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Biomedical subjects

R P Sloan

Publications and source records attributed to R P Sloan.

At least 19 recordsLinked to original sources
PubMed2001

Relation between depression after coronary artery bypass surgery and 12-month outcome: a prospective study.

BACKGROUND: The association of depression with cardiac events has been investigated mainly in community cohorts, in patients undergoing catheterisation, or in patients who have had myocardial infarction. We have assessed the effect of depression on outcomes after coronary artery bypass graft (CABG) surgery. METHODS: In a prospective study, we followed up for 1 year 207 men and 102 women, who had undergone coronary artery bypass graft surgery. We assessed depression with a structured psychiatric interview (diagnostic interview schedule) and a questionnaire (Beck depression inventory) before discharge. Cardiac events included angina or heart failure that needed admission to hospital, myocardial infarction, cardiac arrest, percutaneous transluminal coronary angioplasty, repeat CABG, and cardiac mortality. Non-cardiac events consisted of all other reasons for mortality or readmission. FINDINGS: 63 patients (20%) met modified diagnostic statistical manual IV criteria for major depressive disorder. At 12 months, 17 (27%) of these patients had a cardiac event compared with 25 of 246 (10%) who were not depressed (p<0.0008). Five variables had significant univariate associations with cardiac events: sex, living alone, low ejection fraction (<0.35), length of hospital stay, and depression. In a Cox proportional-hazard model with these five and two other variables of cardiac severity, major depressive disorder (risk ratio 2.3 [95% CI 1.17-4.56]), low ejection fraction (2.3 [1.07-5.03]), and female sex (2.4 [1.24-4.44]) were associated with adverse outcomes. Depression did not predict deaths or admissions for non-cardiac events. INTERPRETATION: Depression is an important independent risk factor for cardiac events after CABG surgery.

Age Distribution↗
PubMed2001

Physiologic responses to cognitive challenge during pregnancy: effects of task and repeat testing.

Physiological responses to stress during pregnancy are believed to influence birth outcomes. Researchers have studied pregnant women in laboratory stressor paradigms to investigate these associations, yet normative data on cardiovascular and respiratory responses to laboratory challenge during pregnancy are not yet established. To begin to establish such normative data, this study examined the effects of task and repeat stressor exposure on reactivity in third-trimester pregnant women. Thirty-one healthy pregnant women (mean age=27 years; range 18-36) between the 33rd and 39th week of pregnancy, were instrumented for continuous electrocardiography, blood pressure (BP), and respiration data. Subjects rested quietly for a 5-min baseline and then performed both a mental arithmetic stressor and a Stroop color-word-matching task, each 5 min in length and each followed by a 5-min recovery period. The order of the tasks was counterbalanced. After each 5-min period, subjects rated the period on a 10-point stress scale. Averaged across task type and challenge period, systolic and diastolic BP and respiration rate increased significantly in response to cognitive challenge, but heart rate (HR) did not. When data were examined for task and period effects, the following results emerged: the Stroop task elicited significantly greater systolic BP and HR reactivity than the arithmetic task, yet subjects rated the arithmetic task as more stressful. Averaged across task type, subjects showed greater systolic BP reactivity during the second challenge period compared to the first. Finally, women's BP tended to drift upward and did not return to baseline during the first recovery period. These findings indicate that averaging data across tasks and periods can obscure the time course of response patterns that may be important in the study of associations between maternal stress and perinatal development, as well as in other research on reactivity to repeat stress exposure.

Adolescent↗
PubMed2001

Enhanced stress reactivity in paediatric anxiety disorders: implications for future cardiovascular health.

The aim was to clarify the developmental nature of associations between psychiatric illness and risk for cardiovascular disease by investigating differences in cardiac functioning between youth with anxiety disorders and healthy controls. Twenty-two children meeting DSM-IV criteria for either separation anxiety disorder, overanxious disorder, panic disorder/panic attacks, or social phobia and 12 healthy controls underwent continuous electrocardiogram and respiration rate monitoring during a 15 min baseline period and 15 min of exposure to 5% CO(2). Heart rate (HR) and high frequency heart rate variability (HRV), a non-invasive measure of cardiac parasympathetic control, were calculated. Youth with anxiety disorders had higher and less fluctuating HR during baseline. Data also suggested that probands showed diminished overall changes in HRV during baseline and CO(2) inhalation relative to controls. However, as respiration rate affects HRV, these findings were confounded by changes in respiration elicited by CO(2) inhalation. The data suggest that youth with anxiety disorders experience an elevated and less fluctuating HR in the face of a novel situation, possibly due to a failure to appropriately modulate HRV. In adults, sustained elevations in HR in conjunction with deficient vagal modulation predicts risk for future cardiovascular disease. As such, the current data suggest that the presence of an anxiety disorder may identify youth who exhibit autonomic profiles that place them at risk for cardiac disease.

Administration, Inhalation↗
PubMed2000

Heart rate variability in depressive and anxiety disorders.

Loss of normal autonomic nervous system control of heart rate and rhythm is an important risk factor for adverse cardiovascular events. After myocardial infarction, reduction in beat-to-beat heart rate variability, a measure of cardiac autonomic innervation by the brain, is a strong predictor of death. With loss of vagal innervation, as is noted in patients with severe neuropathy and in heart transplant recipients, there is loss of heart rate variability. It is speculated that decreased parasympathetic innervation exposes the heart to unopposed stimulation by sympathetic nerves. Individuals with high hostility scores and patients with anxiety or depressive disorders have low heart rate variability and may be at increased risk for cardiovascular death associated with coronary heart disease and arrhythmias. After myocardial infarction, depressed patients exhibit higher mortality rates compared with nondepressed patients. Men with "phobic anxiety," a construct that appears to overlap substantially with panic disorder, also have higher rates of sudden cardiac death and coronary artery disease than control populations. The reduction in autonomic nervous system control to the heart may be one link between psychopathology and heart disease. Although tricyclic antidepressants reduce heart rate variability, at least one study has suggested that, in patients with panic disorder, treatment with the selective serotonin reuptake inhibitor paroxetine normalizes heart rate variability. Hence there is potential for the treatment of psychiatric disorders to affect positively the development and course of cardiovascular disease.

Anxiety Disorders↗
PubMed2000

Maternal stress responses and anxiety during pregnancy: effects on fetal heart rate.

This study examined the effect of an acute maternal stress response and anxiety on fetal heart rate. Seventeen healthy, 3rd-trimester pregnant women (mean age = 26 +/- 6 years) were instrumented for continuous electrocardiography, blood pressure (BP), respiration, and fetal heart rate (HR). Subjects completed the state anxiety subscale of the State Trait Personality Inventory (STPI), then rested quietly in a semirecumbent position for a 5-min baseline period, followed by either a 5-min arithmetic or Stroop color-word task. Over the entire 5-min stress period and when averaged across all subjects, the stressors led to significant increases in maternal systolic BP and respiratory rate but changes in maternal HR, diastolic BP, and fetal HR were not significant. However, when subjects were dichotomized into groups that had above or below average anxiety scores [ANX(+) and ANX(-)], both groups had similar respiration rate increases to the stressors, but the BP and fetal heart rate (FHR) responses were significantly different. Women in the ANX(-) group had significantly greater BP responses compared to women in the ANX(+) group whereas the fetuses of ANX(+) women showed significant HR increases and the fetuses of ANX(-) women exhibited nonsignificant decreases. These findings suggest that women's acute emotional reactivity during pregnancy can influence fetal HR patterns and that a stress-induced increase in maternal BP is not the primary signal by which a women's stress response is transduced to her fetus. The results are consistent with the hypothesis that maternal psychological variables may shape the neurobehavioral development of the fetus.

Adult↗
PubMed2000

Mixed-effects models in psychophysiology.

The current methodological policy in Psychophysiology stipulates that repeated-measures designs be analyzed using either multivariate analysis of variance (ANOVA) or repeated-measures ANOVA with the Greenhouse-Geisser or Huynh-Feldt correction. Both techniques lead to appropriate type I error probabilities under general assumptions about the variance-covariance matrix of the data. This report introduces mixed-effects models as an alternative procedure for the analysis of repeated-measures data in Psychophysiology. Mixed-effects models have many advantages over the traditional methods: They handle missing data more effectively and are more efficient, parsimonious, and flexible. We described mixed-effects modeling and illustrated its applicability with a simple example.

Algorithms↗
PubMed1999

Changes in autonomic regulation with age: implications for psychopharmacologic treatments in children and adolescents.

Developmental changes in the cardiovascular system could have an impact on risks associated with psychopharmacological interventions. Children may be more vulnerable to adverse cardiac events due to immaturity in autonomic control of the heart. These changes are incompletely understood and are characterized in this study. A consecutive series of 70 boys, aged 6-14 years, was recruited. Developmental variation in the autonomic nervous system was evaluated by assessing heart period variability (HPV), pulse, and blood pressure in response to orthostasis. Increased age correlated significantly with greater heart rate and diastolic blood pressure response to orthostasis. HPV at rest and in response to tilt did not significantly correlate with age. Boys with family histories of hypertension had a significantly greater blood pressure response to orthostasis. These findings suggest that developmental age-related changes in the sympathetic nervous system, as reflected by changes of pulse and blood pressure response to tilt, occur across this age range. Parasympathetic changes, as reflected by HPV, do not. In light of these findings, more research is needed on children's and adolescents' relative cardiac risk with psychotropic medications as opposed to adults'.

Adolescent↗
PubMed1999

Cardiovascular effects of desipramine in children and adults during exercise testing.

OBJECTIVE: In light of recent reports of sudden death in children being treated with desipramine (DMI), 3 of which were associated with physical exercise, the authors examined the effects of DMI on exercise in children and adults before and during DMI treatment. METHOD: Before treatment, 22 subjects (9 children, 13 adults) participated in a graded treadmill exercise test. Outcome measures included exercise tolerance, cardiovascular, and electrocardiographic parameters at progressive intensity levels and serum norepinephrine (NE) levels before and after exercise testing. Subjects were then treated with DMI, titrated to an average DMI dosage of 3 mg/kg, and underwent repeated exercise testing. RESULTS: DMI treatment was associated with a significant elevation of circulating NE levels in the pre-exercise assessment. Exercise tolerance was not affected by DMI, and blood pressure and heart rate effects were modest. The cardiovascular impact of DMI treatment was similar in children and adults. One 31-year-old subject exhibited a brief episode of ventricular tachycardia associated with exercise during DMI treatment. CONCLUSIONS: DMI has only minor effects on the cardiovascular response to exercise, and these effects do not appear age-related. However, DMI may increase the risk of exercise-associated arrhythmias in rare individuals.

Adolescent↗
PubMed1999

Effects of desipramine on autonomic input to the heart.

OBJECTIVE: To examine the impact of age on the effects of desipramine (DMI) on autonomic input to the heart. METHOD: Twenty-four-hour electrocardiograms were obtained from 42 subjects, aged 7 to 66 years, while off and on DMI. To obtain measures of autonomic input to the heart, heart rate variability was assessed via spectral analysis of RR interval variability. RESULTS: DMI treatment was associated with a significant increase in 24-hour mean heart rate and significant decreases in RR interval variability in all spectral bands, including in the high-frequency band, which provides a measure of parasympathetic input to the heart. RR interval variability was greater in younger individuals both off and on DMI. CONCLUSIONS: DMI treatment was associated with a marked decline in RR interval variability, indicating that DMI affects autonomic input to the heart. Specifically, DMI reduced parasympathetic input, which, in theory, may increase vulnerability to arrhythmias. However, the magnitude of DMI's impact on RR interval variability did not vary with age.

Adolescent↗
PubMed1998

Heart period variability and psychopathology in urban boys at risk for delinquency.

To examine associations between heart period variability (HPV) and psychopathology in young urban boys at risk for delinquency, a series of 697-11-year-old younger brothers of adjudicated delinquents received a standardized psychiatric evaluation and an assessment of heart period variability (HPV). Psychiatric symptoms were rated in two domains: externalizing and internalizing psychopathology. Continuous measures of both externalizing and internalizing psychopathology were associated with reductions in HPV components related to parasympathetic activity. These associations could not be explained by a number of potentially confounding variables, such as age, ethnicity, social class, body size, or family history of hypertension. Although familial hypertension predicted reduced HPV and externalizing psychopathology, associations between externalizing psychopathology and HPV were independent of familial hypertension. Psychiatric symptoms are associated with reduced HPV in young urban boys at risk for delinquency.

Blood Pressure↗
PubMed1998

Multiple metabolic syndrome is associated with lower heart rate variability. The Atherosclerosis Risk in Communities Study.

OBJECTIVE: To test at the population level whether people with multiple metabolic syndrome (MMS) disorders have reduced cardiac autonomic activity (CAA). RESEARCH DESIGN AND METHODS: We examined the association between the level of CAA and MMS disorders, at the degree of clustering and the segregate combination levels, using a random sample of 2,359 men and women aged 45-64 years from the biracial, population-based Atherosclerosis Risk in Communities (ARIC) Study. Supine resting 2-min beat-to-beat heart rate data were collected. High-frequency (HF) (0.15-0.35 Hz) and low-frequency (LF) (0.025-0.15 Hz) spectral powers, the ratio of LF to HF, and the SD of all normal R-R intervals (SDNN) were used as the conventional indices of heart rate variability (HRV) to measure CAA. The MMS disorders included hypertension, type 2 diabetes, and dyslipidemia. RESULTS: HRV indices were significantly lower in individuals with MMS disorders. The multivariable adjusted mean HF was 0.85 (beat/min)2 in subjects with all three MMS disorders, in contrast to 1.31 (beat/min)2 in subjects without any MMS disorder. At the segregated combination level, the multivariable adjusted means +/- SEM of HF were 1.34 +/- 0.05, 1.16 +/- 0.05, 1.01 +/- 0.17, and 1.34 +/- 0.05 (beat/min)2, respectively, for subjects without any MMS disorder, with hypertension only, with diabetes only, and with dyslipidemia only, and the means +/- SEM of HF were 0.93 +/- 0.04, 0.70 +/- 0.15, and 1.20 +/- 0.05 (beat/min)2, respectively, for subjects with diabetes and hypertension, diabetes and dyslipidemia, and hypertension and dyslipidemia. An increase in fasting insulin of 1 SD was associated with 88% higher odds of having a lower HF. The pattern of associations was similar for LF and SDNN. CONCLUSIONS: These findings suggest that MMS disorders adversely affect cardiac autonomic control and a reduced cardiac autonomic control may contribute to the increased risk of subsequent cardiovascular events in individuals who exhibit MMS disorders.

Arteriosclerosis↗
PubMed1997

Cardiac autonomic control is inversely related to blood pressure variability responses to psychological challenge.

Blood pressure exhibits variability (BPV) at low (0.02- to 0.07-Hz), mid (0.07- to 0.15-Hz)-, and high (0.15- to 0.50-Hz) frequencies. Evidence suggests that BPV responses to challenge are inversely related to cardiac autonomic control. We tested this hypothesis by examining the BPV responses to psychological stressors in 22 normal subjects who differed in cardiac control, operationalized as resting heart period variability (HPV). HPV and BPV were measured noninvasively or a beat-to-beat basis. The stressors produced a significant increase in heart rate and a small but significant increase in diastolic blood pressure. As predicted, the changes in BPV in response to the stressors were inversely related to resting HPV. The results are interpreted in terms of a model of cardiovascular control that holds that BPV originates from feedforward effects of central control of the heart, feedback effects mediated through the baroreflexes, and direct sympathetic vascular effects.

Adult↗