A simple and rapid method for identification of lesions at high risk for the no-reflow phenomenon immediately before elective coronary stent implantation.

We aimed to design a rapid and reliable method to identify coronary lesions at high risk for the no-reflow phenomenon before elective coronary stent implantation using integrated backscatter intravascular ultrasound (IB-IVUS). The no-reflow phenomenon occurring during elective percutaneous coronary intervention (PCI) worsens patient prognosis, regardless of whether the phenomenon is transient or persistent. We retrospectively studied 353 coronary lesions to identify factors potentially promoting the no-reflow phenomenon, including lesion location and severity. We also performed component analysis by two- and three-dimensional IB-IVUS before elective stent implantation. The cutoff values of the true lipid volume and estimated lipid volume (lipid area at the minimal lumen diameter site × total stent length) for the no-reflow phenomenon were determined by receiver operating curve analysis. Type C lesions, regardless of location and a thrombolysis in myocardial flow grade of 0, were risk factors for the no-reflow phenomenon during PCI. The estimated lipid volume was significantly correlated with the true lipid volume (R 2 = 0.778, p < 0.0001). The cutoff value of the estimated lipid volume for the no-reflow phenomenon was 132.6 mm3 (area under the curve = 0.719), and the predictive value was equivalent to that of the true lipid volume. Lesions with an estimated lipid volume of ≥132.6 mm3 had a significantly higher risk of the no-reflow phenomenon during elective stent implantation (odds ratio, 4.35; 95 % confidence interval, 1.67-12.7; p = 0.0024). The simple and rapid measurement of the estimated lipid volume immediately before stenting during PCI constitutes a reliable predictor of lesions at high risk for the no-reflow phenomenon.

Irreversible deterioration of estimated glomerular filtration rate in patients with acute myocardial infarction after primary percutaneous coronary intervention.

Contrast-induced nephropathy is a possible complication after primary percutaneous coronary intervention (PCI) for acute myocardial infarction (MI). Deterioration of renal function is reported to be generally reversible. However, renal insufficiency worsens the prognosis for some patients with primary PCI. We evaluated sequential changes in renal function before primary PCI and until the chronic phase. We retrospectively studied 302 patients who had undergone PCI for acute MI. Renal function was evaluated based on estimated glomerular filtration rates (eGFRs) measured at the following four points: before PCI, within 1 week after PCI, at discharge from the hospital, and 180-365 days after MI. Patients were classified into the preserved eGFR group and the reduced eGFR group according to the median eGFR change from the basal level after PCI. Changes in eGFR in the two groups had significantly different time courses. In the preserved eGFR group, eGFR values during the chronic phase did not differ from the values obtained before PCI. In contrast, eGFRs in the reduced eGFR group did not recover to pre-PCI basal levels, with the median decrease being 10.3 mL/min/1.73 m2. The eGFR change after PCI was the strongest predictor of eGFR change during the chronic phase. In the reduced eGFR group, incidence of major adverse cardiac events was significantly higher (logrank: p = 0.048), and the hazard ratio was 2.28 (95 % confidence interval 1.02-5.60). A decline in eGFR after primary PCI for acute MI is not uncommon, and it appears to remain irreversible, even during the chronic phase.

Should increasing the dose or adding an AT1 receptor blocker follow a relatively low dose of ACE inhibitor initiated in acute myocardial infarction?

OBJECTIVE: Based on currently available clinical evidence, we should use high-dose angiotensin converting enzyme inhibitor (ACE-I) for patients with acute myocardial infarction (MI), initiating it at incremental doses to avoid excessive hypotension. Recent animal studies with acute MI models failed to demonstrate the superiority of the combination therapy of ACE-I and angiotensin receptor blocker (ARB) to high-dose ACE-I treatment with comparable blood pressure reductions, which however might be attributed to the initiation of the targeted doses from the beginning. The aim of this study was to compare the effect of increasing the dose of ACE-I with that of adding ARB following a relatively low dose of ACE-I on the survival and left ventricular (LV) remodeling after MI. METHODS: Rats underwent left coronary artery ligation and were treated with either ACE-I temocapril (5 mg/kg/day) or vehicle for 2 weeks, which was initiated 3 days after the surgery. The rats treated with temocapril were further randomly assigned to receive either high-dose temocapril (10 mg/kg/day) or combination therapy (temocapril 5 mg/kg/day+olmesartan 2.5 mg/kg/day), which was continued for another 6 weeks. RESULTS: Both treatments similarly reduced the blood pressure, improved survival and ameliorated LV enlargement. In contrast, several parameters of LV function were significantly ameliorated only by the high-dose ACE-I but not by the combination therapy. CONCLUSIONS: After the initiation of a relatively low dose of ACE-I in acute MI, increasing the dose of ACE-I or adding ARB may equally improve survival and LV remodeling in the setting of an equal hypotensive effect. Further study with a longer treatment protocol is required to determine whether the several favorable effects on LV function elicited only by the high-dose ACE-I treatment provide further beneficial effects on survival and LV remodeling compared with the combination therapy.

The systemic inflammation-based Glasgow Prognostic Score as a prognostic factor in patients with acute heart failure.

AIMS: By combining C-reactive protein and serum albumin concentrations, the Glasgow Prognostic Score (GPS) provides valuable predictions of prognosis in patients with cancer. Both systemic inflammatory response and malnutrition are also common in patients with heart failure. We evaluated the efficacy of the GPS for predicting the prognoses of patients with acute decompensated heart failure (ADHF). METHODS: We investigated 336 patients who were admitted with ADHF. The GPS (0, 1, and 2) was defined as follows: patients with both elevated C-reactive protein (>1.0 mg/dl) and hypoalbuminemia (<3.5 g/dl) were allocated a score of 2, patients with only one of these biochemical abnormalities were allocated a score of 1, and patients with neither of these abnormalities were allocated a score of 0. RESULTS: During the follow-up period (mean ±â€ŠSD: 504 ±â€Š471 days), 71 patients (21.1%) died. Relative to a GPS of 0, the hazard ratios for all-cause death were 3.40 (95% confidence interval 1.81-6.45) for a GPS of 2 and 1.97 (95% confidence interval 1.06-3.66) for a GPS of 1, as determined using adjusted Cox proportional-hazards analysis. CONCLUSIONS: The GPS, which is based on systemic inflammation, is useful for predicting the prognoses of hospitalized patients with ADHF.