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The incidence of chronic heart failure (CHF) increases with the aging of the population and with the improvement in survival of patients with hypertension, coronary heart disease and diabetes, diseases which constitute the most common causes for the development of CHF. Despite the significant improvement in the treatment of patients with CHF, mortality in recent years has improved slightly. The primary treatment method for chronic heart failure is pharmacotherapy, but it has limitations. The existing data encourages to look for new treatment methods for CHF, replacing or enhancing traditional ones while constituting a low nuisance for patients. New non-pharmacological methods, including therapies based on the use of stem cells, molecular therapy, modern devices supporting the heart such as cardiac contractility modulation, spinal cord stimulation, carotid sinus nerve stimulation, cervical and intracardiac atrioventricular nodal vagal stimulation, implantable monitoring devices and wearable cardioverter-defibrillator or the treatment of comorbid diseases such as hypertension and sleep dis- orders could be of particular importance.

Peripheral (brachial) pulse pressure normally exceeds central (aortic) pulse pressure but is a less powerful predictor of cardiovascular risk. The difference between the 2 variables, called pulse pressure amplification, has never been specifically studied between the proximal and distal aorta in coronary patients. Our goal was to determine aortic pulse pressure amplification in subjects at high coronary risk, with emphasis on associated renal and inflammatory factors. Blood pressure was measured invasively in the ascending aorta, abdominal aorta (at the level of kidneys), and iliac artery in 101 subjects (mean age, 63+/-11 years; 61 men) undergoing coronary angiography. Independently of age, sex, and the presence of coronary stenosis, the increase of pulse pressure between the ascending and terminal aorta was over 10 mm Hg (P<0.001), whereas mean blood pressure remained unchanged. Pulse pressure amplification did not differ significantly between patients with and without coronary artery stenosis. Irrespective of confounding variables, high pulse pressure measured in the ascending aorta and at the level of renal arteries (but not in the iliac artery) was independently related to proteinuria. The increase in pulse pressure from the ascending aorta to the renal level was negatively associated with leukocyte count, even after multivariate adjustment (beta coefficient, -0.19; 95% CI, -0.39 to 0.0; P<0.05). Increased plasma creatinine and aortic pulse wave velocity were independently and positively correlated (beta coefficient, 0.36; CI, 0.18 to 0.54; P<0.001). Independently of coronary atherosclerosis, aortic pulse pressure integrates the predictive value of aortic, inflammatory, and renal factors.