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A 47-year-old man with Degos' disease was examined by echocardiography, which showed hypokinesis of the apical left ventricular wall with pericardial effusion. To evaluate the myocardial perfusion and coronary flow reserve, 201Tl scintigraphy and intracoronary Doppler flowmetry were performed. The coronary flow reserve was not decreased nor was there angiographical coronary stenosis, although a pressure study revealed constrictive dysfunction of both ventricles. The constrictive pericarditis might have been induced by pericardial vasculitis, thereby causing the left ventricular wall motion abnormality.

Although myocarditis from a series of autopsies of patients with systemic lupus erythematosus was frequently observed, the incidence of clinically apparent myocardial dysfunction was low. A 30-year-old woman with systemic lupus erythematosus was examined by echocardiography. An acoustic densitometry was followed at the left ventricular posterior wall throughout the clinical course. A decrease in the magnitude of cyclic variation of integrated backscatter (IB) was observed before treatment. Following the combined treatment, steroid and cyclophosphamide, a repeated ultrasonic tissue characterization showed an increase in the magnitude of cyclic variation of IB. It is thought that ultrasonic tissue characterization may be a useful method to evaluate the impairment of contraction, and to follow up the clinical course of myocardial involvement in systemic lupus erythematosus.

This report presents a case of multiple myeloma with a mass lesion on the pericardium and pericardial effusion. The response to intrapericardial combination chemotherapy (cisplatin and betamethasone) was evaluated by repeated transesophageal echocardiograms. Following the treatment, complete resolution of the tumor and effusion were observed for 6 months after which the patient died of bacterial pneumonia. Intrapericardial combination chemotherapy can be an effective treatment for myelomatous involvement of the pericardium.

Aortic damage during the prediabetic stage of diabetes mellitus (DM) was investigated in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, as an animal model of type II DM. In 30 OLETF and 30 nonDM rats, an oral glucose tolerance test was performed at 10, 20 and 30 weeks of age. At 15 and 30 weeks, intravascular ultrasound images and aortic pressure were recorded and the stiffness parameter beta was calculated. The aortic walls were excised at 5, 15 and 30 weeks for histopathology and the measurement of hydroxyproline. At 10 weeks, blood glucose (mg/dl) and insulin concentrations (ng/ml) of the OLETF rats (2h; 168+/-30 and 0.82+/-0.15) were significantly high (nonDM: 118+/-15; p = 0.02 and 0.16+/-0.64; p = 0.003). At the prediabetic stage (15 weeks), beta in the OLETF rats (2.5+/-0.9) was larger than in nonDM rats (1.4+/-0.4; p = 0.0006), and the collagen (hydroxyproline) content/dry weight (mg/g) of the aortic wall was significantly higher in OLETF (33.5+/-3.1) than in nonDM rats (28.7+/-3.5; p<.05). Histopathological examination showed that from 15 weeks of age the medial wall thickness increased gradually. In the prediabetic stage, collagen accumulation may contribute to impairment of aortic wall stiffness in the OLETF rats, which would accelerate the aging process in the aortic wall.

Although the enhancement of tissue plasminogen activator (tPA) induced thrombolysis by ultrasound has been reported to be augmented by ultrasound contrast agents (UCA), few data exist regarding its process. The present study evaluated the effect of a galactose based UCA on the efficacy of ultrasonic enhancement of tPA thrombolysis and observed the serial changes in the acoustic property and histopathology. A catheter-type transducer capable of ultrasound emission in both continuous (CW) and pulsed wave (PW) was used. The tPA thrombolysis was studied in 30 artificial white thrombi, which were assigned to 4 study groups based on insonation modes and with and without UCA. Each sample was suspended in 100ml saline in a beaker. Five minutes after tPA (8000U) administration, ultrasound was applied for 10min. For the UCA-treated groups, UCA (0.25g) was added 5 min after the start of ultrasound exposure. The alteration of the thrombus was monitored with echography. Weight reduction of the thrombus was -25+/-6% in PW and -30+/-7% in CW, which was significantly enhanced by UCA treatment, 40+/-3% (p<0.005) in PW+UCA and -43+/-7% (p<0.005) in CW+UCA. The area of thrombus echo image minimally decreased with ultrasound alone (-12+/-6%: PW, -23+/-11%: CW). In the UCA groups, UCA induced a remarkable reduction of size (-36+/-3%: PW+UCA, -43+/-7%: CW+UCA) with a high-echo intensity in the superficial layer of the thrombus, where multiple cavity formation was observed by light microscope. UCA markedly enhanced the effect of ultrasound on tPA thrombolysis. The altered acoustic property and corresponding histological microcavity formation in the shallow layer within the thrombus suggests that UCA augmented infiltration of tPA into the thrombus.

A 47-year-old woman with a left-sided Kent bundle showed marked reduction of the ventriculoatrial conduction time during extrastimuli at the right ventricular apex and outflow tract. The degree of reduction was greater than 6 years ago. A 'supernormal conduction' in the ventricle and the Kent bundle could have been responsible for this phenomenon.

Cell-mediated immunity has been implicated in the pathogenesis of vascular cell injury in patients with atherosclerotic aortic aneurysms. To clarify the immunologic mechanisms involved, we examined the expression of a cytolytic factor, perforin, in infiltrating cells from aortic tissue samples taken from 6 patients with atherosclerotic aortic aneurysms. Immunohistochemical studies showed that the infiltrating cells consisted mainly of macrophages, natural killer (NK) cells, cytotoxic T lymphocytes (CTLs), and T helper cells, and that perforin was expressed in NK cells and CTLs. Immunoelectron microscopic studies demonstrated that the infiltrating cells released massive amounts of perforin directly on to the surface of arterial vascular cells. These findings provide the first direct evidence that some of the infiltrating cells in the aortic tissue consist of killer cells, and strongly suggest that these killer cells, especially NK cells and CTLs, may play a critical role in the vascular cell injury caused by atherosclerotic aortic aneurysm by releasing perforin.

A 52-year-old man with inflammatory disease of unknown origin but no specific laboratory abnormalities was referred to our hospital. He has subsequently diagnosed as having adult Still's disease. During an episode of severe inflammation he suffered reversible myocardial damage as revealed by electrocardiography, echocardiography and 201Tl myocardial scintigraphy; this was ameliorated by treatment with steroids and immunosuppressive drugs. No significant stenosis of the coronary artery was observed on coronary angiography. Interstitial mononuclear infiltration was apparent in the right ventricle on endomyocardial biopsy. Myocardial injury with adult Still's disease, which may result in heart failure, has rarely been reported. We report a case of adult Still's disease with myocardial dysfunction that may have been caused by microangiopathy.

Coronary angiographic and risk factor (RF) characteristics were analyzed in 133 Japanese patients with ischemic heart disease (IHD) who were less than 40 years old and who had undergone coronary angiography (CAG) during the past 10 years at six university hospitals in the Tokyo area. We compared the coronary angiographic characteristics of the subject group with those of 216 controls with coronary sclerosis detected by CAG who were more than 40 years old (older control group) and the RF characteristics with those of 133 sex- and age-matched volunteers (younger control group). Sixty seven percent of the subjects (89 cases) were diagnosed as having myocardial infarction (MI) and 33% (44 cases) had angina pectoris (AP). Coronary artery disorders in this group consisted of 103 (77%) cases of coronary sclerosis, 20 (15%) cases of coronary spasm and 10 (8%) cases of miscellaneous diseases, eg, possible vasculitis with connective tissue disease, congenital anomalies, etc. The incidences of significant (> or = 75%) sclerotic narrowing in 0 vessels (31%) and 1 vessel (49%) in the subject group were significantly (p < 0.01) higher than those in the older control group, while the incidence of multivessel disease was significantly (p < 0.05) less in the subject group than in the older control group. The incidences of the following coronary risk factors were significantly (p < 0.05) higher in the subjects than in the younger controls: smoking (83% vs 35%), hypercholesteremia (44% vs 10%), obesity (31% vs 9%), hypertension (29% vs 3%), familial IHD (28% vs 7%) and diabetes mellitus (19% vs 2%). Thus, zero- or single-vessel disease predominated in the younger subject group and the prevalence of coronary risk factors was significantly higher in the subject.

A 35-year-old woman was hospitalized due to frequent attacks of syncope immediately after the ringing of a bell or alarm clock. Her standard electrocardiograms showed a long QT interval (QTc = 0.56 s) with a bizarre T-wave inversion in precordial leads. After admission, a total of 9 events of syncope were observed. Malignant ventricular tachyarrhythmia (torsade de pointes, ventricular flutter or fibrillation) was recorded during each episode, and DC shock was required to abolish such tachyarrhythmias on 3 occasions. On monitored electrocardiograms, an additional 8 events of ventricular tachycardia without syncope were also detected. Auditory stimuli appeared to be involved in the initiation of malignant ventricular arrhythmia. Immediately after auditory stimuli, changes in the QT interval and T-wave morphology resulted in ventricular premature beats, leading to ventricular tachycardia. The episodes of syncope or malignant ventricular arrhythmia were frequently observed early in the morning and near midnight. She had been treated with various types of antiarrhythmic agents, and propranolol was the most effective in preventing ventricular arrhythmia. These findings indicate that auditory stimuli may cause ventricular arrhythmia and subsequent cardiac syncope, or even sudden cardiac death, in some patients with long QT syndrome.

Using a high-frequency ultrasound intravascular imaging system we evaluated the intravascular echo image by comparing it with histological findings in 57 arterial segments of 17 autopsy cases. Moreover, in 8 dogs we estimated the arterial elastic property by observing the change of the arterial section accompanying a reduction of arterial pressure due to hemorrhage (H) or nifedipine infusion (N). The characteristics of the intravascular echograms were as follows: 1) In a normal artery the arterial wall consisted of the inner high echoic, the medial low echoic and the outer high echoic layers. 2) In an aged artery the fibrous thickened intima was seen as the low echo layer giving an echo about the same as that of the normal media, and the intensity of the echo from the degenerated media was lower than that of the normal media. 3) In atheroma the echo intensity of the elastic fiber-rich region was higher than that of the surrounding region, while the calcified region showed as a brighter echo with outer echo free space due to shadowing. We measured the arterial radius, area and circumferential length on the intravascular echo image and calculated the arterial wall tension-circumferential length and the pressure-arterial area relationships. By analysing each relation, we obtained the stiffness and compliance parameters, respectively. The stiffness parameter with N was lower than that with H [(1.5 +/- 0.5) x 10(-2) vs (2.8 +/- 0.9) x 10(-2)] and the compliance parameter with N was higher than that with H (0.92 +/- 0.28 vs. 0.46 +/- 0.12).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute left main coronary artery (LMCA) occlusion is rare and typically fatal. According to the recent literature, only three cases have been reported surviving emergent coronary artery bypass grafting (CABG) for acute myocardial infarction (AMI) caused by total LMCA occlusion. We report the case of a 52-year-old man presenting with total occlusion of the LMCA associated with acute anterolateral myocardial infarction and cardiogenic shock. The patient's dominant right coronary artery did not supply the collaterals to the left coronary system. After ineffective thrombolysis the patient underwent successful emergent CABG for the management of uncontrollable cardiogenic shock. Emergent CABG, though controversial, appears to be a feasible approach for patients with AMI in life-threatening situations, when other attempts at reperfusion have been unsuccessful.

1) Captopril was orally administered in a dose of 12.5 mg to 12 patients with congestive heart failure to follow changes in its blood concentration and determine changes in clinical test values. 2) The blood concentration of captopril reached its peak in 2 h after medication, the mean value being 274 ng/ml and the half-life 3.16 h. The Tmax and T1/2 were found to be extended as compared with those of normal humans and hypertensive patients that had been reported. No significant differences were noted between Group I of mild cases and Group II of serious cases. 3) Following administration of captopril, a rise in angiotensin I and renin activity and a reduction in aldosterone were noted. These were found to be correlated or inversely correlated with the changes in the blood concentration of captopril. Greater changes were noted in Group II than in Group I. All clinical test values in each group tended to return to the control value 6h after the administration.

Doppler echocardiography has become a very useful and widely employed imaging technique for evaluating valvular regurgitation, and has thus lead to the discovery of regurgitation in unexpected subjects. In this study, we examined left-sided valvular regurgitation in 31 healthy subjects, 35 patients with hypertension and 43 patients with old myocardial infarction by Doppler echocardiography. Aortic regurgitation was found in 3% of healthy subjects, 8% of hypertensive patients and 5% of patients with myocardial infarction. Mitral regurgitation was found in 35% of healthy subjects, 69% of hypertensive patients and 84% of patients with myocardial infarction. The pathogenesis of mitral regurgitation in hypertension is considered to be the impairment of the mitral leaflets, since neither anatomical nor functional abnormalities were found in the subvalvular mitral apparatus. Left ventricular dilatation and asynergy near the papillary muscles were related to the pathogenesis of mitral regurgitation in myocardial infarction. Mitral regurgitation in healthy subjects and hypertensive patients was mild and resistant to afterload stress, suggesting that it was less pathological. On the other hand, mitral regurgitation in myocardial infarction was easily worsened by afterload stress. Doppler echocardiography has thus provided us with new insights into valvular regurgitation in healthy subjects and patients without rheumatic valvular disease.

Regurgitant flows in valvular diseases were evaluated by a pulsed Doppler flowmeter combined with an electronic beam sector scanning echocardiograph. The apparatus which was newly developed by us allowed the simultaneous demonstration of a sample site on a two-dimensional echocardiogram with flow measurement. Doppler signals of regurgitant flow were recorded as uni-directional or bi-directional wide frequency band signals. The locations, where regurgitant flow signals were detected, were depicted on the corresponding two-dimensional echocardiogram. This procedure was referred to as "a flow mapping technique" for non-invasive visualization of the distribution of regurgitant flow. In 12 patients with mitral regurgitation due to mitral valve prolapse detected by the pulsed Doppler technique, the regurgitant flow was distributed to the opposite side of the prolapsing mitral leaflet. The transmission of the regurgitant murmur was well consistent with the direction of the regurgitant flow. In 14 patients with aortic regurgitation, the distribution of aortic regurgitant flow visualized by the flow mapping technique closely coincided with that obtained by cineaortography. Based on the distribution of the regurgitation, the severity of the regurgitation could be precisely evaluated by the Doppler technique. Regurgitant flow signals were detected in the right atrium in all 13 patients with tricuspid regurgitation diagnosed by right ventriculography. We found 4 patients who did not show Carvallo's sign but in whom were detected regurgitant flow signals by the Doppler technique. In all of them, tricuspid regurgitation was proven at surgery. These results indicate that the Doppler technique presented here has an obvious clinical advantage in detecting and evaluating regurgitant flow in valvular diseases.

Plasma volume (PV) and extracellular fluid volume (ECF) were determined in 7 patients with essential hypertension (controls) and in 10 patients with primary aldosteronism, while on a high Na diet (342 mEq/day) and on a low Na diet (12 mEq/day). The volume studies were repeated in 6 of the primary aldosteronism patients during treatment with spironolactone for over 3 months. Plasma renin activity (PRA), plasma aldosterone concentration (PAC), cortisol concentration, and serum Na and K concentrations were measured in all patients while on a Na-restricted diet (85 mEq/day) as well as on high-Na and low-Na diets. There were no significant changes in arterial pressure during different Na diets in any groups of patients with essential hypertension, or primary aldosteronism with and without spironolactone therapy. Spironolactone treatment normalized the arterial pressure in patients with primary aldosteronism at all Na intakes. These patients had greater values for PV and ECF than did those with essential hypertension. Spironolactone treatment reduced PV during the low-Na diet, but did not alter it during the high-Na diet. Spironolactone did not produce significant changes in ECF during either the high-Na or low-Na diets. Although there were no changes in PV and ECF in patients with primary aldosteronism due to changes in Na intake, both PV and ECF were significantly less in these patients during spironolactone treatment and in patients with essential hypertension during low-Na intake than during high-Na intake. With primary aldosteronism, PRA was depressed and PAC was elevated when compared to essential hypertension, these were not altered by different Na diets in the patients with primary aldosteronism as they were in those with essential hypertension. During treatment with spironolactone the PRA was restored to normal and showed normal changes with variations in dietary Na, but PAC remained elevated during spironolactone. Plasma cortisol was the same among those with essential hypertension and patients with untreated and spironolactone-treated primary aldosteronism. Serum K was less in untreated primary aldosteronism during all Na diets than in essential hypertension, but during spironolactone it was restored to normal. These results suggest that in primary aldosteronism the reduction in arterial pressure by spironolactone treatment does not occur simply by reductions in body fluid volumes. The long-term treatment of patients with primary aldosteronism with spironolactone does not inhibit the production of aldosterone, possibly because of enhanced activity of the renin-angiotensin system and an increase in serum K.

1) Intracardiac flows were investigated by bi-directional pulsed Doppler technique with a combined use of the two-dimensional echocardiography. The flow at sampling sites in the heat and great vessels were correctly identified on the two-dimensional echocardiograms. 2) Soundspectrographic analysis of the flow Doppler signals was useful in obtaining information about flow modes and in differentiating flow signals from those of valves. 3) In healthy subjects, intracardiac flow revealed a laminar mode. As a matter of interest, a flow toward the aorta, which is a cranially turned flow, was found at the center and at the outflow tract of the left ventricle from mid to late diastole. 4) In mitral stenosis, the central stream at the stenotic portion exhibited an almost laminar and rapid flow. A good coincidence in flow mode was observed between clinical cases of mitral stenosis and experimental stenosis. 5) Disturbed flows were observed in the following diseased conditions. The diastolic regurgitant flow in the left ventricular outflow tract and mitral inflow in aortic regurgitation, the regurgitant flow into the left atrium and the diastolic mitral inflow in mitral regurgitation, the ejection flow in hypertrophic cardiomyopathy with outflow tract obstruction, and the tricuspid inflow in atrial septal defect. 6) Mechanisms of intracardiac flow dynamics were also discussed.

Effects of the intracerebroventricular (IVT) infusion of a subpressor dose (3 ng/kg/min) of angiotensin II (ang II) on the pressor responses to intravenous (IV) infusions of ang II and to IV bolus injections of norepinephrine (NE) were studied in conscious rats. This study was undertaken to determine whether activations of the brain renin-angiotensin system alter pressor responsiveness to IV infusions of ang II and IV injections of NE in the conscious state. Pressor responses to IV infusions of ang II and IV injections of NE were potentiated by the concurrent IVT infusion of the subpressor dose of ang II. Plasma renin activity (PRA), plasma corticosterone (B), and plasma prolactin concentration (PRL) were also measured before and during the IVT infusion of the subpressor (3 ng/kg/min) or the pressor (50 ng/kg/min) dose of ang II in order to determine the mechanisms for this pressor hyperresponsiveness to vasoconstrictor substances. The IVT subpressor dose of ang II increased PRA, but did not significantly change B and PRL. The IVT pressor dose of ang II decreased PRA and increased B, but did not significantly change PRL. These results suggest that the brain renin-angiotensin system plays an important role in pressor responsiveness to IV ang II and NE. Although the mechanisms are not fully understood, pressor hyperresponsiveness to IV ang II and NE by an intracerebroventricularly administered subpressor dose of ang II may be related to increased sympathetic outflow, because of the increment in PRA.

In this study, transmitral flow velocity during the diastolic period was non-invasively measured to assess diastolic behavior of the left ventricle by pulsed Doppler flowmetry combined with electronic beam sector-scanning echocardiography. The velocity pattern was found to have 2 wave components: one appears in the early diastolic rapid filling phase (R wave) and the other in the late diastolic phase. The peak of the early diastolic inflow velocity (peak EFV), the deceleration rate of the R wave (DC), and the peak of the late diastolic inflow velocity (peak LFV) were compared in healthy subjects as the control, patients with hypertension, hypertrophic cardiomyopathy and definite old myocardial infarction. Normal peak EFV and DC, 61.3 +/- 6.7 cm/sec and 355 +/- 67 cm/sec2, respectively, were markedly reduced in patients with hypertension (50.0 +/- 10.0 cm/sec and 265 +/- 75 cm/sec2), hypertrophic cardiomyopathy (48.8 +/- 10.7 cm/sec and 205 +/- 78 cm/sec2), and myocardial infarction (46.1 +/- 12.0 cm/sec and 240 +/- 84 cm/sec2). Among all disease groups the DC was most significantly reduced in the hypertrophic cardiomyopathy groups. Normal peak LFV, 39.9 +/- 11.0 cm/sec, was significantly increased in patients with hypertension (54.3 +/- 10.7 cm/sec) and myocardial infarction (50.0 +/- 11.0 cm/sec), but not in patients with hypertrophic cardiomyopathy (42.0 +/- 8.4 cm/sec). The ratio peak LFV/peak EFV was significantly greater in all disease groups than in the normal group. These findings indicate that impaired early diastolic filling in all disease groups was compensated by enhanced atrial contraction in patients with hypertension and myocardial infarction, and by prolonged rapid filling in patients with hypertrophic cardiomyopathy. Left ventricular wall thickness was better correlated with DC in patients with hypertension (r = -0.76, p less than 0.01) than in patients in the other groups, which indicates that the left ventricular wall thickening is a more important factor in determining diastolic behavior of the ventricle in hypertension than in hypertrophic cardiomyopathy and myocardial infarction. Thus, the pulsed Doppler technique was proved to be useful in assessing ventricular diastolic events non-invasively.

In order to study the entrainment phenomenon in various forms of clinical and experimental tachycardia, overdrive pacing was performed in clinical paroxysmal supraventricular tachycardia (PSVT) of Wolff-Parkinson-White syndrome (6 cases), atrial flutter (AF-6 cases), ventricular tachycardia (VT-2 cases), experimental AF induced by Rosenblueth's method (5 dogs), and in VT induced by aconitine (5 dogs). Progressive fusion was demonstrated in all but aconitine-induced VT. After cessation of pacing, the first tachycardia complex showed no fusion at all, but the timing of the complex varied depending on the recording sites of the electrogram. The tachycardia complex occurred at the pacing rate only when the electrogram was recorded at the upstream of the pacing site along the reentry circuit in PSVT and experimental AF. In clinical VT, the complex appeared progressively later as the pacing rate was increased. In aconitine-induced experimental VT, the complex occurred at its original tachycardia rate originating from the site where aconitine was applied. In reentrant tachycardia, entrainment could be observed even when all three of the diagnostic criteria proposed by Brugada et al. were not fulfilled. The mechanism of tachycardia can be assessed by entrainment, although the proposed criteria should be reevaluated.

A case of Stokes-Adams syndrome, caused by a high degree AV block due to repetitive concealed conduction in the AV node, was presented. Experimental study in dogs with impaired AV conduction by verapamil showed that the favourable conditions for appearance of "repetitive" concealed conduction were as follows: 1) prolonged effective refractory period (ERP) of the AV node, 2) atrial stimulations applied at or just inside of ERP of the AV node successively (deeper penetration of concealed conduction), 3) a prolonged preceding PQ interval (slower speed of concealed conduction) and 4) overdrive suppression of subsidiary pacemaker(s). In clinical cases with apparently normal AV conduction but with prolonged ERP of the AV node, atrial excitations with suitable timing may cause repetitive concealed conduction, resulting in a high degree AV block and Stokes-Adams syndrome.

Diurnal rhythm studies were performed on 11 patients with congestive heart failure. Blood samples were taken for the determination of aldosterone, cortisol and plasma renin activity every 4 hours from 12:00 a.m. to 12:00 a.m. the following day. Following this control study, a second diurnal rhythm study was conducted under dexamethasone treatment (0.5 mg of dexamethasone every 4 hours for 48 hours). In the control study, aldosterone and cortisol fluctuated showing a diurnal rhythm with the lowest value in the evening and the highest value in the morning. Plasma renin activity rhythm was indistinct. Fluctuations in plasma renin activity were not parallel with aldosterone. Dexamethasone treatment suppressed cortisol to less than 1 microgram/100 ml. Aldosterone values decreased significantly in the morning (p less than 0.01); this was accompanied by the abolishment of aldosterone rhythm. Plasma renin activity rhythm remained indistinct following administration of dexamethasone. These results suggest that adrenocorticotrophic hormone plays an important role in the control of aldosterone diurnal rhythm in patients with congestive heart failure.

The cardiac content and plasma concentration of atrial natriuretic polypeptide (ANP) in hypertensive rats were measured by using radioimmunoassay for ANP. The animals used in this study were young (5-week-old) and adult (12- to 14-week-old) spontaneously hypertensive rats (SHR), stroke-prone SHR (SHR-SP) and normotensive control Wistar-Kyoto rats (WKY). Most immunoreactive ANP in the cardiac extract of the hypertensive rats (both SHR and SHR-SP) was found to be predominantly gamma-form as well as that of WKY. Cardiac ANP content in adult SHR and SHR-SP was significantly lower than in adult WKY (p less than 0.01), although there were no differences among three groups in young rats. Similar tendencies were also observed for plasma ANP concentration. The level of plasma in adult hypertensive rats was significantly lower or tended to be lower than in adult normotensive rats. Furthermore, a high negative correlation was present between blood pressure and cardiac ANP content (r = 0.748, p less than 0.01) and between blood pressure and plasma ANP concentration (r = 0.608, p less than 0.01) in all adult rats but there were no such relationships in young rats. The present study suggests that atrial natriuretic polypeptide may contribute to the pathogenesis or maintenance of high blood pressure in the genetic hypertensive rats.

We evaluated the influence of right ventricular (RV) pressure overload on RV and left ventricular (LV) filling using Doppler echocardiography in cor pulmonale. The LV and RV inflow signals were recorded by Doppler flowmetry. The end-diastolic (ED) and end-systolic (ES) LV short axis images were detected by 2-dimensional echocardiography in 20 healthy subjects and in 36 cases of chronic pulmonary disease (CPD) with pulmonary hypertension. We measured (1) the ratio of the peak velocity of inflow due to atrial contraction to the peak velocity of rapid inflow (A/R), (2) the deceleration half-time of rapid inflow (delta TD), (3) the corrected radius of curvature (cRC) of the interventricular septum (IVS) at ES and ED, and (4) the percent change of length of 16 radial grids (%CL) using the fixed method on the ED and ES short axis images. In 17 of 36 patients with CPD, we measured the systolic pulmonary artery pressure (sPAP), the cardiac index (CI), the mean pulmonary capillary wedge pressure (mPCWP), the end-diastolic right ventricular pressure and the partial oxygen pressure of arterial blood (PaO2). The results were as follows: in CPD, (1) both the RV and the LV diastolic behavior were impaired as shown by increased A/R (1.04 +/- 0.20, 0.98 +/- 0.17, respectively) and prolonged delta TD (115 +/- 20, 100 +/- 17 msec, respectively), (2) the IVS was flattened at ED (cRC of IVS = 0.67 +/- 0.12), (3) the IVS wall motion was impaired (%CL of IVS = 133 +/- 13), (4) the sPAP had an adequate correlation with RV A/R (r = 0.80, p less than 0.01), RV delta TD (r = 0.59, p less than 0.05), LV A/R (r = 0.82, p less than 0.01), LV delta TD (r = 0.61, p less than 0.05), cRC of IVS (r = 0.67, p less than 0.01), %CL of IVS (r = -0.59, p less than 0.05). There was no significant correlation between the LV diastolic behavior and the CI, the mPCWP, the PaO2. It is concluded that the impairment of RV diastolic behavior was caused by the decreased RV compliance due to RV free wall hypertrophy. Moreover, the RV pressure overload interfered with the IVS motion during diastole, this regional impairment of diastolic behavior of the IVS subsequently causing impairment of LV diastolic filling.

Two clinically-observed patterns in the response curve relating coupling intervals of premature atrial stimulation to return cycles were experimentally reproduced and studied by microelectrode techniques in the sinoatrial preparations of rabbit hearts. The progressive prolongation pattern of the return cycles with shortening of coupling intervals was associated with progressive depressions both of atriosinus conduction and sinus node automaticity. The progressive shortening pattern of the return cycles was associated with progressive shortening in the duration of sinus node action potential in two-thirds of the preparations and with pacemaker shift in the remaining one-third of them. Possible "sinus node reentry" was demonstrated. The mechanisms and clinical implications of these phenomena were discussed.

Since it is still controversial as to whether or not atrial natriuretic peptide (ANP) antagonizes norepinephrine (NE)-induced vasoconstriction, we examined the interactions of ANP and NE with respect to renal circulation. (I) Although ANP infusion at 25 ng/kg/min for 40 min caused a decrease in total peripheral resistance (-11%, p less than 0.01) in 34 patients with cardiovascular disease and 15 normotensives (NTs), renal vascular resistance (RVR) was not reduced consistently by ANP. However, there was a negative correlation between changes in RVR and the preinfusion plasma NE level (r = -0.51, p less than 0.001). (II) When NE infusion into 6 NTs at 100 ng/kg/min was followed by ANP infusion, urinary Na excretion was increased to a greater degree than that by ANP infusion alone (+234% vs +34%, p less than 0.01). Furthermore, ANP brought about a recovery in NE-induced falls in renal blood flow (+40%) and glomerular filtration rate (+38%, both p less than 0.05). These effects were attributed to both a decrease in calculated renal afferent resistance and an increase in efferent resistance (-43% and +17%, respectively, p less than 0.05). Thus, increased sympathetic nervous activity seems to augment the renal effects of ANP, and the antagonistic effects of ANP to NE-induced preglomerular vasoconstriction may counteract Na retention caused by excessive sympathetic tone.