A change in muscle length significantly alters the developed tension in mammalian cardiac muscle compared to that in skeletal muscle fibers. The intracellular mechanisms related to the length-dependent change in developed tension have been studied using Ca²⁺ indicators in intact preparations; a crossbridge-dependent change in the affinity of troponin-C for Ca²⁺ is a possible mechanism. This hypothesis is further supported by the measurement of Ca²⁺ bound to troponin-C in skinned preparations. The molecular mechanism of the cross-bridge-dependent change in the affinity of troponin-C for Ca²⁺ is not fully understood although the studies which employ the substitution of troponin-C in skinned preparations, transgenic animals and in an animal model with heart disease have been performed. We reviewed the current studies by analyzing the intracellular mechanism responsible for the length-dependent change in tension development in mammalian cardiac muscle.

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The macula densa, a plaque of specialized tubular epithelial cells located in the distal tubule, monitors the NaCl concentration of the tubular fluid and sends an as of yet unidentified signal to control glomerular hemodynamics. In this mechanism, called tubuloglomerular feedback (TGF), an increase in NaCl concentration at the macula densa constricts the glomerular afferent arteriole and thus decreases the single-nephron GFR. Along with the myogenic response, TGF significantly contributes to renal autoregulation. In addition, the macula densa also controls the rate of renin release, and hence the level of angiotensin II. Studies indicate that an appropriate interaction between TGF and the renin-angiotensin system is essential for body fluid and electrolyte homeostasis in the face of rather big variations in daily salt intake. Thus, alterations in TGF may play an important role in the pathogenesis/pathophysiology of various diseases such as hypertension, diabetes mellitus and congestive heart failure.

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We assessed the long-term outcome of medical therapy in 453 patients who underwent coronary angiography in the period from September 1973 to February 1984, and who had a significant stenotic lesion (75% or more stenosis) in a single coronary artery. The mean follow-up period was 9.8 years. The 5-and 10-year survival rates were, respectively, 96.0% and 91.3% in these patients, and these survival rates were comparable to the cumulative survival rates in the age-matched healthy male controls determined on the basis of overall death. Cardiac death occurred in 35/453 patients (7.7%) with single-vessel disease (SVD), and non-fatal myocardial infarction occurred in 17 patients (3.8%) during the follow-up period. The incidence of cardiac events, which was defined as cardiac death and nonfatal myocardial infarction, was as low as 1.2% per year. The survival rates were compared in terms of the presence or absence of myocardial infarction, the type of the coronary artery with stenosis, and proximal versus distal location of the stenotic lesion in the left anterior descending artery (LAD). The survival rates were similarly high in both assessed groups, with no significant differences. Patients with SVD treated medically had a good prognosis, except for those patients with decreased left ventricular function (ejection fraction≤40%).
These factors should be taken into consideration when selecting therapies for patients with SVD.

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Although experimental studies have demonstrated that reduced glutathione (GSH) is involved in cellular protection from deleterious effects of oxygen free radicals (OFRs) in ischemia and reperfusion, there are controversial data on the correlation between the levels of erythrocyte GSH and the ischemic process. To clarify, we determined the erythrocyte GSH levels in 21 patients with acute myocardial infarction (AMI), aged 39-70, who were not given thrombolytic therapy and 21 age- and sex- matched healthy controls. Samples of blood were taken on days 1, 3, 5 and 7 from AMI patients and on the same days from the controls.
The GSH levels of patients with AMI were significantly depressed by 11.5% as compared to the controls on the second day after infarction (7.44±1.71 vs 8.41±1.54U/gHb p<0.05). Although the total mean of GSH levels for all days was lower (3.8%) in patients than in the controls, this finding did not reach statistical significance (7.41±1.71 vs 7.71±1.27U/gHb, ns). There was no correlation between the erythrocyte GSH levels and cardiac enzyme concentrations, infarct localization, hemodynamic status according to Killip classification and the frequency of ventricular arrhythmias.
This preliminary work suggests that depressed GSH levels may be associated with an enhanced protective mechanism to oxidative stress in AMI. Measurements of erythrocyte GSH can be helpful in the estimation of oxidative stress in the course of AMI. However, further research must be done to determine the primary scavenger in AMI by analyzing all the enzymes and substrates involved in the endogeneous system that controls the effects of OFRs.

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This study examined 12 VTs in 8 patients who underwent radiofrequency (RF) catheter ablation for ventricular tachycardia (VT) associated with non-ischemic underlying heart diseases, and who were followed-up for more than 24 months after ablation. The site of VT origin was determined to be within a narrow site (within 1.0×1.0cm) in 5 VTs (4 patients), but VT originated from a wide origin (more than 1.0×1.0cm) in the other 5 VTs (3 patients). The remaining patient had two macroreentrant VTs revolving around an anatomical obstacle in both the clockwise and counterclockwise directions. Two of 5 VTs originating from a narrow site were successfully ablated by 2-3 RF applications. In VT associated with a wide origin, two perpendicular linear RF lesions with 6.0±1.8 RF applications were required to ablate the VT. Eight of the 12 VTs (66.7%) were finally ablated by RF current (30-50 watts), and they did not recur during the follow-up period of 31.2±6.5 months.
An excellent long-term outcome is expected, even in VT associated with non-ischemic underlying heart disease, if VT is successfully treated by RF ablation.

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The aim of the study was to classify the value of endomyocardial biopsies taken from the right ventricular septum in patients with ventricular tachyarrhythmias originating from the right ventricle.
In a cohort of 62 young patients (mean age 35.6 years) 4-5 endomyocardial biopsies were taken from the right ventricular septum and myocardial atrophy, fibrosis and lipomatosis were analysed qualitatively and semi-quantitatively. Much interest was focused on the arrangement and type of fibrosis. Lipomatosis, myocardial atrophy and a finer form of fibrosis surrounding individual myocytes or groups of myocytes were judged as the typical histopathological findings of arrhythmogenic right ventricular dysplasia.
The cohort of patients was subdivided clinically into idiopathic right ventricular outflow tract tachycardia (n=50) and arrhythmogenic right ventricular dysplasia (n=12).
In the group of arrhythmogenic right ventricular dysplasia pathological findings were found in 92% with typical fibrolipomatosis in two cases, severe fibrosis (>40% per biopsy) in 5 cases, a finer form of fibrosis surrounding individual myocytes without lipomatosis in two cases and a slight interstitial or subendocardial fibrosis in two cases. In only one patient the endomyocardial biopsy was normal.
In right ventricular outflow tract tachycardia normal endomyocardial biopsy findings predominated (80%). In two cases lipomatosis without fibrosis was a more or less normal finding, and in two other cases a slight interstitial or subendocardial fibrosis was found. Fibrosis was judged to be moderate or severe with discrete signs of inflammation in only two cases; in a long-term follow-up these two patients developed typical features of idiopathic dilated cardiomyopathy.
Endomyocardial biopsies taken exclusively from the right ventricular septum were able to distinguish between right ventricular outflow tract tachycardia and arrhythmogenic right ventricular dysplasia, although the typical finding of fibrolipomatosis in cases with arrhythmogenic right ventricular dysplasia was rare. Characteristics of fibrosis are the key to the correct diagnosis provided that histopathological analysis is based on experienced qualitative criteria (type and arrangement of fibrosis).
In conclusion, qualitative and semi-quantitative analyses of endomyocardial biopsies are far better than computerized quantitative methods. Biopsies from the free right ventricular wall cannot be generally recommended if a correct definition of arrhythmoge the right ventricular dysplasia in endomyocardial biopsies from the right ventricular septum is used.

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The absolute potential value of Wilson's central terminal was calculated at 2 msec intervals during a cardiac cycle in 60 clinical cases. Starting from the body surface potential data at 128 thoracic locations, the effect of immersion of the body into an infinite conductor on the surface potential was calculated to obtain values with reference to zero potential at infinity. The conductivity of the outside medium was then made to approach zero.
Comparison of the result with the original map showed nearly a constant shift of the potential, corresponding to the voltage of Wilson's terminal. In addition, the cardiac vector was calculated as the first approximation of the cardiac electromotive force and the lead vector of Wilson's terminal was obtained in order that the scalar product of the cardiac vector and the lead vector approximated the observed voltage of Wilson's terminal.
The results indicate that the voltage of the Wilson electrode depended on the surface voltage with a peak value near the maximal QRS force in most of the cases. The peak voltage of Wilson's terminal was either positive or negative, and was 0.15mV in absolute value on average. Voltage variations of Wilson's terminal during a cardiac cycle were 0.20mV as an average of all cases. The voltage of Wilson's terminal also depended on the direction of the equivalent cardiac vector. The lead vector of Wilson's terminal was found to be directed superiorly in most of the cases. The average magnitude of the lead vector of Wilson's terminal was 0.097Ω/cm, which corresponded to about 1/4 of that of lead I.

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The third heart sound (S3) is often present in children and adolescents but is not present in most adults. Applying at the left ventricle a mathematical model, the mechanism of the disappearance of S3 was studied employing the frequency analysis of the sound and echocardiographic data. The existence of a significant correlation between the spectrum energy of S3 and the diameter and thickness of the left ventricle at the moment of S3 in 25 healthy subjects (aged 21±7 years) allowed us to interpret the origin of S3 based on a viscoelastic oscillating system. Once the left ventricle starts vibrating it behaves as a simple physical model composed of a mass (m), a spring (k) and a viscous element. The abrupt deceleration of the blood mass (m) against the left ventricular walls (k) triggers the vibration of the system according to the equation Fd=1/2π√4k/m•√1-ξ2, where Fd is the natural damped frequency and ζ is the damping factor. The equation shows that the vibrating system can oscillate only if ζ is <1. During the growth of the individual the increased myocardial mass may lead to augmented viscous forces causing a gradual increase in ζ until the system becomes overdamped and consequently unable to vibrate causing the disappearance of S3.

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The use of transesophageal pulsed Doppler echocardiography provides an ideal approach for determining both pulmonary venous flow and transmitral flow. This approach thus provides information about the flow of blood into and out of the left atrium. We designed a new method for separately evaluating left atrial functions on the basis of the time-velocity integrals of pulmonary venous flow and transmitral flow using transesophageal pulsed Doppler echocardiography, assuming that the cross-sectional areas of the mitral ring during the left ventricular diastolic phase and of the four pulmonary venous orifices throughout a cardiac cycle were constant and that the blood flows of the four pulmonary veins exhibited identical velocity profiles. Good correlation was observed between the indices of left atrial function (i.e. left atrial reservoir, conduit and forward contractile volume) using this new method of analysis of Doppler echocardiographic data and those of a conventional method using contrast angiography. In conclusion, transesophageal pulsed Doppler echocardiography provided satisfactory information about left atrial function, and our new method may be one of the most practical techniques for estimating individual left atrial functions.

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Most of the patients in this study with spinal muscular atrophy were found to have tremors of the isoelectric line in the electrocardiogram (ECG) tracings. There were a total of 47 cases of SMA (mean age 40.8 months). All three types of SMA had a similar incidence (about 80%) of tremors in the tracings (p=0.885). In 7 cases the ECG tremors had an intermittent pattern.ECG tremors were commonly found in the majority of SMA patients and this finding, though non-specific, may suggest a possible SMA diagnosis.

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The first heart transplantation in New Zealand was performed on December 2, 1987. This study covers all forty-five transplantations that were performed in New Zealand at Green Lane Hospital from that time through January 1994.
Eleven patients from that group have died. The 30 day and 1, 2 and 4 year survival rates were found to be 91.1, 86.7, 80.0 and 75.6%, respectively.
The mean waiting period of the patients for heart transplantation was 61.9 days. Only pulmonary vascular resistance was a statistically significant risk factor for early death after cardiac transplantation. Ischemic time was not a significant risk factor in this study.

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Nitric oxide (NO) production is reduced in patients with essential hypertension and in some experimental models. We have investigated the effect of trichiormethiazide and captopril on NO synthase (NOS) activity and glomerular damage in the kidney of deoxycorticosterone acetate (DOCA)-salt hypertensive rats. DOCA-salt rats were induced with weekly injections of DOCA (30mg/kg body weight (BW)) and 1% saline in drinking water after right nephrectomy. As antihypertensive therapies, CAP (captopril, 40mg/kg BW) and TCM (trichlormethiazide, 10mg/kg BW) were given after induction of DOCA-salt hypertension. The increased blood pressure was significantly lowered by TCM, but not by CAP after 5 weeks. Nitrite production in kidney slices was suppressed in DOCA-salt rats, and immunoreactivity for both braintype NOS (B-NOS) in macula densa and endothelial-type NOS (EC-NOS) in renal vessels was decreased. TCM significantly increased the nitrite production in the kidney slices and B-NOS immunoreactivity, whereas these changes were less in CAP. Glomerulosclerosis score was significantly higher in DOCA-salt rats, and TCM ameliorated renal damage more effectively than CAP. These results indicate that the reduced nitrite production in the kidney of DOCA-salt hypertensive rats was increased more effectively by trichlormethiazide than by captopril, via increased immunoreactivity for B-NOS in the macula densa, and prevented renal damage.

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We report a 64-year-old man who complained of headache without chest pain at the onset of acute myocardial infarction (AMI). He had no history of chest pain or headache. Severe headache in this case was the first symptom of AMI. The headache was reproduced during stress test. During the angioplasty procedure, he also complained of headache without vasospastic change in the coronary artery. These findings suggest that the headache which accompanied AMI or myocardial ischemia in this case was due to referred pain rather than a generalized vasospastic disorder.

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We report the case of a 38-year-old man who had idiopathic ventricular fibrillation (VF) which initiated by abnormally short-coupled ventricular premature beats. VF was successfully prevented by the combination of pilsicainide, propranolol, and verapamil. In particular, the effects of pilsicainide are assumed to exert an important effect in controlling this arrhythmia. Class Ic drugs may be effective for preventing VF initiated by short-coupled VPBs.

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The patient was a 50-year-old woman with primary chylopericardium. Triglyceride rich chyloid fluid was continuously drained from the pericardial space through an indwelling catheter. A surgical procedure was scheduled since a medium chain triglyceride diet was insufficient to control the fluid accumulation. Before the operation, inflammatory signs were apparent around the indwelling catheter and the catheter was removed immediately. The inflammation was easily treated with antibiotics, and the pericardial effusion no longer accumulated during a follow-up period of 10 months.
The inflammatory process may have caused fibrin production and tissue adhesion in the pericardial cavity, and these might have prevented an accumulation of chyloid fluid and occluded the connection between the thoracic duct and the pericardial cavity.

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