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The effects of recombinant alpha-human atrial natriuretic peptide (alpha-hANP) infusion an acute left ventricular dysfunction provoked by exercise were examined in 14 men with coronary artery disease. Patients performed symptom-limited, graded exercise on a supine bicycle ergometer. Plasma alpha-hANP and guanosine 3',5'-monophosphate (cyclic GMP) concentrations as well as hemodynamic variables were measured at rest, during and after exercise. In 14 patients whose pulmonary artery wedge pressure was > 20 mm Hg at peak exercise, the same exercise protocol was repeated at 30 minutes after starting intravenous alpha-hANP infusion (0.05 microgram.kg-1.min-1). In 8 of these patients, a Webster thermodilution catheter was advanced into the coronary sinus for measurement of coronary sinus blood flow. From the control exercise test, plasma alpha-hANP concentration increased from 86 +/- 20 pg/ml at rest to 188 +/- 32 pg/ml at peak exercise (p < 0.001), and plasma cyclic GMP concentration increased from 4.8 +/- 1.9 pmol/ml at rest to 7.2 +/- 2.9 pmol/ml at peak exercise (p < 0.001). Both plasma alpha-hANP and cyclic GMP concentrations showed a significant positive correlation with pulmonary artery wedge pressure during control exercise. With alpha-hANP infusion, systolic and diastolic pulmonary artery pressures and pulmonary artery wedge pressure were significantly decreased at all time points during exercise testing. Heart rate was increased and systolic blood pressure was significantly decreased at rest and at 3 minutes of exercise. Diastolic blood pressure, systemic vascular resistance, and pulmonary vascular resistance were significantly decreased at rest.(ABSTRACT TRUNCATED AT 250 WORDS)

We compared cardiohemodynamic response to dynamic exercise in 32 patients with exercise-induced silent or symptomatic myocardial ischemia. All patients had coronary artery disease without prior myocardial infarction and left ventricular hypertrophy. Patients underwent supine leg-exercise testing and received right heart catheterization. All patients exhibited ischemic ST-segment depression on electrocardiogram during exercise testing. They were classified retrospectively into two groups according to the absence (n = 10, group 1) or presence (n = 22, group 2) of chest pain induced by exercise. There was no significant difference between groups in the magnitude of peak ST-segment depression. Pulmonary artery wedge pressure at peak exercise was significantly lower (p < 0.01), and the cardiac index was significantly higher (p < 0.01), in group 1 versus group 2. Our results indicate that exercise-induced left ventricular dysfunction is less severe in patients with silent myocardial ischemia than in those with symptomatic ischemia.

To determine whether the postexercise systolic blood pressure (SBP) response is a useful marker of left ventricular filling abnormalities, supine leg exercise testing was conducted in 14 control subjects and 70 patients with coronary artery disease (CAD). An abnormal postexercise SBP response (the ratio of SBP after 3 min of recovery to the peak exercise SBP) was defined as 0.85 or more, which represented the cutoff point with the highest sensitivity and specificity for prediction of pulmonary artery wedge pressure (PAWP) of at least 20 mmHg at peak exercise in CAD patients. There was a significant difference between the SBP ratios of the two groups (Control, 0.72 +/- 0.05; CAD, 0.86 +/- 0.13; p < 0.01). There was no significant difference between the PAWP of the two groups at rest, but the PAWP at peak exercise was significantly higher in the CAD group (20.2 +/- 8.9 mmHg) than in the control group (11.5 +/- 4.0 mmHg)(p < 0.01). PAWP at peak exercise was > or = 20 mmHg in 35 (50%) of the 70 CAD subjects. The SBP ratio was significantly correlated with PAWP at peak exercise (r = 0.67, p < 0.01) in the CAD group, but not in the control group. An SBP ratio of > or = 0.85 showed a sensitivity of 80% and a specificity of 80% for predicting a peak exercise PAWP of > or = 20 mmHg in CAD patients.(ABSTRACT TRUNCATED AT 250 WORDS)

To evaluate the clinical significance of simple heart rate-adjusted ST segment depression (delta ST/delta HR) in the diagnosis of coronary artery disease, 42 patients with stable exertional angina underwent supine leg exercise testing and cardiac catheterization. During exercise, heart rate, a multilead electrocardiogram, and pulmonary artery wedge pressure were recorded. The sensitivity and accuracy of the delta ST/delta HR criteria (greater than or equal to 3.0 microV/beat/min) were significantly greater than the conventional analysis of ST segment depression criteria (greater than or equal to 0.2 mV) for detecting three-vessel coronary artery disease at a matched specificity of 72% (100% versus 46%, 81% versus 64%, p less than 0.01). A significant linear correlation was found between maximum pulmonary artery wedge pressure increments during exercise (delta PAWP) or Gensini score and the delta ST/delta HR (delta PAWP: r = 0.51, p less than 0.001; Gensini score: r = 0.47, p less than 0.001). There were no statistically significant differences in the delta PAWP or Gensini score between patients with three-vessel disease who had delta ST/delta HR greater than or equal to 3.0 microV/beat/min and those with one- or two-vessel disease who had delta ST/delta HR greater than or equal to 3.0 microV/beat/min (delta PAWP: 18.1 +/- 2.0 versus 21.9 +/- 3.3, p = NS; Gensini score: 68.5 +/- 6.6 versus 66.3 +/- 11.3, p = NS). These findings demonstrate that delta ST/delta HR is more useful than a conventional analysis of ST segment depression for identifying not only anatomically severe coronary artery disease but also functionally severe coronary artery disease.

To define the factors that affect an abnormal postexercise systolic blood pressure (SBP) response and to verify the diagnostic value of that response in patients with coronary artery disease (CAD), we studied 33 normal subjects, eight patients with hypertension who had no CAD, and 42 patients with documented CAD who underwent supine leg exercise testing. SBP recovery ratios were derived by dividing the values obtained 1 and 3 minutes after exercise by the peak value. The upper normal limit of the SBP ratio was defined by two standard deviations from the mean for 33 normal subjects. The specificity of this criterion for identifying patients with CAD was 97% and the sensitivity was 60%. None of the eight patients with hypertension showed an abnormal postexercise SBP response. At peak exercise the pulmonary artery wedge pressure was significantly greater in the patients with CAD having an abnormal response. In multiple regression analysis the exercise pulmonary artery wedge pressure, the exercise SBP, and the systemic vascular resistance after exercise were determining factors for an abnormal SBP response. Three-vessel disease was more common in patients with an abnormal response. Results of this study indicate that an abnormal postexercise SBP response appears to be determined by (1) the extent of exercise-induced impairment of left ventricular function and (2) peripheral vascular tone during recovery. This study also suggests that this criterion can increase the specificity of supine exercise testing in patients with CAD including those with hypertension and might provide a marker for the severity of impaired left ventricular function by exercise in CAD.

To assess the accuracy of the exercise-induced decrease in the ratio of peak flow velocity in atrial systole to that in early diastole (A/E) for predicting an elevation of left ventricular filling pressure, supine bicycle ergometer exercise testing was performed in 27 consecutive patients with coronary artery disease. Doppler-derived transmitral flow velocities were recorded at rest and immediately after exercise. A/E decreased during exercise in 16 patients (group A) and increased in 11 (group B). Pulmonary artery wedge pressure (PAWP) increased notably from 7 mm Hg at rest to 26 mm Hg at peak exercise in group A (p less than 0.001). In contrast, PAWP increased slightly from 6 mm Hg to 10 mm Hg in group B (p less than 0.05). The cardiac index at peak exercise in group A was significantly lower than that in group B (p less than 0.05). These findings suggest that patients with an exercise-induced decrease in A/E might not increase their cardiac output. A significant negative correlation between PAWP and A/E was observed in patients with PAWP over 20 mm Hg (r = -0.74; p less than 0.005). The exercise-induced decrease in A/E showed a sensitivity of 100%, a specificity of 73%, and a predictive accuracy of 85% in detecting patients with PAWP over 20 mm Hg. These findings show that Doppler recordings of transmitral flow velocities during dynamic exercise can provide useful information concerning exercise-induced left ventricular dysfunction associated with markedly elevated filling pressures.

To investigate whether or not myocardial free fatty acid (FFA) uptake is useful for early recognition of exercise-induced myocardial ischemia compared with myocardial lactate uptake, we studied in 8 patients with stable effort angina pectoris by measuring hemodynamic and metabolic parameters during supine multistage bicycle ergometer exercise (BEx). Analysis of FFA composition was performed by high performance liquid chromatography. The exercise endpoint in the control study was moderate chest pain in all cases. In all cases, BEx testing using the same method, duration and workload was repeated 1.5 hours after the oral administration of 6 mg of nilvadipine (a new calcium antagonist). Exercise time of the subjects studied was 463 +/- 40 sec (mean +/- SE, 180-540 sec). After administration of nilvadipine, chest pain was not induced in 6 patients and was lessened in severity in 2 patients. Mean ST segment depression was 0.21 +/- 0.05 mV in the control period and it was significantly reduced to 0.08 +/- 0.03 mV after nilvadipine administration (p less than 0.05). Myocardial FFA uptake decreased from 21.1 +/- 4.4% at rest to 8.1 +/- 2.1% at peak exercise in the control study (p less than 0.05). Myocardial lactate uptake was unchanged at rest and peak exercise in the control study (21.6 +/- 2.7 vs 22.2 +/- 3.3%). After administration of nilvadipine, myocardial FFA uptake did not change during BEx (25.3 +/- 2.7 at rest and 21.3 +/- 3.6% at peak exercise). At peak exercise, myocardial FFA uptake increased significantly after administration of nilvadipine (21.3 +/- 3.6 vs 8.1 +/- 2.1%, p less than 0.05). In FFA composition, the percentage of each of 12 FFA did not change during myocardial passage at rest and peak exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

The risk factors for ischemic heart disease (IHD) in 35 Tibetan highlanders were investigated and compared with those in 30 age- and sex-matched healthy Japanese controls. Although Tibetans had remarkably high hematocrit values, and a decrease of eicosapentaenoic acid in both serum total lipids and serum phospholipid (PL) possibly due to their diet, they were considered to have a low incidence of IHD from our door-to-door study. These positive risk factors are likely counteracted by other negative risk factors as follows; Tibetans rarely exhibited systolic hypertension, and had lower levels of serum cholesterol and serum apolipoprotein (apo) B, and apo B/apo A-I ratio. In addition, Tibetan highlanders showed a decreased level of palmitic acid and an increased level of linoleic acid in serum PL which may protect against atherosclerosis.

Attempts were made to prepare antisera monospecific for Lp(a) lipoprotein and to investigate the distribution of subjects according to plasma levels of Lp(a) in Japanese controls and patients with coronary heart disease or cerebral infarction. Positive plasma reactions to the double diffusion test for Lp(a) (Ouchterlony) were observed in 32.3% of the healthy Japanese subjects, which is similar to results previously reported in western countries. The plasma threshold level of 17 mg/dl was considered an appropriate point for dividing subjects into positive and negative groups depending on reactions to the double diffusion test. When subjects were divided into two groups at 17 mg/dl, a significant association was found between a high plasma level of Lp(a) and either coronary heart disease or cerebral infarction in the distribution of the cortical artery. These results suggest that Lp(a) may play an important part as a risk factor for coronary heart disease and cerebral infarction.

To estimate the accuracy of cardiac output measured by continuous wave Doppler echocardiography from the suprasternal notch and the utility of this method for evaluating left ventricular function during dynamic exercise, simultaneous thermodilution and Doppler cardiac output were measured in 34 patients with coronary artery disease during multistage ergometer exercise in the supine position. Cardiac output was measured at rest and during each stage of exercise. Twenty-five of the 34 patients whose thermodilution curves were adequate for analysis were studied during exercise. The correlation coefficient for the two methods was 0.85 at rest and 0.84 during exercise. Differences between the two methods were not significant at rest but were significant during exercise, with the thermodilution method giving the higher values. Underestimation by the Doppler method is probably due to technical problems and changes in aortic diameter during exercise. The 25 patients were classified into two groups according to pulmonary artery wedge pressure at peak exercise. There were 11 patients in Group 1 pressure (greater than or equal to 20 mm Hg at peak exercise) and 14 in Group 2 pressure (less than 20 mm Hg at peak exercise). There were significant differences in the change in cardiac index and in peak aortic velocity from rest to peak exercise between the two groups. A significant linear correlation between the percent change in peak aortic velocity and in pulmonary artery wedge pressure from rest to peak exercise was observed (r = -0.66, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

This study investigated whether the measurement of plasma free fatty acids (FFAs) could assist in the early detection of exercise-induced myocardial ischemia. Fifteen subjects with effort angina pectoris underwent angina-limited supine bicycle ergometer exercise testing. Myocardial FFA extraction decreased significantly from 22.8 +/- 3.1% at rest to 7.7 +/- 1.5% at peak exercise (p less than 0.05). Myocardial lactate extraction showed no significant change between rest and peak exercise. After control exercise testing, 8 subjects were given a single oral dose of nilvadipine (6 mg) and then again underwent exercise testing for the same duration. Nilvadipine lessened or abolished chest pain and there was less depression of the ST segment at peak exercise. Furthermore, myocardial FFA extraction showed no significant change between rest and peak exercise after nilvadipine administration. These results suggest that myocardial FFA extraction can be used to assess the presence of exercise-induced myocardial ischemia at an earlier stage than myocardial lactate extraction.