Flow-mediated Dilation In Patients Research Articles

Effects of lowering dialysate sodium on flow-mediated dilatation in patients with chronic kidney disease

This study examined the effects of low dialysate sodium on endothelial dysfunction (ED) as measured by flow-mediated dilatation (FMD) of brachial artery in haemodialysis (HD) patients. Thirty HD patients (17 men; mean age: 48.4 ± 17.8 years) were studied. Subjects underwent two consecutive 6-week HD periods. Dialysate sodium was 143 mEq/L in the first period (standard Na HD) and 137 mEq/L in the second period (low Na HD). After each period, we performed FMD, echocardiographic evaluation and 24-h ambulatory blood pressure monitoring (ABPM). Interdialytic weight gain (IDWG), levels of pre- and post-dialysis blood pressure (BP), and dialysis-related symptoms were monitored during the study. Per cent FMD was significantly greater (P < 0.05) after low Na HD (9.3 ± 6.2) compared with standard Na HD (5.7 ± 6.2). IDWG was significantly lower during low Na HD (2.35 ± 0.86 kg versus 2.71 ± 0.89 kg; P < 0.001). BP control was improved during low Na HD, as assessed by ABPM (128.2/77.5 mmHg versus 132.4/80.8 mmHg). Dialysis-related symptoms were more frequent during low Na HD (P < 0.05). There was no change in left ventricular mass after reducing dialysate sodium. Reducing dialysate sodium concentration reduced ED, and provided better control of IDWG and BP, but increased dialysis-related symptoms.

Clinical correlates of endothelial function in chronic heart failure

There is a close link between heart failure and endothelial dysfunction. Brachial flow-mediated dilation (FMD) is a validated non-invasive measure of endothelial function. The aim of this study was to investigate the clinical correlates of FMD in patients with chronic heart failure (CHF). We evaluated 60 CHF outpatients (age 62 ± 14 years; 49 males, NYHA class 2.2 ± 0.7, left ventricular ejection fraction, LVEF, 33 ± 8%) taking conventional medical therapy (ACE-inhibitors and/or ARBs 93%, beta-blockers 95%) and in stable clinical conditions. The maximum recovery value of FMD was calculated as the ratio of the change in diameter (maximum-baseline) over the baseline value. As compared with patients with a higher FMD, those with FMD below the median value (4.3%) were more frequently affected by ischemic cardiopathy (50 vs. 23%; p = 0.032) and diabetes mellitus (20 vs. 3%; p = 0.044), had a higher NYHA class (2.5 ± 0.5 vs. 1.9 ± 0.7; p < 0.001) and NT-proBNP (2,690 ± 3,690 vs. 822 ± 1,060; p = 0.001), lower glomerular filtration rate estimated by Cockcroft-Gault (GFRCG: 63 ± 28 vs. 78 ± 25; p = 0.001) and LVEF (29 ± 8 vs. 37 ± 9; p = 0.001), as well as more frequently showing a restrictive pattern (40 vs. 7%; p = 0.002). In a multivariate regression model (R (2) = 0.48; p < 0.001), FMD remained associated only with the NYHA class (p = 0.039) and diabetes mellitus (p = 0.024). This study demonstrates that a better functional status and absence of diabetes mellitus are associated to higher FMD regardless of the etiology of the cardiac disease.

Evaluation of carotid intima-media thickness and flow-mediated dilatation in middle-aged patients with nonalcoholic fatty liver disease

BackgroundNonalcoholic fatty liver disease (NAFLD) has a high prevalence in the general population and is the most common liver disease in Western countries. It is a feature of metabolic syndrome and is characterized by excessive accumulation of fat in the liver cells.MethodsWe examined 84 consecutive middle-aged (under 45 years) patients with NAFLD and 65 control subjects matched for age, gender, and body mass index to determine carotid intima-media thickness (CIMT) and flow-mediated dilatation (FMD) in the brachial artery.ResultsThere was a statistically significant difference between CIMT and percentage increase in FMD in the patient group (P = 0.002; r = 0.33) when compared with the control group (P = 0.97; r = 0.005). The mean ± standard deviation CMIT was 0.65 ± 0.09 mm in patients and 0.55 ± 0.07 mm in controls. This difference was statistically significant (P = 0.001). Mean FMD in patients was 6.4% and 15.7% in controls. This difference was statistically significant (P = 0.001).ConclusionThis study shows that pure NAFLD without metabolic syndrome in middle-aged subjects is strongly associated with morphological (CIMT) and physiological (FMD) changes. These findings may have an important role in increasing cardiovascular risk in these patients.

Enhanced External Counterpulsation Improves Peripheral Artery Flow-Mediated Dilation in Patients With Chronic Angina: A Randomized sham-Controlled Study

Enhanced External Counterpulsation Improves Peripheral Artery Flow-Mediated Dilation in Patients With Chronic Angina: A Randomized sham-Controlled Study

Enhanced External Counterpulsation Improves Peripheral Artery Flow-Mediated Dilation in Patients With Chronic Angina

Background— Mechanisms responsible for anti-ischemic benefits of enhanced external counterpulsation (EECP) remain unknown. This was the first randomized sham-controlled study to investigate the extracardiac effects of EECP on peripheral artery flow-mediated dilation. Methods and Results— Forty-two symptomatic patients with coronary artery disease were randomized (2:1 ratio) to thirty-five 1-hour sessions of either EECP (n=28) or sham EECP (n=14). Flow-mediated dilation of the brachial and femoral arteries was performed with the use of ultrasound. Plasma levels of nitrate and nitrite, 6-keto-prostaglandin F 1α , endothelin-1, asymmetrical dimethylarginine, tumor necrosis factor-α, monocyte chemoattractant protein-1, soluble vascular cell adhesion molecule, high-sensitivity C-reactive protein, and 8-isoprostane were measured. EECP increased brachial (+51% versus +2%) and femoral (+30% versus +3%) artery flow-mediated dilation, the nitric oxide turnover/production markers nitrate and nitrite (+36% versus +2%), and 6-keto-prostaglandin F 1α (+71% versus +1%), whereas it decreased endothelin-1 (−25% versus +5%) and the nitric oxide synthase inhibitor asymmetrical dimethylarginine (−28% versus +0.2%) in treatment versus sham groups, respectively (all P &lt;0.05). EECP decreased the proinflammatory cytokines tumor necrosis factor-α (−16% versus +12%), monocyte chemoattractant protein-1 (−13% versus +0.2%), soluble vascular cell adhesion molecule-1 (−6% versus +1%), high-sensitivity C-reactive protein (−32% versus +5%), and the lipid peroxidation marker 8-isoprostane (−21% versus +1.3%) in treatment versus sham groups, respectively (all P &lt;0.05). EECP reduced angina classification (−62% versus 0%; P &lt;0.001) in treatment versus sham groups, respectively. Conclusions— Our findings provide novel mechanistic evidence that EECP has a beneficial effect on peripheral artery flow-mediated dilation and endothelial-derived vasoactive agents in patients with symptomatic coronary artery disease.

Association of abacavir and impaired endothelial function in treated and suppressed HIV-infected patients

HIV-infected patients have accelerated atherosclerosis. Abacavir has been associated with increased risk of cardiovascular events, for reasons that remain to be elucidated. As endothelial dysfunction is central to the pathogenesis of atherosclerosis, we tested the hypothesis that current treatment with abacavir is associated with impaired endothelial function. We studied a cohort of 61 antiretroviral-treated patients who had undetectable plasma HIV RNA levels. Endothelial function was assessed by measuring flow-mediated dilation (FMD) of the brachial artery. We compared FMD in patients treated with or without abacavir, while adjusting for traditional risk factors and HIV-specific characteristics. The median age was 50 years (interquartile range 45-57). The median duration of HIV infection was 18 years, and the median CD4 cell count was 369 cells/microl. Thirty patients (49%) were receiving abacavir. Overall, the median FMD in the HIV-infected patients was low (3.5%; interquartile range 2.3-5.6%). The FMD was lower in the abacavir-treated patients than those not on abacavir (2.8 vs. 4.9%, P = 0.01). After adjustment for traditional risk factors, HIV-specific factors, and baseline brachial artery diameter, current abacavir use was independently associated with lower FMD (P = 0.017). Duration of therapy and CD4 cell count were not associated with reduced FMD. Endothelial function, a central mechanism in atherosclerosis and a marker of cardiovascular risk, is impaired among antiretroviral-treated patients with undetectable viral loads. Current use of abacavir was independently associated with impaired endothelial function. This finding suggests that abnormal endothelial function may underlie the clinically observed increased risk in myocardial infarction among abacavir-treated patients.

Endothelial Function in Lacunar Infarction: A Comparison of Lacunar Infarction, Cerebral Atherosclerosis and Control Group

Background: There are conflicting evidences on endothelial function in lacunar infarction. This may be attributed to the effects of risk factors on the vascular smooth muscle. To test endothelial function only in patients with lacunar infarction, we evaluated the endothelium-dependent and -independent vasodilatation of the brachial artery. Methods: We enrolled consecutive patients with lacunar infarction defined by clinical characteristics and MRI findings. The control group included age- and sex-matched patients with hypertension who do not have any history of clinical stroke, coronary artery disease or peripheral vascular disease. Endothelial function was evaluated using flow-mediated dilatation (FMD) and nitrogen-mediated dilatation (NMD) of the brachial artery. FMD and NMD were examined by an experienced vascular sonographer using a high-resolution ultrasound. Intracranial stenosis was defined as flow gap or >50% reduction in vessel diameter on MRA. Results: FMD was 6.6 ± 4.5% in the lacunar infarction group and 12.2 ± 4.6% in the control group (p = 0.000). NMD was 14.3 ± 4.9% in the lacunar infarction group and 13.8 ± 4.9% in the control group (p = 0.37). FMD in patients with lacunar infarction and intracranial arterial stenosis was 6.4 ± 3.9%, and FMD in patients with lacunar infarction was only 6.9 ± 5.5%. In the control group, it was 12.2 ± 4.6%. Conclusion: FMD was low in patients with lacunar infarction. NMD was similar between the lacunar infarction group and the control group. These results are suggestive of pure endothelial dysfunction in lacunar infarction. Endothelial dysfunction was as severe in lacunar infarction as in intracranial arterial stenosis.

Brachial arterial flow mediated dilation in acute ischemic stroke

Brachial arterial flow-mediated dilation (FMD) reflects endothelium-dependent vasodilation function. FMD is diminished in patients with endothelial dysfunction (ED). Our aim was to investigate the relationship between FMD and outcome for patients with acute ischemic stroke. We measured FMD in 120 consecutive patients (58.3% male, median age 73 years) with acute ischemic stroke within the first 48 h of onset of the stroke, using high-resolution ultrasonography. FMD was calculated as the relationship between basal diameter of the brachial artery before (d(1)) and after (d(2)) transient vascular occlusion (300 mmHg for 4 min) was measured using a sphygmomanometer (FMD = d(2) - d(1)/d(1) x 100). Poor outcome was defined as modified Rankin Scale at 3 months >2. FMD was categorized according to ROC analysis and we defined ED as FMD < or = 4.5%. Thirty-three patients (27.5%) had ED. Median % FMD was 9.12 (7.48). FMD negatively correlated to stroke severity (P = 0.045). Median FMD was significantly lower [4.5 (2.3, 10.3) vs. 9.4 (5.6, 15.1), P = 0.003] for patients with poor outcome (n = 38). The adjusted odds ratio of poor outcome for FMD < or = 4.5% was 3.03 (95% CI, 1.09-27.3). Impaired FMD in patients with acute ischemic stroke is associated with poor outcome.

Total occlusion of the infarct-related coronary artery correlates with brachial artery flow-mediated dilation in patients with ST-elevation myocardial infarction

Occlusion of the coronary artery is the main cause of ST-elevation myocardial infarction (STEMI). In some patients, it is followed by early spontaneous thrombolysis. In this study, we tried to determine whether spontaneous thrombolysis in the infarct-related artery (IRA) correlates with the state of the endothelium, which we assessed using the brachial artery flow-mediated dilation (FMD) test. 52 patients with STEMI were included in the study. Based on the results of coronary angiography performed during the first three days of STEMI, the patients were divided into two groups: Group I (n=33), consisting of patients with remaining total occlusion of the IRA, and Group II (n=19), consisting of patients with spontaneous thrombolysis. We assessed the endothelial function, using the brachial artery FMD test. In Group I, during the first three days of STEMI, brachial artery FMD results were significantly lower than those in Group II: 5.41+/- (3.23-7.41)% versus 10.81+/-(8.00-14.89)%, respectively; P=0.000036. After 7-14 days, this difference disappeared because of significant elevation of the FMD levels in the first group. Group I was characterized by higher levels of high sensitive C-reactive protein (CRP), cholesterol, and cholesterol-LDL and lower usage of angiotensin-converting enzyme (ACE) inhibitors before STEMI. The data presented above reveal that spontaneous coronary thrombolysis in patients with acute STEMI is associated with a preserved endothelium-dependent vasodilator response in the brachial artery. It can depend on the levels of hs-CRP, of fasting glucose, and of ACE-inhibitors from previous treatment.

Efficacy of Nebivolol on Flow-Mediated Dilation in Patients With Slow Coronary Flow

Slow coronary flow (SCF) is the phenomenon of slow progression of angiographic contrast in the coronary arteries in the absence of stenosis in the epicardial vessels in some patients presenting with chest pain. There are no definite treatment modalities for patients with SCF. Our aim was to investigate the efficacy of nebivolol in patients with slow coronary flow by monitoring its effects on endothelial function and different markers of inflammation. Forty-two patients (16 females, 26 males; mean age, 55 +/- 10) with slow coronary flow (SCF) were included in the study. After baseline assessment, the patients were administered nebivolol 5 mg once daily. After 12 weeks of nebivolol therapy, the biochemical and ultrasonographic examinations were repeated. Chest pain relief was detected in 38 patients after treatment (90%). Systolic and diastolic blood pressure and high sensitive CRP were significantly decreased after nebivolol therapy. Among brachial artery dilation variables that reflect endothelial function, basal resistive index (RI), post-flow mediated dilation RI, and post-nitrate mediated dilation RI were significantly decreased after therapy. Nebivolol is effective at improving endothelial function in patients with SCF. It controls chest pain, decreases CRP, and has favorable effects on brachial artery dilation variables in patients with coronary slow flow.

Flow-mediated dilation in patients with coronary artery disease is enhanced by high dose atorvastatin compared to combined low dose atorvastatin and ezetimibe: Results of the CEZAR study

BackgroundEffects independent from cholesterol reduction on vascular function are considered to importantly contribute to the beneficial effects of statin therapy in cardiovascular disease. We aimed to evaluate the effect of high versus low dose atorvastatin on endothelial dysfunction in patients with coronary artery disease (CAD) in a setting of comparable cholesterol reduction. Methods and resultsFifty-eight patients with CAD were randomly assigned to double-blind treatment for 8 weeks with atorvastatin 80mg per day (A80) or atorvastatin 10mg+ezetimibe 10mg per day (A10E10), respectively. Flow-mediated vasodilation (FMD) of the brachial artery, nitroglycerin-mediated endothelium-independent vasodilation (NMD), lipid, C-reactive protein (CRP) plasma concentrations and urinary 8-iso-prostaglandin F2alpha excretion were measured before and after treatment. Total cholesterol, triglycerides and LDL-cholesterol levels were significantly reduced with no difference between A80 and A10E10. A80 caused significantly stronger improvement of FMD compared to A10E10 (absolute change FMD: A80+2.7±3.0% (post vs. pre p<0.001), A10E10+0.6±2.9% (post vs. pre p=0.25), A80 vs. A10E10 p=0.018). NMD was improved by A80 but not by A10E10 (absolute change NMD: A80+2.7±4.6%, A10E10+0.7±3.5%, p=0.12). Both treatment groups caused a comparable reduction of CRP and did not effect urinary 8-iso-prostaglandin F2alpha excretion. There was no correlation between FMD or NMD change and LDL-cholesterol change in either treatment group. ConclusionsThe present findings clearly suggest that in the presence of comparable LDL-lowering effects of both treatment forms, LDL-cholesterol independent effects of high dose atorvastatin therapy account for the improvement of endothelium-dependent vasodilation in patients with stable CAD.

Daily intake of thiamine correlates with the circulating level of endothelial progenitor cells and the endothelial function in patients with type II diabetes

Our objective was to determine the relationships between levels of different dietary nutrients intake with circulating endothelial progenitor cells (EPC) and vascular endothelial function in type II diabetic patients. We studied the daily dietary nutrients intake, the numbers of circulating CD34(+)/KDR(+) EPC and CD133(+)/KDR(+) EPC and brachial artery flow-mediated dilation (FMD) in 88 diabetic patients without prior cardiovascular diseases and 91 sex- and age-matched controls. Compared with controls, diabetic patients had lower CD133(+)/KDR(+) EPC count (48.3 +/- 5.2 vs. 84.6 +/- 7.6/microL, p < 0.001), CD34(+)/KDR(+) EPC count (311 +/- 41 vs. 412 +/- 36/microL, p = 0.045), and FMD (2.54 +/- 0.37% vs. 5.46 +/- 0.47%, p < 0.001). After adjusted for age, sex, smoking history, body weight, hemoglobin A1c level, total calorie intake, other dietary vitamin intake, use of antihypertensives, and lipid lowering agents, a higher intake of thiamine was significantly associated with a higher level of circulating CD34(+)/KDR(+) EPC (beta = 0.49, p = 0.028) and CD133(+)/KDR(+) EPC (beta = 0.45, p = 0.037) in diabetic patients, but not in controls. Furthermore, an increased intake of thiamine from 1st to 4th quartile in diabetic patients independently predicted an absolute increase in FMD by 1.29% (p = 0.026, relative increase = 63.5%). This study demonstrated that daily thiamine intake was positively correlated with the circulating number of EPCs and FMD in patients with type II diabetes, independent of other dietary nutrients intake.

Oxidative DNA Damage Is Significantly Correlated With Flow-Mediated Dilation in Patients With Coronary Artery Disease

BackgroundOxidative DNA damage was increased in patients with coronary artery disease (CAD) and correlated with the severity of the disease. Endothelial dysfunction plays a major role in atherosclerotic process. The...

Successful lower extremity angioplasty improves brachial artery flow-mediated dilation in patients with peripheral arterial disease

Peripheral arterial disease (PAD) is associated with systemic impaired flow-mediated dilation (FMD) and increased risk for cardiovascular events. Decreased FMD may be caused by a decrease in arterial shear stress due to claudication and inflammation due to muscle ischemia and reperfusion. We assumed that endovascular revascularization of lower limb arterial obstructions ameliorates FMD and lowers inflammation through improvement of peripheral perfusion. The study was a prospective, open, randomized, controlled, single-center follow-up evaluation assessing the effect of endovascular revascularization on brachial artery reactivity (FMD) measured by ultrasound, white blood cell (WBC) count, high-sensitive C-reactive protein (hs-CRP), and fibrinogen. We investigated 33 patients (23 men) with chronic and stable PAD (Rutherford 2 to 3) due to femoropopliteal obstruction. Variables were assessed at baseline and after 4 weeks in 17 patients (group A) who underwent endovascular revascularization and best medical treatment, and in 16 patients (group B) who received best medical treatment only. FMD did not differ between group A and B (4.96% +/- 1.86% vs 4.60% +/- 2.95%; P = .87) at baseline. It significantly improved after revascularization in group A (6.44% +/- 2.88%; P = .02) compared with group B at 4 weeks of follow-up (4.53% +/- 3.17%; P = .92), where it remained unchanged. The baseline ankle-brachial index (ABI) was similar for group A and B (0.63 +/- 0.15 vs 0.66 +/- 0.10; P = .36). At 4 weeks of follow-up, ABI was significantly increased in group A (1.05 +/- 0.15; P = .0004) but remained unchanged in group B (0.62 +/- 0.1). WBC counts of the two groups were comparable at baseline (group A: 7.6 +/- 2.26 x 10(6)/mL and group B: 7.8 +/- 2.02 x 10(6)/mL, P = .81). In group A, the leukocyte count significantly decreased after angioplasty from 7.6 +/- 2.26 to 6.89 +/- 1.35 x 10(6)/mL (P = .03). For group B, WBC count did not differ significantly compared with baseline (7.76 +/- 2.64 x 10(6)/mL; P = .94). No effects were observed on hs-CRP or fibrinogen from endovascular therapy. Endovascular revascularization with reestablishment of peripheral arterial perfusion improves FMD and reduces WBC count in patients with claudication. Revascularization may therefore have clinical implications beyond relief of symptoms, for example, reducing oxidative stress caused by repeated muscle ischemia or increased shear stress due to improved ambulatory activity.

Effects of oral niacin on endothelial dysfunction in patients with coronary artery disease: Results of the randomized, double-blind, placebo-controlled INEF study

High-density-lipoproteins-cholesterol (HDL-C) is invertedly related to the incidence of cardiovascular events. Recent studies suggest that HDL-C directly improves endothelial function. Nicotinic acid (niacin) effectively raises serum HDL-C. We therefore hypothesized that treatment with niacin improves endothelial dysfunction in patients with coronary artery disease (CAD). One hundred seven patients with CAD were randomly assigned to double-blinded treatment for 12 weeks with extended-release (ER)-niacin 1000 mg/day (N) or placebo (C), respectively. Flow-mediated dilation (FMD) of the brachial artery, nitroglycerin-mediated endothelium-independent dilation (NMD) and serum lipid concentrations were measured before and after treatment. Triglycerides ( P = 0.013), low-density-lipoprotein-cholesterol (LDL-C) ( P = 0.013) and HDL-C ( P < 0.0001) were altered by N compared to C. Niacin treatment was without effect on FMD or NMD, respectively, compared to placebo. However, post-hoc subgroup analysis revealed an improvement in FMD in patients with low HDL-C at baseline (absolute change in FMD (mean ± S.D.) N: +3.25 ± 3.88%, C: +1.03 ± 2.71% in low tertile HDL-C ≤45 mg/dl. P = 0.047). The present findings indicate that ER-niacin treatment improves endothelial dysfunction in patients with CAD and low HDL-C, but not with normal HDL-C.

Reduction of C-reactive protein with isoflavone supplement reverses endothelial dysfunction in patients with ischaemic stroke

To investigate the effect of oral isoflavone supplement on vascular endothelial function in patients with established cardiovascular disease. A randomized, double-blinded, placebo-controlled trial was performed to determine the effects of isoflavone supplement (80 mg/day, n = 50) vs. placebo (n = 52) for 12 weeks on brachial flow-mediated dilatation (FMD) in patients with prior ischaemic stroke. Compared with controls, FMD at 12 weeks was significantly greater in isoflavone-treated patients [treatment effect 1.0%, 95% confidence interval (95% CI) 0.1-2.0, P = 0.035]. Adjusted for baseline differences in FMD, isoflavone treatment was independently associated with significantly less impairment of FMD at 12 weeks (odds ratio 0.32, 95% CI 0.13-0.80, P = 0.014). The absolute treatment effect of isoflavone on brachial FMD was inversely related to baseline FMD (r = -0.51, P < 0.001), suggesting that vasoprotective effect of isoflavone was more pronounced in patients with more severe endothelial dysfunction. Moreover, isoflavone treatment for 12 weeks resulted in a significant decrease in serum high-sensitivity (hs)-C-reactive protein level (treatment effect -1.7 mg/L, 95% CI -3.3 to -0.1, P = 0.033). Nevertheless, isoflavone did not have any significant treatment effects on nitroglycerin-mediated dilatation, blood pressure, heart rate, serum levels of fasting glucose and insulin, haemoglobin A1c, and oxidative stress as determined by serum superoxide dismutase, 8-isoprostane, and malondialdehyde (all P > 0.05). This study demonstrated that 12 week isoflavone treatment reduced serum hs-C-reactive protein and improved brachial FMD in patients with clinically manifest atherosclerosis, thus reversing their endothelial dysfunction status. These findings may have important implication for the use of isoflavone for secondary prevention in patients with cardiovascular disease, on top of conventional interventions.

The Acute Effect of Cardiac Pacing Mode on Endothelial Vasodilation: Prospective, Double‐Blind, Cross‐Over, Comparative Clinical Study

Compared to atrioventricular sequential pacing, ventricular demand pacing is known to have somewhat more deleterious hemodynamic effects, which probably arise from increased sympathetic tonus and inappropriate baroreceptor activation. Endothelial function is affected by various local and systemic factors including baroreceptor activity. The aim of this study was to explore whether cardiac pacing would have any effect on endothelial functions. Twelve patients (six male, mean age: 75 +/- 9 years) with previously implanted DDD or VDDcardiac pacemakers were included. All patients had stable atrial rhythms during the study. Patients were randomized to either atrial-based pacing mode (VDD or DDD) or ventricular demand pacing mode (VVI) first, and then cross-over was performed with the other pacing mode. Endothelial function was assessed by brachial artery ultrasonography. Basal diameter of the brachial artery, and both flow-mediated dilation (FMD) and endothelium-independent vasodilation with nitroglycerin were measured 1 hour after each pacing mode. Compared to atrial-based pacing mode, ventricular demand pacing was associated with a significantly worse FMD both as absolute and percentage values (0.17 +/- 0.09 mm vs 0.28 +/- 0.11 mm, P = 0.015 and 4.84 +/- 2.37 % vs 7.00 +/- 2.88 %, P = 0.028, respectively). However, there was no significant difference in nitroglycerin-mediated vasodilation values between the two pacing sessions. Acute ventricular demand pacing (VVI pacing) is clearly associated with attenuation of FMD in patients with atrial-based pacing systems. The attenuation of endothelial vasodilation might have a role in hemodynamic and clinical deterioration in patients with VVI pacemakers.

Transient Limb Ischemia Induces Remote Preconditioning and Remote Postconditioning in Humans by a K ATP Channel-Dependent Mechanism

Conclusion: Remote postconditioning (RPostC) is inducible by transient limb ischemia and is as effective as remote ischemic preconditioning (RIPC) for preventing endothelial ischemic–reperfusion (IR) injury. Summary: Ischemic postconditioning and ischemic preconditioning are mechanisms that may protect tissues from injury during IR. In ischemic preconditioning, short periods of IR are applied before a prolonged ischemic insult. In ischemic postconditioning, there is a modified schedule of reperfusion that uses intermediate restoration of flow after prolonged episodes of ischemia (Physiol Rev 2003;83:1113-51; Basic Res Cardiol 2005;100:295-310). Both ischemic preconditioning and ischemic postconditioning share similar mechanisms. In both forms of intervention, survival kinases and mitochondrial adenosine triphosphate (ATP)-sensitive potassium+ (KATP) channels are activated as part of the process of IR tissue protection. It is also known that protection from IR injury can be achieved by application of ischemia to remote sites during an injurious ischemic event. This is termed remote postconditioning (RPostC). In this study, the authors used an in vivo model of endothelial IR injury to determine whether RPostC occurs in humans and if it shares similar mechanisms with RIPC. The authors assessed endothelial function by flow-mediated dilatation before and after 20 minutes of arm ischemia, followed by reperfusion. Remote ischemic preconditioning was induced by conditioning cycles of 5 minutes of ischemia and reperfusion on the contralateral leg or arm before IR. Remote postconditioning induction conditioning cycles were administered during the ischemic phase of IR. The dependence of RIPC and RPostC on KATP was determined with use of oral glibenclamide. Ischemia–reperfusion reduced flow-mediated dilatation in healthy volunteers (baseline, 9.3% ± 1.2% vs post-IR, 3.3% ± 0.7%; P < .0001). Ischemia–reperfusion also caused a significant reduction in flow-mediated dilatation in patients with atherosclerosis (baseline, 5.5% ± 0.6% vs post-IR, 2.3% ± 0.5%; P < .01). These reductions were prevented by RIPC in healthy volunteers (post-IR plus RIPC, 7.2% ± 0.5%, P < .0001 vs post-IR) and in atherosclerotic patients (P < .01 vs post-IR). Reduction was also prevented by RPostC (post-IR plus RpostC, 8.0% ± 0.5%; P < .0001 vs post-IR). Glibenclamide blocked the protective effects of both RPost C and RIPC. Comment: The study may have huge implications. It suggests that in patients undergoing an ischemic event (myocardial infarction, stroke, acute mesentery ischemia or acute limb ischemia), the ischemia–reperfusion injury may be modified by producing transient limb ischemia at a remote site before and after revascularization of the critically ischemic tissue. It should be possible to easily test the effect of this relatively benign stimulus on patients with acute ischemic events.

Prognostic value of flow-mediated dilatation following myocardial infarction

BackgroundRisk stratification for subsequent cardiovascular events following a myocardial infarction (MI) is an important area of research. Previous findings indicate flow-mediated dilatation (FMD) may be a valuable prognostic indicator. This study investigates the prognostic value of FMD in patients suffering an uncomplicated MI. MethodsOne hundred and seventy nine post-MI patients [110male/69 female, mean age: 64.8±10.0 years, ejection fraction: 51.9±12.2%] were included in this analysis. Ultrasound images of the brachial artery were used to determine FMD following reactive hyperemia. Subjects were tracked for subsequent cardiovascular events [myocardial infarction, heart failure, additional interventions (percutaneous coronary intervention, coronary artery bypass)] following data collection via medical chart review. ResultsThere were 45 subsequent cardiovascular events during a mean tracking period of 13.7 (±9.5) months. Receiver operating characteristic (ROC) curve analysis revealed a diagnosis of diabetes (ROC area: 0.67, p=0.001, 95% confidence interval: 0.58–0.77) and percent change in arterial diameter (ROC area: 0.63, p=0.01, 95% confidence interval: 0.53–0.73, optimal threshold: ≤/>4.5%) were prognostically significant. Kaplan–Meier analysis revealed the event-free survival rate for subjects without diabetes and an arterial diameter change >4.5%, without diabetes and percent change in arterial diameter ≤4.5%, with diabetes and percent change in arterial diameter >4.5% and with diabetes and percent change in arterial diameter ≤4.5% was 88.7%, 78.4%, 67.7% and 38.5%, respectively (Log-rank: 24.9, p<0.0001). ConclusionsNon-invasive FMD is a potential risk factor after MI and may add information to conventional risk stratification. This will need to be tested in further studies.

The Effect Of Uncomplicated Percutaneus Coronary Intervention On Brachial Artery Flow Mediated Dilatation in Patients With Stable Angina Pectoris

The Effect Of Uncomplicated Percutaneus Coronary Intervention On Brachial Artery Flow Mediated Dilatation in Patients With Stable Angina Pectoris