Miyuki Tsuchihashi

The incidence and risk factors of cholesterol embolization syndrome, a complication of cardiac catheterization: a prospective study

Abstract Objectives We sought to determine the incidence of cholesterol embolization syndrome (CES) as a complication of cardiac catheterization and to identify risk factors associated with this disease. Background Cholesterol embolization syndrome is a systemic disease caused by distal showering of cholesterol crystals after angiography, major vessel surgery, or thrombolysis. Methods We prospectively evaluated a total of 1,786 consecutive patients 40 years of age and older, who underwent left-heart catheterization at 11 participating hospitals. The diagnosis of CES was made when patients had peripheral cutaneous involvement (livedo reticularis, blue toe syndrome, and digital gangrene) or renal dysfunction. Results Twenty-five patients (1.4%) were diagnosed as having CES. Twelve patients (48%) had cutaneous signs, and 16 patients (64%) had renal insufficiency. Eosinophil counts were significantly higher in CES patients than in non-CES patients before and after cardiac catheterization. The in-hospital mortality rate was 16.0% (4 patients), which was significantly higher than that without CES (0.5%, p Conclusions Cholesterol embolization syndrome is a relatively rare but serious complication after cardiac catheterization. Elevated plasma levels of pre-procedural CRP are associated with subsequent CES in patients who undergo vascular procedures.

Critical Role of Monocyte Chemoattractant Protein-1 Receptor CCR2 on Monocytes in Hypertension-Induced Vascular Inflammation and Remodeling

Activated monocytes are present in the arterial walls of hypertensive patients and animals. Monocyte chemoattractant protein-1 (MCP-1), which controls monocyte function through its receptor (CCR2), is implicated in hypertensive inflammatory changes in the arterial wall. The role of CCR2 expression on monocytes in hypertension-induced vascular remodeling, however, has not been addressed. We hypothesized that CCR2 on monocytes is critical in hypertension-induced vascular inflammation and remodeling. Hypertension was induced by infusion of angiotensin II (Ang II) into wild-type mice, CCR2-deficient (CCR2−/−) mice, and bone marrow-transferred mice with a leukocyte-selective CCR2 deficiency (BMT-CCR2−/−). In wild-type mice, Ang II increased CCR2 intensity in circulating monocytes, which was prevented by an Ang II type-1 (AT1) receptor blocker or blunted in AT1 receptor–deficient mice. Enhanced CCR2 intensity on monocytes was observed in hypertensive patients and rats, and was reduced by treatment with the Ang II receptor blocker, supporting the clinical relevance of the observation in mice. In CCR2−/− and BMT-CCR2−/− mice, Ang II–induced vascular inflammation and vascular remodeling (aortic wall thickening and fibrosis) were blunted as compared with control mice. In contrast, Ang II–induced left ventricular hypertrophy developed in CCR2−/− and BMT-CCR2−/− mice. The present study suggests that CCR2 expression in monocytes has a critical role in vascular inflammation and remodeling in Ang II–induced hypertension, and possibly in other forms of hypertension.

In-hospital and one-year outcomes for patients undergoing percutaneous coronary intervention for acute myocardial infarction

Previous studies have identified risk factors for short- and long-term outcomes for patients undergoing percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI). However, it remains unknown whether they can be generalized to current PCI practice for a broader cohort of patients. We analyzed the follow-up information (mortality and revascularization procedures) obtained from a nationwide Japanese registry during 1997 of a total of 2,211 patients with AMI who underwent PCI at 143 facilities. Demographic, clinical, angiographic, and procedural variables were submitted to statistical analysis to detect the risk factors of adverse outcomes. In-hospital and 1-year mortality rates were 7.1% and 10.9%, respectively. The most important risk factor for in-hospital death was attempted PCI of the left main (LM) coronary artery. Further independent risk factors for death were left ventricular (LV) dysfunction (ejection fraction </=40%), LM disease, older age, multivessel disease, cerebrovascular disease, and diabetes. The receiver-operating characteristics curve for the predicted probability of death was 0.88, indicating a good ability to discriminate high-risk patients. Independent risk factors for 1-year postdischarge mortality were LV dysfunction, older age, renal failure, multivessel disease, and diabetes. The incidence of the need for repeat PCI or bypass surgery was significantly higher in patients with multivessel and LM disease. PCI is a valuable treatment strategy for a broad spectrum of patients with AMI. However, the mortality for patients with LM disease and poor LV function is still high even using current practice standards.