The role of β-adrenoceptor antagonists (β-blockers) in cardiovascular therapy has been subject to diverse trends and changes over the decades. With the advent of a wide variety of excellent drugs for the treatment of antihypertension, β-blockers have been relegated from the first-line treatment of essential hypertension. However, they remain the drugs of first choice in recommendations from the respective medical societies for heart failure, coronary artery disease, and atrial fibrillation as well as in hypertension complicated with heart failure, angina pectoris, or prior myocardial infarction. When indicated, cardioselective β-blockers should be prescribed in patients with diabetes mellitus or chronic obstructive pulmonary disease. We review the available evidence for the use of β-blockers in clinical conditions in which recommendations can be made for everyday practice.

The chemokine receptor CXCR3 and associated CXC chemokines have been extensively investigated in several inflammatory and autoimmune diseases as well as in tumor development. Recent studies have indicated the role of these chemokines also in cardiovascular diseases. We aimed to present current knowledge regarding the role of CXCR3-binding chemokines in the pathogenesis of atherosclerosis and during acute myocardial infarction.

Acute ischemic events occur most frequently at dawn and in the early hours of the morning. The development of these severe clinical events exhibits a temporal relationship with changes in various hemodynamic, prothrombotic, and hormonal processes. The authors highlight not only these relationships but also the potential protective effect of increased bradykinin levels and the inhibition of different angiotensin II (AT-II) receptors (AT2, AT4) against unfavorable prothrombotic influences, which—based on studies to date—decreases the risk of acute cardiovascular events. Comparisons are presented between the different effects of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers on factors that influence thrombus formation and myocardial infarction risk.

The aim of this study was to develop a simplified model of FFR calculation (FFR sim ) derived from three-dimensional (3D) coronary angiographic data and classic fluid dynamic equations without using finite element analysis.Methods and results: Intracoronary pressure measurements were performed by pressure wire sensors.The lumens of the interrogated vessel segments were reconstructed in 3D. The coronary artery volumetric flow was calculated based on the velocity of the contrast material. Pressure gradients were computed by classic fluid dynamic equations. The diagnostic power of the simplified computation of the FFR (FFR sim ) was assessed by comparing the results with standard invasive FFR measurements (FFR meas ) in 68 vessels with a single stenosis. We found a strong correlation between the FFR sim and the FFR meas (r=0.86, p<0.0001). The sensitivity and specificity for predicting the abnormal FFR of ≤0.80 (indicating haemodynamically significant stenosis) were 90% and 100%, respectively. The area under the curve (AUC) was 0.96. To achieve 100% negative and positive predictive values we defined the FFR sim >0.88 and the FFR sim ≤0.8 ranges. In our patient population, these ranges were found in 69% of the cases. Conclusions:According to our simplified model, the invasive FFR measurement can be omitted without misclassification in pre-specified ranges of the calculated FFR sim .

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