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Abstract: Background and aims: The prognostic impact of admission uric acid (UA) levels in patients with acute myocardial infarction (AMI) is controversial. We assessed the prognostic role of in-hospital UA changes in patients with AMI. Methods and results: We studied 375 consecutive patients (320 males, mean age 62.6 years) with AMI (232 with ST elevation MI) within 12 h of symptoms' onset. UA levels were daily measured throughout hospitalization and their admission and peak values were recorded. End-points were 30-day and 1-year mortality. Mortality rate at 30 days was 7.2% and at 1 year 10.9%. Patients who died within 30 days exhibited higher peak UA (10.24 mg/dl vs. 7.06 mg/dl, p < 0.001) and absolute UA elevation (1.7 mg/dl vs. 0.7 mg/dl, p < 0.001). Optimal values for predicting 30-day mortality were 9.65 mg/dl for peak UA and 2.35 mg/dl for UA elevation. Concerning 1-year mortality, deceased patients had higher peak UA levels (9.71 mg/dl vs. 7 mg/dl, p < 0.001) and absolute UA elevation (1.5 mg/dl vs. 0.6 mg/dl, p < 0.001). Optimal values for predicting 1-year mortality were 9.55 mg/dl for peak UA and 1.1 mg/dl for UA elevation. With Cox regression analysis peak UA (adjHR 1.157, p = 0.030) and UA elevation (adjHR 1.288, p = 0.009) were independent predictors of 30-day mortality. Similarly, peak UA levels (adjHR 1.204, p = 0.001) and UA elevation (adjHR 1.213, p = 0.001) predicted 1-year mortality. Conclusions: In patients with AMI peak rather than admission UA levels, and absolute in-hospital UA elevation predict both 30-day and 1-year mortality. Serial in-hospital UA measurements add prognostic information in AMI patients. [Copyright &y& Elsevier]

Abstract: Background and aims: Emerging evidence suggests that the soluble receptor for advanced glycation end-products (sRAGE) is implicated in the development of vascular disease. We investigated the interrelationships of sRAGE with albumin to creatinine ratio (ACR) and arterial stiffness in essential hypertension. Methods and results: In 309 untreated non-diabetic hypertensives, ACR values were determined as the mean of three non-consecutive morning spot urine samples and aortic stiffness was evaluated on the basis of carotid to femoral pulse wave velocity (c-f PWV). In all subjects, venous blood sampling was performed for the estimation of sRAGE levels. Patients with low (n = 155) compared to those with high sRAGE values (n = 154) had greater 24-h systolic BP (140 ± 8 vs. 134 ± 7 mmHg, p < 0.0001), exhibited higher ACR (36.3 ± 51.6 vs. 17.2 ± 1.2 mg g−1, p < 0.0001) and c-f PWV (8.3 ± 1.5 vs. 7.8 ± 1.1 m s−1, p = 0.003), independently of confounding factors. Multiple regression analyses revealed that age, male sex, 24-h systolic BP and sRAGE were the ‘independent correlates’ of ACR (R 2 = 0.493, p < 0.0001), while age, 24-h systolic BP and sRAGE were the ‘independent correlates’ of c-f PWV (R 2 = 0.428, p < 0.0001). Conclusion: In hypertensives, decreased sRAGE levels are accompanied by pronounced albuminuria and arterial stiffening. The association of sRAGE with ACR and c-f PWV suggests involvement of sRAGE in the progression of hypertensive vascular damage. [Copyright &y& Elsevier]

Coronary flow reserve (CFR) is impaired and urinary albumin excretion is increased in patients with essential hypertension. Our aim was to investigate the associations between CFR and cardiac and renal damage in hypertensives. For this purpose we studied 37 never-treated hypertensives (57.9 years old, 16 men) without chest pain but with a positive ischemia stress test result and normal coronary arteries on coronary angiogram. CFR was calculated by a 0.014-inch Doppler guidewire (Flowire, Volcano, San Diego) in the left anterior descending artery in response to bolus intracoronary administration of adenosine (60 μg) as the ratio of hyperemic to basal average peak velocity of the distal vessel. All participants underwent complete echocardiographic study including left ventricular diastolic function evaluation by tissue Doppler imaging (peak early diastolic velocity/peak atrial systolic velocity) and determination of the albumin-to-creatinine ratio (ACR). Hypertensives with low CFR (<2.5, n = 22) compared to those with high CFR (n = 15) exhibited a larger left ventricular mass index by 10.9 g/m(2) (p = 0.045) and ACR values by 10 mg/g (p <0.001). CFR was negatively correlated with logACR (r = -0.511, p = 0.001). LogACR (beta -0.792, p <0.001), male gender (beta 0.313, p = 0.005), left ventricular mass index (beta -0.329, p = 0.007), and peak early diastolic velocity/peak atrial systolic velocity (beta 0.443, p <0.001) were the only independent predictors of CFR in linear regression analysis (adjusted R(2) = 0.672). In conclusion, never-treated asymptomatic hypertensives who exhibit impaired CFR and angiographically normal epicardial arteries are characterized by intrarenal vascular damage as reflected by increased ACR. These findings suggest a plausible role of ACR estimation in the identification of hypertensive subjects with early coronary microvascular dysfunction. [ABSTRACT FROM AUTHOR]

BACKGROUND: Microalbuminuria reflects a state of widespread vascular dysfunction, whereas obstructive sleep apnea (OSA) further promotes atherosclerotic damage in hypertension. STUDY DESIGN: Cross-sectional. SETTING & PARTICIPANTS: In an outpatient hypertensive unit, 62 untreated hypertensive patients (aged 48 +/- 7 years; office blood pressure [BP], 151 +/- 8/97 +/- 7 mm Hg) with OSA and 70 hypertensive patients without OSA (apnea hypopnea index [AHI] < or = 5) matched for age, sex, smoking status, body mass index, and 24-hour pulse pressure were studied. PREDICTOR VARIABLE: Hypertension and OSA compared with hypertension without OSA. OSA defined as AHI greater than 5, documented by polysomnography. OUTCOME VARIABLE: Albuminuria assessed by urinary albumin-creatinine ratio (ACR). MEASUREMENTS: Participants underwent polysomnography, ambulatory BP monitoring, echocardiography, routine metabolic profile assessment, and glomerular filtration rate estimation, whereas ACR was measured from 2 nonconsecutive morning spot urine samples. RESULTS: Hypertensive patients with OSA compared with those without OSA showed increased 24-hour diastolic BP (87 +/- 7 versus 85 +/- 7 mm Hg; P = 0.03) and nighttime pulse pressure (50 +/- 10 versus 45 +/- 10 mm Hg; P = 0.008), but did not differ regarding metabolic profile and estimated glomerular filtration rate. Albuminuria was greater by 57% in patients with OSA compared with those without OSA: log(10)ACR, 1.1 +/- 0.2 versus 0.7 +/- 0.4 mg/g; P < 0.001). In the entire study population, log10(ACR) correlated with log10(AHI) (r = 0.35; P < 0.001), minimum oxygen saturation during sleep (r = -0.33; P < 0.001), 24-hour pulse pressure (r = 0.38; P < 0.001), and nighttime pulse pressure (r = 0.21; P =0 .01). In a multivariable linear regression model, independent predictors of ACR were AHI (beta = 0.36; P < 0.001) and 24-hour pulse pressure (beta = 0.25; P = 0.01). LIMITATIONS: Cross-sectional study. CONCLUSIONS: Albuminuria increases within the normal range in hypertensive individuals with OSA compared with those without OSA proportionally to OSA severity independently of confounders. The association of upper-airway dysfunction with albuminuria and pulsatile hemodynamic load may provide an explanatory mechanism for the OSA-related risk in hypertension. Copyright © 2008 National Kidney Foundation, Inc. [ABSTRACT FROM AUTHOR]

BACKGROUND: Major depression (MD) is a key feature in heart failure (HF), and it is unclear whether common antidepressive medications interact with cardiovascular drugs used for the treatment of patients with MD and HF, affecting their efficacy. We examined the impact of MD on long-term survival of patients with end-stage severe HF. We also evaluated the interaction between antidepressive medication and beta-blockers on the clinical outcome of these patients. METHODS AND RESULTS: The study population consisted of 250 patients with end-stage severe HF. Sixty-one percent of these patients suffered MD and were receiving selective serotonin reuptake inhibitors (SSRIs), serotonin norepinephrine reuptake inhibitors (SNRIs), or tricyclic antidepressants (TCA). All patients were followed prospectively for 18 months. The primary end point was cardiovascular death. At baseline, patients with severe MD had higher serum interleukin 6 (P < .05) and soluble vascular cell adhesion molecule (P < .01). During the follow-up, 167 cardiovascular deaths were reported, and MD was 1 of the major predictors of cardiovascular death (P = .031), whereas treatment with angiotensin receptor inhibitors and statins were also important negative predictors of mortality (P = .036 and P = .039, respectively). Although beta-blockers had a borderline nonsignificant effect on cardiovascular mortality in the overall population, they had a striking beneficial effect among those patients with major depression receiving SSRIs (P = .006), whereas they had a negative effect on mortality in those patients receiving SNRIs/TCAs (P = .025). CONCLUSIONS: MD is an independent predictor of cardiovascular death in patients with end-stage HF. beta-blockers are associated with lower cardiovascular mortality in patients with end-stage HF and depression only when they are combined with SSRIs. [ABSTRACT FROM AUTHOR]

In a population of 162 patients with currently untreated essential hypertension, those with microalbuminuria (n = 75) had significantly impaired elastic properties of the proximal ascending thoracic aorta compared with their normoalbuminuric counterparts (n = 87), whereas urinary albumin excretion was a significant predictor of aortic mechanics in the entire population. Impaired aortic mechanics in microalbuminuric hypertensives were not fully accounted for by clustering of classic risk factors for atherosclerosis, and constitute a finding that may entail additional long-term cardiovascular risk in this subgroup of patients. [ABSTRACT FROM AUTHOR]

Abstract: Background: The majority of cardiovascular events in patients undergoing PCI arise from the progression of NCL during the long-term follow-up period. The purpose of the study was to investigate the clinical and angiographic factors related to the progression of non-culprit lesions (NCL) of patients undergoing percutaneous coronary interventions (PCI). Methods: One hundred and seventeen patients that underwent two coronary angiograms with a time interval greater than 3 months were enrolled. All patients underwent PCI as a treatment for the culprit lesion. In the second coronary angiography we investigated whether they had a new culprit lesion clearly differentiated from the one of the first angiogram. The demographic characteristics, the clinical syndrome responsible for the first PCI and the procedural characteristics were recorded. Quantitative coronary angiography was performed at the culprit lesion of the second angiography and in the same lesion in the first angiography. Results: Multivariate analysis showed that the independent variables for the development of a significant lesion at the follow-up requiring intervention were: the presence of complex lesion (53.78% vs 36.22%, p <0.001, OR=39.42), acute myocardial infarction (AMI) at the initial diagnosis (36.3% vs 32.4%, p <0.001, OR=3.9), and smoking (46.15% vs 53.84%, p =0.03, OR=0.29). Conclusions: Patients with AMI and complex morphology of NCL have increased risk for a new intervention after successful PCI. Smoking at the time of the follow up, was associated with fewer coronary interventions. [Copyright &y& Elsevier]

Pulmonary balloon valvuloplasty results in improvement in the right coronary artery blood flow velocity pattern and the volumetric flow in patients with pulmonary valve stenosis. These changes are closely related to concomitant changes in right ventricular systolic pressure. [ABSTRACT FROM AUTHOR]