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Hypertension. 1997;30:1279-1283

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(Hypertension. 1997;30:1279-1283.)
© 1997 American Heart Association, Inc.

Articles

Susceptibility to Pain in Hypertensive and Normotensive Patients With Coronary Artery Disease

Response to Dental Pulp Stimulation

Colomba Falcone; Carla Auguadro; Renato Sconocchia; Luigi Angoli

From the Department of Medicine, Section of Cardiology, University Hospital, Pavia, Italy.

Correspondence to Colomba Falcone, MD, Department of Medicine, Section of Cardiology, IRCCS Pol. S. Matteo, University Hospital, P.le Golgi, 1, 27100 Pavia, Italy.


*    Abstract
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 *Abstract
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Abstract An association between a decreased responsiveness to varying painful stimuli and arterial hypertension both in animals and in humans has been documented. The relationship between essential hypertension and silent myocardial ischemia in coronary artery disease (CAD) populations is not well understood. The aims of this study in CAD patients with and without essential hypertension were (1) to determine dental pain threshold and reaction to tooth pulp stimulation and (2) to ascertain whether hypertensive CAD patients differ from normotensive ones in reactivity to pain. This study involved 182 patients who were affected by mild and moderate hypertension (G1) and 174 normotensive patients (G2). The inclusion criteria were reproducible exercise-induced myocardial ischemia, CAD documented at angiography, and dental formula suitable for pulp test. All patients underwent an ergometric stress test, coronary angiography, and pulp test. Our CAD hypertensive patients showed a lower prevalence of angina during daily life (64.8% in G1 versus 81.6% in G2, P<.05) and a higher incidence of exercise-induced silent myocardial ischemia (60.4% in G1 versus 48.8% in G2, P<.05) than the normotensive group. The mean anginal pain intensity, which was suffered both during spontaneous transitory episodes of ischemia and/or during acute myocardial infarction, was significantly lower in G1 than in G2 patients (P<.05). During pulp test, 31.8% of G1 and 13.7% of G2 referred no symptoms, even at the highest current intensity of 500 mA. The hypertensive patients with symptoms during pulp test had a higher mean dental pain threshold and lower mean threshold reaction and maximal reaction than did the normotensive symptomatic ones. In patients of both groups, a positive correlation between the mean maximal reaction during pulp test and the prevalence of angina during daily life was also found. In conclusion, patients with CAD and essential hypertension differ from normotensive CAD patients in reactivity to pain. Significantly higher pain thresholds and lower reactions to tooth pulp stimulation characterized patients with increased blood pressure values.


Key Words: myocardial ischemia • dental pulp test • coronary artery disease


*    Introduction
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 *Introduction
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The literature reports a generalized hyposensitivity to pain in patients without symptoms during myocardial ischemia.1 2 3 4 5 A variety of stimulating techniques has demonstrated a higher pain threshold in these subjects, and this finding suggests that the lack of symptoms may partially be explained by individual differences in pain threshold.6 7 8 9 10 11 A reduced pain perception has also been documented in hypertension during various experimental methods of pain induction.12 13 14 15 Electrical dental pulp stimulation (pulp test, PT) has been used to test pain threshold in humans.8 11 16 Dental pain provoked by electrical stimuli is short in duration and does not result in permanent tissue damage; because the test current increases progressively, the PT allows quantification of pain threshold.

The aims of this study in a large population of coronary artery disease (CAD) patients with and without hypertension were to (1) determine dental pain threshold and reaction to tooth pulp stimulation (PT) and (2) ascertain whether hypertensive CAD patients differ from normotensive ones in reactivity to pain.


*    Methods
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 *Methods
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Patient Selection
The study involved 182 patients affected by essential hypertension (from mild to moderate hypertension) and 174 normotensive patients, all of whom were referred to our laboratory to perform an ergometric stress test because of definite or possible ischemic heart disease. The criteria for inclusion in this study were reproducible exercise-induced myocardial ischemia, CAD documented by angiography, and dental formula suitable for PT, as documented by a dental check-up.

All the patients were questioned about both their family history of hypertension and cardiovascular disease and their smoking habits. The study excluded patients with blood pressure values >=200/120 mm Hg at rest, secondary forms of hypertension, history of stroke, severe valvular disease, congestive heart failure, diabetes mellitus, peripheral neuropathy, unstable angina, or clinical conditions that did not permit temporary withdrawal of therapy. Female patients were also excluded from the study.

In basal conditions, three measurements of blood pressure were taken with a standard sphygmomanometer with the patient in the supine position; a standard 12-lead electrocardiogram (ECG) was also recorded. All tests were performed in pharmacological washout: calcium channel blocking agents and nitrates were suspended 48 hours before. No patient was receiving therapy with ß-adrenergic blocking agents at the time of the study. The ß-blockers had been gradually reduced and stopped 1 week before our examination. No patient received digitalis. Informed written consent for all tests was obtained from all subjects. The present study was approved by the ethics committee of our hospital.

Pulp Test
For PT, which was performed immediately before the ergometric stress test, all patients were at rest and in comfortable conditions. The patients were examined with an electrical tooth pulp stimulator, which is commonly used in dentistry to assess pulp vitality. On the morning of the PT, all patients underwent a prior dental checkup to exclude tooth fractures, abrasions, caries, fillings, or significant periodontal disease. As described previously, the pulp tester used for this study (Digilog Demetron Research Corp) was designed to deliver a current impulse of increasing intensity from 10 to 500 mA; a scale of 0 to 9 was displayed on the instrument to indicate the intensity of the stimuli.8 The stimulator was applied on at least two healthy upper incisors and on one inferior incisor through a metal cylinder that was placed on the enamel surface; an electrode paste was applied to the cylinder for improved contact, and the circuit was closed by the hand of the operator in contact with the lips of the patient. All patients had previously been instructed to indicate the commencement of dental pain by lifting a hand. Immediately after the test interruption, the patients were asked to grade the intensity of the pain they experienced on a scale of 1 to 10. Dental pain threshold was defined as the minimal current intensity level that elicited any pulp sensation (10 to 500 mA; on the tester, 1 to 9). All patients were applied the highest current intensity (500 mA; on the tester, 9). Threshold reaction (mean pain intensity at dental pain threshold) and maximal reaction (pain intensity at the maximal stimulation) were determined for all patients. The lack of sensation at the maximal stimulation of 500 mA was defined as reaction 0. Blood pressure values were recorded both immediately before the beginning of the test and during the tooth pulp stimulation.

Ergometric Stress Test
A multistage bicycle ergometric stress test was performed in all patients in the supine position with an initial workload of 25 W and subsequent stepwise increments of 25 W every 3 minutes at a pedaling frequency of 60 rpm. Standard 12-lead ECG and blood pressure were recorded initially in basal conditions with the patient lying in the supine position for 10 minutes and subsequently just before the test, at the end of each stage, at the appearance of ECG signs of ischemia and/or of anginal pain, at peak exercise, and every 3 minutes during recovery. Three ECG leads (D3,V5V6) were monitored continuously and displayed on an oscilloscope throughout the test. During the test, the patients were continuously asked about the appearance of angina or other symptoms. A positive ECG response was defined as the occurrence of at least 1 mm ST depression compared with the baseline tracing. Ischemia threshold was defined as the appearance of 1 mm flat or downsloping ST-segment depression 0.08 second after J-point in comparison with baseline ECG; angina threshold was defined as the time of the first appearance of chest pain during the test. Exercise test was interrupted at the occurrence of any of the following conditions: moderate to severe angina, dyspnea, exhaustion, ST-segment depression >3 mm, and major arrhythmias. The double product (heart ratexsystolic blood pressure) was calculated in basal conditions, at the ischemia and angina threshold, and at peak exercise.

Pain Assessment
In the patients who experienced the occurrence of chest pain during the ergometric stress test, the intensity of the anginal pain was graded on a scale of 1 to 10. The patients were also asked to retrospectively grade, on the same scale, the anginal pain intensity which they had experienced previously during acute myocardial infarction and/or during spontaneous episodes of angina pectoris occurring in daily life.

Angiography Study
All patients underwent cardiac ventriculography and Sones selective coronary arteriography not more than 1 month before or subsequent to the ergometric stress test. Left ventriculography was performed before coronary arteriography in the 30° right anterior oblique projection; ventricular volumes and left ejection fraction were calculated by the standard area-length method. Multiple views of each coronary artery were filmed: significant coronary artery disease was defined as the presence of >=50% stenosis in a major coronary vessel.

Statistical Analysis
The characteristics of the two groups are reported as mean±SD. The differences between the means were evaluated by Student's t test for variables normally distributed. Statistical evaluation was made by variance and regression analysis, both of which used computerized SPSS (Statistical Package for the Social Sciences). The Mann-Whitney test was used for two independent nonparametric samples. A value of P<.05 was considered to be statistically significant.


*    Results
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 *Results
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Patients were classified into two groups on the basis of the presence or absence of arterial hypertension, as recorded in the given case history and as confirmed by the measurements performed before exercise stress testing. Group 1 (G1) consisted of 182 hypertensive male patients and group 2 (G2) of 174 normotensive male patients.

Clinical Features
History of angina was present in 118 patients (64.8%) of G1 (29 on effort, 9 at rest, 7 unstable, and 73 mixed) and in 142 patients (81.6%) of G2 (48 on effort, 15 at rest, 9 unstable, and 70 mixed) (Table 1Down). The mean anginal pain intensity, which was suffered during spontaneous episodes of angina occurring in daily life, was lower in G1 than in G2 patients (P<.05). Of patients without anginal symptoms during daily life, 24 of G1 and 13 of G2 referred experienced dyspnea, 3 of G1 and 1 of G2 had a history of syncope, 15 of G1 and 8 of G2 showed silent myocardial ischemia during a routine physical examination, and 22 of G1 and 10 of G2 showed ECG signs of effort ischemia in postmyocardial infarction evaluation. The prevalence of a previous myocardial infarction was similar in patients of both groups, whereas the mean pain intensity during acute myocardial infarction, as retrospectively graded by the single patients, was significantly lower in the hypertensive patients than in the normotensive ones (P<.05). A significantly higher prevalence of painless myocardial infarction was observed in the hypertensive patients (P<.05).


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  		Table 1. Clinical Features of 356 Male CAD Patients With and Without Essential Hypertension

Exercise Stress Test
The exercise stress test was positive for myocardial ischemia in all patients, as inclusion criterion. Silent myocardial ischemia was observed in 110 patients (60.4%) of G1 and in 85 (48.8%) of G2 (P<.05). The characteristics of the two groups are reported in Table 2Down. The double products, both in basal conditions and at peak exercise, were higher in the hypertensive than in the normotensive patients. The double products both at the ischemia threshold and pain threshold were similar between the two groups. ST-segment depression was also similar in both groups of patients.


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  		Table 2. Ergometric Characteristics of Hypertensive and Normotensive Patients

Pulp Test
During PT, 58 patients (31.8%) of G1 and 24 (13.7%) of G2 experienced no pain, even at the highest current intensity (threshold 0, P<.01). The 124 hypertensive patients who felt dental pain during PT had a higher mean dental pain threshold, a lower mean threshold reaction, and a lower mean maximal reaction (6.6±2.3, 3.8±1.5, and 4.5±1.6, respectively) than did the normotensive symptomatic ones (5.2±4.8, Mann-Whitney 0.0018; 4.7±3.1, Mann-Whitney 0.0002; and 6.6±1.9, Mann-Whitney 0.0000, respectively) (Fig 1Down).



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  		Figure 1. PT response in hypertensive and normotensive patients. Hypertensive patients who experienced symptoms during tooth pulp stimulation had a higher mean dental pain threshold and a lower mean threshold reaction and maximal reaction than did the normotensive symptomatic patients. Bars, SD.

Both in hypertensive and in normotensive patients, a statistical correlation was found between the mean maximal reaction during PT and the prevalence of symptoms during daily life (P=.031 and P=.028, respectively). The higher the dental pain intensity was at the maximal tooth pulp stimulation, the higher was the prevalence of angina during daily life.

In hypertensive patients, mean basal diastolic blood pressure was significantly correlated with mean dental pain threshold, with mean threshold reaction, and with mean maximal reaction (P=.048, P=.005, and P=.005 respectively), whereas the mean basal systolic blood pressure was not. No significant variations in blood pressure values were observed during tooth pulp stimulation in comparison with the baseline values.

Coronary Arteriography
The extent of CAD did not differ statistically between the two groups of patients (Table 3Down). Left ventricular end-diastolic volume and left ventricular end-diastolic pressure were higher in the hypertensive patients than in the normotensive ones (P<.05), whereas no difference between the two groups of patients was observed in the ejection fraction.


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  		Table 3. Hemodynamic and Angiographic Findings in 356 CAD Patients


*    Discussion
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 up arrowAbstract
 up arrowIntroduction
 up arrowMethods
 up arrowResults
 *Discussion
down arrowReferences
 
Significantly higher pain thresholds and lower reactions in response to tooth pulp stimulation were documented in our hypertensive CAD patients than they were in the normotensive CAD ones. The hypertensive patients also showed a lower anginal pain perception both during transitory episodes of myocardial ischemia and/or during acute myocardial infarction than the normotensive CAD ones, confirming a generalized decreased pain perception in CAD patients who have increased arterial blood pressure values.

The literature demonstrates an association between a diminished responsiveness to painful stimuli and arterial hypertension, a finding that suggests a relationship between the central mechanisms involved in pain modulation and arterial blood pressure regulation.17 18 19 20 21 22 23 24 25 A delayed response to noxious stimuli (such as hot plate, electric shock, or mechanical force applied to a limb) has also been reported in experimentally hypertensive animals.12 15 18 20 21 22 26 27

In patients with high blood pressure, CAD may be present but clinically silent.28 29 30 The relationship between essential hypertension and silent myocardial ischemia is not fully understood. The prevalence of silent myocardial ischemia in CAD populations varies from 16% to 70%.2 3 9 31 32 33 34 In a recent work, Siegel et al35 reported a 27% prevalence of silent myocardial ischemia in hypertensive subjects who showed neither clinical nor angiographic evidence of CAD. In our hypertensive population with angiographic evidence of CAD, the incidence of exercise-induced silent myocardial ischemia was 60.4%. Patients with high arterial blood pressure showed significantly lower prevalence of anginal symptoms during daily life than did the normotensive ones. Mean anginal pain intensity, both during transitory episodes of ischemia occurring in daily life and during previous acute myocardial infarction, proved to be significantly lower in hypertensive patients than in the normotensive ones. Moreover, the prevalence of painless myocardial infarction was significantly higher in patients with hypertension. During exercise-induced myocardial ischemia, the double product at the ischemia threshold was not different between the two groups of patients: the similar severity and distribution of the CAD between patients with and without arterial hypertension may justify this finding. The greater double product at peak exercise that was observed in the hypertensive group may be related to the sudden rise in blood pressure during stress. The higher incidence of silent ischemia that was observed in the hypertensive group was not correlated with a different entity of ST-segment depression at peak of exercise.

Pulp Test Response in Hypertensive and Normotensive CAD Patients
In this study, the reactivity to dental pulp stimulation was quantified and correlated with the prevalence of symptoms during daily life in both groups of patients. In the hypertensive subjects, the use of the tooth pulp stimulation confirmed the existence of a relationship between increased arterial blood pressure and decreased pain perception.23 36 37 38 39 Also, in CAD populations, the PT showed significant differences in dental pain threshold and reaction between patients with silent myocardial ischemia and the ones with symptomatic ischemia.8 11

In the present study, the prevalence of patients who remained asymptomatic during PT, even at the maximum tooth pulp stimulation of 500 mA, was significantly higher in the hypertensive than in the normotensive group. When they were symptomatic, the hypertensive patients had a higher mean dental pain threshold and a lower mean threshold reaction and maximal reaction than the normotensive symptomatic subjects. In this population, a positive correlation between the prevalence of angina during daily life and the maximal reaction to tooth pulp stimulation was found both in the hypertensive and in the normotensive groups.

Although several hypotheses about the phenomenon of hypertension-associated hypalgesia have been proposed, the underlying causes of this decreased responsiveness to noxious stimuli in hypertensive subjects remain to be fully identified. Several anatomic, physiological, and pharmacological findings support the hypothesis of a relationship between the various central mechanisms that are involved in pain modulation and in arterial blood pressure regulation; various studies have described an association, or at least a partial overlap, between the brain circuits involved in the control of blood pressure and pain perception.21 23 40 41 42 43 Several investigators have reported an involvement of the baroreceptor reflex arc in the phenomenon of hypertension-related analgesia: carotid sinus baroreceptor denervation in rats was found to abolish the hypalgesic behavior associated with an acute rise in blood pressure.18 24 25 Furthermore, the activation of cardiopulmonary baroreceptor afferent input induced by increased central venous pressure was found to be associated with a hypalgesic response in the rat.43 44 There is the possibility that the baroreceptor-mediated modulation of pain perception may represent one aspect of a more widespread capacity of the baroreflex system to inhibit the central nervous system processes. In fact, several lines of evidence suggest that blood pressure–related antinociception may be due to attenuated transmission of noxious stimuli to the spinal level; this attenuation may be due to descending inhibitory influence from brain stem sites that is involved in cardiovascular regulation and pain modulation.43

In our hypertensive group, the response to PT (dental pain threshold, threshold reaction, and maximal reaction) was found to correlate with diastolic blood pressure values but not with systolic ones. The diastolic pressure is probably one of the most important factors that may influence the baroreceptor reflex arc function, thus playing an important role in the adaptive somatosensory response of the body to stressful events. In fact, the chronic elevation of blood pressure could exert a tonic inhibitory influence on nociception, which is mediated by the baroreceptor reflex arc, resulting in a decreased pain perception.

It has been suggested that endogenous opioid peptides also play a role in blood pressure regulation under stressful physiological conditions.45 Zamir et al19 reported that rats with differing congenital susceptibility to hypertension have abnormally high levels of endogenous opioid activity in the pituitary gland, in the hypothalamus, and in the cervical spinal cord; the role of endogenous opioid peptides in the development and maintenance of hypertension is, however, less clear.

Conclusion
Our results demonstrated that patients with documented CAD and essential hypertension differ from normotensive CAD patients in reactivity to pain. Significantly higher dental pain threshold and lower reaction to pulp stimulation characterized our hypertensive patients. Arterial hypertension seems to be an additional factor in the modulation of pain perception in CAD patients.

Received November 13, 1996; first decision January 10, 1997; accepted April 29, 1997.


*    References
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 up arrowIntroduction
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 *References
 

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