In order to investigate the usefulness of percutaneous transluminal coronary angioplasty (PTCA) on subsequent left ventricular (LV) function in patients with acute myocardial infarction (AMI), regional ejection fraction (REF) was calculated from the left ventriculogram and compared in the acute and chronic phases (4 weeks after infarction) in 19 successful cases of PTCA (group A). In addition, 15 successful cases of intracoronary thrombolysis (PTCR) (group R) and 14 unsuccessful cases (group U) were also analyzed in this study.
From the results, the following points were elucidated.
(1) REF of group A in the chronic phase showed a significant increase compared to that in the acute phase (10±18% vs 20±19%, p<0.01), and this was similar to that observed in group R (9±19% vs 21±16%, p<0.01).
(2) All cases in group A showed a significant increase in REF (p<0.02), if recanalization occurred within 3 hours after the onset of AMI. Some cases in the 3-6 hour recanalization group showed a decrease in REF.
(3) In group A, only patients with subtotal occlusion on the initial coronary angiogram showed a significant increase in REF 4 weeks later (p<0.01), whereas patients with total occlusion on the initial coronary angiogram showed no significant increase in REF.
(4) In group A, only patients recanalized between 3 and 6 hours showed a severe degree of prolonged contrast staining immediately after successful recanalization following PTCA.
Thus, chronic phase regional wall motion was markedly improvedby PTCA in those cases with residual flow. In contrast, abrupt recanalization after PTCA might causally decrease regional wall motion due to hemorrhagic infarction, if it is performed in cases with total occlusion.

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To evaluate ventricular filling and interactions between right and left ventricles in patients with old myocardial infarction, right and left ventricular time-volume curves were analyzed from a cineangiographic study of 10 normal subjects (Group 1), 10 patients with old anterior myocardial infarction (Group 2) and 10 patients with old inferior myocardial infarction (Group 3). Volumes of both ventricles were calculated from each frame over an entire cardiac cycle using Simpson's method. From time-volume curves, peak ejection rates, peak filling rates and atrial kick rates were obtained for both ventricles and these parameters were normalized by end-diastolic volume. All patients were in sinus rhythm with heart rates less than 80 beats/min. There were no significant differences among the 3 groups in end-diastolic pressure of both ventricles and mean pulmonary artery pressure. Left ventricular ejection fractions were significantly lower in Groups 2 and 3 than in Group 1 (p<0.001, p<0.005, respectively), although there were no significant differences in end-diastolic volume indexes of either ventricle among the 3 groups. Peak left ventricular ejection rate and peak filling rates of the left and right ventricles were lower in Group 2 than in Group 1 (p<0.01, p<0.05, p<0.01, respectively) and peak filling rate of the right ventricle in Group 2 correlated with the peak filling rate of the left ventricle and left ventricular ejection fraction (r=0.64, r=0.64, respectively). Peak filling rate of the right ventricle in Group 2 correlated inversely with left ventricular peak negative dp/dt (r=-0.72), but no correlation was found between peak filling rate of the right ventricle and left ventricular end-diastolic volume index or mean pulmonary artery pressure. Peak ejection rate of the left ventricle and peak filling rates of both ventricles in Group 3 were lower than in Group 1 (p<0.02, p<0.02, p<0.01, respectively) and no correlation was found between peak filling rates of both ventricles. Wall motion of the right ventricular septal portion was slightly reduced in 5 patients in Group 2. In all patients in Group 3, right ventricular wall motion centering around the right ventricular diaphragmatic portion was reduced. These results suggest that in old inferior myocardial infarction, right ventricular wall motion abnormality results in impaired right ventricular filling, whereas in old anterior myocardial infarction, right ventricular filling is reduced indirectly due to impaired left ventricular filling.

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The purpose of this study was to evaluate the acute effects of sublingual nifedipine (10mg) on left ventricular systolic function (ejection fraction, peak ejection rate, time to peak ejection rate) and diastolic function (peak filling rate, time to peak filling rate, filling fraction during rapid filling) at rest and during exercise using radionuclide angiography in 17 patients with ischemic heart disease. The results of the study were as follows. Diastolic indexes in the patient group were significantly different from the values in the control group at rest and during exercise. Peak filling rate and filling fraction improved significantly after nifedipine administration. These values did not show significant differences from the values in normal subjects which were obtained before nifedipine administration. The peak filling rate during exercise after nifedipine administration increased significantly, although the value was lower than that in the control group. At rest, systolic indexes in the patient group showed abnormal values, although the differences from the control values were not significant. Ejection fraction and peak ejection rate were significantly lower than those in the control group during exercise. After nifedipine administration, peak ejection rate at rest and during exercise, and ejection fraction at rest in the patient group improved significantly. Seven of 17 achieved the same exercise workloads as control conditions without symptoms or ECG changes. These data suggest that nifedipine improved left ventricular systolic and diastolic dysfunction, as well as exercise tolerance in patients with ischemic heart disease.

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Three cases of chronic rheumatic heart disease with involvement of all four valves are presented. The involvement of tricuspid and pulmonary valves was suspected clinically and was confirmed by two-dimensional echo, Doppler, hemodynamic and angiographic findings. These findings were also verified surgically and histopathologically in 2 cases. One of the cases died after cardiac catheterization; the other 2 cases were treated surgically with success.

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Heat stable adenosine 3', 5'-monophosphate (cAMP)-dependent pro-tein kinase (PK) inhibitor was extracted and partially purified from hu-man heart tissue. One unit of inhibitor was defined as the amount necessary to produce 50% inhibition of the PK activity of 50p mole/min. The eluate from Sephadex G-75 showed a specific activity of 41units/mg, with purification of 390-fold and recovery of 23%. The molecular weight was 29, 000 by gel filtration and S_{20, w} was 1.4, similar to that of rabbit skeletal muscle PK inhibitor. At the purification step involving trichlor-acetic acid precipitation, the specific activity was not significantly differ-ent between tissue from the atria and ventricles. However, the particu-late fraction of ventricular homogenate yielded a specific activity that was 3 times higher than that of the supernatant. Kinetic analysis showed that the inhibition was noncompetitive with respect to ATP, historic and cAMP. In the presence of inhibitor the binding of cAMP to PK was increased. This is consistent with the concept that the inhibitor directly interacts with the catalytic subunit of PK, and modifies the physiological action of cyclic AMP.

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The effects of sodium dichloroacetate (DCA) on the activity of the pyruvate dehydrogenase complex (PDH) and the mechanical function of the isolated ischemic rat heart were investigated. Ischemia was induced by restriction of coronary flow. Perfusion with DCA caused a decrease in the tension developed (DT) and the maximal rate of tension development (+dT/dt max), and an increase in the resting tension (RT) at low flow rates (0.6 and 0.15ml/min). However, it did not affect the DT or +dT/dt max of normoxic hearts (3ml/min) or hearts at zero flow rate. DCA increased PDH activity in hearts at all flow rates. It was concluded that this effect of DCA was associated with a decrease in lactate production, rather than an increase in the lactate/pyruvate ratio.

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The electrophysiological effects of flecainide on the action potential were examined in guinea pig ventricular muscles using microelectrode recording methods. Under the control conditions, flecainide (0.5-1μg/ml) did not alter the resting potential, action potential duration (APD) or effective refractory period (ERP). The major effect of flecainide was on maximum upstroke velocity (Vmax), which was depressed in a dose-dependent manner. In high [K⁺] medium (potassium concentration=10mM), Vmax was depressed by 16.8% at a concentration of 1.0μg/ml (8.8% in normal [K⁺]o). In metabolic acidosis (pH=6.89), it was depressed by 15.7% at the same concentration of the drug (8.3% in normal condition). The changes in ERP and ERP/APD_90% in high [K⁺]o and metabolic acidosis were not significantly different from the normal condition. After hypoxic perfusion for 15min, Vmax depression by flecainide was 16.3% (7.4% in control medium). The increase of ERP/APD_90%, was also greater in hypoxia. These data indicate that the most prominent effect of flecainide is Vmax depression which is enhanced under the high K⁺, acidic and hypoxic conditions. Therefore, it is suggested that flecainide may be most effective for ventricular arrhythmias occurring in myocardial ischemia.

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A 54-year-old man had palpitations on swallowing without any esoph-ageal or heart disease. Electrophysiological findings, including an A wave in the high right atrial leads appearing prior to the A wave on His bundle electrogram, revealed that the arrhythmia was paroxysmal supraventricular tachycardia originating in an ectopic focus of the atrium with intraventricular aberration. Treatment with verapamil, 120mg/day, reduced his symptoms in spite of an insignificant decrease in the arrhythmia observed with Holter dynamic electrocardiography.

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We present a case of tricuspid annulus calcification, documented by fluoroscopy, chest X-ray and cross sectional echocardiography. This case is interesting for two reasons:
1) Tricuspid annulus calcification is extremely rare and very few cases have been reported.
2) It is the third case described where two-dimensional echocardiography established the diagnosis of this very rare condition. Previously reported cases of tricuspid annulus calcification are reviewed.

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In SHR, high blood pressure caused concentric cardiac hypertrophy, but not dilated cardiac hypertrophy and also not localized type of hypertrophy. Also the pathological alteration of cardiac hypertrophy with increase of blood pressure(BP) correlated to the alteration of QRS vector(QRSv) or QRS-T angle in vectrocardiography(VCG).

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Development of hypertension in the young SHR may be, in part, related to the decreased urinary Na excretion, whereas the augmented synthesis of renal DA is regarded as a compensatory mechanisms to overcome the impaired natriuresis and an elevation of BP.

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