Charalampos I. Liakos

Purpose Vigorous physical activity may acutely trigger the onset of an acute coronary syndrome especially in sedentary persons with established cardiovascular risk factors such as arterial hypertension. The rupture of an inflamed coronary plaque and the activation of the coagulation cascade are the main underlying mechanisms. The present study aimed to determine the effect of acute exercise on the inflammatory and thrombotic response in patients with arterial hypertension as compared to normotensive peers. Methods After excluding patients with any inflammatory or/and coronary artery disease, a total of 60 non-treated hypertensive patients and 65 normotensive individuals underwent a maximal treadmill exercise testing. Βlood samples were drawn at rest and immediately after peak exercise. High-sensitivity C-reactive protein (hsCRP), serum amyloid A (SAA), white blood cell (WBC), interleukin-6 (IL-6), and total fibrinogen (TF) levels, as well as plasminogen activator inhibitor-1 (PAI-1) activity, were measured. Results All biomarkers increased with exercise, except PAI-1, which decreased (P < 0.05 for the change between resting and peak exercise for all biomarkers). Αfter adjusting for relevant confounders (duration of exercise, metabolic equivalents, systolic BP, and rate-pressure product achieved at peak exercise), the normotensive group had less marked (P < 0.05) exercise-induced changes than the hypertensive group in hsCRP (7.7 vs. 8.6%), SAA (5.6 vs. 11.9%), WBC (45.0 vs. 51.7%), and PAI-1 (−17.3 vs. -20.1%) and a similar (P = NS) change in IL-6 (23.8 vs. 23.0%) and TF (8.5 vs. 8.5%). Conclusion In conclusion, the acute exercise-induced inflammatory and thrombotic response seems to be more pronounced in non-treated hypertensive patients than in normotensive controls. Possible clinical implications of this finding merit further examination.

The ideal approach to the secondary dyslipidemia goal of lowering triglycerides (TG) is not well established. The available ω‐3 fatty acid products differ from each other in composition and content. The purpose of the present study was to investigate the effect of a highly purified eicosapentaenoic acid (EPA) formulation on cardiometabolic biomarkers in high cardiovascular (CV) risk patients. The study included 226 subjects with high TG and ≥1 of the following CV risk factors: arterial hypertension, diabetes mellitus, ultrasound‐documented atheromatosis, peripheral artery disease, previous myocardial infarction, or ischemic stroke. Participants received 2 g EPA twice daily for 3 months, along with typical nutritional counseling. Cardiometabolic hematological parameters (TG, low‐density lipoprotein [LDL], high‐density lipoprotein [HDL], non‐HDL, total cholesterol [TChol], apolipoprotein A₁ [Apo A₁], apolipoprotein B [Apo B], glucose, glycated hemoglobin [HbA₁c], and C‐reactive protein [CRP]) were measured at baseline and at 3 months. The mean patients' age was 61.1 ± 1.4 years and the mean baseline TG was 2.97 ± 0.15 mmol/L. Apart from Apo A₁, all other biomarkers significantly (p < 0.05) improved at 3 months, regardless of sex (except Apo B) and age: TG 1.75 ± 0.09 versus 2.97 ± 0.15 mmol/L, LDL 2.46 ± 0.08 versus 3.05 ± 0.13 mmol/L, HDL 1.22 ± 0.03 versus 1.11 ± 0.03 mmol/L, non‐HDL 3.29 ± 0.10 versus 4.14 ± 0.16 mmol/L, TChol 4.55 ± 0.10 versus 5.15 ± 0.13 mmol/L, Apo A₁ 26.8 ± 9.3 versus 22.5 ± 8.6 μmol/L, Apo B 1.25 ± 0.23 versus 1.29 ± 0.23 μmol/L, glucose 5.66 ± 0.11 versus 5.99 ± 0.17 mmol/L, HbA₁c 5.83 ± 0.1 versus 5.97 ± 0.1% and CRP 1.92 ± 0.2 versus 5.26 ± 2.8 mg/L. In conclusion, adding highly purified EPA product (4 g daily) on nutritional counseling leads to a significant TG reduction. In addition, this treatment appears to have pleiotropic beneficial cardiometabolic actions.

Background/Objective: Vigorous physical activity may acutely trigger the onset of an acute coronary syndrome especially in sedentary persons with established cardiovascular risk factors such as arterial hypertension. The rupture of an inflamed coronary plaque and the activation of the coagulation cascade are the main underlying mechanisms. The present study aimed to determine the effect of acute exercise on the inflammatory and thrombotic response in patients with arterial hypertension as compared to normotensive peers. Methods: After excluding patients with any inflammatory or/and coronary artery disease, a total of 60 non-treated hypertensive patients and 65 normotensive individuals underwent a maximal treadmill exercise testing. Βlood samples were drawn at rest and immediately after peak exercise. High-sensitivity C-reactive protein (hsCRP), serum amyloid A (SAA), white blood cell (WBC), interleukin-6 (IL-6), and total fibrinogen (TF) levels, as well as plasminogen activator inhibitor-1 (PAI-1) activity were measured. Results: All biomarkers increased with exercise, except PAI-1, which decreased (P<0.05 for the change between resting and peak exercise for all biomarkers). The normotensive group had less marked (P<0.05) exercise-induced changes than the hypertensive group in hsCRP (7.7 vs. 8.6%), SAA (5.6 vs. 11.9%), WBC (45.0 vs. 51.7%), and PAI-1 (-17.3 vs. -20.1%) and a similar (P=NS) change in IL-6 (23.8 vs. 23.0%) and TF (8.5 vs. 8.5%). Conclusion: In conclusion, the acute exercise-induced inflammatory and thrombotic response seems to be more pronounced in non-treated hypertensive patients than in normotensive controls. The effect of blood-pressure lowering treatment on the exercise-induced acute phase response remains to be elucidated.

The prevalence of arterial hypertension is high in patients with diabetes mellitus (DM). When DM and hypertension coexist, they constitute a dual cardiovascular threat and should be adequately controlled. Novel antihyperglycemic agents, including sodium-glucose co-transporter 2 (SGLT-2) inhibitors, glucagon-like peptide-1 receptor agonists (GLP-1 RAs), and dipeptidyl peptidase-4 (DPP-4) inhibitors, have recently been used in the treatment of DM. Beyond their glucose-lowering effects, these drugs have shown beneficial pleiotropic cardiovascular effects, including lowering of arterial blood pressure (BP), as acknowledged in the 2019 European Society of Cardiology/European Association for the Study of Diabetes guidelines on diabetes, prediabetes, and cardiovascular diseases. The purpose of this review was to summarize the available information on the BP-reducing effects of these new glucose-lowering drug classes and provide a brief report on underlying pathophysiological mechanisms. We also compare the three drug classes (SGLT-2 inhibitors, GLP-1 RAs, and DPP-4 inhibitors) in terms of their BP-lowering effect and show that the greater BP reduction seems to be achieved with SGLT-2 inhibitors, whereas DPP-4 inhibitors have probably the mildest antihypertensive effect.

Background/Introduction: Target organ damages (TODs) are common in hypertensive patients especially when an impaired glycaemic profile co-exists. Both hypertension and impaired glycaemic profile cause kidney damage that brings on anaemia.

Background Initiation of antihypertensive therapy with a two-drug fixed-dose combination (FDC) in a single tablet may be recommended in patients at high risk of cardiovascular events to improve adherence and effectiveness. Preferred combinations include an angiotensin-converting enzyme inhibitor with a dihydropyridine calcium antagonist. Objective This study assessed adherence to and the safety, tolerance, and effectiveness of the perindopril/amlodipine FDC in Greek patients with hypertension and stable coronary artery disease (CAD) over a 4-month period. Methods A total of 1907 patients with hypertension and CAD (59.1% males) who had recently (≤2 weeks) commenced treatment with the perindopril/amlodipine FDC (5/5, 5/10, 10/5, or 10/10 mg) were studied at baseline and at 1 and 4 months. Adherence to treatment was assessed with the Morisky Medication-taking Adherence Scale (MMAS). Results Seven patients (0.4%) did not attend the scheduled visits. In total, 1607 (84.6%) patients received a constant treatment dose throughout the study. High adherence (MMAS score = 0) was reported by 1592 (83.6%), 1628 (85.7%), and 1477 (77.7%) patients at the second and the third visit and at both visits, respectively. Adverse reactions were reported by only 13 (0.7%) patients, were all minor, and did not result in treatment discontinuation. Office blood pressure (BP) was significantly decreased at the third visit (130.8 ± 8.4/78.2 ± 6.4 mmHg) compared with baseline (156.5 ± 15.0/89.9 ± 9.6 mmHg; p < 0.001), regardless of previous antihypertensive treatment. Patients with grade 1, 2, and 3 hypertension at baseline showed a reduction in BP of 19.3/9.4, 31.5/13.5, and 47.8/22.2 mmHg, respectively (p < 0.001). Uncontrolled hypertension (≥140/90 mmHg) was notably reduced from 90.3% at baseline to 18.5% at the third visit. Conclusions The perindopril/amlodipine FDC is characterized by high adherence and effectiveness, regardless of previous treatment. Degree of BP reduction was related to baseline BP levels. Clinical trials registration number (Protocol Number): IC4 – 05985 – 011 – GRC.

Background: Contrast‐induced nephropathy (CIN) is an acute kidney injury (AKI) defined as serum creatinine (sCr) increase 48 to 72 hours after contrast administration. Because most subjects undergoing invasive cardiac procedures are discharged within 24 hours, sCr is unsuitable for CIN detection.Hypothesis: In the present study we tested the hypothesis that neutrophil gelatinase‐associated lipocalin (NGAL) is superior compared with sCr and other established nephropathy markers in early CIN diagnosis after elective invasive cardiac procedures.Methods: Serum creatinine, urine creatinine, serum cystatin C, urine albumin, urine NGAL (uNGAL), and plasma NGAL were measured at 0, 6, 24, and 48 hours after contrast administration in 100 elective invasive cardiac procedures. Estimated glomerular filtration rate and albumin‐to‐creatinine ratio were calculated. Changes from baseline were considered statistically significant at P < 0.05 and clinically significant when > the biomarker's reference change value. Participants were divided into those with and without clinically significant uNGAL changes (uNGAL positive and negative for AKI, respectively).Results: Thirty‐three individuals were uNGAL positive for AKI. Serum cystatin C changes were statistically and clinically nonsignificant in both groups. Serum creatinine and plasma NGAL were statistically but not clinically elevated 48 hours postcatheterization in the AKI group. Except for contrast volume (higher in AKI group), groups were comparable at baseline (P not significant) regarding cardiovascular risk factors, coronary heart disease, coronary interventions performed, and renal biomarkers. Baseline uNGAL was significantly correlated to estimated glomerular filtration rate and albumin‐to‐creatinine ratio.Conclusions: Urine NGAL is potentially superior compared with conventional nephropathy markers in early CIN diagnosis after elective invasive cardiac procedures. Definition of clinically significant uNGAL changes with reference change value is probably a valuable supplement to statistically defined significant variations.

The purpose of this study was to assess the role of urine α₁‐microglobulin as a marker of hypertension‐induced renal damage compared with estimated glomerular filtration rate, (eGFR), urine albumin, and urine albumin‐to‐creatinine ratio (ACR). Its response on different blood pressure (BP)–lowering drugs was also studied. Sixty never‐treated hypertensive patients (65.0% men, 46.9 years, BP 141.4/94.0 mm Hg) were randomized to an irbesartan (an angiotensin receptor blocker [ARB]) or a diltiazem (a nondihydropyridine calcium channel blocker [CCB])‐based regimen. Patients with diabetes or established cardiovascular, renal, or liver disease were excluded. Blood samples and 24‐hour urine were analyzed at baseline and 6 months after pharmaceutical BP normalization. Serum creatinine was measured and eGFR was calculated. Urine albumin, creatinine, and α₁‐microglobulin were measured and ACR was calculated. Minor changes (P=not significant [NS]) in eGFR were noted during follow‐up in both groups (from 111.0 mL/min/1.73 m² to 108.4 mL/min/1.73 m² in the ARB group and from 111.3 mL/min/1.73 m² to 114.0 mL/min/1.73 m² in the CCB group). Twenty‐four–hour urine indices were all significantly improved (P<.01) in the ARB group (albumin from 19.4 mg/L to 8.2 mg/L, ACR from 21.5 mg/g to 10.0 mg/g, α₁‐microglobulin from 5.06 mg/L to 3.64 mg/L) but not (P=NS) in the CCB group (albumin from 15.6 mg/L to 13.9 mg/L, ACR from 17.6 mg/g to 17.1 mg/g, α₁‐microglobulin from 4.94 mg/L to 4.79 mg/L). These differences between groups remained significant (P<.05) after adjusting for office heart rate and BP. α₁‐Microglobulin was significantly correlated (P<.05) with albumin and ACR both at baseline (r=0.283 and 0.299, respectively) and at the end of follow‐up (r=0.432 and 0.465, respectively) but not (P=NS) with eGFR. It was also significantly related (P<.05) to cardiovascular risk scores (Framingham and HeartScore) both at baseline (r=0.264 and 0.436, respectively) and at the end of follow‐up (r=0.308 and 0.472, respectively). Urine α₁‐microglobulin emerges as a potentially usable marker of hypertension‐induced renal impairment. Its excretion rate and its response to treatment appears similar to that of albumin. Irbesartan but not diltiazem seems to be associated with reduced excretion of α₁‐microglobulin in urine.