Psychological stress and cardiovascular disease

Abstract

There is an enormous amount of literature on psychological stress and cardiovascular disease. This report reviews conceptual issues in defining stress and then explores the ramifications of stress in terms of the effects of acute versus long-term stressors on cardiac functioning. Examples of acute stressor studies are discussed in terms of disasters (earthquakes) and in the context of experimental stress physiology studies, which offer a more detailed perspective on underlying physiology. Studies of chronic stressors are discussed in terms of job stress, marital unhappiness, and burden of caregiving. From all of these studies there are extensive data concerning stressors' contributions to diverse pathophysiological changes including sudden death, myocardial infarction, myocardial ischemia, and wall motion abnormalities, as well as to alterations in cardiac regulation as indexed by changes in sympathetic nervous system activity and hemostasis. Although stressors trigger events, it is less clear that stress "causes" the events. There is nonetheless overwhelming evidence both for the deleterious effects of stress on the heart and for the fact that vulnerability and resilience factors play a role in amplifying or dampening those effects. Numerous approaches are available for stress management that can decrease patients' suffering and enhance their quality of life.

Figure 1. Holter Report During Earthquake

(A and B) Heart rate variability 0 to 15 min before and 15 min after the earthquake, respectively. The histogram shows a decrease in the high-frequency (HF) zone and an increase in the low-frequency (LF)/HF ratio from 0.4 to 2.0. (C and D) A sudden increase in heart rate up to 160 beats/min and sinus tachycardia that persisted for 58 min. NU = normalized units; TP = total power; VLF = very low frequency. Reprinted, with permission, from Huang et al. (1).

Figure 2. Incidence of Pulmonary Embolism Associated With Earthquake

Patients with pulmonary embolism (A to C) and shock in the Niigata-Chuetsu earthquake (D). Pulmonary embolism increased after the earthquake compared with the prior 4 weeks and the corresponding 8 weeks in 2002 and 2003. The number of shocks was cited from the official records of the Niigata-Chuetsu earthquake by Japan Meteorological. p < 0.001 versus prior 4 weeks in *2004 or corresponding 8 weeks in †2002 or ‡2003. Reprinted, with permission, from Watanabe et al. (4).

Figure 3. Daily Cardiac Deaths in Los Angeles Associated With Earthquake

On the day of the earthquake (January 17, 1994), there was a sharp rise in the number of deaths related to atherosclerotic cardiovascular disease (n = 51, relative risk 2.6, 95% confidence interval 1.8 to 3.7). The daily number of deaths related to atherosclerotic cardiovascular disease declined in the 6 days after the earthquake (z = 3.15, p = 0.002). Reprinted, with permission, from Leor et al. (5).

Figure 4. Effect of Public Speaking on Plasma Epinephrine

Plasma epinephrine response to different activities. Each line represents a single subject; the dotted line indicates the mean. Reprinted, with permission, from Dimsdale and Moss (7).

Figure 5. Effect of Mental Stress and Exercise on Regional Myocardial Uptake

Changes in regional myocardial uptake or rubidium-82 and in electrocardiogram in relation to chest pain before and after mental arithmetic or exercise. Control scans show homogeneous regional cation uptake. In the patient above there are defects in uptake (arrows) by the anterior wall with mental arithmetic and exercise, and these changes are accompanied by ST-segment depression and angina. A = anterior wall; FW = left ventricular free wall; S = interventricular septum. Adapted and reprinted, with permission, from Deanfield et al. (9).

Figure 6. Probability of Cardiac Event–Free Survival in Patients With and Without a Stress-Induced Drop in LVEF

Probability of event–free survival as a function of mental stress-induced left ventricular ejection fraction (LVEF) change plotted at 2 prototypical values, 1 standard deviation (SD) below (LVEF change =−12.40%) and 1 SD above (LVEF change =+1.05%) the mean of the entire sample (LVEF change = −6.73%). Curves are adjusted for baseline LVEF, history of myocardial infarction, and age. The risk ratio associated with the lower curve compared with the higher curve is 2.40 (p = 0.02). Reprinted, with permission, from Jiang et al. (12).

Figure 7. Angiogram in Stress Cardiomyopathy

Left ventricular angiogram in diastole (left) and systole (right) in right anterior oblique projection demonstrating wall motion abnormality characteristic of stress cardiomyopathy. At end systole, left ventricular chamber adopts distinctive “short neck with round flask” configuration in which distal (apical) portion is akinetic/hypokinetic whereas, in contrast, the remaining proximal (basal) segment is hypercontractile (sharp area of transition is shown by arrows). Reprinted, with permission, from Sharkey et al. (16).

Figure 8. Effect of Perceived Discrimination on Pressor Sensitivity

Effects of ethnicity and perceived discrimination on diastolic pressor response. For visual purposes, perceived discrimination was dichotomized into high and low groups using median split. Individuals who perceive more ethnic discrimination have greater blood pressure responses to phenylephrine (p < 0.05). DBP = diastolic blood pressure. Reprinted, with permission, from Thomas et al. (29).

Figure 9. Effect of Meditation on HR Response to Infused Isoproterenol

Effects of meditation on chronotropic responses to isoproterenol. (Solid line) Mean ± standard error response to isoproterenol in 93 women; (dotted line) patient's response while meditating; (dashed line) patient's response while instructed not to meditate. BPM = beats/min; HR = heart rate. Reprinted, with permission, from Dimsdale and Mills (39).