Dynamic behavior and autonomic regulation of ectopic atrial pacemakers.

BACKGROUND: Heart rate (HR) variability reflects the neural regulation of normal pacemaker tissue, but the autonomic nervous regulation of abnormal atrial foci originating outside the sinus node has not been well characterized. We compared the HR variability of tachycardias originating from the ectopic foci and the sinus node. METHODS AND RESULTS: R-R-interval variability was analyzed from 24-hour Holter recordings in 12 patients with incessant ectopic atrial tachycardia (average HR 107+/-14 bpm), 12 subjects with sinus tachycardia (average HR 106+/-9 bpm), and 24 age- and sex-matched subjects with normal sinus rhythm (average HR 72+/-8 bpm). Time- and frequency-domain HR variability measures, along with approximate entropy, short- and long-term correlation properties of R-R intervals (exponents alpha(1) and alpha(2)), and power-law scaling (exponent beta), were analyzed. Time- and frequency-domain measures of HR variability did not differ between subjects with ectopic and sinus tachycardia. Fractal scaling exponents and approximate entropy were similar in sinus tachycardia and normal sinus rhythm, but the short-term scaling exponent alpha(1) was significantly lower in ectopic atrial tachycardia (0.71+/-0.16) than in sinus tachycardia (1.16+/-0.13; P<0.001) or normal sinus rhythm (1.19+/-0.11; P<0.001). Abrupt prolongations in R-R intervals due to exit blocks from the ectopic foci or instability in beat-to-beat R-R dynamics were the major reasons for altered short-term HR behavior during ectopic tachycardias. CONCLUSIONS: HR variability obtained by time- and frequency-domain methods does not differ between ectopic and sinus tachycardias, which suggests that abnormal atrial foci are under similar long-term autonomic regulation as normal pacemaker tissue. Short-term R-R-interval dynamics are altered toward more random behavior in ectopic tachycardia, which may result from a specific autonomic disturbance or an intrinsic abnormality of ectopic atrial pacemakers.

Prevalence and natural course of ectopic atrial tachycardia.

AIMS: The purpose of this study was to calculate the prevalence of ectopic atrial tachycardia in a population of young asymptomatic males and to assess its natural course both in asymptomatic subjects and in symptomatic hospital patients. METHODS AND RESULTS: 12-lead electrocardiograms (ECG) of 3554 consecutive males applying for a pilot's licence were analysed. ECGs of symptomatic arrhythmia patients at two university hospitals were also analysed. A repeat ECG was taken in cases of ectopic atrial tachycardia to assess the natural course of this arrhythmia. Twelve out of 3554 asymptomatic subjects (prevalence 0.34%) and 17 out of 3700 symptomatic arrhythmia patients (prevalence 0.46%) had ECG evidence of ectopic atrial tachycardia. A repeat ECG was obtained after a mean follow-up of 8+/-3 years in asymptomatic subjects and 7+/-3 years in symptomatic patients. After the follow-up, seven (26%) out of 27 patients were still in a similar ectopic atrial rhythm, 10 (37%) showed a change in P wave morphology and 10 (37%) were in sinus rhythm. Heart rate was significantly slower (mean rate 81+/-19 vs 109+/-17 beats. min-1) in the repeat ECGs. CONCLUSION: Asymptomatic ectopic atrial tachycardia is not an uncommon finding in a population of young males. The majority of patients show slowing of heart rate in the course of time, either with restoration of sinus rhythm or with a change in P wave morphology, suggesting that the ectopic foci undergo gradual degeneration with time.

QT interval and arrhythmic risk assessment after myocardial infarction.

To assess ventricular repolarization features as predictors of ventricular tachyarrhythmias (VT) in patients with previous myocardial infarction, we performed a dynamic study of QT interval from 24-hour electrocardiographic data. QT rate dependence was enhanced in patients with VT when compared with patients without VT.

Association of lipoprotein cholesterol and triglycerides with the severity of coronary artery disease in men and women.

The differences between the lipid profiles of male and female patients and the effect of plasma lipids on the extent of coronary artery disease were evaluated in 122 angiographically assessed coronary artery disease patients (95 males and 27 females) and 60 controls. Both male and female patients had lower HDL-cholesterol and higher total cholesterol, LDL-cholesterol, triglyceride, VLDL-cholesterol and VLDL-triglyceride concentrations than the controls. The VLDL lipid values did not differ significantly between the male patients with different extent of CAD, whereas the VLDL lipid values of female patients tended to increase with an increasing severity of CAD. High Lp(a) (> or = 35 mg/dl) values were more prevalent in patients with > 50% coronary stenosis compared to patients with < 50% stenosis and the controls (29%, 17% and 12%, respectively). The apolipoprotein E phenotypes and epsilon allele frequencies were similar in the patients and the controls. Low HDL-cholesterol and high LDL-cholesterol are CAD risk factors for both sexes. For women, elevated VLDL-triglycerides seem to be an additional risk factor for CAD.

Abnormalities in beat-to-beat dynamics of heart rate before the spontaneous onset of life-threatening ventricular tachyarrhythmias in patients with prior myocardial infarction.

BACKGROUND: Beat-to-beat analysis of RR intervals can reveal patterns of heart-rate dynamics, which are not easily detected by summary measures of heart-rate variability. This study was designed to test the hypothesis that alterations in RR-interval dynamics occur before the spontaneous onset of ventricular tachyarrhythmias (VT). METHODS AND RESULTS: Ambulatory ECG recordings from 15 patients with prior myocardial infarction (MI) who had spontaneous episodes of sustained VT during the recording and VT inducible by programmed electrical stimulation (VT group) were analyzed by plotting each RR interval of a sinus beat as a function of the previous one (Poincaré plot). Poincaré plots were also generated for 30 post-MI patients who had no history of spontaneous VT events and no inducible VT (MI control subjects) and for 30 age-matched subjects without heart disease (normal control subjects). The MI control subjects and VT group were matched with respect to age and severity of underlying heart disease. All the healthy subjects and MI control subjects showed fan-shaped Poincaré plots characterized by an increased next-interval difference for long RR intervals relative to short ones. All the VT patients had abnormal plots: 9 with a complex pattern, 3 ball-shaped, and 3 torpedo-shaped. Quantitative analysis of the Poincare plots showed the SD of the long-term RR-interval variability (SD2) to be smaller in all VT patients (52+/-14 ms; range, 31 to 75 ms) than in MI control subjects (110+/-24 ms; range, 78 to 179 ms, P<.001) or the normal control subjects (123+/-38 ms, P<.001), but the SD of the instantaneous beat-to-beat variability (SD1) did not differ between the groups. The complex plots were caused by periods of alternating sinus intervals, resulting in an increased SD1/SD2 ratio in the VT group. This ratio increased during the 1-hour preceding the onset of 27 spontaneous VT episodes (0.43+/-0.20) compared with the 24-hour average ratio (0.33+/-0.19) (P<.01). CONCLUSIONS: Reduced long-term RR-interval variability, associated with episodes of beta-to-beat sinus alternans, is a highly specific sign of a propensity for spontaneous onset of VT, suggesting that abnormal beat-to-beat heart-rate dynamics may reflect a transient electrical instability favoring the onset of VT in patients conditioned by structurally abnormal hearts.

No difference in cardiac innervation of diabetic patients with painful and asymptomatic coronary artery disease.

OBJECTIVE: To test the hypothesis that diabetic autonomic neuropathy interfering with sensory impulses from the heart by sympathetic denervation is the major cause of the high prevalence of asymptomatic coronary artery disease (CAD) in diabetic patients. RESEARCH DESIGN AND METHODS: We evaluated cardiac sympathetic innervation in a population-based group of 10 asymptomatic diabetic patients with angiographically proven CAD and in an age- and sex-matched group of 10 diabetic patients with symptomatic CAD using [123I]metaiodobenzylguanide (MIBG) scintigraphy. Exercise electrocardiography and myocardial perfusion imaging by 201Tl were used to detect myocardial ischemia, and standard cardiovascular tests were used to diagnose autonomic nervous dysfunction. RESULTS: Thallium scintigraphy revealed perfusion defects in all 10 symptomatic patients and in 9 of the asymptomatic patients. MIBG accumulation defects were found in all cases with painless and with painful disease. In the asymptomatic group, the denervation area exceeded the ischemic area in six cases and areas with total MIBG accumulation defects were seen in four cases. In one case, the MIBG defect was not in the ischemic region. In the symptomatic group, the denervation area exceeded the area of the ischemic region in all cases and areas of total denervation were seen in six cases. The autonomic nervous function tests were abnormal in two asymptomatic and three symptomatic patients with CAD. CONCLUSIONS: Cardiac sympathetic denervation is common in both patients with painful CAD and patients with asymptomatic CAD regardless of diabetic autonomic neuropathy. This finding supports the view that sympathetic innervation of the heart is highly sensitive to ischemia and this profound effect of ischemia masks the potential effects of autonomic neuropathy on sympathetic innervation. Mechanisms leading to the lack of ischemic pain in diabetic patients with CAD are complex and are not solely explained by autonomic neuropathy.

Significance of perfusion of the infarct related coronary artery for susceptibility to ventricular tachyarrhythmias in patients with previous myocardial infarction.

OBJECTIVE: To study the significance of perfusion of the infarct related coronary artery for susceptibility to ventricular tachyarrhythmias in patients with a remote myocardial infarction. SETTING: Tertiary referral cardiac centre. METHODS: Angiographic filling of the infarct related artery was assessed in a consecutive series of 85 patients with different susceptibilities to ventricular tachyarrhythmias after previous (> 3 months) Q wave myocardial infarction: 30 patients had a history of cardiac arrest (n = 16) or sustained ventricular tachycardia (n = 14), and sustained ventricular tachyarrhythmia was inducible in these by programmed electrical stimulation (arrhythmia group); 47 patients had no clinical arrhythmic events and no inducible ventricular tachyarrhythmias during programmed ventricular stimulation (control group). Eight patients without a history of any arrhythmic events were inducible into ventricular tachycardia. RESULTS: The patients in the arrhythmia group were older (63 (SD 8) years) than the control patients (59 (6) years, P < 0.05), and had larger left ventricular volumes in cineangiography (P < 0.01), but ejection fraction, severity of left ventricular wall motion abnormalities, previous thrombolytic therapy, and time from previous infarction did not differ between the groups. Patients with susceptibility to ventricular tachyarrhythmias more often had a totally occluded infarct related artery on angiography (77%) than patients without arrhythmia susceptibility (21%) (P < 0.001), and complete collateral filling of the infarct artery in cases without complete anterograde filling was less common in the arrhythmia group than in the control group (P < 0.001). Patients without a history of malignant arrhythmia but with inducible ventricular tachyarrhythmia also had no or poor perfusion of the infarct artery more often than the patients without inducible arrhythmia (P < 0.001). Logistic multiple regression showed that no or poor anterograde or collateral filling of the infarct related artery was the most powerful predictor of susceptibility to ventricular tachyarrhythmias (P < 0.001). Left ventricular size and function were not independently related to arrhythmic susceptibility. CONCLUSIONS: No or poor angiographic filling of the infarct related artery is closely associated with susceptibility to ventricular tachyarrhythmias late after acute myocardial infarction, suggesting that perfusion of the infarct artery will modify favourably the electrophysiological substrate of the infarct scar independently of the myocardial salvage achieved by early reperfusion.

Effects of perfusion of the infarct-related artery on risk markers of life-threatening arrhytmias in patients with prior myocardial infarction

Programmed electrical stimulation (PES), angiographic studies, Holter recording, 12-lead ECG and signal averaged ECG (SAECG, n=63) were performed in 109 consecutive patients with a prior Q-wave myocardial infarction (MI). Sixty-five patients (59 por cento) had TMI-class ) or 1 antegrade perfusion without significant collateral filling of the infarct related artery (IRA) (=poor persuion) and forty four (41 por cento) had either good antegrade or collateral perfusion of the IRA. The severity of corony artery disease or ejection fraction did not differ between the patients with poor or good perfusion of IRA. Heart rate variability and presence of late potentials on SAECG were also similar between the groups. but the dispersion of the QT interval was prolonged in the patients with poor perfusion of IRA (86 +/- 35 ms vs. 69 +/- 27 ms, p<0.01). The patients with poor perfusion of IRA had more often a clinical history of VT compared to those with good perfusion (68 por cento vs 9 por cento, p<0.01). Patets with good filling of the IRA after a prior MI have a low risk for VT, suggesting that preserved perfusion of the infarct scar stabilizes the electrophysiologic substrate.

Dispersion of QT interval in patients with and without susceptibility to ventricular tachyarrhythmias after previous myocardial infarction.

OBJECTIVES: The aim of this study was to estimate the value of QT dispersion measurement from the standard 12-lead electrocardiogram (ECG) in identifying patients susceptible to reentrant ventricular tachyarrhythmias after a previous myocardial infarction. BACKGROUND: Variability in QT interval duration on the different leads of the 12-lead ECG has been proposed as an indicator of risk for ventricular arrhythmias in different clinical settings, but the value of QT dispersion measurement in identifying patients at risk for reentrant ventricular tachyarrhythmias after myocardial infarction is not known. METHODS: The QT interval duration, QT dispersion and clinical and angiographic variables were compared between 30 healthy subjects; 40 patients with a previous myocardial infarction but no history of arrhythmic events or inducible ventricular tachycardia during programmed electrical stimulation; and 30 postinfarction patients with a history of cardiac arrest (n = 12) or sustained ventricular tachycardia (n = 18) and inducible, sustained monomorphic ventricular tachycardia by electrical stimulation. RESULTS: Dispersion of the corrected QT interval (QTc) differed significantly between the study groups and was significantly increased in patients with susceptibility to ventricular tachyarrhythmias ([mean +/- SD] 104 +/- 41 ms) compared with that in both healthy subjects (38 +/- 14 ms, p < 0.001) and postinfarction patients with no susceptibility to arrhythmias (65 +/- 31 ms, p < 0.001). Maximal QT interval duration was also prolonged in the group with arrhythmias compared with that in the other groups (p < 0.001). Multivariate analysis, including clinical and angiographic variables, QT dispersion and maximal QT interval, showed that QT dispersion was the independent factor that most effectively identified the patient groups with and without susceptibility to ventricular tachyarrhythmias (p < 0.001). CONCLUSIONS: Increased QT dispersion is related to susceptibility to reentrant ventricular tachyarrhythmias, independent of degree of left ventricular dysfunction or clinical characteristics of the patient, suggesting that the simple, noninvasive measurement of this interval from a standard 12-lead ECG makes a significant contribution to identifying patients at risk for life-threatening arrhythmias after a previous myocardial infarction.

Impaired low-frequency oscillations of heart rate in patients with prior acute myocardial infarction and life-threatening arrhythmias.

Myocardial infarction results in abnormal cardiac autonomic function, which carries an increased risk of cardiac mortality, but it is not well known whether autonomic dysfunction itself predisposes patients to life-threatening arrhythmias or whether it merely reflects the severity of underlying ischemic heart disease. To determine the significance of abnormalities of cardiovascular neural regulation on the risk for ventricular tachycardia (VT), heart rate (HR) variability in the time and frequency domain were compared in a case-control study between 30 patients with a prior myocardial infarction and a history of sustained VT (n = 18) or cardiac arrest (n = 12) (VT group) and 30 patients with a prior myocardial infarction but no arrhythmic events (control group). The patient groups were carefully matched with respect to age, sex, location, ejection fraction, number of prior infarctions, number of diseased coronary arteries, and beta-blocking medication. In all patients in the VT group, inducibility into sustained VT was achieved, but none of the control patients had inducible nonsustained or sustained VT during programmed electrical stimulation. Patients in the VT group had a significantly lower SD of the RR intervals (p < 0.01), and reduced ultra low-, very low-, and low-frequency power spectral components of HR variability (p < 0.001 for all) than controls, but the high-frequency component of HR variability did not differ significantly between groups. In multiple regression analysis, reduced very low-frequency power of HR variability was the strongest independent predictor of VT susceptibility.(ABSTRACT TRUNCATED AT 250 WORDS)

Relation between heart rate variability and spontaneous and induced ventricular arrhythmias in patients with coronary artery disease.

OBJECTIVES: The aim of this study was to determine the relation between autonomic control of heart rate and the spontaneous occurrence and inducibility of ventricular arrhythmias in patients with coronary artery disease. BACKGROUND: Low heart rate variability increases the risk of arrhythmic events. It is not known whether impaired autonomic heart rate control reflects alterations in functional factors that contribute to the initiation of spontaneous arrhythmias or whether it is the consequence of an anatomic substrate for reentrant tachyarrhythmias. METHODS: Fifty-four patients with coronary artery disease with a history of sustained ventricular tachycardia (n = 25) or cardiac arrest (n = 29) were studied by 24-h ambulatory electrocardiographic recording and by programmed electrical stimulation. Heart rate variability was compared among the patients with and without spontaneous ventricular arrhythmias and with and without inducibility of sustained ventricular tachyarrhythmias. RESULTS: Eight patients had a total of 21 episodes of sustained ventricular tachycardia on Holter recordings. Standard deviation of RR intervals and low frequency and very low frequency components of heart rate variability were significantly blunted in patients with sustained ventricular tachycardias compared with those without repetitive ventricular ectopic activity (p < 0.05, p < 0.01 and p < 0.05, respectively). However, no significant alterations were observed in heart rate variability before the onset of 21 episodes of sustained ventricular tachycardia. Heart rate variability did not differ between the patients with or without nonsustained episodes of ventricular tachycardia. In patients with frequent ventricular ectopic activity, low frequency and very low frequency power components were significantly blunted compared with those with infrequent ventricular ectopic activity (p < 0.01 and p < 0.001, respectively). Heart rate variability did not differ significantly between the patients with and without inducible sustained ventricular tachyarrhythmias. CONCLUSIONS: Impaired very low and low frequency oscillation of heart rate reflects susceptibility to the spontaneous occurrence of ventricular arrhythmias but may not reflect the instantaneous triggers for life-threatening arrhythmias or a specific marker of the arrhythmic substrate for ventricular tachyarrhythmias.

Asymptomatic coronary artery disease in diabetes: relation to common risk factors, lipoproteins, apoproteins and apo E polymorphism.

The risk factors for asymptomatic coronary artery disease (CAD) were examined in 138 diabetic patients. Following non-invasive screening examinations (exercise electrocardiography, dynamic thallium scintigraphy, 24-h electrocardiographic recording), CAD was confirmed angiographically in 21 symptom-free diabetic subjects with an ischaemic finding in at least one of the non-invasive tests. The prevalence of asymptomatic CAD in this cohort of diabetic patients was 21/132 (16%), which may be an underestimation because 6 patients refused angiography. Risk factors (age, diabetes, smoking, hypertension, serum lipoproteins, apoproteins and apo E phenotypes) were analysed according to the presence or absence of CAD. Multivariate logistic stepwise analysis did not show any definite changes of serum lipids, lipoproteins and apoproteins in type 1 (n = 72) and type 2 (n = 66) diabetic patients with or without asymptomatic CAD. The only factors associated with asymptomatic CAD were the duration of diabetes (P < 0.005) and the age of the patient (P < 0.05). These results suggest that in diabetic patients the major risk factor for premature coronary atherosclerosis is diabetes itself. Assessment of other risk factors does not seem to define any subgroup with asymptomatic CAD.

Apolipoprotein E and B polymorphisms--longevity factors assessed in nonagenarians.

To test if the prevalence of genetic risk factors for coronary heart disease (CHD) is low in individuals who have reached an extremely old age, the allele frequencies of apolipoprotein E (apo E) and B (apo B) polymorphisms and plasma lipoprotein(a) levels were investigated in nonagenarians and in younger control groups. The frequency of the epsilon 4 allele of apo E was significantly lower in the nonagenarians than in the middle-aged and young adults (P < 0.05). Also, the frequency of EcoRI allele R- of apo B was low in the nonagenarians, whereas the allele frequency for the XbaI polymorphism of apo B and plasma lipoprotein(a) concentrations did not differ between the nonagenarians and the younger groups. These findings strongly suggest that the presence of these potential genetic risk factors for CHD, namely the epsilon 4 allele of apo E and the R- allele of apo B, decreases the probability of an individual reaching an extremely old age.

Efficacy of intravenous sotalol for suppressing inducibility of supraventricular tachycardias at rest and during isometric exercise.

The efficacy of intravenous sotalol (1 mg/kg) for suppressing inducibility of supraventricular tachycardias (SVT) with different electrophysiologic mechanisms was studied in 30 consecutive patients referred for an electrophysiologic study because of paroxysmal SVT. Orthodromic SVT using accessory atrioventricular (AV) connection was inducible in 14 patients, AV nodal reentrant SVT in 8, and intraatrial SVT in 8 before administration of sotalol, Isometric handgrip exercise facilitated the inducibility of SVT in 8 patients who were noninducible at rest. After intravenous sotalol, 7 of 14 patients (50%) with orthodromic SVT, 8 of 8 (100%) with AV nodal reentrant SVT, and 8 of 8 (100%) with intraatrial reentrant SVT became noninducible into sustained SVT, Isometric exercise facilitated the inducibility of only 3 nonsustained SVT runs after sotalol infusion, and exercise did not reverse the prolongation of refractory periods of the atrium, AV node, accessory pathway and ventricle caused by sotalol. During a mean follow-up period of 18 +/- 7 months, none of the 14 patients who remained noninducible into sustained SVT during the stress test after intravenous sotalol and tolerated long-term oral sotalol therapy had recurrence of symptomatic SVT. Thus, sotalol is efficacious for suppressing SVT with AV nodal or intraatrial reentrant mechanism, but less efficacious in patients with accessory AV pathway. The beta-blocking and cellular antiarrhythmic effects of sotalol are not significantly reversed by exercise.

Asymptomatic coronary artery disease in diabetes: associated with autonomic neuropathy?

To elucidate the potential association of diabetic autonomic neuropathy with increased prevalence of silent coronary artery disease (CAD), 138 asymptomatic diabetic subjects were screened using exercise ECG. 24-h ambulatory ECG and dynamic thallium scintigraphy. Fourteen patients with exercise-induced myocardial ischaemia and angiographically confirmed CAD (greater than or equal to 50% coronary artery narrowing) were found using this protocol. Their autonomic nervous function was assessed using standard cardiovascular tests and compared with that of 23 consecutive diabetic patients catheterised because of symptomatic CAD (mean New York Heart Association class 3.0). The diabetic patients with symptomatic CAD had more severe coronary atherosclerosis than the diabetic patients with asymptomatic CAD assessed by jeopardy score (P less than 0.01). The groups did not, however, differ with respect to autonomic function tests. Five patients (22%) with symptomatic CAD and 3 patients (21%) with asymptomatic CAD had definite autonomic dysfunction, i.e. two or more abnormal tests. Thus, our results suggest that the frequency of autonomic neuropathy is not increased in diabetic patients with asymptomatic CAD. The contribution of diabetic autonomic neuropathy to the absence of cardiac pain needs further clinical and pathological studies.

Prevalence of asymptomatic myocardial ischaemia in diabetic subjects.

OBJECTIVE: To compare the prevalence of silent myocardial ischaemia associated with coronary artery disease in diabetic subjects with that in controls of similar age and sex. DESIGN: A controlled study in which subjects with positive findings on exercise electrocardiography, 24 hour electrocardiographic recording, or dynamic thallium scintigraphy (diabetics only) underwent coronary angiography. SETTING: Academic medical centre; referral based cardiology clinic. SUBJECTS: 136 Diabetic subjects, of whom 72 (33 women, 39 men (mean age 46.0] were insulin dependent and 64 (19 women, 45 men (mean age 49.3] non-insulin dependent. 80 Controls matched for age and sex; all were clients of the Occupational Health Service of Oulu University Central Hospital or the State Occupational Health Service Station in Oulu in whom diabetes had been excluded by a glucose tolerance test. INTERVENTIONS: Any subject showing signs of myocardial ischaemia was referred for cardiac catheterization. MAIN OUTCOME MEASURES: Exercise electrocardiography and 24 hour electrocardiographic recording were regarded as positive if there were ST depressions of greater than or equal to 1 mm that were planar or downsloping and persisted for 0.08 seconds after the J point. Thallium tomographic imaging. With cardiac catheterisation, coronary artery lesions were classified as significant in half or more of the vessel lumen was narrowed, or insignificant if such narrowing was less than half. RESULTS: 40 (29%) diabetes and four (5%) controls had positive results in one or more of the non-invasive tests. Coronary angiography was performed on 34 of the diabetics (six refused); 12 had significant coronary artery narrowing; seven had unimportant atherosclerosis; 15 had patent coronary arteries. Among the controls only one had unimportant atherosclerosis; the other three had patent arteries. CONCLUSIONS: These results confirm the high prevalence of asymptomatic myocardial ischaemia in diabetics. Non-invasive screening of diabetic subjects, however, does not seem justified because of the low preset probability of the presence of the disease and the inaccuracy of the available test methods.

Effect of coronary artery disease on parasympathetic cardiovascular reflexes in NIDDM patients.

To evaluate the effect of coronary artery disease on parasympathetic cardiac reflexes in patients with non-insulin-dependent diabetes mellitus (NIDDM), we studied standard cardiovascular reflexes in 27 NIDDM patients with coronary artery disease (group 1) and in 21 NIDDM patients with no signs of coronary artery disease (group 2). Groups did not differ with respect to age, duration of diabetes, or presence of retinopathy. The mean +/- SD heart-rate variation in deep breathing was lower in group 1 than in group 2 (11.6 +/- 6.5 vs. 17.1 +/- 9.0 beats/min, P less than 0.05). Heart-rate variation was more often abnormally low (less than or equal to 10 beats/min) in group 1 than in group 2 (48 vs. 19%, P less than 0.05). Thus, the presence of coronary artery disease appears to modify cardiac parasympathetic reflexes in patients with diabetes mellitus and must be kept in mind when interpreting test results.