Polycystic ovary syndrome (PCOS), or Stein-Leventhal syndrome, is a common endocrine disorder defined by two of the three following features: i) oligoovulation or anovulation, ii) clinical and/or biochemical signs of hyperandrogenism, or iii) polycystic ovaries, once the related endocrinological and gynaecological disorders have been excluded. PCOS does not exclusively involve the reproductive apparatus , it has a complex number of systemic relevancy symptoms. It leads to Metabolic Syndrome, with severe consequences on the cardiovascular apparatus. Many clinical studies have underlined the connection between PCOS and the cardiovascular risk profile of such female patients, due to a lipid/glucose altered metabolism, hypertension, systemic inflammatory condition (assessable by markers such as VES, TNF-alfa, citokines and C-reactive protein (hsPCR) levels), and vascular injuries. Considering the early onset of the disease, PCOS could be considered as a real cardiovascular risk factor which affects the quality of life seriously. The current review aimed to point out the main connections between PCOS and cardiovascular risk factors according to the latest findings coming from literature data analysis, and try to depict the great influences that such a common disease can have on the patients’ health integrity.

The influence of thyroid hormones on cardiovascular system is well established. Thyroid diseases can effectively enhance the alteration on cardiovascular system by influencing chronotropic and inotropic actions of the heart; altering the strength and the speed of contraction, the speed of relaxation, the duration of the potential of action, and the duration of the refractory period and atrio-ventricular conduction time; modulating circulation and peripheral vascular beds. One of the more intriguing insights in the connection between thyroid diseases and cardiovascular alterations is related to the evaluation of the influence of thyroid hormones on pulmonary vascular beds. Literature reported several studies regarding the association between both hypothyroidism and hyperthyroidism and the occurrence of increased vascular pulmonary arterial pressure. Nevertheless, the pathogenetic mechanisms able to explain such relationship are not fully understood. Many doubts still persist in the comprehension of the mechanisms of pulmonary hypertension in thyroid diseases. The aim of this review was to provide possible explanation about the possible interaction between pulmonary vascular beds and thyroid function in order to evaluate the possibility of novel perspectives in the general management of patients suffering from thyroid and cardiovascular diseases.

Hyperpolarization and Cyclic Nucleotide (HCN) -gated channels represent the molecular correlates of the “funny” pacemaker current (If), a current activated by hyperpolarization and considered able to influence the sinus node function in generating cardiac impulses. HCN channels are a family of six transmembrane domain, single pore-loop, hyperpolarization activated, non-selective cation channels. This channel family comprises four members: HCN1-4, but there is a general agreement to consider HCN4 as the main isoform able to control heart rate. This review aims to summarize advanced insights into the structure, function and cellular regulation of HCN channels in order to better understand the role of such channels in regulating heart rate and heart function in normal and pathological conditions. Therefore, we evaluated the possible therapeutic application of the selective HCN channels blockers in heart rate control.

Although the survival rate for preterm subjects has improved considerably, due to the progress in the field of perinatal medicine, preterm birth is frequently the cause underlying a series of notorious complications: morphological, neurological, ophthalmological, and renal alterations. In addition, it has recently been demonstrated how low gestational age and reduced foetal growth contribute towards an increased cardiovascular risk in preterm neonates. In fact, cardiovascular mortality is higher among former preterm adults than those born at term. This condition is referred to as cardiovascular perinatal programming. In the light of the above, an early, constant, and prolonged cardiological followup programme should be implemented in former preterm individuals. The aim of this paper was to perform a comprehensive literature review about two new emerging conditions predisposing to an increased cardiovascular risk: prematurity and low weight at birth.

BackgroundPrognostic stratification of elderly patients with chronic obstructive pulmonary disease (COPD) is difficult due to the wide inter-individual variability in the course of the disease. No marker can exactly stratify the evolution and natural history of COPD patients. Studies have shown that leukocyte count is associated with increased risk of mortality in COPD patients. The aim of this study was to evaluate the possible role of relative lymphocyte count as a risk marker for mortality in elderly patients with COPD.Methods and resultsThis is a3-year prospective study. A total of 218patients, mean age 75.2±7 years, with moderate to severe COPD and free from conditions affecting lymphocyte count were enrolled. The population was divided into two groups according to the relative lymphocyte count, with a cut-off of 20%. Eighty-five patients (39%) had a relative lymphocyte count ≤20%. Three-year mortality rates from any cause in patients with relative lymphocyte count ≤ or > 20% were 68 and 51%, respectively (p = 0.0012). Survival curve analysis showed higher mortality in patients with relative lymphocyte count ≤20% (p = 0.0005). After adjustment for age and sex, the hazard ratio for mortality risk according to lymphocyte count was 1.79 (95% confidence interval [CI]: 1.26–2.57, p = 0.0013), even in the analysis limited to the 171 patients without congestive heart failure (1.63; 95% CI: 1.03–2.58, p = 0.038).ConclusionsLow relative lymphocyte count was associated with higher mortality in elderly patients with severe COPD.Electronic supplementary materialThe online version of this article (10.1186/s12890-018-0685-6) contains supplementary material, which is available to authorized users.