Cross correlation of heart rate and respiration versus deep breathing. Assessment of new test of cardiac autonomic function in diabetes.

Cross correlation is a mathematical function whereby spectral analysis is used to describe the relationship between heart-rate fluctuations (256 R-R intervals) and respiration (simultaneously obtained by pneumotacograph). To assess its usefulness for testing autonomic integrity, cross correlation and deep breathing were compared in 141 diabetic subjects (aged 39 +/- 14 yr) and in 77 control subjects (aged 33 +/- 13 yr). To characterize patients, Valsalva maneuver, 30:15 ratio, tilt, and handgrip tests were performed in 96 of these patients; 23 had two or more abnormal tests (group A), 28 had one (group B), and 45 had none (group C). Sensitivity to parasympathetic withdrawal was compared in 9 control subjects (aged 26 +/- 4 yr) by four sequential 0.01-mg/kg i.v. atropine administrations. Reproducibility was compared in 11 control subjects (aged 25 +/- 2 yr) by repeating the tests four times for 2 consecutive days. Considering all 141 patients, cross correlation and deep breathing were less than 2SD of the mean of control subjects in 64 and 36 subjects, respectively. Considering patients who also performed other tests of autonomic function, cross correlation and deep breathing were less than 2SD of the mean of controls in 42 and 30 subjects, respectively (group A, 20 and 15; group B, 12 and 9; group C, 10 and 6). Cross correlation had better reproducibility than deep breathing (C.V. 10.3 vs. 30.6% at 6 breaths/min) and greater sensitivity to atropine (after the 1st injection, cross correlation and deep breathing decreased to 34.6 and 48.2% of baseline values, respectively; P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Load dependence of isovolumic relaxation in intact heart: facts or artifacts?

In order to study the dependence of left ventricular isovolumic relaxation on preload, afterload, and contractility the effects of infusions of dextran, phenylephrine, and dobutamine were assessed in 10 closed chest anaesthetised dogs. Left ventricular and aortic pressures and left ventricular transverse diameters were measured by micromanometers and a tracking sonomicrometer. Isovolumic relaxation time constant was computed by two different single exponential models: the first (time constant Tw) assumed the horizontal asymptote as equal to zero, whereas the second (time constant Tl) assumed a variable asymptote (Pb). To compare the two models, deviations between observed and predicted left ventricular pressures during isovolumic relaxation were computed for both (average squared difference ARSSQw and ARSSQl respectively). Dextran infusion, although increasing preload indexes, did not affect Tl (from 35.1(2.6) to 38.5(2.2) ms, NS) (mean(SEM], but increased Tw (from 28.4(1.4) to 43.8(2.1) ms, p less than 0.001); Pb was significantly shifted upwards (from -7.9(2.4) to +8.2(2.8) mmHg, p less than 0.01). Pb correlated with left ventricular end diastolic pressure (r = 0.71, p less than 0.001). Phenylephrine infusion did not change the isovolumic relaxation time course (Tl from 36.4(3.5) to 46.2(6.1) ms, NS; Tw from 26.8(2.3) to 30.5(2.9) ms, NS) nor Pb (from -9.5(2.3) to -18.7(2.3) mmHg, NS). Dobutamine infusion reduced Tl significantly (from 35.2(3.7) to 25.3(2) ms, p less than 0.02), but did not change Tw (from 27.5(2.4) to 23.3(3.3) ms, NS) nor Pb (from -7.3(1.8) to -8.8(2.3) mmHg, NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Chlamydia pneumoniae and cytomegalovirus seropositivity, inflammatory markers, and the risk of myocardial infarction at a young age.

BACKGROUND: Pathogens causing chronic infections may promote atherosclerosis. The aim of our study was to evaluate the association of Chlamydia pneumoniae (Cp) and cytomegalovirus (CMV) infection and of inflammatory activation with premature myocardial infarction (MI). METHODS: Specific anti-Cp and anti-CMV immunoglobulin G (IgG), fibrinogen, white blood cells (WBC), and C-reactive protein (CRP) were measured in 120 post-MI patients

Acute haemodynamic effects of ibopamine and dopamine on isovolumic relaxation.

The effects of intraduodenal ibopamine (a new orally active inotropic agent claimed to have haemodynamic effects similar to dopamine) on isovolumic relaxation were monitored for 90 min in eight closed-chest anaesthetized dogs. Dopamine and epinine (ibopamine active metabolite) were also infused at graded doses. After 15 min, ibopamine (12 mg/kg) shortened the time constant of isovolumic relaxation, and increased stroke volume and mean aortic pressure. Peak positive dP/dt increased significantly only 10 min later. Heart rate did not change. Dopamine (10 micrograms/kg per min) similarly reduced the time constant, and increased stroke volume, mean aortic pressure, peak positive dP/dt and heart rate. Epinine (10 micrograms/kg per min) caused similar changes in peak positive dP/dt, stroke volume, mean aortic pressure, and accelerated time constant without raising the heart rate. Ibopamine and epinine therefore significantly improved the isovolumic relaxation phase, like dopamine, without however affecting the heart rate.

[Reproducibility of the measurement of thoracic electric impedance]. / Riproducibilità delle misure di impedenza elettrica toracica.

Recordings of thoracic electrical impedance were consecutively taken in 10 normal subjects (age 18-48 years, mean 38.6) two times during the same day, during the following day and after 1 month. The following parameters were evaluated: heart rate, systolic blood pressure, diastolic blood pressure, left ventricular ejection time, pre-ejection time, baseline electrical impedance, DZ positive peak, Q-dZ/dt interval and Heather Index. Data were processed in order to quantify the different source of variability: subjects or biological variability, days, beats. Total variability was expressed in absolute units as coefficient of variation. Results were as follows: Q-dZ/dt interval had the lowest coefficient of variation (7.7%). Inter subject was the largest source of variability for all the indices showed, ranging from 70.5% to 89.3%. On the contrary intraindividual variability was moderate racing from 1% to 2.6% for various impedance measurements. In conclusion, thoracic electrical impedance measurements showed good reproducibility, especially when successive measurements were compared in a same subject.

[The apex cardiogram in normal aged subjects]. / L'apicocardiogramma in soggetti anziani normali.

In 25 healthy subjects aged 60-88 years (mean 74.5) and in 20 healthy subjects aged 16-32 years (mean 23.6) apexcardiographic indices were studied as a function of age. The apex cardiograms (ACG) were obtained using a non-calibrated displacement transducer. With the help of an interactive computer program, 17 ACG indices of systolic and diastolic function were computed. The indices were divided into 2 groups (according to the nomenclature proposed by their Authors): a) systolic indices: electromechanical ventricular interval q-C, systolic upstroke time C-E, time from the beginning of ventricular depolarization to the peak of the first ACG derivative q-dA/dt, time from the onset of systolic slope to the peak of first ACG derivative C-dA/dt, ejection fraction according to Antani et al. 1979 E.F.; b) diastolic indices: electromechanical atrial interval P-a, atrial wave length d.a., height of atrial wave as percent of total ACG deflection a/H, height of atrial wave as percent of total diastolic deflection a/D, ratio of the diastolic wave to the total ACG height D/H, total rapid filling cR, early filling period EFP, rapid filling period RFP, total apexcardiographic relaxation time TART, duration of diastolic period A2-C, total apexcardiographic relaxation time index TARTI and diastolic amplitude time index DATI. Several diastolic indices (a/D, a/H, TART, electromechanical atrial time) were markedly higher (p less than 0.001) or lower (TART and DATI, p less than 0.001) in the older group. Systolic indices showed less significant differences: the electromechanical interval lengthened in the older group (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of mental stress on platelet function in normal subjects and in patients with coronary artery disease.

We studied the effect of emotional stress (mental arithmetic for 10 min) in 10 postinfarction patients and in 10 age-matched apparently healthy subjects as controls. Blood samples for platelet function studies and for the determination of epinephrine levels in serum were taken in basal conditions, at the end of mental stress and after 30 min of recovery. Patients were studied twice, in washout of medications and after oral administration of dipyridamole, 200 mg twice a day for 6 consecutive days. Mental stress induced in patients significant increments in different hemodynamic parameters (heart rate, systolic blood pressure and diastolic blood pressure) and in serum epinephrine levels. Concomitantly, the test produced a significant increase in platelet aggregation (induced by 3 microM ADP or 1 microgram/ml collagen), the formation of circulating platelet aggregates and an increase in plasma thromboxane B2 levels. Hemodynamic parameters and platelet function tests returned to baseline values after 30 min. Similar activation of hemodynamic parameters, similar increase in epinephrine levels and lower increase in platelet function by emotional stress were observed in control subjects. Treatment of patients with dipyridamole had no effect on stress-induced increase in hemodynamic parameters and epinephrine levels, but decreased stress-related platelet activation. These data can contribute to a better understanding of the complex relationships between psychosocial factors, the hemostatic system and vascular disease.

Antithrombin III biological activity and emotional stress in patients with coronary artery disease.

We studied the effect of emotional stress (mental arithmetic for 10 minutes) in ten postinfarction patients and in ten age-matched, apparently healthy subjects as controls. Blood samples for the determination of epinephrine and AT III levels were taken in basal conditions, at the end of mental stress and after 30 minutes of recovery. Mental stress induced a significant increase in epinephrine levels and a significant decrease in AT III levels in control subjects. Both parameters returned to baseline values after 30 minutes of recovery. On the contrary, in postinfarction patients AT III levels of recovery were still significantly lower than those of baseline, suggesting a reduced ability to restore the original concentration of this physiologic inhibitor. Our data can contribute to a better understanding of the complex relationships among phychosocial factors, the haemostatic system and vascular disease.

Psychophysiological stress testing in postinfarction patients. Psychological correlates of cardiovascular arousal and abnormal cardiac responses.

The psychophysiological responses to two mental stress tests (mental arithmetic and an interactive concentration task) were assessed in 168 unmedicated, male, postinfarction patients 36-69 years old. Patients also completed a standard battery of psychological tests. Psychophysiological responses were generally unrelated to age and education. Comparison of patients scoring high (more than 75%) and low (less than 25%) relative to the normal population on psychological measures indicated that heart rate and blood pressure responses to mental stress tests were significantly greater in those reporting low than in those reporting high neuroticism. The study population was subsequently divided into high, medium, and low cardiovascular responders on the basis of rate-pressure product reactions to the two stress tests. The three cardiovascular response groups did not differ in age, interval between myocardial infarction and stress testing, ejection fraction, incidence of exercise-induced ischemia, or ischemic signs during Holter monitoring. However, the high cardiovascular responders were more likely to manifest possible or definite electrocardiographic signs of ischemia or significant arrhythmia during mental stress testing than were the medium or low cardiovascular responders (50% versus 19.6% and 7%, respectively). High cardiovascular responders also reported lower levels of trait anxiety, neuroticism, psychophysiological symptoms, and depression.

Effect of solid detergent washing on values of skin electrical impedance.

We have studied the electrical behaviour of the skin on 20 volunteers, before and after cleaning with solid detergent. The aim was to study one of the possible variables of the measurements. The results have shown that the cleaning has globally reduced the electrical skin parameters of the forehead, without influencing other parts examined (dorsal and palmar surfaces of the hand). The result has been attributed to the elimination of the hydrolipidic film of the surface and in particular that of the sebum of the forehead. The data give an idea as to how to obtain more homogeneous final results, as well as studying the sebum production function.

Platelet activation by emotional stress in patients with coronary artery disease.

We studied the effects of experimentally induced emotional stress (mental arithmetic) on different hemodynamic parameters, catecholamine levels, and serum and platelet function tests in 25 postinfarction patients and in 10 apparently healthy, age-matched control subjects. Mental stress (10 minutes) induced significant increments in heart rate, systolic blood pressure, diastolic blood pressure, double product, and cardiac output, indicating a sympatho-adrenal stimulation that was confirmed by a significant increase in serum epinephrine and norepinephrine levels. All of the effects disappeared at minute 10 of recovery. Concomitantly, the test produced a significant increase in platelet aggregation (induced by 3 microM ADP or 1 microgram/ml collagen), the formation of circulating platelet aggregates, and an increase in thromboxane B2 levels in plasma and serum. These effects were also rapidly reversible. Similar activation of hemodynamic parameters and a similar but less evident increase in platelet function by emotional stress were observed in control subjects. A possible artifact due to factitious platelet activation by catheter sampling was excluded with experiments in which a 40-minute rest was introduced after the baseline period and before mental stress; platelet activation did not occur during baseline or rest periods, only after emotional stress. Furthermore, the antiplatelet drug dipyridamole reduced the stress-induced formation of platelet aggregates in postinfarction patients. These results demonstrate the existence of a direct link between emotional stress and platelet function and offer an explanation of one of the mechanisms through which mental stress may be involved in the development of coronary artery disease.