Giornale italiano di cardiologia最新文献

Due to the growing evidence of clinical benefits conferred by the reduction of low-density lipoprotein cholesterol (LDL-C) levels, the availability of multiple effective lipid-lowering agents, and guideline recommendations, clinicians not infrequently have to manage patients with low or very low LDL-C levels. In clinical practice it is essential to consider that, when LDL-C plasma concentrations are low, the Friedewald formula commonly used for LDL-C level calculation is less accurate, hence risk assessment should be integrated by using different methods for LDL-C level quantification and other parameters, such as non-high-density lipoprotein cholesterol and, where possible, apolipoprotein B, should be measured. As regards the clinical impact of low LDL-C levels, genetically determined hypocholesterolemia forms provide reassuring data on the effects of this condition in the long term, except for the forms with extremely low or undetectable LDL-C levels. Evidence from clinical studies that used highly effective lipid-lowering drugs, such as proprotein convertase subtilisin/kexin type 9 inhibitors, goes in the same direction. In these studies, the incidence of non-cardiovascular adverse events in patients who reached very low LDL-C levels was similar to that in the placebo arm. Overall, the fear of adverse effects should not deter intensive lipid-lowering treatment when indicated to reduce the risk of cardiovascular events.

More than 50 years after its introduction in clinical practice, the increase in the intensity of care offered by the cardiac intensive care units, the shift in the population of patients treated and the wider availability of circulatory supports, still makes the pulmonary artery catheter (PAC) an essential tool for diagnosis, monitoring and prognosis in patients suffering from cardiogenic shock. In this review, we will discuss how to identify those patients who can benefit most from its use, the configuration and the correct insertion technique of a PAC. A pragmatic guide will also be provided for the interpretation of the hemodynamic indexes (direct and calculated) that the PAC is able to reveal as well as a summary of the most common errors in reading or interpreting the pressure curves provided by the PAC. In this article, we will then present a practical guide on how to use the PAC in a modern cardiac intensive care unit.

Hypertension does not recognize obvious pathogenic causes in the majority of patients (essential hypertension). However, a secondary underlying cause of hypertension can be recognized in 5-10% of unselected hypertensive patients, and this prevalence may increase to more than 20% in patients with hypertension that is difficult to control or frankly resistant to treatment. In children, secondary hypertension is most often due to aortic coarctation, distal thoracic or abdominal aortic stenosis, or specific gene mutations. In adults or elderly individuals, secondary hypertension is most often due to atherosclerotic renal artery stenosis, primary hyperaldosteronism, and Cushing's disease or syndrome. Parenchymal nephropathy and hyperparathyroidism can cause hypertension at all ages, while pheochromocytoma and paraganglioma tend to occur more often in adolescents or young adults. In general, secondary hypertension should be suspected in subjects with: (a) onset of hypertension under 30 years of age especially if in the absence of hypertensive family history or other risk factors for hypertension; (b) treatment-resistant hypertension; c) severe hypertension (>180/110 mmHg), malignancy, or hypertensive emergencies; d) rapid rise in blood pressure values in previously well controlled patients. Any clinical signs suspicious or suggestive of hypertension from endocrine causes, a "reverse dipping" or "non-dipping'" profile at 24 h ambulatory blood pressure monitoring not justified by other factors, signs of obvious organ damage may be helpful clues for diagnosis. Finally, patients snoring or with clear sleep apnea should also be considered for possible secondary hypertension.

Sudden cardiac arrest/death in pediatric patients is a rare but potentially preventable event. Cardiomyopathies and channelopathies are the most common causes which are detectable with ECG and transthoracic echocardiography in asymptomatic subjects. Coronary artery anomalies are a rare cause of sudden cardiac arrest/death, but these events suggest that ECG and echocardiography, focused on the site of origin of the coronary arteries, should be both part of the screening tool of young athletes. Finally, the rare cardiac arrest events in young patients with ventricular preexcitation without prior symptoms or markers of high risk suggest that transcatheter ablation should be considered in all pediatric patients with ventricular preexcitation because it can eliminate the small long-term risk of sudden cardiac arrest/death, but a careful consideration of the most appropriate timing is mandatory.

Although mitral annular calcification is a common degenerative condition of the fibrous mitral annulus, tricuspid annular calcification, especially isolated, is rare. We report the case of a 73-year-old male, with a history of hypertension and severe kyphoscoliosis, referred to the emergency department for progressive dyspnea and leg swelling. Echocardiography revealed a dilated right heart with a homogeneous, hyperechoic, crescent shaped mass along the tricuspid annulus. Computed tomography confirmed the calcific nature of the lesion. Right heart catheterization revealed mild pre-capillary pulmonary hypertension and a mild spirometrically-defined restrictive ventilatory defect. Kyphoscoliosis has recently been associated with alterations in cardiac deformation and with an increased risk of restrictive lung disease. In our patient, we hypothesized that both these anomalies could have led to premature tricuspid annular degeneration resulting in a giant tricuspid calcification.

Although there is substantial evidence on the harmful effects of air pollution on human health, these are scarcely considered in the general clinical practice and also in the context of cardiovascular disease prevention. In light of the numerous epidemiological and basic research studies that have demonstrated the unfavorable impact of air pollution on the cardiovascular system, this review aims to bring this aspect to the attention of clinicians. This work describes the main air polluting components that can contribute to the onset and progression of cardiovascular diseases. The pathophysiological mechanisms underlying the impact of pollutants on the cardiovascular system and the available evidence regarding their effect on cardiovascular risk factors are reported. This article also examines the evidence relating to the correlation between environmental pollutants and some specific cardiovascular diseases, including acute coronary syndromes, cerebrovascular diseases, heart failure, and arrhythmias. Finally, the possible strategies to be implemented to limit pollution-induced cardiovascular damage are analyzed.