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Fundamentos: A determinação precisa do colesterol de lipoproteína de baixa densidade (LDL-C) é importante para se alcançar concentrações de LDL-C recomendadas por diretrizes e para reduzir resultados cardiovasculares adversos em pacientes diabéticos. A equação de Friedewald comumente usada (LDL-Cf) produz resultados imprecisos em pacientes diabéticos devido a dislipidemia diabética associada. Recentemente, duas novas equações -Martin/Hopkins (LDL-CMH) e Sampson (LDL-Cs) -foram desenvolvidas para melhorar a precisão da estimativa de LDL-C, mas os dados são insuficientes para sugerir a superioridade de uma equação sobre a outra. Objetivos: O presente estudo comparou a precisão e a utilidade clínica das novas equações de Martin/Hopkins e Sampson em pacientes diabéticos. Método: Foram incluídos no estudo quatrocentos e dois (402) pacientes com diabetes. O risco cardiovascular dos pacientes e as metas de LDL-C foram calculadas por diretrizes europeias. As concentrações de LDL-Cmh, LDL-Cs, e LDL-Cf calculadas foram comparadas à concentração de LDL-C direto (LDL-Cd) para testar a concordância entre essas equações e LDL-Cd. Um P valor <0,05 foi aceito como estatisticamente significativo. Resultados: A LDL-CMH e a LDL-Cs tiveram concordância melhor com o LDL-Cd em comparação com a LDL-Cf, mas não houve diferenças estatísticas entre as novas equações para concordância com o LDL-Cd (Alfa de Cronbach de 0,955 para ambos, p=1). Da mesma forma, a LDL-CMH e a LDL-Cs tinham um grau semelhante de concordância com o LDL-Cd para determinar se o paciente estava dentro da meta de LDL-C (96,3% para LDL-Cmh e 96,0% para LDL-Cs), que eram ligeiramente melhores que a LDL-Cf (94,6%). Em pacientes com uma concentração de triglicérides >400 mg/dl, a concordância com o LDL-Cd foi ruim, independentemente do método usado. Conclusão: As equações de Martin/Hopkins e Sampson mostram uma precisão similar para o cálculo de concentrações de LDL-C nos pacientes com diabetes, e ambas as equações são ligeiramente melhores que a equação de Friedewald.

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Snapshot evaluation of acute and chronic heart failure in real-life in Turkey: A follow-up data for mortality Objective: Heart failure (HF) is a progressive clinical syndrome. SELFIE-TR is a registry illustrating the overall HF patient profile of Turkey. Herein, all-cause mortality (ACM) data during follow-up were provided. Methods: This is a prospective outcome analysis of SELFIE-TR. Patients were classified as acute HF (AHF) versus chronic HF (CHF) and HF with reduced ejection fraction (HFrEF), HF with mid-range ejection fraction, and HF with preserved ejection fraction and were followed up for ACM. Results: There were 1054 patients with a mean age of 63.3±13.3 years and with a median follow-up period of 16 (7-17) months. Survival data within 1 year were available in 1022 patients. Crude ACM was 19.9% for 1 year in the whole group. ACM within 1 year was 13.7% versus 32.6% in patients with CHF and AHF, respectively (p<0.001). Angiotensin-converting enzyme inhibitor/angiotensin receptor blocker, beta blocker, and mineralocorticoid receptor antagonist were present in 70.6%, 88.2%, and 50.7%, respectively. In the whole cohort, survival curves were graded according to guideline-directed medical therapy (GDMT) scores ≤1 versus 2 versus 3 as 28% versus 20.2% versus 12.2%, respectively (p<0.001). Multivariate analysis of the whole cohort yielded age (p=0.009) and AHF (p=0.028) as independent predictors of mortality in 1 year. Conclusion: One-year mortality is high in Turkish patients with HF compared with contemporary cohorts with AHF and CHF. Of note, GDMT score is influential on 1-year mortality being the most striking one on chronic HFrEF. On the other hand, in the whole cohort, age and AHF were the only independent predictors of death in 1 year.

We retrospectively analyzed short- and long-term outcomes of patients who received bailout tirofiban during primary percutaneous intervention (pPCI). A total of 2681patients who underwent pPCI between 2009 and 2014 were analyzed; 1331 (49.6%) out of 2681 patients received bailout tirofiban. Using propensity score matching, 2100 patients (1050 patient received bail-out tirofiban) with similar preprocedural characteristics were identified. Patients who received bailout tirofiban had a significantly higher incidence of acute stent thrombosis, myocardial infarction, and major cardiac or cerebrovascular events during the in-hospital period. There were numerically fewer deaths in the bailout tirofiban group in the unmatched cohort (1.7% vs 2.5%, P = .118). In the matched cohort, in-hospital mortality was significantly lower (1.1% vs 2.4%, P = .03), and survival at 12 and 60 months were higher (96.9% vs 95.2%, P = .056 for 12 months and 95.1% vs 92.0%, P = .01 for 60 months) in the bailout tirofiban group. After multivariate adjustment, bailout tirofiban was associated with a lower mortality at 12 months (odds ratio [OR]: 0.554, 95% confidence interval [CI], 0.349-0.880, P = .012) and 60 months (OR: 0.595, 95% CI, 0.413-0.859, P = .006). In conclusion, bailout tirofiban strategy during pPCI is associated with a lower short- and long-term mortality, although in-hospital complications were more frequent.

In a fraction of patients with mild mitral stenosis, left ventricular systolic function deteriorates despite the lack of hemodynamic load imposed by the dysfunctioning valve. Neither the predisposing factors nor the earlier changes in left ventricular contractility were understood adequately. In the present study we aimed to evaluate left ventricular mechanics using three-dimensional (3D) speckle tracking echocardiography. A total of 31 patients with mild rheumatic mitral stenosis and 27 healthy controls were enrolled to the study. All subjects included to the study underwent echocardiographic examination to collect data for two- and three-dimensional speckle-tracking based stain, twist angle and torsion measurements. Data was analyzed offline with a echocardiographic data analysis software. Patients with rheumatic mild MS had lower global longitudinal (p < 0.001) circumferential (p = 0.02) and radial (p < 0.01) strain compared to controls, despite ejection fraction was similar for both groups [(p = 0.45) for three dimensional and (p = 0.37) for two dimensional measurement]. While the twist angle was not significantly different between groups (p = 0.11), left ventricular torsion was significantly higher in mitral stenosis group (p = 0.03). All strain values had a weak but significant positive correlation with mitral valve area measured with planimetry. Subclinical left ventricular systolic dysfunction develops at an early stage in rheumatic mitral stenosis. Further work is needed to elucidate patients at risk for developing overt systolic dysfunction.

Hypochloremia has recently gained interest as a potential marker of outcomes in patients with heart failure (HF). The exact pathophysiologic mechanism linking hypochloremia to HF is unclear but is thought to be mediated by chloride-sensitive proteins and channels located in kidneys. This analysis aimed to understand whether renal dysfunction (RD) affects the association of hypochloremia with mortality in patients with HF. Using data from a nationwide registry, 438 cases with complete data on serum chloride concentration and 1-year survival were included in the analysis. Patients with an estimated glomerular filtration rate of <60 mL/min/m2 at baseline were accepted as having RD. Hypochloremia was defined as a chloride concentration <96 mEq/L at baseline. For HF patients without RD at baseline, patients with hypochloremia had a significantly higher 1-year all-cause mortality than those without hypochloremia (41.6% vs 13.0%, log-rank p < 0.001) and the association remained significant after multivariate adjustment (odds ratio (OR): 2.55, 95% confidence interval (CI): 1.25–5.21). The evidence supporting the association was very strong in this subgroup (Bayesian Factor (BF)10: 48.25, log OR: 1.56, 95% CI: 0.69–2.43). For patients with RD at baseline, there was no statistically significant difference for 1-year mortality for patients with or without hypochloremia (36.3% vs 29.7, log-rank p = 0.35) and there was no evidence to support an association between hypochloremia and mortality (BF10: 1.18, log OR :0.66, 95% CI: −0.02 to 1.35). In patients with HF, the association between low chloride concentration and mortality is limited to those without RD at baseline.

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