[Familial atrioventricular block].
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Diagnosis, Differential↗
Biomedical subjects
Y Himura
Publications and source records attributed to Y Himura.
[Idiopathic sustained ventricular tachycardia].
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Anti-Arrhythmia Agents↗
Abnormal cardiac sympathetic nerve function in a patient with pheochromocytoma. An analysis using 123I metaiodobenzylguanidine scintigraphy.
A 23-year-old woman with pheochromocytoma had a high level of plasma norepinephrine (NE) (6039 pg/ml) and 123I metaiodobenzylguanidine (MIBG) scintigram showed decreased myocardial retention. After surgical resection, plasma norepinephrine was normalized and the myocardial retention of 123I MIBG gradually improved. These findings suggest that the possibility that the excess of circulating norepinephrine caused by pheochromocytoma could damage the cardiac sympathetic nerve function and 123I MIBG scintigraphy is a useful method of evaluating abnormalities.
3-Iodobenzylguanidine↗
Reversible left ventricular dysfunction associated with Guillain-Barré syndrome--an expression of catecholamine cardiotoxicity?
The patient was a 76-year-old female who had a history of Guillain-Barré syndrome 3 years previously; ST-segment elevation was noted in association with reversible left ventricular dysfunction. Left ventrioculogram and coronary angiograms were normal and ergonovine test was negative during the chronic period of Guillain-Barré syndrome. She was hospitalized again due to the recurrence of Guillain-Barré syndrome. Two days later, ST-segment elevation in leads V2 through V5 prompted us to perform cardiac catheterization, although she did not complain of any chest symptoms. A large akinetic area was found mainly around the apex on left ventriculography, despite the lack of coronary stenoses. Peak creatine kinase and C-reactive protein were 400 IU/ml and 3.5 mg/dl, respectively. Left ventricular dysfunction was normalized within one week. During the acute phase of the cardiac episode, plasma norepinephrine and epinephrine were 1340 pg/ml and 112 pg/ml, respectively. I123 metaiodobenzyl-guanidine myocardial scintigram 3 weeks after the episode showed an extensive apical defect which was improved markedly 3 months later. We think that this reversible left ventricular dysfunction was due to the synergistic toxic effect of mildly increased catecholamine and transiently damaged sympathetic nerve endings in the myocardium, presumably due to Guillain-Barré syndrome.
3-Iodobenzylguanidine↗
Limitations of electrocardiography in the diagnosis of acute myocardial infarction--comparison with two-dimensional echocardiography.
In order to assess the sensitivity of the initial electrocardiogram (ECG) in diagnosing the first attack of acute myocardial infarction (AMI), we compared the findings on ECG and two-dimensional echocardiogram (2-D echo) in 74 patients with single vessel coronary artery disease. Group A consisted of 41 patients with infero-posterior AMI while group B consisted of 33 patients with antero-septal AMI. In group A, 12 patients showed normal ECGs, while 2-D echo failed to reveal abnormal left ventricular wall motion in only 2 patients. In those two patients, the quality of the echocardiogram was poor. In group B, only one patient showed a normal ECG, and all patients showed abnormal left ventricular wall motion on 2-D echo. We conclude that electrocardiography has limitations in diagnosing infero-posterior myocardial infarction especially during the acute phase, but 2-D echo is an additional useful diagnostic procedure.
Echocardiography↗
Short-term effects of naloxone on hemodynamics and baroreflex function in conscious dogs with pacing-induced congestive heart failure.
OBJECTIVES: The purpose of this study was to determine the effects of naloxone on systemic hemodynamics and reflex function in dogs with congestive heart failure induced by rapid pacing. BACKGROUND: We have shown previously that naloxone, an opiate receptor antagonist, improves cardiac output, aortic blood pressure, systolic performance and the baroreflex function in conscious dogs with chronic right-sided congestive heart failure. However, whether endogenous opioids also play a role n mediating the reduction of myocardial and baroreflex function in animals with left heart failure remains controversial. METHODS: We administered naloxone (1 mg/kg body weight) and normal saline solution to 15 dogs with pacing-induced congestive heart failure (225 beats/min for 8 weeks) and 11 control dogs. In addition to systemic hemodynamic measurements, the slope of pressure-area relation obtained from echocardiography with intravenous bolus injection of phenylephrine was taken as a load-independent index of myocardial contractility. Baroreflex function was estimated by the slope of the regression line relating systolic aortic pressure and RR interval. RESULTS: Plasma beta-endorphin levels were elevated in dogs with congestive heart failure. Naloxone administration increased heart rate, mean aortic pressure, first derivative of left ventricular pressure, cardiac output and myocardial contractility in pacing-induced congestive heart failure. These changes correlated significantly with basal plasma beta-endorphin levels and were accompanied by increases in plasma beta-endorphin and catecholamines after naloxone administration. However, unlike the hemodynamic and cardiac effects of naloxone, baroreflex function did not change after naloxone in dogs with congestive heart failure. CONCLUSIONS: The increase in basal plasma beta-endorphin suggests that the endogenous opiate system is activated in left-sided congestive heart failure. Because naloxone improves the systemic hemodynamics and myocardial contractile function under this condition, the endogenous opioids appear to play an important role in mediating the myocardial depression that occurs in heart failure. However, the endogenous opiate system has no apparent effect on the regulation of baroreflex control in heart failure induced by rapid pacing.
Animals↗
Nitroprusside infusion improves arterial baroreflex control of heart rate in dogs with chronic congestive heart failure.
To determine if nitroprusside improves arterial baroreflex responsiveness in chronic congestive heart failure (CHF), we administered nitroprusside to 11 conscious dogs with pacing-induced CHF. Baroreflex sensitivity was determined by plotting the R-R interval against systolic aortic pressure after a bolus injection of phenylephrine (PE). At baseline, dogs with CHF had higher heart rate (HR), increased left atrial blood pressure (BP), and reduced left ventricular (LV) dP/dt as compared with 10 sham-operated normal animals. Baroreflex sensitivity index was significantly lower in CHF dogs, (8.3 +/- 1.3 ms/mm Hg) than normal dogs (25.1 +/- 1.2 ms/mm Hg, p < 0.001). Intravenous (i.v.) administration of nitroprusside (1 microgram/kg/min) to CHF dogs decreased left atrial BP (23 +/- 1-17 +/- 1 mm Hg) and HR (131 +/- 4-115 +/- 4 beats/min), but had no significant effect on either cardiac output (CO) or systolic aortic BP. This resulted in a 58% increase in baroreflex sensitivity index to 13.1 +/- 1.3 ms/mm Hg (p < 0.001); and the change correlated significantly with magnitude of decrease in left atrial BP (r = 0.884, p < 0.001) but not with the increase in R-R interval (r = 0.390, p > 0.10). In contrast, administration of nitroprusside sufficient to decrease left atrial BP (9.0 +/- 1.4-6.4 +/- 1.2 mm Hg) did not alter baroreflex sensitivity (26.4 +/- 3.4-26.4 +/- 3.9 ms/mm Hg) in 5 normal dogs. The results suggest that nitroprusside infusion increases arterial baroreflex sensitivity only in dogs with CHF and that this effect is probably functionally linked to the reductions of cardiac filling pressure.
Animals↗
Beta-adrenoceptor downregulation in pacing-induced heart failure is associated with increased interstitial NE content.
We used the rapid ventricular pacing model to examine myocardial norepinephrine (NE) uptake kinetics in congestive heart failure. Dogs subjected to pacing at 225 beats/min for 8 wk developed heart failure as evidenced by elevated left atrial pressure, depressed first derivative of left ventricular pressure with respect to time, and depressed cardiac output compared with dogs paced at 100 beats/min for 8 wk. Fast-paced dogs also exhibited an elevated plasma NE and reduced myocardial NE content. Myocardial NE uptake kinetics and interstitial NE concentration were measured in vivo using a triple-isotope intracoronary tracer technique. The rate constant of neuronal uptake of NE was significantly depressed in the fast-paced animals (0.224 +/- 0.027 vs. 0.725 +/- 0.097 s-1, P < 0.001), while the interstitial NE concentration was significantly increased in the heart (1.12 +/- 0.15 vs. 0.17 +/- 0.07 ng/ml, P < 0.001). Myocardial beta-adrenoceptor density was significantly reduced in the fast-paced animals (49 +/- 7 vs. 86 +/- 6 fmol/mg, P < 0.001), and there was a significant inverse correlation between beta-adrenoceptor density and interstitial NE concentration. Thus we conclude that excess myocardial interstitial NE content contributes to the abnormalities in the beta-adrenoceptor system.
Algorithms↗
Isoform-specific regulation of myocardial Na,K-ATPase alpha-subunit in congestive heart failure. Role of norepinephrine.
BACKGROUND: Myocardial ouabain-binding sites and Na,K-ATPase activity are reduced in congestive heart failure (CHF), but the mechanisms by which CHF reduces the Na,K-ATPase remain unknown. We proposed to investigate whether the changes are accompanied by isoform-specific reductions of the Na,K-ATPase alpha-subunit proteins in CHF and whether similar changes could be produced by exogenous norepinephrine administration. METHODS AND RESULTS: CHF was induced in dogs by rapid ventricular pacing at a rate of 225 beats per minute for 8 weeks (protocol 1). A second group of dogs were paced at 100 beats per minute and served as controls. In protocol 2, norepinephrine was infused in normal dogs using a subcutaneous osmotic minipump for 8 weeks. The control dogs received normal saline through the pump. Animals were studied after 8 weeks of pacing or norepinephrine infusion. After the baseline hemodynamics and interstitial norepinephrine concentration had been obtained, the hearts were removed for measuring [3H]ouabain-binding sites and Na,K-ATPase alpha-subunit proteins using isoform-specific monoclonal antibodies. RESULTS: Myocardial [3H]ouabain-binding sites were reduced in dogs with CHF and chronic norepinephrine infusion. The Western blot analysis showed that adult canine hearts possess both alpha 1 and alpha 3 isoforms of the Na,K-ATPase alpha-subunit but not the alpha 2 isoform protein. CHF and NE infusion had no effect on the Na,K-ATPase alpha 1-subunit protein but did reduce the alpha 3 isoform protein significantly. In addition, there was a significant inverse correlation between the amount of myocardial alpha 3 isoform protein and interstitial norepinephrine content in the dogs. In contrast, the specific activity of the sarcolemmal marker 5'-nucleotidase did not differ among the groups of animals. CONCLUSIONS: The reduction of myocardial Na,K-ATPase in CHF is limited to the alpha 3 isoform. Furthermore, because similar changes in myocardial ouabain-binding sites and Na,K-ATPase alpha 3 isoform were produced by chronic norepinephrine infusion, the decrease in the Na,K-ATPase in CHF is most likely mediated via excess sympathetic stimulation.
Animals↗
Cardiac noradrenergic nerve terminal abnormalities in dogs with experimental congestive heart failure.
BACKGROUND: We have shown previously that norepinephrine (NE) uptake activity is reduced in the failing right ventricle of animals with right heart failure (RHF) produced by tricuspid avulsion and progressive pulmonary constriction. However, it is unknown whether this defect in neuronal NE uptake is related to reduction of noradrenergic nerve terminals or whether these changes also occur in animals with left heart failure (LHF). It is also unknown whether increased NE release in heart failure contributes to the noradrenergic nerve abnormalities. METHODS AND RESULTS: We measured myocardial NE content. NE uptake function, and noradrenergic nerve profiles in dogs with either RHF or LHF induced by rapid ventricular pacing. NE uptake activity was measured using [3H]NE, and noradrenergic nerve profiles were visualized by glyoxylic acid (SPG)-induced histofluorescence and tyrosine hydroxylase immunocytochemical staining. To study the effects of excess NE, we exposed normal dogs to 8 weeks of chronic NE infusion using subcutaneous osmotic minipumps. RHF and LHF animals exhibited reduced myocardial contractile function and congestive heart failure, as evidence by reduced cardiac output and elevated right atrial pressure. However, unlike that in LHF, left atrial pressure was not increased in RHF. The animals also showed an increase in plasma NE and a decrease in cardiac NE. In addition, SPG-induced histofluorescence correlated significantly with NE uptake activity (r = .712, P < .001) and tyrosine hydroxylase immunoreactive profiles (r = .569, P < .001) in the right ventricles of RHF dogs and in both ventricles of LHF dogs. The numbers of catecholaminergic profiles and tyrosine hydroxylase profiles significantly correlated with cardiac filling pressures. Chronic infusion of NE decreased heart rate in normal dogs but had no effect on either mean aortic pressure or left atrial pressure; like heart failure, it resulted in significant decreases in myocardial NE uptake activity and numbers of SPG-induced catecholaminergic histofluorescence and immunoreactive tyrosine hydroxylase profiles. CONCLUSIONS: Myocardial NE uptake activity was reduced only in the failing ventricles with elevated filling pressure in RHF and LHF. These changes probably were caused by loss of noradrenergic nerve terminals in the failing ventricles, as evidenced by the reductions of catecholaminergic histofluorescence and tyrosine hydroxylase immunostained profiles. Furthermore, since similar reductions of myocardial NE uptake and noradrenergic nerve profiles could be produced by chronic NE infusion in normal dogs, elevated NE levels may play a role in the development of cardiac noradrenergic nerve abnormalities in congestive heart failure.
Animals↗
Comparison of thermodilution and Fick methods for measurement of cardiac output in tricuspid regurgitation.
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Cardiac Output↗
The characteristics of hepatic venous flow velocity pattern in patients with pulmonary hypertension by pulsed Doppler echocardiography.
To determine the characteristic change in the Doppler hepatic venous flow velocity pattern in patients with pulmonary hypertension (PH), 21 patients with PH in sinus rhythm were examined with pulsed Doppler echocardiography. The control group included 13 subjects with chest pain syndrome and normal pulmonary arterial pressure. The hepatic vein Doppler signal was biphasic with one peak during ventricular systole (S wave) and the other in diastole (D wave). A reversed signal was recorded after contraction (A wave). The peak velocity of the A wave (Va), S wave (Vs), and D wave (Vd), the time velocity integral of these waves (VIa, VIs, and VId), the acceleration time (t-AC), and the slope of acceleration (s-AC) in the S wave were measured. Compared with controls the PH group had a higher value of Va (26.88 +/- 10.30 vs 13.41 +/- 3.69 cm/sec; p less than 0.01), VIa (2.55 +/- 1.18 vs 1.20 +/- 0.34 cm; p less than 0.01), VIa/(VIs+VId) (0.34 +/- 0.22 vs 0.14 +/- 0.06; p less than 0.01), and s-AC (372 +/- 156 vs 203 +/- 103 cm/sec2; p less than 0.01). They also had a shorter t-AC (101 +/- 32 vs 136 +/- 27 msec; p less than 0.01). There was a weak correlation between the reversed atrial flow and the right heart pressures (r = 0.43 to 0.66). Thus, the hepatic venous flow velocity pattern by Doppler echocardiography is clinically useful in evaluating pulmonary hypertension.
Adult↗
Importance of left ventricular systolic function in the assessment of left ventricular diastolic function with Doppler transmitral flow velocity recording.
To study the effect of left ventricular systolic function on the Doppler transmitral flow velocity pattern, Doppler echocardiographic variables were correlated with hemodynamic indexes in 11 control subjects and 58 patients with heart disease. All underwent cardiac catheterization performed with use of a Millar micromanometer. The time constant of left ventricular isovolumetric pressure decrease and left ventricular end-diastolic myocardial stiffness was calculated. The 58 patients were classified into two groups according to ejection fraction: group I (n = 30; ejection fraction greater than 55%) and group II (n = 28; ejection fraction less than 50%). Compared with the control subjects, patients in group I had impairment only of left ventricular relaxation (time constant 47 +/- 9 vs. 38 +/- 3 ms; p less than 0.01), whereas patients in group II had, in addition to impaired left ventricular relaxation (time constant 52 +/- 11 vs. 38 +/- 3 ms; p less than 0.01), increased preload, increased pulmonary capillary pressure (12 +/- 8 vs. 5 +/- 3 mm Hg; p less than 0.01) and increased myocardial stiffness (2,018 +/- 980 vs. 1,050 +/- 218 g/cm2; p less than 0.01). In group I, there was a significant partial correlation coefficient between the time constant and deceleration half-time (r = 0.54). In group II, a strong correlation existed between myocardial stiffness and peak atrial filling velocity (r = -0.71) and between myocardial stiffness and the ratio of peak atrial to peak rapid filling velocity (r = -0.71).(ABSTRACT TRUNCATED AT 250 WORDS)
Blood Flow Velocity↗
Left ventricular regional relaxation and its nonuniformity in hypertrophic nonobstructive cardiomyopathy.
BACKGROUND: Regional nonuniformity has been suggested to be closely related to left ventricular (LV) relaxation in diseased heart. The purpose of the present study was to assess LV global and regional relaxation in patients with nonobstructive hypertrophic cardiomyopathy (HCM). METHODS AND RESULTS: Left ventriculography was conducted simultaneously with pressure micromanometry in 10 normal control subjects and 11 patients with nonobstructive HCM. LV silhouettes in the right anterior oblique projection were divided into eight regions, and regional wall stress during isovolumic relaxation was computed for six regions from the midventricle to the apex. In HCM patients, isovolumic relaxation time (IRT) and the time constant of LV pressure decrease (Tp) were greater than in control subjects (IRT, 84 +/- 13 versus 66 +/- 6 msec; Tp, 51 +/- 8 versus 36 +/- 5 msec, respectively; p less than 0.01). In HCM patients, the (-)dP/dt upstroke pattern was convex-downward, and dP/dt(20/60), the ratio of dP/dt values 20 and 60 msec after peak (-)dP/dt, was less than in control subjects (1.46 +/- 0.16 versus 2.15 +/- 0.14, p less than 0.01). These findings suggest that there is impaired LV relaxation in HCM patients. End-systolic regional wall stress was lower, and the time constant of regional stress decrease (Tst) was prolonged for each region in HCM patients compared with control subjects. In the HCM group, Tst tended to be more prolonged in regions with increased wall thickness than in regions with normal wall thickness (60 +/- 15 versus 50 +/- 11 msec, p less than 0.01). The coefficient of variation for Tst values in six areas of the left ventricle was calculated in each subject and was greater in HCM patients than in control subjects (13 +/- 7% versus 7 +/- 3%, p less than 0.05), indicating regional nonuniformity in Tst during isovolumic relaxation in HCM patients. CONCLUSIONS: Significant correlations existed between the coefficients of variation for Tst and Tp (r = 0.80, p less than 0.01), IRT (r = 0.79, p less than 0.01), and dP/dt(20/60) (r = -0.67, p less than 0.05) in the HCM group. Thus, regional nonuniformity is closely related to the impairment of LV relaxation in HCM.
Cardiac Catheterization↗
Hemodynamic efficacy of E-1020 in comparison with dopamine on acute mitral regurgitation in anesthetized dogs.
To evaluate the effects of a new phosphodiesterase inhibitor, E-1020 (1, 2-dihydro-6-methyl-2-oxo-5-(imidazo [1, 2-a] pyridin-6-yl)-3-pyridine carbonitrile hydrochloride monohydrate), on cardiovascular hemodynamics in acute heart failure, we compared its effects with those of dopamine on experimentally produced acute mitral regurgitation in dogs. After the production of mitral regurgitation by transmyocardial chordal sectioning and obtaining a stable state, dopamine (5 micrograms/kg/min) was infused until the peak positive dP/dt (peak (+) dP/dt) increased to about 50% of the predopamine value. After complete recovery, E-1020 (30 micrograms/kg) was infused over 5 min and the data were obtained 10 min later. Both drugs equally increased peak (+) dP/dt, decreased systemic vascular resistance, and increased cardiac output. Left ventricular (LV) end-diastolic pressure, LV end-diastolic segment length (EDL), and mean left atrial (LA) pressure decreased with both drugs. The changes in EDL and mean LA pressure were larger with E-1020 than with dopamine (p less than .01 and p less than .05). Although mean inferior vena caval blood flow volume (mIVCF) increased and mean inferior vena caval pressure decreased with both drugs, the increment of mIVCF was smaller with E-1020 (p less than .001). Thus, E-1020 had not only a positive inotropic effect but also a vasodilatory action both on resistance vessels and on capacitance vessels.
Acute Disease↗
Left ventricular regional wall stress in dilated cardiomyopathy.
Left ventriculography with simultaneous pressure micromanometry was performed in 11 normal control subjects and 17 patients with dilated cardiomyopathy (DCM). Left ventricular silhouettes in the right anterior oblique projection were divided into eight areas, and regional wall stress was computed by Janz's method in each area excluding the two most basal areas. Wall stress was higher in DCM patients than in control subjects (p less than 0.01). The percent area changes from end diastole to end systole in each area were lower in DCM patients than in control subjects (mean for six areas, 22 +/- 14% versus 54 +/- 9%, respectively, p less than 0.01), but the coefficient of variation for the percent area changes in the six areas of the left ventricle in DCM patients was greater than that in control subjects (32 +/- 17% versus 15 +/- 4%, respectively, p less than 0.01), indicating regional differences in hypokinesis. There was a significant negative correlation between end-systolic regional wall stress and percent area change (r = -0.60 to -0.86, p less than 0.05) in each area. Thus, excessive regional afterload may play an important role in causing regional hypokinesis in DCM.
Cardiomyopathy, Dilated↗
Liver function in congestive heart failure: abnormal elevation of serum hepatic enzyme and hepatic venous flow velocity.
Fifty one patients (pts) with various heart diseases and 6 normal subjects (N) were studied. Four of the 51 pts showed unusually high GOT values (greater than 3000 IU) without preceding evidence of acute heart failure, myocardial infarction, or hepatitis. Of these 4 pts, either ventricular tachyarrhythmias, marked bradycardia, or rapid ventricular response with atrial fibrillation (af) were evident a few days prior to the GOT elevation. GOT values returned to below 100 IU within a few days, but hypotension and frequent arrhythmias were sustained in 3 of the 4 pts and these 3 pts died about one month later. The symptoms of the remaining one improved but he too died 9 months later of ventricular fibrillation. A postmortem histological examination revealed centrilobular necrosis of the liver cells. Thus, abnormal GOT elevation may result from hepatic cell necrosis, which is probably due to tissue hypoperfusion caused by severe arrhythmias. Hepatic venous flow velocity (HFV) was measured in the remaining 47 pts and 6N using a pulsed doppler echocardiogram. The HFV curve was biphasic, with the first curve corresponding to the forward flow velocity during ventricular systole (s-HFV) and the second corresponding to ventricular diastole (d-HFV). The ratio of the area under s-HFV curve to the sum of areas under s-HFV and d-HFV curves was defined as the VI ratio. In N, the VI ratio was 0.7 +/- 0.06 whereas the VI ratio in pts in sinus rhythm tended to be above 0.7. This indicated that s-HFV is greater than d-HFV in N while s-HFV is less than d-HFV in pts in sinus rhythm. There was a good negative correlation (n = 15: r = -0.70) between VI ratio and cardiac index (CI) in these pts, suggesting that the contribution of s-HFV to the venous return becomes greater as the cardiac function becomes more impaired. In pts with af, the VI ratio was below 0.5 and there was a good positive correlation (n = 14: r = 0.82) between the VI ratio and CI. This suggested that the s-HFV may be reduced due to a lack of atrial contribution in af so that contribution of d-HFV to venous return becomes greater as the cardiac function becomes more impaired. Thus, the HFV pattern may reflect the abnormality of the cardiac pump function in human beings.
Adult↗
[Diastolic rapid filling in mitral regurgitation].
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Blood Flow Velocity↗