Original Article
Evidence of a Selective Increase in Cardiac Sympathetic Activity in Patients with Sustained Ventricular Arrhythmias
N Engl J Med 1991; 325:618-624August 29, 1991
- Abstract
- Abstract
Background.
Although enhanced efferent cardiac sympathetic nervous activity has been proposed as an important factor in the genesis of ventricular arrhythmias and sudden cardiac death, direct clinical evidence has been lacking.
Methods.
We measured the rates of total and cardiac norepinephrine spillover into the plasma, which reflect, respectively, overall and cardiac sympathetic nervous activity, in 12 patients who had recovered from a spontaneous, sustained episode of ventricular tachycardia or ventricular fibrillation outside the hospital 4 to 48 days earlier. The results were compared with those from three age-matched reference groups without a history of ventricular arrhythmias: 12 patients with coronary artery disease, 6 patients with chest pain but normal coronary arteries, and 12 healthy, normal subjects.
Results.
The patients who had had ventricular arrhythmias had reduced left ventricular ejection fractions, as compared with the patients with coronary artery disease or chest pain (mean [±SE], 46±3 percent vs. 58±4 percent and 69±5 percent, respectively; P<0.003). The rates of total norepinephrine spillover into the plasma were similar in the three reference groups, but 80 percent higher in the patients with ventricular arrhythmias (P<0.005). The rate of cardiac norepinephrine spillover was 450 percent higher in these patients (17±39 pmol per minute, as compared with 32±8 pmol per minute in the normal subjects; P<0.001), a disproportionate increase relative to the increase in total spillover, which indicated selective activation of the cardiac sympathetic outflow. This increase in cardiac norepinephrine spillover was probably caused by a reduction in left ventricular function.
Conclusions.
These results suggest that in some patients major ventricular arrhythmias are associated with and perhaps caused by sustained and selective cardiac sympathetic activation. We speculate that depressed ventricular function was present before the ventricular arrhythmia occurred, and that this resulted In reflex cardiac sympathetic activation, which in turn contributed to the genesis of the arrhythmia. (N Engl J Med 1991; 325:618–24.)
Media in This Article
Figure 1
Norepinephrine Concentration In Arterial Plasma (Upper Panel) and Rate of Total Norepinephrine Spillover (Lower Panel) in the Three Reference Groups (Solid Circles) and the Patients with Ventricular Arrhythmias (Open Circles). Bars indicate mean values.Figure 2
Rates of Cardiac Norepinephrine Spillover into the Plasma in the Three Reference Groups (Solid Circles) and the Patients with Ventricular Arrhythmias (Open Circles). Bars indicate mean values.Article Activity
- Article
SUDDEN cardiac death due to a ventricular tachyarrhythmia is a major component of cardiovascular mortality. The immediate precipitants are unknown, but it is clear that the majority of patients have underlying organic heart disease, most often coronary artery disease1 , 2 and poor left ventricular function.3 4 5 Patients with left ventricular impairment and ischemic heart disease have a high prevalence of ventricular arrhythmias on ambulatory electrocardiographic monitoring and also have a high incidence of sudden cardiac death.5 , 6 Although associations between ventricular arrhythmias, impaired left ventricular function, and sudden death are well established, the precise mechanisms involved are unclear.
The level of cardiac sympathetic activity is an obvious link between impaired left ventricular function and ventricular electrical instability. A relation between sympathetic activation and ventricular arrhythmias has been proposed, largely on the basis of an extensive body of experimental evidence.7 8 9 Direct stimulation of the cardiac sympathetic nerves has been shown to reduce the threshold of ventricular fibrillation in dogs10 and to precipitate ventricular fibrillation in the presence of myocardial ischemia.11 The evidence that cardiac sympathetic activation has an important role in humans is more circumstantial. The favorable effect of β-adrenergic blockers on ventricular arrhythmias12 and the rate of mortality13 , 14 after myocardial infarction and the predictive value of the plasma concentration of norepinephrine for overall mortality in congestive heart failure15 point to the possible clinical importance of the sympathetic nervous system in arrhythmogenesis and sudden cardiac death.
Plasma norepinephrine, however, is an inadequate guide to either overall or cardiac sympathetic activity, for two reasons. First, the plasma level depends not only on the rate of release of norepinephrine but also on the rate of clearance from the plasma pool. In patients with heart failure, for example, approximately 50 percent of the observed increase in the plasma concentration of norepinephrine is due to reduced clearance.16 , 17 Second, the cardiac contribution to the total plasma pool of norepinephrine is comparatively small (approximately 2 to 3 percent),18 and substantial changes in the rate of cardiac norepinephrine release may not be detected if only the plasma concentration is measured.
Our aim in this study was to quantify cardiac sympathetic nervous activity in patients who were at high risk for recurrent major ventricular arrhythmias and sudden death, using the radiotracer kinetic techniques previously developed by our laboratory.18 8,19 The patients were selected because they had recently had a sustained, life-threatening arrhythmia (ventricular tachycardia or fibrillation) not precipitated by acute myocardial infarction. Sympathetic nervous system function in these patients was compared with that in reference populations (patients with coronary artery disease or atypical chest pain and normal subjects) without a history of ventricular arrhythmias. Our hypothesis was that spontaneous, life-threatening ventricular arrhythmias may be associated with and are possibly precipitated by a sustained high level of efferent cardiac sympathetic nervous activity.
Methods
Study Population
In 12 patients who had had spontaneous and sustained life-threatening ventricular arrhythmias outside the hospital 4 to 48 days earlier (mean, 13), we measured total and cardiac norepinephrine spillover into the plasma immediately before a diagnostic electrophysiologic study. Data on this group with ventricular arrhythmias were compared with data on 18 patients undergoing routine diagnostic coronary angiography (12 with angina [the group with coronary artery disease] and 6 with atypical chest pain [the group with chest pain]) and 12 normal, healthy, age-matched volunteers recruited by advertisement. The clinical characteristics of the study subjects are shown in Table 1.Table 1
Clinical Characteristics of the Four Study Groups. None of the subjects in the three reference groups had had a sustained or symptomatic episode of ventricular tachycardia or had previously required cardiopulmonary resuscitation or direct-current cardioversion.The group with ventricular arrhythmias consisted of three patients who had had documented ventricular fibrillation requiring cardiopulmonary resuscitation and direct-current cardioversion and nine who had had ventricular tachycardia, of whom five required cardiopulmonary resuscitation and cardioversion and four were initially treated with intravenous lidocaine. In all the patients with ventricular tachycardia the arrhythmia was documented (by 12-lead electrocardiography in four and at least single-lead electrocardiography in the remaining five). Because the events occurred outside the hospital, the duration of the arrhythmias could only be estimated, on the basis of the report of the ambulance attendant and other records. The duration ranged from 5 to 30 minutes.
The arrhythmias occurred in seven patients while at home, three while at work, one while cycling, and one while resting on the beach. Four patients had a history of ventricular arrhythmias. They and the eight remaining patients in the arrhythmia group had abnormal electrocardiograms at rest. Despite a history of myocardial infarction in nine patients, there was no evidence of acute myocardial infarction in the clinical history, repeated electrocardiography, or enzyme measurements either at the time of or after the presenting arrhythmia. None of the patients were receiving antiarrhythmic drugs at the time of the arrhythmia.
All of the study subjects gave written informed consent, and the study was approved by the Alfred Hospital Ethics Review Committee.
Protocol
Before total and cardiac norepinephrine spillover into the plasma was measured, α- and β-adrenergic blockers, antiarrhythmic agents of all classes, antianginal medications including long-acting nitrates and calcium antagonists, angiotensin-converting—enzyme inhibitors, and diuretic agents were discontinued for at least 24 hours. None of the patients had received central anti-adrenergic agents in the previous four weeks. Tea, coffee, cigarettes, and alcohol were withheld for a minimum of 12 hours before the study. All the patients in the group with ventricular arrhythmias had fully recovered from their arrhythmias and were hemodynamically stable and able to walk at the time of the study.
In the patients, total and cardiac sympathetic nervous activity was assessed during a period of supine rest after the insertion of arterial and venous catheters and before the diagnostic phase of the procedure (programmed electrical stimulation in the 12 patients with ventricular arrhythmias and coronary angiography in the 18 patients with coronary artery disease or chest pain); in the normal subjects it was assessed during a separate research study. Cardiac sympathetic nervous activity was also measured after the programmed electrical stimulation in the patients with ventricular arrhythmias.
Total and Cardiac Norepinephrine Spillover into the Plasma
We measured the spillover into the plasma of norepinephrine from the heart and the body as a whole to estimate the cardiac and overall sympathetic nervous activity (integrated firing rate), on the basis of the relation between the rate of sympathetic-nerve firing in an organ and the overflow of norepinephrine into its venous drainage.20 21 22
At steady state during peripheral intravenous infusion of a tracer dose of tritiated norepinephrine (0.7 μCi of levo-[7–3H] norepinephrine per minute; specific activity, 12 to 20 Ci per millimole; New England Nuclear, Boston), total norepinephrine spillover into the plasma and total plasma norepinephrine clearance were calculated19 according to the following equations: total norepinephrine spillover equals the rate of infusion of tritiated norepinephrine (expressed as disintegrations per minute) per minute divided by the specific activity of plasma norepinephrine in disintegrations per minute per picogram; and total norepinephrine clearance equals the rate of infusion of tritiated norepinephrine (expressed as disintegrations per minute) per minute divided by the plasma concentration of tritiated norepinephrine in disintegrations per minute per milliliter.
The rate of norepinephrine spillover from the heart was calculated according to the Fick principle, corrected for the fractional extraction of tritiated norepinephrine across the heart16 , 18 , 23. cardiac norepinephrine spillover equals the plasma norepinephrine concentration in the coronary sinus minus the arterial plasma norepinephrine concentration, added to the arterial plasma concentration times the fractional extraction of tritiated norepinephrine in a single passage through the heart, and the result multiplied by the coronarysinus plasma flow in milliliters per minute.
Arterial and coronary-sinus sampling was performed according to our previously published methods.16 A 7-French coronarysinus thermodilution catheter (type CCS-7U–90B, Webster Laboratories, Baldwin Park, Calif.) was introduced into the coronary sinus through an antecubital venous sheath. Coronary-sinus plasma flow was derived from thermodilution-determined blood flow and the hematocrit.24
Catecholamine Assays
Samples of coronary-sinus and arterial blood were transferred immediately to ice-chilled tubes containing reduced glutathione (5 ml of blood for estimation of endogenous norepinephrine) or lithium heparin (10 ml for estimation of tritiated norepinephrine). The samples were then centrifuged at 4°C, and the plasma was separated for storage at —70°C until assayed. The plasma concentration of endogenous norepinephrine was measured by the method of Peuler and Johnson25 and the concentration of tritiated norepinephrine by liquid scintillation counting after extraction with alumina, as previously described.19
Left Ventricular Volume and Ejection Fraction
Left ventricular dimensions were determined by planimetry from single-plane left ventriculograms in the right anterior oblique projection during routine catheterization of the left ventricle. The left ventricular volume and ejection fraction were measured with a computerized image-analysis system (Cardio-500, Kontron Bildanalyse, Munich, Germany).
Statistical Analysis
The data are expressed as means±SE. The data were found to be compatible with a normal distribution. Statistical significance was assessed by one-way analysis of variance. Multiple comparisons between groups were performed with Scheffé's test.26 To test whether the observed increase in cardiac norepinephrine spillover in the group with ventricular arrhythmias was a function of the left ventricular ejection fraction, we performed an analysis of covariance. The null hypothesis was rejected if P<0.05.
Results
There were no significant differences in age, sex, weight, heart rate at rest, or blood pressure among the groups (Tables 1 and 2Table 2
Hemodynamic Characteristics and Left Ventricular Function.), although patients in the group with ventricular arrhythmias had reduced left ventricular ejection fractions (46±3 percent, as compared with 58±4 percent and 69±5 percent in the groups with coronary artery disease and chest pain, respectively; P<0.003). The left-ventricular end-diastolic—volume index was significantly greater in the groups with ventricular arrhythmias and coronary artery disease than in the group with chest pain, whereas the end-systolic—volume index was increased only in the group with ventricular arrhythmias (P<0.003) (Table 2). Three patients in the group with ventricular arrhythmias and two in the group with coronary artery disease were in New York Heart Association functional class III.The concentration of norepinephrine in arterial plasma was similar in the normal subjects and the patients with chest pain or coronary artery disease (1195±141, 958±206, and 1293±126 pmol per liter, respectively), but it was 69 percent higher on average in the group with ventricular arrhythmias (2031±320 pmol per liter, P<0.01) (Fig. 1Figure 1
Norepinephrine Concentration In Arterial Plasma (Upper Panel) and Rate of Total Norepinephrine Spillover (Lower Panel) in the Three Reference Groups (Solid Circles) and the Patients with Ventricular Arrhythmias (Open Circles). Bars indicate mean values. and Table 3Table 3
Plasma Kinetics of Cardiac Norepinephrine.). Levels of epinephrine in arterial plasma were similar in the four groups (453±60 pmol per liter in the normal subjects, 425±76 pmol per liter in the patients with chest pain, 377±38 pmol per liter in those with coronary artery disease, and 409±76 pmol per liter in those with ventricular arrhythmias). The rate of total norepinephrine spillover into the circulation was elevated by 80 percent in the group with ventricular arrhythmias as compared with the normal group (P<0.005) (Fig. 1). Multiple-comparison testing revealed that only data on the group with ventricular arrhythmias differed significantly from data on the other groups (P<0.005). Total norepinephrine clearance did not differ among the four groups (1.73±0.12, 1.75±0.14, 1.60±0.15, and 1.95±0.21 liters per minute, respectively), which explained the nearly parallel increases in arterial-plasma norepinephrine concentration and norepinephrine release to the circulation in the patients with ventricular arrhythmias.Cardiac norepinephrine spillover at rest was similar in the normal subjects and the patients with chest pain or coronary artery disease, but it was markedly elevated in the patients with ventricular arrhythmias, by an average of 450 percent (176±39 pmol per minute, as compared with 32±8 pmol per minute in the normal subjects; P<0.001) (Fig. 2Figure 2
Rates of Cardiac Norepinephrine Spillover into the Plasma in the Three Reference Groups (Solid Circles) and the Patients with Ventricular Arrhythmias (Open Circles). Bars indicate mean values. and Table 3). Cardiac norepinephrine spillover was elevated disproportionately more than total norepinephrine spillover, providing evidence of selective activation of the sympathetic nerves to the heart. The increase in cardiac norepinephrine spillover in the patients with ventricular arrhythmias was independent of changes in coronarysinus plasma flow and neuronal reuptake of norepinephrine, as measured by the fractional extraction of tritiated norepinephrine by the heart (Table 3). There was no relation between the level of total or cardiac norepinephrine spillover and the time elapsed since the ventricular arrhythmia.Programmed ventricular stimulation of the right ventricular apex and outflow tract at a basic cycle length of 600 msec, with up to three premature impulses (EP-2 Clinical Stimulator, Digital Cardiovascular Instruments, San Jose, Calif), induced ventricular tachycardia in 8 of the 12 patients in the group with ventricular arrhythmias (sustained in 6 of them). The mean cardiac norepinephrine spillover at rest in this subgroup was 206±65 pmol per minute. For 10 of the 12 patients, measurements of total and cardiac norepinephrine spillover were repeated 10 minutes after the conclusion of the electrophysiologic study. Neither total nor cardiac sympathetic activation was significantly influenced by the procedure (levels before and after testing, 3688±573 vs. 3534±650 pmol per minute and 189±47 vs. 210±76 pmol per minute, respectively).
To examine the relation between left ventricular function and cardiac norepinephrine spillover over a broader range of left ventricular function, we pooled data from this study with data from patients previously studied in our laboratory, including data on cardiac norepinephrine spillover from 12 patients with symptoms and signs of severe congestive heart failure and left ventricular ejection fractions significantly lower than in the group with ventricular arrhythmias.16 We found a significant exponential inverse relation between cardiac norepinephrine spillover and left ventricular ejection fraction that accounted for 63 percent of the observed variance in the data (the log of the cardiac norepinephrine spillover equaled 2.763 minus 0.019 times the ejection fraction; r = 0.79, SE = 0.32, P<0.0001) (Fig. 3Figure 3
Cardiac Norepinephrine Spillover, Plotted as a Function of the Left Ventricular Ejection Fraction, Measured from a Single-Plane Left Ventriculogram in the Right Anterior Oblique Projection during Routine Left Ventricular Catheterization.), suggesting that the higher levels of cardiac norepinephrine spillover observed in the patients with ventricular arrhythmia may have been due to impairment of left ventricular function.Analysis of covariance was performed to assess the influence of left ventricular impairment on cardiac norepinephrine spillover. With the historical heart-failure group included, left ventricular ejection fraction was the main determinant of the higher levels of cardiac norepinephrine spillover observed in the group with ventricular arrhythmias. As shown in the inset in Figure 3, however, 3 of the 12 patients in the group with ventricular arrhythmias had levels of cardiac norepinephrine spillover above the upper 95 percent confidence limit for their left ventricular ejection fractions.
Discussion
This study provides evidence of marked sustained activation of the sympathetic nervous system, specifically to the heart, in patients who have recovered from a life-threatening ventricular arrhythmia. In such patients we observed a nearly fivefold increase in cardiac norepinephrine spillover into the plasma, as compared with levels in normal, healthy, age-matched subjects at rest or in patients with chest pain undergoing diagnostic cardiac catheterization. The increase in cardiac norepinephrine spillover in the patients with ventricular arrhythmias was due to an increase in norepinephrine release and therefore in cardiac sympathetic nervous activation. Other possible causes of higher norepinephrine overflow, such as a flow-dependent increase in norepinephrine washout27 , 28 or faulty neuronal reuptake of norepinephrine,29 were excluded, since neither coronary-sinus plasma flow nor the cardiac extraction of tritiated norepinephrine, which is dictated by neuronal uptake,30 differed significantly between the group with ventricular arrhythmias and the other three groups.
The extent and selectivity of cardiac sympathetic activation observed in the patients with ventricular arrhythmias were not apparent from the global measures of sympathetic nervous activity, concentration of norepinephrine in arterial plasma, or rate of total norepinephrine spillover. Values for these variables overlapped substantially with the corresponding values in the reference groups. The reasons for this are two. First, the heart contributes only a small percentage of the total norepinephrine released into the plasma, so that even substantial increases in cardiac norepinephrine release can easily remain undetected by measurements of norepinephrine in arterial plasma.28 Second, the sympathetic nervous system is organized into regional outflows, with each outflow capable of different responses to a variety of physiologic and pathophysiologic stimuli.28 Global measures of sympathetic activity do not identify the sources of norepinephrine release and cannot delineate the regional patterns of sympathetic nervous activation.
It is unlikely that the extent of cardiac sympathetic activation observed in our patients who had had ventricular arrhythmias was simply a consequence of those arrhythmias. The electrophysiologic study and the measurements of sympathetic activity occurred on average 13 days after the episodes of arrhythmia. Levels of norepinephrine spillover in the patients studied soonest after the arrhythmia did not differ from the levels in patients studied up to 48 days later. Moreover, it seems improbable that the selective cardiac sympathetic activation in the group with ventricular arrhythmias could be explained by any greater anticipatory anxiety associated with an electrophysiologic study than with coronary angiography. The plasma epinephrine concentration (an indicator of adrenal medullary activation by stress)31 was not significantly different in the group undergoing the electrophysiologic study.
An important issue is whether the increase in cardiac sympathetic activity in the patients with ventricular arrhythmias was attributable to reflex sympathetic stimulation in the setting of impaired left ventricular function. The relation between sympathetic activation and cardiac performance is complex and not well understood. Some investigators have found a significant inverse correlation between plasma norepinephrine concentration and left ventricular function,32 , 33 whereas others have not.34 Leimbach et al.33 found no correlation between the left ventricular ejection fraction and the level of muscle sympathetic nervous activity recorded in the peroneal nerve in patients with heart failure. Using cardiac norepinephrine spillover, a more direct measure of cardiac sympathetic nervous activity, we found an exponential inverse relation between cardiac sympathetic activation and the left ventricular ejection fraction. This relation is important because it indicates that the higher levels of cardiac norepinephrine spillover observed in our patients with ventricular arrhythmias were explained mostly by reduced left ventricular function. We were not able to measure the left ventricular ejection fraction in our patients before the episodes of ventricular arrhythmia. The measurements were made after the life-threatening arrhythmia, and it is possible that the arrhythmia itself contributed to the depression of ventricular function. We speculate, however, that depressed ventricular function present before the arrhythmia resulted in reflex cardiac sympathetic activation, which then contributed to the genesis of the arrhythmia.
Sympathetic overactivity has previously been implicated in lethal ventricular arrhythmia and sudden death. To date, the most persuasive evidence supporting the pathophysiologic role of sympathetic activation in the genesis of ventricular arrhythmias has come from studies examining the effects of direct stimulation or denervation of the cardiac sympathetic nerves and ganglia and the protective influence of pharmacologic blockade of receptors. β-Adrenergic blockers have been shown to reduce the vulnerability of the myocardium to ventricular arrhythmias during acute ischemia35 and to reduce ventricular ectopy,12 reinfarction, and mortality after myocardial infarction. 13 , 14 , 36 Potential benefit has also been suggested with respect to sudden and nonsudden death in patients with ventricular tachyarrhythmias in the setting of left ventricular dysfunction37 and with respect to survival in patients with congestive cardiac failure.38
These findings suggest a role for cardiac sympathetic activation in ventricular arrhythmias that occur outside the hospital. Although such activation is unlikely to be the sole determinant of major ventricular arrhythmias, it may increase the propensity of other triggering events to result in symptomatic, life-threatening ventricular arrhythmias. Whether measurements of cardiac sympathetic nervous activity such as those employed in the present study will be of clinical use in predicting which patients are at high risk for ventricular arrhythmias remains to be determined. Improved prediction of the risk of major ventricular arrhythmias could have important therapeutic implications for the long-term care of patients with left ventricular impairment, particularly since modern drug therapy has been of little benefit in reducing the incidence of sudden death.
Supported by the National Heart Foundation of Australia and by an Institute Grant from the National Health and Medical Research Council of Australia to the Baker Medical Research Institute.
We are indebted to Gavin W. Lambert, B.S., and Elizabeth M. Dewar, B.S., for technical assistance; to Dr. Anthony M. Dart for thoughtful suggestions and assistance in the statistical analysis of the data; and to the staff of the Department of Cardiology, Alfred Hospital, for their patience and cooperation.
Source Information
From the Alfred and Baker Medical Unit, Baker Medical Research Institute, and the Department of Cardiology, Alfred Hospital, Melbourne, Australia. Address reprint requests to Dr. Meredith at the Human Autonomic Function Laboratory, Baker Medical Research Institute, Box 348, Prahran, Melbourne 3181, Australia.
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