Clinical and Angiographic Features of Patients With Out-of-Hospital Cardiac Arrest and Acute Myocardial Infarction.

BACKGROUND: Sudden cardiac arrest is a serious complication of acute myocardial infarction (MI). Although in-hospital mortality from MI has decreased, the mortality of MI patients complicated with out-of-hospital cardiac arrest (OHCA) remains high. However, the features of acute MI patients with OHCA have not been well known. OBJECTIVES: We sought to characterize the clinical and angiographic features of acute MI patients with OHCA comparing with those without OHCA. METHODS: We retrospectively analyzed 480 consecutive patients with acute MI undergoing percutaneous coronary intervention. Patients complicated with OHCA were compared with patients without OHCA. RESULTS: Of the patients, 141 (29%) were complicated with OHCA. Multivariate analysis revealed that age (odds ratio [OR]: 0.8; 95% confidence interval [CI]: 0.7 to 0.9 per 5 years; p < 0.001), estimated glomerular filtration rate (OR: 0.8; 95% CI: 0.7 to 0.8 per 10 ml/min/1.73 m2; p < 0.001), peak creatine kinase-myocardial band (OR: 1.3; 95% CI: 1.2 to 1.4 per 102 U/l; p < 0.001), calcium-channel antagonists use (OR: 0.4; 95% CI: 0.2 to 0.7; p = 0.002), the culprit lesion at the left main coronary artery (OR: 5.3; 95% CI: 1.9 to 15.1; p = 0.002), and the presence of chronic total occlusion (OR: 2.9; 95% CI: 1.5 to 5.7; p = 0.001) were significantly associated with OHCA. CONCLUSIONS: Younger age, no use of calcium-channel antagonists, worse renal function, larger infarct size, culprit lesion in the left main coronary artery, and having chronic total occlusion were associated with OHCA.

Prognostic impact of nutritional status and physical capacity in elderly patients with acute decompensated heart failure.

AIMS: Nutritional status as well as physical capacity is related to prognosis in patients with heart failure. The purpose of this study was to explore a simple prognostic indicator in patients with acute decompensated heart failure (ADHF) by including both nutritional status and physical capacity. METHODS AND RESULTS: Patients hospitalized with ADHF (N = 203; mean age, 81 years) were enrolled. We evaluated the geriatric nutritional risk index (GNRI) on hospital admission and at discharge. A GNRI score < 92 was defined as malnutrition. Physical capacity was evaluated by simple walking test to determine if patients could walk 200 m, with a Borg scale score ≤ 13, without critical changes in vital signs. Primary endpoints were mortality and heart failure rehospitalization within 2 years. A total of 49% and 48% of patients showed malnutrition on admission and at discharge, respectively. Malnutrition at discharge was more strongly related to mortality [hazard ratio (HR) 3.382, 95% confidence interval (CI) 1.900-6.020, P < 0.0001)] than that on admission (HR 2.448, 95% CI 1.442-4.157, P = 0.001) by univariable analysis. Malnutrition at discharge was related to mortality (HR 2.370, 95% CI 1.166-4.814, P = 0.02), but malnutrition on admission was not related (HR 1.538, 95% CI 0.823-2.875, P = 0.18) by multivariable analysis. Almost half of patients (45%) could not walk 200 m, which was significantly related to mortality by univariable analysis (HR 3.303, 95% CI 1.905-5.727, P < 0.0001), but was not by multivariable analysis (HR 1.990, 95% CI 0.999-3.962, P = 0.05). The combined index including both GNRI and simple walking test was an independent and stronger predictor of mortality than either index alone by multivariable analysis (HR 2.249, 95% CI 1.362-3.716, P < 0.01). Neither malnutrition nor low physical capacity was related to heart failure rehospitalization by univariable analysis (HR 0.702, 95% CI 0.483-1.020, P = 0.06; HR 1.047, 95% CI 0.724-1.515, P = 0.81, respectively). Malnutrition at discharge significantly reduced heart failure rehospitalization by multivariable analysis (HR 0.431, 95% CI 0.266-0.698, P < 0.01). When patients were classified into Group G (both nutritional status and physical capacity at discharge were good), Group E (either was good), and Group B (both were bad), mortality rates were significantly different among the groups (log rank P < 0.0001). CONCLUSION: A simple indicator including both nutritional status and physical capacity may predict 2 year mortality in elderly patients with ADHF.

Relation of Chronic Total Occlusion to In-Hospital Mortality in the Patients With Sudden Cardiac Arrest Due to Acute Coronary Syndrome.

Although the presence of chronic total occlusion (CTO) has been associated with long-term mortality in the patients with ST-segment elevation myocardial infarction, the influence of having CTO on in-hospital mortality in sudden cardiac arrest (SCA)-acute coronary syndrome (ACS) patients has not been reported. Therefore, we examined the association between the presence of CTO and in-hospital mortality in those patients. Consecutive 106 SCA-ACS patients who received coronary angiography were retrospectively included. The factors associated with in-hospital mortality were analyzed. Among 106 patients, 40 (38%) patients died during hospitalization. Multivariate analysis revealed presence of CTO dependent on infarct-related artery (IRA-dependent-CTO) (hazard ratio [HR] = 2.88, p = 0.004), diabetes mellitus (HR = 2.04, p = 0.044), percutaneous cardiopulmonary support use (HR = 2.22, p = 0.045), successful recanalization (HR = 0.31, p = 0.004), and peak creatine kinase muscle-brain fraction (HR = 1.11, p < 0.001) were significantly associated with mortality. In conclusion, presence of IRA-dependent-CTO was significantly associated with in-hospital mortality in SCA-ACS patients.

Quantitative Assessment of Fluid Accumulation Using Bioelectrical Impedance Analysis in Patients With Acute Decompensated Heart Failure.

BACKGROUND: Acute decompensated heart failure (ADHF) is generally considered to be a problem of fluid volume overload, therefore accurately quantifying the degree of fluid accumulation is of critical importance in assessing whether adequate decongestion has been achieved. The aim of this study was to develop and validate a method to quantify the degree of fluid accumulation in patients with ADHF. METHODS AND RESULTS: Using multi-frequency bioelectrical impedance analysis (BIA), we measured extracellular water (ECW) volume in 130 ADHF patients on admission and at discharge. We also predicted optimal ECW volume using original equations based on data from 60 control subjects without the signs of HF. Measured/predicted (M/P) ratio of ECW in ADHF patients was observed to decrease from 1.26±0.25 to 1.04±0.17 during hospitalization (P<0.001). The amount of ECW volume reduction was significantly correlated with reduction in body weight (r=0.766, P<0.001). On multivariate analysis, higher M/P ratio of ECW at discharge was associated with increased risk of ADHF readmission or cardiac death within 6 months after discharge. CONCLUSIONS: Multi-frequency BIA-measured ECW was found to offer valuable information for analyzing the pathophysiology of ADHF, and may be a useful guide in the management of this disease.

Porphyrin accumulation in mitochondria is mediated by 2-oxoglutarate carrier.

Heme (Fe-protoporphyrin IX), an endogenous porphyrin derivative, is an essential molecule in living aerobic organisms and plays a role in a variety of physiological processes such as oxygen transport, respiration, and signal transduction. For the biosynthesis of heme or the mitochondrial heme proteins, heme or its biosynthetic precursor porphyrin must be transported into mitochondria from cytosol. The mechanism of porphyrin accumulation in the mitochondrial inner membrane is unclear. In the present study, we analyzed the mechanism of mitochondrial translocation of porphyrin derivatives. We showed that palladium meso-tetra(4-carboxyphenyl)porphyrin (PdTCPP), a phosphorescent porphyrin derivative, accumulated in the mitochondria of several cell lines. Using affinity latex beads, we showed that 2-oxoglutarate carrier (OGC), the mitochondrial transporter of 2-oxoglutarate, bound to PdTCPP, and in vitro PdTCPP inhibited 2-oxoglutarate uptake into mitochondria in a competitive manner (Ki = 15 microM). Interestingly, all types of porphyrin derivatives examined in this study competitively inhibited 2-oxoglutarate uptake into mitochondria, including protoporphyrin IX, coproporphyrin III, and hemin. Furthermore, mitochondrial accumulation of porphyrins was inhibited by 2-oxoglutarate or OGC inhibitor. These results suggested that porphyrin accumulation in mitochondria is mediated by OGC and that porphyrins are able to competitively inhibit 2-oxoglutarate uptake into mitochondria. This is the first report of a putative mechanism for accumulation of porphyrins in the mitochondrial inner membrane.