Low-flow, low-gradient severe aortic stenosis despite normal ejection fraction is associated with severe left ventricular dysfunction as assessed by speckle-tracking echocardiography: a multicenter study.

BACKGROUND: Low-flow low-gradient (LFLG) is sometimes observed in severe aortic stenosis (AS) despite normal ejection fraction, but its frequency and mechanisms are still debated. We aimed to describe the characteristics of patients with LFLG AS and assess the presence of longitudinal left ventricular dysfunction in these patients. METHODS AND RESULTS: In a multicenter prospective study, 340 consecutive patients with severe AS and normal ejection fraction were studied. Longitudinal left ventricular function was assessed by 2D-strain and global afterload by valvulo-arterial impedance. Patients were classified according to flow and gradient: low flow was defined as a stroke volume index ≤35 mL/m(2), low gradient as a mean gradient ≤40 mm Hg. Most patients (n=258, 75.9%) presented with high-gradient AS, and 82 patients (24.1%) with low-gradient AS. Among the latter, 52 (15.3%) presented with normal flow and low gradient and 30 (8.8%) with LFLG. As compared with normal flow and low gradient, patients with LFLG had more severe AS (aortic valve area=0.7±0.12 cm(2) versus 0.86±0.14 cm(2)), higher valvulo-arterial impedance (5.5±1.1 versus 4±0.8 mm Hg/mL/m(2)), and worse longitudinal left ventricular function (basal longitudinal strain=-11.6±3.4 versus -14.8±3%; P<0.001 for all). CONCLUSIONS: LFLG AS is observed in 9% of patients with severe AS and normal ejection fraction and is associated with high global afterload and reduced longitudinal systolic function. Patients with normal-flow low-gradient AS are more frequent and present with less severe AS, normal afterload, and less severe longitudinal dysfunction. Severe left ventricular longitudinal dysfunction is a new explanation to the concept of LFLG AS.

Prognostic value of ischaemia-modified albumin in patients with non-ST-segment elevation acute coronary syndromes.

BACKGROUND: Ischaemia-modified albumin (IMA) is a new sensitive diagnostic biochemical marker of myocardial ischaemia. The purpose of the study was to analyse the prognostic value of IMA in patients admitted for non-ST-segment elevation acute coronary syndromes (NSTE ACS). METHODS: Consecutive patients admitted for NSTE ACS in our institution were prospectively included. IMA, cardiac troponin I (TnI) and C-reactive protein (CRP) were measured in all patients within 3h of last chest pain. The clinical combined endpoint was major adverse cardiac events (MACE) including cardiac death, nonfatal myocardial infarction (MI) and recurrent ischaemia leading to urgent revascularization. The independent prognostic impact of IMA on occurrence of the combined endpoint during hospitalization and at 1 year was tested by a logistic regression model and was systematically adjusted for other known clinical and biological predictors. RESULTS: Seventy-nine patients were enrolled. Nine (11.4%) patients experienced the combined endpoint during hospitalization and 16 (20.2%) during 1-year follow-up. Median IMA level was significantly higher in patients with MACE during hospitalization (115 [93-126]U/mL versus 100 [42-138]U/mL; p=0.007) and at 1 year (114 [93-126]U/mL versus 97 [42-138]U/mL; p<0.001). After adjustment for conventional prognostic risk factors, IMA remained an independent predictor of MACE both during hospitalization (odds ratio [OR]: 1.08; 95% confidence interval [CI]: 1.01-1.16; p=0.03) and at 1 year (hazards ratio [HR]: 1.07; 95% CI: 1.03-1.12; p=0.003). CONCLUSION: Baseline levels of IMA were associated with both short- and long-term cardiovascular (CV) events in patients admitted for NSTE ACS.

High post-treatment platelet reactivity is associated with a high incidence of myonecrosis after stenting for non-ST elevation acute coronary syndromes.

High post-treatment platelet reactivity (HPPR=adenosine diphosphate [ADP] 10 microM-induced platelet aggregation >70%) identifies low responders to dual antiplatelet therapy with increased risk of recurrent cardiovascular (CV) events after stenting for non-ST elevation acute coronary syndromes (NSTE-ACS). This study was designed to compare the incidence of periprocedural myocardial infarction (MI) after stenting for NSTE-ACS patients between non-responders to dual antiplatelet therapy defined by HPPR and normo-responders. One hundred ninety NSTE-ACS consecutive patients undergoing coronary stenting were included in this prospective study. They received 250 mg aspirin and a 600 mg loading dose of clopidogrel at least 12 hours (h) before percutaneous coronary intervention (PCI). A single post-treatment blood sample was obtained before PCI to analyze maximal intensity of ADP-induced platelet aggregation, and troponin levels were analyzed before PCI, and 12 and 24 h after PCI. Troponin I was considered elevated if >0.4 ng/ml. HPPR was present in 22% of patients (n=42). Periprocedural MI occurred significantly more frequently in patients with HPPR than in the normo-responders (43% vs. 24%, p=0.014). After being correlated with recurrent ischemic events after stenting for NSTE-ACS, the HPPR seems to be also a marker of increased risk of periprocedural MI for NSTE-ACS patients.