SUMMARYDiabetic retinopathy (DR) is an early and frequent marker of other vascular complications of diabetes and its relation with coronary ischemia is known. The aim of the present study was to evaluate the association between DR and indices of coronary artery disease (CAD) severity and extent determined by coronary angiography.Sixty-nine diabetic patients undergoing coronary angiography for suspected CAD were evaluated. The severity and extent of CAD were scored from coronary angiograms by using 3 scores. Retinopathy was graded by fundus examination.There were differences in the severity score, extent score, number of vessels with disease, duration of diabetes, diabetes therapy, history of previous myocardial infarction (MI), and serum creatinine level among patients with and without DR. CAD severity was associated with the presence of DR (r: 0.53, P < 0.001), grade of DR (r: 0.52, P < 0.001), duration of diabetes (r: 0.28, P: 0.019), history of previous MI (r: 0.36, P: 0.002); and serum creatinine level (r: 0.24, P: 0.049) where the presence of DR was the only independent factor related to the severity score in multivariate analysis (r: 0.48, P < 0.001). The parameters related to the extent score were the presence of DR (r: 0.50, P < 0.001); grade of DR (r: 0.48, P < 0.001); previous MI (r: 0.37, P: 0.002) and age of the patient (r: 0.26, P: 0.033). Factors independently related to the extent score in multivariate analysis were the presence of DR (r: 0.37, P: 0.001), previous MI (r: 0.30, P: 0.006), and age of the patient (r: 0.22, P: 0.003).Among diabetics who are suspected of having CAD, those with retinopathy have more diffuse and severe coronary atherosclerosis, compared with diabetics without retinopathy. This cannot be explained by a longer duration or inferior control of the disease. (Int Heart J 2005; 46: 639-646)

No abstract

Background:Coronary artery ectasia (CAE) is defined as localized or diffuse dilatation of the coronary arteries. There are scarce data about the role of inflammation in CAE. In the present study, the plasma soluble adhesion molecules intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) levels in CAE were investigated. Methods: The study population (n = 67) consisted of four groups. Group 1: patients with normal coronary artery (NCA); group 2: patients with isolated ectasia without stenotic lesion; group 3: patients with obstructive coronary artery disease (OCAD) without CAE; group 4: patients with both OCAD and CAE. Results: Plasma concentrations of ICAM-1 and VCAM-1 were higher in patients with isolated ectasia than in cases with NCA (p < 0.001 and p < 0.001, respectively). Compared with OCAD patients, patients with CAE had significantly elevated concentrations of ICAM-1 and VCAM-1 (p < 0.001 and p < 0.05, respectively). The levels of ICAM-1 and VCAM-1 of the CAE and OCAD group were higher than in patients in the OCAD group (p < 0.05 and p < 0.05, respectively). We detected a positive correlation between the presence of CAE and the levels of ICAM-1 and VCAM-1. Multivariate logistic regression analyses revealed a significant independent relation between the presence of CAE and ICAM-1 and VCAM-1. Conclusion: We found elevated plasma levels of ICAM-1 and VCAM-1 in patients with CAE and OCAD + CAE compared with subjects with NCA and OCAD. These data strongly suggest that more severe vascular wall inflammation may play a role in the pathogenesis of CAE.

Elevated NLR and increased LVESD were independent prognostic factors in predicting persistent LV dysfunction in patients with PPCM. The NLR might assist in identifying high risk patients with PPCM.

RV function significantly improved after corrective surgery. Quantitative echocardiographic examination provides accurate estimation when deciding for corrective surgery and also should be used in the assessment of postoperative improvement.

These findings support the idea that LVDD may develop in patients with MetS even in the absence of hypertension. In addition, co-existence of hypertension with MetS contributes to further worsening of diastolic functions.

Patients with severe aortic regurgitation frequently present with angina pectoris. The exact pathophysiology for angina in aortic regurgitation is not clear. Left ventricular hypertrophy and myocardial blood supply-demand mismatch have been the suggested mechanisms to explain ischemia. However, no conclusive clinical study exists to define the incidence of ischemia in patients with severe aortic regurgitation and normal coronary arteries. We, therefore, investigated the frequency of myocardial ischemia in relation to left ventricular hypertrophy or dilatation in patients with severe aortic regurgitation and normal coronary arteries. We reviewed the medical records of all patients (n = 311) with aortic valve replacement due to aortic regurgitation between 2007 and 2010. We selected subjects with normal coronary arteries (n =182) for the study purpose, and we identified 35 patients who underwent myocardial perfusion scintigraphy prior to the coronary angiography (19 female and 16 male subjects; age 45.0 ± 8.9 years). Left ventricular hypertrophy and dilatation were detected in 9 (26%) and 5 (14%) patients, respectively. Myocardial perfusion scintigraphy showed evidence of ischemia in 10 (29%) patients with normal coronary arteries. The presence of ischemia did not relate to the presence of left ventricular hypertrophy and/or dilatation. As a potential mechanism, aortic regurgitation causes backflow of blood from the aorta into the left ventricle, hence disturbs coronary flow dynamics. In conclusion, myocardial ischemia is common (nearly one-third) among patients with severe aortic regurgitation even in the absence of coronary obstruction, left ventricular hypertrophy and/or dilatation.

No abstract