Five hundred and forty-eight patients who sustained their first acute myocardial infarction (AMI) were admitted to the coronary care unit (CCU). Ninety-eight of them were known diabetics. The diabetic patients were younger, 50±12 vs. 64±18 years of age (p<0.05), and the proportion of females in their group was higher than in the nondiabetics, 44% vs. 33.4% (p<0.05). The in hospital mortality rate was 30% for diabetics and 16% for nondiabetics (p<0.001). Diabetics had a higher percentage of mortality caused by left ventricular failure (LVF) (p<0.025) and a tendency for more frequent complete A-V block (p<0.01) compared to nondiabetics. Obesity and a positive family history for coronary heart disease were more prevalent in the diabetic group (both p<0.01).
The echocardiographic assessment of left ventricular function, performed in 125 consecutively admitted patients (25 diabetics and 100 nondiabetics) on the 3rd-5th post-infarct day, showed that the indices of myocardial contractility, that is, E point septal separation (EPSS), ejection fraction (EF) and fractional shortening (FS) were far more impaired in diabetics than in nondiabetics (p<0.01, p<0.005, p<0.005, respectively). No significant difference was found in the prevalence of dyskinetic, akinetic and hypokinetic segments between the two categories of patients, suggesting no difference in the amount of myocardial mass affected by the AMI.
Our results indicate that the increased incidence of LVF developed in diabetics after an AMI compared to nondiabetics may be caused by other factors, probably some form of latent diabetic cardiomyopathy as a result of either small vessel disease or metabolic disorder.

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The blood pressure, electrocardiographic findings and serum total cholesterol of Tongans, characterized by extreme obesity, were compared with those of Japanese employees of a trading firm in Tokyo. The prevalence of cardiovascular diseases in Tongans as far as assessed by these measurements was rather low for their excessive obesity. It is unclear whether the relatively low prevalence rate of cardiovascular diseases among the Tongans is due to genetic factors which might be considered an ethnological difference, or to environmental factors. Reducing weight is very difficult for many obese people. Accordingly, if "healthy obesity" exists, elucidation of its mechanism will be glad tidings for obese persons. However, the most prevalent diseases among the Tongans were the same as those of the developing countries. Consequently, imitating the Tongan lifestyle does not necessarily assure the longevity of obese persons of developed nations, although it may decrease the risk of the cardiovascular diseases.

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To study the acute effects of ISDN, nifedipine, propranolol and placebo on cardiac function in patients with myocardial ischemia and to characterize their hemodynamic effects by PANOVA, we repetitively performed exercise radionuclide angiography (RNA) following random assignment of each drug in 20 patients with effort angina pectoris. We obtained exercise response curves of hemodynamic parameters determined by RNA. ANOVA was performed to analyze the sizes (average height) of those response curves, and PANOVA (principal component analysis, PCA, combined with ANOVA) to analyze differences in the profiles (patterns) of the curves.
By conventional analysis of variance followed by a Scheffe type multiple comparison, end-diastolic volume after ISDN, which was significantly smaller than those after the other drugs at rest (p<0.01), was similar to those after nifedipine and propranolol during exercise (96.4±4.6ml/m2 vs. 94.8±5.1ml/m² and 97.1±4.9ml/m², respectively). Systemic vascular resistance after nifedipine, which was also significantly lower than those after the other drugs at rest (p<0.05), was not different from that after placebo during exercise (16.9±1.1 units vs. 18.7±1.3 units). Thus, this analysis was considered insufficient to fully differentiate the characteristics of each drug.
By PANOVA, the profiles of LVEF with these three antianginal drugs were similar, and significantly differentiated from that of placebo (p<0.05). This indicated that the antianginal effect could be represented by the profiles of the response curves of LVEF, using PANOVA. Evaluating the underlying hemodynamic mechanisms of these drugs by PANOVA, ISDN was significantly differentiated from nifedipine and propranolol by the profile of end-diastolic volume (p<0.05). The characteristics of nifedipine were clearly demonstrated by the size and profile of systemic vascular resistance, and those of propranolol were also differentiated by the size and profile of the double product and P-V index.
Hence, it is concluded that with the aid of PANOVA, the changes in hemodynamic parameters during ischemia can be evaluated in a manner that is highly effective in differentiating the characteristics of the effects of antianginal drugs in patients with angina pectoris.

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It is not clear whether hemodynamic and other benefits from dualchamber pacing also exist in elderly patients.
We studied a group of 18 elderly patients (mean age 74±4 yrs) with exercise testing in DDD and VVI modes in a randomized way to compare the effects of these pacing modes on exercise capacity, atrial rate and exercise-induced arrhythmias. Patients were selected when complete heart block was present without clinical evidence of sinus node dysfunction.
Significant differences were observed: atrial rate was lower during exercise in DDD-mode (p<0.01); exercise time and cumulative load increased (p<0.05); maximal oxygen uptake was improved (p<0.05). Some of these differences were less clear in a subgroup with replacement of a VVI-device by DDD-stimulation.
No differences could be observed in severity of exercise-induced arrhythmias. No evidence of sinus node dysfunction was found during exercise. Reprogramming of atrial sensitivity was required in 3 patients, with reprogramming to DVI because of paroxysmal atrial fibrillation once. Two patients died within a mean follow-up period of 13 months. Sinus rhythm was present at the most recent evaluation in all patients, including the patient stimulated in the DVI mode.
Physiologic stimulation is of value for elderly patients with an active life style and complete heart block. Reprogramming to another pacing mode is only seldom necessary.

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Out of 20 subjects selected for refractory arrhythmias, amiodarone therapy (200mg/day) was efficacious in 85%. No statistically significant variations in electrocardiographic parameters (QTc) were observed; similarly, there was little evidence of side effects 1 year after initiation of treatment. These results were most likely due to the low daily dosage administered. We observed:
1) a significant increase in rT3 levels;
2) a decrease in TT3;
3) a uniform homeostasis of free fraction (FT₃; FT₄)
These effects are all characteristic patterns of a "Low T3 Syndrome". The dosage of circulating amiodarone in 6 patients with borderline hormonal status (3 hyper-and 3 hypothyroidism) was not found to be an efficacious test for therapeutic monitoring. Identification of a statistically significant linear regression relationship between cumulative dose of amiodarone and rT₃ levels may be a useful test in clinical practise for establishing more appropriate therapeutic dosages. Furthermore, it provides a guideline for threshold levels (maximum rT₃=100-110ng/dl) which are in close association with several side effects.

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The electrocardiographic characteristics of P waves from patients having more than two episodes of transient atrial fibrillation (T-af) were examined during an episode-free period. The P waves of these patients recorded from the X Y Z leads of Frank's lead system on high-speed and high-gain recordings revealed longer durations than those of the normal control subjects (p<0.001), while the standard 12 lead ECG did not show any difference in width between the 2 groups. The configuration of the P loops on VCGs showed abnormal irregularities, such as bites or notches, in 16 of 28 cases of the T-af group. The maximum magnitudes of the P loops in VCGs and those in SVECGs were greater in the T-af group than those in the normal group (p<0.05). Body surface maps during atrial excitation showed that the duration of the anterior maximum was longer than that of the left maximum, and that the values of both maxima of the T-af group were longer than those of the normal group (p<0.01). These findings suggest the presence of intra-atrial conduction disturbances in patients with this disease, which might contribute to the genesis of this arrhythmia. Furthermore, these electrocardiographic characteristics of the P waves in the T-af group can be used as predictive and diagnostic signs of this arrhythmia even during an episode-free period.

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We performed an electrophysiologic study (EPS) in 8 patients who had received corrective surgery for tetralogy of Fallot. The mean age was 30 years. An average of 15 years had elapsed after corrective surgery. Two patients had episodes of syncope. ECG showed normal sinus rhythm in 7 patients and atrial fibrillation in 1, and all had complete right bundle branch block. All patients had ventricular premature beats of grade 3 or higher of Lown's classification. Overdrive suppression test was performed in 6 patients. Corrected sinus node recovery time (CSNRT) ranged from 230msec to 510msec. Wenckebach block of atrioventricular nodal conduction occurred at rates of 130 to 170 bpm during atrial pacing. The H-V interval was prolonged to 60msec in 1 patient, but was below 55msec in the others. Programmed stimulation induced ventricular tachycardia (VT) in 3 patients, nonsustained VT in 2 and sustained VT in 1. In 2 of 3 patients, delayed potential or fragmentations were recorded in the outflow tract of the right ventricle. During the follow-up period of 20 months, 2 patients died suddenly. Their CSNRTs and H-V intervals were normal. Ventricular tachyarrhythmia seems to be important as a cause of late sudden death after repair of tetralogy of Fallot.

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To evaluate pathologic features of myocardial infarction of the right ventricle (MI-RV), we analyzed 106 autopsy cases with transmural myocardial infarction (MI) (fresh in 46 cases and healed in 60). Anterior MI was observed in 47, posterior MI in 54 and lateral in 5. There were 13 cases (12%) with MI-RV (anterior in 1 case and posterior in 12), which included 10 cases with fresh MI and 3 with healed MI. All cases with MI-RV had associated transmural interventricular septal infarction. Of the 13 cases with MI-RV, 9 (69%) had right ventricular dilatation (RVD) and 2 had right ventricular hypertrophy. Extensive MI-RV (more than 1/3 of the right ventricle) was observed in 8 (89%) of those with RVD. Of 93 cases of MI without MI-RV, 14 (16%) had RVD. The incidence of RVD was greater in cases with MI-RV than in those without (p<0.005). All 12 cases with posterior MI-RV had significant (_??_75%) narrowing of the right coronary artery (RCA), and 19 cases (87%) of those with posterior MI without MI-RV, had similar lesions.
In conclusion, the incidence of RVD and significant narrowing of RCA was greater in cases with posterior MI-RV than in those with posterior MI.

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Guyton indicates that the contribution of venous resistance to venous return resistance is magnified by the compliance ratio (_??_30) of the venous compartment to the arterial compartment. Therefore, even a slightly increased venous resistance sensitively decreases venous return and hence cardiac output in the circulatory equilibrium. However, Guyton's diagram does not allow an easy and explicit evaluation of the effect of venous resistance on cardiac output. The circulatory equilibrium can be visualized graphically by Togawa's four quadrant diagram. However, Togawa's diagram does not include venous resistance. Therefore, I modified Togawa's diagram to incorporate venous resistance in the first quadrant for the cardiac output curve. The new diagram shows easily and explicitly that venous resistance sensitively tilts down either the venous return curve or the cardiac output curve and markedly decreases venous return and cardiac output.

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The volume of air moved into the trachea due to ventricular activity-a record of which is the pneumocardiogram (PNCG)-is always less than true stroke volume. A new method of investigating this relationship consists of inducing a known volume change (ΔV_in) within the thorax and measuring the volume of air (ΔV_out) recorded with a pneumotachograph connected to the trachea. The range of ΔV_in was from 4ml to 36ml. A linear relationship (mean r=0.98, p<0.001) between ΔV_out and ΔV_in was observed in 19 anesthetized, intubated dogs: ΔV_out=(f)ΔV_in, where f=0.53±0.09 (mean±SD). The coeff=icient, f, ranged from 0.40 to 0.71. These results demonstrate that although f is subject-dependent, ΔV_out reliably reflects changes in ΔV_in. It is suggested that the technique of inducing a known volume change within the thorax and measuring the volume of air recovered from the trachea could be used as a method for calibrating the pneumocardiogram to obtain stroke volume.

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A case of arrhythmogenic right ventricular dysplasia with frequent episodes of ventricular tachycardia (VT) in a 57-year-old man is reported, His electrocardiogram showed a normal axis and inverted T waves in V₁-V₃ during sinus rhythm and a left bundle branch block pattern during VT. The VT could be terminated by either intravenous administration of lidocaine or procainamide or by cardioversion. Echocardiogram and right ventriculography showed reduced wall motion of the apex and infundibulum of the dilated right ventricle. No evidence of ischemic heart disease was found by left ventriculography, coronary arteriography and RI scintigraphy. A prominent late potential following the QRS complex was recorded by averaging and magnifying the surface electrocardiogram. The combination of oral mexiletine and disopyramide partially suppressed the VT attacks and relieved the subjective symptoms, however the late potential remained almost unchanged.

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A 61-year-old man with hypertrophic obstructive cardiomyopathy with asymptomatie ventricular tachycardia underwent electrophysiologic study. Double extrastimuli at the right ventricular outflow tract induced polymorphic ventricular tachycardia which degenerated into fibrillation. After intravenous administration of 50mg of disopyramide, the pressure gradient in the outflow tract disappeared, but the tachycardia inducing zone appeared at the right ventricular apex. Although disopyramide may be used in patients with hypertrophic cardiomyopathy to relieve the intraventricular pressure gradient, it should be used only after evaluating its safety and efficacy electrophysiologically.

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A case of a 24-year-old man with the contracted form of primary endocardial fibroelastosis diagnosed by left ventricular endomyocardial biopsy showing a markedly thickened endocardium with fibroelastic proliferation is reported. He had no evident symptoms of congestive heart failure except for shortness of breath on moderate exertion. Echocardiogram showed thickened and dense echoes from the left side of the septum and from the posterior left ventricular endocardium. Hemodynamic and angiographic studies revealed marked elevation of right and left ventricular end-diastolic pressures with dip and plateau pressure contours, moderate pulmonary hypertension, left atrial enlargement and mild mitral regurgitation. Further elevation of right and left ventricular diastolic pressures and pulmonary artery pressure was observed at the second evaluation after 5 years. Our patient suggests that primary endocardial fibroelastosis should be included in the differential diagnosis of adult patients with obscure types of cardiac disease.

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Two-dimensional and Doppler echocardiographic findings in a 67-year-old man with endomyocardial fibrosis (EMF) are described. The two-dimensional echocardiogram showed typical features of EMF, right ventricular endomyocardial calcification, a thickened right ventricular wall, obliteration of the apex of the right ventricle and marked dilatation of the right atrium. In addition, premature opening of the pulmonary valve was observed during late diastole. The Doppler echocardiogram revealed forward flow from the right ventricle to the pulmonary artery, indicating the conduit state of the right ventricle. These findings were supported by cardiac catheterization and autopsy. Thus, two-dimensional and Doppler echocardiography are useful not only in making the diagnosis, but also in understanding the hemodynamic condition in EMF.

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