Heart failure with preserved ejection fraction (HFpEF), which currently represents approximately 50 % of heart failure (HF) cases, is common and associated with high morbidity and mortality. Understanding the epidemiology of HFpEF has been difficult due to the challenges in HFpEF diagnosis and the heterogeneous etiologies and pathophysiologies that underlie HFpEF. Nevertheless, several high-quality epidemiology and observational registry studies of HFpEF demonstrate that an increasing prevalence of HFpEF in both the outpatient and inpatient settings, coupled with a lack of evidence-based effective treatments for HFpEF, is resulting in an emerging epidemic of HFpEF. In this review, we discuss the emerging HFpEF epidemic, focusing on: (1) reasons for the rising prevalence of HFpEF; (2) the abnormalities in cardiac structure and function that dictate the transition from risk factors to HFpEF; (3) novel HFpEF mechanisms that may underlie the increase in HFpEF prevalence; (4) prognosis of HFpEF; and (5) risk prediction in HFpEF. We conclude with 10 unanswered questions on HFpEF epidemiology that will be important areas for future investigation.

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Grayanotoxins are known to occur in the honey pro duced from the nectar of Rhododendron ponticum growing on the mountains of the eastern Black Sea region of Turkey. Two cases of honey intoxication are presented here. Both patients experienced severe bradycardia and hypotension following ingestion of honey which was brought from Trabzon, Turkey. Microscopical examination of the honey demonstra ted Rhododendron ponticum tétrades. Anesthetized albino rats were injected intrapcritoneally with toxic honey extracts in amounts equivalent to 1 or 5 g honey/kg b.w. Dose-dependent hypotension, bradycar dia and respiratory rate depression were observed.

Overweight and obesity are well-established risk factors for most cardiovascular diseases (CVD), including coronary heart disease (CHD), heart failure (HF), and atrial fibrillation. Despite the strong link between excess adiposity and risk of CVD, growing evidence has demonstrated an obesity paradox in patients with CVD. This phenomenon is characterized by a better prognosis in overweight and mildly obese CVD patients than their leaner counterparts. Moreover, the worst outcomes are often incurred by underweight CVD patients, followed by those of normal weight or severely obese. The obesity paradox is now a well-established phenomenon across different types of CVD, and it occurs regardless of age and ethnicity of patients, and severity of CVD. Physical inactivity and low cardiorespiratory fitness (CRF) have long been recognized as major risk factors for CVD. In contrast, high levels of physical activity (PA) and CRF largely neutralize the adverse effects of excess adiposity and other traditional CVD risk factors, including hypertension, metabolic syndrome, and type-2 diabetes. Higher CRF also results in better CVD outcomes across different BMI groups and significantly alters the obesity paradox in patients with HF and CHD. Prognostic benefits of overweight/obesity tend to be limited to unfit patients with HF and CHD, and the obesity paradox usually disappears with improved levels of CRF. Nevertheless, increased PA and exercise training, to maintain or improve CRF, are effective, safe, and proven strategies for primary and secondary prevention of CVD in all weight groups. In this review, we discuss the current concepts of individual and combined contributions of fatness and fitness to CVD risk and prognosis. We then examine the influence of fitness on the obesity paradox in individuals with CVD.

Heart failure with preserved ejection fraction (HFpEF) is a common clinical syndrome associated with high rates of morbidity and mortality. Due to the lack of evidence-based therapies and increasing prevalence of HFpEF, clinicians are often confronted with these patients and yet have little guidance on how to effectively diagnose and manage them. Here we offer 10 key lessons to assist with the care of patients with HFpEF: (1) Know the difference between diastolic dysfunction, diastolic heart failure, and HFpEF; (2) diagnosing HFpEF is challenging, so be thorough and consider invasive hemodynamic testing to confirm the diagnosis; (3) a normal B-type natriuretic peptide does not exclude the diagnosis of HFpEF; (4) elevated pulmonary artery systolic pressure on echocardiography in the presence of a normal ejection fraction should prompt consideration of HFpEF; (5) use dynamic testing in evaluating the possibility of HFpEF in patients with unexplained dyspnea or exercise tolerance; (6) all patients with HFpEF should be systematically evaluated for the presence of coronary artery disease; (7) use targeted treatment for HFpEF patients based on their phenotypic classification; (8) treat HFpEF patients now by treating their comorbidities; (9) understand the importance of heart rate in HFpEFlower is not always better; and (10) do not forget to consider rare diseases ("zebras") as causes for HFpEF when evaluating and treating patients. Taken together, these 10 key lessons can help clinicians care for challenging patients with HFpEF while we eagerly await the results of ongoing HFpEF clinical trials and observational studies.

Cardiovascular events occur more frequently in sodium-sensitive patients with essential hypertension; recently, sodium sensitivity was shown to be a cardiovascular risk factor independently of other classic factors such as blood pressure and cigarette smoking This study examined the relationship between salt sensitivity status and target organ damage in hypertensive patients. Ninety-six patients (35 men, 61 women) with moderate essential hypertension were studied for salt sensitivity status and the presence of target organ damage, including hypertensive retinopathy, serum creatinine, creatinine clearance, and urinary albumin excretion (UAE). Four different patterns of left ventricular anatomic adaptation were identified by categorizing patients according to the values of left ventricular mass index and relative wall thickness by the means of echocardiography. Forty-five (47%) patients were shown to be salt-sensitive, in contrast to 51 (53%) salt-resistant subjects. Serum creatinine and UAE were significantly higher in the group of salt-sensitive hypertensives (P < .05 and P < .001, respectively). Left ventricular mass index (LVMI), relative wall thickness (RWT), and left atrial index (LAI) were all significantly higher in the group of salt-sensitive hypertensive patients. Concentric hypertrophy was significantly more prevalent in the salt-sensitive group (37.8% v 11.8%; P < .01). The prevalence of hypertensive retinopathy in the salt-sensitive group was 84.4%, in contrast to 59.6% in the salt-resistant group (P < .01). Multivariate regression analysis revealed salt sensitivity as a significant predictor of LVMI, RWT, and UAE, independently of age, body mass index, and mean blood pressure. In conclusion, salt-sensitive hypertensive patients are more prone to develop severe hypertensive target organ damage that may enhance their risk of renal and cardiovascular morbidity.

Grayanotoxins are known to occur in honey produced from the nectar of Rhododendrons of the family Ericaceae. Grayanotoxins extracted from honey sample obtained from a patient who experienced severe bradycardia and hypotension after ingesting two tablespoonfuls corresponded to Rhododendron ponticum tetrades. Anaesthetized albino rats were injected with honey extract intracerebroventricularly or intraperitoneally. The intracerebroventricular dose was equivalent to 50 mg honey and i.p. doses were equivalent to 50 mg, 1 mg kg-1 and 5 g kg-1 honey. Marked bradycardia and respiratory rate depression were observed in rats injected with extract equivalent to 1 and 5 g kg-1 honey i.p. and in rats injected with 50 mg i.c.v., but not in rats given 50 mg i.p. In bilaterally vagotomized animals, grayanotoxin-contaminated honey extract was not bradycardic. These results suggest that the sites of cardiac and respiratory actions are within the central nervous system, and that the bradycardic effect of grayanotoxin is mediated by vagal stimulation at the periphery.

Hypertension (HTN) is a global health problem and a leading risk factor for cardiovascular disease (CVD) morbidity and mortality. The hemodynamic overload from HTN causes left ventricular (LV) remodeling, which usually manifests as distinct alterations in LV geometry, such as concentric remodeling or concentric and eccentric LV hypertrophy (LVH). In addition to being a common target organ response to HTN, LV geometric abnormalities are well-known independent risk factors for CVD. Because of their prognostic implications and quantifiable nature, changes in LV geometric parameters have commonly been included as an outcome in anti-HTN drug trials. The purpose of this paper is to review the relationship between HTN and LV geometric changes with a focus on (1) diagnostic approach, (2) epidemiology, (3) pathophysiology, (4) prognostic effect and (5) LV response to anti-HTN therapy and its impact on CVD risk reduction.