To evaluate the prevalence of coronary artery disease (CAD) in patients with spinal cord injury (SCI), 47 clinically asymptomatic SCI patients received thallium-201 myocardial perfusion single photon emission computed tomography (Tl-201 SPECT) after dipyridamole administration for the diagnosis of CAD. There were 4 groups as follows; group 1: 13 patients with quadriplegia and complete SCI, group 2: 11 patients with quadriplegia and incomplete SCI, group 3: 11 patients with paraplegia and complete SCI, and group 4: 12 patients with paraplegia and incomplete SCI. There were no significant differences in sex distribution, ages, SCI duration, or CAD risk factors among the SCI patients in the 4 groups. All Tl-201 SPECT images were interpreted by the agreement of 2 experienced nuclear medicine physicians without prior knowledge of the patients' histories. A total of 30 of 47 (63.8%) SCI patients had abnormal Tl-201 SPECT findings. Among the 4 groups of SCI patients, those in groups 1 and 4 had the significantly highest and lowest prevalences of abnormal Tl-201 SPECT findings, respectively. We concluded that combined quadriplegia and complete SCI is an important CAD risk factor in SCI patients based on the objective evidence of intravenous dipyridamole cardiac stress testing with Tl-201 SPECT.

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The Tei index is an echocardiographic index of combined systolic and diastolic function, calculated as isovolumetric relaxation time plus isovolumetric contraction time divided by ejection time. The aim of this study was to define the correlation of the Tei index with left ventricular dilatation and mortality in patients with acute myocardial in-farction (AMI).
A total of 77 patients (58 men, 19 women) with a mean age of 53 ± 12 years, who had presented with an AMI in our clinic between June 2001 and February 2002 were compared with a control group of 88 healthy subjects (63 men, 25 women) with a mean age of 55 ± 6 years. Echocardiographic evaluation was carried out within 24 hours and the third month of AMI, using a 3.5 MHz probe with pulse wave Doppler recordings by the adult cardiac mode of an Acuson C 256 echocardiograph.
There were statistically significant differences between the 2 groups in all echocardiographic parameters, except mitral A wave. Thirteen patients died during the follow-up period of 3 months. The Tei index was significantly higher in the patients who died compared with those who survived (0.70 ± 0.10 versus 0.61 ± 0.10; P < 0.001). The patients who had heart failure after AMI had a mean Tei index value of 0.76 ± 0.27, whereas the patients who did not have heart failure after AMI had a significantly lower Tei index value of 0.60 ± 0.32 (P < 0.05). Patients were divided into 2 groups according to their Tei index. Patients with a > 0.60 Tei index had significantly higher end-systolic and end-diastolic volumes compared to patients with a < 0.60 Tei index (P < 0.001 for both) in the acute phase of AMI. Within 3 months, patients with a Tei index < 0.60 had a significant reduction in end-diastolic volumes (P < 0.01), whereas the end-diastolic volumes did not change significantly in patients with an index > 0.60 (P = 0.19).
The Tei index is an important indicator of left ventricular dysfunction and death after AMI. A greater Tei index at the onset of AMI is associated with a higher incidence of subsequent cardiac death, CHF, and progressive LV remodeling.

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Coronary heart disease (CHD) is recognized as a lifestyle-related disease and is the second leading cause of death in Japan. However, the cardiac risk factor profile of young patients with CHD has not been clarified in suburban areas of Japan. Our study aimed to determine metabolic and lifestyle risk factors in young patients and compare them with older patients living in suburban areas of Nagano Prefecture.
A multicenter study was conducted in 86 young (aged less than 40 years) and 91 older (aged 50 years and over) patients diagnosed with CHD from 1992 to 2002. There was a strong association between obesity and the occurrence of CHD events in young patients (odds ratio = 3.61, P = 0.006). Lifestyle in the young patients was characterized by a lack of physical activity and regular physical activity was found to decrease the risk of the CHD events in these patients (odds ratio = 0.31, P = 0.030). In older patients, hypertension was identified as an independent risk factor for CHD events.
The results of the present study have demonstrated that obesity and a lack of regular physical exercise are independent risk factors for CHD events in younger patients. Thus, the data may be useful for the effective screening of high-risk individuals and the development of educational programs for the prevention of CHD, especially in younger Japanese.

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We previously reported that continuous intravenous (IV) administration of nicorandil (NIC) inhibits QT dispersion (QTd). However, no prior study has evaluated the efficacy of NIC when administered orally to acute myocardial infarction (AMI) patients following continuous IV administration.
Thirty patients with anteroseptal infarction in whom revascularization was performed successfully within 6 hours of AMI onset were included in the study and assigned to one of 3 groups: group A (continuous IV administration of NIC), group B (continuous IV and oral administration of NIC), and group C (no treatment with NIC). After 24 hours, QTd in groups A and B was significantly decreased compared to QTd in group C (P < 0.01) (group A, 58.1; group B, 58.2; and group C, 81.3). The QTd obtained 3 months later was significantly shorter in group B subjects who were orally administered NIC, and QTd before percutaneous coronary intervention (PCI) was restored in group A, in which no NIC had been administered orally [group A, 66.7; group B, 54.1; and group C, 73.9; P < 0.05 (group A versus group B) and P < 0.01 (group B versus group C)].
The effects were evaluated by comparing different routes of administration. Continuous IV and subsequent oral administration of NIC inhibited prolongation of QTd, suggesting that these effects may prevent the occurrence of cardiac events during both the acute and chronic phases of AMI.

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Intracardiac electrograms are important for discrimination of tachyarrhythmia by implantable cardioverter defibrillators (ICD). A low R-wave can cause not only undersensing of ventricular tachyarrhythmia but also inappropriate discharges due to oversensing of unexpected signals because of its characteristic sensing algorithm. Therefore, this study aimed to investigate adverse events associated with R-wave amplitude. We included 115 consecutive patients followed-up over one year after implantation of a transvenous ICD system. The status of the ICD was checked every 3 months and intracardiac ventricular electrograms were analyzed. The decrease in R-wave amplitude was high in arrhythmogenic hypertrophy cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy (ARVC), and sarcoidosis. Low R-waves (< 5.0 mV) were observed in 13 patients at a follow-up of 15 ± 16 months after implantation, and the mean R-wave was 3.0 ± 0.8 mV. The frequency of low R-waves was high in ARVC (38%), sarcoidosis (33%), and dilated cardiomyopathy (17%). All of the dilated cardiomyopathy patients with low R-waves had severe left ventricular dysfunction. Inappropriate ICD therapy resulting from T-wave oversensing occurred in 7 patients and the R-wave was < 5.0 mV in 6 of the patients. The frequency of inappropriate therapy was high in patients with sarcoidosis. In 3 patients, inappropriate therapy caused ventricular tachyarrhythmia. In conclusion, decreases in R-wave amplitude occurred in some progressive cardiac disorders and caused inappropriate ICD discharges having arrhythmogenicity. Physicians should attempt to obtain a high R-wave amplitude during ICD implantation and careful follow-up is required, especially in patients with ARVC or sarcoidosis.

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Increased platelet activity plays a key role in atherothrombotic events. Persistent platelet activity has been reported in patients with atrial fibrillation (AF) following myocardial infarction and in the chronic phase after ischemic stroke. However, platelet activity in patients with AF remains clear. This study investigated platelet reactivity (expressed by CD62p) in patients with chronic nonvalvular (NV) AF. Expression of CD62p was measured by flow cytometry in 62 consecutive patients with chronic NVAF (defined as sustained AF > 6 months) and no previous embolic events. The CD62p expression was also evaluated in 20 healthy subjects. Expression of CD62p was not different between AF patients and healthy subjects (P = 0.970). Additionally, CD62p expression did not differ between patients with and patients without the following atherosclerotic risk factors: hypertension, current smoking, and hypercholesterolemia (all P values > 0.1). Furthermore, CD62p expression did not differ between patients taking and not taking the following medications: warfarin, a statin, or an angiotensin converting enzyme inhibitor/angiotensin II receptor blocker (all P values > 0.2). However, diabetes mellitus (DM) was strongly associated with increased CD62p expression (P < 0.0001). Multiple linear regression analysis demonstrated that only DM independently predicted increased CD62p expression (r² = 0.509, regression coefficient = 3.044, P < 0.0001). In conclusion, compared to healthy subjects, CD62p expression was not significantly enhanced in chronic NVAF patients. However, CD62p expression was substantially elevated in diabetic patients with chronic NVAF.

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Although catecholaminergic polymorphic ventricular tachycardia (CPVT) is associated with fatal ventricular arrhythmias and sudden death, the ECG findings are not fully understood. In this paper, we report on alterations in the U-wave.
Seven patients from 6 families with CPVT in which bidirectional tachycardia and polymorphic VT were induced by exercise or isoproterenol infusion visited our hospitals. VT was not inducible by programmed electrical stimulation. A novel gene mutation of the ryanodine receptor 2 (RyR2) was confirmed in 2 families.
In one of these patients, U-wave alternans was observed following ventricular pacing at 160 beats/min. In the other patient, U-wave alternans was observed during the recovery phase after the exercise stress test, which was terminated because of polymorphic VT. In both cases, leads V₃-V₅ were the leads showing alternans most clearly. In the third patient, a negative U-wave became positive following a pause from sinus arrest and a change in T-wave was also noted.
Since such findings were not found in the other subjects who underwent electrophysiologic study, isoproterenol infusion or exercise stress testing, the phenomenon seems to be relevant to the underlying pathogenesis of CPVT. The genesis and significance of U-wave alteration need to be determined.

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Both left ventricular (LV) hypertrophy and insulin resistance (IR) have often been demonstrated in patients with essential hypertension (EH). Insulin may exert a direct growth promoting effect on cardiomyocytes rather than affecting the LV internal diameter. The purpose of this study was to examine the effect of IR on LV geometry.
We enrolled 105 patients (71 females, mean age, 49.2 ± 13.6 years) with recently diagnosed and untreated hypertension (blood pressure > 140 and/or 90 mmHg, fasting glucose < 110 mg/dL), and grouped them as normal (N) (39 patients, 26 females, mean age, 48.5 ± 14.7 years) if all M-mode echocardiographic measurements were within normal limits, concentric remodeling (CR) (22 patients, 15 females, mean age, 50.5 ± 14.8 years) if relative wall thickness was increased but left ventricular mass index (LVMI) was normal, concentric hypertrophy (CH) (13 patients, 9 females, mean age, 50.3 ± 10.8 years) if both ventricular thicknesses and the LVMI were increased, and eccentric hypertrophy (EH) (31 patients, 21 females, mean age, 48.6 ± 12.9 years) if ventricular thicknesses were normal, but LVMI was increased. Transthoracic echocardiography was performed in all subjects, and interventricular septal thickness (IVS), posterior wall thickness (PWT), sum of wall thickness (SWT), left ventricular end-diastolic internal diameter (LVED), relative wall thickness (RWT), and LVMI were recorded. Blood samples for routine biochemical examination and fasting insulin levels were obtained and then the homeostasis model assessment (HOMA) index was calculated by the formula: HOMA Index = Fasting Blood Glucose (mg/dL) × Immunoreactive Insulin (μU/mL)/405, for the assessment of IR.
There were no significant differences among the groups with respect to age, blood pressure (BP) levels, fasting blood glucose (FBG), LDL-cholesterol (LDL-C), HDL-cholesterol (HDL-C), total cholesterol (TC), or triglyceride (TG) levels. Insulin levels were significantly higher in the CR and CH groups in comparison with the N group (P = 0.004), and the HOMA index was higher in the CH group compared to the N group (P = 0.024). In Pearson's correlation analysis, insulin was found to be directly correlated with IVS (r = 0.29, P = 0.002), SWT (r = 0.25, P = 0.009), and RWT (r = 0.33, P = 0.0001). The HOMA index was also directly correlated with IVS (r = 0.33, P = 0.001), SWT (r = 0.29, P = 0.002), and RWT (r = 0.29, P = 0.003).
Cardiac changes in hypertensive patients include increased LVMI and altered LV geometry. The concentric LV geometry seen in hypertensive patients might be mediated, at least in part, by increased insulin levels and the HOMA index.

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Plasma atrial (ANP) and brain (BNP) natriuretic peptide levels were compared to determine if transmitral flow velocity pattern is an instantaneous marker of body fluid balance in anuric patients on hemodialysis (HD).
We measured plasma ANP and BNP levels and performed Doppler echocardiography in 38 anuric patients before and after HD. Patients with valvular disease, left ventricular systolic dysfunction having a fractional shortening < 0.3, arrhythmia, or left ventricular hypertrophy were excluded. The relationships between plasma ANP or BNP levels and the transmitral flow velocity pattern were evaluated. We also determined if the magnitude of the decrease in plasma ANP level was related to that in the early peak of transmitral flow velocity (peak E). The mean age of the subjects was 61.1 ± 9.7 years.
The ANP level of 213.6 ± 146.1 pg/mL was related to peak E of 61 ± 15 cm/s before HD (R = 0.504, P < 0.001), but not after HD. Plasma ANP level was not related to peak late transmitral flow velocity (peak A) or peak E/peak A before or after HD. BNP level was not related to the transmitral flow velocity pattern. The magnitude of decrease in hANP level during HD was significantly related to that in peak E (R = 0.342, P < 0.05).
Before HD, peak E was related to the plasma ANP level, reflecting volume overload. Change in peak E showed a weak relationship with that of plasma ANP level in the same HD patient. The measurement of peak E during a HD session may potentially enable the assessment of hydration status during HD.

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The objective of the present study was to examine the relationship between markers of inflammation, such as high-sensitivity C-reactive protein (hsCRP) and erythrocyte sedimentation rate (ESR), and brachial-ankle pulse wave velocity (baPWV), an indicator of arterial stiffness, in Japanese men.
We studied 269 male subjects (mean age, 53 years) who entered our health check-up program. Subjects who were receiving any medication were excluded from the study. baPWV was measured using a volume-plethysmographic apparatus (Form /ABI; Colin, Co. Ltd., Komaki, Aichi, Japan). In addition to routine laboratory tests including ESR, serum levels of hsCRP were determined by a highly sensitive ELISA technique.
baPWV was significantly correlated with age (r = 0.41, P < 0.0001), height (r = − 0.21, P = 0.0006), body weight (r = − 0.17, P = 0.007), mean blood pressure (r = 0.66, P < 0.0001), pulse pressure (r = 0.56, P < 0.0001), heart rate (r = 0.25, P < 0.0001), ln (ESR) (r = 0.20, P = 0.001), fasting blood glucose (r = 0.23, P = 0.0001), and ln (serum hsCRP) (r = 0.23, P = 0.0002). baPWV in the highest tertile of ESR was significantly higher than that in the lowest tertile of ESR (P = 0.005). baPWV in the highest tertile of serum hsCRP was significantly higher than those in the lowest tertile (P = 0.002) and the middle tertile of serum hsCRP (P = 0.02). In multiple regression analysis, baPWV significantly correlated with ln (serum hsCRP) independently of other clinical variables that showed a significant correlation with baPWV.
baPWV is significantly associated with serum levels of hsCRP in Japanese men, suggesting that inflammation is involved in arterial stiffening.

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The objective of the present study was to explore the effect of carvedilol treatment on metabolic parameters in patients with metabolic syndrome. A total of 77 patients ≥ 20 years of age (59 females, 18 males, mean age, 52.3 ± 10.3) with stage 1 hypertension who fulfilled at least 3 of the metabolic syndrome criteria proposed by NCEP-ATP III were included in this prospective, randomized, controlled study. Patients were randomly assigned to receive daily treatment with carvedilol (n = 27, 12.5 mg/day orally for the first 2 days and 25 mg/day thereafter), atenolol (n = 26, 50 mg/day orally), or doxazosin (n = 24, 2 mg/day orally) for 90 days. Doses were doubled at the end of the 3rd week in patients whose blood pressure was inadequately controlled and amlodipine 10 mg was added to the treatment if the target blood pressure was still not reached at the end of week 6. The biochemical parameters and insulin sensitivity based on the HOMA-IR model were evaluated at baseline and at the end of treatment. Similar reductions in systolic and diastolic blood pressure were observed in all groups (P > 0.05). A significant decrease in HDL cholesterol levels occurred in the doxazosin and atenolol groups compared to the carvedilol group (percent change: −5.6 ± 13.5 and −8 ± 9.8 versus −0.1 ± 12.2, respectively; P < 0.05) and a significant increase in apolipoprotein A1 level was observed in the carvedilol group compared to the doxazosin and atenolol groups (percent change: +4.3 ± 9.6 versus −0.5 ± 10.6 and −2.3 ± 6.6, respectively; P < 0.05). There were no significant differences among the groups with respect to other parameters. It is concluded antihypertensive treatment with carvedilol in patients with metabolic syndrome effectively reduces blood pressure without adversely affecting metabolic parameters.

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An attenuated heart rate recovery (HRR) immediately after exercise has been shown to be predictive of mortality. It is not known whether HRR predicts mortality when measured in patients with heart failure. The present study was undertaken to evaluate the ability of HRR to predict mortality in patients with heart failure.
We studied 84 NYHA class II or III chronic congestive heart failure patients who had a left ventricular ejection fraction ≤ 40%. All patients underwent symptom limited cardiopulmonary exercise testing. The value for the HRR was defined as the difference in heart rate between peak exercise and one-minute later; a value ≤ 18 beats per minute was considered abnormal. The patients were divided into 2 groups according to the value of HRR. Those with abnormal HRR were assigned to group I and those with normal HRR were assigned to group II. The 2 groups were compared with each other regarding baseline characteristics and exercise capacity assessed by peak VO₂.
There were 26 patients (31%) in group I and 58 patients (69%) in group II. Group II patients had better performance on treadmill exercise testing than group I patients. They had greater exercise duration (7.5 ± 3.8 minutes versus 5 ± 3.5 minutes, P = 0.006), better heart-rate reserve (79 ± 25% versus 63 ± 27%, P = 0.01), and higher values of maximal heart-rate (141 ± 18 beats/min versus 132 ± 17 beats/min, P = 0.04). Group II patients also had higher peak VO₂ values (16.8 ± 4.4 mL/kg/min versus 14.4 ± 3.6 mL/kg/min, P = 0.01). When we separated the groups according to beta-blocker usage, beta-blockers had no prominent effect on HRR.
In the follow-up period (mean 14.1 ± 6.1 months), the presence of abnormal HRR and lower peak VO₂ (≤ 14 mL/kg/min) were the only significant predictors of mortality in our patient population (adjusted hazard ratio [HR] 5.2, 95% CI, 1.3 to 24, P = 0.03 and adjusted HR 13, 95% CI, 2.1 to 25.6, P = 0.005, respectively).
It seems that the attenuated HRR value one minute after peak exercise appears to be a reliable index of the severity of exercise intolerance in heart failure patients and this study supports the value of HRR as a prognostic marker among heart failure patients referred for cardiopulmonary exercise testing for prediction of prognosis.

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The aim of this study was to investigate whether electrical stimulation of skeletal muscles could represent a rehabilitation alternative for patients with chronic heart failure (CHF). Thirty patients with CHF and NYHA class II-III were randomly assigned to a rehabilitation program using either electrical stimulation of skeletal muscles or bicycle training. Patients in the first group (n = 15) had 8 weeks of home-based low-frequency electrical stimulation (LFES) applied simultaneously to the quadriceps and calf muscles of both legs (1 h/day for 7 days/week); patients in the second group (n = 15) underwent 8 weeks of 40 minute aerobic exercise (3 times a week). After the 8-week period significant increases in several functional parameters were observed in both groups: maximal VO₂ uptake (LFES group: from 17.5 ± 4.4 mL/kg/min to 18.3 ± 4.2 mL/kg/min, P < 0.05; bicycle group: from 18.1 ± 3.9 mL/kg/min to 19.3 ± 4.1 mL/kg/min, P < 0.01), maximal workload (LFES group: from 84.3 ± 15.2 W to 95.9 ± 9.8 W, P < 0.05; bicycle group: from 91.2 ± 13.4 W to 112.9 ± 10.8 W, P < 0.01), distance walked in 6 minutes (LFES group: from 398 ± 105 m to 435 ± 112 m, P < 0.05; bicycle group: from 425 ± 118 m to 483 ± 120 m, P < 0.03), and exercise duration (LFES group: from 488 ± 45 seconds to 568 ± 120 seconds, P < 0.05; bicycle group: from 510 ± 90 seconds to 611 ± 112 seconds, P < 0.03). These results demonstrate that an improvement of exercise capacities can be achieved either by classical exercise training or by home-based electrical stimulation. LFES should be considered as a valuable alternative to classical exercise training in patients with CHF.

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A 62 year-old-woman presented with a right bundle branch block (RBBB) and left axis deviation (LAD) tachycardia. Radiofrequency (RF) energy was delivered to the left posterior fascicle (LPF) where 2 presystolic Purkinje potentials (P1 and P2) preceding onset of the QRS complex were recorded. During RF energy applications, the QRS morphology of the tachycardia changed from RBBB and LAD to RBBB and right axis deviation without termination of the tachycardia. The Purkinje potential was observed following the QRS complex during the tachycardia because of conduction block of the LPF distal to the reentry circuit due to RF catheter ablation.

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Focal left atrial tachycardias (AT) originating from the mitral annulus-aorta (MA-Ao) junction are rare and their mechanisms are unclear. We report a 35-year-old male with successful ablation of an exercise-induced focal AT due to triggered activity originating from the MA-Ao junction. The AT occurred spontaneously during treadmill exercise testing and was easily induced by an atrial extrastimulus and atrial burst pacing after intravenous administration of isoproterenol. The AT was terminated by an atrial extrastimulus as well as a bolus of 5 mg of adenosine 5'-triphosphate. The coupling intervals of the extrastimuli that induced the AT were positively correlated with the interval between the extrastimuli and the first beat of the AT, suggesting the triggered activity as a tachycardia mechanism. The AT was successfully eliminated by a focal ablation at the MA-Ao junction with the earliest atrial activation where fractionated atrial potentials were recorded. The MA-Ao junction should be recognized as an important arrhythmogenic region.

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A 24 year-old male who presented with palpitations and presyncopal attacks had monomorphic ventricular tachycardia and a well-defined huge mass within the inferoposterior wall of the left ventricle proved by transthoracic echocardiography. The mass was completely resected and shown to be proliferative angiomatosis by histopathologic examination. This is the first reported case of primary left ventricular angiomatosis in the literature.

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A 69-year-old male patient with type 1 diabetes mellitus had been under treatment at our outpatient clinic since the age of 65. He had previously undergone surgery for esophageal cancer at the age of 55; the excised portion of the esophagus was replaced by a retrosternal gastric tube. He was admitted to our hospital for suspected pneumonia on April 8, 2004. An electrocardiogram (ECG) on admission showed marked ST depression in leads V₁ and V₂, and prominent negative T waves in leads I and aVL; however, the T waves unexpectedly flattened after 2 minutes and the ST depression resolved after about 4 hours. On January 7, 2005, we performed a deep breathing test to analyze the effects of movements of the thoracic wall and intrathoracic structures on the ECG. In this test, deep inspiration induced ST depression reaching 0.5 mV in leads V₁ to V₃; this resolved on switching to deep expiration. ECG changes together with chest computed tomography images supported the concept that the ST-T abnormalities were induced by cardiac compression caused by expansion of the gastric tube between the sternum and heart. We have reviewed 7 other similar reported cases.

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