Preload affects left ventricular pump function through the FrankStarling curve by changing sarcomere length. However, common indices of preload, such as end-diastolic volume, or pressure, or stress, do not necessarily reflect sarcomere length, Ultimately, this depends on the elastic stiffness constant (k) and end-diastolic stress (σ), which are not in simple relation with the above mentioned indices. An index of preload is proposed, (kσ)^(1/k). This index has been evaluated in 148 patients with different degrees of hemodynamic overload, and in 24 normal subjects. The preload index was found to be 1.448±0.034 in normal subjects. However, in the other patients evaluated preload index increased in mitral insufficiency (1.490±0.035), in decompensated aortic insufficiency (1.490±0.89) and in dilated cardiomyopathy (1.52±0.125), and markedly decreased in aortic stenosis (1.367±0.039) and in hypertrophic cardiomyopathy (1.41±0.034). It was always positively related to the afterload, measured as peak systolic stress. No positive relationship was found with end-diastolic volume nor pressure. Therefore, preload as a compensatory mechanism is differently recruited in response to various degrees of hemodynamic overload and parallels the afterload, in agreement with the concept of preload-afterload mismatch.

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Exercise electrocardiography with or without thallium-201 scintigraphy was performed (pre-hospital discharge) in 66 asymptomatic survivors of a first inferior myocardial infarction (IMI). Although coronary angiography revealed an 82% incidence of multivessel coronary artery disease (MV-CAD) in the total cohort, the sensitivity of exercise ECG for MVCAD in the group with absent anterior ST-depression in the acute phase was low (11%). In contrast the presence of acute phase anterior STsegment depression improved the yield for MV-CAD to 55%.
Forty-six patients agreed to a symptom-limited exercise ECG plus/minus thallium imaging at 8-10 weeks post IMI. The sensitivity of detecting MV-CAD improved by 15% in patients with no acute phase anterior ST-segment depression and 16% in patients with acute phase anterior ST-segment depression. At each exercise protocol, thallium improved the sensitivity of exercise in detecting ischemia in the noninfarct zone.
It is concluded that following IMI, a high percentage of asymptomatic patients whose acute phase ECG showed anterior ST-segment depression will have MV-CAD detected by heart-rate limited and, more so, by symptom-limited exercise ECG. The detection rate will double in patients with no anterior ST-segment depression if exercise testing is delayed until 8-10 weeks post IMI.

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In order to detect silent impairment of the heart due to diabetes mellitus, the signal-averaging electrocardiograms (ECG) of 21 healthy subjects and 22 diabetic patients without ventricular tachycardia were compared. The QRS duration in the signal-averaging ECG was longer in diabetic patients than in the normal subjects (87.3ms vs. 114.5ms, p<0.01). Moreover, late potentials in the terminal portion of the QRS complex were observed in 7 diabetic patients (32%), but in only one normal subject (5%, p<0.01). These findings suggested that patients with diabetes mellitus frequently have intraventricular conduction disturbances, presumably due to diabetic microangiopathy.

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The purpose of this prospective study was to compare two methods of evaluating antihypertensive treatment efficacy: the traditional sphygmomanometric method and automatic home recording. Thirty hypertensive patients were studied who had been on antihypertensive therapy for at least 3 months. In the first 3 weeks of study their therapy was left unchanged and their diastolic blood pressures, measured with the traditional sphygmomanometer (weekly morning visit in the outpatient clinic; three successive recordings at 5-min intervals; subject seated), were always higher than 95mmHg. During the following 8 weeks, the physician tried to reduce diastolic blood pressure to not greater than 90mmHg by changing or increasing the therapy. Before and after any modification in therapy, noninvasive, automatic home, blood pressure monitorings for 24 hours were obtained and analyzed with Halberg's method of single cosinor, but were not made available to the physician until the end of the study. Automatic recordings showed that 18 patients had already had a circadian diastolic mesor ≤90mmHg under the original drug regimen. By changing or increasing the therapy, no additional pressure decrease was seen in the home pressure recordings of the whole group of patients, whereas the sphygmomanometric diastolic pressures of 15 patients fell under 90mmHg. Our study provides additional evidence that casual sphygmomanometric measurements can be misleading when one tries to assess the efficacy of antihypertensive therapy, and a cause of potential overtreatment.

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A mathematical model has been derived to describe cardiac contraction. This model assumes (1) a linear end-systolic force-length relation for the intact left ventricular (LV) myocardium with proportionality constant Ec, and (2) that the rate of increase in the number of active cross-bridges is proportional to the number of cross-bridges capable of being activated at that moment with a proportionality constant Ka. Quantitative evaluation of this model was performed using parameter values measured in the normal human LV. The model predictions agreed well with many earlier experimental data concerning the myocardial force-time relation, myocardial force-velocity-length relation, systolic time interval-afterload relation, time-varying elastance concept, several LV end-systolic relations, and LV dP/dt_max-end-diastolic volume relation. Moreover, two important basic properties of contractile proteins, i.e., the maximal force-generating capacity and the rate of activation of cross-bridges, were evaluated in the model from the values of Ec and Ka, respectively. Although no definitive biological proof has yet been provided for the assumptions, this model might mathematically integrate the myocardial and ventricular dynamics over the entire systole and then provides a new method for evaluation of the human LV systolic function from two basic properties of active cross-bridges.

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The concept of end-systolic myocardial stiffness permits the quantification of preload effects on fiber shortening and changes in the slope (max E_av) of the end-systolic stress-strain relation, which, if linear, reflect changes in the inotropic state. As an application of this new concept, the end-systolic stress-strain and shortening-afterload relations were evaluated on the basis of data from dogs studied during development of perinephritic hypertension. End-systolic stress-strain relations were linear before and 2 weeks after the induction of hypertension and the end-systolic pressure-diameter relations were not always linear. The shortening-afterload relations obtained directly from raw data points displayed enhanced contractility in the hypertensive state under betaadrenergic receptor blockade. However, the preload-corrected shortening-afterload relations demonstrated that contractility was unchanged in hypertension. Hypertensive hearts operated at higher preload than normotensive hearts at any afterload levels. This discrepancy between the conventional method without preload-correction and the preloadcorrected analysis indicates the importance of preload- correction on shortening-afterload relations in hypertension.

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The effects of a new thromboxane A₂ synthetase inhibitor (DP-1904) on electrical stability of the heart were tested in anesthetized, open chest dogs. The incidence of spontaneous ventricular arrhythmias, ventricular refractory period and ventricular fibrillation threshold (VFT) during ligation of the left anterior descending coronary artery (LAD) for 180min and after reperfusion were measured as indices of stability. Ventricular fibrillation and ventricular tachycardia occurred spontaneously after ligation of LAD in 56% of 9 control dogs and 29% of 7 dogs which received intravenous DP-1904 (100mg) before ligation of LAD (n.s.). In the control group, the ventricular refractory period decreased in the ischemic region; consequently, the difference in refractory period duration between the ischemic and non-ischemic regions (i.e., dispersion) increased 30min after coronary ligation (7±9ms vs 32±17ms, p<0.05). The dispersion at 30min after coronary ligation, though, was not affected in the DP-1904 treated group (2±4ms vs 10±9ms, n.s.). The VFT (determined with pulse trains) decreased from 28±5mA to 15±11mA (p<0.05) 30min after coronary ligation in the control group, but was not affected (30±0mA vs 27±4mA) in the DP1904 group. The plasma concentration of thromboxane B₂ decreased after DP-1904 administration (baseline vs 30min after coronary ligation: 475±165pg/ml vs 165±74pg/ml, n=3, p<0.05), while the concentration of 6-keto-prostaglandin F_1α increased gradually. In conclusion, DP-1904 prevents a decline in electrical stability in the ischemic region of the canine heart during coronary occlusion.

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The venous blood flow in the great cardiac vein (GCV) was meas-ured with an ultrasonic transit-time flowmeter during brief occlusion of major branches of the coronary arteries in open-chest dogs. Occlusion of the right coronary artery did not affect GCV outflow. GCV outflow vanished when the left anterior descending artery (LAD) was occluded proximal to the bifurcation of the septal artery. When the LAD was occluded distal to the septal artery, the GCV flow reduction averaged 70%. Occlusion of the left circumflex artery resulted in a slight but significant decrease, followed by an increase in GCV outflow. Partial occlusion of the coronary sinus or GCV by a catheter resulted in a decrease in outflow. This suggests that the absolute value of coronary venous flow obtained by the thermodilution technique should be evaluated carefully.

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A case of a 73-year-old man with variant angina who developed chest pain and shock following an injection of sodium bicarbonate and hydrocortisone is reported. The electrocardiogram (ECG) during the chest pain attack revealed ST elevation in leads II, III and aV_F. It returned to a normal pattern 10min later. Coronary angiography, performed 2 hours after the anginal attack, showed no significant coronary arterial stenosis. One month later, an injection of ergonovine (16μg) into the right and left coronary arteries induced spasms in segments 4 and 13, with ischemic ECG changes. Possible causes of the anginal attack are a coronary arterial spasm induced by the allergic reaction to hydrocortisone and/or serum alkalosis due to the sodium bicarbonate injection triggered by hyperventilation.

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A 43-year-old woman with progressive external ophthalmoplegia developed a bifascicular block and dilatation of the right ventricle during 4 years of follow-up. Histochemical and electron microscopy studies detected mitochondrial abnormalities in ocular, skeletal muscle and cardiac biopsies. This case registers disease progression from the external ocular to the skeletal and cardiac muscles. Mitochondrial DNA was deleted in relation to the morphological abnormality.

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We describe an extremely rare case of secundum atrial septal defect with aortic stenosis and coronary artery disease showing a single second heart sound throughout the respiratory cycle by echocardiogram with simultaneous phonocardiogram. Aortic valve closure corresponded to the single second heart sound. We were unable to detect pulmonary valve closure (PVC) on echocardiogram. Because of the presence of pulmonary hypertension, the pulmonary component of the second heart sound (P₂) was presumed to be increased in intensity, and the PVC-P₂ interval was thought to be abbreviated. Carotid pulse tracing showed a prolongation of the left ventricular ejection time. We concluded that the single second heart sound was due to both prolongation of left ventricular systole and pulmonary hypertension.

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A case of patent ductus arteriosus (PDA) in an 80 years old female is presented. This is the oldest case reported in Japan and the most elderly case of newly diagnosed PDA in the world. Features of PDA in the elderly are reviewed.

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