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Arterial hypertension and stroke are strong independent risk factors for the development of cognitive impairment and dementia. Persistently elevated blood pressure (BP) is known to impair cognitive function, however onset of new cognitive decline is common following a large and multiple mini strokes. Among various forms of dementia the most prevalent include Alzheimer’s disease (AD) and vascular dementia (VaD) which often present with similar clinical symptoms and challenging diagnosis. While hypertension is the most important modifiable vascular risk factor with antihypertensive therapy reducing the risk of stroke and potentially slowing cognitive decline, optimal BP levels for maintaining an ideal age-related mental performance are yet to be established. Cognition has improved following the use of at least one representative agent of the major drug classes with further neuroprotection with renin angiotensin inhibitors and calcium channel blockers in the hypertensive elderly. However, a reduction in BP may worsen cerebral perfusion causing an increased risk of CV complications due to the J-curve phenomenon. Given the uncertainties and conflicting results from randomized trials regarding the hypertension management in the elderly, particularly octogenarians, antihypertensive approaches are primarily based on expert opinion. Herein, we summarize available data linking arterial hypertension to cognitive decline and antihypertensive approach with potential benefits in improving cognitive function in elderly hypertensive patients.

Trimethylamine-N-oxide (TMAO) has been suggested as a marker and mediator of cardiovascular diseases. However, data are contradictory, and the mechanisms are obscure. Strikingly, the role of the TMAO precursor trimethylamine (TMA) has not drawn attention in cardiovascular studies even though toxic effects of TMA were proposed several decades ago. We assessed plasma TMA and TMAO levels in healthy humans (HH) and cardiovascular patients qualified for aortic valve replacement (CP). The cytotoxicity of TMA and TMAO in rat cardiomyocytes was evaluated using an MTT test. The effects of TMA and TMAO on albumin and lactate dehydrogenase (LDH) were assessed using fluorescence correlation spectroscopy. In comparison to HH, CP had a two-fold higher plasma TMA (p < 0.001) and a trend towards higher plasma TMAO (p = 0.07). In CP plasma, TMA was inversely correlated with an estimated glomerular filtration rate (eGFR, p = 0.002). TMA but not TMAO reduced cardiomyocytes viability. Incubation with TMA but not TMAO resulted in the degradation of the protein structure of LDH and albumin. In conclusion, CP show increased plasma TMA, which is inversely correlated with eGFR. TMA but not TMAO exerts negative effects on cardiomyocytes, likely due to its disturbing effect on proteins. Therefore, TMA but not TMAO may be a toxin and a marker of cardiovascular risk.

H ypertension contributes significantly to the high cardiovascular morbidity and mortality rates worldwide. While acknowledging the complexity and multifactorial pathogenesis of hypertension, it has been suggested that activation of the sympathetic nervous system (SNS) is an important contributor in at least 50% of cases.1 Persistent sympathetic activation initiates and sustains elevated blood pressure (BP) via various pathways, including renal (sodium and water retention), humoral (activation of the renin-angiotensin system), peripheral (vasoconstriction), and other mechanisms. 1 Sustained sympathetic activation has also been closely linked to a range of clinical adverse consequences, such as left ventricular hypertrophy, progression of renal disease, and others. Catheter-based renal denervation (RDN) is a relatively novel therapeutic approach used primarily in the context of resistant hypertension aimed at targeting sympathetic overactivity commonly encountered in these patients. 2 Indeed, we and others have demonstrated that RDN reduces both renal sympathetic activity (by ≤42% in obese hypertensive dogs and by ≤47% in patients with resistant hypertension 3,4 ) and muscle sympathetic nerve Abstract-Overactivation of renal sympathetic nervous system and low-grade systemic inflammation are common features of hypertension. Renal denervation (RDN) reduces sympathetic activity in patients with resistant hypertension. However, its effect on systemic inflammation has not been examined. We prospectively investigated the effect of RDN on monocyte activation and inflammation in patients with uncontrolled hypertension scheduled for RDN. Ambulatory blood pressure, monocyte, and monocyte subset activation and inflammatory markers were assessed at baseline, 3 months, and 6 months after procedure in 42 patients. RDN significantly lowered blood pressure at 3 months (150.5±11.2/81.0±11.2 mm Hg to 144.7±11.8/77.9±11.0 mm Hg), which was sustained at 6 months (144.7±13.8/78.6±11.0 mm Hg). Activation status of monocytes significantly decreased at 3 months (P<0.01) and 6 months (P<0.01) after the procedure. In particular, classical monocyte activation was reduced at 6 months (P<0.05). Similarly, we observed a reduction of several inflammatory markers, including monocyte-platelet aggregates (3 months, P<0.01), plasma monocyte chemoattractant protein-1 levels (3 months, P<0.0001; 6 months, P<0.05), interleukin-1β (3 months, P<0.05; 6 months, P<0.05), tumor necrosis factor-α (3 months, P<0.01; 6 months, P<0.05), and interleukin-12 (3 months, P<0.01; 6 months, P<0.05). A positive correlation was observed between muscle sympathetic nerve activity and monocyte activation before and after the procedure. These results indicate that inhibition of sympathetic activity via RDN is associated with a reduction of monocyte activation and other inflammatory markers in hypertensive patients. These findings point to a direct interaction between the inflammatory and sympathetic nervous system, which is of central relevance for the understanding of be...

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Background A large number of chemotherapy‐induced cardiovascular complications were discovered in studies over the last several decades. The focus of the majority of these studies was left ventricular (LV) remodeling. The aim of this article was to provide a comprehensive overview of potential mechanisms of chemotherapy‐induced right ventricular (RV) remodeling and summarize clinical studies on this topic. Hypothesis Chemotherapy induces RV structural, functional, and mechanical changes. Methods We searched PubMed, MEDLINE, Ovid and Embase databases for studies published from January 1990 up to September 2016 in the English language using the following keyword “chemotherapy,” “heart,” “right ventricle,” “anthracyclines,” and “trastuzumab.” Results The existing research show that RV remodeling occurs simultaneously with LV remodeling, which is why RV remodeling should not be neglected in the overall cardiac assessment of patients treated with chemotherapy, and especially those protocols that involve anthracyclines and trastuzumab. Investigations showed that these agents could significantly impact RV structure, function, and mechanics. These medications induce fibrosis of the RV myocardium, RV dilatation, decline in RV systolic function, worsening of its diastolic function, and finally impairment of RV mechanics (strain). The mechanisms of chemotherapy‐induced RV remodeling are still not entirely clear, but it is considered that direct destructive influence of chemotherapy on myocardium, oxidative stress, endothelial dysfunction, and negative impact on pulmonary circulation could significantly contribute to RV impairment. Conclusions Chemotherapy induces the impairment of RV structure, function, and mechanics by different complex mechanisms.

SLOWB training improves cardiorespiratory capacity and appears to slow the progression of HFrEF. Further long-term outcome studies are required to confirm the benefits of paced breathing in HFrEF.