Jitsuki Tsuzuki

Diagnostic usefulness of postexercise systolic blood pressure response for detection of coronary artery disease in patients with electrocardiographic left ventricular hypertrophy

Patients with left ventricular (LV) hypertrophy often have a positive result on exercise testing despite a normal coronary arteriogram. This indicates that exercise-induced ST depression is not always an accurate indicator of the presence of coronary artery disease (CAD) in such patients. We evaluated the usefulness of the postexercise systolic blood pressure (BP) response for detection of CAD in 51 patients with both electrocardiographic evidence of LV hypertrophy and positive ST depression on treadmill exercise testing. Coronary cineangiograms showed normal coronary arteries in 23 patients (45%) (group 1) and significant CAD in 28 patients (55%) (group 2). The systolic BP ratio (systolic BP at 3 minutes of recovery divided by systolic BP at peak exercise) was significantly higher in group 2 than in group 1 (1.01 +/- 0.19 vs 0.80 +/- 0.09; p < 0.001). Analysis of the relative cumulative frequency revealed that a systolic BP ratio of 0.86 was the cutoff point for distinguishing a patient with CAD from one with normal coronary arteries. The sensitivity, specificity, and accuracy of a systolic BP ratio > or = 0.86 for detection of CAD in patients with LV hypertrophy were 79%, 83%, and 82%, respectively. Our results suggest that the use of an abnormal BP ratio, in combination with ST depression, improves the accuracy of treadmill exercise testing for detecting CAD in patients with electrocardiographic evidence of LV hypertrophy.

Prognostic value of abnormal postexercisesystolic blood peessure response: Prehospital discharge test after myocardial infarction in Japan

To assess the prognostic value of an abnormal postexercise response in systolic blood pressure (SBP), treadmill exercise testing was performed in 217 survivors of acute myocardial infarction at an average of 9.3 weeks after infarction. During the mean follow-up period of 4 years, cardiac events were noted in 34 patients (16%), including cardiac death in 13 (6%), nonfatal reinfarction in 12 (6%), and coronary artery bypass graft surgery in nine (4%). An abnormal postexercise SBP response was defined as the ratio of SBP at 3 minutes of recovery to peak exercise SBP of 0.9 or more, on the basis of the cutoff point with the highest sensitivity and specificity to predict cardiac events. An abnormal postexercise SBP response occurred in 90 patients (42%). Patients with an abnormal postexercise SBP response had more exercise-induced myocardial ischemia. more left ventricular impairment, and more extensive coronary artery lesions than those without. Cox proportional hazards model demonstrated that the abnormal postexercise SBP response was ranked first in ability to predict cardiac death (p = 0.025, relative risk 15.41). Bypass surgery was associated with an abnormal postexercise SBP ratio (p less than 0.05). Nonfatal reinfarction could not be predicted by any clinical or exercise variables. In conclusion, an abnormal postexercise SBP response could be useful for predicting cardiac death and the need for bypass surgery after myocardial infarction. This response is probably the result of myocardial ischemia and left ventricular impairment.

Correlation between the direction of the interventricular septum estimated with transmission computed tomography and the initial QRS vectors.

A correlative study was performed to relate the interventricular septal angle (As degrees) evaluated by transmission computed tomography to the azimuth of initial QRS vectors in 52 patients. Patients were divided into five groups: RV volume overloading (RVO), RV pressure overloading (RSO), LV volume overloading (LVO), LV pressure overloading (LSO), and normal control with no cardiopulmonary disease. For measurement of As degrees, the leftward and forward directions were designated as zero and 90 degrees, respectively. The mean value of As degrees was significantly smaller in RVO (14.4 degrees) and RSO (41.1 degrees) than in normal controls (50.4 degrees) and in LVO (53.2 degrees). The mean value of the azimuth of the initial 12-msec instantaneous QRS vectors (H 12 degrees) was significantly smaller in RVO (80.5 degrees), RSO (81.7 degrees), and LSO (81.3 degrees) than in normal controls (113.8 degrees and in LVO (113.7 degrees). A significant linear correlation was shown between As degrees and H12 degrees in a combined group consisting of RVO, LVO, and normal controls (r = 0.70, p less than 0.001), and also in another combined group consisting of RSO, LSO, and normal controls (r = 0.52, p less than 0.01). It was concluded that the orientation of the interventricular septum was one of the major determinants of the direction of initial QRS vectors, especially in patients with ventricular volume overload or without cardiopulmonary disease.

Effect of the autonomic blockade on the automaticity of the A-V junctional pacemaker in awake dogs**

The effect of the autonomic blockade on the automaticity of the A-V junctional pacemaker was evaluated in 15 awake dogs with experimentally induced A-V junctional rhythm. The duration of asystole after overdrive (D.A.O.) in these dogs was prolonged significantly in accordance with increase in the drive rate, and the mean +/- SD of the D.A.O. reached 4.7 +/- 1.1 seconds (N = 15) after overdrive at 2.5 times the spontaneous heart rate. After administration of atropine (0.4 mg/kg; i.v.) to eight dogs, the mean +/- SD of the D.A.O. at the same rate decreased from 4.5 +/- 0.9 to 3.4 +/- 1.2 seconds. After administration of practolol (0.5 mg/kg; i.v.) to the seven other dogs, the mean +/- SD of the D.A.O. at the same rate increased remarkably from 4.9 +/- 1.3 to 9.4 +/- 3.0 seconds. Intravenous injection of practolol (0.5 mg/kg) had no effect upon the D.A.O. in the five dogs with sinus rhythm. Thus, it is suggested that (1) the sympathetic nerve might play a more important role in regulating the automaticity of the A-V junctional pacemaker than the vagus and (2) it physiologically might take over 5.0 seconds for the A-V junctional pacemaker to initiate an escape beat during longstanding sinus arrest, if a marked dysfunction of the A-V junctional pacemaker occurs due to a decrease in tension of the sympathetic nerve.

Overdrive suppression in diagnosis of sick sinus syndrome.

A criterion to determine the indication for pacemaker implantation in the sick sinus syndrome by overdrive suppression is proposed. Overdrive suppression was performed in 10 patients with the sick sinus syndrome (SSS) and another 10 patients with normal sinus rhythm (NSR) who served as controls. In the SSS group, 9 patients had complained of such severe symptoms as Adams-Stokes attack and/or congestive failure and were referred to our laboratory for pacemaker implantation. One other patient, an apparently robust young man (20 years old) referred for detailed cardiac examination, had no remarkable symptoms except for arrhythmias, but was found dead two months later. Atrial pacing for overdrive suppression was carried out at first at various rates ranging from 60 to 180 beats/min for 15 sec, and then at a rate of 100 beats/min for various durations ranging from 5 to 180 sec. After cessation of the atrial pacing, asystolic pauses were measured and the maximum (maximum pause) among the pauses obtained was used as a parameter indicating depression of cardiac automaticity. The maximum pause in the SSS group ranged from 5.6 to 9.0 sec (mean +/- SD = 7.0 +/- 1.2), WHILE THOSE IN THE NSR group ranged from 0.7 to 1.5 sec (mean +/- SD = 1.2 +/- 0.14). Therefore, the maximum pause was considered not only to reflect the severity of the symptoms necessitating pacemaker implantation in the 9 patients of the SSS group but to have warned us of sudder death in another patient. We concluded that overdrive suppression is useful as a supplementary challenge to determine indications for pacemaker implantation for the sick sinus syndrome, and that prolongation of the maximum pause beyond 5.0 sec is the critical level for pacemaker implantation.

Characteristic findings on the standard 12-lead ECG in patients with the fasciculoventricular Mahaim fiber

Standard 12-lead electrocardiograms with a Q wave in lead V1 were obtained from 32 subjects without organic cardiac disease and analyzed for features that might characterize an abnormal atrioventricular conduction through the fasciculoventricular Mahaim fiber. Following an infusion of ajmaline, the Q wave in V1 vanished abruptly and changed to an rS pattern in the 12 ajmaline responders. Discriminant analysis was performed to distinguish the ajmaline responders from the others. The explanatory variables were number of precordial leads with the abnormal Q wave, existence of the septal q waves, existence of the slurring of the Q wave in V1, existence of clockwise rotation, and existence of high voltage (RV5 + SV1 > 3.5 mV). Three variables, the absence of the septal q waves, the presence of the slurring, and the absence of clockwise rotation, were found to predict a positive response to ajmaline (discriminant probability = 77%). These findings associated with the Q wave in V1 suggest that the fasciculoventricular fiber may be present.

Comparative evaluation of depressed automaticity in sick sinus syndrome by Holter monitoring and overdrive suppression test

To ascertain whether the long cardiac pauses on the Holter ECGs of patients with the sick sinus syndrome were related to the spontaneously occurring overdrive suppression, the heart rates for the 12 seconds preceding the cardiac pauses longer than 5 seconds were compared with that averaged for 24 hours. Even in six out of seven patients with bradycardia-tachycardia syndrome the former rate was not significantly greater than the latter, indicating that episodes of such long cardiac pauses may not result from spontaneously occurring overdrive suppression. This observation was also consistent with the result that no statistically significant correlation was obtained between the maximum pauses measured from Holter ECGs of sick sinus syndrome and those obtained by the overdrive suppression test. In conclusion, many episodes of long life-threatening cardiac pauses observed in sick sinus syndrome may be attributed to accidental depression of the sinus nodal and subsidiary pacemaker activity rather than to spontaneously occurring overdrive suppression; therefore, Holter monitoring may be useful as an additional tool for diagnosis of sick sinus syndrome.

Long-term effects of niceritrol on serum lipoprotein(a) and lipids in patients with high levels of lipoprotein(a)

The long-term effects of niceritrol on lipoprotein(a) (Lp[a]), lipids, apolipoproteins, and fibrinogen and fibrinolytic factors were evaluated in 20 outpatients who had serum Lp(a) levels higher than 20 mg/dL. The mean ( +/- SE) levels of Lp(a) decreased from 33.6 +/- 2.3 mg/dL to 23.5 +/- 3.5 mg/dL after 12 months of niceritrol treatment (P < 0.01). Serum levels of triglycerides and apolipoprotein E decreased significantly and high-density lipoprotein cholesterol (HDL-C) increased significantly after 12 months (P < 0.05). There were no significant changes overall in fibrinogen and fibrinolytic factors, although fibrinogen concentrations showed a tendency to decrease with treatment. PAI-1 levels decreased significantly (P < 0.05) after 6 months of niceritrol treatment. A significant correlation of percent reduction between Lp(a) and apolipoprotein B levels (P < 0.01) was observed, suggesting that the Lp(a)-lowering effects of niceritrol may be due to niceritrol inhibition of apolipoprotein B synthesis, the major apolipoprotein of Lp(a). The ability of niceritrol to decrease Lp(a) levels and increase HDL-C levels, together with its tendency to lower fibrinogen levels, may help prevent coronary events in patients with high levels of Lp(a).

Influence of left ventricular preload reduction by hemodialysis on the Doppler-derived left ventricular filling profile

Hemodialysis caused an average 3.2-liter volume loss, but blood pressure and heart rate did not change significantly. Hemodialysis diminished the left atrial dimension (35±5 to 31±5 mm; p>0.001), indicating that it reduced left ventricular preload. These results indicate that the atrial contribution to ventricular filling was more effective afterwards than before hemodialysis and that under depressed left ventricular diastolic function, the atrial contribution decreased as preload increased further

Evaluation of left atrial rhythm with pulsed Doppler echocardiography.

SummaryTo evaluate the origin of ectopic atrial rhythms, the beginning of atrioventricular inflow due to left and right atrial ejection was estimated using the pulsed Doppler combined with two-dimensional echocardiography. In ten normal controls, the beginning of transtricuspid flow due to atrial ejection preceded that of transmitral by 0 to 40 msec with an average of 22 msec. In contrast, the beginning of right atrial ejection flow lagged behind that of left atrial by 40 to 80 msec in case 1 and by 20 to 50 msec in case 2 of ectopic atrial rhythm. The significant delay of atrioventricular inflow due to right atrial ejection in these two patients strongly suggests that the ectopic atrial rhythm is of left atrial origin. The pulsed Doppler echocardiography is considered to be a useful clinical tool for noninvasive evaluation of the left atrial rhythm.