Daiji Saito

Early Afterdepolarization Abolished by Potassium Channel Opener in a Patient with Idiopathic Long QT Syndrome

Abolished Early Afterdepolarization by Nicorandil. We describe a 17‐year‐old boy with idiopathic long QT syndrome and repeated syncopal episodes. Early afterdepolarization (EAD) in the monophasic action potential (MAP) was demonstrated in the posterior septum of the left ventricle. Injection of the potassium channel opener nicorandil decreased KAD and shortened MAP duration. The syncopal episodes due to ventricular fibrillation disappeared after administration of the potassium channel opener.

Effects of oral theophylline on sick sinus syndrome

OBJECTIVES We sought to determine the effect of theophylline on cardiac pauses in sick sinus syndrome. BACKGROUND Sick sinus syndrome, a relatively benign condition, is usually treated with pacemaker implantation without any proved effectiveness. Thus, an appropriate pharmacologic therapy would be useful. METHODS Theophylline (200 to 400 mg/day for 1 month) was initially administered orally to 17 patients with sick sinus syndrome, which is manifested by sinus pauses of > 2.5 s. Eleven of the 17 patients subsequently received theophylline for an additional 8 to 37 months. Twenty-four-hour Holter recordings were obtained before treatment, at the end of 1 month of treatment and then at 6-month intervals. RESULTS Theophylline decreased the frequency of sinus pauses from 256 +/- 230 to 23 +/- 62 pauses per 24 h and decreased the duration of the longest pauses from 4.7 +/- 1.8 to 2.2 +/- 0.97 s after 1 month of treatment. Subjective symptoms associated with cardiac pauses disappeared in 16 of 17 patients. Ventricular premature beats increased in frequency but did not last longer than two beats. Three patients experienced adverse effects. Nine of the 11 patients receiving long-term treatment had a good outcome, but 2 patients required a pacemaker because of the reappearance of long sinus pauses. CONCLUSIONS The results suggest that oral theophylline may be beneficial for the treatment of patients with sick sinus syndrome.

Papillary fibroelastoma in the left ventricular outflow tract.

SummaryWe report a case of a papillary fibroelastoma originating from the left ventricular endocardium in the outflow tract which was discovered by echocardiography in an asymptomatic patient. Two echocardiographic features were observed: (1) the tumor surface was smooth, and characteristic papillary formation was not detected; and (2) the outline of the mass was clearly defined as a dense echo, with the central, radiolucent, portion surrounded by a highly refractive linear echo at the level of the maximum diameter of the mass. The excised tumor was covered with a gelatinous substance that masked multiple papillae on the surface, but its echolucent center could not be explained by the pathology of the tumor which was solid centrally. Our case indicates that a papillary fibroelastoma may sometimes show echocardiographic findings similar to those of a myxoma, although other investigators have not noted the smooth surface and the echolucent center makes it indistinguishable from a myxoma. Thus, in some cases, it is difficult to distinguish papillary fibroelastoma from myxoma by echocardiography.

Primary pulmonary hypertension improved by long-term oral administration of nifedipine.

of left ventricular dimensions on endocardial and epicardial QRS amplitude and ST-segment elevations during acute myocardial ischemia. Circulation 61:679, 1980. 3. Berman JL, Wynne J, Cohn PT: Multiple-lead QRS changes with exercise testing. Diagnostic value and hemodynamic implications. Circulation 61:53, 1980. 4. Kilpatrick D: Exercise vectorcardiography in diagnosis of ischemic heart disease. Lancet 2:332, 1976. 5. Willems JC, Poblete PF, Pipberger HV: Day-to-day variation of the normal orthogonal electrocardiogram and vectorcardiogram. Circulation 45:1957, 1972. 6. Holland RP, Arnsdorf MF: Solid angle theory and the electrocardiogram: Physiologic and quantitative interpretations. Prog Cardiovasc Dis 19:431, 1977.

Reperfusion through balloon catheter to minimize myocardial infarction during the interval between failed percutaneous transluminal coronary angioplasty and emergency coronary artery bypass grafting

SummaryA 65-year-old man was admitted with chest pain. A diagnosis of spastic angina was made because of symptoms of recurrent anginal attacks associated with ST-segment elevations in the electrocardiogram. A selective coronary arteriogram revealed a 90% diameter narrowing of the proximal left anterior descending coronary artery (LAD). No angiographically visible collaterals from the right coronary artery to the LAD were observed. The ventriculogram showed normal contraction of the left ventricle with an ejection fraction of 65%. Percutaneous transluminal coronary angioplasty (PTCA) failed resulting in total occlusion of the stenosis. Repeat PTCA at a higher pressure and of longer duration failed to redilate the artery. Reperfusion with the blood from the femoral artery through the balloon catheter, which was used for the PTCA, was carried out until coronary artery bypass grafting (CABG). Blood flow rate of perfusion was approximately 25 ml/min. Reperfusion through the balloon catheter reduced chest pain and ST-segment elevations in the electrocardiogram. The patient tolerated the operative procedure well and his post-operative course was uncomplicated. The interval between the acute occlusion and revascularization by CABG was approximately 4 1/4 h. The ventriculogram taken 56 days after the CABG demonstrated normal contraction of the anterior wall of the left ventricle with an ejection fraction of 63%. Abnormal Q waves did not appear in precordial leads of the electrocardiogram after the surgery. The thallium scintigram showed no perfusion defects.In conclusion, this case suggested that autologous blood reperfusion through balloon cathether would be worth attempting in some cases for minimization of myocardial infarction during the interval between failed PTCA and emergency CABG.

Apical hypertrophy associated with rapid T wave inversion on the electrocardiogram

SummaryA 53-year-old man who had no chest pain and no family history of heart disease demonstrated a rapid T wave change on an electrocardiogram, from a positive T wave to a giant negative T wave, within 1 year. Echocardiography showed no left ventricular hypertrophy before or after the T wave change. Cine-magnetic resonance imaging revealed focal apical hypertrophy after the appearance of the giant negative T wave. Although T wave inversions sometimes develop within a short period in patients with hypertrophic cardiomyopathy, they are rare in a patient without hypertension or chest pain.

Autoregulation by the right coronary artery in dogs with open chests; comparison with the left coronary artery

Experiments were conducted to study autoregulatory responses of the right and left coronary arteries in dogs with open chests. The right and left circumflex coronary artery were cannulated and perfused with blood from the femoral artery via a pressurized reservoir. The perfusion pressure was varied in steps over a wide range and coronary blood flow rates were measured. Both the right and left coronary arteries exhibited autoregulation but the pressure at the lower end of the autoregulatory range was lower in the right (39.8±9.1 mm Hg) than in the left circumflex coronary artery (57.6±14.5 mm Hg). The slope of the pressure-flow relationship in the autoregulatory range was less steep in the right than the left circumflex coronary artery. The closed-loop gain when the perfusion pressure was less than 100 mm Hg was greater in the right than in the left circumflex coronary artery. Increases in the right ventricular afterload produced by pulmonary artery constriction decreased the closed-loop gain, shifted the autoregulatory range upward and to the right, and made the slope steeper. These results indicate that more effective autoregulation is carried out by the right than the left circumflex coronary artery.

Morning increase in hemodynamic response to exercise in patients with angina pectoris

SummaryThe present study was conducted to determine whether or not there is diurnal variation in the hemodynamic responses to stimuli that increase myocardial oxygen demand, and the effects of such variation on electrocardiograms (ECG). Fifteen patients with angina pectoris, 17 patients with old myocardial infarction, and 8 healthy controls were examined in this study. Graded exercise stress testing was conducted in the supine position, once in the morning and once in the afternoon, using a bicycle ergometer. A standard 12-lead ECG was recorded before, immediately after, and 3, 5, and 10 min after the end of the exercise. The exercise ECG and blood pressure changes were compared among the groups and, within each group, the results after morning and afternoon exercise were compared. Hemodynamic responses, including heart rate, blood pressure, and the pressure-rate product, showed greater increases in the morning than in the afternoon in angina patients and controls, in association with greater depression of the electrocardiographic ST-segment. In contrast, patients with old myocardial infarction exhibited no difference in hemodynamic responses or the ST-pattern from morning to afternoon. The results suggest that diurnal variation of hemodynamic responses to increased oxygen demand may explain, at least partly, why myocardial ischemia of effort angina is more severe in the morning than in the afternoon.

Reactive hyperaemic flow characteristics of the right coronary artery compared to the left anterior descending coronary artery in the open-chest dog

Reactive hyperaemia, the cardiovascular response to transient occlusion of a vessel, was examined and compared in the right coronary artery (RCA) and the left anterior descending coronary artery (LAD) in the same heart of an open-chest dog. First, to study the relationship between reactive hyperaemia and occlusion time in the RCA and LAD, respective flows were measured and reactive hyperaemia was induced with different occlusion times. Occlusion time required for half the maximum peak percentage reactive hyperaemic flow (%PRH), t1/2, for the RCA was approximately twice that of the LAD: 11.4±2.3 s versus 5.9±1.4 s. Maximum %PRH of the RCA was significantly greater than that of the LAD while the percentage repayment of the RCA was lower than that of the LAD. Augmentation of right ventricular oxygen consumption shortened t1/2 and increased percentage repayment significantly. Second, to determine “critical pressure”, which was defined as the perfusion pressure below which reactive hyperaemia was abolished completely, the RCA and LAD were perfused through a shunt from the carotid artery, perfusion pressure was varied in the range of 100 to 20 mmHg and reactive hyperaemia was induced. Critical pressure in the RCA was significantly lower than in the LAD: 32.2±5.7 mmHg versus 41.5±5.0 mmHg. These results suggest that the RCA has a greater flow reserve than the LAD. These results were consistent with the difference of oxygen metabolism between the right and left ventricles. The difference of oxygen metabolism between the two ventricles would, at least partly, account for these results.

The Role of Adenosine on Myocardial Reactive Hyperemia

The present study was conducted to test the hypothesis that activation of adenylate cyclase participates in myocardial reactive hyperemia by release of adenosine during brief coronary occlusions using forskolin and 8-phenyltheophylline (8-PT). We also examined the possible contribution of membrane-bound 5′-nucleotidase to the synthetizing of adenosine. Intracoronary infusion of α, β-methylene adenosine 5-diphosphate (AOPCP) was used for this purpose. Forskolin increased flow debt repayments by about 25% following 15-, 20- and 30-s coronary occlusions, but with 8-PT, forskolin-induced increments in the flow debt repayments diminished significantly (P < 0.05). Further, AOPCP infusion attenuates flow debt repayment by about 30% following coronary occlusions of 15 s or longer (P < 0.05). Neither forskolin, 8-PT, nor AOPCP affected blood pressure, heart rate, or myocardial oxygen consumption. These results suggest that adenosine is involved in myocardial reactive hyperemia through an activation of adenylate cyclase, and that ecto-5′-nucleotidase participates in producing adenosine of the interstitial myocardial space.