Silent myocardial ischaemia (SMI) is defined as objective evidence of ischaemia without angina (or equivalent symptoms) in the presence of coronary artery disease, differing from silent coronary artery disease. Silent myocardial ischaemia represents the majority of episodes of myocardial ischaemia at Holter monitoring. During transient myocardial ischaemia, the symptoms appear after the contraction anomalies of the left ventricle and after the ECG changes. The cause of silent myocardial ischaemia is still not well established. The severity and duration of ischaemia have been theorized as important elements in the SMI mechanism. Another possible mechanism responsible for SMI is represented by changes in the perception of painful stimuli with an increased pain threshold. Finally, a neuronal dysfunction of the diabetic, in post-infarction or a cardiac neuronal 'stunning' could play a role in SMI. In the pre-stent era, the SMI was associated with a worse prognosis. In patients with diabetes mellitus, SMI seems to be more represented because autonomic dysfunction is present in this category of patients. In conclusion, SMI is more frequent than symptomatic ischaemia. However, despite the presence of countless studies on the subject, it is not clear today whether medical therapy has equalized the risk and what the real prognosis of SMI is.The sodium-glucose co-transporter-2 (SGLT2) inhibitors are a new class of oral anti-diabetic drugs acting through the inhibition of renal reabsorbtion of glucose. Three important randomized clinical trial in diabetic patients receiving SGLT2 inhibitors (vs. placebo), demonstrated a significant reduction of major adverse cardiovascular events, but only in patients with known atherosclerotic disease, and a clear-cut and early reduction in hospital admissions for heart failure in patients in primary as well as secondary prevention settings. This latter information prompted the design of a recent study the DAPA-HF (Dapagliflozin And Prevention Of Adverse-outcomes In Heart Failure) trial, comparing dapagliflozin vs. placebo, and showing a significant reduction of clinical relevant episodes of heart failure in patients with reduced left ventricular ejection fraction, regardless the presence of diabetes mellitus. The mechanism by which the SGLT2 inhibitors exert their anti-heart failure action is not well understood but appears to be independent from its hypoglycaemic action. These results, along with the scarcity of adverse side effects of the drug, render dapagliflozin a new tool in the treatment of heart failure.The relationship between arterial hypertension and cognitive decline, two among the conditions with higher prevalence in the elderly population, has gained significant interest, in the scientific community, during the last few years, stemming from the numerous epidemiologic, experimental, and therapeutic evidences suggesting a non-casual correlation between the two conditions. In fact, the brain, for its substantial metabolic and functional complexity, is more susceptible to the harmful effect of high blood pressure than the other target organs. Chronic ischaemic impairment, microvascular damage, and neurodegenerative phenomena are the likely pathophysiologic basis for the correlation between hypertension and cognitive decline. Vascular dementia and Alzheimer's disease, the two prominent forms of senile dementia, seem to represent the end result of the chronic exposure, during the lifetime, to harmful stimuli, among which the most relevant are the cardiovascular risk factors, at least from an epidemiological perspective. Evidences from interventional studies, although limited, seems to support the concept that to limit the spread of senile dementia, the early optimization of the control of cardiovascular risk factors, first and foremost hypertension, is crucial. The occurrence of a variable degree of mental decline, till overt dementia, in the hypertensive patient, represents the final step of a pathophysiologic process that began many years before. There is, then, the clear opportunity to control the pathophysiologic mechanisms leading to cognitive decline in the hypertensive patient.Despite optimal medical therapies, there is currently a persistent residual cardiovascular risk. The most likely pathway responsible for this residual risk has been identified in the inflammatory state. Recent studies have confirmed that inflammation increases cardiovascular risk independently from LDL cholesterol levels. Addressing traditional risk factors, such as obesity, cigarette smoking, diabetes, arterial hypertension, and dyslipidaemia, also provides an important reduction of the levels of inflammation. Nonetheless, inflammation is also a target for specific and focused therapeutic interventions. Recent studies have outlined an association between oral hygiene, sleep deprivation, and nutritional patterns on the one hand, with the development of multi-districts atherosclerosis and/or adverse cardiovascular events on the other. These lifestyle patterns appear to be involved in fostering inflammation associated with atherosclerosis. There is, however, a persistent need for further studies to clarify whether such associations with cardiovascular disease are direct and causal, and if they are all channelled through vascular inflammation.In the percutaneous treatment of coronary stenoses, it is essential to take into account the presence of calcifications as this influences the short- and long-term post-procedural outcomes. Today in the catheterization laboratory, there are several tools for the treatment of calcium; exploiting the different operating mechanisms, possibly even combining them together, is part of a modern approach to coronary angioplasty that aims to optimize results. To this end, each procedure must be properly planned and, in this perspective, intracoronary imaging (such as optical coherence tomography and intravascular ultrasound) is an essential aid to guide the procedure and show results.High blood pressure (BP) is a leading cause of chronic kidney disease (CKD) and at the same time represents its most frequent complication. https://www.selleckchem.com/products/pluripotin-sc1.html High BP is an independent risk factor for advanced CKD; on the other hand, at least 40% of patients with normal glomerular filtration rate (GFR) and virtually all patients with GFR less then 30 mL/min are hypertensive. CKD and microalbuminuria are powerful risk factors for cardiovascular morbidity and mortality. Consequently, in uraemic hypertension, it is of utmost importance to carefully manage both high BP and microalbuminuria, in order to slow down the progression of kidney damage and to reduce the incidence of cardiovascular events. The first purpose of the medical treatment in hypertensive patients is to normalize BP, regardless of the drug used. Nevertheless, some drugs have an 'additional' nephroprotective effect at the same BP target achieved. In this regard, first-line drugs are definitely renin-angiotensin-aldosterone inhibitors, mainly for their proved efficacy in reducing hypertension-related kidney damage and proteinuria.