We are surrounded by factors called free radicals (FR), which attach to the molecules our body is made of, first among them the endothelium. Even though FR are to a certain extent a normal factor, nowadays we face an escalating increase in these biologically aggressive molecules. The escalating formation of FR is linked to the increased usage of man-made chemicals for personal care (toothpaste, shampoo, bubble bath, etc.), domestic laundry and dish-washer detergents, and also an ever wider usage of drugs (both prescription and over the counter), especially if they are to be used long-term (years). In addition, tobacco smoking, processed foods, pesticides, various chronic infectious microbes, nutritional deficiencies, lack of sun exposure, and, finally, with a markedly increasing impact, electromagnetic pollution (a terribly destructive factor), can increase the risk of cancer, as well as endothelial dysfunction, owing to the increased production of FR that they cause. All these factors create endothelial damage, but the organism may be able to repair such damage thanks to the intervention of the immune system supported by antioxidants. However, one other factor can perpetuate the state of inflammation, namely obesity and metabolic syndrome with associated hyperinsulinemia. In this review, the role of FR, with a special emphasis on their origin, and of antioxidants, is explored from the perspective of their role in causing atherosclerosis, in particular at the coronary level.

Cardiovascular drugs are widely used for the prevention and treatment of various cardiac and vascular disorders. However, some of these drugs can also cause adverse effects on the kidney, leading to acute or chronic renal dysfunction, electrolyte imbalances, and increased mortality. The mechanisms of drug-induced renal toxicity vary depending on the type and class of the drug, the dose and duration of exposure, and the patient’s characteristics and comorbidities. In this review, we summarize the current knowledge on the renal effects of some common cardiovascular drugs, such as diuretics, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, calcium channel blockers, beta-blockers, antiplatelet agents, anticoagulants, and statins and proton-pump inhibitors. We also discuss the clinical implications and management strategies for preventing or minimizing drug-induced nephrotoxicity, as well as the potential role of oxidative stress in its pathogenesis.

Background: Apical hypertrophic cardiomyopathy (ApHCM) is a rare form of hypertrophic cardiomyopathy which predominantly affects the apex of the left ventricle. The diagnosis can be challenging due to several factors, ranging from no typical clinical and electrocardiogram (EKG) findings to potential difficulties in executing and interpreting the echocardiographic examination.Case presentation: We report the case of an 84-year-old woman who came to our echo-lab to undergo a routine echocardiogram. She had a history of permanent atrial fibrillation, paced rhythm and previous episodes of heart failure (HF), allegedly explained by a diagnosis of hypertensive heart disease that had been confirmed many times over the previous 20 years. The clinical examination and the EKG were unremarkable. The echocardiographic images were poor quality. But a senior cardiologist, expert in imaging and echocardiography, noted the lack of delineation of the endocardial border of the left ventricular (LV) apex region. Contrast echocardiography was performed and severe apical hypertrophy discovered.Conclusion: ApHCM can be a challenging diagnosis. Contrast echocardiography must always be applied in cases of poor delineation of the LV apical endocardial border at baseline echocardiography. Timely detection and appropriate lifestyle intervention might slow the development of LV hypertrophy, and possibly minimize and delay heart failure (HF) related symptoms and arrhythmias. The prognosis remains relatively benign during long term follow-up.

Background: To verify whether the severity of coronary stenosis could be non-invasively assessed by enhanced transthoracic coronary echo Doppler in convergent color Doppler mode (E-Doppler TTE) over a wide range of values (from mild to severe). Methods: Color-guided pulsed wave Doppler sampling in the left anterior descending coronary artery (LAD) was performed in 103 diseased LAD segments (corresponding to 94 patients examined) as assessed by quantitative coronary angiography (QCA) or intracoronary ultrasound (IVUS). The E-Doppler TTE examinations consisted of measuring the velocity (vel) at the stenosis site and a reference adjacent segment. Then the continuity equation (C-Eq) was applied to calculate the percent cross-sectional area reduction (%CSA) at the stenosis site. The applied formula was: %CSA = 100 × (1 − [TVIref × 0.5]/TVIs). TVI = the time velocity integral at the stenosis [s] and the reference site [ref], respectively); 0.5 = the correcting factor for a parabolic profile was used only when the % accelerated stenotic flow was >122% (AsF = diastolic peak vel at first site − diastolic peak vel at second site/diastolic peak vel at second site × 100). Results: E-Doppler TTE feasibility was 100%. Doppler and QCA/IVUS-derived %CSA stenosis showed very good agreement over a large range of values (from mild to severe), with no significant bias; the maximum difference between QCA/IVUS and transthoracic Doppler %CSA was mostly around 20% with a few patients exceeding this limit (limits of agreement = −27.53 to 23.5%). The scattering was slightly larger for the non-significant stenoses. The correlation was strong (r = 0.89, p < 0.001). Conclusion: E-Doppler TTE is a feasible and reliable method for assessing the severity of LAD stenosis by applying the C-Eq.

Cardiovascular drugs are widely used for the prevention and treatment of various cardiac and vascular disorders. However, some of these drugs can also cause adverse effects on the kidney, leading to acute or chronic renal dysfunction, electrolyte imbalances, and increased mortality. The mechanisms of drug-induced renal toxicity vary depending on the type and class of the drug, the dose and duration of exposure, and the patient’s characteristics and comorbidities. In this review, we summarize the current knowledge on the renal effects of some common cardiovascular drugs, such as diuretics, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, calcium channel blockers, beta-blockers, antiplatelet agents, anticoagulants, and statins and proton-pump inhibitors. We also discuss the clinical implications and management strategies for preventing or minimizing drug-induced nephrotoxicity, as well as the potential role of oxidative stress in its pathogenesis.