Peripheral Vascular Endothelial Dysfunction in Patients With Angina Pectoris and Normal Coronary Arteriograms

Lekakis, John; Papamichael, Christos; Vemmos, Costas; Voutsas, Anastasios; Stamatelopoulos, Stamatios; Moulopoulos, Spyridon D.

doi:10.1016/s0735-1097(97)00542-1

Cited by 97 publications

(66 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Because this reduction occurred, however, together with and in relation to an increase in arterial wall thickness, an alteration in arterial wall structure is presumably involved. This alteration could originate from the reduced nitric oxide secretion that can be seen in diabetes [39], because firstly nitric oxide has been shown to oppose proliferation of vessel wall tissue in vitro [40] and secondly endothelial function has been found to be inversely related to carotid artery wall thickness both in studies of animals and humans in vivo [41,42]. It could, however, also be due to the insulin given exogeneously because insulin is known to be a growing factor for vascular wall tissues [43].…”

Section: Discussionmentioning

confidence: 99%

Early impairment of large artery structure and function in Type I diabetes mellitus

et al. 1999

View full text Add to dashboard Cite

Diabetes mellitus is associated with an increased risk of atherosclerosis [1]. Atherosclerosis is responsible for the increased rate of coronary heart disease, cerebrovascular disease and peripheral artery disease typical of diabetes mellitus [2±13]. It is not, however, well established how early alterations in large artery function, that may preceed the appearance and favour the progression of atherosclerotic lesions, i. e. a reduced arterial distensibility, occur in diabetic patients [14±16]. This is because most studies on arterial distensibility have been done in Type II (non-insulindependent) diabetes mellitus, where it is difficult to separate the arterial stiffening due to abnormalities Diabetologia (1999) Abstract Aims/hypothesis. Diabetes mellitus is associated with an increased incidence of atherosclerosis. How early functional and structural alterations of large arteries that may preceed atherosclerosis occur in the course of this disease has, however, never been conclusively documented. Methods. We evaluated arterial wall distensibility in the radial artery, common carotid artery and abdominal aorta in 133 patients (aged 35.4 ± 0.9 years, means ± SEM) with Type I (insulin-dependent) diabetes mellitus and no macrovascular complications. Arterial distensibility was derived from continuous measurements of arterial diameter through echotracking techniques and use of either the Langewouters (radial artery) or the Reneman (carotid artery and aorta) formula. The same echotracking techniques enabled us to obtain radial artery and carotid artery wall thickness. Data were compared with those from 70 age-matched normotensive control subjects. Results. In diabetic patients arterial distensibility was consistently less (p < 0.01) than in control subjects, the reduction averaging 26 %, 14 % and 25 % for the radial artery, carotid artery and aorta, respectively. This was accompanied by an increase (p < 0.01) in both radial and carotid artery wall thickness. The changes were more pronounced in patients with microalbuminuria, retinopathy or neuropathy or both. They were evident also in those without microvascular complications. This was the case also when subjects in whom diabetes was associated with hypertension (n = 30) were excluded from data analysis. Carotid and aortic wall abnormalities showed a relation with the duration of disease and blood pressure whereas radial artery abnormalities showed a relation with glycated haemoglobin. Conclusion/interpretation. Type I diabetes is characterised by diffuse arterial wall stiffening and thickening which progress with the severity of the disease but can clearly be seen also in the absence of any diabetic-related complication. This suggests that in diabetes stiffening and thickening are an early marker of vascular damage. [Diabetologia (1999) 42: 987± 994]

show abstract

Section: Discussionmentioning

confidence: 99%

Early impairment of large artery structure and function in Type I diabetes mellitus

et al. 1999

View full text Add to dashboard Cite

show abstract

“…However, MFR did not relate to endothelial dysfunction in isolated subcutaneous resistance arteries as measured by acetylcholine-induced vasodilatation. Impaired FMD has been demonstrated in patients with microvascular angina and coronary artery disease, 11 and has been related to coronary endothelial dysfunction in patients evaluated for coronary artery disease. 37 Our results extend these findings to hypertensive patients without coronary heart disease, but with LV hypertrophy on electrocardiogram.…”

Section: Vasodilatory Dysfunctionmentioning

confidence: 99%

“…medium-sized conduit arteries 8 and in resistance arteries. 9,10 Nonhypertensive patients with symptoms of angina pectoris, but with normal coronary angiograms, have decreased flow-mediated dilatation (FMD) in the brachial artery during reactive hyperaemia, 11 as well as increased minimal forearm vascular resistance (FVR), 12 suggesting parallel vascular dysfunction in the coronary and peripheral vasculature. This parallel vascular dysfunction has also been identified by Leschke et al, 13 who found increased minimal FVR in hypertensive patients with reduced MFR.…”

Section: Introductionmentioning

confidence: 99%

Association between vascular dysfunction and reduced myocardial flow reserve in patients with hypertension: a LIFE substudy

et al. 2004

View full text Add to dashboard Cite

Impaired myocardial flow reserve (MFR) has been demonstrated in hypertension, and has been associated with peripheral vascular changes. We investigated whether MFR was impaired and associated with structural and/or functional vascular changes in hypertensive patients without evidence of coronary artery disease (CAD). We measured left ventricular (LV) mass index by echocardiography and MFR by positron emission tomography in 33 unmedicated, hypertensive patients with electrocardiographic LV hypertrophy without CAD, and 15 age-and gender-matched normotensive subjects. We also measured 24-h ambulatory blood pressure, minimal forearm vascular resistance (MFVR) by plethysmography, media:lumen ratio in isolated, subcutaneous resistance arteries by myography, intima-media crosssectional area of the common carotid artery, and flow-mediated (FMD) and nitroglycerin-induced dilatation (NID) of the brachial artery by ultrasound. Compared to the controls, the patients had impaired MFR (2.4 (95% CI 1.95-2.8) vs 3.4 (2.7-4.2), Po0.01) due to increased resting myocardial blood flow (MBF) (0.82 (0.73-0.91) vs 0.65 (0.56-0.75) ml/g min), and decreased dipyridamole-stimulated MBF (1.80 (1.55-2.1) vs 2.3 (1.80-2.8) ml/g min, both Po0.05). The difference in resting MBF disappeared (80 (74-87) vs 86 (74-97) ll/ kg mmHg, NS) when normalized for blood pressure and heart rate. MFR correlated negatively to median 24-h systolic blood pressure (r ¼ À0.50, Po0.01) as well as to LV mass index (r ¼ À0.45, Po0.05) and MFVR in men (r ¼ À0.47, Po0.05), and positively to FMD (r ¼ 0.44, Po0.05) and NID (r ¼ 0.40, Po0.05). Hypertensive patients with electrocardiographic LV hypertrophy without CAD had impaired MFR associated with cardiovascular hypertrophy and vasodilatory dysfunction. This suggests that MFR is impaired by LV hypertrophy and structural/functional vascular damage in the coronary and noncoronary circulation.

show abstract

“…Microvascular dysfunction appears to be part of a systemic process 33,34) . The functional capacity of the myocardial microcirculation may be assessed by CFR, and GFR may in part reflect and rely on the integrity of the renal microvascular bed.…”

Section: Discussionmentioning

confidence: 99%

A Reduction of Coronary Flow Reserve Is Associated With Chronic Kidney Disease and Long-Term Cardio-Cerebrovascular Events in Patients With Non-Obstructive Coronary Artery Disease and Vasospasm

Sakamoto¹,

Iwaya²,

Owada³

et al. 2012

FJMS

View full text Add to dashboard Cite

: Background : Coronary flow reserve (CFR) provides essential information about the coronary microvasculature. Chronic kidney disease (CKD) is a risk factor for cardio -cerebrovascular diseases. We hypothesized that low CFR is associated with CKD and long -term cardio -cerebrovascular events in the patients without obstructive coronary artery diseases and vasospasm. Method and Results : In this study, 73 patients suspected with coronary artery disease but had no epicardial coronary stenosis and vasospasm were enrolled. There were 13 CKD patients and CFR was measured using the Doppler flow wire methods in the left anterior descending artery. CFR was significantly lower in CKD group than non -CKD group (3.13±0.6 vs. 4.00±1.1, P= 0.007). From multivariate logistic regression analysis, the independent factor associated with the presence of CKD was only CFR (odds ratio 3.85, 95% confidence interval 1.27 -11.70, P=0.017). In the patients with low CFR (≤2.8), cardio -cerebrovascular events were more common than those with normal CFR (CFR >2.8). Besides, in the patients who had both low CFR and CKD, longterm cardio -cerebrovascular events were more likely to occur than those with normal CFR or non -CKD. Conclusions : Our data suggest that low CFR is associated with CKD and cardio -cerebrovascular events in the patients without coronary stenosis and vasospasm.

show abstract

Peripheral Vascular Endothelial Dysfunction in Patients With Angina Pectoris and Normal Coronary Arteriograms

Cited by 97 publications

References 28 publications

Early impairment of large artery structure and function in Type I diabetes mellitus

Early impairment of large artery structure and function in Type I diabetes mellitus

Association between vascular dysfunction and reduced myocardial flow reserve in patients with hypertension: a LIFE substudy

A Reduction of Coronary Flow Reserve Is Associated With Chronic Kidney Disease and Long-Term Cardio-Cerebrovascular Events in Patients With Non-Obstructive Coronary Artery Disease and Vasospasm

Contact Info

Product

Resources

About