Background: Patients with chronic heart failure (CHF) are characterized by endothelial dysfunction, partly due to increased oxidative stress. Since folic acid exerts potential antioxidant activity, the present study was designed to evaluate the impact of folic acid supplementation on endothelial function, as well as on markers of chronic inflammation and oxidative-stress. Methods and Results: 20 patients with CHF were included in this randomized, double blind, placebo-controlled study to receive folic acid (5 mg/day) or placebo for 1 month, on top of standard optimal therapy. Despite a significant increase in plasma folate levels (from 6.9 ± 3.2 to 163.2 ± 147.7 ng/ml, p < 0.01) and a significant reduction in homocystein plasma concentration (from 14.8 ± 3.5 to 12.0 ± 2.0 mmol/L p = 0.011) in the folate-group, endothelial function, as assessed non-invasively by flow mediated vasodilatation, was not significantly affected (from 3.8 ± 1.7% to 4.1 ± 2.1%, p = 0.64). Oxidative stress and inflammation parameters did not change significantly after folate substitution. However, 4 weeks of treatment with 5 mg folic acid significantly decreased diastolic blood pressure (DBP) as compared to baseline from 76.1 ± 12.2 to 69.5 ± 7.2mmHg; p = 0.03). A not-significant decrease in systolic blood pressure (SBP) was also observed (from 115 ± 10.5 to 111 ± 12.8mmHg; p = 0.06). There was no change in blood pressure after placebo (SBP from 113.8 ± 8.9 to 116 ± 5.1mmHg, p = 0.36 DBP from 68.9 ± 7.2 to 71.0 ± 6.9mmHg p = 0.13). Conclusion: Chronic treatment with folic acid (5 mg/day) over one month did not improve endothelial function and oxidative as well as inflammatory parameters in patients with CHF. However a significant reduction in arterial blood pressure has been observed.

Background: Recent data demonstrates beneficial effect of cocoa on cardiovascular health, especially on vascular and platelet function, as well as on blood pressure and insulin resistance, most likely due to an increase in nitric oxide (NO) bioavailability. Patients with congestive heart failure (CHF) are characterized by impaired endothelial and platelet function and an increase in oxidative stress. Therefore flavonoid-rich cocoa has the potential to positively affect vascular function in these patients. Methods and Results: In this double blind, randomized trial, we prospectively assessed, the effect of flavonoid-rich, commercially available, dark chocolate on endothelial and platelet function in 20 patients with congestive heart failure in the short-term (2 hours after ingestion of 40 g) and in the long-term (4 weeks, 80 g daily). Endothelial function was assessed non-invasively by flow-mediated vasodilatation (FMD) of the brachial artery. FMD significantly improved from 4.98 ± 1.95 to 6.86 ± 1.76% after 2 hours, as well as after chronic treatment for 4 weeks (from 4.98 ± 1.95 to 6.86 ± 1.76%). Cocoa-free chocolate had no effect. Platelet adhesion significantly decreased from 3.9 ± 1.32 to 2.99 ± 1.31% after 2 hours, but remained unchanged after 4 weeks. Conclusion: Flavonoid-rich chocolate acutely and chronically improves vascular function in patients with CHF. These beneficial effects were paralleled by a significant short-term effect on platelet adhesion.

The endocannabinoid system is a physiological system, which is responsible for the control of glucose and lipid-metabolism, as well as for the regulation of the body weight. The endocannabinoid receptors are distributed both in the central and peripher nervous system. Different studies provide evidence that an hyperactive endocannabinoid system is involved in the development of different cardiovascular risk factors. The pharmacological blockade of these cannabinoid receptors may represent a new approach for cardiometabolic risk management.

Das Endocannabinoidsystem ist ein physiologisches System, welches unter anderem für die Kontrolle des Energiegleichgewichtes, den Glukose- und Lipidmetabolismus sowie für die Regulation des Körpergewichtes verantwortlich ist. Die Endocannabinoid- Rezeptoren sind sowohl im zentralen Nervensystem als auch in der Peripherie verteilt. Durch verschiedene Studien wird belegt, dass ein hyperaktives Endocannabinoidsystem für die Entwicklung verschiedener kardialer und metabolischer Risikofaktoren von Bedeutung ist. Die medikamentöse Blockierung des Cannabinoid-1- Rezeptors kann einen neuen Ansatz zur Beeinflussung von kardiometabolischer Risikofaktoren darstellen.

Introduction.Recent studies raised the question about cardiovascular safety of selective cyclooxygenase (COX)-2 inhibitors and traditional non-steroidal anti-inflammatory drugs (NSAIDs), in patients with coronary artery disease in particular.Physicians now frequently use paracetamol instead of NSAIDs, despite its weaker analgesic effect, because this drug is considered to be cardiovascular safe.However, data prospectively addressing cardiovascular safety of paracetamol are still lacking.Aim.To evaluate the impact of paracetamol on 24-hour ambulatory blood pressure monitoring (ABPM) and endothelial function.Methods.24 patients with coronary artery disease were included in this randomized, double-blind, crossover study.Patients received paracetamol (3x1g/d) for 2 weeks followed by placebo or vice versa on top of standard cardiovascular therapy.Between the 2 treatment periods a 2-week washout period was scheduled.At baseline and after each treatment period, endothelial function, as assessed by flowmediated dilation of the brachial artery and ABPM were obtained.Results.Treatment with acetaminophen resulted in a significant increase of systolic (SBP, from 120.1±11.7 to 122.4±12.3mmHg,p=0.03) and diastolic (DBP, from 72.2±7.4 to 74±8.6mmHg, p=0.04) 24-hour BP and heart rate (HR, from 65.8±7.5 to 68.1±8.1 b/min p=0.04), whereas there was no change after placebo (SBP from 120.4±11.7 to 120.1±10.2;and DBP from 73.1±7.6 to 72.7±6.6mmHg,HR from 66.6±8.65 to 68±8.1 b/min, p=ns for all parameters).No significant change in flow-mediated and in nitroglycerin-induced vasodilation was observed after paracetamol and placebo.Conclusions.This study for the first time demonstrates that paracetamol induces a significant increase in 24-hour blood pressure and heart rate in patients with coronary artery disease indicating that careful risk benefit analysis needs to be undertaken for all anti-inflammatory agents

Bei Patienten mit arterieller Hypertonie liegt eine Endotheldysfunktion vor. Eine reduzierte Verfügbarkeit von gefäßerweiterndem Stickstoffmonoxid (NO) sowie ein Überschuss an vasokonstriktiven Substanzen (z. B. Endothelin oder Angiotensin II) sind als Ursache der gestörten endothelabhängigen Vasodilatation anzusehen. Das Vorhandensein einer Endotheldysfunktion korreliert mit kardiovaskulären Ereignissen und hat auch prognostische Bedeutung. Die Reduktion des Blutdrucks per se ist nicht ausreichend, um die Endothelfunktion zu verbessern. Die verschiedenen Substanzklassen der Antihypertensiva beeinflussen die Gefäßfunktion in unterschiedlicher Art und Weise.