Hamsters with coronary vasospasm are at increased risk from stress.

Abstract

Results of earlier experiments suggested that hamsters with inherited heart disease were at a higher risk of succumbing to stress during the vasospastic, lesion-forming period of their lives rather than later when the process of congestive heart failure had begun. To test this hypothesis, we stressed cardiomyopathic hamsters (CMH) whose ages differed by about 3 months; the younger of the two groups of stressed hamsters was in the vasospastic phase of the disease. The stressor was cold immobilization in which stressor intensity was manipulated using two durations of cold exposure. Log rank survival curves revealed no difference in mortality with the more intense stressor. However, significantly fewer of the older hamsters succumbed to the less intense stressor (46% as compared with 85% of the younger CMHs). Examination of the hearts in the experiment where mortality rate was the same for both groups revealed evidence of cardiac dilatation, indicative of heart failure, only in the older hamsters following stress. Since the younger hamsters did not show these changes and since they, but not the older animals, have coronary microvascular spasm and an increased susceptibility to stress, it would appear that the process of coronary vasospasm should be viewed as an independent and additional risk factor in determining the consequences of stress. Because of the effects of stress in the younger cardiomyopathic hamster, we believe that a neural link--which can be activated by stress--may be involved in the pathogenetic process of coronary vasospasm.

Effects of Psychological and Social Factors on Organic Disease: A Critical Assessment of Research on Coronary Heart Disease

“…Other animal models have been utilized to study the effects of stress on hearts with preexisting disease. In this regard, a series of studies (Natelson et al 1991, McCabe et al 2000 demonstrated that stress could worsen the effects of heart failure and cardiac death in a hamster model with inherited heart disease. With regard to cardiac arrhythmias and sudden death, studies by Verrier and colleagues (Verrier & Lown 1984) have shown that stress can lower the threshold for malignant arrhythmias in dogs with induced coronary artery blockage.…”

Effect of trimetazidine and verapamil on the cardiomyopathic hamster myosin phenotype

“…The BIO 14:6 Syrian cardiomyopathy hamster (CMH) is a widely used model of both cardiac and skeletal abnormalities (Kagiya et al , 1991; Davidoff & Gwathmey, 1994). Abnormal cellular calcium homeostasis and spasms of the microcirculation, producing transient focal ischaemia, have been postulated to be at the origin of the cell death in these animals (Natelson et al , 1991; Conway et al , 1994). In the heart, cell loss is associated with compensatory ventricular hypertrophy and the degree of hypertrophy correlates with the myosin isoform restructuring (see Kitsis & Scheuer, 1988; Lompré et al , 1991 for reviews).…”

The Role of Stressor Intensity in Influencing the Course of Heart Disease in Cardiomyopathic Hamsters

“…Additionally, different stressor intensities produced different survival curves in 2.5-and 5-month CMHs; younger hamsters, in their lesion-forming period, were at an increased risk from stress (9). These data suggested that stressor intensity may play an important role in pathological outcomes of hamster heart disease following stress.…”