[Induction of mucosal immunity to mycobacterial heat shock protein (hsp) 65 by colonic inoculation of plasmid DNA encoding hsp65].

Mycobacterial heat shock protein (hsp) 65 has more than 50% sequence homology with human hsp60 and immune responses against mycobacterial hsp65 may cross-react with human hsp60 and could cause autoimmune diseases including inflammatory bowel diseases (IBD). Since the colonic mucosa is a main inflammatory site in IBD, mucosal immunity to hsp65 may be more important for the mucosal inflammation than systemic immunity to hsp65. We inoculated plasmid DNA (pDNA) encoding mycobacterial hsp65 (pACB-hsp 65) into the colon of Wistar rats and evaluated the mucosal humoral immune response and the effect of these immune responses on the colonic mucosa. Four weeks after pDNA inoculation, significantly elevated titers of hsp65-specific IgA antibody were seen in fecal extracts of rats immunized intra-colonic mucosa with pACB-hsp65 (40 +/- 9 U/ml), whereas the fecal IgA antibody titers of rats inoculated intradermal with pACB-hsp65 did not arise (8 +/- 5 U/ml). Colonic inoculation of pACB-hsp65 induced systemic and mucosal immune responses to hsp65. However, macroscopic and histological examinations of the colonic mucosa inoculated with pACB-hsp65 showed no evidence of mucosal damage. These results suggested that the mucosal immunity to hsp65 on the colonic mucosa may not play a crucial role in the induction of colonic mucosal inflammation as was seen in IBD.

Determining the optimum dose for the intravenous administration of nicardipine in the treatment of acute heart failure--a multicenter study. The Nicardipine Heart Failure Study Group.

Nicardipine is a potent arteriolar vasodilator with a negligible negative inotropic effect. Although intravenous administration of this drug has been reported to be effective in the treatment of heart failure, the optimal dose by this route is not clear. This study was designed to determine the optimum dose for the intravenous infusion of nicardipine in the treatment of heart failure. In Trial 1, nicardipine was administered intravenously at a dose of 0.5 microgram/kg per min to 14 patients with acute heart failure. The dose was increased to 1.0 microgram/kg per min in 13 cases with marked improvement at 2 h. In Trial 2, nicardipine was administered in a double-blind manner to 53 patients at 3 different rates of infusion for 2 h: 1.0 (Group 1, n = 19), 2.0 (Group 2, n = 15), and 3.0 (Group 3, n = 19) micrograms/kg per min. Neither heart rate nor mean right atrial pressure changed in any of the 3 groups. Favorable hemodynamic effects were evident in all groups beginning 30 min after the start of infusion, with an increase in cardiac index (control vs 2 h after infusion, L/min per m2) (Group 1: 2.2 +/- 0.4 vs 3.1 +/- 0.8, Group 2: 2.2 +/- 0.4 vs 2.9 +/- 0.5, Group 3: 2.3 +/- 0.3 vs 3.1 +/- 0.7, all p < 0.01 compared to the control) and a decrease in diastolic pulmonary artery pressure (Group 1: 26 +/- 10 vs 19 +/- 7, Group 2: 27 +/- 10 vs 20 +/- 8, Group 3: 26 +/- 7 vs 18 +/- 5 mmHg, all p < 0.01). The decrease in systolic pressure was greatest in Group 3 (Group 1: 141 +/- 31 vs 119 +/- 18, Group 2: 149 +/- 25 vs 118 +/- 17, Group 3; 147 +/- 27 vs 107 +/- 14 mmHg, all p < 0.01 compared to control, and p < 0.05 between Groups 1 and 3). The intravenous drip infusion of nicardipine is effective in the treatment of heart failure by inducing an increase in cardiac output and a decrease in pulmonary artery wedge pressure. The optimal dose in this study was 1.0 microgram/kg per min.

Effects of a new calcium channel blocker, MPC-1304, on blood pressure, serum lipoproteins and serum carbohydrate metabolism in patients with essential hypertension.

The effects of MPC-1304, a new calcium channel blocker, on blood pressure, serum lipoproteins, and carbohydrate metabolism were compared with those of atenolol in a group of patients with mild to moderate essential hypertension. Systolic and diastolic pressures were significantly decreased by both MPC-1304 and atenolol administration. Serum levels of apolipoproteins A-I and A-II were significantly increased after 8-12 weeks of MPC-1304 treatment, but were unchanged during a similar period of atenolol treatment. Neither drug induced any significant change in other lipoprotein parameters, fasting blood sugar, immunoreactive insulin, C-peptide or HbA1c. No serious side-effects or abnormal laboratory values were observed during the course of administration of either drug. These findings indicated that MPC-1304 is as efficacious as an antihypertensive drug and is without adverse effect on lipoprotein or carbohydrate metabolism.

Effect of bevantolol and propranolol on serum lipids in patients with essential hypertension.

In patients with essential hypertension, the beta-blockers bevantolol or propranolol were administered once or twice a day for twelve weeks to evaluate the effects on blood pressure, and lipid metabolism. Both systolic and diastolic blood pressure decreased significantly in response to both bevantolol and propranolol. The pulse-rate also decreased significantly in both groups. Total cholesterol did not change significantly in both groups. Triglycerides increased significantly in the bevantolol group. HDL cholesterol decreased significantly in the propranolol group. The LDL cholesterol/HDL cholesterol ratio increased significantly in the propranolol group, while no significant increase was observed in the bevantolol group. The apolipoprotein B/A ratio was elevated in the propranolol group. No serious side-effects were noted during the study in both groups. These results indicate that bevantolol is an effective antihypertensive drug with fewer unfavorable effects on lipid metabolism than propranolol.

Intracardiac thrombi in both the right atrium and right ventricle after acute inferior-wall myocardial infarction.

We present a case of inferior-wall myocardial infarction associated with thrombi in both the right ventricle and right atrium. Routine transthoracic echocardiography could not detect these thrombi while transesophageal echocardiography provided an excellent image of the thrombi. The right atrium or right ventricle may be the site for thrombi, presumably due to both right ventricular and right atrial infarction in acute inferior-wall infarction.

A model study of time- and voltage-dependent effects of class I antiarrhythmic drugs in guinea-pig papillary muscles as related to external potassium concentration.

1. A piecewise exponential three-state model previously introduced by the authors in 5.4 mmol/l was intended to apply to states with different [K+]o and with a different drug. Using the conventional microelectrode technique the effects of 20 mumol/l mexiletine (MEX), 5 mumol/l aprindine (APR), 20 mumol/l quinidine (QUI), 5 mumol/l flecainide (FLE), 5 mumol/l E-0747 (dl-6-chloro-2,2'-dimethyl-1'-[3-(4-hydroxypiperizino)propyl]spiro [chroman-4,4'-imidazolidine]-2',5'-dione hydrochloride and 100 mumol/l QX-222, a quaternary derivative of lidocaine, on action potentials (APs) in guinea-pig papillary muscles were studied. Specific objects of the study were (1) steady state Vmax values at various frequencies (all drugs), (2) the recovery process of Vmax in premature responses (MEX) and (3) Vmax changes during a train of stimulation at 1 Hz after a rest period (all other drugs) in 2.7 and 10 mmol/l [K+]o. Further, those of APR alone and APR plus 1 mmol/l nicorandil (NIC), which shortened action potential durations (APDs) specifically, were investigated on the above items (1) and (3) in 5.4 mmol/l [K+]o. 2. All the drugs reduced the Vmax of APs frequency-dependently and, except QX-222, more markedly in 10 mmol/l [K+]o than in 2.7 mmol/l [K+]o at 1 Hz. 3. The rate constants estimated from the model fitting characterized MEX and APR and the other drugs as predominantly inactivated and activated channel blockers, respectively. The calculated rate of onset of block, lambda T, does not differ much between the three [K+]o levels. lambda T shows that APR belongs to class Ia rather than class Ib.(ABSTRACT TRUNCATED AT 250 WORDS)

Age-related modification of regional left ventricular filling in normal subjects.

Left ventricular diastolic filling has been reported to be impaired with advancing age in normal subjects. To investigate the influence of regional ventricular diastolic asynchrony on global ventricular filling as a function of age and to assess the location of asynchronous regions within the left ventricle, radionuclide ventriculography was conducted in 48 normal subjects aged 15 to 73 years. Left ventricular regional filling was assessed by dividing the left ventricular region of interest into 4 quadrants, from which global, septal, apical and lateral time-activity curves and first-derivative curves were derived. Indexes of global left ventricular systolic function at rest did not correlate with age. However, indexes of global early diastolic filling declined significantly with age; peak filling rate normalized to end-diastolic volume (r = -0.42; p < 0.01), to stroke volume (r = -0.48; p < 0.001) and to peak ejection rate (r = -0.47; p < 0.001) decreased with advancing age. Global time to peak filling rate also increased with aging (r = 0.41; p < 0.01). Early diastolic asynchrony was measured as the sum of the absolute values of the time differences from global peak filling rate to that in each of three quadrants (delta TPFR). delta TPFR increased with age (r = 0.37; p < 0.01). Global peak filling rate normalized to end-diastolic volume (r = -0.40; p < 0.01), to stroke volume (r = -0.45; p < 0.01) and to peak ejection rate (r = -0.51; p < 0.001) decreased significantly with increasing delta TPFR. Time to peak filling rate of the lateral region occurred first (163 +/- 33 ms), followed by the apical (184 +/- 38 ms) and finally the septal region (195 +/- 35 ms). With regard to the sequence of regional filling, this suggests that a physiologic asynchrony exists in resting condition in normal subjects. Times to peak filling rate in the septal and apical regions were modestly correlated with age (r = 0.29; p < 0.05, r = 0.30; p < 0.05 respectively), but that in the lateral region did not show significant correlation with age. This may indicated that the effects of advancing age on the regional filling differ in regions within the left ventricle. These results suggest that aging alters left ventricular early diastolic filling in association with the increase in physiologic asynchrony.

Effect of the combination of anticoagulant and thromboxane synthetase inhibitor (Y-20811) or receptor blockade (S-1452) on preventing thrombotic cyclic coronary flow reduction in dogs with coronary stenosis.

We examined the hypothesis that combined actions of anticoagulant (heparin) and Y-20811, thromboxane A2 synthetase inhibitor (TXSI), or S-1452, receptor blockade (TXRB), can provide better antithrombotic protection than TXSI or TXRB alone. In 20 of 33 dogs instrumented, placement of a critical stenosis at a focus of coronary vascular injury initiated a reproducible cyclic coronary flow reduction (CCFR). TXSI (1 mg/kg, IV) perfectly inhibited CCFR in 6 of 10 dogs (60%), and was associated with a significant decrease in 11-dehydro-TXB2 (85 +/- 8% of control; p < 0.05) and an increase in 6-keto-PGF1 alpha (155 +/- 38%; p < 0.05) in coronary sinus blood samples. In the remaining 4 dogs, additional administration of heparin (2000 IU) completely abolished CCFR. On the other hand, TXRB (1 mg/kg, IV) perfectly inhibited CCFR in 7 of 10 dogs (70%), and was accompanied by a significant increase in 6-keto-PGF1 alpha (214 +/- 65%; p < 0.05) and unchanged TXB2 level. In the remaining 3 dogs, additional administration of heparin (2000 IU) completely abolished CCFR. Thus, the combination of anticoagulant and TXSI or TXRB were more effective than TXSI or TXRB alone in abolishing thrombotic CCFR, suggesting that the combination might be effective for treating patients with impending myocardial infarction.

Genetic analysis of dilated cardiomyopathy--HLA and immunoglobulin genes may confer susceptibility.

To identify genetic factors in the immune system which control the susceptibility to dilated cardiomyopathy (DCM), HLA class II DNA typing was performed in 61 Japanese patients, using PCR/SSO probe analyses. The frequencies of HLA-DQB1*0503 (15% vs 5%; RR = 3.06, chi 2 = 7.19) and DQB1*0604 (21% vs 10%; RR = 2.41, chi 2 = 6.20) were significantly increased and that of HLA-DQB1*0502 (RR = 1.74) was slightly increased in the DCM patients. The frequency of DQB1*0303 (16% vs 31%; RR = 0.44, chi 2 = 5.16) was significantly decreased in the patients. The increased HLA-DQB1 alleles have a histidine residue in common at the 30th codon for the HLA-DQ beta chain. Among the genetic markers studied by Southern blot analyses, IGLV (immunoglobulin lambda light chain, pV3.3) showed a strong association with DCM, i.e. A2/A2 genotype was found in 37.7% of patients whereas it was observed in only 18.9% of the control subjects (RR = 2.6, chi 2 = 7.77). The frequency of this genotype was higher in patients under age 45 years at the time of diagnosis (45.5%, RR = 3.6, chi 2 = 10.02). These results suggest that HLA and immunoglobulin genes are closely linked to susceptibility to DCM.

Dilated cardiomyopathy with special reference to humoral immunity.

The question of whether the etiology of DCM is immune or autoimmune has been increasingly discussed. Abnormal findings on humoral immunity in DCM were investigated, especially those regarding anti-heart antibodies (AHA), IgG subclasses and soluble interleukin-2 receptor (sIL-2R). The heterophile type AHA was detected in 64.7% of cases by the indirect immunofluorescence technique (IF) with rat heart, by indirect IF with human heart AHA in 57.8% of cases, and by thin-layer chromatogram with human glycolipids AHA in 44% of cases. Also, 57.1% of the specimens were found to bind IgG on perimyocytes by direct IF with biopsy specimens taken from patients with DCM. The epitope of an antigen which reacted with the heterophile type AHA is a Gal alpha 1-3Gal structure. 200 Kd, 70 Kd and 40 Kd antigens were reacted with AHA detected by indirect IF with human heart. The possible mechanisms of AHA in the pathogenesis could be either complement dependent cytotoxicity or interference to cardiac metabolism. The concentration of sIL-2R and IgG3 in sera from patients with DCM were elevated. These results suggest that immunological abnormalities occur continuously in DCM.

Dynamic determinants of left ventricular early diastolic filling in old myocardial infarction.

The determinants of left ventricular early diastolic filling were assessed in 15 patients with old myocardial infarction. The left atrial pressure (LAP) and left ventricular pressure (LVP) were simultaneously measured by a Millar's multisensor micromanometer with the pusled Doppler mitral inflow velocity at baseline and during angiotensin infusion (20 ng/kg/min). Cardiac output was measured by a thermodilution method. LV peak systolic pressure and end-diastolic pressure were significantly (p less than 0.001) increased during angiotensin infusion from 137 +/- 19 to 170 +/- 21 mmHg and from 13.3 +/- 5.9 to 20.4 +/- 6.2 mmHg, respectively. Cardiac index was significantly decreased during angiotensin infusion. Heart rate, diastolic time, and peak positive dP/dt were unchanged. Although the LA-LV peak pressure gradient[(LAP-LVP) max] was unchanged (from 2.8 +/- 1.0 to 3.0 +/- 1.4 mmHg), the pressure gradient interval (the interval between the first and second points of transmitral pressure crossover) was significantly (p less than 0.001) decreased from 154 +/- 38 to 117 +/- 26 msec during angiotensin infusion. Peak early diastolic mitral inflow velocity (peak E) and the time-velocity integral of E wave (Ei) were significantly decreased during angiotensin infusion from 51 +/- 10 to 45 +/- 11 cm/sec (p less than 0.002) and from 7.47 +/- 1.96 to 5.70 +/- 1.66 cm (p less than 0.001), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of changing afterload and inotropic states on inner and outer ventricular wall thickening.

Effect of changing afterload and inotropic states on inner and outer ventricular wall thickening. Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H109-H116, 1992.--To study the differing behaviors of the inner (IH) and outer halves (OH) of the left ventricular (LV) free wall during an increasing afterload and changing inotropic states, we determined the LV pressure (LVP) and transmural (TM) and OH wall thickness (WTTM and WTOH) by sonomicrometry in 11 anesthetized dogs. The percent systolic wall thickening (% delta WT) and the fractional contribution (FC) were calculated. At rest, % delta WT of TM, IH, and OH were 22 +/- 1 (mean +/- SE), 33 +/- 3, and 13 +/- 2 (P less than 0.01 vs. IH), respectively. The FC of IH and OH were 74 +/- 5 and 29 +/- 4% (P less than 0.01 vs. IH), respectively. During increasing afterload by aortic constriction (AC) without drugs, % delta WT in IH was reduced to 22 +/- 2%, associated with unchanged % delta WT in OH (12 +/- 3%), whereas the FC of IH and OH were not altered from resting values. During AC with dobutamine infusion (3 micrograms.kg-1.min-1), the % delta WT and FC in each layer were not reduced from resting values. On the other hand, during AC with propranolol (2 mg bolus iv), the reduction of % delta WT in IH was greater (from 29 +/- 4 to 15 +/- 6%, P less than 0.01) than that in OH (from 11 +/- 2 to 10 +/- 3%; P less than 0.01 vs. IH). The FC in the IH was decreased (56 +/- 16%) by AC with propranolol, so that the difference in FC between IH and OH became insignificant (FCOH 40 +/- 13%, P greater than 0.1 vs. FCIH).(ABSTRACT TRUNCATED AT 250 WORDS)

Advances in transesophageal echocardiography for the evaluation of atherosclerotic lesions in thoracic aorta--the effects of hypertension, hypercholesterolemia, and aging on atherosclerotic lesions.

We assessed atherosclerotic lesions in the thoracic aorta in 166 consecutive patients (aged 56 +/- 13 years) by transesophageal echocardiography, and investigated the influences of hypertension, hypercholesterolemia and age on the prevalence of such lesions. Satisfactory images were obtained of all the thoracic aorta, except for a small part of the ascending aorta, by use of a biplane transesophageal probe. We defined atherosclerotic lesions as increased echogenicity of the intima (intimal thickening), raised plaque, calcification, ulceration, or aneurysms. Lesions were observed in 97 patients (58%). The incidence of lesions in patients with hypertension (81%) or hypercholesterolemia (80%) was significantly greater than in those without both conditions (37%, p less than 0.005). The incidence of lesions was significantly increased among patients over 60 years old compared with that in patients under 60 (76% vs 42%, p less than 0.005). Patients without either hypertension or hypercholesterolemia showed a marked increase in the incidence of lesions with age (16% at less than 60 yrs vs. 67% at greater than 60 yrs), and no significant influence of these conditions on the incidence of lesions was found in patients over 60. We conclude that hypertension and hypercholesterolemia might be important risk factors for the development of atherosclerotic lesions in the thoracic aorta in relatively younger patients. Age appears to become a more important determinant of such lesions in Japanese patients over 60 years old irrespective of blood pressure and serum cholesterol levels.

Absence of atrial contraction and exercise in patients with isolated atrial fibrillation.

The aim of the study was to assess the effect of absence of atrial contraction during exercise. During the incremental ergometer exercise tests, heart rate, oxygen uptake, and oxygen pulse in patients with isolated atrial fibrillation were compared with those in control subjects at rest, at the exercise level of gas exchange anaerobic threshold, and at peak exercise. The study population consisted of 51 subjects aged 40 years or more: 12 patients with isolated atrial fibrillation and 39 control subjects with normal sinus rhythm. Heart rate in control subjects was lower than that in patients with isolated atrial fibrillation, at rest, anaerobic threshold, and peak exercise (74 +/- 12 vs 85 +/- 8 beats/min at rest, 108 +/- 16 vs 134 +/- 18 beats/min at anaerobic threshold, and 151 +/- 16 vs 173 +/- 22 beats/min at peak exercise, all p less than 0.01). During exercise, oxygen uptake in patients with isolated atrial fibrillation was not significantly different from that in control subjects. Oxygen pulse in patients with isolated atrial fibrillation was lower than that in control subjects during exercise (6.45 +/- 2.04 vs 7.84 +/- 1.63 ml/beat at anaerobic threshold, 7.79 +/- 2.28 vs 9.16 +/- 1.79 ml/beat at peak exercise, both p less than 0.05). In patients with isolated atrial fibrillation, the oxygen pulse might be reduced due to the lack of atrial contraction during exercise. However, the oxygen uptake that represents the exercise capacity would be preserved with the increase in heart rate.

[A case of polyangiitis overlap syndrome].

A 25 year old man was admitted to our hospital on June 1, 1989 because of general fatigue and pleural effusion. He had noticed purpuras and nodules on his bilateral lower legs in July 1988. He was admitted to Nihon University Hospital and was diagnosed as allergic granulomatous angiitis. Methylprednisolone was administered. In March, 1989, a nodular shadow was detected in his lung CT films. From the findings of TBLB a granulomatous lesion was suspected. However, his clinical course was rather stable so he was discharged from the hospital. Two months later, he was suffered from fever and general fatigue. On his chest X ray film pleural effusion was detected in the lower part of his left lung. The nodular shadow was increasing gradually. Laboratory findings on his admission showed leukocytosis, thrombocytosis, elevated CRP and a high titer of RA factor. He was diagnosed as hypersensitivity angiitis in a broad sense based on his biopsy findings of the skin lesion. Furthermore, the diagnosis of an early stage of Wegener's granulomatosis (WG) or limited type of WG was also made from the clinical course of his lung lesion. The combination therapy with cyclophosphamide and methylprednisolone was started. It was so effective that the nodule of his left lung was almost disappeared. It seems that this case is one of the polyangiitis overlap syndrome proposed by Fauci.

Effects of digoxin, propranolol, and verapamil on exercise in patients with chronic isolated atrial fibrillation.

STUDY OBJECTIVE: The aim was to evaluate the effects of digoxin, propranolol, and verapamil on exercise in patients with chronic isolated atrial fibrillation. DESIGN: Patients with chronic isolated atrial fibrillation underwent maximal exercise testing before and after the administration of digoxin, propranolol, or verapamil. Heart rate, oxygen uptake and oxygen pulse were observed at rest, at gas exchange anaerobic threshold, and at peak exercise. SUBJECTS: The subjects were 10 patients (aged 48-78 years, mean age 60, SD 9, years) with chronic isolated atrial fibrillation. MEASUREMENTS AND MAIN RESULTS: During exercise without medication, the heart rate was 85 (SD 8) beats.min-1 at rest, 127(19) at the level of anaerobic threshold, and 175(17) at peak exercise. With digoxin, heart rate was reduced to 75(9) beats.min-1 at rest (control v digoxin, p less than 0.01). However, reduction of heart rate was not seen at anaerobic threshold or at peak exercise. With propranolol, heart rate was 63(7) beats.min-1 at rest, 99(16) at anaerobic threshold, and 138(28) at peak exercise (control v propranolol, all p less than 0.01). Heart rate with verapamil was 70(13) beats.min-1 at rest, 107(30) at anaerobic threshold, and 138(28) at peak exercise (control v verapamil, p less than 0.05 at rest and at anaerobic threshold, p less than 0.01 at peak exercise. Neither digoxin, nor propranolol, nor verapamil changed the oxygen uptake during exercise. Without medication, oxygen pulse was 6.5(2.0) ml.beat-1 at anaerobic threshold and 7.7(2.1) ml.beat-1 at peak exercise. With digoxin, the change of oxygen pulse, versus without medication, was not significant at rest or at anaerobic threshold but was increased at peak exercise, at 8.3(2.1) v 7.7(2.1) ml.beat-1, p less than 0.05. With propranolol, oxygen pulse was increased to 8.2(1.9) ml.beat-1 at anaerobic threshold and 9.2(2.3) ml.beat-1 at peak exercise (control v propranolol, both p less than 0.01). With verapamil, oxygen pulse was increased to 8.7(1.8) ml.beat-1 at anaerobic threshold and 10.0(2.1) ml.beat-1 at peak exercise (control v verapamil, both p less than 0.01). CONCLUSIONS: Digoxin was effective in reducing heart rate at rest, but failed to reduce it during exercise. Propranolol and verapamil reduced heart rate at all levels of exercise as well as at rest. Oxygen uptake during exercise (total exercise capacity) was not reduced with propranolol or verapamil; this was thought to have been accomplished by an increased oxygen pulse.

Characteristics of blood flow velocity patterns of central systemic veins in healthy adults assessed by Doppler echocardiography.

To evaluate the differences in shape and phase lag of the flow velocity curves in the superior (SVC) and inferior (IVC) venae cavae and the hepatic vein (HV), Doppler echocardiographic examination was performed in 40 healthy adults (aged 20 to 67 years, mean +/- SD: 39 +/- 12 years). Flow velocity patterns in each vein were characterized by 4 major deflections: S wave, a systolic forward flow; D wave, a diastolic forward flow; A wave, a small backward flow or reduction of diastolic forward flow due to atrial contraction; and O wave, a small backward flow or reduction of forward flow after the second heart sound. Except for a reduced phasic flow in a collapsed IVC, the venous flow velocity recordings in each vein demonstrated very similar pulsatile patterns and small differences in mean time lags of less than 50 msec. In general, the lowest values of peak A/peak S, peak O/peak S and peak D/peak S were observed in HV flow and the highest in IVC flow. Backflows of A and O waves were prominent in HV flow, but small and least frequent in IVC flow. These data suggest that the baseline of the central venous flow recordings might shift downward in HV flow and upward in IVC flow. However, even if both the baseline shift and amplitude of the flow curve were normalized in each venous flow velocity curve, apparent differences in shape of the flow velocity curves would remain. We concluded that the characteristics and differences of each central venous flow velocity pattern should be noted in studies of these areas.

Mechanism of augmented left atrial pump function in myocardial infarction and essential hypertension evaluated by left atrial pressure-dimension relation.

To analyze left atrial (LA) pump function in normal subjects, in patients with essential hypertension and in patients with a healed myocardial infarction, LA dimension (aortic-root echogram) and pressure (catheter-tip manometer) were simultaneously recorded in 25 patients (8 normal subjects, 7 with hypertension and 10 with myocardial infarction). The pressure-dimension relation of the left atrium was composed of 2 loops: the A loop (expressing the pump function of the left atrium) and the V loop. LA dimension at the beginning of active LA shortening was significantly greater in hypertensive subjects (33 +/- 3 mm) and in those with myocardial infarction (32 +/- 4 mm) than in normal subjects (28 +/- 3 mm) (p less than 0.01, p less than 0.05, respectively). The area of the A loop significantly increased in subjects with hypertension (48 +/- 3 mm Hg.mm, p less than 0.01) and in subjects with myocardial infarction (29 +/- 10 mm Hg.mm, p less than 0.05), compared with normal subjects (20 +/- 8 mm Hg.mm). The mean fractional shortening velocity of the left atrium significantly increased in subjects with hypertension, compared with normal subjects and those with myocardial infarction (p less than 0.05 for both). LA peak wall tension during the LA active contraction period significantly increased with hypertension and with myocardial infarction, compared with normal subjects (p less than 0.01, p less than 0.05, respectively). The area of the A loop was directly proportional to the LA dimension at the beginning of active LA shortening (r = 0.53), p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

[Reliability of the exercise ECG in detecting silent ischemia in patients with prior myocardial infarction].

To assess the reliability of the exercise ECG in detecting silent ischemia, ECG results were compared with those of stress-redistribution thallium-201 single-photon emission computed tomography (SPECT) in 116 patients with prior myocardial infarction and in 20 normal subjects used as a control. The LV was divided into 20 segmental images, which were scored blindly on a 5-point scale. The redistribution score was defined as thallium defect score of exercise subtracted by that of redistribution image and was used as a measure of amount of ischemic but viable myocardium. The upper limit of normal redistribution score (= 4.32) was defined as mean +2 standard deviations derived from 20 normal subjects. Of 116 patients, 47 had the redistribution score above the normal range. Twenty-five (53%) of the 47 patients showed positive ECG response. Fourteen (20%) of the 69 patients, who had the normal redistribution score, showed positive ECG response. Thus, the ECG response had a sensitivity of 53% and a specificity of 80% in detecting transient ischemia. Furthermore, the 116 patients were subdivided into 4 groups according to the presence or absence of chest pain and ECG change during exercise. Fourteen patients showed both chest pain and ECG change and all these patients had the redistribution score above the normal range. Twenty-five patients showed ECG change without chest pain and 11 (44%) of the 25 patients had the abnormal redistribution. Three (43%) of 7 patients who showed chest pain without ECG change had the abnormal redistribution score. Of 70 patients who had neither chest pain nor ECG change, 19 (27%) had the redistribution score above the normal range. Thus, limitations exist in detecting silent ischemia by ECG in patients with a prior myocardial infarction, because the ECG response to the exercise test may have a low degree of sensitivity and a high degree of false positive and false negative results in detecting silent ischemia.