A high degree of heart rate (HR) variability is found in compensated hearts with good function, whereas HR variability can be decreased with severe coronary artery disease, congestive heart failure, aging and diabetic neuropathy. To test the hypothesis that HR variability is a predictor of long-term survival after acute myocardial infarction (AMI), the Holter tapes of 808 patients who survived AMI were analyzed. Heart rate variability was defined as the standard deviation of all normal RR intervals in a 24-hour continuous electrocardiogram recording made 11 +/- 3 days after AMI. In all patients demographic, clinical and laboratory variables were measured at baseline. Mean follow-up time was 31 months. Of all Holter variables measured, HR variability had the strongest univariate correlation with mortality. The relative risk of mortality was 5.3 times higher in the group with HR variability of less than 50 ms than the group with HR variability of more than 100 ms. HR variability remained a significant predictor of mortality after adjusting for clinical, demographic, other Holter features and ejection fraction. A hypothesis to explain this finding is that decreased HR variability correlates with increased sympathetic or decreased vagal tone, which may predispose to ventricular fibrillation.

Decreased heart rate variability and its association with increased mortality after acute myocardial infarction

A consistent link appears to exist between predominance of vagal or sympathetic activity and predominance of HF or LF oscillations, respectively: RR variability contains both of these rhythms, and their relative powers appear to subserve a reciprocal relation like that commonly found in sympathovagal balance. In this respect, it is our opinion that rhythms and neural components always interact, just like flexor and extensor tones or excitatory and inhibitory cardiovascular reflexes, and that it is misleading to separately consider vagal and sympathetic modulations of heart rate. In humans and experimental animals, functional states likely to be accompanied by an increased sympathetic activity are characterized by a shift of the LF-HF balance in favor of the LF component; the opposite occurs during presumed increases in vagal activity. In addition, LF oscillation evaluated from SAP variability appears to be a convenient marker of the sympathetic modulation of vasomotor activity. Although based on indirect markers, the exploration in the frequency domain of cardiovascular neural regulation might disclose a unitary vision hard to reach through the assemblage of more specific but fragmented pieces of information.

Cardiovascular neural regulation explored in the frequency domain.

Background The early hours of the morning after awakening are associated with an increased frequency of events such as myocardial infarction and ischemic stroke. The triggering mechanisms for these events are not clear. We investigated whether autonomic changes occurring during sleep, particularly rapid-eye-movement (REM) sleep, contribute to the initiation of such events. Methods We measured blood pressure, heart rate, and sympathetic-nerve activity (using microneurography, which provides direct measurements of efferent sympathetic-nerve activity related to muscle blood vessels) in eight normal subjects while they were awake and while in the five stages of sleep. Results The mean (±SE) amplitude of bursts of sympathetic-nerve activity and levels of blood pressure and heart rate declined significantly (P<0.001), from 100 ±9 percent, 90 ±4 mm Hg, and 64 ±2 beats per minute, respectively, during wakefulness to 41 ±9 percent, 80 ±4 mm Hg, and 59 ±2 beats per minute, respectively, during stage 4 of non-REM sl...

https://www.nejm.org/doi/pdf/10.1056/NEJM199302043280502

Sympathetic-Nerve Activity during Sleep in Normal Subjects

The purpose of this study was to relate baroreflex sensitivity to age and arterial pressure in 61 male and 20 female untreated subjects, aged 19-66 years, whose mean arterial pressures ranged from 70 to 150 mm Hg. In this selected group of subjects there was no correlation between age and arterial pressure. The index of sensitivity used was the increase in pulse interval which occurs reflexly in response to a rise in systolic pressure induced by the intravenous injection of phenylephrine and is measured as the increase in pulse interval in milliseconds per mm Hg rise in systolic blood pressure. It ranged from 1.9 to 48.9 msec/mm Hg. Increasing age and arterial pressure act independently to reduce baroreflex sensitivity. Eight subjects who had normal blood pressure at the time of testing but whose pressure had been elevated in the past, had reflex sensitivities significantly less than expected in persons of the same age and mean arterial pressure. The heart rate in these subjects was not significantly different from that in the controls; the heart rate of the 12 hypertensive subjects aged under 40 years was significantly faster than that of age-matched normotensive subjects but not that of older hypertensive subjects.

Effect of age and high blood pressure on baroreflex sensitivity in man.

Background Despite the clinical importance of atrial fibrillation (AF), the development of chronic nonvalvular AF models has been difficult. Animal models of sustained AF have been developed primarily in the short-term setting. Recently, models of chronic ventricular myopathy and fibrillation have been developed after several weeks of continuous rapid ventricular pacing. We hypothesized that chronic rapid atrial pacing would lead to atrial myopathy, yielding a reproducible model of sustained AF. Methods and Results Twenty-two halothane-anesthetized mongrel dogs underwent insertion of a transvenous lead at the right atrial appendage that was continuously paced at 400 beats per minute for 6 weeks. Two-dimensional echocardiography was performed in 11 dogs to assess the effects of rapid atrial pacing on atrial size. Atrial vulnerability was defined as the ability to induce sustained repetitive atrial responses during programmed electrical stimulation and was assessed by extrastimulus and burst-pacing techniqu...

Chronic Rapid Atrial Pacing Structural, Functional, and Electrophysiological Characteristics of a New Model of Sustained Atrial Fibrillation

The control of arterial pressure during sleep was studied in 13 untreated, unsedated subjects aged 20 to 46, including 7 with hypertension. Arterial pressure was measured directly. A transient rise of arterial pressure up to 30 mm Hg was produced by the sudden intravenous injection of 0.25 to 2 µg of angiotensin. Linear plots were obtained in 10 of 13 subjects when the systolic pressures of successive pulses during the pressure rise were plotted against the pulse intervals which began the next beat. The relationship was disturbed by movement or arousal, and was better when pulse intervals falling in inspiration were discarded. The slope of the line (milliseconds of cardiac slowing per millimeter rise in systolic pressure) in the awake subject ranged from 2 to 15.5 msec/mm Hg, and from 4.5 to 28.9 during sleep. Reflex sensitivity was highest in dreaming sleep. In 7 of 10 subjects, baroreflex sensitivity increased significantly during sleep; in 6, the prevailing arterial pressure was inversely correlated wi...

Reflex Regulation of Arterial Pressure during Sleep in Man: A Quantitative Method of Assessing Baroreflex Sensitivity

Sudden intravenous injections of small amounts of angiotensin or phenylephrine were given to 30 subjects to produce modest, brief increases in directly measured systemic arterial pressure. A plot of each systolic pressure against the second succeeding cardiac cycle length produced a linear distribution, the slope of which was expressed as the millisecond increase in cycle length per mm Hg rise in systolic pressure. The slope is an index of baroreflex sensitivity and was found to have an average value of 12.8 in 18 subjects without hypertension and 2.8 in 12 others with hypertension. When all results were pooled, there was an inverse relationship between the resting mean arterial pressure and slope of the baroreflex regression lines. The findings demonstrate reduced sensitivity of the baroreflexes in hypertension, with respect to control of heart rate. A distinction is made between this change in sensitivity and simple resetting of the reflex.

Diminished Baroreflex Sensitivity in High Blood Pressure

Excerpt An investigation was made of the fall in blood pressure that occurs during a night's sleep. The stage of sleep was identified from the electroencephalogram (five channels), the electrooculo...

Harley S. Smyth

Papers

Reflex Regulation of Arterial Pressure during Sleep in Man: A Quantitative Method of Assessing Baroreflex Sensitivity

Diminished Baroreflex Sensitivity in High Blood Pressure

A Quantitative Assessment of Baroreceptor Reflex Sensitivity in Man, Awake and Asleep.