Takanori Yasu

Peak C-Reactive Protein Level Predicts Long-Term Outcomes in Type B Acute Aortic Dissection

Acute aortic dissection (AAD) is associated with an inflammatory reaction, as evidenced by elevated inflammatory markers, including C-reactive protein (CRP). The association between the peak CRP level and long-term outcomes in type B AAD has not been systematically investigated. The purpose of this study was to investigate whether the peak CRP level during admission predicts long-term outcomes in type B AAD. We conducted a clinical follow-up study of type B AAD. We divided the study population into 4 groups according to the tertiles of peak CRP levels (T1: 0.60 to 9.37 mg/dL; T2: 9.61 to 14.87 mg/dL; T3: 14.90 to 32.60 mg/dL; and unavailable peak CRP group). Multivariate Cox regression analysis was applied to investigate whether the tertiles of peak CRP predict adverse events even after adjusting for other variables. A total of 232 type B AAD patients were included in this analysis. The median follow-up period was 50 months. CRP reached its peak on day 4.5±1.7. Mean peak CRP values in T1, T2, and T3 were 6.4±2.4, 12.0±1.5, and 19.5±4.0 mg/dL, respectively. There were 65 events (39 deaths and 26 aortic events) during the follow-up. T3 and T2 (versus T1) were strong predictors of adverse events (T3: hazard ratio: 6.02 [95% CI: 2.44 to 14.87], P=0.0001; T2: hazard ratio: 3.25 [95% CI: 1.37 to 7.71], P=0.01) after controlling for all of the confounding factors. In conclusion, peak CRP is a strong predictor for adverse long-term events in patients with type B AAD.

Elevation of plasma placental growth factor in the patients with ischemic cardiomyopathy

BACKGROUND Placental growth factor (PlGF), which is a member of the vascular endothelial growth factor family, stimulates angiogenesis and collateral growth in ischemic tissues. In addition, PlGF has been known to be a useful biomarker of vascular inflammation. This study was undertaken to examine whether plasma PlGF levels were increased in patients with congestive heart failure (CHF). METHODS Ninety-eight patients with systolic heart failure (ejection fraction <40%) and twenty control subjects were enrolled. The patients were divided into four subgroups according to the criteria of NYHA functional class. Plasma PlGF, tumor necrosis factor (TNF)-alpha, brain natriuretic peptide (BNP), norepinephrine, high-sensitive C-reactive protein (hs-CRP) were determined. RESULTS In analysis of all the subjects, there was no significant difference in plasma PlGF levels among the subgroups of NYHA classes and the controls. In the ischemic cardiomyopathy (ICM) patients, however, plasma PlGF levels were significantly increased according to the severity of NYHA class; control: 8.9+/-0.5; NYHA I: 9.4+/-1.1, NYHA II: 9.7+/-1.9, NYHA III: 14.6+/-1.2, NYHA IV: 17.9+/-1.9 pg/ml (p=0.0006). Plasma PlGF levels correlated positively with BNP (r=0.53, p=0.0003) and hs-CRP (r=0.23, p=0.02) in the ICM patients, whereas there was not any correlation between plasma PlGF levels and other variable values in the non-ICM patients. CONCLUSIONS In the ICM patients, plasma PlGF levels are increased according to the severity of heart failure. These results may indicate that augmented release of PlGF is involved in the pathogenesis of cardiomyopathy derived from chronic myocardial ischemia.

Determinants of long-term mortality in patients with type B acute aortic dissection.

BACKGROUND Type B acute aortic dissection (AAD) carries a high short- and midterm mortality rate; however, knowledge related to long-term outcome is largely incomplete. The objective of this study was to identify long-term predictors including antihypertensive medications in type B AAD. METHODS We conducted a clinical follow-up study on 202 type B AAD patients. Univariate and multivariate Cox regression analyses were performed to identify predictors of mortality. RESULTS There were 44 postdischarge deaths in 202 consecutive type B AAD patients with a median follow-up of 55 months. In univariate Cox regression analysis, age (10 year incremental: hazard ratio (HR) 1.82, 95% confidence interval (CI) 1.35-2.46, P < 0.0001), previous myocardial infarction or angina pectoris (HR 3.93, 95% CI 1.72-8.99, P = 0.001), and impaired renal function (HR 4.90, 95% CI 2.48-9.65, P < 0.0001) were predictors of death. Calcium channel blockers (CCBs), beta-blockers, and angiotensin-converting enzyme (ACE) inhibitors as antihypertensive medications at discharge were predictors of increased survival. In multivariate Cox regression analysis, CCBs were a significant predictor of increased survival (vs. no antihypertensive medication at discharge: HR 0.38, 95% CI 0.15-0.97, P = 0.04). Impaired renal function was a significant predictor of death (HR 3.41, 95% CI 1.58-7.33, P = 0.002). No antihypertensive medication at discharge group was significantly associated with increased mortality (vs. 1 class of antihypertensive medication: HR 9.51, 95% CI 1.85-48.79, P = 0.007). CONCLUSIONS Impaired renal function was a predictor for adverse outcome in patients with type B AAD. The use of CCBs as antihypertensive medication at discharge was associated with increased survival.

Clinical features of early recurrent myocardial infarction

Recurrence of myocardial infarction, especially when occurring early after the prior one, carries a significant morbidity and mortality rate. The aim of this study was to investigate the characteristics of patients who experienced recurrence under secondary prevention therapy. Case record review identified myocardial infarction patients who had a history of previous myocardial infarction within 5 years. Hospital chart records, initial laboratory data, medications, and type of infarction were reviewed. Patients were divided into two groups according to the interval of recurrence: an early group (recurrence within 1 year), and a late group (recurrence after more than 1 year). A total of 89 patients were included in the analysis; 40 patients in the early group, and 49 patients in the late group. Mean age in the early group and late groups was 67.3 ± 11.9 and 59.4 ± 8.9, respectively (P = 0.001). Mean body mass index in the early and late groups was 22.1 ± 3.6 and 25.0 ± 3.3, respectively (P < 0.001). There were fewer current smokers in the early group (7.5% vs 44.9%, P < 0.001) and more stent thrombosis (17.5% vs 2%, P = 0.02), as compared with the late group. The in-hospital mortality rate tended to be higher in the early group (7.5% vs 0%, P = 0.09). Multiple logistic regression revealed that smoking status (odds ratio [OR] 0.09, 95% confidence interval [CI] 0.02−0.49, P = 0.005), HDL cholesterol level (5 mg/dl increase: OR 1.34, 95% CI 1.04−1.74, P = 0.03), and stent thrombosis (OR 35.59, 95% CI 2.13−595.49, P = 0.01) had significant associations with early recurrence. Early recurrence of myocardial infarction was associated with stent thrombosis, a higher HDL cholesterol level, and a lower frequency of smoking. Early recurrence had a trend toward higher mortality than late recurrence.

Effects of Thiazolidinediones on In-Stent Restenosis: A Review of IVUS Studies

Patients with metabolic syndrome or type 2 diabetes are at high risk of in-stent-restenosis, although drug-eluting stents reduce the in-stent restenosis rate and target lesion revascularization rate to less than half compared with bare metal stents.(Mintz GS, et al. J Am Coll Cardiol 2006) Most clinical trials of systemic pharmacotherapies with ACE inhibitors, statins and antiplatelet agents to reduce restenosis have yielded disappointing results. Proliferation of vascular smooth muscle cells is the predominant mechanism of neointimal hyperplasia leading to restenosis. Insulin resistance is a major factor in metabolic syndrome and type 2 diabetes, and has been demonstrated to represent an independent risk factor for in-stent-restenosis.(Piatti P, et al. Circulation 2003) Thiazolidinediones are insulinsensitizing agents, and reportedly inhibit proliferation of vascular smooth muscle cells in vitro and in animal studies. Recent studies, including our own, (Katayama et al. Am Heart J 2007; Takagi et al. J Am Coll Cardiol Intv 2009) have highlighted the beneficial effects of thiazolidinediones in reducing neointimal growth after stent implantation. We review herein IVUS studies regarding the effects of thiazolidinedione therapy on in-stent restenosis after coronary stent implantation.