Biomedical subjects

R Nagai

Publications and source records attributed to R Nagai.

At least 181 records · Page 10Linked to original sources

PubMed2000

Effect of enalapril on exhaled nitric oxide in normotensive and hypertensive subjects.

We investigated whether an angiotensin-converting enzyme (ACE) inhibitor increases the production of nitric oxide (NO) in exhaled air in normotensive and hypertensive subjects. In study 1, 8 normotensive male subjects received a single oral dose of enalapril (5 mg) or nitrendipine (10 mg) in a crossover manner. Exhaled air was collected at baseline, and at 2, 4, and 8 hours after administration of the drug. In study 2, 10 normotensive subjects (6 men and 4 women) and 10 hypertensive subjects (6 men and 4 women) received a single oral dose of enalapril (5 mg). Exhaled air was collected at baseline and at 2 and 4 hours after administration of the drug. In study 1, enalapril significantly increased the NO release rate from the lung in normotensive subjects (36.9+/-5.1 pmol/s at baseline versus 58.3+/-7.3 pmol/s at 4 hours, P<0.01). Nitrendipine did not change the NO release rate. In study 2, enalapril significantly increased the release of NO from the lung in normotensive subjects (40.4+/-6.0 pmol/s at baseline versus 70. 3+/-11.4 pmol/s at 4 hours, P<0.01) but not in hypertensive subjects. ACE inhibition increased NO production from the lung in normotensive subjects but not in hypertensive patients. The reduction of angiotensin II production and/or the accumulation of bradykinin in the pulmonary tissue may be responsible for increased NO production in components of the lung, such as the pulmonary vascular endothelium, bronchial epithelial cells, macrophages, nasopharyngeal cells, and neurons. However, the effects of ACE inhibition on NO production from the lung differ between hypertensive subjects and normotensive subjects.

Adult↗

PubMed2000

Disruption of the klotho gene causes pulmonary emphysema in mice. Defect in maintenance of pulmonary integrity during postnatal life.

Homozygous mutant klotho (KL(-/-)) mice exhibit multiple phenotypes resembling human aging. In the present study, we focused on examining the pathology of the lungs of klotho mice and found that it closely resembled pulmonary emphysema in humans both histologically and functionally. Histology of the lung of KL(-/-) mice was indistinguishable from those of wild-type littermates up to 2 wk of age. The first histologic changes appeared at 4 wk of age, showing enlargement of the air spaces accompanied by destruction of the alveolar walls, and progressed gradually with age. In addition to these changes, we observed calcium deposits in type I collagen fibers in alveolar septa and degeneration of type II pneumocytes in 8- to 10-wk-old KL(-/-) mice. Pulmonary function tests revealed prolonged expiration time in KL(-/-) mice, which is comparable with the pathophysiology of pulmonary emphysema. The expression level of messenger RNA for type IV collagen, surfactant protein-A and mitochondrial beta-adenosine triphosphatase was significantly increased in KL(-/-) mice, which may represent a compensatory response to alveolar destruction. Additionally, the heterozygous mutant klotho mice also developed pulmonary emphysema late in life, around 120 wk of age. These findings indicate that klotho gene expression is essential to maintaining pulmonary integrity during postnatal life. The klotho mutant mouse is a useful laboratory animal model for examining the relationship between aging and pulmonary emphysema.

Aging↗

PubMed2000

Endothelin-1 is a potent activator of nonselective cation currents in human bronchial smooth muscle cells.

The effects of endothelin (ET)-1 on cultured human bronchial smooth muscle cells (HBSMC) were investigated and compared with those of histamine, using the patch clamp techniques and measurements of intracellular Ca(2+) ([Ca(2+)](i)). Both ET-1 and histamine caused an initial transient elevation of [Ca(2+)](i) by Ca(2+) mobilization, followed by a sustained rise due to Ca(2+) entry. Nicardipine inhibited the sustained phase, but La(3+) abolished it. With low ethyleneglycol-bis-(beta-aminoethyl ether)-N,N'-tetraacetic acid (EGTA) and K(+) internal solutions, both ET-1 and histamine induced a sustained depolarization from approximately -40 to -20 mV. Under voltage clamp conditions, both drugs transiently activated an outward K(+) current at a holding potential of 0 mV. Additionally, with a Cs(+) internal solution, they elicited another transient inward current, frequently followed by current oscillations. These transient currents were blocked by high EGTA or heparin. With high EGTA and Cs(+) internal solutions, both drugs activated a long-lasting inward current. The reversal potential of these agonist-induced currents was approximately 0 mV and was not altered by the replacement of internal or external concentration of Cl(-), suggesting that the inward current was a nonselective cation current (I(cat)). The half-maximal effective concentration to activate I(cat) was 12 nM for ET-1 and 11 microM for histamine. La(3+) and Cd(2+) abolished these agonist-induced I(cat). The effects of ET-1 on [Ca(2+)](i) and I(cat) could be blocked by combined pretreatment with BQ-123 and BQ-788. Sarafotoxin S6c also increased [Ca(2+)](i) and activated I(cat). By polymerase chain reaction of reverse transcribed RNA, we detected both ET-A and ET-B receptor messenger RNA. These results provide the first evidence that ET-1 is a potent activator of I(cat) in HBSMC via ET-A and ET-B receptors, and the activation of I(cat) plays an important role in ET-1-induced Ca(2+) entry in human airways.

Bronchi↗

PubMed2000

Restored insulin-sensitivity in IRS-1-deficient mice treated by adenovirus-mediated gene therapy.

Insulin resistance is commonly observed both in overt diabetes and in individuals prone to, but not yet manifesting, diabetes. Hence the maintenance or restoration of insulin sensitivity may prevent the onset of this disease. We previously showed that homozygous disruption of insulin receptor substrate-1 (IRS-1) in mice resulted in insulin resistance but not diabetes. Here, we have explored the mechanism of systemic insulin resistance in these mice and used adenovirus-mediated gene therapy to restore their insulin sensitivity. Mice expressing the IRS-1transgene showed almost normal insulin sensitivity. Expression of an IRS-1 mutant (IRS-1Deltap85) lacking the binding site for the p85 subunit of phosphatidylinositol 3-kinase (PI3K) also restored insulin sensitivity, although PI3K is known to play a crucial role in insulin's metabolic responses. Protein kinase B (PKB) activity in liver was decreased in null mice compared with the wild-type and the null mice expressing IRS-1 or IRS-1Deltap85. In primary hepatocytes isolated from null mice, expression of IRS-1 enhanced both PI3K and PKB activities, but expression of IRS-1Deltap85 enhanced only PKB. These data suggest that PKB in liver plays a pivotal role in systemic glucose homeostasis and that PKB activation might be sufficient for reducing insulin resistance even without full activation of PI3K.

Adenoviridae↗

PubMed2000

ADAMTS-1: a metalloproteinase-disintegrin essential for normal growth, fertility, and organ morphology and function.

A disintegrin and metalloproteinase (ADAM) represents a protein family possessing both metalloproteinase and disintegrin domains. ADAMTS-1, an ADAM family member cloned from cachexigenic colon adenocarcinoma, is unusual in that it contains thrombospondin type I motifs and anchors to the extracellular matrix. To elucidate the biological role of ADAMTS-1, we developed ADAMTS-1-null mice by gene targeting. Targeted disruption of the mouse ADAMTS-1 gene resulted in growth retardation with adipose tissue malformation. Impaired female fertilization accompanied by histological changes in the uterus and ovaries also resulted. Furthermore, ADAMTS-1(-/-) mice demonstrated enlarged renal calices with fibrotic changes from the ureteropelvic junction through the ureter, and abnormal adrenal medullary architecture without capillary formation. ADAMTS-1 thus appears necessary for normal growth, fertility, and organ morphology and function. Moreover, the resemblance of the renal phenotype to human ureteropelvic junction obstruction may provide a clue to the pathogenesis of this common congenital disease.

ADAM Proteins↗

PubMed2000

Renovascular hypertension observed in a patient with antiphospholipid-antibody syndrome.

The antiphospholipid-antibody syndrome is associated with an increased incidence of arterial and venous thrombosis. Although renal infarction has been observed in these patients, stenotic lesions of the renal artery associated with the antiphospholipid-antibody syndrome have not been reported. A 47-year-old male with a history of hypertension for 7 years developed blurred vision secondary to thrombotic occlusion of the central retinal artery. Laboratory and radiologic examinations revealed renal dysfunction, a positive anticardiolipin antibody, and narrowing of the right renal artery. Successful percutaneous transluminal renal artery angioplasty resulted in normalization of the blood pressure and recovery of renal function.

Angioplasty, Balloon, Coronary↗

PubMed2000

Unclassified connective tissue disease presenting as cardiac tamponade: a case report.

This report describes a case of cardiac tamponade as the initial manifestation of unclassified connective tissue disease (UCTD). A 68-year-old Japanese woman was admitted to hospital because of dyspnea and edema. She had undergone a radical left mastectomy for the treatment of breast cancer 18 years before. On admission, bilateral leg edema, hepatomegaly, and a paradoxical pulse were noted on physical examination. The erythrocyte sedimentation rate was elevated and the C-reactive protein was 2.8 mg/dl. Antinuclear antibodies and anti-SS-A/Ro antibodies were present. The scl-70 and anticentromere antibodies were elevated. Chest radiography showed cardiomegaly. Echocardiography revealed a large pericardial effusion, but the pericardial fluid did not contain malignant cells or bacteria. She did not meet the diagnostic criteria for any known connective tissue diseases, so was diagnosed with cardiac tamponade due to UCTD. Prednisolone (30 mg/day) was administered, which resulted in a gradual resolution of the pericardial effusion. Although connective tissue diseases are known to cause pericardial effusion, cardiac tamponade as the initial manifestation of the disease in the absence of other symptoms is quite rare.

Aged↗

PubMed2000

Prediction of functional recovery after revascularization in coronary artery disease using (18)F-FDG and (123)I-BMIPP SPECT.

STUDY OBJECTIVES: Clinical studies comparing fatty acid and glucose metabolism in relation to functional recovery of ischemic myocardium after coronary revascularization are scarce. This study evaluated the recovery of regional and global left ventricular function after coronary revascularization in relation to uptake patterns of beta-methyl-iodophenyl-pentadecanoic acid (BMIPP) and fluorodeoxyglucose (FDG) in patients with ischemic myocardial dysfunction. METHODS: Patients with ischemic regional wall motion abnormality underwent baseline viability imaging with (18)F-FDG, (123)I-BMIPP, and (99m)Tc- methoxyisobutylisonitrile, and the regions with evidence for maintained tissue viability were revascularized. Mismatch of uptake score between two different single-photon emission CT (SPECT) images in the same myocardial region was graded as low or high mismatch. Regional and global left ventricular functional changes after revascularization were analyzed in relation to mismatch severity and difference of total uptake score in each SPECT image pair. A total of 33 vessels in 30 patients related to the asynergic regions were revascularized, and a total of 100 myocardial segments perfused by the revascularized vessels were analyzed. RESULTS: Segments showing high metabolic mismatch (FDG/BMIPP) had lowest regional wall motion score at baseline, representing the most severely impaired ischemic myocardium, and had highest improvement in regional wall motion score after revascularization. Difference of total uptake score between FDG and BMIPP showed a significant positive correlation with difference of ejection fraction between pre- and postrevascularization (r = 0.774, p < 0.0001). CONCLUSIONS: Combined metabolic SPECT imaging with FDG and BMIPP has the potential to identify severely impaired ischemic myocardium leading to more efficient therapeutic management of patients with coronary artery disease.

Aged↗

PubMed2000

The clinical significance of reversed flow in the main pulmonary artery detected by doppler color flow imaging.

BACKGROUND: Using Doppler color flow imaging, abnormal flow patterns were reported to occur with pulmonary artery (PA) dilation. We have frequently observed red signals in the main PA, suggesting reversed flow (RF) in patients without overt pulmonary hypertension. The clinical implication of these signals has not been extensively studied. PATIENTS AND METHODS: We studied 191 of 412 patients referred for echocardiography (99 men and 92 women; mean +/- SD age, 62 +/- 13 years), in whom the main PA diameter had been adequately measured. If a red signal was observed by color flow imaging, a pulsed Doppler echocardiogram of the red signal was recorded simultaneously. The presence of the red signal was correlated with the PA diameter and the PA systolic pressure determined using the modified Bernoulli equation. In 54 patients who also underwent cardiac catheterization studies, the red signal was correlated with PA and pulmonary capillary wedge (PCW) pressures, and with pulmonary vascular resistance. RESULTS: Red signals adjacent to the medial PA border were detected in parallel with systolic blue signals in 127 patients (66%). Pulsed Doppler recordings revealed that they were caused by RF occurring immediately after the forward systolic signal and persisted in diastole. The PA diameter (28 +/- 4.8 mm) and the estimated PA systolic pressure (34 +/- 16 mm Hg) of patients with the RF signal were significantly greater (p < 0.001 and p < 0.05, respectively) than those of patients without the signal (22 +/- 2.5 mm and 28 +/- 6.0 mm Hg, respectively). Among patients who had hemodynamic studies, PA and PCW pressures were significantly higher (p < 0.05) in the 41 patients with the RF signal (22 +/- 12 mm Hg vs 15 +/- 2.6 mm Hg and 11 +/- 5.5 mm Hg vs 8 +/- 3.1 mm Hg, respectively). CONCLUSION: : RF signals in the main PA occur mostly as a result of PA dilation, which may be caused by primary pulmonary hypertension or chronic elevation of left atrial pressure in left-sided cardiac abnormalities.

Aged↗

PubMed2000

Intracoronary serum smooth muscle myosin heavy chain levels following PTCA may predict restenosis.

Recently a novel biochemical method that uses an immunoassay to quantitate serum smooth muscle myosin heavy chain (SMMHC) levels was developed for diagnosis of aortic dissection.) The purpose of this study was to determine whether SMMHC released from the coronary arterial wall can be used to predict restenosis after percutaneous transluminal coronary angioplasty (PTCA). Fifty-two consecutive patients undergoing successful PTCA for single vessel disease were examined (40 men, 12 women, 63 +/- 8 years). Intracoronary blood samples were obtained distal to the lesion, and from the femoral artery after PTCA. In 10 patients, blood samples were taken immediately after the final balloon inflation, and 10 and 20 minutes after PTCA. SMMHC levels were measured by ELISA using SMMHC-specific monoclonal antibodies. Follow-up coronary angiography was performed 3 months after PTCA. Intracoronary serum SMMHC levels were significantly higher than those obtained from the femoral artery (10.6 +/- 1.5 vs 2.1 +/- 0.1 ng / ml, p < or = 0.001). Of 40 patients without apparent dissection, the 23 patients who did not develop restenosis in the follow-up study were found to have had higher levels of intracoronary SMMHC levels immediately after PTCA compared to the 17 patients with restenosis (15.2 +/- 2.9 vs 7.1 +/- 1.2 ng /ml, p < or = 0.05). We suggest that elevated intracoronary SMMHC levels after PTCA may reflect the extent of injury to the arterial wall. Intracoronary SMMHC may be a possible biochemical marker for the prediction of restenosis.

Aged↗

PubMed2000

Screening for cardiac dysfunction in asymptomatic patients by measuring B-type natriuretic peptide levels.

Early diagnosis and treatment of heart failure lead to improved survival; pre-clinical detection would thus be beneficial. A non-invasive biochemical testing method would indeed be ideal to screen for the condition. In the present study, we sought to determine whether circulating levels of B-type natriuretic peptide (BNP) correlate with cardiac function in asymptomatic subjects. 294 consenting asymptomatic subjects were examined. BNP levels in elevated patients (> 18.4 pg / ml) showed significant correlation with echocardiographic parameters of the systolic and diastolic functions (EF r = -0.51, FS r = -0.50, E/A r = 0.42, p < 0.01). Moderate correlation with the CTR on chest X-ray was also seen (r = 0.23, p < 0.01). Multiple regression analysis showed numerous echocardiographic and hemodynamic parameters including those of systolic and diastolic function in addition to left ventricular wall thickness, blood pressure and serum creatinine levels to be significantly associated with raised BNP levels. Elevated BNP levels reflect cardiac function (both systolic and diastolic) in the asymptomatic population. Detection of cardiac dysfunction by the non-invasive biochemical test may prove useful in early pre-clinical diagnosis of heart failure.

Atrial Natriuretic Factor↗

PubMed2000

Augmented responses of angiotensin I and II in patients with ischemic heart disease: relation to left ventricular function.

To evaluate the effects of left ventricular (LV) dysfunction upon the sympathetic nervous and renin-aldosterone-angiotensin systems, neurohormonal factors were measured in patients with ischemic heart disease. Eleven patients were divided into two groups by their LV ejection fraction based on previous catheterization; preserved (EF > or = 60%) and impaired (EF < 60%) LV systolic function groups. They performed supine ergometer exercise and blood samples were drawn at rest and at peak exercise. After dynamic exercise, plasma norepinephrine was significantly (p < 0.05) increased in patients with preserved LV function, whereas it was not altered in patients with impaired LV function (norepinephrine 20.8 +/- 20.5 vs 45.8 +/- 41.9, respectively). We observed no differences in basal or peak levels of neurohormonal factors, including plasma renin activity, aldosterone, and brain natriuretic peptide (BNP), between the groups. Although the plasma levels of angiotensin I and II were not different in the two groups at rest or at peak exercise, their increasing ratios from rest to peak exercise were significantly higher in patients with impaired LV function compared to those with preserved LV function (angiotensin I; -18.6 +/- 31.0% vs 64.8 +/- 66.5%, p < 0.05, angiotensin II; -5.9 +/- 41.2% vs 60.7 +/- 40.4% , p < 0.05). These results suggest that the increasing ratios of angiotensin I and II are superior to BNP as predictors of LV dysfunction, and that the sympathetic nervous system has already been activated even at rest and did not respond to dynamic exercise in patients with LV dysfunction in ischemic heart disease.

Aged↗

PubMed2000

Serum levels of vascular endothelial growth factor and transforming growth factor-beta1 in patients with atrial fibrillation undergoing defibrillation therapy.

We have previously reported that pulsatile mechanical stretch in vitro induced rapid secretion of vascular endothelial growth factor (VEGF) by cultured cardiac myocytes and that the stretch-induced secretion of VEGF was mainly mediated by secretion of transforming growth factor (TGF)-beta1 by cardiac myocytes in an autocrine fashion. To investigate whether tachycardia-induced mechanical overload increases serum levels of VEGF and TGF-beta1, we investigated the serum levels of VEGF and TGF-beta1 in patients with atrial fibrillation undergoing defibrillation therapy. The serum VEGF level before defibrillation was significantly increased in 13 out of 20 patients (89.48 +/- 16.09 pg/ml [mean +/- SE]). After defibrillation, the serum VEGF level in these 13 patients significantly (p = 0.019) decreased (65.04 +/- 16.61 pg/ml [mean +/- SE]), although it increased slightly in one patient. The serum TGF-beta1 level before defibrillation therapy (13.01 +/- 1.97 pg/ml [mean +/- SE]) in these 12 patients also decreased after defibrillation therapy (11.47 +/- 2.06 pg/ml [mean +/- SE]). The changes in serum VEGF level significantly correlated with those in the serum TGF-beta1 level in these 12 patients (r = 0.73, p < 0.05, n = 12). Our data suggest that tachyarrhythmia-induced mechanical overload can increase the serum VEGF level, which can be a useful clinical marker for relative myocardial oxygen shortage in such patients.

Aged↗

PubMed2000

Effects of antihypertensive therapy on blood pressure and left ventricular hypertrophy in patients with severe hypertension.

The mechanisms responsible for regression of left ventricular (LV) mass with antihypertensive therapy in patients with severe hypertension remain unclear. This study was designed to examine whether systolic and diastolic blood pressures are associated with changes in LV mass. Eighteen patients with essential hypertension whose average seated diastolic blood pressure was >or = 110 mm Hg were enrolled in the study. All patients were administered antihypertensive therapy and underwent M-mode echocardiography before and after 6 months of treatment. In all patients, antihypertensive treatment significantly reduced systolic blood pressure from 175 +/- 21 mm Hg at baseline to 143 +/- 22 mm Hg at 6 months (p < 0.001), and diastolic blood pressure from 116 +/- 7 mm Hg at baseline to 92 +/- 20 mm Hg at 6 months (p < 0.001). LV mass index at 6 months was significantly reduced compared to its baseline value (p < 0.05). Change (value at 6 months-value at baseline) in systolic and diastolic blood pressures correlated positively with the change in LV mass index (r = 0.61, p < 0.01 and r = 0.71, p < 0.001, respectively). The patients were divided into responders. whose LV mass regressed by > or = 10% (n = 9), and nonresponders, whose LV mass regressed by < 10% (n = 9). Systolic (p < 0.001) and diastolic (p < 0.001) blood pressures. interventricular septal thickness (p< 0.05), posterior wall thickness (p < 0.001), and LV mass index (p < 0.001) were significantly decreased in the responders, but not in the nonresponders, at 6 months compared with those at baseline. Systolic (p < 0.05) and diastolic (p < 0.05) blood pressures in nonresponders were significantly higher than those in the responders at 6 months. The changes in systolic and diastolic blood pressures did not correlate with the change in LV mass index in the responders or the nonresponders. The regression of LV mass is strongly affected by reducing blood pressure. This is the first study using antihypertensive therapy to demonstrate that a change in blood pressure correlates positively with changes in LV mass index in severely hypertensive patients.

Adult↗

PubMed2000

C-reactive protein as a prognostic marker in lymphocytic myocarditis.

The prognosis of patients with lymphocytic myocarditis (LM) is poor with the combined endpoint of death or transplant in the Myocarditis Treatment trial being 56% at 5 years. Physicians often have difficulty determining the prognosis in an individual patient. Patients with LM may have ongoing myocardial inflammation. We evaluated the ability of a serum marker of inflammation to predict prognosis in patients with LM. Serum concentrations of C-reactive protein (CRP) were measured in patients with LM. Thiry-one patients with clinical and histologic evidence of LM were evaluated. Patients with coronary artery disease, and idiopathic dilated and secondary cardiomyopathies were excluded. Overall mortality and morbidity from congestive heart failure was assessed at 28 days. The mean plasma CRP concentrations in the five patients who died within the 28-day follow-up period were significantly higher than in those patients who survived (17.4 +/- 5.6 vs 5.9 +/- 3.3 mg/ml, p < 0.05). The CRP concentration was positively correlated with plasma levels of lactic dehydrogenase and the New York Heart Association functional class. Routine measurement of CRP may be a useful tool for determining the prognosis in patients with LM.

Adolescent↗

PubMed2000

Evaluation of the heart with magnetic resonance imaging.

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.

Blood Flow Velocity↗

PubMed2000

Prolongation of QT interval and ventricular septal hypertrophy.

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 abnormalities 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 degrees) was significantly lower (p < 0.05) than in the control group (46+/-26 degrees). 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 > or = 12 min, 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.

Adult↗

PubMed2000

Is the QT interval an indicator of autonomic state?

Prolonged QT interval is suggested to indicate an increased risk of sudden cardiac death in certain clinical conditions such as diabetes mellitus. We investigated whether the individual QT interval is an indicator of an autonomic state. An ambulatory 24-hour ECG was recorded in 53 subjects from different clinical backgrounds. Power spectral components of heart rate variability (HRV) and the QT interval were regressively obtained at a heart rate of 60, 70, 80, 90, or 100 beats per minutes (bpm). Log values of the high-frequency component of HRV (HF: 0.15-0.50 Hz, a scale of cardiac parasympathetic tone) failed to show a relationship with the QT interval. In contrast, the QT interval at a heart rate of 90 bpm and 100 bpm showed a significant correlation with the log values of the low-frequency component (LF: 0.04-0.15 Hz) and the log[LF/HF], i.e., a putative scale of sympathetic tone (100 bpm: QT vs logLF: r = 0.414, p < 0.005, QT vs log[LF/HF]: 0.416, p < 0.002). Also, attenuated rate-dependent QT shortening was associated with greater logLF and log[LF / HF] values at a heart rate of 80, 90, or 100 bpm. These results suggest that the QT interval at a moderate heart rate (approximately 90-100 / min) and the degree of rate-dependent QT shortening are related to individual sympathetic tone.

Autonomic Nervous System↗