SUMMARYSeveral studies have suggested that an increased high sensitivity C-reactive protein (hsCRP) level is a strong independent predictor of increased risk for atherosclerotic cardiovascular mortality and morbidity. Reduced heart rate variability (HRV) has also been reported to predict cardiovascular events such as sudden death and myocardial infarction in apparently healthy subjects. The aim of this cross-sectional study was to test the possible correlation between variation of the R-R interval as one of the markers of HRV and serum hsCRP levels in a general population in Japan.Resting, supine, 2-minute, beat-to-beat heart rate data were collected in 823 randomly selected participants enrolled in our cohort study. The coefficient of variation of the R-R interval (CVrr) was obtained as a parameter of HRV. To determine which factors predict the presence of low CVrr (below the 5 percentile) in this group, we performed a multivariate logistic regression analysis using cardiovascular risk factors and an elevated hsCRP level as independent variables.The lowest CVrr group showed significantly higher hsCRP levels compared to those of other quartiles (P < 0.01). After adjustment for confounding factors such as age, heart rate, obesity, hypercholesterolemia, and hypertension by multivariate logistic analysis, an elevated hsCRP level (OR = 3.11, 95%CI; 1.27-7.60: P < 0.02) was a significant independent predictor of low CVrr.The results of the present study indicate that an increased serum hsCRP level is significantly associated with reduced CVrr in this general population. It is conceivable that the parasympathetic nerve withdrawal and inflammation could interact with each other, resulting in the progression of atherosclerotic cardiovascular disease. (Int Heart J 2006; 47: 867-876)
A 69-year-old man with prior myocardial infarction (hypertension; dyslipidemia; smoking; no diabetes; and no history of allergy, autoimmune disease, or vasculitis) underwent sirolimus-eluting stent (SES) implantation (3.0 mm in diameter; 33 mm in length) for chest pain on exertion with chronic total occlusion of the left anterior descending coronary artery (LAD) ( Figure 1A through 1C and Video 1). Intravascular ultrasound examination after SES implantation demonstrated well-expanded stent struts without evidence of incomplete stent apposition (ISA) ( Figure 1D through 1F).Follow-up angiography at 8 months after initial SES implantation demonstrated multifocal contrast staining outside the stent contour with no evidence of angiographic restenosis ( Figure 2A and Video 2). Subsequently, at 16 months after stenting, coronary angiography showed that the areas of contrast staining outside the stent contour increased in size ( Figure 2B and Video 3). At 23 months after stenting, coronary artery aneurysm (CAA) formation was demonstrated in the midportion of the SES ( Figure 2C and Video 4). The first 8-month angiography was a protocol-driven follow-up study for the index LAD lesion. The second 16-month angiography was also a protocol-driven follow-up study for the circumflex coronary artery lesion treated 8 months before. Similarly, the third 23-month angiography Figure 1. Baseline angiographic and intravascular ultrasound findings. A, Chronic total occlusion of the proximal LAD before percutaneous coronary intervention (arrow); B, collateral flow into the LAD from the right coronary artery (arrow); C, LAD after SES (3.0 mm in diameter; 33 mm in length) implantation (arrows); D through F, intravascular ultrasound images after SES implantation demonstrating well-expanded stent struts without evidence of incomplete stent apposition.
Several studies have demonstrated that pulmonary vascular abnormalities precede alterations in aortic circulation downstream in animal models of heart failure. The relationship between increased pulmonary vascular resistance (PVR) and agonist-induced limb vasodilatory response remains unknown in patients with congenital cardiovascular shunt lesions (CSL). The authors hypothesized that patients with CSL and severely elevated PVR will show a defective vasomotor response in the peripheral vascular bed. To examine this hypothesis we measured forearm blood flow (FBF) responses to the endothelium-dependent vasodilator acetylcholine and the endothelium-independent vasodilator sodium nitroprusside. The values for these FBF responses were compared with PVR in adult patients with CSL (n=20) and healthy age- and sex-matched controls (n = 15). When patients with CSL were divided into 2 subgroups by median value of PVR, in the lower PVR subgroup, acetylcholine-induced FBF changes were selectively and significantly lower than in the healthy control group (p <0.05). In the higher PVR subgroup, FBF responses to both acetylcholine and sodium nitroprusside were significantly blunted compared to healthy controls (both p < 0.01). In addition, when FBF changes above baseline for each dose of acetylcholine and sodium nitroprusside were cumulated and used as acetylcholine response and sodium nitroprusside response, the sensitivity and specificity for identifying patients with Eisenmenger's type of CSL was 100% and 80% by acetylcholine response, and 67% and 80% by sodium nitroprusside response, respectively. In conclusion, adult CSL patients with elevated PVR and severe pulmonary arterial hypertension showed generalized vasodilator dysfunction in the forearm vasculature. This result suggests that upper limb resistance vessel dysfunction may be an indicator for advanced stage of adult patients with CSL.
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