Circadian Variation of Ambulatory Myocardial Ischemia

Krantz, David S.; Kop, Willem J.; Gabbay, Frances H.; Rozanski, Alan; Barnard, Marie; Klein, Jacob; Pardo, Y; Gottdiener, John S.

doi:10.1161/01.cir.93.7.1364

Cited by 83 publications

(22 citation statements)

References 42 publications

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“…In some patients orthostatic hypertension is another possibility [46]. Our finding is compatible with the results of other studies which have demonstrated that postural changes on awakening may trigger myocardial ischemia [47]. …”

Section: Discussionsupporting

confidence: 92%

Potential Triggering Factors of Intracerebral Hemorrhage

Passero

Ciacci²,

Reale³

2001

Cerebrovasc Dis

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The distributions of intracerebral hemorrhage (ICH) according to place of onset, degree of physical activity at onset and potential triggering factors were analyzed in 848 patients with ICH. Patients were grouped according to the presumed cause of ICH: hypertensive ICH, secondary ICH and ICH of undetermined origin. The influence of demographic and temporal factors on the relative frequency of events was also assessed. In 30% of the cases, ICH occurred during inactivity or sedentary activity, in 50% during light exertion and in 20% during moderate/vigorous exertion. During inactivity or sedentary activity, hypertensive ICH was significantly less frequent than secondary ICH (OR 0.32; 95% CI 0.21–0.47) and undetermined ICH (OR 0.36; 95% CI 0.23–0.55), whereas during moderate or vigorous exertion hypertensive ICH was more frequent than secondary (OR 1.88; 95% CI 1.16–3.05) and undetermined ICH (OR 2.29; 95% CI 1.31–4.00) Potential triggering factors were observed in 27% of patients and were significantly more frequent in patients with hypertensive ICH than in patients with secondary ICH (OR 2.90; 95% CI 1.85–4.54) or undetermined ICH (OR 2.44; 95% CI 1.54–3.87). Our findings suggest that many potential external triggers that act mainly by raising blood pressure may interact, and their concurrence may favor cerebral hemorrhage, particularly in hypertensive patients. In many cases, these circumstances of increased risk may be mitigated by preventive measures.

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Section: Discussionsupporting

confidence: 92%

Potential Triggering Factors of Intracerebral Hemorrhage

Passero

Ciacci²,

Reale³

2001

Cerebrovasc Dis

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“…For instance, myocardial ischemia during daily life shows a characteristic circadian rhythm. 219 Even though exogenous factors (ie, the amount of physical and mental activity) trigger episodes of myocardial ischemia, 208,209,219 Krantz et al 219 demonstrated that the circadian rhythm of myocardial ischemia also appears to have an endogenous component, as demonstrated in Figure 7. Understanding the factors driving this apparent endogenous component could help further elucidate the pathophysiology of mental stress-induced ischemia.…”

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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“…We also showed that 458 nm light exposure caused a lower DSBP and DDBP compared with exposure to 550 nm light, which might be associated with the color effect of 458 nm light. Previous studies showed that the risk of myocardial infarction, stroke, and sudden death shows a peak in the early morning (Marler et al, 1989;Muller et al, 1989;Kranz et al, 1996), and the morning shift in cardiac sympatho-vagal balance may be involved in this increased risk of cardiovascular incidents at that time (Furlan et al, 1990;Esler, 2000). The relaxing effect of 458 nm light might be useful in the avoidance of such incidents.…”

Section: Discussionmentioning

confidence: 99%