The heart as an integrated muscle and pump system: triple control and subdivision of the cardiac cycle.
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Biomedical subjects
Publications and source records attributed to S U Sys.
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Cardiac endothelial cells, regardless of whether they are from endocardial or from coronary (micro)vascular origin, directly modulate performance of the subjacent cardiomyocytes, resulting in control of the onset of ventricular relaxation and rapid filling of the heart. This review summarizes major features of the morphology, embryology, and comparative physiology of cardiac endothelial cells as well as the experimental observations on how cardiac endothelial cells affect the mechanical performance of the heart. As for the underlying mechanisms of the interaction between cardiac endothelial cells and cardiomyocytes, two working hypotheses have been postulated over the past years; (1) interaction mediated through a trans-endothelial physicochemical gradient for various ions (active blood-heart barrier), and (2) interaction mediated through the release by the cardiac endothelial cells of various cardioactive substances, eg, nitric oxide, endothelin, and prostacyclin. These two mechanisms may act in concert or in parallel.
Alinidine, a new compound with a bradycardic action, has a rate-decreasing and stabilizing action on the spontaneous contractions of single rat ventricular cardiac cells with a partially skinned and leaky sarcolemmal membrane but with a well-functioning sarcoplasmic reticulum. In the intact multicellular cat papillary muscle, alinidine delays the onset of mechanical activation at concentrations that hardly affect peak mechanical performance and the relaxation phase. From these results, we postulate that alinidine has a stabilizing action on activation, in particular on the release of calcium from the intracellular membranous system, with minimal effects on the total amount released and on the calcium reuptake or process of inactivation.
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.
OBJECTIVE: To determine by how far worsening outpatient clinical parameters can affect outcome after aortic valve replacement, in patients with preserved left ventricular function and symptomatic aortic valve disease. PATIENTS AND METHODS: Five hundred patients with aortic valve disease underwent aortic valve replacement using a bioprosthesis. In 348 patients, another procedure was added. The preoperative outpatient parameters were investigated for their effect on hospital and long-term mortality. A Fisher exact, Kaplan-Meier univariate and Cox proportional hazard analysis were used. RESULTS: A retrospective follow-up of 2022 patient years was obtained. Five preoperative parameters were found to be more present in patients with a decreased left ventricular function: 1) severity of symptoms, 2) previous myocardial infarction, 3) conduction defects, 4) aortic valve regurgitation and 5) increasing need for medication. In patients with an ejection fraction of 50% or more, logistic regression analysis showed that hospital mortality increased with need for medication (p=0.004), previously performed CABG (0.015), increase in symptoms (p=0.018) and myocardial infarction (p=0.034). A Kaplan-Meier analysis revealed aortic valve regurgitation (p=0.017) and increased need for medication (p=0.012) as significant on long-term survival. Presence of a previous myocardial infarction showed a trend (p=0.062). A Cox' proportional hazard analysis showed for global mortality increased need for medication (p=0.010) and previous myocardial infarction (p=0.018) as independent factors and for long-term mortality, this was aortic valve regurgitation (p=0.001). CONCLUSIONS: Results after aortic valve replacement deteriorate with the presence of valve regurgitation, a preoperative myocardial infarction, increasing need for medication or severity of symptoms, even for an ejection fraction of 50% or more. Anamnesis with special care to the degree of symptoms and increasing need for medication early in the valve disease could lead to early referral, thereby reducing number of patients with severe symptoms and improving postoperative results.