Acute heart failure registry from high-volume university hospital ED: comparing European and US data.

BACKGROUND: Acute heart failure (AHF) is associated with a poor prognosis. OBJECTIVES: The objectives of this study are to describe mechanisms of AHF and to identify the predictors for all-cause mortality by patients admitted for hospitalization by emergency departments (EDs) as well as to compare European and American data. METHODS: We designed a prospective registry of consecutively admitted patients for AHF to a high-volume university hospital ED during a 1-year period (n=202; age, 75±11 years; 51% men; ejection fraction, 38%±15%). RESULTS: The major causes of AHF were coronary artery disease, often with concomitant mitral regurgitation, hypertension, or atrial fibrillation (>90% of cases). At admission, 24.9% of patients had preserved ejection fractions (>50%); and only 7.7% fulfilled the definition of diastolic AHF. The 30-day and long-term mortality (median follow-up, 793 days) were 20.3% and 31.0%, respectively. A low systolic blood pressure (P=.006), reduced ejection fraction (P=.044), and low serum hemoglobin level (P<.01) emerged as the strongest predictors of all-cause mortality. In patients with AHF without acute myocardial infarction (MI) (63.9%), prescription, at discharge, of statins (P<.05) was independently associated with all-cause mortality. CONCLUSIONS: The patient's blood pressure, ejection fraction, and hemoglobin values, at admission, were identified as the strongest predictors of all-cause mortality. In AHF not triggered by acute MI, long-term use of statins may be associated with reduced survival. The prevalence of diastolic AHF is low. The American AHF population had similar baseline characteristics; needed fewer intensive care unit admissions; had a better 30 days of prognosis, lower incidence of MI, and de novo AHF diagnoses. In a similar subgroup, we observed similar incidences of inotropic support and mechanical ventilation. Our results could not be generalized to all patients with AHF admitted to US EDs.

Lack of an association between connexin-37, stromelysin-1, plasminogen activator-inhibitor type 1 and lymphotoxin-alpha genes and acute coronary syndrome in Czech Caucasians.

BACKGROUND: The majority of acute coronary syndrome (ACS) cases cannot be explained by the analysis of commonly recognized risk factors; thus, the analysis of possible genetic predispositions is of interest. The genes for connexin-37, stromelysin-1, plasminogen activator-inhibitor type 1 (PAI-1) and lymphotoxin-alpha are among many presently known candidate genes that are associated with risk factors for ACS. OBJECTIVE: To identify the potential impact of the functional variants of connexin-37, stromelysin-1, PAI-1 and lymphotoxin-alpha on ACS in a Caucasian Czech population. METHODS: A total of 1399 consecutive patients (1016 men and 383 women) with ACS from five coronary care units located in Prague (Czech Republic) were analyzed; a representative sample of 2559 healthy individuals (1191 men and 1368 women) were also genotyped and served as controls. RESULTS: The gene variants analyzed were not significantly associated with the prevalence of ACS or the classical risk factors of ACS development such as high plasma lipid levels, hypertension, diabetes, high body mass index or smoking. CONCLUSION: In a Caucasian Czech population sample, genetic variants of connexin-37, stromelysin-1, PAI-1 and lymphotoxin-alpha were not significantly associated with a predisposition toward ACS.

Heart failure with preserved ejection fraction in outpatients with unexplained dyspnea: a pressure-volume loop analysis.

OBJECTIVES: The aim of the present study was to diagnose heart failure with preserved ejection fraction (HFPEF) in outpatients with unexplained chronic dyspnea and to elucidate its underlying mechanisms in this population using invasive pressure-volume loop analysis. BACKGROUND: The diagnosis of HFPEF in stable outpatients with unexplained dyspnea is difficult. METHODS: Thirty patients (age 67 +/- 8.6 years, 27% males) with preserved left ventricular (LV) ejection fraction (>50%) and unexplained chronic New York Heart Association functional class II to III dyspnea underwent heart catheterization. Patients with significant coronary artery stenosis (>50%) were excluded. Pressure-volume loops were assessed using a conductance catheter at rest, hand-grip exercise, leg lifting, and nitroprusside and dobutamine infusion. RESULTS: Twenty (66%) patients showed LV end-diastolic pressure >16 mm Hg (HFPEF), whereas the remaining 10 patients served as controls. Patients with HFPEF had significantly higher end-diastolic stiffness (0.205 +/- 0.074 vs. 0.102 +/- 0.017, p < 0.001) at rest, and their end-diastolic pressure-volume relationship showed a consistent upward and leftward shift during all hemodynamic interventions compared with controls. Regarding the underlying mechanism of HFPEF, 14 (70%) patients had markedly increased end-diastolic stiffness, which was considered a sufficient single pathology to induce increased LV end-diastolic pressure. Four (20%) patients showed a concomitant presence of moderately increased stiffness and severe LV dyssynchrony, and the remaining 2 (10%) patients, with normal stiffness, showed significant exercise-induced mitral regurgitation at hand-grip exercise. If the invasive pressure measurements were absent, only 5 (25%) of the outpatients with HFPEF fulfilled the European Society of Cardiology definition of HFPEF. CONCLUSIONS: A significant proportion of stable outpatients with unexplained chronic dyspnea may have HFPEF. In the patients whom we studied, increased LV stiffness, dyssynchrony, and dynamic mitral regurgitation were the major mechanisms underlying development of HFPEF.

A FTO variant and risk of acute coronary syndrome.

BACKGROUND: The FTO gene plays an important role in the determination of body weight and BMI and it has been suspected of being associated with all-case mortality. METHODS: We have analyzed the FTO rs17817449 variant in consecutive 1092 male patients with acute coronary syndrome (ACS) and in 1191 randomly selected Caucasian individuals (population controls). RESULTS: The FTO variant was significantly associated with BMI both in controls (P<0.02) and ACS patients (P<0.01). In both groups, BMI was highest in GG homozygotes and lowest in TT homozygotes. There was a significant difference between the ACS patients and controls in the frequency of the FTO genotype GG (21.4% vs. 15.9%, P<0.005). FTO GG homozygotes had a significantly increased risk of ACS, compared with TT homozygotes which was independent of age and BMI (odds ratio 1.49, 95% confidence interval 1.16-1.93). The odds ratio of ACS patients for the GG genotype remained significant even after the exclusion of diabetics (100 controls and 339 ACS patients), with OR 1.32 (95% CI 1.01-1.72). CONCLUSIONS: This study provides an evidence of an association between the FTO variant and risk of ACS in Caucasian males.