We investigated the correlation between left ventricular filling pressure and the extent of ischemic or infarcted myocardium in 39 patients with coronary artery disease: 25 with angina pectoris (group A) and 14 with old myocardial infarction but without overt transient myocardial ischemia (group B). Hemodynamic parameters were measured at rest and during exercise. The extent and severity scores of ischemia or infarct were calculated using thallium-201 (²⁰¹Tl) myocardial single-photon emission computed tomography. In group A, the extent and severity scores of ischemia were strongly correlated with pulmonary artery wedge pressure at peak exercise (r=0.71, p<0.001, r=0.62, p<0.01, respectively). In group B, the extent and severity scores of the infarct were significantly correlated with left ventricular ejection fraction (r=-0.81, p<0.001, r=-0.77, p<0.01, respectively), but were not correlated with pulmonary artery wedge pressure. Since no relationship was found between the extent of infarct and left ventricular filling pressure, dynamic exercise appears to elicit a different compensatory mechanisms in nonischemic myocardium for exerciseinduced transient ischemia and in noninfarcted myocardium for old infarction. The compensatory mechanism inpatients with old myocardial infarction may be affected by ventricular remodeling.

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To assess the role of atrial and brain natriuretic peptides (ANP, BNP) in maintaining cardiac performance at rest and during exercise in patients with cardiac dysfunction, we measured plasma levels of ANP and BNP during ²⁰¹Tl dynamic exercise testing in 32 patients with angiographically proven old myocardial infarction (OMI) and 35 normal control subjects (CS). Plasma levels of ANP and BNP at rest were significantly higher in patients with OMI than in CS (AMP, 42.6±19.3 vs 19.4±2.4 pg/ml, p<0.01; BNP, 53.4±32.5 vs 2.8±0.8 pg/ml, p<0.01, respectively). Correlations were found between plasma levels of these peptides and left ventricular ejection fraction (LVEF), cardiac index (CI), pulmonary capillary wedge pressure (PCWP) and left ventricular end-diastolic pressure (LVEDP) in patients with OMI. In addition, a strong positive correlation was found between plasma levels of these peptides and the severity score obtained from ²⁰¹Tl myocardial scintigraphy. During exercise, both ANP and BNP significantly increased in patients with OMI. However, in CS, although ANP increased, BNP remained unchanged. The changes in plasma levels of ANP or BNP from at rest to peak exercise correlated with LVEF, CI, PCWP, LVEDP and the severity score in patients with OMI. These findings indicate that ANP and BNP play an important role in maintaining cardiac performance at rest and during exercise in patients with cardiac dysfunction.

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We studied the causes of exercise-induced ST-segment elevation. Group I consisted of 15 patients with anterior myocardial infarction in the absence of a coronary artery luminal narrowing of 75% or more. Group II consisted of 36 patients with predominantly exertional angina and a luminal narrowing of 90% or more in the left anterior descending coronary artery in the absence of previous myocardial infarction. In group I, exercise-induced ST-segment elevation occurred frequently during treadmill exercise (15/15, 100%). None of the patients showed ²⁰¹Tl redistribution. The standard deviation of the phase in radionuclide ventriculography increased during bicycle exercise. Of group II patients, only those with 99% narrowing and poor collaterals showed exercise-induced ST-segment elevation (13/14, 93%), whereas none of those with complete occlusion or 99% narrowing and good collaterals, or 90% narrowing showed ST-segment elevation. In group II, patients with exercise-induced ST-segment elevation showed lower ²⁰¹Tl uptake during exercise and washout in the territory of the diseased vessel than those without exercise-induced ST-segment elevation. In conclusion, wall motion abnormalities may cause exercise-induced ST-segment elevation independently of myocardial ischemia. In patients with predominantly exertinal angina, exercise-induced ST-segment elevation may be a marker for 99% narrowing with poor collaterals and severe myocardial ischemia.

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Nicorandil is a hybrid of a nitrate and a potassium channel opener, and has a potent vasodilatory effect on coronary arteries. The effects of intracoronary injection of nicorandil on coronary circulation were examined in 12 adult patients with angiographically normal or near-normal left coronary arteries to determine the optimal dose of this agent. The intracoronary injection of nicorandil (up to 1 mg over 1 min) dilated left coronary artery segments in a dose-dependent manner, with no significant effects on systemic hemodynamic parameters. The percent increase in the epicardial coronary artery diameter with 1 mg nicorandil 31±5%, mean±SEM) was not significantly different from that with 0.3 mg sublingual nitroglycerin (39±55%). Coronary sinus venous oxygen saturation increased immediately after the intracoronary injectin of 1mg nicorandil, and then returned to the baseline level within 3 min. Neither arrhythmias nor conduction disturbances were observed. These results indicate that dilatation of the epicardial coronary artery was achieved with intracoronary nicorandil in a dose-dependent manner (up to 1 mg over 1 min) without any adverse effects in man, and the dilatory effect on coronary resistance vessels was of short duration.

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Previous studies have reported that patients with hypertrophic cardiomyopathy (HCM) are prone to sudden death. In this study, we retrospectively assessed the prognosis and any influencing factors in 83 patients (66 male, 17 female) with HCM. Twenty-two patients were obstructive, 40 were non-obstructive, 18 were apical HCM and 3 were unclassified. Four of the 83 cases progressed to left ventricular dilatation and dysfunction during the follow-up period. The mean age was 51.2 years (range 16 to 73) and the mean duration of follow-up was 6.7 years (range 0.3 to 15.1). The 5- and 10-year survival rates were 98% and 89%, respectively. Five patients died; 3 from cardiac events (two sudden deaths and one due to congestive heart failure) and 2 from malignant diseases. The lack of a family history of sudden death and the amplitude of the S wave in lead V₁ (less than 2.0 mV) were associated with a favorable prognosis. None of the patients who were diagnosed before age 50 died, but this observation was not statistically significant. None of the patients with apical HCM died, but the classification of HCM was not significantly associated with the prognosis. None of the patients without medication died and medical treatment did not influence the prognosis. Sex, family history of HCM, the patient's symptoms and physical signs, NYHA classification of cardiovascular disability, thickness of the septum and the posterior wall of the left ventricle, dimension of the left atrium, and the left and right ventricles in echocardiogram, amplitude of the R wave in lead V₅, the depth of the negative T wave and atrial fibrillation did not influence the prognosis.

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OBJECTIVES: We investigated the effect of chronic administration of an angiotensin II type-1 receptor antagonist in the development of heart failure due to volume overload in rats. METHODS: Aortocaval fistula (AVF), a model of volume overloaded heart failure, was induced in rats by our newly developed technique using a simple and rapid 18-gauge needle multipuncture. After 3 weeks of oral administration of an angiotensin II receptor antagonist TCV-116, 1 mg/kg per day, we evaluateeift ventricular dilatation. We also compared the effect of TCV-116 with that of an angiotensin-converting enzyme inhibitor delapril, 1 g/L in drinking water. RESULTS: AVF heart failure produced by our technique exhibited significant increases in the left ventricular end-diastolic pressure (LVEDP)(12±1 vs 4±1 mmHg, p<0.05), right atrial pressure (RAP)(5.0±0.6 vs 1.0±0.4 mmHg, p<0.05), right ventricular systolic pressure (RVSP)(58±6 vs 33±1 mmHg, p<0.05), left ventricular weight (LVW)(3.00±0.13 vs 2.09±0.04 g/kg BW, p<0.05), right ventricular weight (RVW)(0.93±0.05 vs 0.59±0.01 g/kg BW, p<0.05), and left ventricular end-diastolic volume index (LVEDVI) (2.55±0.14 vs 0.80±0.12 ml/kg BW, p<0.05) as compared with these values in shamoperated rats. There were no differences in shunt ratio between untreated and TCV-116- and delapril-treated AVF groups. TCV-116 improved these hemodynamics, as did delapril (TCV-116 vs delapril: LVEDP 8±1 vs 8±1, RAP: 3.8±0.6 vs 2.3±1.4, RASP: 50±2 vs 46±3, LVW: 2.53±0.11 vs 2.52±0.15, RVW: 0.80±0.04 vs 0.77±0.06, LVEDVI: 1.67±0.15 vs 1.70±0.17). CONCLUSION: These results suggest that AVF rats with volume overload produced by a new multipuncture method exhibit both right- and left-side heart failure. Angiotensin II type-1 receptor antagonist as well as angiotensin converting enzyme inhibitor attenuate the development of this type of heart failure in rats.

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This study was designed to assess the changes in left ventricular (LV) diastolic filling and to evaluate the dynamic determinants of LV diastolic filling during coronary reperfusion after acute myocardial ischemia. We examined LV diastolic pressure-volume relations (D-PVRs) using the conductance catheter technique with a high-fidelity micromanometer, and the transmitral flow using transesophageal pulsed Doppler echocardiography in 9 open-chest anesthetized dogs with the pericardium opened. We measured early diastolic peak flow velocity(E), late diastolic peak flow velocity (A), the ratio of peak E to peak A (E/A), operational chamber compliance at the minimum LV pressure [(dV/VdP)nadir], and the time constant of LV relaxation (TC). Acute regional myocardial ischemia was produced by occluding the proximal portion of the left anterior descending coronary artery. Data were acquired at baseline, 10 min after acute myocardial ischemia, and after 15 and 90 min of reperfusion under left atrial pacing at 100 beats/min. During myocardial ischemia, D-PVRs shifted upward and rightward on the same curvilinear relationship compared with that at baseline (LV end-diastolic pressure (LVEDP) from 7.3 to 10.5 mmHg, LVEDV from 25 to 31 ml, both p<0.01), accompanied by a decrease in peak E and E/A (E from 41 to 25 cm/sec, E/A from 1.7 to 1.1, both p<0.01) and a prolongation of TC (from 25.4 to 30.3 msec, p<0.01). After coronary reperfusion, D-PVRs returned to baseline accompanied by an improvement in the peak E and E/A ratio. No significant changes in peak A were observed in any of the stages. There was no correlation between peak E and TC, however, a significant positive correlation was observed between peak E and (dV/VdP)nadir (r=0.76, p<0.01). In conclusion, this study demonstrated that, using pulsed Doppler echocardiography, the improvement of diastolic filling after coronary reperfusion was based mainly on changes in early diastolic filling, and that LV operational chamber compliance at early diastole, rather than a LV relaxation property, might play an important role in determining early diastolic filling during coronary reperfusion.

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