Transient left ventricular dysfunction during provocative mental stress in patients with coronary artery disease

LaVeau, Paul J.; Rozanski, Alan; Krantz, David S.; Cornell, Carol E.; Cattanach, Lynn; Zaret, Barry L.; Wackers, Frans J. Th.

doi:10.1016/0002-8703(89)90064-1

Cited by 80 publications

(23 citation statements)

References 29 publications

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“…These techniques include those used to measure left ventricular function (radionuclide ventriculography [195][196][197][198][199] [ Figure 4], echocardiography, 200 assessment of left ventricular changes by either a stationary probe 201 and ambulatory VEST 202 ) and Figure 3. Schematic of pathophysiological effects of acute psychosocial stress.…”

Section: Induction Of Myocardial Ischemiamentioning

confidence: 99%

“…Specifically, stress that is more emotionally laden and/or personally relevant, such as a speaking assignment concerning personal faults, results in a significantly greater frequency and magnitude of inducible left ventricular wall motion abnormalities than does more nonspecific mental stress, such as the performance of mental arithmetic or the Stroop Color-Word task. 195 Because the mean heart rate increases of Ϸ15 to 20 bpm during laboratory-modeled public speaking 201 are far less than those of real-life speaking experiences, 205,206 this and similar tasks may underestimate the potential potency of mental stress in certain real-life situations. 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).…”

Section: Induction Of Myocardial Ischemiamentioning

confidence: 99%

“…Maximal heart rate and blood pressure responses are generally observed at the near onset of mental stress, and ischemic abnormalities are induced relatively rapidly during laboratory mental stress. 201 By contrast, laboratory exercise is always presented to patients in a graded fashion. However, when healthy individuals were exercised to a high workload without warm-up, ST-segment depression was induced in a significant number of subjects.…”

Section: Induction Of Myocardial Ischemiamentioning

confidence: 99%

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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%

Section: Induction Of Myocardial Ischemiamentioning

confidence: 99%

Section: Induction Of Myocardial Ischemiamentioning

confidence: 99%

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

1999

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“…The acute effect of mental stress on vasomotion is not surprising, as mental stress in coronary artery disease patients is known to trigger transient ischemia and regional flow disturbances. [17][18][19][20] It remains unclear, however, whether chronic stress contributes to the development of vasomotor abnormalities and whether such effects are secondary to or independent of heart rate, blood pressure, plasma lipids, or concomitant plaque size.…”

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Psychosocial factors impair vascular responses of coronary arteries.

et al. 1991

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Background. Four sets of monkeys were used to examine the effect of chronic psychosocial disruption and diet on dilator responses of coronary arteries.Methods and Results. One set consisted of monkeys consuming monkey chow and living in a stable social setting (nonatherosclerotic controls, n=6). Three sets consumed an atherogenic diet for 14 months followed by one of three treatments for the next 16 months: 1) a high-cholesterol diet and housed in unstable social groups (n =9); 2) a low-cholesterol diet and housed in unstable (n=8); or 3) stable groups (n=10). Quantitative coronary angiography revealed that intracoronary infusion of acetylcholine resulted in a change of diameter (versus infusion of 5% dextrose in water) of +4±1% in control monkeys and -11+4% in unstable monkeys consuming a high-cholesterol diet (p<0.05). In monkeys consuming the cholesterollowering diet, the change in artery diameter was +2±4% in stable and -10±4% in unstable social conditions (p<0.05) despite a similar plaque size (0.4±0.2 and 0.5±0.1 mm2) and total plasma cholesterol concentrations (179±+9 and 172+±6 mg/dl), respectively. The arterial response to nitroglycerin was similar among all groups of monkeys.Conclusions. We conclude that chronic social disruption is associated with relative arterial

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“…A isquemia desenvolvida durante estresse mental correlaciona-se com um aumento reativo maior da resistência vascular periférica do que com o aumento da freqüência cardíaca e débito cardíaco, quando comparada com a isquemia esforço-induzida 23,31,32 . A isquemia induzida por estresse mental acompanha-se de disfunção diastólica 33 , aumento do volume de ventrículo esquerdo e redução da fração de ejeção de ventrículo esquerdo, que ocorre com o início do estresse, havendo um rebote imediatamente após seu término 23,34 . A redução da fração de ejeção pode ser atribuída ao aumento da pós-carga imposta ao ventrículo esquerdo, à diminuição da contratilidade ou a ambos, não guardando relação com a freqüência cardíaca, pressão arterial, débito cardíaco, sexo ou idade 30 .…”

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Estresse Mental e Sistema Cardiovascular

Loures¹,

Sant'anna²,

Baldotto³

et al. 2002

Arq. Bras. Cardiol.

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AtualizaçãoO estresse mental ou emocional é um dos maiores problemas das sociedades modernas. Em uma situação de estresse, o organismo humano redistribui suas fontes de energia, antecipando uma agressão iminente. Esse mecanismo de adaptação é vantajoso se realmente houver perigo iminente. Entretanto, se esse estado persistir por muito tempo, o dano será inevitável.A cultura popular há muito associa o estresse agudo e crônico com o desenvolvimento de doenças, corroborado por inúmeros estudos epidemiológicos e experimentais, que demonstram uma ligação entre o estresse mental e o aparecimento e curso de muitas doenças, desde simples infecções virais, até úlceras gástricas e neoplasias. O sistema cardiovascular possui ampla participação na adaptação ao estresse, sofrendo por isso as conseqüências da sua exacerbação. A suspeita de que estados de estresse mental agudos e crônicos sejam fatores de risco para maior morbimortalidade por doença cardiovascular é antiga. Entretanto, a adequada comprovação científica deste fato somente vem sendo obtida mais recentemente. Muitos profissionais ainda encaram com certo ceticismo esta associação, encontrando dificuldade em valorizá-la na prática clínica, embora o estresse mental seja uma das principais queixas de pacientes.Alterações fisiológicas produzidas pelo estresse mental -A vida consiste de um equilíbrio dinâmico, constantemente alternando estados de estresse e homeostase. Desta forma, as forças que alteram a homeostase são equilibradas por respostas adaptativas geradas pelo organismo. Os organismos multicelulares se adaptam a essas situações através de complexas alterações neurais, humorais e celulares, envolvendo múltiplos órgãos e tecidos. O organismo humano desenvolveu um sistema complexo, constituído por componentes do sistema nervoso central, incluindo os neurônios do núcleo paraventricular hipotalâmico, que produzem o hormônio de liberação da corticotrofina, núcleos noradrenérgicos do tronco cerebral com seus componentes periféricos, o eixo hipotálamo-hipófise-adrenal e o sistema nervoso autônomo, cuja principal função é manter a homeostase no repouso e em situações de estresse. Este sistema exerce importante influência em muitas funções vitais, como a respiração, o tônus cardiovascular e o metabolismo intermediário, que também são alteradas por estados de estresse.Os fundamentos para o atual interesse envolvendo as conseqüências fisiopatológicas do estresse provêm dos achados de Cannon, que descreveu a reação de luta ou fuga, caracterizada por intensa descarga adrenérgica na presença de uma ameaça. Mais tarde, Seyle descreveu uma resposta mais generalizada, marcada pela ativação do eixo hipotálamo-hipofisário-adrenal 1 . Atualmente, as pesquisas se focalizam na importância da interpretação subjetiva do estresse e em suas repercussões nos diversos sistemas de forma aguda e crônica.O sistema cardiovascular participa ativamente das adaptações ao estresse (quadro I), estando portanto sujeito às influências neuro-humorais. As respostas cardiovasculares resultam principa...

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Transient left ventricular dysfunction during provocative mental stress in patients with coronary artery disease

Cited by 80 publications

References 29 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

Psychosocial factors impair vascular responses of coronary arteries.

Estresse Mental e Sistema Cardiovascular

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