It is known that the QT interval is longer in women than men. Estrogen is reported to account for the QT interval prolongation in several studies conducted with hormone replacement therapy (HRT) in postmenopausal women. Along with this, there are conflicting data as regards the effects of HRT on QT interval and dispersion. Moreover, there is no evidence about the effect of HRT on exercise QT parameters.
We compared QT parameters obtained from surface electrocardiograms during resting and peak exercise before and after 6 months of HRT consisting of estrogen plus progesterone in healthy postmenopausal women. Twenty-four healthy postmenopausal women were given 0.625 mg/day conjugated estrogens and 2.5 mg/day medroxyprogesterone acetate for 6 months. Exercise stress testing using the Bruce protocol was performed before and after HRT. QT maximum, minimum, dispersion and corrected QT maximum, minimum and dispersion were calculated during resting and peak exercise.
HRT resulted in a significant increase in estradiol plasma levels from 24±10 pg/mL to 117±66 pg/mL (P<0.001). There was no significant difference in resting QT parameters after HRT, whereas QT dispersion and corrected QT dispersion were significantly increased during peak exercise (20±7 versus 25±10 ms; P<0.05, 33±12 versus 41±16 ms; P<0.05, respectively). Nonetheless, the other exercise QT parameters were unchanged.
The resting QT parameters are not affected by long term HRT consisting of estrogen plus progesterone, which leads to an increase in QT dispersion and corrected QT dispersion during peak exercise.

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The clinical and laboratory findings of eight (20%) cases of cardiac involvement of 39 patients with sepsis caused by S. aureus (Staphylococcus aureus) were reviewed retrospectively. Our purpose was to emphasize the importance of the cardiac findings in patients with sepsis caused by S. aureus in childhood. The ages of the patients ranged from 6 to 14 years. All patients had pericardial effusion which was confirmed by echocardiographic (ECHO) examination in all cases except the one in whom ECHO examination could not be performed because he died 2.5 days after admission to the hospital. This patient also had myocarditis and heart failure. Aside from these, mitral insufficiency was diagnosed in the other patient; it was accepted as a sequela of rheumatic fever acquired previously. Open pericardial drainage was conducted successfully in the case who had a progression to cardiac tamponade. In the other patients pericardial effusion completely resolved with supportive and antibiotic therapy one to two weeks. Two of eight patients died from sepsis and septic shock; the mortality rate was 25%. Our findings show that cardiac involvement was fairly high (20%) in S. aureus sepsis in childhood. Therefore, it is suggested that children with S. aureus sepsis should be carefully monitored for cardiac involvement.

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There have been no previous studies that clearly demonstrate the effects of training on the relation between exercise capacity and vasodilatory capacity in skeletal muscle. This study was performed to clarify the effects of short-term, moderate-intensity physical training on exercise tolerance and vasodilatory capacity in cardiac patients.
We studied 21 patients after acute myocardial infarction, coronary artery bypass grafting, or valve replacement. Each patient performed symptom-limited incremental exercise tests before and after a 2-week training program of moderate-intensity exercise. A cycle ergometer was used for both the training and exercise tests. Blood pressure measurement and respiratory gas analysis were continuously performed during the tests. Cardiac output was also measured using a dye-dilution method at rest and every 2 minutes during incremental exercise. Reactive hyperemic calf blood flow was measured at rest.
After the training program, the subjects attained a significant decrease in systemic vessel resistance and significant increases in oxygen uptake and cardiac output at peak exercise. Changes in reactive hyperemic calf blood flow were significantly correlated with the changes in cardiac output, systemic vascular resistance, and the kinetics of oxygen uptake during warm-up exercise.
By improving the peripheral vasodilatory capacity in these patients, short-term, moderate-intensity physical training was found to improve the cardiovascular adaptation not only at peak exercise, but also during the onset of exercise.

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Moderate chronicexercise attenuates the elevation of blood pressure in young spontaneously hypertensive rats. In order to elucidate the physiological process of the effects of exercise, we examined the involvement of nitric oxide, angiotensin II, and superoxide dismutase in this process. Rats were exercised by voluntary running in a wheel-cage for 10 weeks. Systolic blood pressure in the exercised rats (195±4 mmHg, n=27) was significantly (p<0.05) lower than in the post-control rats (212±3 mmHg, n=28). The concentration of total plasma nitrite was significantly higher in exercised rats (14.9±1.5μmol l^-1) than in the post-control rats (9.9±0.7 μmol l^-1, p<0.05). Superoxide dismutase activity in the exercised rats was significantly higher (p<0.05) than in the post-control rats (thoracic aorta: 4.6±0.3 U mg protein^-1 vs 3.6±0.3 U mg protein ^-1, heart: 12.7±0.6 U mg protein^-1 vs 10.2±0.6 U mg protein^-1, p<0.05). The plasma angiotensin II concentration was higher in the post-control rats (74.4±14.0 pg mL^-1) than in the exercised rats (45.0±6.4 pg mL ^-1, p<0.05), and in the pre-control rats (47.2 ±6.0 pg mL^-1). The results suggest that exercise acts to decrease the level of superoxide by increasing superoxide dismutase activity in the aorta and heart and to decrease levels of angiotensin II, both of which, in turn, increase the effective concentration of nitric oxide. We conclude that the combination of these effects with the increased NO formation resulted in the low blood pressure seen in the exercised rats.

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Considerable attention has been focused on both highly oxidized low-density lipoprotein (ox-LDL) and mildly oxidized LDL (mox-LDL) as important risk factors for cardiovascular disease. Further, 5-hydroxytryptamine (5-HT) appears to play a crucial role in the development of atherosclerotic plaque. We assessed the interaction of oxidatively modified LDL and its major oxidative components, ie, hydrogen peroxide (H₂O ₂), lysophosphatidylcholine (LPC), and 4-hydroxy-2-nonenal (HNE) with 5-HT on DNA synthesis in vascular smooth muscle cells (VSMCs). Growth-arrested rabbit VSMCs were incubated in serum-free medium with native LDL, mox-LDL, ox-LDL (all 50 ng/mL), H₂O₂ (0.5 μM), LPC (1 μM), or HNE (0.1 μM) for 24 hours followed by 5-HT (5 μM) for another 24 hours. DNA synthesis in VSMCs was measured by [³H]thymidine incorporation. Significant effects on [³H]thymidine incorporation were observed in VSMCs incubated with mox-LDL (129%), ox-LDL (129%), H₂O₂ (119%), LPC (115%), HNE (127%), or 5-HT (183%) in contrast with native LDL (113%). The mitogenic effect of 5-HT was potentiated by mox-LDL, ox-LDL, H₂O₂, LPC, or HNE (183 to 365%, 274%, 304%, 339%, or 273%, respectively) but not by native LDL (240%). The mitogen-activated protein kinase (MAPK) kinase inhibitor PD98059 (10 μM) signficantly inhibited the mitogenic effect of 5-HT but did not influence the effects of mox-LDL, ox-LDL, H₂O₂, LPC, or HNE. The intracellular antioxidant N-acetylcysteine (400 μM) siginificantly inhibited the mitogenic effects of mox-LDL, ox-LDL, H₂O₂, LPC, and HNE but not that of 5-HT. Our results suggest that mox-LDL, ox-LDL, and their major components H₂O ₂, LPC, and HNE act synergistically with 5-HT in inducing VSMC DNA synthesis via MAPK and redox-sensitive pathways, contributing to the development of atherosclerotic plaque.

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Adenosine is a powerful direct coronary vasodilator with a very short half-life that has been shown to be effective in avoiding and reversing no reflow. We report an immediate successful recanalization of an occluded major side branch after stenting with acute intracoronary adenosine administration. The beneficial effect of adenosine may imply that the side branch occlusion (SBO) in this case could be due to spasm or distal embolization of the atherosclerotic debri ending up with no flow.
We believe that adenosine could be helpful in at least some cases of SBO and therefore may be worth attempting.

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Percutaneous coronary intervention was performed in a severely tortuous right coronary artery (RCA). Immediately after straightening its tortuousity by using two guidewires, angiographic slow flow, ischemic electrocardiographic changes, and anginal pain developed. This is a rare case who had severe myocardial ischemia caused by the accordion phenomenon.

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In a patient referred for the evaluation of non-sustained monomorphic ventricular tachycardia on Holter recordings, ventricular fibrillation was electrically induced during electrophysiologic study. Despite the absence of structural heart diseases, his ECG revealed J wave and ST segment elevation in the inferior leads, which showed circadian variation and were augmented by the sodium channel blocker, pilsicainide. This case might lead us to notice a new concept, a 'latent' type of variant Brugada syndrome, and these ECG findings and changes might serve as its diagnostic sign.

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We report a case of mitochondrial cardiomyopathy in a Japanese boy who presented with severe cardiac heart failure and died 6 days after admission. The onset of mitochondrial cardiomyopathy often occurs very early in childhood and has a rapid downward course.

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Cardiovascular disease is a major cause of mortality and morbidity in patients with acromegaly. We describe the case of a 43-year-old man with acromegaly who presented with severe congestive heart failure. Treatment with the somatostatin analog octreotide improved cardiac function with an increase in left ventricular ejection fraction (LVEF) from 11% to 27%. LVEF further increased to 43% after trans-sphenoidal surgery. Recovery was uneventful. We emphasize the need for early diagnosis and effective treatment of acromegaly to prevent cardiovascular complications. Octreotide therapy or trans-sphenoidal surgery, if possible, should be considered to control cardiac function even in acromegalic patients with severe congestive heart failure.

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A 48-year-old Turkish male presented with worsening angina and a painful left hand eight years after coronary artery bypass surgery. Coronary angiography showed extensive coronary atherosclerosis with patent vein grafts to his diagonal branch and right coronary arteries. There was a severe narrowing lesion in the left subclavian artery before the origin of the left internal mammary artery (LIMA), which appeared patent. Percutaneous subclavian angioplasty and stent implantation to the left subclavian artery stenosis restored normal flow to the left hand and the LIMA with abolition of his ischemic hand symptom and marked improvement of his angina.

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