To elucidate the mechanism of reduced exercise tolerance in the supine position, 14 patients with coronary artery disease were studied by both supine ergometer exercise and upright treadmill exercise. Maximal oxygen consumption in the supine position amounted to 80% of that in the upright position (1110 ± 453 vs 1387 ± 470 ml/min; p < 0.001). Maximal cardiac output was identical in both positions (12.07 ± 4.44 vs 12.55 ± 4.49 l/min; ns). Maximal arteriovenous oxygen difference in the supine position amounted to 83% of that in the upright position (9.22 ± 1.92 vs 11.14 ± 1.88 vol%; p < 0.01). thus, the lower maximal oxygen consumption in the supine position was not caused by the decreased cardiac output but by the impaired augmentation of arteriovenous oxygen difference. Lactate concentration at the same oxygen consumption was higher in the supine position, which means early augmentation of anaerobic metabolism. We concluded that the aerobic capacity in the supine position was significantly lower than that in the upright position in patients with coronary artery disease, and the impaired utilization of transported oxygen was considered to be one of the mechanisms of the decreased aerobic capacity in the supine position.

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To assess the effect of dibutylyl cyclic AMP (DBcAMP) on patients with congestive heart failure (CHF) in comparison with dobutamine and captopril, these three agents were administered to 9 patients with CHF. DBcAMP was infused at a rate of 0.2 mg/kg·min for 30 min, dobutamine was infused at a rate of 8 μg/kg·min and captopril 25 mg was administered orally. Hemodynamic and echocardiographic studies were performed before and after administration of each agent. Systolic arterial pressure (SAP) fell with DBcAMP and captopril but rose with dobutamine. Cardiac output (CO) rose and systemic vascular resistance (SVR) fell with each agent but the magnitude of the change was greater with DBcAMP than with the other two agents. Left ventricular end-systolic dimension decreased and percent fractional shortening increased with all these drugs. Comparing DBcAMP and captopril, although the degree of change in CO was closely correlated with that in SVR by captopril, the degree of increase in CO by DBcAMP was more than that expected from the degree of the decrease of SVR. Comparing DBcAMP and dobutamine, SAP and pressure rate product increased with dobutamine, but the former fell and the latter was not changed by DBcAMP. Arrhythmia was not increased by DBcAMP, though it was markedly increased by dobutamine. In conclusion, the magnitude of positive inotropic and vasodilator effect So DBcAMP is thought to be useful for the treatment of CHF.

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Arrhythmogenic right ventricular dysplasia (ARVD) is a recently identified clinical entity and its diagnosis rests on documentation of ventricular tachycardia (VT) of right ventricular origin and morphologic changes of the right ventricle. However, the diagnosis of ARVD is difficult noninvasively and often requires angiography. The usefulness of equilibrium radionuclide ventriculography as a noninvasive method for the diagnosis of ARVD has not been fully evaluated. We performed equilibrium radionuclide ventriculography in 7 patients with ARVD, 10 normal subjects and 9 patients with dilated cardiomyopathy (DCM). The right ventricular ejection fraction (EF) in patients with ARVD (25 ± 8%, mean ± SD) was lower (p < 0.001) than that in normal subjects (56 ± 7%) but was not significantly different from that in patients with DCM (32 ± 10%). The left ventricular EF in patients with ARVD (57 ± 12%) was lower (p < 0.05) than that in normal subjects (70 ± 7%), but higher (p < 0.001) than that in patients with DCM (27 7%). These findings suggest that ARVD is a specific from of DCM which predominantly affects the right ventricle and that equilibrium radionuclide ventriculography may be a useful noninvasive method for the diagnosis of this disorder. In addition, we present a family in which 3 of 6 siblings were affected by ARVD, suggesting that some genetic factors may be involved in the etiology of this disorder.

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To assess the effect of afterload on the left ventricular pressure (LVP) fall during isovolumic relaxation period (IRP) in man, we examined the peak (-)dP/dt, (-)dP/dt upstroke pattern if IRP, and time constant (T) in 15 patients [normal (N) : 5, valvular heart disease (VHD) : 5, dilated cardiomyopathy (DCM) : 5]. LVP and echocardiographic internal diameter were measured simultaneously at rest and after about 30 mmHg increment of LV peak systolic pressure (PSP) by drip infusion of angiotensin (20 ng/kg/min). After augmentation in afterload, heart rate (HR) increased slightly in VHD. T increased significantly (p < 0.05) in N (from 32 ± 3 to 39 ± 4 ms) and DCM (from 56 ± 18 to 72 ± 12 ms), but not in VHD (from 41 ± 5 to 46 ± 8 ms) probably due to increased HR. LV end-systolic dimension had the same trend as T. Although there was no significant change in peak (-)dP/dt in N (from 1937 ± 385 to 1945 ± 189 mmHg/s), VHD (from 1521 ± 210 to 1730 ± 462 mmHg/s), or DCM (from 814 ± 143 to 814 ± 131 mmHg/s), the (-)dP/dt upstroke pattern during IRP became nonexponential in N and more downward convex in VHD or DCM. Thus, these changes of T and (-)dP/dt upstroke pattern suggest the afterload dependence of LVP fall during IRP in normal and diseased hearts.

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Both the resting thallium-201 imaging and resting gated radionuclide ventriculography were conducted in the left anterior oblique view in 35 patients with isolated disease of the left anterior descending coronary artery (LAD), and the corresponding involved region was compared from two differing perspectives, one measuring regional ventricular function and the other regional myocardial perfusion. In the thallium-201 imaging, the thallium activity in the septal or apical region supplied by the LAD was calculated as an activity ratio between the mean value of the normally perfused lateral region and that of the septal or apical region, and was called relative thallium uptake (%T1 uptake). In the gated radionuclide ventriculographic study, a computer program subdivided the image of the left ventricle into 4 regions. The time-activity and first-derivative curves were computed in the septal and apical regions. Significant positive correlations were present between the %T1 uptake and the ejection fraction or peak ejection rate both in the septal and apical regions, indicating that the regional systolic function diminishes progressively as the perfusion abnormality increases. However, positive but poor and scattering correlations were found between the %T1 uptake and the peak filling rate, and there were no significant correlations between the %T1 uptake and the filling period in these affected regions. Thus, we could suppose that the regional systolic function is closely related to the regional %T1 uptake which probably reflects the amount of the residual viable myocardium, but there is the possibility that the regional diastolic filling function may be not so much related to the amount of the viable myocardium as is systolic function or may be modulated by some factors other than the amount of the regional viable myocardium.

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Impairment of mitochondrial respiration in early myocardial ischemia was studied with special reference to myocellular irreversible injury. The technique used was total ligation of the left anterior descending coronary artery, followed by reconstruction of coronary blood flow, in the dog. State 3 respiratory activity reduced significantly to 76% of that of the non-ischemic myocardium in subendocardial muscle (Endo) as early as 30 min after occlusion, and at 60 min to 84% in the subepicardium (Epi). The activity was not recovered by reperfusion. The activity of complex I of sonicated submitochondrial particles decreased at 30 min to 67% in Endo and at 60 min to 71% in Epi, and was not recovered by reperfusion. Complex II and IV activities were kept in the control level until 60 min of ischemia. DNP-stimulated ATPase activity reduced to 79% in Endo at 15 min and to 70% in Epi at 30 min, but recovered significantly by reperfusion until 30 min of ischemia. Mitochondrial respiratory activity was impaired irreversibly in ischemia for 30 min in Endo and this spread to Epi later. Degradation of complex I is considered to be one of the causes of myocardial irreversibility in early ischemia.

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IN the lung overperfused by dextran 70, it is not known how intravascular blood volume and extravascular water volume increase as a function of pulmonary microvascular pressure. To determine their characteristics, we produced an overperfusion state (high pressure and high blood flow) by infusing dextran 70 (100 ml/kg over 30 min) into 15 anesthetized dogs. Using the thermal and dye dilution technique, we simultaneously estimated the pulmonary blood volume (PBV) and the extravascular lung thermal volume (EVLTV), and correlated mathematically these variables with pulmonary artery end-diastolic pressure (PAEDP). Here, we defined PAEDP as the pulmonary microvascular pressure. From the values determined before, during and after dextran 70 infusion, we obtained the following exponential relations. PBV(ml/kg) = 30{1 - 0.902(e-^{0.021 PAEDP(mmHg)})} EVLTV(ml/kg) = 5.15(e-<0.027 PAEDP(mmHg)>) From these mathematical relations, we conclude that: (1) the pulmonary blood volume increases rapidly at low pressure and slowly at high pressure; and (2) the pulmonary extravascular water volume increases slowly at low pressure and then increases rapidly at high pressure. In addition, this equation indicates that the critical pressure from which the pulmonary extravascular water volume exceeds the upper limit of its normal volume is about 17 mmHg in PAEDP. Infusion of dextran 70 increased plasma macromolecular osmotic pressure from 20.8 0.6 (mean SD) mmHg before infusion to 43.7 1.4 mmHg after infusion. Therefore, dextran 70 does not change the critical microvascular pressure against pulmonary edema.

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The QRS area map, which is obtained by time integration of the QRS potential, is assumed to correlate with the ventricular activation time (VAT) map. Using 16 mongrel dogs, the QRS area map and VAT map from cardiac and body surface were compared during sinus rhythm and left and right ventricular endocardial pacing. The cardiac surface QRS area map resembled the cardiac surface VAT map, and it was considered useful to estimate the excitation sequence. The body surface QRS area map localized the stimulus site more easily during pacing than the body surface VAT map. Therefore, it was considered useful to determine the site at which a ventricular extra-systole occurs. The QRS area map proved to be more reproducible than the VAT map.

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Ischemic and reperfusion injuries to the myocardium were evaluated by measuring cardiac function and the calcium binding capacity of the sarco-plasmic reticulum (SR) and by studying the myocardial protective effect of nicorandil. While undergoing cardiopulmonary bypass, dogs were subjected to 120-min global myocardial ischemia and then to 120-min reperfusion. Group I hearts were arrested with untreated potassium cardioplegic solution; Group II with the same solution containing 2 mg/L and Group III with the same plus 10 mg/L of nicorandil. Group III exhibited better recovery from ischemic and reperfusion injuries than Group I with recovery rates of LV dp/dt max (95.0 ± 28.9% vs 61.1 ± 30.4, p < 0.05) and LV negative dp/dt max (69.0 ± 12.5% vs 46.8 ± 21.7, p < 0.05). The 3 groups showed a marked decrease in the max calcium binding capacity during ischemia compared with the Control Group but exhibited no further decrease after reperfusion. After ischemia and reperfusion, Group III (30.4 ± 9.13 mol Ca/mg protein, 30.0 8.50) demonstrated a significantly higher binding capacity than Group I (17.0 2.41 and 18.3 1.01, p 0.05), while Group II did not. These results suggest that ischemia is more injurious to the calcium binding capacity of SR than reperfusion and that 10 mg/L of nicorandil added to the cardioplegic solution preserves SR function and enhances the recovery of cardiac function.

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Incubation of [³H] inositol-labeled cultured rat aortic vascular smooth muscle cells with angiotensin II caused the dose- and time-dependent formation of inositol mono-, bis- and trisphosphates. Under these conditions, adenosine triphosphate (ATP) stimulated the formation of these inositol phosphates. The maximal reaction velocities obtained by ATP and angiotensin II were roughly the same. The doses of ATP giving half maximal and maximal reaction velocities were about 100 μM and 1 mM, respectively. This action of ATP was mimicked by other nucleotides such as adenosine diphosphate (ADP) and guanosine triphosphate (GTP), but these nucleotides were far less effective than ATP. Adenosine monophosphate (AMP), adenosine, guanosine diphosphate (GDP), guanosine monophosphate (GMP), deoxythymidine trisphosphate (dTTP), and cytosine triphosphate (CTP) were almost ineffective. The formation of inositol phosphates induced by ATP was inhibited partially by pretreatment of the cells with pertussis toxin. This toxin ADP-ribosylated a protein with a molecular mass of about 40, 000. These results indicate that ATP induced the phospholipase C-mediated hydrolysis of phosphoinositides probably via P₂-purinoceptors in rat aortic vascular smooth muscle cells, and suggest that a pertussis toxin-sensitive GTP-binding protein is involved at least partially in the coupling of this receptor to the phospholipase C in this cell type.

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The lumen of the coronary artery after thrombolysis using urokinase was successfully observed in patients with acute myocardial infarction. A white flapping material, resembling a ruptured atherosclerotic plaque, was seen.

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