Elevated plasma beta-endorphin levels in patients with congestive heart failure.

Recent experimental studies show that the opioid system is important to the pathophysiology of cardiovascular impairment in congestive heart failure. Plasma beta-endorphin levels were measured in 37 patients with congestive heart failure and compared with those of 21 age- and gender-matched normal subjects. The relation of plasma beta-endorphin levels and cardiac function at rest and exercise capacity was assessed in 17 of the patients with dilated cardiomyopathy. Exercise capacity was determined by symptom-limited maximal treadmill exercise with expired gas analysis. Plasma beta-endorphin levels were elevated and correlated with the patients' New York Heart Association functional cardiac status (control: 14.0 +/- 4.4 pg/ml; class II: 17.9 +/- 3.6 pg/ml; class III: 28.3 +/- 8.8 pg/ml; class IV: 46.7 +/- 14.6 pg/ml, mean +/- SD). No relation was found between plasma beta-endorphin levels and left ventricular systolic performance as assessed by M-mode and Doppler echocardiography. Plasma beta-endorphin levels were negatively correlated with cardiac output determined by Doppler echocardiography and positively correlated with systemic vascular resistance (r = -0.733, r = 0.747, respectively, both p less than 0.001), but not correlated with calf blood flow as measured by a plethysmography. A good correlation was found between plasma beta-endorphin levels at rest and exercise capacity. The correlations with peak oxygen consumption, anaerobic threshold, and peak rate-pressure product were r = -0.721, -0.672, and -0.674, respectively (p less than 0.01). The data show that plasma beta-endorphin levels are elevated in patients with congestive heart failure and reflect, to some degree, the severity of the disease.

Paradoxical forearm vasodilatation and haemodynamic improvement during cardiopulmonary baroreceptor unloading in patients with congestive heart failure.

1. To examine the contribution of paradoxical reflex forearm vasodilatation during unloading of cardiopulmonary baroreceptors to systemic haemodynamics, the responses of central and peripheral haemodynamics during lower-body negative pressure were measured in 24 patients with chronic congestive heart failure (New York Heart Association functional class II-IV) and were compared with those of 10 normal subjects. 2. Lower-body negative pressure of less than -20 mmHg caused a significant forearm vasoconstriction in normal subjects but not in patients with congestive heart failure. In the individual cases, however, eight patients (subgroup A) had a significant forearm vasoconstriction, whereas 10 patients (subgroup B) had a paradoxical forearm vasodilatation. The remaining six patients had a blunted forearm vascular response. Baseline pulmonary capillary wedge pressure (26 +/- 3 versus 20 +/- 1 mmHg, means +/- SEM) and left ventricular wall stress in end-diastole (57 +/- 6 versus 37 +/- 4 g/cm2) were significantly (P < 0.05) higher in subgroup B than in subgroup A. 3. During lower-body negative pressure of -20 mmHg, the plasma level of noradrenaline, systemic vascular resistance and cardiac index did not change significantly in subgroup A. In subgroup B, however, during this orthostatic stimulus systemic vascular resistance fell significantly from a baseline value of 2023 +/- 109 to 1740 +/- 110 dyn s-1 cm-5 (P < 0.01) and cardiac index increased significantly from a baseline value of 2.0 +/- 0.1 to 2.5 +/- 0.2 1 min-1 m-2 (P < 0.01) despite there being no significant change in the plasma level of noradrenaline. 4. After treatment, a second bout of lower-body negative pressure was applied to seven patients in subgroup B. The forearm vascular response to the second bout of lower-body negative pressure was normalized. 5. These data suggest that the patients with more severe heart failure show a paradoxical forearm vasodilatation during mild lower-body negative pressure and that this altered cardiopulmonary baroreflex control of the circulation serves to improve the depressed cardiac performance.

[Impaired cardiopulmonary baroreflex control of forearm vascular resistance in hypertrophic cardiomyopathy].

We tested the hypothesis that the cardiopulmonary baroreflex control of forearm vascular resistance is impaired in patients with hypertrophic nonobstructive cardiomyopathy (HNCM). Forearm vascular responses to lower body negative pressures (LBNP) at -20 mmHg and -40 mmHg and to lower body positive pressure (LBPP) at +20 mmHg and +40 mmHg were compared between 11 patients with HNCM and 6 normal subjects. Forearm blood flow was measured with a strain gauge plethysmograph and forearm vascular resistance was calculated by dividing mean blood pressure by forearm blood flow. The left ventricular end-diastolic dimension and the left atrial dimension changed with the increases in LBNP and LBPP in patients with HNCM and in normal subjects. The ranges of these changes were similar in the 2 groups. Mean blood pressure and heart rate did not change during LBNP and LBPP. LBNP increased but LBPP decreased forearm vascular resistance in normal subjects, but neither LBNP nor LBPP changed the resistance in patients with HNCM. Increases in the resistance to cold pressor tests did not differ between the 2 groups. In patients with HNCM, there was a negative correlation between forearm vascular resistance at LBNP -20 mmHg and the left ventricular wall thickness (r = -0.81, p < 0.01). These results suggest that the cardiopulmonary baroreflex control of forearm vascular resistance is impaired in hypertrophic cardiomyopathy and that this impairment may be associated with left ventricular wall thickness.

[Precordial ST segment depression in acute inferior myocardial infarction: the importance of posterolateral wall infarction].

To determine whether precordial ST segment depression during acute inferior myocardial infarction indicates posterolateral wall ischemia, anatomical predominance of coronary circulation was examined by coronary angiography and evaluated in 43 patients who experienced first acute inferior myocardial infarction. Among patients who underwent intracoronary thrombolysis within six hours from the onset of symptoms, the infarct-related artery was the right coronary artery (RCA) in 35. In addition, their early 12-lead electrocardiographic features were compared with those in eight patients having the infarct-related left circumflex coronary artery (group Cx). Thirty-five patients with RCA obstruction were categorized in four groups: Four patients with left predominant type (group L), 10 with balanced type (group B), five with right super-predominant type (group SR), and 16 with right intermediate type (group RI). Seventeen of the 21 patients in groups SR and RI demonstrated precordial ST segment depression, whereas it was present in only six of the 14 patients in groups L and B (p less than 0.05). Of the 29 patients in groups SR, Cx and RI, total ST segment depression in leads V1 through V4 (sigma ST) was greater in the 14 patients in groups L and B (p less than 0.05) than in other groups. Furthermore, in these 29, all patients in groups SR and Cx had greater sigma ST than did the patients in group RI (p less than 0.05). There was no significant difference in sigma ST between groups SR and Cx. Precordial ST segment depression did not correlate with concomitant disease of the left anterior descending artery and was not a mirror image of ST segment elevation in inferior leads. On thallium-201 scintigraphy, additional perfusion defects of the posterolateral wall were present in all eight patients in group Cx and in ten of the 21 patients in groups SR and RI. Thus, precordial ST segment depression during acute inferior myocardial infarction seemed to be affected by the pattern of coronary circulation. It was concluded that this ST depression represents more extensive involvement of the posterolateral wall in patients with right predominant coronary circulation as well as in those with left circumflex artery obstruction.

Correlation between initial potentials on a signal-averaged P-wave and indice of electrophysiologic measurements in the right atrium.

The aim of this study was to determine whether initial potentials of the P-wave on a signal-averaged electrocardiogram (SAE) during sinus rhythm reflect indices of electrophysiologic measurements in the high lateral right atrium. A total of 67 patients underwent P-wave signal averaging during electrophysiologic testing. The correlation between root mean square voltages for the initial 10 and 20 msec of the P-wave on the SAE and indices of electrophysiologic measurements, sinus node recovery time (SRT) and sinoatrial conduction time (SACT), obtained from programmed stimuli, was evaluated. It was found that the initial potentials of the P-wave on the SAE correlated negatively with SRT and SACT (-0.37 < or = r < or = -0.30). It was concluded that the initial potentials correlated with indices of electrophysiologic measurements, although the statistical significance was weak.

[Blood flow patterns in the left ventricle in patients with myocardial infarction and ventricular aneurysm: evaluation using real-time two-dimensional Doppler echocardiography].

To evaluate how the intraventricular blood flow is affected by the size of a left ventricular aneurysm and ventricular dysfunction, systolic left ventricular blood flow patterns were evaluated using two-dimensional Doppler flow images (real-time 2-D Doppler echo). The subjects consisted of 10 normal controls, 35 patients with anteroseptal infarction, two patients with inferior infarction and five patients with anteroseptal-inferior infarctions. The systolic period was divided into three subsets; early, mid- and end-systole. Forty-two patients with myocardial infarction were classified into three groups according to the left ventricular inflow patterns on real-time 2-D Doppler echo using the apical left ventricular long-axis approach; i.e., inflow signals confined to early systole (Group I), visualized up to mid-systole (Group II) and end-systole (Group III). Left ventricular end-diastolic dimension (LVDd), left ventricular end-systolic dimension (LVDs), and % non-contractile circumference (delta L) were calculated by the same echocardiographic approach. Ejection fraction (EF) was calculated by left ventricular cineangiography using the Simpson's method. The left ventricular inflow Doppler signals in the normal controls and Group I turned in the apex and then directed toward the left ventricular outflow tract during late diastole and early systole. Significant differences in EF were observed among the three groups. EF in Group I, II and III was 53 +/- 9%, 41 +/- 8% and 29 +/- 7%, respectively. However, LVDd, LVDs and delta L had the largest values in Group III and the smallest values in Group I. LVDd, LVDs and delta L were smallest in Group I and largest in Group III. In the normal controls, the left ventricular inflow signals proceeded to the apex and directed toward the left ventricular outflow tract in the early systolic period. Various changes in the inflow pattern were observed in patients with myocardial infarction and severe wall motion abnormalities, including delayed timing in proceeding from the apex to the left ventricular outflow tract, stagnant blood at the apex and further inflow of blood toward the apex even during end-systole. The patients with sustained inflow during late systole had hypofunction of the left ventricle as demonstrated by smaller EF and larger LVDd, LVDs, and delta L. In conclusion, the observation of intracardiac blood flows by real-time 2-D Doppler echo is of help in evaluating the severity of myocardial infarction.

[Clinical significance of precordial ST segment depression during acute inferior myocardial infarction].

To investigate the mechanisms and clinical significance of precordial (V1-V4) ST segment depression during acute inferior myocardial infarction, stress thallium-201 scintigrams and coronary angiograms were obtained within four to eight weeks after the onset of myocardial infarction in 37 patients experiencing their first acute inferior myocardial infarction. Among 18 patients with precordial ST depression (group 1), 11 with concomitant disease of the left anterior descending artery (LAD) had positive results on exercise test, whereas in seven patients without LAD lesion, only two had positive exercise test (p less than 0.01). In 19 patients without precordial ST depression (group 2), 11 had severe stenosis in the LAD. However, among these 11 patients, only two had positive exercise tests. Patients with precordial ST depression demonstrated a higher frequency of positive exercise tests than those without it (p less than 0.01). On stress thallium-201 scintigraphy, a perfusion defect involving the inferior wall was present in all patients, but additional anterior wall ischemia was present in only five of the 18 patients in group 1. These five patients had chest pain on exercise tests and a severe stenosis greater than 90% in the LAD. There was no significant difference in the frequency of additional posterolateral wall infarction between groups 1 and 2. In 18 patients in group 1, sigma ST (total degrees of ST segment depression in leads V1, V2, V3, and V4 in the acute stage) was significantly greater in 11 patients with LAD lesion than in seven without (p less than 0.05), and sigma ST greater than five mm was observed in 12 of 13 patients who had additional anterior wall ischemia and posterolateral wall infarction on stress thallium-201 scintigraphy (p less than 0.05). Myocardial revascularization, such as aortocoronary bypass surgery or percutaneous transluminal coronary angioplasty (PTCA), was performed in six of the 18 patients in group 1 in the chronic stage, but in only one of the 19 patients in group 2. Thus, in patients with initial acute inferior myocardial infarction, those with precordial ST depression seemed to be a high-risk group. It was suggested that, during the early stage of myocardial infarction, this abnormality on electrocardiograms is related to the summation of effects of anterior wall ischemia and posterolateral wall infarction. Furthermore, the sigma ST evaluation is useful in differentiating a mirror image of inferior wall infarction from anterior wall ischemia and posterolateral wall infarction as the mechanism of precordial ST depression.

[Cardiopulmonary exercise test in patients with DDD pacemaker: report of two cases with increased exercise capacity by decreased ventricular tracking limit rate setting].

We reported 2 patients with complete A-V block with a DDD pacemaker whose exercise capacity was increased by decreased ventricular tracking limit rate setting (VTL) of their pacemakers. Cardiopulmonary exercise test was used for estimating exercise capacity. Case 1: A 15-year-old girl complained of fainting. Her electrocardiogram (ECG) revealed complete A-V block (atrial rates 100/min, ventricular rates 39/min). After implantation of a DDD pacemaker and the VTL setting at 152/min, her bradycardia disappeared, however, she complained of dyspnea after a few minutes' walk. We performed symptom-limited cardiopulmonary exercise test with a motor-driven treadmill. When the pacing rate reached VTL (152/min), ECG suddenly changed to approximately 2:1 pacing (80/min) and the patient complained of dyspnea. Concomitant rapid increases in VE, VCO2 and RQ suggested that dyspnea was caused by the marked change in pacing rates on VTL. With the lowered VTL (110/min), there was no rapid increase in VE, VCO2 and RQ, and dyspnea subsided when the pacing rate reached VTL. At the same time, the peak VO2 and exercise time were increased by 15% and 8%, respectively. Case 2: A 47-year-old man complained of syncope. His ECG revealed complete A-V block (atrial rates 100/min, ventricular rates 33/min). After a DDD pacemaker implantation (VTL: 150/min), he experienced dyspnea while walking up the stairs in his office. Like in Case 1, when the VTL was lowered from 150/min to 110/min, both the peak VO2 and exercise time were increased by 11%.(ABSTRACT TRUNCATED AT 250 WORDS)