 = 65%) and cardiovascular death(RR = 1.02, 95%CI: 0.93-1.11, I2 = 0%). DPP-4 inhibitors resulted in a non-significant decrease in the risk for fatal and non-fatal stroke(RR = 0.96, 95%CI: 0.85-1.08, I2 = 0%) and coronary revascularization(RR = 0.99, 95%CI: 0.90-1.09, I2 = 0%), Finally, DPP-4 inhibitors demonstrated a neutral effect on the risk for hospitalization due to unstable angina(RR = 1.00, 95%CI: 0.85-1.18, I2 = 0%). As far as cardiac arrhythmias are concerned, DPP-4 inhibitors did not significantly affect the risk for atrial fibrillation(RR = 0.95, 95%CI: 0.78-1.17, I2 = 0%), while they were associated with a significant increase in the risk for atrial flutter, equal to 52%(RR = 1.52, 95%CI: 1.03-2.24, I2 = 0%). DPP-4 inhibitors did not have a significant impact on the risk for any of the rest assessed cardiac arrhythmias.CONCLUSION DPP-4 inhibitors do not seem to confer any significant cardiovascular benefit for patients with T2 DM, while they do not seem to be associated with a significant risk for any major cardiac arrhythmias, except for atrial flutter. Therefore, this drug class should not be the treatment of choice for patients with established cardiovascular disease or multiple risk factors, except for those cases when newer antidiabetics(glucagon-like peptide-1 receptor agonists and sodium-glucose cotransporter-2 inhibitors) are not tolerated, contraindicated or not affordable for the patient.     

Vulnerable plaque: the challenge to identify and treat it

In order to understand, treat, and prevent acute coronary syndromes we need to improve our ability to identify the rupture-prone, vulnerable atherosclerotic coronary plaque. The diagnostic modalities that are currently available to clinical practice have not fulfilled this expectation, and newer diagnostic techniques based on the recently identified features of the vulnerable plaque are quite promising. Coronary angiography, intravascular ultrasound, and angioscopy have been used in the clinical arena of interventional cardiology with several limitations regarding the identification of the vulnerable plaque. Thermography, optical coherence tomography, elastography, Raman spectroscopy, and infrared spectroscopy are used in clinical trials and the results are encouraging. Ultrafast computed tomography and magnetic resonance imaging have the advantage of being noninvasive. With our progress in the identification of the rupture-prone vulnerable coronary plaque, we will be able to identify patients that are at high risk and will benefit from a more aggressive therapeutic approach.     

Diverse associations of microalbuminuria with C-reactive protein, interleukin-18 and soluble CD 40 ligand in male essential hypertensive subjects

BACKGROUND: Microalbuminuria (MA) and low-grade inflammation constitute emerging markers of subclinical atherosclerosis. We investigated whether urinary albumin excretion, expressed as the albumin-to-creatinine ratio (ACR), is associated with high sensitivity C-reactive protein (hs-CRP), interleukin (IL)-18, and soluble CD40 ligand (sCD40L), in hypertensive subjects. METHODS: The study population consisted of 108 nondiabetic male patients with newly diagnosed untreated stage I to II essential hypertension (aged 44.6 years, office blood pressure [BP] 148/95 mm Hg). According to ACR values determined as the average of two nonconsecutive overnight spot urine samples, subjects were divided into microalbuminurics (n = 28) (mean ACR = 30 to 300 mg/g) and normoalbuminurics (n = 80) (mean ACR <30 mg/g). RESULTS: Although microalbuminurics as compared to normoalbuminuric hypertensives had greater hs-CRP levels (2.55 +/- 1.18 v 1.45 +/- 0.52 mg/L, P < .0001), independently of confounding factors, these two groups did not differ regarding IL-18 and sCD40L values (P = not significant [NS] for both cases). In the entire population, ACR exhibited a positive correlation with hs-CRP (r = 0.623, P < .0001), whereas there was no association with both IL-18 and sCD40L (P = NS for both cases). When multiple linear regression analysis was performed, it was revealed that age, body mass index, office systolic BP, total cholesterol, and hs-CRP levels were significant independent predictors of the ACR (P < .05). CONCLUSIONS: In essential hypertensive subjects, MA is accompanied by elevated hs-CRP levels, but not by augmented IL-18 and sCD40L concentrations, suggesting activation of different inflammatory pathways in the progression of renal and cardiovascular atherosclerotic disease. The pathophysiologic mechanisms of these associations remain to be further elucidated in future studies.     

Association between TNF-alpha -308G>A polymorphism and the development of acute coronary syndromes in Greek subjects: the CARDIO2000-GENE Study.

PURPOSE: We investigated the association of a polymorphism within the promoter of TauNuF-alpha locus at the position -308 on the likelihood of having acute coronary syndromes (ACS) in Greek adults. METHODS: We studied demographic, lifestyle, and clinical information in 237 hospitalized patients (185 males) with a first event of an ACS and 237 matched by age and sex (controls) without any clinical evidence of coronary heart disease. Genotyping was performed by PCR-RFLP analysis. RESULTS: The genotype frequencies were in patients, 87% (n = 206), 12% (n = 29), and 1% (n = 2) for G/G, G/A, and A/A, and in controls, 96% (n = 227), 4% (n = 10), and 0% (n = 0) for G/G, G/A, and A/A, respectively (P = 0.04). After adjusting for age and sex, as well as various potential confounders, we observed that G/A or A/A genotypes were associated with 1.94-fold higher odds (95% CI 1.06 to 3.68) of ACS compared to G/G homozygotes. No gene to-gender or to-clinical syndrome interactions were observed. Further subgroup analysis showed that the distribution of TNF-alpha -308G>A polymorphism was associated with the presence of family history of CHD in patients, but not in controls. In particular, in G/A and A/A patients 17.2% reported family history of CHD, whereas in G/G patients, 34.5% reported family history (P = 0.036). CONCLUSIONS: Our findings may state a hypothesis of an association between the -308G>A TNF-alpha polymorphism the development of ACS and the presence of family history of CHD, in Greece.