Short-term physical training improves ventilatory response to exercise after coronary arterial bypass surgery.

The issue of whether exercise training improves exercise hyperpnea in patients after coronary arterial bypass graft (CABG) surgery has not been fully explored. Effects of short-term physical training on ventilatory response and cardiac output during exercise in patients following coronary arterial bypass grafting surgery is studied. Thirty-four patients underwent exercise training for 2 weeks after the second postoperative week (Ex group); 23 stayed sedentary (Sed group). Ventilatory and cardiac output response during the cardiopulmonary exercise test was measured before and after the training period. The minute ventilation-carbon dioxide output (VE-VCO2) slope decreased from 38.9+/-8.1 to 35.1+/-6.7 (p<0.05) in the Ex group, but failed to decrease in the Sed group (39.7+/-11.1 to 41.5+/-11.4). Cardiac output during exercise at 20W and at peak exercise, and peak oxygen pulse (VO2/HR) increased significantly only in the Ex group after training. There was a correlation between improvement of the VE-VCO2 slope and peak cardiac output during the training interval (r=-0.47) in the Ex group. Short-term physical training after CABG improves ventilatory response to exercise and increases cardiac output during exercise. Improvement of cardiac output is correlated with a decreased value of the VE-VCO2 slope.

Effects of physical training on the recovery of the autonomic nervous activity during exercise after coronary artery bypass grafting: effects of physical training after CABG.

Analysis of heart rate variability (HRV) can identify patients at risk of sudden cardiac death after myocardial infarction. The present study examined the effect of 2 weeks of supervised aerobic exercise training on the recovery of the autonomic nervous activity, exercise capacity, and cardiac output (CO) after coronary artery bypass grafting (CABG). Twenty-eight patients were randomly divided into the training group or the control group and performed exercise tests at 1 week, 3 weeks, 3 months, 6 months and 1 year after CABG. The HRV was measured, and the high-frequency component of HRV was used as an index of parasympathetic nerve activity (PNA); the plasma norepinephrine concentration (NE) was used as an index of sympathetic nervous activity. Cardiac output was also measured. In the training group, peak VO2, peak CO and PNA during exercise had improved at 3 weeks, but there was no improvement in these indices in the control group. NE decreased 1 week after CABG in both groups. These results indicate that physical training soon after CABG improves not only the exercise capacity, but also PNA.

Impaired heart rate response during incremental exercise in patients with acute myocardial infarction and after coronary artery bypass grafting: evaluation of coefficients with Karvonen's formula.

Heart rate (HR) response during exercise in patients with ischemic heart disease was evaluated, and the appropriateness of Karvonen's method for determining rehabilitation exercise target HR was investigated. The study group comprised 24 patients with acute myocardial infarction (AMI) and 37 patients who had undergone coronary artery bypass grafting (CABG). Cardiopulmonary exercise testing (CPX) was performed with a cycle ergometer and changes in HR (deltaHR)/changes in work rate (deltaWR) and interval changes of the coefficient of Karvonen's formula were evaluated. In the AMI group and the CABG group, deltaHR/deltaWR were significantly lower than those of age-matched control subjects (p<0.01). Karvonen's coefficients ranged from 0.37 to 0.54 when calculated from actual peak HR and 0.21 to 0.32 calculated from the predicted peak HR. An impaired HR response was found in patients with AMI and those who had had CABG up to 6 months previously. Because the Karvonen's coefficient values, which ranged from 0.6 to 0.8, were elevated for these patients, and considering the data from the CPX, increased exercise is recommended for such cases.

[Factors affecting exercise capacity after coronary bypass grafting].

In order to determine the contribution of cardiac reserve and the peripheral muscle to exercise capacity in patients after Coronary Artery Bypass Grafting (CABG), 19 patients (18 males, 1 female, mean age 63.3 +/- 7.1 years, mean numbers of grafting 2.5 +/- 0.8) performed exercise tests at 1 week, 3 weeks, and 3 months after CABG. Ventilatory gas was analyzed throughout the testing and anaerobic threshold (AT) and peak oxygen uptake (peak VO2) was determined. During exercise testing, the cardiac index (CI) was measured, and the change in CI during exercise, delta CI = (CI at peak exercise) (CI at rest), was calculated. O2 delivery was derived from the product of CO and the oxygen content of arterial blood at peak exercise. The sectional area of the thigh muscles at the level of 10 cm above the patella was measured using a computed tomography before each test. Average peak VO2 at 1 week after CABG was 867 +/- 171 ml/min and it increased to 1,214 +/- 246 ml/min at 6 months. Average AT did not change from 1 week to 3 weeks, however, it increased significantly from 665 +/- 122 ml/min at 3 weeks to 873 +/- 181 ml/min at 6 months. The muscle area of the thigh increased significantly from 170 +/- 24 cm2 at 3 weeks after CABG to 186 +/- 27 cm2 at 3 months. delta CI showed a tendency to increase from 6.6 +/- 1.2 l/min/m2 at 1 week after CABG to 7.3 +/- 1.3 l/min/m2 at 3 weeks, and also showed a tendency to increase from 3 weeks to 6 months. Peak VO2 and AT correlated to delta CI at 1 weeks and also it correlated significantly to both the muscle area of the thigh and delta CI at 3 weeks, 3 months, and 6 months after CABG. The delta value of peak VO2 from 1 week to 3 weeks showed a significant correlation to those of delta CI and O2 delivery. Moreover, the delta values of peak VO2 and AT from 3 weeks to 3 months showed a correlation to those of delta CI and O2 delivery. These results suggest that both cardiac reserve and peripheral factors contribute to the exercise capacity up to 3 months after CABG, and, in particular, O2 delivery are important to increase exercise capacity.

A case of a pseudomalfunction of a DDD pacemaker.

DDD pacemaker pseudomalfunction occurred in a 65-year-old man. This was due to premature ventricular contraction (PVC) response option and cross-talk detection window, which are designed to protect against pacemaker related tachycardia or cross-talk. Pseudomalfunction disappeared by eliminating PVC response option.

Detection of rotavirus antigen in tracheal aspirates of infants and children with pneumonia.

Clinical manifestations of respiratory tract infection often precede or coincide with rotavirus gastroenteritis in infants and children. To investigate the possible association between respiratory tract manifestations and rotavirus infection, the authors determined human rotavirus (HRV) antigen and respiratory syncytial virus (RSV) antigen in tracheal aspirates of 58 children with clinically diagnosed pneumonia by enzyme-linked immunosorbent assay (ELISA) and immunofluorescent antibody techniques. HRV antigen was detected in 16 out of the 58 cases (27.6%) and RSV antigen was found positive in 27 cases (46.5%). In four cases both HRV and RSV antigens were detected. The results of our study suggest that rotavirus may occasionally by one of the etiologic agents of acute lower respiratory infections of infants and children and that rotavirus infection may be transmitted via respiratory route. However, further extensive studies are needed for confirmation of the association between rotavirus and respiratory tract infection.

Clinical significance of exercise-induced negative U-waves in patients with anterior myocardial infarction.

To elucidate the clinical significance of the exercise-induced negative U-wave (NU) in patients with anterior myocardial infarction, we compared the angiographic and scintigraphic findings in 15 patients with and 20 patients without NU, and obtained the following results: 1) On coronary angiography, all patients in the NU (+) group showed over 90% stenosis or total occlusion of the left anterior descending coronary artery (LAD). In the latter cases moderate to abundant collaterals were visualized on the anterior wall. In contrast, such a tendency was not observed in the NU (-) group. 2) Segments composed of viable myocardium (estimated by preservation of contraction at rest and T1-201 redistribution after exercise) numbered 30 of 45 segments (67%) in the NU (+) group, and 13 of 60 segments (22%) in the NU (-) group. Segments composed of lost myocardium (estimated by loss of contraction at rest and persistent defect in T1-201 uptake) numbered 7 of 45 segments (16%) in the NU (+) group, and 38 of 60 segments (63%) in the NU (-) group. 3) Exercise-induced NU was frequently observed on R-wave preserved leads with ST depression, but was also observed over abnormal Q waves, ST elevation and in isolation in some instances. 4) In 3 patients, preexisting exercise-induced NU was no longer observed and a transient stress-induced T1-201 defect disappeared after successful LAD revascularization. In conclusion, exercise-induced NU on precordial leads in patients with anterior myocardial infarction may be a sign suggesting the presence of jeopardized, but still salvageable, myocardium in the infarcted area.

Radiotherapy in China today.

The treatment of cancer by radiation in China began in the early 1930's. However, up to 1949, its development was very slow. Following Liberation, the growth of this specialty has been extremely rapid, as shown by the kind of modern radiotherapeutic equipment that is available today in many centers of our country. Currently almost every province has a cancer center with a good radiotherapy department and consequently, treatment results have improved over the past years. Due to the large number of patients seen in every radiotherapy department, many types of cancers are treated each day; thus clinical trials can be concluded in a shorter time. The author will show the kind of work that is being achieved in China in general, and Shanghai in particular.

Ischaemia-induced negative U waves in electrocardiograms (an experimental study in canine hearts).

To confirm the clinical impression that negative U waves are a sign of myocardial ischaemia, and to study their possible mechanism, we performed open chest experiments on dogs with the following results. (1) A negative U-wave tended to appear the peripheral rather than the central portion of the cyanotic zone following coronary artery occlusion; (2) it also appeared temporarily at the central ischaemic area after release of coronary artery occlusion; (3) it became apparent or accentuated with augmentation of left ventricular performance at a postextrasystolic beat; and (4) it was eliminated by infusion of K+-free Tyrode solution, but appeared after an infusion of high K+-Tyrode solution into the regional coronary artery. These results indicate that negative U waves are a sign of myocardial ischaemia, which may be related not only to simple myocardial stretching but also to contraction and external high K+ in the ischaemic area.

Handgrip-induced negative U-wave in electrocardiogram of hypertensive subjects.

To study clinical significance and possible mechanism of negative U-wave observed in hypertensive patients, we applied handgrip test (HG) to 35 patients with hypertension and 20 age-matched normal subjects. HG was sustained for 3 min at 50% of maximum voluntary contraction. ECG recording and measurement of blood pressure were made before, during, and after HG. During HG, systolic blood pressure was 188.7 +/- 3.4 mmHg (mean +/- SE) and diastolic blood pressure was 114.8 +/- 2.1 mmHg in hypertensives, while 145.3 +/- 2.6 mmHg and 93.8 +/- 1.1 mmHg in normals; the difference between hypertensives and normals was statistically significant (p less than 0.001). Incidence of HG-induced negative U-wave was 0% in normals, while 68.6% in hypertensives. In hypertensive subjects, HG-induced negative U-wave appeared in 24 of the 28 patients (85.7%) with minimum to moderate left ventricular hypertrophy shown by ECG and/or UCG findings (QRS-T angle greater than 130 degrees with left high voltage: left ventricular wall thickness greater than 12 mm). Further we recorded UCG during HG in 14 subjects. In 4 patients, negative U waves appeared simultaneously with increase in left ventricular dimension during diastole. In the remaining 10 cases that included both normals and hypertensives, however, neither increase in left ventricular end diastolic dimension nor negative U waves were observed. Thus we conclude that HG-induced negative U waves may be caused by stretch of the ventricular wall resulting from acute left ventricular volume overload.

Contribution of vagal tone to initiation and termination of ventricular tachycardia: report of three cases.

The role of vagus nerve in modulating ventricular dysrhythmia has recently been emphasized. We report here on two patients who had ventricular tachycardia (VT) which was terminated and converted to sinus rhythm by either eyeball pressure or a Valsalva maneuver. Moreover, in one of these patients and in a third patient, VT was initiated following administration of vagolytic agents. This supports the view that the parasympathetic nervous system does modulate the electrical activity of the human ventricle.

Effects of K+ and K+-induced polarization on (dV/dt)max, threshold potential, and membrane input resistance in guinea pig and cat ventricular myocardium.

We studied the non-membrane potential-dependent effect of K+ on (dV/dt)max and threshold potential in guinea pig and cat ventricular myocardium. Membrane potential (MP) was changed uniformly in segments (length less than or equal to 1.0 mm) of papillary muscles by applying extracellular polarizing current pulses across a single sucrose gap. Control [K+]o was 5.4 mM and test [K+]o values were 2.0, 10.0, 11.5, 13.0, 16.2, 20, 22, and 24.0 mM. Each muscle was studied under four conditions: (1) control [K+]o and unaltered (control level) resting MP (Em); (2) one of the test [K+]o values and the unaltered (test level) Em; (3) the same test [K+]o and Em held at the control level; (4) control [K+]o and Em held at the test level. At all [K+]o greater than or equal to 11.5 mM, (dV/dt)max showed a decrease significantly (P less than 0.01) greater than the corresponding MP-dependent decrease in both guinea pig and cat myocardium. This non-MP-dependent decrease averaged 7.5% at 11.5 mM, 26.5% at 13.0 mM, 37.2% at 16.2 mM, and 22.7% at 20.0 mM. At [K+]o greater than or equal to 20.0 mM, (dV/dt)max was predominantly slow-channel-dependent; it was increased by hyperpolarization to -110 mV at [K+]o = 20 and 22 mM but not at [K+]o = 24mM. Threshold potential became progressively less negative with increasing [K+]o, but this effect was dependent only on MP. The membrane input resistance (rm) was determined by two opposing factors: at a given [K+]o, rm increased with depolarization; and at a given MP, rm decreased with increasing [K+]o. Our study shows that non-MP-dependent depression of (dV/dt)max in the ventricular myocardium occurs at [K+]o concentrations that may be encountered in vivo.

Maximal rate of the left ventricular pressure fall (peak negative dP/dt) in early stage of myocardial ischemia following experimental coronary occlusion.

Short-term, repeated myocardial ischemia was produced in 20 opened-chest anesthetized dogs by left anterior descending (LAD) branch occlusion. Left ventricular pressure (LVP) and its dP/dt were recorded by Satham SF-1 transducer, and isometric local force (F) was measured by a Walton-Brodie strain gauge arch sewn onto LV free wall. In all experiments, within a few beats after LAD occlusion, peak negative dP/dt started to diminish its amplitude, reaching a nadir after 20-30 sec (63 +/- 5% of control, 9 dogs). It recovered to 83 +/- 3% of control level in 45 sec and remained essentially unchanged thereafter. This change preceded those of LVP and max dP/dt, which showed only minor falls. In 6 dogs, changes by occluding root of LAD were compared with those by its branch occlusion. The greater the extent of ischemia, the more marked and prolonged were the changes. While F in the ischemic center (Fc) rapidly lost its contractile activity following LAD occlusion, F in marginal zone between infarcted and non-infarcted region (Fm) showed variable extent and different time-course of its diminution. Thus, it was concluded that the change in peak negative dP/dt following LAD occlusion was one of the sensitive signs of early ischemic changes, and was attributed at least in part to characteristic changes in contractile activity of myocardium surrounding the ischemic injury.