Background and objectives AKI is associated with major adverse kidney events (MAKE): death, new dialysis, and worsened renal function. CKD (arising from worsened renal function) is associated with a higher risk of major adverse cardiac events (MACE): myocardial infarction (MI), stroke, and heart failure. Therefore, the study hypothesis was that veterans who develop AKI during hospitalization for an MI would be at higher risk of subsequent MACE and MAKE.Design, setting, participants, & measurements Patients in the Veterans Affairs (VA) database who had a discharge diagnosis with International Classification of Diseases, Ninth Revision, code of 584.xx (AKI) or 410.xx (MI) and were admitted to a VA facility from October 1999 through December 2005 were selected for analysis. Three groups of patients were created on the basis of the index admission diagnosis and serum creatinine values: AKI, MI, or MI with AKI. Patients with mean baseline estimated GFR,45 ml/min per 1.73 m 2 were excluded. The primary outcomes assessed were mortality, MAKE, and MACE during the study period (maximum of 6 years). The combination of MAKE and MACE-major adverse renocardiovascular events (MARCE)-was also assessed.Results A total of 36,980 patients were available for analysis. Mean age6SD was 66.8611.4 years. The most deaths occurred in the MI+AKI group (57.5%), and the fewest (32.3%) occurred in patients with an uncomplicated MI admission. In both the unadjusted and adjusted time-to-event analyses, patients with AKI and AKI+MI had worse MARCE outcomes than those who had MI alone (adjusted hazard ratios, 1.37 [95% confidence interval, 1.32 to 1.42] and 1.92 [1.86 to 1.99], respectively).Conclusions Veterans who develop AKI in the setting of MI have worse long-term outcomes than those with AKI or MI alone. Veterans with AKI alone have worse outcomes than those diagnosed with an MI in the absence of AKI.

Abstract-Prehypertensive individuals are at increased risk for developing hypertension and cardiovascular disease compared with those with normal blood pressure. Early compromises in left ventricular structure may explain part of the increased risk. We assessed echocardiographic and exercise parameters in prehypertensive individuals (nϭ790) to determine associations between exercise blood pressure and left ventricular structure. The exercise systolic blood pressure at 5 metabolic equivalents (METs) and the change in blood pressure from rest to 5 METs were the strongest predictors of left ventricular hypertrophy. We identified the systolic blood pressure of 150 mm Hg at the exercise levels of 5 METs as the threshold for left ventricular hypertrophy. There was a 4-fold increase in the likelihood for left ventricular hypertrophy for every 10-mm Hg increment in systolic blood pressure beyond this threshold 2,3 It is estimated that substantial reductions in hospitalizations, nursing home admissions, and deaths would be realized if prehypertension is eliminated 4 or the progression from prehypertension to hypertension is prevented.The factors involved in the increased risk are not well defined. Prehypertension may mark the beginning of a progressive remodeling of the left ventricle that may go unnoticed for years. Increased left ventricular mass (LVM) is an independent predictor of cardiovascular disease and mortality. 5-7 Naturally, reversing or retarding the rate of progression from prehypertension to hypertension and preventing target-organ injury is desirable.Daytime ambulatory systolic BP is directly associated with LVM and is a stronger predictor of it than resting BP. 8,9 This suggests that the impetus for increased LVM is an elevated hemodynamic load during routine daily activities. Because the metabolic demand of most routine daily activities is within 5 metabolic equivalents (METs), 10 the BP taken during an exercise tolerance test (ETT) at the workload of 5 METs is likely to reflect the hemodynamic load during daily activities. Thus, this exercise BP may be used as a practical and relatively inexpensive predictor of increased risk for left ventricular hypertrophy (LVH) in prehypertensive individuals.Moderate and high-fit prehypertensive individuals exhibit significantly lower ambulatory BP, 11 exercise BP, and heart rate (HR) at submaximal and absolute workloads 12 when compared with unfit. We also reported significantly lower exercise BP at the absolute submaximal workloads of 3 to 6 METs 13 and LVM 14 in hypertensive patients after 16 weeks of low-to-moderate intensity exercise training. Collectively, these findings support that moderate increases in cardiorespiratory fitness may result in lower BP, HR, and hemodynamic

Systemic hypertension and physical exercise are both associated with cardiac adaptations. The impact is most prominent on the left side of the heart, which hypertrophies leading to left ventricular hypertrophy. This article reviews structural and functional cardiac changes seen in hypertensive and athlete's hearts. | INTRODUCTIONChronically or intermittently elevated blood pressure (BP) increases systemic pressure and volume overload, with increased workload on the left ventricle and ultimately left ventricular (LV) hypertrophy (LVH). The normal left ventricle size (Table 1) undergoes several types of anatomical cardiac structural adaptations varying from concentric remodeling, eccentric remodeling, concentric hypertrophy, and eccentric hypertrophy to a combination of concentric and eccentric hypertrophy.1 Hypertensive LVH is a well-recognized risk factor for heart failure, myocardial infarction, arrhythmias, sudden cardiac death, and stroke. 2-4 Physical activity increases heart rate and BP. Regularly performed sports or physical activities of substantial volume and intensity lead to cardiac changes that meet the characteristic criteria for LVH, especially in highly trained individuals. 5,6 However, cardiac adaptations in response to increased physical activity, referred to as "athlete's heart," differ from the cardiac changes resulting from the pathologically elevated BP in hypertension. The objective of this review is to discuss and contrast the pathological and physiological cardiac adaptations associated with hypertension and chronic exercise. 7,8 | HYPERTENSIVE HEARTChronic, untreated systemic arterial hypertension leads to end organ damage. 3,4,8 The heart in chronic hypertension responds to the increased hemodynamic load with structural and functional changes.The structural changes include hypertrophy of existing myocytes and addition of sarcomeres together with an increase in connective tissue, ultimately leading to an overall increase in ventricular mass. 3,9,10 LV structural changes can include concentric or eccentric remodeling, concentric or eccentric hypertrophy, or a combination of concentric or eccentric hypertrophy, 1 with a varying combination of increase in LV wall thickness and LV diastolic and systolic dimensions (Table 2).In a recent publication from the Dallas Heart Study where 31% of the population was hypertensive, the prevalence of concentric LVH was much higher than that of eccentric hypertrophy. LVH was present in 730 (30%) of the 2458 patients, classified as indeterminate in 404, isolated thick (concentric) hypertrophy in 289, dilated (eccentric) hypertrophy in 30, and both thick and dilated hypertrophy in seven patients. On follow-up, outcome was worse in patients with dilated (eccentric) hypertrophy than in those with isolated thick (concentric) hypertrophy and worst in those who had a combination (both thick and dilated hypertrophy) of the two types of hypertrophy. 11In addition to structural changes, functional compensations with neurohormonal recruitment of sympathetic or renin-...

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HRR at 2 min post exercise is strongly and inversely associated with all-cause mortality. Exercise capacity affects HRR-associated mortality substantially and should be considered when applying HRR to estimate mortality.

Increased left ventricular mass is a predictor of subsequent kidney dysfunction and should be considered in renal risk stratification in a broad spectrum of men with high cardiovascular risk.

When acute kidney injury accompanies pneumonia, postdischarge outcomes are worse than either diagnosis alone. Patients who survive a pneumonia hospitalization and develop acute kidney injury are at high risk for major adverse kidney events including death and should receive careful follow-up.

Recent evidence demonstrates that masked hypertension (MH) is a significant predictor of cardiovascular disease, while apelin and relaxin are two novel factors with a significant role in vascular regulation. Apelin is an adipokine that elicits endothelium-dependent vasorelaxation and reduces arterial blood pressure, while relaxin is a protein hormone that induces the production of nitric oxide and vascular endothelial growth factor and inhibits endothelin and angiotensin II. This study aimed to investigate whether apelin and relaxin plasma levels are affected in patients with MH and compare the findings with those of healthy normotensives. One hundred-thirty (60 men, 70 women) healthy patients with a mean age of 45AE12 years who had clinic blood pressure <140/90 mmHg were studied. The whole study population underwent 24-hour ambulatory blood pressure monitoring (ABPM). According to the ABPM recordings, 24 individuals (8 men, 16 women) had MH and the remaining 106 patients (52 men, 54 women) had normal ABPM recordings. Apelin and relaxin plasma levels were determined in both groups (enzyme-linked immunosorbent assay method). The apelin (220AE121 vs 315AE147 pg/mL, P=.001) and relaxin (35.2AE6.7 vs 56.8AE13.6 pg/mL, P<.001) plasma levels were significantly lower in the masked hypertensive group compared with normotensive controls. Our findings suggest that patients with masked hypertension have significantly lower apelin and relaxin levels. This observation may have prognostic significance for future cardiovascular events in patients with MH and needs further investigation. J Clin Hypertens (Greenwich). 2013;15:333-336. ª2013 Wiley Periodicals, Inc.The phenomenon of masked hypertension (MH) is defined as a clinical condition when patient office blood pressure (BP) is <140/90 mm Hg but ambulatory or home BP readings are in the hypertensive range.