After compensating for two kinds of motion artifacts caused by cardiac beating and respiration, cardiac magnetic resonance (MR) imaging is now feasible for the diagnosis of various cardiac diseases. Taking cost-effectiveness into consideration, this paper reviews the experiences of preferable indications of cardiac MR imaging by demonstrating the characteristic preciseness and uniqueness that play an important role in obtaining time-volume curves consisting of the theoretically most accurate measurements of left and right ventricular volumes, in overall evaluation of the left ventricular apex and the right ventricle, in delineating the wide range of the coronary arterial tree, in measuring the most precise blood flow volume through the cross-sectional images of the vessels, and in assessing the spatial derivative of the blood flow velocity at the vessel wall, i.e., wall shear rate.

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Many cardiac surgeries are performed with blood cardioplegia. However, some studies suggest that activated neutrophils form blood cardioplegia can cause reperfusion injury. In this study we assessed myocardial protection using a leukocyte-depleted cardioplegic solution. Patients undergoing elective coronary artery bypass grafting (CABG) with continuous blood cardioplegia were divided into two groups: the LD group, which received leukocyte-depleted blood cardioplegia (n = 11); and the control group, which received nonfiltered blood cardioplegia (n = 11). IL-6, IL-8, CK-MB, and troponin T were measured in the coronary sinus blood immediately after the release of the aortic cross-clamp. Cytokine concentrations were also measured upon the patient's return to the ICU. The total dopamine and dobutamine doses, hemodynamic measurements after surgery, and the leukocyte filtration rate were also measured. During antegrade cardioplegia infusion, leukocytes were almost completely removed (filtration rate: 85.8 ± 4.0%). However, during terminal warm cardioplegia, leukocyte removal decreased (filtration rate: 39.9 ± 7.8%). Immediately after the release of the aortic cross-clamp, plasma CK-MB and troponin T concentrations were significantly lower in the LD group (17.7 ± 1.9 U / l and 0.017 ± 0.002 ng / ml, respectively) than in the control group (30.3 ± 3.6 U / l and 0.072 ± 0.029 ng / ml, respectively). The IL-6 and IL-8 concentrations were similar in the LD group and the control group. After the return to the ICU, the CK-MB and troponin T concentrations were similar in the two groups. No significant differences were found in the total doses of dopamine or dobutamine after surgery in the two groups (99 ± 77 vs 101 ± 128 μ g / kg / min). No significant differences were found in the hemodynamic parameters after surgery in the two groups. In patients undergoing CABG with continuous blood cardioplegia, leukocyte-depleted blood cardioplegic solution may attenuate reperfusion injury.

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Dobutamine (DOB) stress two-dimensional echocardiography is an established method for the detection of viable myocardium, but conventional assessment of wall motion is subjective. We measured quantitatively the left ventricular systolic velocities along the longitudinal axis by pulsed Doppler tissue imaging (DTI). In 30 patients with previous myocardial infarction, pulsed DTI focused on the infarct area was performed from an apical two- or four-chamber view before and during DOB (10 μg / kg / min) stress one day before coronary angioplasty. We calculated peak systolic velocity (S), regional pre-ejection period (PEP, the time interval from the onset of QRS to the onset of systolic wave) and regional ejection time (ET). Left ventriculography was obtained before and 3 months after coronary angioplasty to assess regional wall motion. Improvement of abnormal wall motion was observed in 19 patients (group P) but not in 11 (group N). Group P had significantly larger S and smaller PEP / ET than group N during DOB stress, although there were no significant differences in these indices between the groups at baseline. As a consequence, group P had a significantly larger percent change in S and a smaller percent change in PEP / ET than group N (164 ± 39 vs 117 ± 20 % and 88 ± 17 vs 116 ± 29%, respectively, p < 0.01). It is suggested that the quantitative measurement of longitudinal systolic velocities during DOB stress by DTI is useful for the precise assessment of myocardial viability.

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We evaluated the factors that determine the heart rate response to exercise in 60 patients with atrial fibrillation (25 men and 35 women, with a mean age of 61 ± 10 years) who underwent symptom limited cardiopulmonary exercise testing with blood sampling of atrial natriuretic peptide (ANP), 2-dimensional echocardiography and cardiac catheterization. Atrial muscles resected during the Maze operation were examined histologically in 12 patients. The heart rate response to exercise depended on the severity of the atrial organic injury, which was expressed as left atrial diameter, ANP secretion during the maximal exercise testing and the histological findings of atrial tissue. Conversely, we believe that the severity of the atrial injury can be predicted from the heart rate response to exercise in patients with atrial fibrillation.

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To assess right atrial appendage (RAA) flow and its possible relationship to left atrial appendage (LAA) flow in chronic nonvalvular atrial fibrillation (AF), transesophageal echocardiography (TEE) was performed in 26 patients with chronic nonvalvular AF (group I). For the purpose of comparison, an additional group of 27 patients with chronic valvular AF due to mitral stenosis (group II) was analyzed. The clinically estimated duration of AF in group I was significantly longer than that of group II (8.7 ± 3.4 versus 2.7 ± 1.1 years). Although right atrial size and RAA maximal area were larger in group I than those in group II, left atrial size was larger in group II than that in group I. Group II had larger LAA maximal areas than group I, but this difference did not reach statistical significance. The two groups were not different with respect to the RAA or LAA emptying velocities. Significant correlations were observed between echocardiographic parameters of the two atria in patients with nonvalvular AF (r range, 0.4 to 0.7). In contrast, in patients with valvular AF, no correlation was observed between the echocardiographic parameters of the two atria (appendage emptying velocity, r = 0.38, p = 0.051; atrial size, r = - 0.03, p = 0.89; maximal appendage area, r = 0.07, p = 0.75, respectively). There were no significant differences in the presence of right and left atrial spontaneous echo contrast and thrombus between the groups. All of the right and left atrial thrombi were confined to their respective appendages and were found in the atria with spentaneous echo contrast. Both RAA and LAA thrombi were present in one patient. In conclusion, our findings suggest that AF could affect both atria equally in nonvalvular AF, in contrast to valvular AF. Therefore, the assessment of RAA function as well as LAA may be important in patients with chronic nonvalvular AF.

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Long QT syndrome (LQTS) is a prime example of interplay between molecular biology, cellular physiology, and organ physiology. Both the congenital and acquired forms of LQTS are due to intrinsic and / or acquired abnoma1ities of the ionic currents responsible for cardiac repolarization. We analyzed the QTc interval, QRS axes and interventricular septal thickness (IVST) in 41 patients who had a prolonged QT interval on routine electrocardiography (ECG) (5 females and 36 males, mean age 65 ± 13 years). The QRS axis of patients in the LQTS group (27 ± 49°) was significantly lower (p < 0.05) than in the control group (46 ± 26°). However, the IVST in the LQTS group (10 ± 2 mm) was significantly thicker than in the control group (9 ± 1 mm) (p < 0.05), while the WTd was not significantly different. The QTc interval in patients with ventricular septal hypertrophy (IVST ≥ 12 mm, 478.8 ± 7.9 msec) was significantly longer (p < 0.05) than in the normal group (IVST < 12 mm, 472.1 ± 17.5 msec). In conclusion, the results of this preliminary study suggest that prolongation of the QT interval on ECG should prompt screening for electrocardiographic evidence of ventricular hypertrophy in patients with this disease.

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Transcatheter closure of an interatrial septal defect (ASD) with a CardioSEAL device was successfully performed on 12 Taiwanese children. There were five boys and seven girls, aged from 3.6-13.9 (8.3 ± 3.2) years and with body weight of 15-57 (33.7 ± 14.7) kgs. After one year of follow-up studies, which included physical examination, ECG, chest X-ray and echocardiography, complete closure of ASD was achieved in nine (75%) patients. Two children with a trivial residual shunt were asymptomatic and without audible cardiac murmur. A girl had a small residual left to right atrial shunt by color Doppler echocardiography, but without audible cardiac murmur. There were no immediate or intermediate complications. Transcatheter implantation of the CardioSEAL device is a safe and proper treatment for children with non-complicated small to medium secundum ASD.

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Action potential duration (APD) in rabbit ventricular myocardium shortens after a rest period (postrest shortening). However, the effects of preceding stimulus frequency on the postrest shortening have not been elucidated. We recorded transmembrane action potentials (TAPs) and monophasic action potentials (MAPs) from the rabbit ventricle. In in vitro experiments, repetitive regular stimuli (S1) at cycle lengths ranging between 500 to 3000 ms were followed by a single extrastimulus (S2) at a coupling interval of 5000 ms. A decrease in S1S1 interval resulted in a progressive shortening of the duration of TAP (TAPD) elicited by S2 (S2-TAPD), which was potentiated by increasing extracellular calcium concentration ([Ca²⁺] _o) or application of ouabain and was inhibited by lowering [Ca ²⁺]_o or verapamil. Application of ryanodine was most effective in lengthening S2-TAPD following a short S1S1 interval. 4-aminopyridine and E4031 caused marked lengthening of S2-TAPD when S1S1 was long. However, the lengthening effect was attenuated and disappeared with a shorter S1S1 interval. In in vivo experiments, regular ventricular pacing (S1) at cycle lengths ranging between 250 to 1000 ms was followed by a single extrastimulus (S2) with a coupling interval (S1S2) of 1500 ms. A decrease in the S1S1 interval also resulted in progressive shortening of the duration of MAP elicited by S2. Our results indicate that the postrest shortening is potentiated by an increase in the preceding stimulus frequency in the rabbit ventricle, in which the function of sarcoplasmic reticulum may play a significant role.

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The mechanism through which nitric oxide (NO) mediates cardiac myocyte death during acute cardiac rejection has not been fully delineated. We sought to determine whether NO promotes myocardial apoptosis and contributes to graft failure during acute cardiac rejection in a murine model. Heterotopic cardiac transplantation was performed from Balb / c (H-2^d) to C3H / He mice (H-2^k). Recipients were treated with aminoguanidine (AG) at 400 mg / kg every day after surgery. As references, we used isografts in Balb / c mice with and without AG treatment (400 mg / kg / day). Graft survival, histological changes and serum NO levels were assessed. Intra-graft apoptosis was evaluated using a DNA fragmentation detection assay (TUNEL method) and DNA laddering. Significant prolongation of graft survival was observed in allografts treated with AG in comparison with nontreated allografts. Serum NO levels, which peaked on day 7 in nontreated allografts, were significantly decreased in AG-treated allografts. AG treatment decreased the number of apoptotic cells and lowered the ratio of the apoptotic cardiac myocytes in contrast to that of the apoptotic infiltrating cells. DNA laddering was clearly detected in nontreated allografts but was suppressed in AG-treated allografts. Inhibition of NO production by AG prolonged murine cardiac allograft survival. The decrease in intra-graft apoptotic activity paralleled histological improvement. Cardiac myocyte death which occurs through an apoptotic process mediated by NO contributes to graft failure during acute cardiac rejection.

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We investigated the effect of a monoclonal antibody against CD2 molecules (OX34) in preventing the induction of experimental autoimmune myocarditis (EAM) induced by immunizing Lewis rats with cardiac myosin. Administration of OX34 before immunization, on Days -6, -4, -2 and 0, completely prevented EAM. On the other hand, treatment with OX34 just before the appearance of myocardial lesions, on Days 9, 11, 13 and 15, had only a partial effect in preventing the disease. Flow cytometric analysis of lymph node cells showed that CD3⁺ T cells were immediately depleted with the administration of OX34 but had largely recovered on Day 21. Lymph node cells in OX34-treated rats had no proliferative responses to cardiac myosin-rod, but the proliferation was restored when recombinant IL-2 was added. Ultimate production of the anti-myosin antibody was not inhibited by the treatment with OX34. These results suggest that the prevention of EAM by administering the anti-CD2 monoclonal antibody OX34 resulted from T cell depletion during the induction phase, and might in addition result from T cell anergy of Th1, but not Th2 cells.

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A 45-year-old Japanese man with paroxysmal atrial fibrillation (AF) developed acute anteroseptal myocardial infarction (MI). He had used 1 % topical minoxidil (RiUP®) once a day for 4 months before the onset of MI for treatment of baldness. Coronary angiography demonstrated severe stenosis at the proximal portion of the left anterior descending coronary artery with a filling defect. Electrocardiographic monitoring revealed paroxysmal AF and sinus bradycardia with sinus arrests, suggestive of sick sinus syndrome. Topical minoxidil is now widely used for the treatment of male pattern baldness. Although it may be difficult to relate topical use of minoxidil to myocardial ischemia, a greater awareness of its toxicity will be necessary, and patients with cardiovascular disorders should be excluded from the therapy.

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We report the case of a young Turkish man with a transient ischemic attack secondary to a rare cardiac tumor, papillary fibroelastoma. The tumor was diagnosed by 2-dimensional echocardiography and treated surgically.

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A 16-year-old Japanese male diagnosed with congestive heart failure (CHF) due to dilated cardiomyopathy was treated by conventional intensive treatment such as intravenous infusion of diuretics, catecholamines, and phosphodiesterase inhibitors with vasodilators. However, he developed a low output syndrome with appearances of hyponatremia and hypochloremia. As a consequence, intravenous infusion of carperitide (synthetic atrial natriuretic peptide) was added to the therapy. Thereafter his symptoms and hemodynamic parameters promptly and dramatically improved without significant diuresis, and this amelioration persisted for more than 20 days without drug intolerance. This outcome suggests that use of carperitide may be a safe and efficacious means to reduce cardiac preload without hypotension and tachycardia in patients with refractory CHF in whom intensive treatment has already been performed.

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Blunt chest trauma causing isolated right atrial tear and cardiac tamponade in three patients is reported. All three patients presented with hypotension, elevated central venous pressure and altered consciousness. Echocardiographic examination demonstrated pericardial effusion in all three cases. All three patients underwent operation with a median sternotomy approach without using cardiopulmonary bypass. At operation, two patients had one tear in the right atrium, the other had two tears in the right atrium. All three patients recovered uneventfully. Early use of echocardiography to detect the presence of hemopericardium and cardiac tamponade in patients with suspected atrial rupture following blunt chest trauma is advocated.

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