Comparative Assessment of the Heart's Functioning by Using the Akabane Test and Classical Methods of Instrumental Examination.

Acupuncture physicians have studied the application of reflexotherapy to cardiology. However, no one has investigated the connection of ancient Chinese diagnostic methods with modern tools. A total of 102 patients (54 men and 48 women) with heart pathology, namely, sick-sinus syndrome, Wolff-Parkinson-White syndrome, and atrioventricular blockade, were studied using the usual instrumental methods (transesophageal electrophysiological study of the heart, echocardiography), after which they underwent Akabane thermopuncture testing as in traditional Chinese medicine. The results of cardio examination from one side of the Akabane test with that from the other side were compared by means of a multiple stepwise regression analysis. We revealed the effects on the characteristic pattern of acupuncture channel lesions inherent in a definite heart pathology, i.e., the most vulnerable acupuncture channel (AC), of such factors as disturbances of the contractile, conductive, or automatic heart functions, and changes in the chambers' size or circulation volume. Сhanges in the indices of the left and the right branches of these channels usually reflect the opposing natures of the changes in these indicators, which should be considered in reflexotherapy. The main value of the Akabane test along with the use of mathematical analysis lies in early, quick, and inexpensive detection of the above-mentioned heart disturbances.

Cost-effectiveness of dual-chamber pacing compared with ventricular pacing for sinus node dysfunction.

BACKGROUND: Compared with single-chamber ventricular pacing, dual-chamber pacing can reduce adverse events and, as a result, improve quality of life in patients paced for sick sinus syndrome. It is not clear, however, how these benefits compare with the increased cost of dual-chamber pacemakers. METHODS AND RESULTS: We used 4-year data from a 2010-patient, randomized trial to estimate the incremental cost-effectiveness of dual-chamber pacing compared with ventricular pacing and then projected these findings over the patients' lifetimes by using a Markov model that was calibrated to the first 5 years of in-trial data. To assess the stability of the findings, we performed 1000 bootstrap analyses and multiple sensitivity analyses. During the first 4 years of the trial, dual-chamber pacemakers increased quality-adjusted life expectancy by 0.013 year per subject at an incremental cost-effectiveness ratio of 53,000 dollars per quality-adjusted year of life gained. Over a lifetime, dual-chamber pacing was projected to increase quality-adjusted life expectancy by 0.14 year with an incremental cost-effectiveness ratio of approximately 6800 dollars per quality-adjusted year of life gained. In bootstrap analyses, dual-chamber pacing was cost-effective in 91.9% of simulations at a threshold of 50,000 dollars per quality-adjusted year of life and in 93.2% of simulations at a threshold of 100,000 dollars. Its cost-effectiveness ratio was also below this threshold in numerous sensitivity analyses that varied key estimates. CONCLUSIONS: For patients with sick sinus syndrome requiring pacing, dual-chamber pacing increases quality-adjusted life expectancy at a cost that is generally considered acceptable.

Sinus node recovery time assessment by the overdrive suppression test employing an intravenous injection of disopyramide phosphate.

Although sinus node recovery time (SNRT) assessment by the overdrive suppression test (ODST) is important in detecting sick sinus syndrome (SSS), its sensitivity is still inadequate. We have evaluated the effect of intravenous injection (i.v.) of disopyramide phosphate (DP) in ODST. The subjects were 30 SSS patients (64.9 +/- 10.0 years old). If SNRT was <2,000 ms or the corrected SNRT (CSNRT) was < 1,000 ms, ODST was repeated after DP i.v. (2 mg. kg(-1), < or = 100 mg in total). Eleven normal subjects (59.3 +/- 9.0 years old) were also studied. Although SNRT was <2,000 ms or the CSNRT was < 1,000 ms in 13 of the 30 SSS patients (43%), SNRT was prolonged from 1,510 +/- 300ms to 3,400 +/- 1,160 ms (P<0.01), and CSNRT from 510 +/- 190 to 2,470 +/- 1,470 ms (P<0.01) after DP i.v. in these patients. Thus, SNRT was > or = 2,000 ms and the CSNRT was > or = 1,000 ms in 27 of 30 SSS patients (90%) after DP i.v. Using a combination of overdrive suppression and intravenous injection of disopyramide phosphate, the corrected sinus node recovery time was diagnostic (>525 ms) in 29 of the 30 patients (97%). In contrast, SNRT and CSNRT were shortened in the normal subjects during ODST after DP i.v. (P<0.01). The plasma concentration of DP estimated in nine patients was 4.1 +/- 1.0 microg.ml(-1). No serious side effect occurred. ODST employing DP i.v. is safe and seems to be highly effective in diagnosing SSS.

Electrophysiologic assessment of calcium channel blockers in transplanted hearts: an experimental study.

The effects of calcium channel blockers on automaticity, conduction, and refractoriness were studied in a model of heterotopic heart transplantation in dogs, which combined an innervated heart (recipient) and a denervated one (donor). Following the surgical procedure, 0.2 mg/kg verapamil (n = 10), 0.15 mg/kg diltiazem (n = 10), or 5 microg/kg + 30 microg/kg/h nifedipine (n = 10) was administered intravenously. In basal situation and after drug administration, each heart was assessed for AV interval, cycle length, sinoatrial conduction time, atrioventricular node antegrade block point, and atrioventricular node and ventricular refractory periods; electrocardiographic PR and QT intervals and QRS complexes; systemic arterial, pulmonary artery, central venous, and pulmonary capillary wedge pressures; and cardiac output. The depressor effects of these calcium channel blockers on automaticity, refractoriness, and conduction were more intense in the transplanted hearts, very possibly because of the absence of adrenergic reflexes mediated by the autonomic nervous system; in particular, verapamil produced a great depression of sinus automaticity in a large number of cases.

Sinus node recovery time assessment revisited: role of pharmacologic blockade of the autonomic nervous system.

Sinus node recovery time assessment is used to diagnose clinically significant sinus node dysfunction (SND) when Holter has failed to prove a relationship between sinus bradyarrhythmias and symptoms, but consensus has not been reached as to the value of including assessment after pharmacologic blockade of the autonomic nervous system. This issue was addressed in the present study performed on 52 patients with syncope or presyncope/dizziness (n = 48), sinus bradyarrhythmias (n = 45), or both (n = 41). Group 1 consisted of 13 patients with a proven relationship between symptoms and sinus bradyarrhythmias. Group 2 consisted of 39 patients with suspected SND. The protocol included three pacing periods at two pacing rates and was performed at baseline (n = 52), after single doses of atropine and propranolol (0.02 mg/kg and 0.1 mg/kg, respectively) (n = 41), and again after a second dose (n = 29). The sensitivity of prolonged recovery times was 77% in group 1. Among group 2 patients, 56% had prolonged recovery times at baseline (79% when including the results after the first dose of drugs). The second dose did not contribute diagnostic information, but it caused significant adverse reactions in 7 of 29 patients (P < 0.001). These 7 patients were all older than 60 years. Assessment of sinus node recovery time after pharmacologic blockade of the autonomic nervous system thus increases the sensitivity of the method in patients with suspected SND and normal baseline results. However, only 50% of the initially suggested doses of atropine and propranolol is sufficient and eliminates the risk for significant adverse reactions.

Assessment of sinus node function in patients with congenital long QT syndrome.

Sinus node function was evaluated in 4 patients with congenital long QT syndrome suffering from recurrent episodes of syncope and ventricular arrhythymias. Three of the 4 patients had bradycardia at rest on a 24-hour ECG. Sinus node function was examined by the atrial overdrive suppression test and the atrial premature stimulation test. Corrected sinus node recovery time (CSNRT) was prolonged in all patients. Total sinoatrial conduction time was also prolonged in 2 of the 4 patients. In all patients with abnormally high values, these values returned to normal after atropine administration, except in one patient. His prolonged CSNRT remained high after atropine administration, indicating abnormal automaticity such as that seen in sick sinus syndrome. These results show that sinus node function in congenital long QT syndrome is often associated with autonomic dysfunction, and sometimes with intrinsic disturbances of sinoatrial conduction.

Reliability of transesophageal pacing in the assessment of sinus node function in patients with sick sinus syndrome.

The purpose of this study was to find out whether transesophageal pacing could be utilized for assessment of sinus node function in patients with sick sinus syndrome (SSS). In 17 patients with SSS (study group) we compared the results of sinus node tests obtained both in the basal state and after pharmacological autonomic blockade by endocavitary stimulation and, 24 hours later, by transesophageal pacing. In another group of 17 patients with SSS (control group), we compared the results obtained by two endocavitary studies. In "study group", sinus cycle length (SCL) and corrected sinus node recovery time (CSRT) did not show significant differences between the two studies both in the basal state and after autonomic blockade, whereas sinoatrial conduction time (SACT) was more prolonged during esophageal pacing (P less than 0.01). In "control group", sinus node measures did not show significant differences between the two studies. In the "study group," the following coefficients of correlation were obtained in the basal state; SCL, r = 0.65, CSRT, r = 0.57, SACT, r = 0.52 and after autonomic blockade: SCL, r = 0.95, CSRT, r = 0.62 and SACT, r = 0.53. In the basal state, the correlation for SCL and CSRT between the two studies was lower in the "study group" than in the "control group" (P less than 0.05), whereas after autonomic blockade the correlation for sinus node measures did not show significant differences between the two groups of patients. These data suggest that transesophageal study influences the autonomic tone regulating the sinus node; however, it is not responsible for important variations in sinus node measures.(ABSTRACT TRUNCATED AT 250 WORDS)

Assessment by autonomic blockade of age-related changes of the sinus node function and autonomic regulation in sick sinus syndrome.

Age-related changes of the sinus node (SN) function and the autonomic influence on the SN function were evaluated in 65 patients with sick sinus syndrome (range 14 to 84 years). Heart rate (HR), corrected SN recovery time and sinoatrial conduction time were measured before (basic) and after (intrinsic) autonomic blockade (propranolol 0.2 mg/kg plus atropine 0.04 mg/kg intravenously). Percent of autonomic chronotropies of the SN function were calculated by the following formulas: (1)--(intrinsic HR--basic HR/intrinsic HR) X 100; (2) (intrinsic corrected SN recovery time--basic corrected SN recovery time/intrinsic corrected SN recovery time) X 100; (3) (intrinsic sinoatrial conduction time--basic sinoatrial conduction time/intrinsic sinoatrial conduction time) X 100. Basic HR, basic corrected SN recovery time and basic sinoatrial conduction time did not vary with age. Intrinsic HR decreased with age, but this correlation was weak (r = -0.54, p less than 0.001). Intrinsic corrected SN recovery time and intrinsic sinoatrial conduction time tended to increase with age (r = 0.26, p less than 0.05; r = 0.29, p less than 0.05, respectively). Percent chronotropies of HR, corrected SN recovery time and sinoatrial conduction time were negative values in younger patients and positive values in elderly patients; they correlated positively with age (r = 0.59, p less than 0.001; r = 0.60, p less than 0.001; r = 0.43, p less than 0.001, respectively). Thus, the basic SN function did not change with age, while the intrinsic SN function deteriorated with age.(ABSTRACT TRUNCATED AT 250 WORDS)

Pathophysiological characteristics, diagnostic problems and assessment of sinus node dysfunction.

Based on clinical and experimental experience, sick sinus syndrome can be divided into two groups: intrinsic and autonomic neurovegetative pacemaker dysfunction. Sinus node activity is characterized electrophysiologically by automaticity, recovery and sinoatrial conduction. The automaticity of the sinus pacemaker cell groups and sinus recovery can be differentiated properly under experimental conditions. Studies of the electrophysiological characteristics showed the basic functional parameters to be normal in autonomic sinus dysfunction. Diagnosis is either based on clinical observation or on the data of Holter monitoring, the electrophysiological methods being inadequate for diagnosing this neurovegetative form of sick sinus syndrome. On the other hand, intrinsic-organic sinus dysfunction can be diagnosed by electrophysiological tests. If completed by complex pharmacological studies, in this organic form of sick sinus syndrome, even the severity of the intrinsic injuries can be assessed quantitatively. This division provides a logical basis for a proper selection and evaluation of the differential diagnostic procedures, while information on the aetiopathology of sinus dysfunction and on the degree of the functional injuries of the electrophysiological structure of the heart provides an adequate basis for therapy.

Pre- and postoperative electrophysiologic assessment of children with secundum atrial septal defect.

Sinus node (SN) and atrioventricular node (AVN) dysfunction after repair of atrial septal defect (ASD) may be caused by inherent nodal abnormalities and not related to altered hemodynamics. To assess the preoperative prevalence and postoperative persistence of nodal dysfunction, 21 consecutive children, mean age 5.4 years, underwent electrophysiologic evaluations before ASD repair. Preoperative SN recovery time was prolonged in 11 patients and was associated with abnormal AVN response to rapid atrial pacing in 5. There were no significant differences in age, hemodynamic values or shunt size between children with normal and those with abnormal nodal function. Atrial and AVN refractory periods were normal. The ASD was repaired in 9 children with SN dysfunction. Electrophysiologic studies performed 4 to 16 months after surgical correction showed improvement in all electrophysiologic values. However, SN function remained abnormal. Significant decreases were observed in atrial (p less than 0.05) and AVN (p less than 0.05) refractory periods, with increased atrial conduction velocity (p less than 0.01) and AVN Wenckebach response to atrial pacing (p less than 0.01). ASD repair improved nodal and atrial muscle electrophysiologic function, theoretically by relieving stress on atrial impulse propagation. SN and AVN dysfunction may persist as an inherent part of the ASD complex.

New application of direct sinus node recordings in man: assessment of sinus node recovery time.

Sinus node recovery time (SNRT) is frequently used to assess sinus node function in patients with suspected sick sinus syndrome (SSS). Although SNRT is assumed to reflect sinus node automaticity, this assumption remains unproven. The purpose of this study was (1) to test the hypothesis that SNRT in patients with and without SSS reflects sinus node automaticity, and (2) to assess the role of sinoatrial conduction time in the measurement of SNRT. A total of 16 patients (mean +/- SD age 63 +/- 9 years), seven of which had SSS, form the basis of this report. An electrogram of the sinus node was obtained for each of the 16 patients, and overdrive pacing was performed in each at cycle lengths of 1000 to 300 msec. SNRT was measured (1) on the sinus node electrogram (direct method, measuring SNRTd) as the interval from the last pacing stimulus artifact to the onset of the upstroke slope of first postpacing sinus beat and (2) on the high right atrial electrogram (indirect method, measuring SNRTi). Results were as follows: (1) The longest SNRTd was significantly shorter than the longest SNRTi (989 +/- 304 vs 1309 +/- 356 msec, p less than .001). (2) For the first postpacing sinus beat there was a significant prolongation of sinoatrial conduction time as compared with that for sinus beats before pacing (319 +/- 152 vs 99 +/- 35 msec, p less than .001). Sinoatrial conduction time normalized within 3.6 +/- 0.96 postpacing sinus beats. (3) At the pacing cycle length that resulted in the longest recovery time, sinus node depression was seen in 56% of patients, sinus node acceleration was noted in 26%, and no appreciable change in sinus node automaticity was observed in 19%. (4) Sinoatrial conduction time for the sinus beat before pacing and that for the first postpacing beat was longer in patients with SSS when compared with in patients without SSS. (5) In patients with SSS the abnormal SNRTi, when corrected for the degree of prolongation of sinoatrial conduction time for the first postpacing beat, became normal in five of six patients. We conclude that (1) SNRTi reflects both sinus node automaticity and sinoatrial conduction time, whereas SNRTd reflects sinus node automaticity, (2) overdrive atrial pacing results in marked prolongation of sinoatrial conduction time for the first postpacing beat, which is longer in patients with SSS when compared with in those without SSS, and (3) in patients with SSS the inference of abnormal sinus node automaticity on the basis of a prolonged corrected SNRTi is usually incorrect.

Diagnostic assessment of recurrent syncope.

The definitive diagnosis of a cardiac arrhythmia as the basis for syncope is made by electrocardiographic monitoring during a syncopal episode. In the absence of this evidence, abnormalities demonstrated by an electrophysiologic study may suggest the etiology of syncope. Cardiac electrophysiologic testing in patients with recurrent syncope should probably be limited to patients with underlying cardiac disease. These patients are at a higher risk for sudden death and have a high incidence of electrophysiologic abnormalities. In particular, ventricular tachycardia may be evoked and specific therapy for this abnormality is associated with remission of syncope. In contrast, electrophysiologic studies in patients with no underlying cardiac disease have a very low yield of abnormal findings in the order of 10-20%, and should be performed only when there are reasons to suspect the presence of arrhythmias. Furthermore, in patients with no underlying cardiovascular disease there is a high spontaneous remission rate of syncope and the late incidence of sudden death is low, and related to the presence of other systemic illnesses. At present, the significance of nonsustained ventricular tachycardia or ventricular fibrillation induced during cardiac electrophysiologic studies in patients with no documented arrhythmias is unknown, and further prospective studies are necessary to define appropriate therapy for these patients. Further investigation is also required to clarify the spontaneous remission rate of syncope, as this information is of vital importance in assessing the success of any therapeutic modality.

Value and limitations of clinical electrophysiologic study in assessment of patients with unexplained syncope.

We assessed the value of clinical electrophysiologic study using intracardiac recording and programed electrical stimulation in 34 patients who had unexplained syncope and/or presyncope. All patients had normal electrocardiograms, and no abnormality was detected by clinical examination, ambulatory electrocardiographic recording, or treadmill testing. The electrophysiologic results were diagnostic in four patients (11.8 percent) and led to appropriate therapy that totally relieved symptoms. The results were abnormal but not diagnostic in two patients (5.8 percent) and normal in the remaining 28 patients (82.4 percent). The patients were followed for a mean period of 15 months (range two to 44) after electrophysiologic testing. Sixteen patients (47 percent) had no further episodes in the absence of any intervention. In four patients (11.8 percent), a definitive diagnosis was made during follow-up. In seven patients, permanent pacing was instituted empirically with relief of syncope. Two patients continued to have syncopal spells. We conclude that the diagnostic yield of electrophysiologic testing is low in a patient population that has no electrocardiographic abnormality or clinical evidence of cardiac disease. Empirical permanent pacing in patients with symptoms continuing after our study appeared to be beneficial, but this result is difficult to evaluate because of the high incidence of spontaneous remission in this group. Persistent attempts to document electrocardiographic abnormalities during a typical episode of symptoms appears to be the only definitive way to confirm or exclude an arrhythmic cause of the symptoms.

Exercise assessment of sinoatrial node function following the Mustard operation.

To screen for sinoatrial node dysfunction following the Mustard procedure for transposition of the great arteries, we studied the chronotropic response to graded maximal treadmill exercise in 29 patients at mean 6.7 years after operation. Although 93% of patients had normal resting heart rate (HR), 83% demonstrated significant depression of maximum HR and/or recovery HR after termination of exercise. These findings were similarly present among a subset of 13 patients with normal exercise tolerance. Resting and exercise-induced HR in 10 patients receiving chronic digoxin therapy were no different than in the 19 patients without medication. Sixteen patients with abnormal chronotropic responses to exercise had intracardiac electrophysiologic evaluation which confirmed sinoatrial node dysfunction in nine. Abnormal HR responses did not correlate with clinical symptoms, cardiac arrhythmias, or postoperative hemodynamics. Maximal exercise testing may be a sensitive noninvasive method to identify sinoatrial node dysfunction in postoperative children.

Sinus and atrioventricular nodal function: Preoperative and early postoperative assessment in children.

Ninety-three rapid atrial pacing studies were performed in 38 children to compare preoperative and early postoperative function of the sinus and atrioventricular (AV) nodes. The interval between the preoperative and postoperative studies was under 6 months in the majority of patients. Postoperative studies were performed within 48 hours of operation and between 4 and 8 days after operation. Sinus nodal function as measured by sinus nodal recovery time (SNRT) was an unreliable index in determining depression since the number who improved postoperatively (10/55) was nearly equal to the number that worsened (12/55). The majority who had abnormal function postoperatively demonstrated a junctional rather than sinus recovery focus. This finding appears a more definitive and more reproducible indicator of sinus node depression in the postoperative patient. Postoperative AV nodal function was decreased (as measured by the cycle length [CL] at which Wenckebach periodicity occurred) in 15 of 55 studies (27%) of the entire group. There was nearly an equal chance for improvement (24%) in function. This also applied to those patients who had sequential studies. Therefore, this method of assessment for AV nodal function was unreliable, or else the operation did not affect the node significantly. The latter is unlikely in view of late postoperative data. The greatest utility of this test was to determine the capability for AV conduction in certain patients with slow escape rhythms in the absence of surface P waves, and to differentiate complete heart block from AV dissociation when atrial activity was absent. Despite the variability of effects on the sinus and AV nodes in these patients, those who demonstrated depression had a significantly higher incidence of dysrhythmias (80% of patients with sinus nodal depression and 100% of patients with AV nodal depression).