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Biomedical subjects

R Kirkeeide

Publications and source records attributed to R Kirkeeide.

10 recordsLinked to original sources
PubMed2000

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.

BACKGROUND: 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. METHODS AND RESULTS: 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. CONCLUSIONS: 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.

Adult↗
PubMed2000

Pressure-derived fractional flow reserve to assess serial epicardial stenoses: theoretical basis and animal validation.

Background-Fractional flow reserve (FFR) is an index of stenosis severity validated for isolated stenoses. This study develops the theoretical basis and experimentally validates equations for predicting FFR of sequential stenoses separately. Methods and Results-For 2 stenoses in series, equations were derived to predict FFR (FFR(pred)) of each stenosis separately (ie, as if the other one were removed) from arterial pressure (P(a)), pressure between the 2 stenoses (P(m)), distal coronary pressure (P(d)), and coronary occlusive pressure (P(w)). In 5 dogs with 2 stenoses of varying severity in the left circumflex coronary artery, FFR(pred) was compared with FFR(app) (ratio of the pressure just distal to that just proximal to each stenoses) and to FFR(true) (ratio of the pressures distal to proximal to each stenosis but after removal of the other one) in case of fixed distal and varying proximal stenoses (n=15) and in case of fixed proximal and varying distal stenoses (n=20). The overestimation of FFR(true) by FFR(app) was larger than that of FFR(true) by FFR(pred) (0.070+/-0.007 versus 0.029+/-0.004, P<0.01 for fixed distal stenoses, and 0.114+/-0.01 versus 0.036+/-0. 004, P<0.01 for fixed proximal stenoses). This overestimation of FFR(true) by FFR(app) was larger for fixed proximal than for fixed distal stenoses. Conclusions-The interaction between 2 stenoses is such that FFR of each lesion separately cannot be calculated by the equation for isolated stenoses (P(d)/P(a) during hyperemia) applied to each separately but can be predicted by more complete equations taking into account P(a), P(m), P(d), and P(w).

Animals↗
PubMed1998

Social relations and extent and severity of coronary artery disease. The Stockholm Female Coronary Risk Study.

AIMS: Social relations have been repeatedly linked to coronary heart disease in men, even after careful control for standard risk factors. Women have rarely been studied and results have not been conclusive. We investigated the role of social support in the severity and extent of coronary artery disease in women. METHODS AND RESULTS: One hundred and thirty-one women, aged 30 to 65 years, who were hospitalized for an acute coronary event and were included in the Stockholm Female Coronary Risk Study, were examined with computer assisted quantitative coronary angiography. Angiographic measures included presence of stenosis greater than 50% in at least one coronary artery (severity) and the number of stenoses greater than 20% within the coronary tree (extent). Social factors included two measures of social support, which were previously shown to predict coronary disease in prospective studies of men. After adjustment for age, lack of social support was associated with both measures of coronary artery disease. With further adjustment for smoking, education, menopausal status, hypertension, high density lipoprotein and body mass index, the risk ratio for stenosis greater than 50% in women with poor as compared to those with strong social support was 2.5 (95% confidence interval 1.2 to 5.3; P=0.003). Also, women with poor social support had more stenoses obstructing at least 20% of the coronary lumen with multivariate adjustment, but the difference from women with strong support was only of borderline significance (P=0.09). CONCLUSION: The findings suggest that lack of social support contributes to the severity of coronary artery disease in women, independent of standard risk factors.

Adult↗
PubMed1997

Lipoprotein(a) as a determinant of coronary heart disease in young women.

BACKGROUND: Lipoprotein(a) [Lp(a)] appears to be a risk factor for coronary heart disease (CHD) in men. The role of Lp(a) in women, however, is less clear. METHODS AND RESULTS: We examined the ability of Lp(a) to predict CHD in a population-based case-control study of women 65 years of age or younger who lived in the greater Stockholm area. Subjects were all patients hospitalized for an acute CHD event between February 1991 and February 1994. Control subjects were randomly selected from the city census and were matched to patients by age and catchment area. Lp(a) was measured 3 months after hospitalization by use of an immunoturbidometric method (Incstar) calibrated to the Northwest Lipid Research Laboratories (coefficient of variation was < 9%). Of the 292 consecutive patients, 110 (37%) were hospitalized for an acute myocardial infarction, and 182 were hospitalized (63%) for angina pectoris. The mean age for both patients and control subjects was 56 +/- 7 years. Of participants, 74 patients (25%) and 84 control subjects (29%) were premenopausal. The distributions of Lp(a) were highly skewed in both patients and control subjects, with a range from 0.001 to 1.14 g/L. Age-adjusted odds ratio for CHD in the highest versus the lowest quartile of Lp(a) was 2.3 (95% confidence interval [CI], 1.4 to 3.7). After adjustment for age, smoking, education, body mass index, systolic blood pressure, total cholesterol, triglycerides, and HDL, the odds ratio was 2.9 (95% CI, 1.6 to 5.0). The odds ratios were similar when myocardial infarction and angina patients were compared with their respective control subjects. The odds ratios were 5.1 (95% CI, 1.4 to 18.4) and 2.4 (95% CI, 1.3 to 4.5) in premenopausal and postmenopausal women, respectively. CONCLUSIONS: These results suggest that Lp(a) is a determinant of CHD in both premenopausal and postmenopausal women.

Adult↗
PubMed1995

Comparative validation of quantitative coronary angiography systems. Results and implications from a multicenter study using a standardized approach.

BACKGROUND: Computerized quantitative coronary angiography (QCA) has fundamentally altered our approach to the assessment of coronary interventional techniques and strategies aimed at the prevention of recurrence and progression of stenosis. It is essential, therefore, that the performance of QCA systems, upon which much of our scientific understanding has become integrally dependent, is evaluated in an objective and uniform manner. METHODS AND RESULTS: We validated 10 QCA systems at core laboratories in North America and Europe. Cine films were made of phantom stenoses of known diameter (0.5 to 1.9 mm) under four experimental conditions: in vivo (coronary arteries of pigs) calibrated at the isocenter or by use of the catheter as a scaling device and in vitro with 50% contrast and 100% contrast. The cine films were analyzed by each automated QCA system without observer interaction. Accuracy and precision were taken as the mean and SD of the signed differences between the phantom stenoses, and the measured minimal luminal diameters and the correlation coefficient (r), the SEE, the y intercept, and the slope were derived by their linear regression. Performance of the 10 QCA systems ranged widely: accuracy, +0.07 to +0.31 mm; precision, +/- 0.14 to +/- 0.24 mm; correlation (r), .96 to .89; SEE, +/- 0.11 to +/- 0.16 mm; intercept, +0.08 to +0.31 mm; and slope, 0.86 to 0.64. CONCLUSIONS: There is a marked variability in performance between systems when assessed over the range of 0.5 to 1.9 mm. The range of accuracy, intercept, and slope values of this report indicates that absolute measurements of luminal diameter from different multicenter angiographic trials may not be directly comparable and additionally suggests that such absolute measurements may not be directly applicable to clinical practice using an on-line QCA system with a different edge detection algorithm. Power calculations and study design of angiographic trials should be adjusted for the precision of the QCA system used to avoid the risk of failing to detect small differences in patient populations. This study may guide the fine-tuning of algorithms incorporated within each system and facilitate the maintenance of high standards of QCA for scientific studies.

Algorithms↗
PubMed1992

Improved stenosis geometry by quantitative coronary arteriography after vigorous risk factor modification.

This study is a randomized, controlled, blinded, arteriographic trial to determine the effects of a low-cholesterol, low-fat, vegetarian diet, stress management and moderate aerobic exercise on geometric dimensions, shape and fluid dynamic characteristics of coronary artery stenoses in humans. Complex changes of different primary stenosis dimensions in opposite directions or to different degrees cause stenosis shape change with profound effects on fluid dynamic severity, not accounted for by simple percent narrowing. Accordingly, all stenosis dimensions were analyzed, including proximal, minimal, distal diameter, integrated length, exit angles and exit effects, determining stenosis shape and a single integrated measure of stenosis severity, stenosis flow reserve reflecting functional severity. In the control group, complex shape change and a stenosis-molding characteristic of statistically significant progressing severity occurred with worsening of stenosis flow reserve. In the treated group, complex shape change and stenosis molding characteristic of significant regressing severity was observed with improved stenosis flow reserve, thereby documenting the multidimensional characteristics of regressing coronary artery disease in humans.

Adult↗
PubMed1990

Potential role of coronary vasoconstriction in ischaemic heart disease: effect of exercise.

Coronary vasomotion plays an important role in the regulation of coronary perfusion at rest and during exercise. Normal coronary arteries show coronary vasodilation of the proximal (+20%) and distal (+40%) vessel segments during supine bicycle exercise. However, patients with coronary artery disease show exercise-induced vasoconstriction of the stenotic vessel segments. The exact mechanism of exercise-induced stenosis narrowing is not clear but might be related to a passive collapse of the disease-free vessel wall (Venturi mechanism), elevated plasma levels of circulating catecholamines, an insufficient production of the endothelium-derived vasorelaxing factor or increased platelet aggregation due to turbulent blood flow with release of thromboxane A2 and serotonin. Various vasoactive drugs, such as nitroglycerin and calcium antagonists, prevent exercise-induced stenosis vasoconstriction. An additive effect on coronary vasodilation of the stenotic vessel segment was observed after combination of nitroglycerin with diltiazem. Thus, exercise-induced stenosis narrowing plays an important role in the pathophysiology of myocardial ischaemia during dynamic exercise. The antianginal effect of vasoactive substances can be explained--besides the effect on pre- and afterload--by a direct action on coronary stenosis vasomotion.

Angiography↗
PubMed1984

[Hemodynamics of coronary stenoses].

Under physiological conditions the resistance component of large epicardial coronary branches is very small in relation to total coronary resistance and can be neglected. The pressure losses across minor stenoses can be compensated by a decrease of resistance in the more peripheral coronary bed (autoregulation). This compensatory mechanism is limited to luminal obstructions less than 85%. Above this limit, when collateral vessels are not available, perfusion of the periphery becomes a function of the flow across the stenosis. As a consequence coronary reserve becomes abolished with an increasing obstruction. Coronary reserve describes an increase of coronary flow up to a factor of five, which, under normal conditions, is induced by dilation of resistors (arterioles) in the coronary bed. After exhaustion of coronary reserve the hemodynamic impact of a vascular narrowing can be expressed as the pressure loss across a coronary lesion (delta p). delta p is composed of viscous losses (AV) that are in linear relation to flow and inertial components that are related to the square of flow (B). Accordingly pressure loss across a stenosis can be expressed in a general form as delta p = AV X Q + B X Q2. In vitro data show that an approximation of delta p can be calculated on the basis of stenosis geometry including normal and minimal diameter, length, angle of entrance and exit, velocity of flow, viscosity and density of blood. Pressure losses across a stenosis can be divided in three components: the entrance, the narrow part, and the exit. Turbulence arises at the exit. This fact leads to a variable interaction of consecutive vascular lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗