No abstract

Fractional flow reserve derived from pressure measurements correlates more closely to relative flow reserve derived from PET than angiographic parameters. This validates in humans the use of fractional flow reserve as an index of the physiological consequences of a given coronary artery stenosis.

Previous research showed: a) emotional distress is a risk factor for mortality after myocardial infarction (MI) and b) emotional distress is linked to stable personality traits. In this study, we examined the role of these personality traits in mortality after MI. Subjects were 105 men, 45 to 60 years of age, who survived a recent MI. Baseline assessment included biomedical and psychosocial risk factors, as well as each patient's personality type. After 2 to 5 (mean, 3.8) years of follow-up, 15 patients (14%) had died. Rate of death for patients with a distressed personality type (11/28 = 39%) was significantly greater than that for patients with other personality types (4/77 = 5%) (p < .0001). Patients with this personality type tend simultaneously to experience distress and inhibit expression of emotions. Low exercise tolerance, previous MI (p < .005), anterior MI, smoking, and age (p < .05) were also associated with mortality. A logistic regression model including these biomedical factors had a sensitivity for mortality of only 27%. The addition of distressed personality type in this model more than doubled its sensitivity. Of note, among patients with poor physical health, those with a distressed personality type had a five-fold mortality risk (p < .005). Consistent with the findings of other investigators, depression (p < .005), life stress, use of benzodiazepines (p < .01), and somatization (p < .05) were also related to post-MI mortality. These psychosocial risk factors were more prevalent in the distressed personality type than in the other personality types (p < .001-.05). Multiple logistic regression indicated that these psychosocial factors did not add to the predictive value of the distressed personality type. Hence, an important personality effect was observed despite the low power. This suggests that personality traits may play a role in the detrimental effect of emotional distress in MI patients.

In the present review, we adopted the viewpoint of the physiologist looking at the global function of the heart, during relaxation and diastole, as an integrated muscle-pump system. We first focused our attention on properties of relaxation and diastole at the subcellular (SR, contractile proteins), cellular, and multicellular scales of cardiac muscle and then at the scale of the ventricle and intact global heart. At each lower scale we derived properties from experimental facts and examined the extent to which these properties could be extrapolated conceptually to the higher scale. From this muscle-pump approach, we learned that a general and fundamental property of relaxation of the heart as a muscle-pump system is load dependence, i.e., the mutually independent behavior of the time patterns of slow force decline and pressure fall and of rapid lengthening and rapid filling. Load dependence is found at all hierarchic scales, irrespective of whether it is examined under strictly isotonic-isometric or isometric-isotonic or auxotonic loading conditions and despite often substantial nonuniformity. Relaxation is governed by the interaction of the loading conditions and the two major determinants of the inactivation process, i.e., Ca2+ reuptake by the SR and the properties of the contractile proteins. Load dependence is the mere mechanical expression of the unequal contribution, during the two phases of relaxation, of these three interacting determinants of relaxation (load, SR, and contractile proteins). During force decline in isolated muscle and pressure fall in the ventricle, the properties of the contractile proteins predominate over load and SR; during muscle lengthening and rapid ventricular filling, load and SR become more important. As the relative importance of the phenomena above is different during pressure fall in comparison to rapid filling, it is not surprising that directional changes in pressure fall may not predict those in filling. We also saw that the overall time pattern of pressure fall in contrast to rapid filling may sometimes be markedly altered, e.g., with simultaneous increases in peak-dP/dt, indicating more rapid early pressure relaxation, and prolonged time constant tau, indicating slower late pressure relaxation, or vice versa. From this muscle-pump approach, it should also be remembered that optimal efficiency of the heart limits the extent to which nonuniformity may exist. At all hierarchic scales, variations in the degree of nonuniformity, however small, constitute an important physiological modulator of performance throughout systole and diastole.(ABSTRACT TRUNCATED AT 400 WORDS)

NO and cGMP induced a concentration-dependent biphasic contractile response. The myocardial contractile effects of NO and cGMP were modulated by the status of EE and by concomitant cholinergic or adrenergic stimulation.

Primary diastolic dysfunction or failure is a distinct pathophysiologic entity. It results from increased resistance to ventricular filling, which leads to an inappropriate upward shift of the diastolic pressure-volume relation, particularly during exercise (exercise intolerance). The causes of diastolic failure are inappropriate tachycardia, decreased diastolic compliance and impaired systolic relaxation. Impaired (incomplete or slowed) systolic relaxation must be conceptually distinguished from compensatory prolonged systolic contraction (delayed or retarded relaxation). Optimal therapy will depend on the type of disease, the phase during the course of a given disease and the coexistence and relative contribution of various (de)compensatory processes. Treatment may consist of bradycardic, remodeling and lusitropic drugs.

EARLY DETECTION of impaired relaxation has been emphasized recently for the evaluation of global and regional ventricular function in patients with heart disease. Although early relaxation abnormalities have been found in various cardiac diseases, the underlying mechanisms are not as yet fully understood. Given the recent progress in our understanding of relaxation of the heart,' these mechanisms can now be discerned more easily. We will first summarize our present knowledge of relaxation of cardiac muscle or, more specifically, how relaxation is controlled by the three following interacting determinants: (1) load, (2) (in)-activation, and (3) nonuniform distribution of load and (in)activation in space and in time. Then, the concept of triple control will be extended to that of the intact heart in situ as a pump. We will also review how multiple factors, acting either alone or in concert depending on the nature of the disease, underlie early relaxation abnormalities in patients with heart disease. Finally, measurements of ventricular relaxation will be critically discussed in view of these newer concepts. Mechanical aspects of relaxation of isolated cardiac musclePerformance of the heart during the contraction phase, both as a muscle and as a muscle-pump system, is regulated through two distinct but interrelated functions, namely heterometric autoregulation or control by changes in load (volume and/or pressure) and homeometric autoregulation or control by changes in contractility. Although regulation of performance by changes in load is conceptually related to heterometric autoregulation and regulation of performance by changes in contractility to homeometric autoregulation, these concepts are not quite identical. By the same token, although changes in contractility are usu- Received Jan. 5, 1983; revision accepted Sept. 29, 1983. 190 ally believed to be the mechanical expression of changes in activation, the concepts of contractility and activation should not be used interchangeably. Given the complexity of the intact heart, one should also take into account some degree of nonuniform distribution of the former two mechanisms as a third important physiologic determinant of performance.We have recently learned that a similar triple control mechanism also operates during the relaxation phase. Relaxation of the heart, both as a muscle and musclepump system, is governed by the continuous interplay of the sensitivity of the contractile system to the prevailing load and the dissipating activation (inactivation). ' For a given set of loading conditions, relaxation can be modulated by subtle alterations of the load dependence due to changes in the underlying dissipation of activation. Alternatively, for a given load dependence, and hence unchanged dissipation of activation, relaxation will be influenced by alterations of the prevailing load. As in the contraction phase, this control of relaxation is continuously modulated by the regional and temporal nonuniform distribution of load and inactivation. Within a given...

In the present study, cutoff values of FFRmyo and translesional pressure gradients are established from the relation between intracoronary pressure-derived indexes and ECG signs of myocardial ischemia during maximal exercise. These values can be helpful for clinical decision making in cases with dubious angiographic results. Furthermore, our data support the concept that stenosis physiology is better reflected by hyperemic than by basal measurements.