Usefulness of adenosine triphosphate-atropine stress echocardiography for detecting coronary artery stenosis.

There have been few studies on adenosine triphosphate (AT) stress echocardiography. The AT stress test may have fewer adverse effects than the adenosine stress test. The addition of atropine to AT echocardiography may enhance the sensitivity for detection of coronary artery disease (CAD). The purpose of this study was to determine the utility of AT-atropine echocardiography for detection of CAD. The group studied consisted of 112 patients with suspected CAD. Sixty-one patients did not have a history of prior myocardial infarction (group I) and 51 patients did (group II). AT was infused intravenously at 180 microg/kg/min for 14 minutes. Atropine (0.25 mg intravenously, repeated up to maximum total dose of 1 mg) was administered starting after 8 minutes of AT infusion. Ischemic response was defined as new or worsening wall motion abnormality occurring during the infusion. The sensitivity and specificity for detection of CAD were assessed using the representative echocardiograms during single AT infusion and AT-atropine infusion. Sixty-two patients had CAD. Fifty-eight patients (52%) developed minor side effects that resolved promptly. The rate-pressure product (10(3)/mm Hg beats/min) was significantly increased at 12 minutes of infusion (12.4+/-3.2) compared with that at baseline (9.1+/-2.3) and that at 6 minutes of infusion (9.4+/-2.1). The sensitivity for detection of CAD was 45% for AT echocardiography and 74% for AT-atropine echocardiography. The specificity was 94% for AT echocardiography and 90% for AT-atropine echocardiography. The sensitivity and specificity of AT-atropine echocardiography was 78% and 93%, respectively, in group I, and 70% and 86%, respectively, in group II. In conclusion, AT-atropine stress echocardiography seems to be well tolerated, safe, and useful for detection of CAD.

Right ventricular stiffness measured by a new method without volume estimation in coronary artery disease.

This study was designed to measure the right ventricular (RV) stiffness (delta P/ delta V) with a new method without estimating the RV volume itself. RV stiffness has rarely been measured due to the difficulty in estimating the RV volume. Without measuring RV volume itself, stiffness can be determined by measuring its volume change (delta V). Tricuspid filling flow volume, which is the diastolic RV delta V, is measurable by using Doppler echocardiography. Thus, RV stiffness may possibly be obtained from Doppler echocardiography combined with high-fidelity RV pressure. Subjects consisted of 8 controls, 8 patients with angina pectoris, 8 with anterior, 8 with posterior, and 8 with inferior prior myocardial infarction. Tricuspid annular dimension was measured by 2-dimensional echocardiography and the tricuspid annular area was calculated. Velocity-time integral of the tricuspid filling flow during the late diastole was measured by pulsed Doppler echocardiography. Then, the late diastolic RV delta V was obtained as the product of the tricuspid annular area and the integral. The late diastolic RV pressure rise (delta P) was also measured with a micromanometer catheter. The RV elastic chamber stiffness constant ([delta P/ delta V]/P) was obtained by dividing simple stiffness by the mean RV pressure during late diastole. The RV elastic chamber stiffness constant did not significantly differ among controls, patients with angina pectoris, and those with anterior and posterior myocardial infarction (0.0054 +/- 0.0009 vs 0.0057 +/- 0.0018 vs 0.0064 +/- 0.002 vs 0.0052 +/- 0.0019 ml-1). However, it was significantly increased in patients with inferior myocardial infarction (0.010 +/- 0.004 ml-1, p < 0.01 or 0.05) compared with those in the other 4 groups. These results suggest (1) that RV stiffness can be measured with a new method without RV volume estimation, and (2) that this new method is useful in evaluating RV diastolic pathophysiology in patients with coronary artery disease.

Comparison of transthoracic Doppler echocardiography and natriuretic peptides in predicting mean pulmonary capillary wedge pressure in patients with chronic atrial fibrillation.

The purpose of this study was to assess whether transthoracic Doppler echocardiography and serum natriuretic peptide levels could predict mean pulmonary capillary wedge pressure (PCWP) in patients with chronic atrial fibrillation. We examined mitral flow velocity and pulmonary venous flow (PVF) velocity patterns in 32 patients with chronic atrial fibrillation. Plasma A-type and B-type natriuretic peptide (ANP, BNP, respectively) levels in the peripheral vein were measured. Significant correlations were observed between mean PCWP and the following: peak velocity (r = 0.51) and deceleration time (r = -0.65) of the mitral flow; peak velocity (r = 0.64) and deceleration time (r = -0.80) of the PVF; BNP (r = 0.60); and ANP (r = 0.36). Stepwise multiple linear regression analysis selected PVF deceleration time and mitral flow deceleration time as independent predictors of PCWP. A cutoff value of PVF deceleration time of < or =150 ms and a mitral flow deceleration time of < or =100 ms predicted a mean PCWP of > or =18 mm Hg, with a sensitivity of 100% and 80% and a specificity of 96% and 85%, respectively. In conclusion, PVF deceleration time and mitral flow deceleration time obtained from transthoracic Doppler echocardiography are more accurate predictors of mean PCWP than values obtained with natriuretic peptides in patients with chronic atrial fibrillation.

Electromyographic diagnosis of the carpal tunnel syndrome.

Sensory conduction velocities of the median nerve were studied from digit to palm and from palm to wrist in normal subjects and in patients with the carpal tunnel syndrome. Definite slowing was noted in the palm to wrist segment, even in the early carpal tunnel syndrome. It was noted that 37% of normal women over 40 years of age had electrophysiological evidence of the carpal tunnel syndrome.

Motor unit estimation in a muscle supplied by the radial nerve.

The number of motor units in a muscle, the abductor pollicis longus (APL), supplied by the radial nerve was estimated. In 40 APL muscles of control subjects, the mean number of motor units was found to be 421 +/- 99 (SD). Ten patients underwent conventional EMG examination to confirm the clinical suspicion of denervation in radial nerve territory. All presented a significant reduction in the number of motor units in the APL muscle. These results show that this method is useful in the evaluation of muscles supplied by the radial nerve.

Incidence, severity, and time-course of motoneurone dysfunction in myotonic dystrophy: their significance for an understanding of anticipation.

The numbers of functioning motor units and the amplitudes of the maximum evoked muscle responses have been measured in 198 muscles of 102 patients with myotonic dystrophy. Losses of units could be demonstrated in most of the extensor digitorum brevis and thenar muscles but less commonly in the hypothenar groups. A more proximal limb muscle, the soleus, was also shown to be involved frequently. Investigation of two premature infants withmyotonic dystrophy also revealed reductions of functiong units; in one infant clinical improvement was associated with increased muscle innervation. Repeated examinations of 10 adult patients disclosed an abnormal decline in neuromuscular function below the age of 60 years. The reduction in functioning units amounted to approximately 3% of the mean control value per annum. Analysis of 19 families showed that the severity of neuromuscular involvement was nearly always greater in members of later generations. If the predicted deterioration was also taken into account, the results strongly suggested that anticipation was a true genetic phenomenon rather than an artefact of selection. The combined results are considered to strengthen the concept of motoneurone dysfunction as the major pathogenetic factor in this form of dystrophy.

An autopsy case of multiple leucoencephalitis showing hemiatrophy of the brain.

A 39-year-old female died 25 years after the onset of epileptic seizure. In the clinical course, she suffered epileptic seizures, left hemiparesis and muscular atrophy of the left upper extremity, psychological character change, dementia, forced laughter and hallucinatory and delusional states. Pathologically, severe changes were found in the right hemisphere consisting of lesions of white matter with myelin loss, especially in the frontal, temporal and occipital lobes. Gliosis was diffusely observed in the white matter excepting areas with severe changes. In some parts of the cortex, the cytoarchitecture was destroyed and in this area, blood vessels numerously increased. In the left occipital white matter, perivascular infiltration mainly consisting of lymphocytes was observed with numerous fat granule cells and gemystocytic astrocytes around them. The present case may belong to the category of multiple leucoencephalitis, however, it had many characteristic features, such as a long clinical course (25 years) and pathologically revealed hemiatrophy of the brain.

[Clinical study of spinal cord compression due to metastatic epidural tumors].

Eleven patients with spinal cord compression due to metastatic epidural tumors were analyzed. Primary tumors were Hodgkin's disease, non-Hodgkin's lymphoma, multiple myeloma (two patients each), cervical cancer, malignant melanoma, gastric cancer, lung cancer, and neuroblastoma (one patient each). It was felt that myelography is the most important diagnostic test, although CT scan and bone scan may give further diagnostic information in some patients. Six patients were treated with decompressive laminectomy and postoperative radiotherapy, and five with radiotherapy alone. Regardless of the pretreatment neurological status and the type of treatment given, the functional prognosis in our small series of patients appeared to be favorable for radiosensitive tumors such as malignant lymphoma and multiple myeloma.

Transesophageal Doppler echocardiographic assessment of systolic and diastolic coronary blood flow velocities at baseline and during adenosine triphosphate-induced coronary vasodilation in chronic aortic regurgitation.

Few reports exist on the changes in systolic and diastolic coronary flow velocities (CFVs) at baseline and during coronary vasodilation in patients with chronic aortic regurgitation (AR). We examined the left anterior descending CFVs in 21 patients with AR (11 patients with mild AR and 10 patients with moderate to severe AR), 9 patients without AR (no AR group), and 6 patients who had undergone surgery for moderate to severe AR (postoperation group) with transesophageal Doppler echocardiography. Adenosine triphosphate (ATP) was infused into a peripheral right arm vein at four different doses (35, 70, 100, and 140 micrograms/kg/min). Coronary flow velocity response in systole and diastole was calculated as the ratio of systolic peak and mean and diastolic peak and mean CFVs during maximal ATP infusion to those at baseline. The systolic peak and mean CFVs and the diastolic peak and mean CFVs at baseline were significantly increased in the moderate to severe group compared with those in the other groups (p < 0.05, respectively). Systolic and diastolic CFVs were significantly increased during ATP infusions in the four groups. No significant differences of systolic and diastolic CFVs were observed among the four groups during maximal ATP infusion. The coronary flow velocity response calculated from the peak and mean diastolic CFVs were significantly decreased in the moderate to severe group (1.6 +/- 0.3 and 1.7 +/- 0.4) compared with those in the other three groups (3.6 +/- 0.7 and 3.2 +/- 1.1 in the no AR group, 2.6 +/- 0.6 and 2.5 +/- 0.4 in the mild group, and 2.5 +/- 0.7 and 2.4 +/- 0.6 in the postoperation group) (p < 0.05, respectively). In conclusion, the systolic and diastolic left CFVs at baseline appeared to be significantly increased in patients with moderate to severe chronic AR. However, the velocities during coronary vasodilation by ATP were equal to those in other groups, resulting in a decrease of coronary flow velocity response in systole and diastole.

Influence of left ventricular filling profile during preceding control beats on the occurrence of pulse deficit caused by ventricular premature contractions.

This study was designed to investigate whether the left ventricular filling profile during preceding control beats significantly affects the pulse deficit caused by ventricular premature contractions (VPCs). The study group consisted of 18 patients (10 men, eight women, 15-85 years old) who underwent electrophysiological catheterization because of sinus bradycardia. Using a temporary pacing lead inserted in the right ventricular apex, isolated VPCs with various coupling intervals were produced by electrical stimulation of the right ventricle. During the production of the VPCs, the mitral filling flow velocity using pulsed wave Doppler echocardiography, the femoral arterial pressure curve and the electrocardiogram were simultaneously recorded. The right ventricle was stimulated 800, 750, 700, 650, 600, 550, 500, 450 and 400 ms after the triggered control beat QRS complex. Pulse pressures during VPCs gradually decreased in relation to the shortening of the extrasystolic beat coupling interval. The longest coupling interval for each subject, which caused complete abolition of the pressure pulse during the VPC, was defined as the pulse deficit coupling interval. The early to late diastolic velocity-time integral ratio (Ei/Ai ratio) of the mitral filling flow velocity during the control beats which precede the VPC was obtained as an index expressing the left ventricular filling profile. The Ei/Ai ratio of the mitral filling flow velocity ranged from 0.7 to 4.5 (1.8 +/- 1.0). The pulse deficit coupling interval ranged from 440 to 640 ms (510 +/- 60 ms).(ABSTRACT TRUNCATED AT 250 WORDS)

Transesophageal Doppler echocardiographic assessment of left coronary blood flow velocity in chronic aortic regurgitation.

Assessment of systolic and diastolic coronary blood flow velocities (FVs) in patients with aortic regurgitation (AR) has remained a clinical challenge. We recorded left anterior descending coronary blood FV in 21 patients with chronic AR an in 6 control subjects using transesophageal pulsed Doppler echocardiography. In 7 patients FV was measured 4.0 +/- 5.2 months after aortic valve replacement. Peak and mean FVs during systole and diastole and systolic/diastolic ratios of these FVs were determined. Left ventricular (LV) mass index was calculated by means of standard M-mode echocardiography. In patients with severe AR, peak and mean systolic FVs were significantly increased (34 +/- 8 cm/sec and 21 +/- 6 cm/sec, respectively) compared with FVs in the control group (15 +/- 4 and 12 +/- 3 cm/sec, respectively) and in patients with mild AR (17 +/- 3 cm/sec and 13 +/- 2 cm/sec, respectively). Peak and mean systolic FVs were also significantly increased in severe AR (54 +/- 13 cm/sec and 33 +/- 9 cm/sec, respectively) compared with FVs in the control (30 +/- 8 cm/sec and 21 +/- 5 cm/sec, respectively) and mild AR groups (30 +/- 5 cm/sec and 21 +/- 4 cm/sec, respectively). Peak systolic and diastolic FVs were correlated significantly with LV mass index (r = 0.72 and r = 0.73, respectively). Systolic and diastolic FVs and LV mass index were significantly decreased, normalized or both after aortic valve surgery. In conclusion, LV mass seems to have an effect on the significantly increased systolic and diastolic left coronary blood FV pattern in patients with chronic, severe AR. Increased systolic and diastolic FV appears to be normalized in the late period after surgery.