Diffuse Narrowing Of Coronary Arteries Research Articles

Abstract 18728: Plasma Heparin Cofactor II Activity is a Predictor of Diffuse Coronary Artery Narrowing in Patients with Diabetes Mellitus

Background: Heparin cofactor II (HCII) is a major physiological inhibitor of thrombin action. We previously reported high plasma HCII was protective against in-stent restenosis after coronary stenting and carotid atherosclerosis. Furthermore, we reported that HCII was a predictor of cardiovascular events in patients with coronary heart disease. Kataoka et al reported patients with DM had smaller coronary vessel and longer diseased segment than those with impaired glucose tolerance (IGT) and normal glucose tolerance. HCII and morphologic characteristics of diabetic coronary was unknown. Methods: We enrolled 20 diabetic patients examined by coronary angiography, sequentially (13 males and 7 females; age, 67.9+/-10.4yrs, HbA1c>/=7.0%). Coronary cinearteriography was analyzed by quantitative coronary angiography (QCA) with Cardiovascular Measurement System (CCIP-310/W). Segment diameter<1.5mm as diseased lesions were determined. And diseased lesion length and HCII activity were analyzed, statistically. Results: The mean plasma level of HCII activities was 101.4+/-18.6%. And the mean of diseased lesion length was 13.7+/-12.0mm. Multivariate analysis showed age, low-HDLemia, smoking habit and disease period of DM were positively correlated with ALL, and HCII activity was negatively correlated. Univariate analysis showed HCII activity was negatively correlated with ALL, and disease period of DM was positively. That is, HCII activity and disease period of DM were correlated with lesion length of coronary artery diffuse-narrowing in diabetic patients. . Conclusions: The results suggested that low level of plasma HCII activity was correlated with diffuse coronary artery narrowing in patients with diabetic mellitus.

Quantitative Coronary Angiographic Studies of Patients With Angina Pectoris and Impaired Glucose Tolerance

We investigated the morphological characteristics of coronary arteries in patients with impaired glucose tolerance (IGT) using computer-assisted quantitative coronary angiography. IGT is an independent risk factor for cardiovascular disease. However, the morphological changes developing in the coronary arteries of patients with IGT remain unknown. A total of 534 patients with angina pectoris were studied. Of these, 144 patients were being treated for diabetes. The remaining 390 patients were classified as follows depending on the results of a 75-g oral glucose tolerance test: normal glucose tolerance (NGT) (n = 117), impaired fasting glucose (n = 3), IGT (n = 136), and diabetes pattern (preclinical diabetes) (n = 134). The diameters of the middle section of all major coronary artery segments were measured and averaged to determine the averaged vessel diameter (AVD). We defined segments of a diameter of < or = 1.5 mm as diseased lesions and determined the averaged lesion length (ALL). AVD and ALL were significantly different among patients with IGT and those with NGT. Patients with diabetes (preclinical and/or treated) had smaller AVD and longer ALL than those with IGT. By multivariate analysis, postprandial glucose levels were shown to be independently associated with an AVD <3.0 mm and an ALL >20 mm. Diffuse coronary artery narrowing develops not only in patients with diabetes but also in those with IGT. This morphological change is associated with postprandial hyperglycemia.

Frequency and clinical implications of fluid dynamically significant diffuse coronary artery disease manifest as graded, longitudinal, base-to-apex myocardial perfusion abnormalities by noninvasive positron emission tomography.

Diffuse coronary atherosclerosis is the substrate for plaque rupture and coronary events. Therefore, in patients with mild arteriographic coronary artery disease without significant segmental dipyridamole-induced myocardial perfusion defects, we tested the hypothesis that fluid dynamically significant diffuse coronary artery narrowing is frequently manifest as a graded, longitudinal, base-to-apex myocardial perfusion abnormality by noninvasive PET. In this study, 1001 patients with documented coronary artery disease by coronary arteriography showing any visible coronary artery narrowing underwent rest-dipyridamole PET perfusion imaging. Quantitative severity of dipyridamole-induced, circumscribed, segmental PET perfusion defects was objectively measured by automated software as the minimum quadrant average relative activity indicating localized flow limiting stenoses. Quantitative severity of the graded, longitudinal, base-to-apex myocardial perfusion gradient indicating fluid dynamic effects of diffuse coronary artery narrowing was objectively measured by automated software as the spatial slope of relative activity along the cardiac longitudinal axis. In patients with mild arteriographic disease without statistically significant dipyridamole-induced segmental myocardial perfusion defects caused by flow-limiting stenoses compared with normal control subjects, there was a graded, longitudinal, base-to-apex myocardial perfusion gradient significantly different from normal control subjects (P=0. 001) that was also observed for moderate to severe dipyridamole-induced segmental perfusion defects (P=0.0001), indicating diffuse disease underlying segmental perfusion defects; 43% of patients with or without segmental perfusion defects demonstrated graded, longitudinal, base-to-apex perfusion abnormalities beyond +/-2 SD of normal control subjects, indicating diffuse coronary arterial narrowing by noninvasive PET perfusion imaging.

Diffuse Narrowing of Coronary Arteries in Diabetic Patients: The Earliest Phase of Coronary Artery Disease

Coronary arteries in diabetic patients appear to be narrower than in normal subjects, but this has not been examined systematically. To investigate this hypothesis we reviewed the data of 711 consecutive patients with angiographically ‘normal coronary arteries’. Excluded were patients with valvular, myocardial or pericardial disease, and patients with hypertension or hyperlipidemia. Thirteen diabetic patients (10 men) and 22 nondiabetic persons (8 men) constituted the study and control groups, respectively. The diameters of the coronary arteries and their branches were measured and adjusted for body surface area. The sum of the proximal left anterior descending (LAD), circumflex and right coronary arteries (RCA) was calculated and defined as total coronary diameter (TCD). The sum of the distal LAD, first diagonal, first marginal and distal RCA was calculated and defined as total distal coronary diameter (dTCD). The clinical data of both groups were comparable. Adjusted TCD for body surface area was 5.4 ± 1.1 and 6.5 ± 1.1 mm/m² (p < 0.05) in diabetics and nondiabetics, respectively, and adjusted dTCD was 4.9 ± 1.2 and 6.1 ± 1.2 mm/m² (p = 0.01) in diabetics and normal subjects, respectively. Specific arteries and branches that were significantly smaller in diabetics included: left main coronary artery, distal LAD, first diagonal, proximal RCA, distal RCA, right ventricular branch, and posterolateral and posterior descending artery of RCA origin. Gender was not a confounding factor since the control group had a larger proportion of women and still larger arteries than the diabetic group. In conclusion, coronary arteries and their branches in diabetic patients have smaller diameters than normal subjects. This may be due to increased coronary tone, diffuse mild atherosclerosis or both.

Ergonovine-induced constrictions of epicardial coronary arteries in conscious dogs: alpha-adrenoceptors are not involved.

The effect of i.v. ergonovine tartrate infusions (0.05-20 micrograms/kg/min, 12 minutes duration) on coronary arteries was studied in 14 conscious dogs instrumented to continuously measure vascular diameter by an ultrasonic dimension gauge using 10-MHz piezoelectric crystals. Ergonovine induced a biphasic coronary response: small, transient dilation during the first minutes of infusion, followed by slowly developing constriction reaching its maximum 5 to 15 minutes after the end of the infusion and persisting at this level for at least 10 minutes. The threshold dosage for significant constriction was 0.05 microgram/kg/min. A dosage of 5 micrograms/kg/min (cumulative 60 micrograms/kg, corresponding to 35 micrograms/kg ergonovine maleate) caused a decline in mean left circumflex artery diameter by 137 +/- 15 micrometers (= 4.6%) without significantly altering heart rate, plasma catecholamines or plasma renin activity. Coronary venous O2 saturation did not decline, indicating the absence of coronary resistance vessel constriction. The epicardial artery constriction was not attenuated by a vasopressin antagonist. Under adrenergic blockade (2 mg/kg phentolamine and 2 mg/kg nadolol) or under ganglionic blockade (5 mg/kg pentolinium tartrate), ergonovine (5 micrograms/kg /min) caused substantial elevation in mean arterial pressure, while the decline in coronary artery diameter was attenuated. When this increase in arterial pressure was prevented by appropriate bleeding, the ergonovine-induced coronary constriction was not diminished by adrenergic or ganglionic blockade. The serotonin antagonist methysergide (0.5 mg/kg) completely abolished the ergonovine-induced coronary artery vasomotion. It is concluded that ergonovine in dogs causes an epicardial coronary artery constriction comparable to the diffuse coronary artery narrowing in men not suffering from variant angina pectoris. These constrictions are not mediated by an adrenergic mechanism.

Type III hyperlipoproteinemia: A quantitative study demonstrating severe diffuse coronary artery narrowing by atherosclerotic plaques including frequent severe narrowing of the left main

Type III hyperlipoproteinemia: A quantitative study demonstrating severe diffuse coronary artery narrowing by atherosclerotic plaques including frequent severe narrowing of the left main

Coronary and peripheral arterial responses to ergometrine in patients susceptible to coronary and oesophageal spasm.

Vascular responses to ergometrine were compared in groups of patients subject to coronary artery spasm, or oesophageal spasm, or neither. We measured the degree of diffuse narrowing at different coronary artery sites (not in spasm), and the rise in blood pressure. The data provide no evidence for a generalised sensitivity to alpha-adrenergic stimulation underlying either of these two clinical entities. The left main stem was narrowed significantly less than the three main branches of the coronary artery tree. The degree of diffuse coronary artery narrowing was not influenced by the presence or absence of minor (less than or equal to 50%) fixed stenotic lesions, nor by the initial calibre of the arteries. Ergometrine did not alter arterial lactate concentration or lactate extraction in the absence of coronary spasm.