Frequency of ST-segment depression produced by mental stress in stable angina pectoris from coronary artery disease

Barry, Joan; Selwyn, Andrew P.; Nabel, Elizabeth G.; Rocco, Michael; Mead, Kimberely; Campbell, Stephen; Rebecca, George S.

doi:10.1016/0002-9149(88)90112-9

Cited by 123 publications

(31 citation statements)

References 13 publications

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“…Recall of angry events is also a laboratory trigger of myocardial ischemia, 196 which supports the epidemiological study of anger by Mittleman et al 194 These laboratory studies are complemented by ambulatory ECG studies that demonstrate an association between psychological stress and/or negative emotions and the occurrence of myocardial ischemia during daily-life circumstances (Figure 5). [207][208][209] Like ischemia induced during mental stress testing in the laboratory, transient ischemic episodes out of hospital are overwhelmingly silent and occur at relatively low heart rate elevations. 210 Furthermore, patients who manifest myocardial ischemia during laboratory mental stress are also more likely to manifest myocardial ischemia during ambulatory ECG monitoring of daily-life activity.…”

Section: Induction Of Myocardial Ischemiamentioning

confidence: 99%

Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

1999

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Abstract-Recent studies provide clear and convincing evidence that psychosocial factors contribute significantly to the pathogenesis and expression of coronary artery disease (CAD). This evidence is composed largely of data relating CAD risk to 5 specific psychosocial domains: (1) depression, (2) anxiety, (3) personality factors and character traits, (4) social isolation, and (5) chronic life stress. Pathophysiological mechanisms underlying the relationship between these entities and CAD can be divided into behavioral mechanisms, whereby psychosocial conditions contribute to a higher frequency of adverse health behaviors, such as poor diet and smoking, and direct pathophysiological mechanisms, such as neuroendocrine and platelet activation. An extensive body of evidence from animal models (especially the cynomolgus monkey, Macaca fascicularis) reveals that chronic psychosocial stress can lead, probably via a mechanism involving excessive sympathetic nervous system activation, to exacerbation of coronary artery atherosclerosis as well as to transient endothelial dysfunction and even necrosis. Evidence from monkeys also indicates that psychosocial stress reliably induces ovarian dysfunction, hypercortisolemia, and excessive adrenergic activation in premenopausal females, leading to accelerated atherosclerosis.Also reviewed are data relating CAD to acute stress and individual differences in sympathetic nervous system responsivity. New technologies and research from animal models demonstrate that acute stress triggers myocardial ischemia, promotes arrhythmogenesis, stimulates platelet function, and increases blood viscosity through hemoconcentration. In the presence of underlying atherosclerosis (eg, in CAD patients), acute stress also causes coronary vasoconstriction. Recent data indicate that the foregoing effects result, at least in part, from the endothelial dysfunction and injury induced by acute stress. Hyperresponsivity of the sympathetic nervous system, manifested by exaggerated heart rate and blood pressure responses to psychological stimuli, is an intrinsic characteristic among some individuals. Current data link sympathetic nervous system hyperresponsivity to accelerated development of carotid atherosclerosis in human subjects and to exacerbated coronary and carotid atherosclerosis in monkeys.Thus far, intervention trials designed to reduce psychosocial stress have been limited in size and number. Specific suggestions to improve the assessment of behavioral interventions include more complete delineation of the physiological mechanisms by which such interventions might work; increased use of new, more convenient "alternative" end points for behavioral intervention trials; development of specifically targeted behavioral interventions (based on profiling of patient factors); and evaluation of previously developed models of predicting behavioral change. The importance of maximizing the efficacy of behavioral interventions is underscored by the recognition that psychosocial stresses tend to cluster together. ...

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Section: Induction Of Myocardial Ischemiamentioning

confidence: 99%

Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

1999

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“…Mental stress is furthermore known to precipitate angina pectoris and myocardial ischemia in patients with CHD both during laboratory testing and in daily life (Rozanski et al 1988; Barry et al 1988).…”

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confidence: 99%

Mental Stress Impairs Endothelial Vasodilatory Function by a Beta-Adrenergic Mechanism

et al. 2007

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Mental stress has been shown to impair endothelium-dependent vasodilation (EDV) in the human forearm. The aim of this study was to investigate if this response could be blunted by local infusions of beta-blockade (propranolol), alpha-blockade (phentolamine), or neurogenic blockade. Thirty-one young healthy volunteers underwent forearm blood flow (FBF) measurements, using venous occlusion plethysmography, during local intra-arterial infusions of metacholine (MCh; inducing EDV) and sodium nitroprussid (SNP; inducing endothelial-independent vasodilation [EIDV]), respectively. These measurements were repeated during a 5-min mental arithmetic stress test without (n = 8) or with concomitant local infusion of propranolol (n = 7) or phentolamine (n = 8) in the forearm or during axillary plexus blockade (n = 8). An index of endothelial vasodilatory function (EFI) was calculated as the EDV to EIDV ratio. Mental stress impaired EDV significantly (p < .05), and as a result, EFI was significantly reduced (p = .02). This effect on EFI could be blocked by propranolol and neurogenic blockade but not by phentolamine (p < .05). Thus, impairment of endothelial vasodilatory function induced by mental stress could be blocked by beta-adrenergic, but not alpha-adrenergic, receptor blockade.

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“…Emotional stress has been identified as a significant risk factor for triggering cardiac ischaemic episodes (Barry et al 1988). In the present study we have investigated firstly, whether stimulation in the PAG is associated with electrocardiographic signs of ischaemia and secondly, whether PAG-evoked changes in the ECG waveform could be modulated by activation of neurones in nucleus raphe magnus (NRM): a source of inhibitory input to the PAG (Schenberg & Lovick, 1995).…”

Section: Department Of Physiology University Of Birmingham Birminghmentioning

confidence: 96%

Cardiovascular/Respiratory Control

1998

The Journal of Physiology

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We have previously shown that reflex bradycardia occurs when subatmospheric pressure is applied to the surgically isolated upper airway of the decerebrate paralysed rabbit (Nolan et al. 1997). However, upper airway negative pressure also evokes reflex changes in phrenic nerve activity, so the reduction in heart rate could be secondary to changes in central respiratory activity. We set out to determine whether the reflex cardioinhibitory response t o upper airway negative pressure could be demonstrated in hypocapnic apnoea.Experiments were performed in adult New Zealand White rabbits. Anaesthesia was induced with Saffan (Glaxovet, 4 mg kg-1 LV.) and maintained with halothane (1-2% inspired concentration). The internal carotid arteries were tied and a pre-collicular decerebration performed. and artificial ventilation instituted via a low cervical tracheostomy. We recorded the electrocardiogram and the electrical activity of the cut central end of the left phrenic nerve. Pressures in the range 0 to -30 cmH 2 0 were applied for 5 s to the entire upper airway through cannulae sealed into the external nares and rostral trachea. The ventilator was disconnected during negative pressure stimuli to eliminate phasic pulmonary stretch receptor activity.When animals were hyperventilat ed so that the phrenic nerve was electrically silent (pHa = 7,526 ± 0'06, P a . co , = 22, 2 ± 4'7, mean ± S .D., n = 13) upper airway negative pressure caused bradycardia: -30 cmH 2 0 pressure applied to the upper airway increased R-R interval from 257 ± 8 to 325 ± 19 ms (mean ± S.E.M., n = 13 , P= 0'002, ANOVA and Student-Newman-Keuls test). When carbon dioxide was added to the inspired gas to restore normal rhythmic phrenic nerve activity (pHa = 7'373 ± 0'03, Pa,co, = 34'8 ± 4'0, mean ± S .D., n = 4), the application of -30 cmH 2 0 pressure to the upper airway increased R-R interval from 308 ± 25 to 458 ± 90 ms (mean ± S .E.M ., n = 4). The response in normocapnia was statistically significantly larger (P = 0'01) than that observed in these animals in hypocapnic apnoea. No significant response remained, either in hypocapnia (n = 9) or normocapnia (n = 3), after bilateral section of the superior laryngeal nerves.We conclude that upper airway negative pressure causes reflex bradycardia in the absence of a central respiratory rhythm in hypocapnic apnoea. These data suggest that Journal of Physiology (1998) 511.P upper airway distortion exerts a direct influence on the neural control of heart rate, and the responses to upper airway negative pressure are not secondary to changes in central respiratory activity. Use of positive pressure breathing (PPB) to protect fast jet aircrew against hypoxia at high altitudes is limited by circulatory collapse, due to peripheral pooling of blood and progressive loss of fluid from the circulation. These effects can be reduced by applying lower body counter pressure (LBCP). Unpublished studies suggest that improved protection may be provided by increasing the inflation pressure of LBCP above that of PPB. Wi...

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Frequency of ST-segment depression produced by mental stress in stable angina pectoris from coronary artery disease

Cited by 123 publications

References 13 publications

Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

Mental Stress Impairs Endothelial Vasodilatory Function by a Beta-Adrenergic Mechanism

Cardiovascular/Respiratory Control

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