Following the administration of recombinant human erythropoietin (rHuEPO) to 18 patients undergoing hemodialysis. the hematocrit (Ht) increased from 19.7±1.8 to 31.0±2.0%. The incidence of hypertension according to the criteria of WHO was 11.1%. The systolic blood pressure (SBP) increased significantly from 120±21 to 129±26 mmHg (p<0.01) and diastolic blood. pressure (DBP) increased from 67±14 to 73±12mmHg (p<0.05). The cardiac Index (CI) decreased significantly from 4.07±1.13 to 3.56±0.88 L/min/m² (p<0.05). Total peripheral resistance index (TPRI) and blood volume (BV) increased significantly from 1.725±406 to 2.170±643 dynes/sec/cm^-5/m² (p<0.001) and from 78.9±11.2 to 87.8±14.8ml/kg (p<0.005) respectively. Pulse rate (PR) decreased significantly from 73.0±10.7 to 65.9±7.8 beats/min (p<0.01). Patients who developed a blood pressure (BP) elevation of 10% or more for the mean blood pressure (MBP) showed a slight and insignificant decrease in CI from 3.65±1.12 to 3.49±1.06L/min/m². which clearly contrasted to that in another group of patients who showed a reduced increase in MBP and a significant reduction in CI from 4.50±1.03 to 3.63±0.72L/min/m² (p<0.05). Stroke volume index (SVI) was unchanged in both groups but PR decrease significantly in the latter group. A significant increase in TPRI or BV was observed equally in both groups. The change in MBP significantly correlated with that in CI in all cases (r=0.64, p<0.01). The present study indicates that the correction of anemia with rHuEPO is associated with an increase in TPRI in all cases in chronic hemodialysis patients and BP elevation is regulated by the change in CI.

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Indices of left ventricular ejection and diastolic filling were measured by cineventriculography in 11 patients with non-insulin dependent diabetes mellitus without significant coronary stenosis and 11 control subjects without diabetes mellitus. Indices of left ventricular ejection. such as ejection fraction and peak ejection rate, were the same in the two groups. The left ventricular end-diastolic volume index and the rapid filling volume index were significantly smaller. the peak filling rate was lower. the left ventricular end-diastolic pressure was higher and the modulus of left ventricular chamber stiffness was larger in the diabetic patients than in the control subjects. These results indicate that left ventricular chamber stiffness is increased in patients with non-insulin dependent diabetes mellitus.

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The purpose of this study was to evaluate the acute and chronic stability of the atrial screw-in lead. In this study, we used CPI model 4165, 4166, and 4266 porous tip screw-in leads in 32 patients (12 for AAI pacing and 20 for DDD pacing). All of these leads were fixed to the free wall of the right atrium and used as the unipolar type. Acute voltage and current thresholds, lead impedance. P-wave amplitude, and chronic threshold were measured. Early and late complications were also investigated. The average acute stimulation thresholds at 0.6 msec pulse width were 0.82±0.43 V and 1.1±0.6 mA. Mean lead impedance was 627.2±83.1 ohms, and mean P wave amplitude was 3.1±1.1 mV. After an average follow-up period of 32 months (range: 2-72 months), we found the results of the chronic threshold study to be satisfactory. The thresholds were usually below 0.1 msec pulse width with the nominally programmed pacemaker output. Only one patient required a higher output due to an increased threshold. With regard to complications, neither lead dislodgment nor cardiac perforation was observed. In conclusion, acute and chronic thresholds were satisfactory and no serious complications occurred. Therefore the atrial screw-in lead has long-term reliability and stability.

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Forty patients (36 men and 4 women) with life-threatening arrhythmia received an implantable cardioverter defibrillator (ICD). Mean age was 63 years (range. 46 to 80 years). All patients had structural heart disease, with coronary artery disease in 32 patients, idiopathic cardiomyopathy in 7 patients, and hypertensive heart disease in 1 patient. Mean left ventricular ejection fraction was 29±13%. The clinical arrhythmia was out-of-hospital cardiac arrest in 14 patients (35%), symptomatic sustained ventricular tachycardia in 21 patients (53%), and episodes of syncope without documented spontaneous ventricular arrhythmia but ventricular tachycardia that was easily provoked at the time of electrophysiologic testing in 5 patients (13%). Sustained ventricular tachycardia was induced in 37 patients (93%) at basic electrophysiologic testing. The average number of drug failures was 2.9±1.4 per patient. One patient (2.5%) died perioperatively because of intractable ventricular tachycardia and ventricular fibrillation. During a median follow-up period of 5.5 months (range 2-21 months) 2 sudden deaths occurred. No patient had a serious complication during the follow-up period. Ten patients (25%) received antiarrhythmic drugs to suppress spontaneous ventricular tachycardia. Appropriate shock treatment was received by 18 patients (45%), and inappropriate shock treatment was received by 2 patients (5%). Several issues regarding use of the ICD must be considered, but the device seems to be useful, and it is associated with an accept-able rate of complications and good long-term success at the present time.

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Cardiac membranes from 26-, 52- and 104-week-old Wister rats were used to investigate the age-related alterations in the β-adrenergic receptor-adenylyl cyclase system. The densities and affinities of β-adrenoceptors did not change with aging. There were no significant changes in the total amount of stimulator G-protein (G_s), and in G_s activity measured in a reconstitution assay using human platelet membranes. The major isoform of G_sα, however, changed from a 45.000 to 52.000 dalton peptide with aging. The total amount of pertussis toxin substrates (G_i2 and G_o) decreased significantly with aging. This finding was supported by the fact that pertussis toxin-induced potentiation of adenylyl cyclase activity was markedly reduced in the aged group. The activity of catalytic protein assessed by forskolin-stimulated adenylyl cyclase activity was de-creased at 104 weeks. On the other hand, GTP analogue-stimulated adenylyl cyclase activity was significantly potentiated in the same group. These results suggest that the decreased sensitivity to catecholamines observed in aged hearts is mainly due to a dysfunction of catalytic protein, and that decreased G_i activity partially compensates for this catalytic dysfunction.

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One hundred and thirty-four cases of Wolff-Parkinson-White syndrome were studied to evaluate the relative usefulness of electrocardiography (ECG). electrophysiological studies (EPS), body surface mapping (BSM). gated blood-pool phase analysis (nuclear studies), and vectrocardiography (VCG) in the localization of the accessory pathway (ACP). In comparison with the final localization verified by intraoperative studies. 93.4% in 8-region ACP localization (97.7% in 4-region ACP localization) could be correctly localized by ECG using our criteria. 83.9% (86.8%) by EPS. 82.6% (95.8%, ) by BSM. 78.8% (87.7%) by nuclear studies, and 67.3% (78.0%) by VCG. It was concluded that: (a) ACP can be localized preoperatively with considerable accuracy by using our simple ECG criteria. (b) The EPS method has some limitation, especially with respect to 8-region ACP localization. (c) Our observation showed no evidence that BSM. VCG, or nuclear studies were superior to ECG in ACP localization. (d) Among the 5 methods studied. ECG and EPS appear to be the appropriate procedures for preoperative ACP identification.

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A 48-year-old man with severe variant angina refractory to conventional treatment with calcium antagonists and nitrates, or prazosin, or trihexyphenidyl hydrochloride, became symptom free rapidly when treated with denopamine, a adrenergic beta-1 agonist. Denopamine may prove to be an additional therapeutic agent in the management of severe variant angina. Therefore the response to denopamine and the lack of response to prazosin in this patient suggests that not only the adrenergic alpha receptor but also the adrenergic beta-1 receptor plays an important role in the production of coronary spasm, at least in some patients.

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A 44-year-old man with an unruptured aneurysm originating from the right coronary cusp is reported. The patient was asymptomatic and a heart murmur and abnormal electrocardiogram were discovered incidentally. Echocardiography and aortography showed an unruptured aneurysm of the right coronary cusp. Surgical correction was successful using a Dacron patch and aneurysmal wall.

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We present a case of restrictive cardiomyopathy which progressed over a 10 month period. A 69-year-old female was admitted because of acute inferior myocardial infarction; hemodynamically, she was in Forrester subset I. Cardiac catheterization performed 4 weeks post-infarction showed markedly increased left ventricular end-diastolic and pulmonary wedge pressures. Left ventricular ejection fraction was 66% with postero-basal akinesis and minimal mitral regurgitation. The right coronary artery was completely occluded with good collateral circulation from the intact left coronary artery. Doppler echocardiography 4 weeks post-infarction showed pseudo-normalization of the A/E ratio of peak mitral flow velocity in atrial systole (A) to peak mitral flow velocity in early diastole (E). Preload reduction by nitroglycerin increased the A wave. Ten months post-infarction, the patient was re-admitted due to congestive heart failure. The A/E ratio was unchanged, however the A wave no longer increased after the same dose of nitroglycerin. We have hypothesized that dehydration and/or the vigorous use of a nitrate, in the acute phase of myocardial infarction, masked an underlying restrictive cardiomyopathy which progressed in the 10 months post-infarction.

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We experienced a rare case of a patient with acute myocardial infarction. It was rare in that a piece of tissue, probably a remnant valve of the inferior vena cava in the right atrium, was dislodged by the Swan-Ganz catheter during a right heart catheterization study in the chronic phase of the disease. As far as we know, no other such case has been reported. Such remnants are considered to be present in 2 to 3% of the general population. Therefore, it is necessary to determine the presence or absence of a remnant before cardiac catheterization and to modify the procedure. such as by changing the catheter's approach, when a remnant is present.

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We applied transcoronary chemical ablation of the atrioventricular (AV) node to a patient with uncontrollable paroxysmal supraventricular tachycardia (PSVT). Through an angioplasty dilatation catheter. 99%, ethanol at a dose of 1.0ml was selectively infused into the AV nodal artery. Complete AV block with junctional escape rhythm occurred. Two weeks later. the treadmill exercise test was performed according to a modified Bruce protocol. The patient tolerated for 12min. and the heart rate increased to 85 beats/min. His bundle electrocardiogram showed that the AV block resulted from atrio-Hisian block. Neither atrial nor ventricular extrastimulus could induce the tachycardia. It appeared that chemical ablation was a good method for controlling medically resistant PSVT. Elevation of serum creatine kinase was observed when ethanol overflowed during the ablation procedure. Occlusion of branches of the AV artery and mild hypokinesis in the inferobasal wall of the left ventricle were seen.

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Myocardial blood flow (MBF). tissue ATP content. mitochondrial respiratory function and mitochondrial ultrastructure were examined in 62 adult mongrel dogs weighing 6-14kg in which acute myocardial ischemia had been produced under anesthesia. The left anterior descending coronary artery was dissected free for ligation before the first diagonal branch. MBF was measured before coronary ligation and 60 min following ligation. Then, samples of myocardium were taken and subjected to tissue ATP content assay. mitochondrial respiratory function measurement respiratory control index (RCI) and rate of oxygen consumption in state III (QO₂III): and electron microscopic examination. Mitochondrial morphologic injury was evaluated quantitatively according to Schaper's criteria. MBF was significantly correlated with tissue ATP content. mitochondrial respiratory function and mitochondrial ultrastructural change. When MBF was less than 20ml/min/100g. tissue ATP content (1.86±1.21 μmol/g wet weight) and mitochondrial respiratory function (RCI 2.51±0.59) were significantly lower than in the non-ischemic area (ATP 4.52±1.11. RCI 3.82±0.37) and, mitochondrial ultrastructural injury had deteriorated significantly at an MBF below 40 ml/min/100g. In conclusion, our findings show that when MBF is reduced, mitochondrial ultrastructural changes precede the depression in mitochondrial oxidative phosphorylation.

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We investigated the basal levels and responses of cyclic GMP (cGMP) derived from perfused mesenteric arteries to acetylcholine (ACh) and sodium nitroprusside (SNP) in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY) at different ages, in order to evaluate the basal and stimulated release of endothelium-derived relaxing factor (EDRF) from the resistance vessel during the development of hypertension. The mesenteric arteries were removed from 8-, 12- and 20-week-old WKY and SHR, and were perfused with Krebs-Henseleit solution containing 0.2 mM isobutyl methyl xanthine. The effluents from the perfused arteries were corrected before and after infusions of graded doses of ACh or SNP, and the levels of cGMP were measured. The basal levels of cGMP from the msenteric arteries in the 12- and 20-week-old SHR were significantly lower than those in age-matched WKY. A negative correlation was observed between the basal levels of cGMP and the systolic blood pressure in SHR, but not in WKY, among all ages. On the other hand, there were no differences in the responses of cGMP to infusion of ACh between the WKY and SHR at each age. Moreover, the responsiveness of cGMP to in-fusion of SNP in the 12-week-old SHR was much higher than that in age-matched WKY. These data suggest that the basal cGMP formation in the arteries which may reflect the basal release of EDRF is reduced in older SHR and is associated with the development of hypertension, and that the stimulated ralease of EDRF is not associated with the development of hypertension.

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Effects of nicorandil (2-nicotinamidoethyl nitrate), a nitrate derivative with a K⁺ channel-opening action, on endothelin-1 (ET)-induced effects on peripheral blood vessels were studied using a hind-limb perfusion preparation in rats. ET injected into this circuit increased the perfusion pressure for more than 30 min following a transient, initial vasodepression of the perfusion system. The magnitude of both responses was dose-dependent. Pretreatments with nicorandil infused into this preparation significantly attenuated both the initial vasodilation and the sustained vasoconstriction caused by ET. The initial vasodepression caused by ET could be mediated by the release of endothelium-derived relaxing factor (EDRF). The sustained phase would be due to increased intracellular calcium elicited by ET. Nicorandil inhibited both the initial and the sustained phase of the ET-responses, probably by inhibition of intracellular phosphoinositide metabolism in both endothelium and vascular smooth muscle cells.

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In a study of the aortic component of the second heart sound (A2) intensity. using 10 dogs, miniature cardiac accelerometers were attached to the exposed left ventricle (LV) at the apex, and to the surface of proximal aorta, to obtain LV and aortic surface acceleration. Manometer tipped catheters were used to detect aortic systolic pressure and diastolic pressure and time constant of left ventrucular pressure fall "T". Drugs (Nitroprusside. Dobutamine and Methox-amine) altered aortic pressure, LV contraction and LV relaxation. When T was ±35% of control, the aortic systolic pressure and diastolic pressure were good predictors of A2 intensity. When LV relaxation was impaired, increasing T>135% of control, the A2 intensity for any given aortic pressure was reduced. When relaxation was hyperactive, decreasing T<65% of control, A2 intensity was increased. Aortic pressure/T which assessed both aortic pressure and relaxation ability. is a better determinant of A2 intensity than aortic systolic pressure or aortic diastolic pressure alone.

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