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Kidney disease is linked to the development of cardiovascular disorders, further increasing morbidity and mortality in this high-risk population. Thus, early detection of myocardial damage is imperative in order to prevent devastating cardiovascular complications within this patient group. Over the years, cardiac biomarkers have been identified and are now widely used in everyday clinical practice. More specifically, available data suggest that cardiac troponin and its regulatory subunits (TnT, TnI, and TnC) reflect the injury and necrosis of myocardial tissue. While cTnC is identical in cardiac and skeletal muscle, TnT and TnI constitute cardiac-specific forms of troponin, and, as such, they have been established by international societies as biomarkers of cardiac damage and diagnostic indicators for acute myocardial infarction. Elevations in the levels of both cardiac troponins (cTnT and cTnI) have been also reported in asymptomatic patients suffering from chronic kidney disease. Therefore, if abnormal, they often generate confusion among clinicians regarding the interpretation and clinical significance of their numerical values in emergency settings. The aim of this review is to explore the reasons behind elevated troponin levels in patients with chronic kidney disease and identify when these elevated levels of biomarkers indicate the need for urgent intervention, considering the high cardiovascular risk in this patient group. [ABSTRACT FROM AUTHOR]

Automated office blood pressure (AOBP) measurement, attended or unattended, eliminates the white coat effect (WCE) showing a strong association with awake ambulatory blood pressure (ABP). This study examined the difference in AOBP readings, with and without 5 minutes of rest prior to three readings recorded at 1‐min intervals. Cross‐sectional data from 100 randomized selected hypertensives, 61 men and 39 women, with a mean age of 52.2 ± 10.8 years, 82% treated, were analyzed. The mean systolic AOBP values without preceding rest were 127.0 ± 18.2 mm Hg, and the mean systolic AOBP values with 5 minutes of preceding rest were 125.7 ± 17.9 mm Hg (P =.05). A significant order effect was observed for the mean systolic BP values when AOBP without 5 minutes of preceding rest was performed as the first measurement (130.0 ± 17.7 vs 126.5 ± 16.2, P =.008). When we used a target systolic AOBP ≥ 130 mm Hg, awake ABP yielded lower readings, while at a target systolic AOBP value of < 130 mm Hg higher awake ABP values were obtained. Our findings indicate that systolic AOBP can be initially checked without any preceding rest and if readings are normal can be accepted. Otherwise, when AOBP is ≥ 130 mm Hg, measurements should be rechecked with 5 minutes of rest. [ABSTRACT FROM AUTHOR]

Brain natriuretic peptide (BNP) is a peptide hormone secreted by cardiomyocytes in response to atrial or ventricular wall stretch and/or pressure overload. It promotes a number of systemic effects, including vasodilatation, increase in urinary output and sodium excretion, as well as inhibition of the sympathetic nervous system and the renin-angiotensin-aldosterone system. Plasma BNP levels have been reported to be elevated in patients with left ventricular hypertrophy, congestive heart failure, acute coronary syndromes, atrial fibrillation, and impaired renal function. Moreover, elevated BNP levels have been shown to be a strong predictor of morbidity and mortality in patients with heart failure. Interestingly, it has also been found that the N-terminal peptide of BNP is slightly superior to BNP for predicting death or re-hospitalization for heart failure. Presumably, it is the longer half-life of N-terminal fragment of braintype natriuretic peptide (NT-pro-BNP) that may promote it as a more accurate index of ventricular stress and therefore a better predictor of prognosis. [ABSTRACT FROM AUTHOR]

Atrial Fibrillation (AF) is the most common cardiac arrhythmia in clinical practice and its prevalence increases markedly with advancing age, worldwide. Almost every primary care physician, internist, or cardiologist, has dealt with stroke or with other complications of AF. Still, its management remains a hot issue for clinicians and the debate over which treatment strategy is the best is ongoing. Moreover, AF increases significantly the total cardiovascular (CV) morbidity and mortality. Despite a great bulk of data in the existing medical literature, the pathophysiology of AF in patients with hypertensive heart disease (HHD) is poorly understood, and the underlying signaling pathways linking hypertension (HTN) to AF remain to be fully elucidated. The scope of this article is to discuss the myocardial anatomical and physiological alterations that occur in HTN, and highlight the proposed electrophysiological mechanisms that cause the hypertensive heart to fibrillate. In addition, we will focus on the latest ESC 2016 guidelines for the risk stratification of AF patients as a tool to guide anticoagulation which represents the mainstay of treatment for AF. Last, the other therapeutic approaches for hypertensives with AF currently adopted for optimal patient management will be reviewed.