Arterial hypertension is an established risk factor for acute coronary syndromes, and physical exertion may trigger the onset of such an event. The mechanisms involved include the rupture of a small, inflamed, coronary plaque and the activation of thrombogenic factors. Blood pressure (BP)-lowering treatment has been associated with beneficial effects on subclinical inflammation and thrombosis at rest and during exercise. This prospective study sought to compare the effect of different antihypertensive drugs on the inflammatory and thrombotic response during exercise. A total of 60 never-treated hypertensive patients were randomized to an angiotensin receptor blocker (ARB)-or non-dihydropyridine calcium channel blocker (CCB)-based regimen. Patients with inflammatory or coronary artery disease were excluded. Six months after pharmaceutical BP normalization, the patients underwent a maximal treadmill exercise testing. High-sensitivity C-reactive protein (hsCRP), serum amyloid A (SAA), white blood cells (WBC), tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6), total fibrinogen (TF) and von Willebrand factor (vWF) levels, as well as plasminogen activator inhibitor-1 (PAI-1) activity were measured in blood samples taken while the patients were at rest and during peak exercise. All of these biomarkers increased with exercise, except PAI-1, which decreased (Po0.05 for the difference between resting and peak exercise for all biomarkers). The ARB group had less marked (Po0.05) exercise-induced changes than the CCB group in hsCRP (5.8% vs. 7.7%), SAA (4.2% vs. 7.2%), WBC (46.8% vs. 52.6%), TNF-a (16.3% vs. 24.3%), TF (9.5% vs. 16.9%) and PAI-1 ( À9.5% vs. À12.3%) but a similar (P ¼ NS) change in IL-6 (39.4% vs. 38.6%) and vWF (29.2% vs. 28.6%). In conclusion, ARBs are most likely more effective than CCBs at suppressing the exercise-induced acute phase response. Potential protection against exercise-related coronary events remains to be elucidated.

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2Delayed blood pressure (BP) and heart rate (HR) decline at recovery post-exercise are independent predictors of incident coronary artery disease (CAD). Delayed BP recovery and exaggerated BP response to exercise are independent predictors of future arterial hypertension (AH). This study sought to examine whether the combination of two exercise parameters provides additional prognostic value than each variable alone. A total of 830 non-CAD patients (374 normotensive) were followed for new-onset CAD and ⁄ or AH for 5 years after diagnostic exercise testing (ET). At the end of follow-up, patients without overt CAD underwent a second ET. Stress imaging modalities and coronary angiography, where appropriate, ruled out CAD. New-onset CAD was detected in 110 participants (13.3%) whereas AH was detected in 41 former normotensives (11.0%). The adjusted (for confounders) relative risk (RR) of CAD in abnormal BP and HR recovery patients was 1.95 (95% confidence interval [CI], 1.28-2.98; P=.011) compared with delayed BP and normal HR recovery patients and 1.71 (95% CI, 1.08-2.75; P=.014) compared with normal BP and delayed HR recovery patients. The adjusted RR of AH in normotensives with abnormal BP recovery and response was 2.18 (95% CI, 1.03-4.72; P=.047) compared with delayed BP recovery and normal BP response patients and 2.48 (95% CI, 1.14-4.97; P=.038) compared with normal BP recovery and exaggerated BP response individuals. In conclusion, the combination of two independent exercise predictors is an even stronger CAD ⁄ AH predictor than its components. J Clin Hypertens (Greenwich). 2013; 15:162-170. Ó2012 Wiley Periodicals, Inc. Electrocardiographic (ECG) exercise testing (ET)remains a valuable tool for cardiovascular risk assessment.1 Although many clinicians typically think of ET only as a measure of ST-segment changes that may reflect ischemia, non-ECG parameters have emerged as stronger independent predictors of coronary artery disease (CAD). 1-4Markers reflecting autonomic nervous system dysfunction can predict cardiovascular events, future arterial hypertension (AH), and mortality. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19] The delayed fall in heart rate (HR) immediately after exercise (delayed HR recovery) has been associated with CAD and death.1-11 The insufficient decline in blood pressure (BP) during recovery has been reported as a predictor of CAD, new-onset AH, and mortality.12-16 The exaggerated BP response to exercise has been related to the risk of future AH. [16][17][18][19] A prospective study aiming to synthesize the clinical importance and evaluate the prognostic value of the combination of the aforementioned non-ECG exercise parameters was conducted. Its purpose was to test the hypothesis that the combination of two established prognostic markers provides an additional predictive value than each variable alone. Specifically, the relative risk (RR) for incident CAD according to HR and BP recovery (one or both abnormal) as well as the RR for new-onset hypertension according ...

Intrarenal hemodynamics depend on blood pressure (BP), heart rate (HR), and smoking. Although BP levels have been associated with kidney function, the effect of HR levels, BP, and HR variability on renal function are less well clarified. This cross-sectional study sought to determine the association of 24-hour BP and HR variability with kidney function in hypertensive patients, stratified by smoking. The study comprised 9600 nondiabetic, never-treated hypertensive individuals without evident renal impairment examined from 1985 to 2014 (aged 53.3AE13.4 years, 55.3% males). The 24-hour systolic BP (SBP) and HR variability were estimated via their coefficient of variation (C V =standard deviation9100/ mean value) derived from ambulatory recording. The C V SBPto-C V HR ratio (C V R) was used as a marker of the interplay between 24-hour SBP and HR variability. Renal function was estimated via 24-hour urine creatinine clearance (CrCl), estimated glomerular filtration rate (eGFR), albumin-to-creatinine ratio (ACR), and 24-hour urine a 1 -microglobulin. After adjustment for age, sex, and smoking, C V SBP was found to be weakly correlated to eGFR (r=À0.017, P=.1) and somewhat more strongly to CrCl, ACR, and a 1 -microglobulin (r=À0.032, 0.072, and 0.065; P=.002, <.001 and <.001, respectively). C V HR was much better related to renal function, with stronger adjusted correlations to CrCl, eGFR, ACR, and a 1 -microglobulin (r=0.185, 0.134, À0.306, À0.247; all P<.001, respectively). C V R also showed equally good adjusted correlations (r=À0.175, À0.125, 0.336, 0.262; all P<.001, respectively). Most adjusted correlations for C V HR and C V R were even better in smokers (r=0.213, 0.158, À0.332, À0.272 and À0.183, À0.118, 0.351, 0.275, respectively; all P<.001). C V HR and C V R emerge as better related to kidney function than C V SBP, especially in smokers. The correlation of C V HR and C V SBP to renal function is inverse to each other. ACR and a 1 -microglobulin are better related to variability indices than CrCl and eGFR. However, causal relations cannot be proved. J Clin Hypertens (Greenwich). 2015;17:938-943. ª 2015 Wiley Periodicals, Inc.

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2The purpose of this study was to assess the role of urine a 1 -microglobulin as a marker of hypertension-induced renal damage compared with estimated glomerular filtration rate, (eGFR), urine albumin, and urine albumin-to-creatinine ratio (ACR). Its response on different blood pressure (BP)-lowering drugs was also studied. Sixty never-treated hypertensive patients (65.0% men, 46.9 years, BP 141.4/94.0 mm Hg) were randomized to an irbesartan (an angiotensin receptor blocker [ARB]) or a diltiazem (a nondihydropyridine calcium channel blocker [CCB])-based regimen. Patients with diabetes or established cardiovascular, renal, or liver disease were excluded. Blood samples and 24-hour urine were analyzed at baseline and 6 months after pharmaceutical BP normalization. Serum creatinine was measured and eGFR was calculated. Urine albumin, creatinine, and a 1 -microglobulin were measured and ACR was calculated. Minor changes (P=not significant [NS]) in eGFR were noted during follow-up in both groups (from 111.0 mL/min/1.73 m 2 to 108.4 mL/min/1.73 m 2 in the ARB group and from 111.3 mL/min/1.73 m 2 to 114.0 mL/min/1.73 m 2 in the CCB group). Twenty-four-hour urine indices were all significantly improved (P<.01) in the ARB group (albumin from 19.4 mg/L to 8.2 mg/L, ACR from 21.5 mg/g to 10.0 mg/g, a 1 -microglobulin from 5.06 mg/L to 3.64 mg/L) but not (P=NS) in the CCB group (albumin from 15.6 mg/L to 13.9 mg/L, ACR from 17.6 mg/g to 17.1 mg/g, a 1 -microglobulin from 4.94 mg/L to 4.79 mg/L). These differences between groups remained significant (P<.05) after adjusting for office heart rate and BP. a 1 -Microglobulin was significantly correlated (P<.05) with albumin and ACR both at baseline (r=0.283 and 0.299, respectively) and at the end of follow-up (r=0.432 and 0.465, respectively) but not (P=NS) with eGFR. It was also significantly related (P<.05) to cardiovascular risk scores (Framingham and HeartScore) both at baseline (r=0.264 and 0.436, respectively) and at the end of follow-up (r=0.308 and 0.472, respectively). Urine a 1 -microglobulin emerges as a potentially usable marker of hypertension-induced renal impairment. Its excretion rate and its response to treatment appears similar to that of albumin. Irbesartan but not diltiazem seems to be associated with reduced excretion of a 1 -microglobulin in urine.

Hypercalcemic crisis associated with the development of acute respiratory distress syndrome (ARDS) has been rarely documented in the literature. Most cases have been described in patients suffering from malignancies or renal failure with the presence of metastatic calcifications being a prominent feature. Only three cases of ARDS have been reported to date in patients with hypercalcemic crisis due to primary hyperparathyroidism (PHPT). Herein, we report a 72-year-old patient with PHPT that presented with severe hypercalcemic crisis and developed ARDS. He had mild chronic kidney disease and at presentation he had extremely high levels of serum calcium (22.5 mg/dl) and parathormone (3822 pg/ml). After receiving medical treatment for hypercalcemia and the initiation of hemodialysis, he developed ARDS with a fatal outcome, without the presence of pancreatitis, sepsis or heart failure. Although very rare, ARDS should be taken into account as a possible complication of parathyroid crisis, especially in patients with excessive calcium and parathormone levels.