Cardiovascular injury induced by sympathetic catecholamines

Haft, Jacob I.

doi:10.1016/0033-0620(74)90039-5

Cited by 251 publications

(93 citation statements)

References 46 publications

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“…One hypothesis is that the heightened sympathetic arousal and catecholamine secretion induced by anger are damaging to the heart and its vasculature and also play a role in the development of atherosclerotic lesions. Excessive circulating catecholamines (eg, epinephrine and norepinephrine) are known to cause direct damage to the endothelium and heart muscle 15,16 and to disrupt the electrical rhythm of the heart. 17 Further, studies have confirmed that the presence of catecholamines is associated with increased platelet adhesion and aggregation, 18 lipid mobilization, 19 and activation of macrophages, 20 each of which has been implicated in the complex process of atherogenesis, stemming from endothelial injury and ending in the formation of atherosclerotic lesions.…”

Section: Discussionmentioning

confidence: 99%

Anger Proneness Predicts Coronary Heart Disease Risk

Williams

Paton²,

Siegler³

et al. 2000

Circulation

227

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Background-Increased research attention is being paid to the negative impact of anger on coronary heart disease (CHD). Methods and Results-This study examined prospectively the association between trait anger and the risk of combined CHD (acute myocardial infarction [MI]/fatal CHD, silent MI, or cardiac revascularization procedures) and of "hard" events (acute MI/fatal CHD). Participants were 12 986 black and white men and women enrolled in the Atherosclerosis Risk In Communities study. In the entire cohort, individuals with high trait anger, compared with their low anger counterparts, were at increased risk of CHD in both event categories. The multivariate-adjusted hazard ratio (HR) (95% CI) was 1.54 (95% CI 1.10 to 2.16) for combined CHD and 1.75 (95% CI 1.17 to 2.64) for "hard" events. Heterogeneity of effect was observed by hypertensive status. Among normotensive individuals, the risk of combined CHD and of "hard" events increased monotonically with increasing levels of trait anger. The multivariate-adjusted HR of CHD for high versus low anger was 2.20 (95% CI 1.36 to 3.55) and for moderate versus low anger was 1.32 (95% CI 0.94 to 1.84). For "hard" events, the multivariate-adjusted HRs were 2.69 (95% CI 1.48 to 4.90) and 1.35 (95% CI 0.87 to 2.10), respectively. No statistically significant association between trait anger and incident CHD risk was observed among hypertensive individuals. Conclusions-Proneness to anger places normotensive middle-aged men and women at significant risk for CHD morbidity and death independent of the established biological risk factors.

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Section: Discussionmentioning

confidence: 99%

Anger Proneness Predicts Coronary Heart Disease Risk

Williams

Paton²,

Siegler³

et al. 2000

Circulation

227

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“…It has been hypothesized that high levels of arousal over a period of time may engender chronic changes in the cardiovascular system, including increases in serum lipids Y (e.g., cholesterol), myocardial lesions, arterial occlusion, and blood platelet aggregation, important factors in atherogenesis (Glass, 1983;Eliot, 1979;Haft, 1974;Raab, Chaplin, & Bajusc, 1989;Ardlie, Glew, & Schwartz, 1968). These effects have been observed in animals (Manuck, Kaplan, & Clarkson, 1983a;1985a) and also in acute and chronic studies of humans (Frankenhaeuser, 1983;Henry, 1983;Herd, 1981;Schneiderman, 1983), primarily using male subjects.…”

Section: Chaptermentioning

confidence: 99%

“…A 1 portion of this data will be discussed here. (Glass, 1983;Eliot, 1979;Haft, 1974; Raab, Chaplin, & Bajusc, 1989; Ardlie, Glew, & Schwartz, 1968). These effects have been observed in animals (Manuck, Kaplan, & Clarkson, 1983a;1985a) and also in acute and chronic studies of humans (Frankenhaeuser, 1983;Henry, 1983;Herd, 1981;Schneiderman, 1983), primarily using male subjects.…”

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confidence: 99%

Anger and denial as predictors of cardiovascular reactivity in women

Emerson

Harrison

1990

J Psychopathol Behav Assess

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Behavioral and physiological reactivity, and its relationship to cardiovascular disease has been studied in men for a number of years, and the expression of anger has been identified as a possible contributing factor. Few studies, however, have focused specifically on the reactivity of women, and those which have suggest that women are less reactive to laboratory tasks than men. For the present study, 45 undergraduate women, ages 19-21 were selected from a larger sample of 135 women to represent three discrete groups: (1) low anger/low denial, (2) high anger/low denial, and (3) low anger/high denial, based on their scores on the State-Trait Anger Expression Inventory, 1 and the Marlowe-Crowne Social Desirability Scale. It was hypothesized that the three groups would show reliable differences in heart rate and blood pressure during presentation of a stressful laboratory stimulus, the Stroop Color and Word Test. Each subject received three counterbalanced conditions: (1) no feedback, (2) error feedback without observer present, (3) error feedback with observer present. As hypothesized, women who reported a high level of denial and a low level of anger exhibited reliably greater systolic blood pressure to the no-feedback condition than subjects who reported low levels of denial and anger. The hypothesis that all groups°w ould display greater reactivity in a condition which T provided error feedback with observation was not supported. (Eliot, Buell & Dembroski, 1982;Obrist, 1981). The reasons for this are still somewhat unclear.Investigations of the etiology and effects of hyperreactivity have followed three independent, yet seemingly related, lines of research. As early as 1911, Walter Cannon addressed the association between anger and the neuroendocrine mediation of the "fight-flight" response, the physiological reactivity associated with the mobilization of energy. Much later, in the early 1950's, investigators studying the relationship between cardiovascular reactivity and hypertension found that Cardiovascular Reactivity 1 compared to normotensives, hypertensive individuals manifested larger systolic blood pressure increases to stimuli which elicited both pain and anger (Schacter, 1957).Concurrently, other researchers utilized a harrassment paradigm with men to study the effects of psychological stress on hypertension. They found that individuals could be grouped according to whether or not they expressed their feelings (especially those of anger and anxiety), and that these groups evidenced differential degrees of reactivity in blood pressure and heart rate (Funkenstein, King, & Drolette, 1954).A third line of investigation focused on coronary heart disease. Friedman and Rosenman (1961) (1982), Contrada (1984), and. A 1 portion of this data will be discussed here. (Glass, 1983;Eliot, 1979;Haft, 1974; Raab, Chaplin, & Bajusc, 1989; Ardlie, Glew, & Schwartz, 1968). These effects have been observed in animals (Manuck, Kaplan, & Clarkson, 1983a;1985a) and also in acute and chronic studies of humans (Franke...

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“…In the case of pressure 20 overload there is an increase in cardiac mass, re-expression of fetal genes, a suppression of genes related to several rate-limiting enzymes in fatty acid oxidation, enhancement of genes related to rate-limiting enzyme for glucose oxidation, and increased reliance on carbohydrate oxidation to enable maintenance of contractile function [8,9]. Also, an increased adrenergic tone in the setting of heart failure not only exerts a direct toxic effect on the myocyte [10] but also causes unfavorable changes in myocardial 25 energy use [11]. With progression of heart failure there is a metabolic remodeling from adaptation to maladaption where regulated metabolic pathways become dysregulated metabolic pathways and the failing heart loses its ability to switch to the most efficient fuel for energy production, thus, becoming an energy-starved heart [4].…”

Section: Introductionmentioning

confidence: 99%

A study of changes in deformation and metabolism in the left ventricle as a function of hypertrophy in spontaneous hypertensive rats using microPET technology

Gullberg

Huesman

Reutter

et al. 2005

Journal of Nuclear Cardiology

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Problem: In the case of hypertrophy caused by pressure overload (hypertension) there is an increase in cardiac mass and modification cardiac metabolism. Aim: This study was designed to study the changes in glucose metabolism, ejection fraction, and deformation in the left ventricle with the progression of hypertrophy in spontaneous hypertensive rats (SHR). Methods: Dynamic PET data were acquired using the microPET II at UC Davis. Two rats were imaged at 10-week intervals for 18 months. Each time a dose of approximately 1-1.5 mCi of F-18-FDG was injected into a normotensive Wistar Kyoto (WKY) rat and the same dose was injected into a SHR rat. Each rat was imaged using a gated dynamic acquisition for 80 minutes acquiring list mode data with cardiac gating of approximately 600-900 million total counts. For the analysis of glucose of metabolism, the list mode data were histogrammed into a dynamic sequence (42 frames over 80 mins). For each time frame, projection data of 1203 140×210 sinograms of 0.582 mm bins were formed by summing the last three gates before and one after the R-wave trigger to correspond to the diastolic phase of the cardiac cycle. Dynamic sequences of 128×128×83 matrices of 0.4×0.4×0.582 mm 3 voxels in x, y, and z were reconstructed using an iterative MAP reconstruction which used a prior that penalized the high frequency components of the reconstruction using appropriate weighting between 26 nearest neighboring voxels. Time activity curves were generated from the dynamic reconstructed sequence for the blood and left ventricular tissue regions of interest which were fit to a 2-compartment model to obtain a least squares fit for the kinetic parameters. For the analysis of deformation, the list mode data were histogrammed into 8 gates of the cardiac cycle, each gate was the total sum of the later 60 mins of the 80 min acquisition. Images of 128×128×83 matrices for each gate were reconstructed using the same iterative MAP reconstruction used to reconstruct the dynamic sequence. The in-plane image dimensions were doubled to 256×256×83 in order to increase the resolution for the Warping analyses. These image data sets were then cropped to 128×128×83. The end-systolic image data sets were designated as the template images and the end-diastole image data sets were designated as the target images, thus providing an analysis of the diastolic relaxation and filling phases of the cardiac cycle. The template images were manually segmented to create surface definitions representing the epi-and endocardial surfaces. Finite element models of the left ventricles were created using the segmented surfaces and defining a transversely isotropic material with fiber angles varying from the epicardial surface to the endocardial surface. A Warping analyses was performed to obtain the LV strain tensor and fiber stretch distributions. Results: In one study, the average first principal Green-Lagrange strain, fiber stretch, ejection fraction, and metabolic rate of F-18-FDG was 0.22, 1.08, 80%, 0.1 for the WKY rat and...

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Cardiovascular injury induced by sympathetic catecholamines

Cited by 251 publications

References 46 publications

Anger Proneness Predicts Coronary Heart Disease Risk

Anger Proneness Predicts Coronary Heart Disease Risk

Anger and denial as predictors of cardiovascular reactivity in women

A study of changes in deformation and metabolism in the left ventricle as a function of hypertrophy in spontaneous hypertensive rats using microPET technology

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