Left ventricular chamber size predicts the race time of Japanese participants in a 100 km ultramarathon.

OBJECTIVE: As a subanalysis of an echocardiographic study performed on 291 Japanese participants in a 100 km ultramarathon, to estimate predictors of race time. METHODS: A total of 247 male participants in a 100 km ultramarathon (age 20-73 years) were examined by echocardiography. Correlations between age, body surface area, monthly running distance, or echocardiographic variables and the race time were examined. RESULTS: According to simple regression analysis, age (r = 0.299, p < 0.0001), monthly running distance (r = -0.388, p < 0.0001), left ventricular end diastolic diameter (r = -0.300, p < 0.0001), and left ventricular end systolic diameter (r = -0.325, p < 0.0001) correlated significantly with the race time. When multiple regression analysis was performed, age (f = 2.364), monthly running distance (f = -0.113), and left ventricular end systolic diameter (f = -2.361) remained significant predictors of the race time. CONCLUSION: Left ventricular diameter predicts the race time for a 100 km ultramarathon, in addition to age and amount of training.

Plasma brain natriuretic peptide in takotsubo cardiomyopathy.

BACKGROUND: Takotsubo cardiomyopathy is a reversible left ventricular dysfunction with symptoms resembling acute myocardial infarction, but without coronary lesions. Patients have wall motion abnormalities (apical akinesis and basal hyperkinesis), and characteristic left ventricular morphology. AIM: To investigate plasma brain natriuretic peptide (BNP) concentrations in takotsubo cardiomyopathy. METHODS: Ten consecutive patients with takotsubo cardiomyopathy underwent cardiac catheterization on their first hospital day, and blood was collected to measure BNP. To evaluate acute basal hyperkinesis, the difference in diameter between systole and diastole was measured at 10 mm below the aortic valve (the deltaBase value). RESULTS: Coronary angiography revealed no significant stenosis in any patient. Initial ejection fraction was 42.2 +/- 7.3%, cardiac index was 1.90 +/- 0.39 l/min/m(2), and plasma BNP was 522.5 +/- 632.9 pg/ml. Ventricular contraction and the ejection fraction were normalized on echocardiography after 17.9 +/- 6.3 days. BNP was significantly correlated with deltaBase, but not with other cardiac parameters. DISCUSSION: Initial deltaBase value seems to be a good indicator of the severity of basal hyperkinesis in patients with takotsubo cardiomyopathy. In contrast to other diagnoses, a high BNP concentration is not associated with a poor prognosis in this condition.

Effects of prolonged strenuous exercise on plasma levels of atrial natriuretic peptide and brain natriuretic peptide in healthy men.

BACKGROUND: Now that marathon racing is growing in popularity, many thousands of enthusiastic athletes are participating in various ultramarathons all over the world each year. However, it remains controversial whether such a sport contributes to the promotion of health. The occurrence of transient cardiac dysfunction and irreversible myocardial injury has been reported in association with such exercise in healthy individuals. Brain natriuretic peptide (BNP) is a cardiac hormone, as is atrial natriuretic peptide (ANP), and its measurement has been widely used for clinical evaluation of cardiac dysfunction. However, little is known about the response of plasma BNP to prolonged strenuous exercise. We hypothesized that confirmation of minimal cardiac dysfunction or myocardial injury may be made by measurements of plasma BNP. METHODS: Levels of plasma ANP, BNP, catecholamines, blood lactate, and serum cardiac troponin T (cTnT) were determined before and after a 100-km ultramarathon in 10 healthy men to examine the effects of the exercise on levels of ANP and BNP and correlations between the natriuretic peptides and cTnT as a marker for myocardial damage. RESULTS: Whereas all variables significantly increased after the race, increased levels of ANP and BNP were most strongly correlated with increases in cTnT levels. The cTnT level after the race was greater than the upper reference limit in 9 of 10 men. CONCLUSIONS: Such exercise significantly increased ANP and BNP levels in healthy men, and the increases could be partially attributed to myocardial damage during the race.

Congenital giant aneurysm of the left atrial appendage mimicking pericardial absence case report.

A 25-year-old man was found to have an abnormal cardiac contour on a chest radiograph, and was referred. Transesophageal echocardiography suggested herniation of the left atrial appendage (LAA) through a gap in the pericardium, and magnetic resonance imaging indicated congenital partial absence of the pericardium. Cardiac dysfunction was caused by compression from the enlarged left atrium and thrombi were thought to be present in the appendage, so surgery was performed. The intraoperative diagnosis was congenital LAA aneurysm. Although distinguishing between congenital LAA aneurysm and congenital absence of the pericardium is reported to be possible with magnetic resonance imaging, we were unable to so in this case.

Influence of angiotensin-converting enzyme gene polymorphism on development of athlete's heart.

BACKGROUND AND HYPOTHESIS: Genetic influence on development of athlete's heart is uncertain. This study investigated whether angiotensin-converting enzyme (ACE) gene polymorphism influenced development of athlete's heart. METHODS: Forty-three participants in a 100-km ultramarathon were classified on the basis of ACE gene polymorphism into a deletion group (n = 26) and an insertion group (n = 17). Echocardiograms were recorded to determine left ventricular end-diastolic and end-systolic diameters, interventricular septal thickness, left ventricular posterior wall thickness, left ventricular mass, and ejection fraction. RESULTS: Left ventricular end-diastolic diameter (65.5 +/- 4.0 mm) and left ventricular mass (369.5 +/- 73.9 g) were significantly larger in the subjects with deletion than in those with insertion (57.4 +/- 4.2 mm, 306.5 +/- 93.7 g). However, no significant differences in the other parameters were noted. CONCLUSIONS: In long-distance runners, ACE gene polymorphism of the D/D and D/I genotypes has a stronger influence on left ventricular hypertrophy than polymorphism of the I/I genotype.

Effect of angiotensin-converting enzyme gene polymorphism on left ventricular remodeling after anteroseptal infarction.

BACKGROUND AND HYPOTHESIS: Genetic influence on cardiac remodeling is uncertain. The purpose of this study is to determine the effects of polymorphism of the angiotensin-converting enzyme (ACE) gene on cardiac remodeling after myocardial infarction. METHODS: The subjects were 43 patients with old anteroseptal myocardial infarction. Based on the polymorphism of the ACE gene, they were classified into a deletion group of 25 patients (D/D genotype in 4 and D/I genotype in 21) and an insertion group of 18 patients (all I/I genotype). Echocardiograms were used to determine left ventricular end-diastolic and end-systolic diameters, interventricular septal and posterior wall thicknesses, left ventricular mass, left atrial diameter, and left ventricular ejection fraction. Blood concentrations of atrial and brain natriuretic peptide were also measured. RESULTS: Left ventricular end-systolic and end-diastolic dimensions, left ventricular mass, and levels of both atrial and brain natriuretic peptide were significantly higher in the deletion group. In contrast, septal thickness, posterior wall thickness, and ejection fraction showed no differences between the two groups. CONCLUSIONS: In patients with old anteroseptal infarction, ACE gene polymorphism of the D/D and D/I genotypes has a stronger influence on left ventricular remodeling than polymorphism of the I/I genotype.

Dynamic changes of QT dispersion as a predictor of myocardial ischemia on exercise testing in patients with angina pectoris.

The difference between the maximum and minimum QT intervals on the standard 12-lead ECG (QT dispersion) may be a significant predictor of serious arrhythmias. Dynamic changes in QTd were determined during exercise-induced ischemia in 15 patients with effort angina (> or = 75% coronary stenosis) and 10 normal individuals. Treadmill exercise testing was performed according to Bruce's protocol and the rate-corrected QT dispersion (QTcd) was calculated using Bazett's formula. The resting QTcd before exercise was similar in the angina patients and the controls. After the first stage of exercise, QTcd was significantly increased in the angina patients (p = 0.035), while it remained near baseline in the controls. Five minutes after completing exercise, QTcd was significantly greater in the angina patients than in the controls (p = 0.011). Furthermore, QTcd values after the first stage of exercise were significantly correlated with the maximum ST depression observed on completing exercise in the angina patients (r = 0.714, p = 0.0028). Because QTd may represent the heterogeneity of ventricular repolarization, its significant exercise-induced increase in the angina patients suggests that myocardial ischemia caused repolarization disorders. The significant correlation between QTcd values after the first stage of exercise (before significant ST depression) and the maximum ST depression on completing exercise suggests that an increase in QTcd preceding ischemic ST depression may predict myocardial ischemia. In addition, even daily activities not causing significant ST changes may increase QTcd and the risk of serious arrhythmia in angina patients.

Influence of exercise on QT dispersion in ischemic heart disease.

UNLABELLED: QT dispersion (QTd: maximum QT interval-minimum QT interval) is associated with severe cardiac arrhythmia and with abnormal ventricular repolarization. We investigated the influence of exercise on QTd in patients with ischemic heart disease. On standard 12-lead electrocardiograms, QTd was measured before and after treadmill exercise in 7 normal subjects, 17 patients with effort angina pectoris (and > or = 75% stenosis on coronary arteriography), and 33 patients with old myocardial infarction. Bazett's formula was used to obtain the corrected QTd (QTcd). The pre-exercise resting QTcd was 45.9 +/- 10.6, 44.3 +/- 15.2, and 74.8 +/- 28.1 msec in the respective groups, being significantly greater in the infarct group (p < 0.05). The QTcd at 5 min after exercise was respectively 49.3 +/- 9.0, 58.8 +/- 19.9, and 75.4 +/- 30.9 msec (p = 0.0347, infarct vs. controls). The difference in QTcd was significant for the angina group before and after physical exercise (p = 0.0003). There was a significant increase of QTcd after exercise in the angina group whether or not the patients were receiving beta-blockers. The infarct patients without beta-blocker therapy showed an increase of QTcd after exercise, while those receiving beta-blockers showed a decrease. The post-exercise difference between these subgroups was significant (p = 0.0351). CONCLUSIONS: QTcd was significantly increased by exercise in the angina group, possibly reflecting impaired repolarization due to ischemia. Inhibition of the increase in QTd by beta-blockers suggested a possible preventive effect on severe arrhythmias due to nonhomogeneous ventricular repolarization.

A randomized trial of aspirin versus cilostazol therapy after successful coronary stent implantation.

Percutaneous transluminal coronary angioplasty (PTCA) is widely used to treat patients with ischemic heart disease, but the procedure involves a number of problems, including acute coronary occlusion and restenosis. Although stents have proved useful for preventing post-PTCA restenosis, especially elastic recoil during the acute phase, no method has yet been established to prevent restenosis caused by vascular smooth muscle cell proliferation in the late phase. Cilostazol selectively inhibits the 3'5'-cyclic-nucleotide phosphodiesterase (PDE) III (cyclic guanosine monophosphate-inhibited PDE) of the cyclic adenosine monophosphate PDE family; it also has antithrombotic and vasodilating effects, as well as an inhibitory effect on vascular smooth muscle cell proliferation through PDE III inhibition. From November 1995 to March 1997, the usefulness of cilostazol versus aspirin in preventing subacute thrombosis and restenosis was studied in 70 patients (55 men and 15 women; 82 total lesions) who had undergone successful elective Palmaz-Schatz stent implantation. Patients were randomly allocated to receive aspirin 81 mg/d (40 patients with 45 lesions) or cilostazol 200 mg/d (30 patients with 37 lesions) alone. There was no difference in patients or angiographic characteristics between these groups. No subacute thrombosis, acute complications (ie, death, emergent coronary artery bypass grafting, or hemorrhagic complications), or drug side effects were found in the cilostazol group. The minimal lumen diameter (mean +/- SD) at follow-up was 1.89 +/- 1.08 mm in the aspirin group (41 lesions, 5.63 +/- 1.74 months after stent implantation) and 2.34 +/- 0.74 mm in the cilostazol group (35 lesions, 5.14 +/- 1.91 months after stent implantation), revealing statistically significant dilatation in the cilostazol group. The restenosis rate was 26.8% in the aspirin group, compared with 8.6% in the cilostazol group; this difference was statistically significant. Administration of cilostazol alone after the implantation of intracoronary Palmaz-Schatz stents was useful for the prevention of subacute thrombosis and restenosis.

Pharmacokinetics of propranolol used for suppressing tachycardia in hyperthyroidism.

The aim of this study was to investigate the pharmacokinetics of propranolol in patients with hyperthyroidism, and its effect on heart rate (HR) using 24 hour-ECG monitoring. Subjects included 9 patients with hyperthyroidism (group H) and 9 euthyroid patients with hypertension selected as the control group (group C). All patients took propranolol at a dosage of 10 mg, 3 times a day for 7 days. Plasma propranolol concentrations were measured on the 7th day of its administration by the HPLC method. Twenty-four hour-ECG monitoring was recorded twice before and after treatment with propranolol. The mean reduction in the minimum HR was 10.7 +/- 3.6 (11.9 +/- 3.6%) in group H and 5.0 +/- 1.6 (9.5 +/- 3.0%) bpm in group C. That in the average HR was 12.2 +/- 3.7 (11.3 +/- 3.1%) in group H and 9.2 +/- 2.2 bpm (13.7 +/- 3.2%) in group C. That in the maximum HR was 16.9 +/- 5.2 (10.9 +/- 3.1%) in group H and 24.4 +/- 2.4 bpm (21.9 +/- 2.1%) in group C. The peak concentration of propranolol in plasma was 10.8 +/- 2.4 ng/ml in group H and 55.3 +/- 14.3 ng/ml in group C (p < 0.01). There was a linear correlation between the reduction in the hourly maximum heart rate and the peak plasma propranolol concentration in group H. Cardiovascular manifestations in hyperthyroid patients were related to sympathetic hypersensitivity and their improvement was not fully obtained by small doses of propranolol.

Prevalence and clinical significance of silent myocardial ischemia in exercise test.

Prevalence of silent myocardial ischemia in exercise test was retrospectively reviewed from 749 tests performed for 513 patients with definite evidence of ischemic heart disease. The clinical significance was studied and absence of transient ischemia, occurrence of transient ischemia with and without pain were observed in 48%, 30% and 22% of the tests, respectively. Anginal pain was frequently observed in exercise tests for patients with severe coronary artery disease and low exercise tolerance. A large number of tests showing ischemic response were discontinued due to symptoms other than anginal pain and hence silent myocardial ischemia could be thought to be a result of ischemic state which does not reach the angina threshold. Silent myocardial ischemia was frequently observed during usual daily life. However, a definite correlation between severity of transient ischemia and presence or absence of chest pain in the same individuals was not obtained from the study. A day to day variation in the angina threshold might be responsible. In general, silent myocardial ischemia was not rare. However, the consistent condition was very unusual. In angina of effort (EA) and old myocardial infarction (OMI), 3.7% and 12.3% were silent, respectively. A higher incidence was obtained in OMI than in EA. This is important for the management of these patients. The mechanism of silent myocardial ischemia and the cause of the different incidence of this state between EA and OMI were not defined and remained to be further studied.

Sono-enterocolonography by oral water administration.

A new ultrasound technique for intestinal examination, named "sono-enterocolonography by oral water administration," was devised. The diagnostic usefulness and limitations of this procedure were studied in 56 subjects including 42 normal patients, 10 patients with 13 colonic polyps and 4 patients with colon carcinomas. Except for the rectum, almost all the intestines were clearly visualized by ultra-sonography as tubular structures filled with water. In every case, ileocecal valve movement was clearly observed dynamically. Eight of the 9 elevated polypoid lesions of the bowel, ranging in size from 10 mm to 20 mm, were detected by this method without any special pretreatment. Although this method may not be indicated for the screening of minute lesions, it may possibly be useful as a supportive diagnostic modality for intestinal disorders, especially in the ileocecal region.

Clinical significance of exercise-induced negative U-waves in patients with anterior myocardial infarction.

To elucidate the clinical significance of the exercise-induced negative U-wave (NU) in patients with anterior myocardial infarction, we compared the angiographic and scintigraphic findings in 15 patients with and 20 patients without NU, and obtained the following results: 1) On coronary angiography, all patients in the NU (+) group showed over 90% stenosis or total occlusion of the left anterior descending coronary artery (LAD). In the latter cases moderate to abundant collaterals were visualized on the anterior wall. In contrast, such a tendency was not observed in the NU (-) group. 2) Segments composed of viable myocardium (estimated by preservation of contraction at rest and T1-201 redistribution after exercise) numbered 30 of 45 segments (67%) in the NU (+) group, and 13 of 60 segments (22%) in the NU (-) group. Segments composed of lost myocardium (estimated by loss of contraction at rest and persistent defect in T1-201 uptake) numbered 7 of 45 segments (16%) in the NU (+) group, and 38 of 60 segments (63%) in the NU (-) group. 3) Exercise-induced NU was frequently observed on R-wave preserved leads with ST depression, but was also observed over abnormal Q waves, ST elevation and in isolation in some instances. 4) In 3 patients, preexisting exercise-induced NU was no longer observed and a transient stress-induced T1-201 defect disappeared after successful LAD revascularization. In conclusion, exercise-induced NU on precordial leads in patients with anterior myocardial infarction may be a sign suggesting the presence of jeopardized, but still salvageable, myocardium in the infarcted area.

Heart rate at onset and termination of paroxysmal atrial fibrillation in apparently healthy subjects.

Eighteen paroxysms were documented on Holter electrocardiogram both at the onset and the termination of paroxysmal atrial fibrillation in 14 apparently healthy subjects. There were large inter- and intraindividual variations and no definite trend was observed in the time and duration of paroxysms. Heart rate at the onset of paroxysms was consistently higher than that at sinus rhythm immediately before atrial fibrillation started. There were 2 patterns in the sequence of heart rate during paroxysms. One was an almost constant heart rate during paroxysms, and the other was a trend toward a decrease in heart rate from the onset to the termination of paroxysms. The duration of paroxysms was within 2 hours in the former group and more than 2 hours in the latter group. There was a reverse correlation between heart rate at the termination of paroxysms and their duration.

Incidence of portal vein thrombosis in liver cirrhosis. An angiographic study in 708 patients.

Portal vein thrombosis was thought to be a common complication of liver cirrhosis in the past. The incidence of angiographically demonstrable portal vein thrombosis was studied in 708 consecutive patients with unequivocal cirrhosis seen in the past 10 yr in whom either transhepatic portography or superior mesenteric arterial portography clearly delineated the major portal vein system. Excluding 2 cases that were thought to be associated with past splenectomy, there were 4 cases of portal vein thrombosis related to cirrhosis, all in a decompensated stage. The calculated incidence of portal vein thrombosis was 0.573% of all cirrhotic patients without splenectomy in the past. They constituted 23.5% of the 17 cases of extrahepatic portal vein obstruction encountered during the same period. There were 78 cases of idiopathic portal hypertension similarly studied angiographically, and the incidence of portal vein thrombosis unrelated to splenectomy was 2.86%. A statistical survey based on 247,728 necropsies recorded in the Japan Autopsy Registries of 1975-1982 showed a 0.05489% incidence of portal vein thrombosis and a 6.58857% incidence of cirrhosis of all types among them, suggesting that portal vein thrombosis is not a common complication of cirrhosis in Japan in recent years.

Esophageal varices: correlation of left gastric venography and endoscopy in patients with portal hypertension.

Selective left gastric venography was performed via percutaneous transheptic catheterization in 100 patients with portal hypertension to study hemodynamics and left gastric collaterals. Flow was hepatofugal in 81 patients, while 63 had varices supplied by the left gastric vein; azygos/hemiazygos collaterals were seen in 27 patients, gastrorenal shunts in 18, and other collaterals in 58. In 79 cases, enlarged, tortuous veins arising from thin parallel vessels at the esophagogastric junction on venography corresponded with varices on endoscopy in both size and course. Venography failed to show small varices which were seen endoscopically, whereas endoscopy often interpreted non-tortuous veins as varices. Using endoscopy as a reference, the sensitivity of venography for varices was 76%, specificity 100%, and accuracy 78%. There was a significant correlation between venographic demonstration of varices and previous hematemesis. Left gastric venography is necessary prior to embolization of varices and is also useful in their diagnosis as well as study of hemodynamics and assessment of bleeding risk.