Analysis of heart rate variability (HRV) can identify patients at risk of sudden cardiac death after myocardial infarction. The present study examined the effect of 2 weeks of supervised aerobic exercise training on the recovery of the autonomic nervous activity, exercise capacity, and cardiac output (CO) after coronary artery bypass grafting (CABG). Twenty-eight patients were randomly divided into the training group or the control group and performed exercise tests at 1 week, 3 weeks, 3 months, 6 months and 1 year after CABG. The HRV was measured, and the high-frequency component of HRV was used as an index of parasympathetic nerve activity (PNA); the plasma norepinephrine concentration (NE) was used as an index of sympathetic nervous activity. Cardiac output was also measured. In the training group, peak VO₂, peak CO and PNA during exercise had improved at 3 weeks, but there was no improvement in these indices in the control group. NE decreased 1 week after CABG in both groups. These results indicate that physical training soon after CABG improves not only the exercise capacity, but also PNA.

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Mitral regurgitation is a significant complication of end-stage cardiomyopathy, and its existence predicts poor survival. In general, it is thought that mitral valve replacement (MVR) alone is ineffective; however, there are few detailed reports of the clinical course of patients who have undergone MVR. Five patients with mitral regurgitation whose preoperative left ventricular end-systolic volume index was more than 100ml/m² were studied. Although their prognosis late after MVR became poor, none of them died within 30 days of the operation. Postoperative cardiac catheterization was performed 6.3±1.1 months after surgery; the end-diastolic volume had reduced (before: 193±26ml/m²; after: 166±34ml/m², p<0.05), but the end-systolic volume had not (before: 110±7ml/m²; after: 112±32ml/m²). The end-systolic wall stress was substantially elevated preoperatively (238±29kdyne/cm²) and tended to increase after surgery (295±96kdyne/cm²). All the patients were able to return to work at some stage postoperatively (their New York Heart Association functional class improved to I or II), but 3 of the 5 patients died suddenly of heart failure at 3.3±1.6 years after surgery and the New York Heart Association functional class of the others worsened to III again. Mitral valve surgery, including MVR, can manage severe end-stage heart disease with mitral regurgitation.

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Chlamydia pneumoniae, a common human respiratory pathogen, has been implicated in the pathogenesis of coronary heart diseases (CHD) in several seroepidemiological studies. The present case-control study investigated the relation between serologic evidence of C. pneumoniae infection and CHD in a Japanese population. Two groups of cases were enrolled: 26 patients with acute myocardial infarction (AMI) and 46 patients with effort angina pectoris (e-AP). Their data were compared with 58 age-matched healthy controls and also compared with 53 patients with vasospastic angina (VSA) as pathological control subjects. Anti-C. pneumoniae specific IgA and IgG antibody titers were measured by enzyme-linked immunosorbent assay (ELISA). The mean indices of IgG-type antibody in AMI and e-AP were not significantly different from those in either the normal controls or VSA group. On the other hand, the mean indices of IgA-type antibody in AMI were significantly higher than in the normal controls (1.39±0.83 in AMI vs 0.84±0.58 in controls, p<0.001) and VSA (1.39±0.83 in AMI vs 1.05±0.61 in VSA, p<0.05) group. However, the differences in the IgA titers in the e-AP group compared with the normal controls did not reach a significant level. The odds ratio associated with the seropositivity of IgA for AMI against the normal controls was 3.89 (95% confidence interval (CI): 1.16-13.10) and that against VSA was 6.90 (95% CI: 1.73-27.52) after adjustment for risk factors for CHD and/or age, sex and smoking status. In 6 patients the elevated IgA titers were sustained even at 3 months after the episode of AMI. These results suggest that seropositivity for IgA-type antibody against C. pneumoniae may be a significant risk factor for the development of AMI. The possible mechanisms include chronic inflammation in the coronary artery due to persistent C. pneumoniae infection.

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Although various risk factors have been implicated in the progression of coronary artery disease (CAD), coronary risk factors specifically related to the long-term prognosis for high-risk CAD have not been determined. The study enrolled 311 consecutive Japanese patients with CAD who underwent diagnostic coronary arteriography and divided them into 2 groups: (i) 135 high-risk patients with either impaired left ventricular function (ejection fraction<50%) or multivessel disease and (ii) 176 low-risk patients with normal left ventricular function and 0-or 1-vessel disease. The prevalence of risk factors including age, gender, smoking, hypertension, diabetes mellitus (DM), obesity and lipid variables were compared between the 2 groups. The prevalence of DM, a serum high-density lipoprotein (HDL)-cholesterol level below 35mg/dl and a serum lipoprotein (Lp) (a) level above 25mg/dl was significantly higher in the high-risk group as compared with the low-risk group. Multiple logistic regression analysis demonstrated that DM (odds ratio (OR): 1.72, 95% confidence intervals (CI): 1.02-2.92, p<0.05), a low HDL-cholesterol level (OR: 2.49, 95% CI: 1.49-4.17, p<0.001) and a high Lp(a) level (OR: 1.68, 95% CI: 1, 02-2.76, p<0.05) were all independent risk factors for high-risk CAD. However, if the patients with 0-vessel disease were excluded from the low-risk group, a low HDL-cholesterol level was found to be the only independent predictor for high-risk CAD (OR: 2.07, 95% CI: 1.15-3.70, p<0.05). Among both men and smokers in this population, a higher Lp(a) level was found to be a significant predictor for high-risk CAD. A low serum level of HDL-cholesterol, a high serum level of Lp(a) and DM were significant predictors of high-risk in patients with CAD. Among patients with a significant coronary stenosis or left ventricular dysfunction, a low serum level of HDL-cholesterol was the only significant predictor for high-risk CAD.

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Monocyte chemoattractant protein-1 (MCP-1) plays an important role in the progression of atherosclerosis in coronary arteries. To examine whether or not plasma antigen levels of MCP-1 are related to restenosis after percutaneous transluminal coronary angioplasty (PTCA), the plasma antigen levels of MCP-1 were measured by enzyme-linked immunosorbent assay (pg/ml) before, 24 and 48h, and 3 months after elective PTCA for stable exertional angina performed between June 1997 and March 1998. Restenosis was defined as recurrence of stenosis greater than 50% of the diameter in the dilated segment at 3-month follow-up angiography. There were no differences in plasma MCP-1 antigen levels before and at 24h after PTCA between restenosis (R; n=27) and norestenosis (N; n=43) groups (R vs N: 633±35 vs 589±34, and 669±41 vs 575±36pg/ml before and at 24h after PTCA, respectively), but plasma MCP-1 antigen levels were higher at 48h and 3 months after PTCA in the R than in N group (R vs N: 678±41 vs 558±35, and 735±35 vs 571±32pg/ml at 48h and 3 months after PTCA, respectively). These data suggest that the MCP-1 production and macrophage accumulation in the balloon-injured site is partially associated with restenosis after PTCA.

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The present study investigated the mechanism of ventricular arrhythmias showing left bundle branch block (LBBB) pattern with an inferior axis. The effects of 3 drugs, adenosine triphosphate (ATP), nicorandil and verapamil, were evaluated in 17 patients. ATP suppressed the arrhythmias in 14 patients and nicorandil suppressed them in 8 of those 14. Verapamil suppressed 5 of the 6 ATP-nicorandil-sensitive arrhythmias. Four patients with ATP- or nicorandil-sensitive arrhythmias were not sensitive to verapamil. On the other hand, 3 of the ATP-insensitive arrhythmias were sensitive to neither nicorandil nor verapamil. The QT intervals and QTc were shortened by nicorandil in 5 of the 6 patients who were sensitive to all 3 drugs. One mechanism of suppression by nicorandil could be related to less Ca⁺⁺ entering the myocardium, which would decrease the duration of the action potential as indicated by the shortened QT intervals. The results suggest that the mechanism of some ventricular arrhythmias is related to triggered activity. Arrhythmias that are sensitive to ATP or nicorandil, but not to verapamil, may be caused by abnormal automaticity. On the other hand, arrhythmias that are insensitive to all 3 drugs might be related to reentry. The features of ventricular arrhythmias with LBBB pattern and inferior axis differ and therefore the causative mechanisms are not the same.

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The study examined the association between aortic wall volume (AWV) detected by enhanced computed tomography and coronary artery atherosclerosis observed on angiography. In 180 cases, AWV was measured as the total wall volume of a 7-cm portion of the descending thoracic aorta distal from the tracheal bifurcation. Coronary artery atherosclerosis was angiographically quantified by both Gensini score, in terms of the severity of coronary artery stenosis, and Extent score, in terms of the severity of coronary artery involvement. Mean AWV values between the patients with significant coronary artery stenosis and those without significant stenosis were 9.83±4.04cm³ and 8.09±2.39cm³, respectively (p<0.001). AWV was a significantly independent variable for significant coronary artery disease (p=0.0097) and an Extent score ≥60 (p=0.0092). Calcification of AWV, however, was not associated with coronary atherosclerosis. The quantification of aortic atherosclerosis was useful for diagnosing coronary artery disease.

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Blood viscosity (η_B) is low in athletes, but the effect of exercise training on η_B during endurance exercise at an anaerobic threshold (AT) intensity in non-athletes is not well known, although it is known that exercise training sometimes induces the hyperviscosity syndrome. Fourteen subjects were recruited and divided into 2 groups: those who trained at an AT intensity for 30min/day, 3 times weekly for 1 year (Group T, n=8), and sedentary subjects (Group C, n=6). The test protocol consisted of a single 30-min treadmill exercise at each individual’s AT intensity, which was determined in advance. The η_B, plasma viscosity (η_P), and hematocrit were measured just before and at the end of the treadmill exercise. The subjects were not allowed to drink any water before exercise. In the Group C subjects, the hematocrit and η_P increased significantly and the η_B tended to increase. However, in the Group T subjects, the hematocrit and η_P did not increase and the η_B decreased significantly. These data indicate that long-term exercise training attenuates the increase in blood viscosity during exercise.

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Heart rate (HR) response during exercise in patients with ischemic heart disease was evaluated, and the appropriateness of Karvonen’s method for determining rehabilitation exercise target HR was investigated. The study group comprised 24 patients with acute myocardial infarction (AMI) and 37 patients who had undergone coronary artery bypass grafting (CABG). Cardiopulmonary exercise testing (CPX) was performed with a cycle ergometer and changes in HR (ΔHR)/changes in work rate (ΔWR) and interval changes of the coefficient of Karvonen’s formula were evaluated. In the AMI group and the CABG group, ΔHR/ΔWR were significantly lower than those of age-matched control subjects (p<0.01). Karvonen’s coefficients ranged from 0.37 to 0.54 when calculated from actual peak HR and 0.21 to 0.32 calculated from the predicted peak HR. An impaired HR response was found in patients with AMI and those who had had CABG up to 6 months previously. Because the Karvonen’s coefficient values, which ranged from 0.6 to 0.8, were elevated for these patients, and considering the data from the CPX, increased exercise is recommended for such cases.

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The present study examined the relation of plasma oxidized low-density lipoprotein (LDL) levels to plasma LDL cholesterol levels and the impairment of endothelium-dependent coronary vasorelaxation in patients with coronary artery disease (CAD). In the first study, the relationship between plasma levels of oxidized LDL and LDL cholesterol were investigated in 88 patients with CAD. In the second study, the changes in the diameter of the left anterior descending (LAD) and the left circumflex (LCX) coronary arteries were measured after intracoronary administration of acetylcholine (15μg) and isosorbide dinitrate (2.5 mg) in 15 patients with CAD. Plasma oxidized LDL levels were determined with a sandwich enzyme-linked immunosorbent assay. Plasma oxidized LDL levels did not correlate with plasma LDL cholesterol levels (r=-0.03, p=NS). The % diameter changes (mean±SEM) in the LAD and LCX after intracoronary acetylcholine were -8.3±3.5% and -10±4.2%, respectively. The % diameter changes in the LAD and LCX after intracoronary isosorbide dinitrate were 23±4.8% and 23±5.1%, respectively. The % diameter changes in the LAD and LCX inversely correlated with plasma oxidized LDL levels after intracoronary acetylcholine (LAD: r=-0.55, p=0.03; LCX: r=-0.59, p=0.02), but were not after intracoronary isosorbide dinitrate. Plasma LDL cholesterol, triglyceride, and high-density lipoprotein cholesterol levels did not correlate with the coronary vasoreaction to acetylcholine. In conclusion, plasma oxidized LDL levels do not correlate with plasma LDL-cholesterol levels and are related to impairment of endothelium-dependent coronary vasodilation in patients with CAD.

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Volume overload results in eccentric cardiac hypertrophy, but it is still unknown how this mechanical overload modulates the inotropic response to exogenous Ca²⁺ or adenylyl cyclase stimulation. Inotropic responsiveness in vivo and the levels of gene expression of Ca²⁺ signaling proteins were studied in rabbit hearts hypertrophied as a result of volume overload at 4 and 12 weeks after arteriovenous shunt formation. In sham-operated control rabbits, left ventricular (LV)+dP/dt was augmented in response to graded doses of CaCl₂. Dose-related changes of LV+dP/dt to CaCl₂ were attenuated significantly in shunt rabbits with volume overload. Forskolin dose-dependently augmented LV+dP/dt in sham rabbits, which was also attenuated significantly in rabbits with volume overload. The mRNA levels of dihydropyridine receptor, Na⁺/Ca²⁺ exchanger, sarcoplasmic reticulum Ca²⁺-ATPase, and ryanodine receptor decreased significantly at 4 and 12 weeks in the volume-overload rabbits compared with the sham rabbits, but the mRNA levels of phospholamban and calsequestrin remained unchanged. Chronic volume overload alters contractile responsiveness to Ca²⁺ or adenylyl cyclase stimulation, and downregulation of steady state mRNA levels of Ca²⁺ signaling proteins might be, at least in part, related to this pathologic process.

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Diadenosine tetraphosphate (AP₄A) can be released from activated platelets and the present study examined its effect on coronary arterial microvessels. The role of purinoceptors in the coronary microcirculation in vivo was also investigated. In open chest dogs, coronary arterioles were observed using a microscope with a floating objective. In Protocol 1, AP₄A (1, 10, 100 and 1, 000μmol/L) was superfused onto the heart surface before and during the superfusion of 10μmol/L of 8-phenyltheophylline (8-PT), a P₁ purinoceptor blocker. In Protocol 2, AP₄A (0.1, 1, 10, and 100 nmol·kg^-1·min^-1) was infused into the left anterior descending coronary artery before and during the superfusion of 10μmol/L of 8-PT. In addition to 8-PT, 30μmol/L of pyridoxalphosphate-6-azophenyl 2′, 4′-disulphonic acid (PPADS), a P_2X purinoceptor blocker in Protocol 3, or 300μmol/L of N^ω-nitro-L-arginine (LNNA) in Protocol 4, was continuously superfused, and 4 doses of AP₄A were cumulatively superfused as in Protocol 1. In Protocol 5, 10μmol/L of α, β-methylene ATP, an agonist of P_2X purinoceptors, was superfused for 60 min. Superfused AP₄A dilated arterioles in a dose-dependent manner. The magnitude of dilatation was greater in smaller arterioles (small vessel ≤150μm: 24.5±2.2% vs large vessel > 150μm: 10.6±1.5% at a dose of 1, 000 μmol/L, p<0.001). On the other hand, intraluminally applied AP₄A also dilated arterioles, but no size dependency was shown. In the presence of 8-PT, vasodilatory responses to superfused and intraluminally applied AP₄A were attenuated and the lower doses of AP₄A constricted arterioles. This vasoconstrictor effect was not affected by PPADS. The vasodilatory effect of the higher doses of AP₄A was almost abolished in the presence of LNNA. α, β-methylene ATP had no effect on coronary microvascular diameters. AP₄A has bidirectional effects on coronary arterial microvessels: vasodilatory effects mediated by P₁ purinoceptors and NO, which might be mediated by P_2Y purinoceptors, and a vasoconstrictor effect, which is not mediated by P_2X purinoceptors.

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Quantitative information is needed on the directly depolarized area (DDA) induced by high-output energy during a precise mapping procedure to detect the origin of a tachycardia. In the present study, a DDA caused by high-output energy was quantitatively evaluated in the exposed canine heart. In 8 dogs, the right atrial and ventricular surfaces were exposed through a right thoracotomy and pacing with various outputs was delivered from the epicardial surface. A comb-shaped 16 polar electrode array and/or a 224 polar mat electrode array were used for recording the epicardial electrograms. The local activation time was measured at each electrode site, and the relationship of the distance between the electrode location from the pacing site and the local activation time was plotted and fitted to a primary regression line. The intercept of the regression line on the horizontal axis was defined as the radius of the ‘DDA’ and this was evaluated at each pacing output. The radius of the DDA was 0.6±0.1mm with a 2V and 3.8±0.2mm with a 10V output when it was evaluated in a direction perpendicular to the fiber orientation of the pectinate muscle, 0.8±0.1mm with a 2V and 4.1±0.3mm with a 10V output in a direction parallel to the pectinate muscle fiber orientation, and 0.9±0.3mm with a 2V and 3.6±0.5mm with a 10V output in the right ventricle. The DDA extended according to the increase in stimulation outputs at all sites, and there was no significant difference in the pacing site or the direction of the stimulation propagation. The DDA caused by high-output energy is a purely physical phenomenon that depends only on stimulation output and tissue resistance. The diameter of the DDA exceeded 4mm (ie, the size of a standard tip electrode for catheter ablation) when pacing was delivered with an output greater than 6V.

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After placing a stent in the main vessel of a bifurcation lesion, it is sometimes necessary to perform further balloon inflation in order to treat an ostial lesion in a side branch. The stent struts may prevent full balloon expansion at the ostium of a side branch, resulting in residual ostial stenosis. The degree of completeness of balloon inflation may vary significantly depending on the stent design and structure. A model of a bifurcation lesion with an angle of 45°was created from acrylic resin. The diameters of the main vessel and the side branch were both 3.5mm. Deployment of the Palmaz-Schatz stent (n=5), NIR stent (n=5) or Multi-Link stent (n=5) was performed in the main vessel with a 3.5-mm balloon catheter inflated to 12 atm. A 3.5-mm balloon catheter was then inflated to 12 atm through the stent struts of the main vessel and into the ostium of the side branch. The degree of completeness of balloon inflation (% balloon expansion) was calculated as (smallest diameter of balloon catheter/reference diameter of balloon catheter)×100%. The minimal lumen diameter (MLD) and cross-sectional area (CSA) at the ostium of the side branch created with the stent struts were also measured. Limited balloon expansion through the struts was observed with the Palmaz-Schatz stent and the NIR stent, but almost full balloon expansion was observed with the Multi-Link stent (% balloon expansion: Palmaz-Schatz stent 80%, NIR stent 60%, Multi-Link stent 94%, p<0.01). The MLD and CSA of the dilated struts, representing the ostium of the side branch, of the Palmaz-Schatz stent (2.2±0.1mm, 4.5±0.3mm²) and the NIR stent (1.8±0.1mm, 3.1±0.3mm²) were significantly smaller compared with those of the Multi-Link stent (3.0±0.2mm, 8.4±0.6mm²) (p<0.01). The struts of the Palmaz-Schatz stent and the NIR stent deployed in the main vessel of a bifurcation prevent full expansion of a balloon catheter inflated at the side branch ostium. In contrast, almost full balloon expansion through the struts of the Multi-Link stent is achieved.

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A 55-year-old man was referred because of congestive heart failure and atrial flutter. A 12-lead electrocardiogram (ECG) showed positive P waves in leads II, III, and aVF with a continuously undulating pattern that lacked an isoelectric baseline. Tachycardia was diagnosed as atypical atrial flutter based on classical criteria. An electrophysiological study and catheter ablation using an electroanatomical system revealed the mechanism of the tachycardia to be focal atrial tachycardia originating from the left atrial roof. This case indicates that focal atrial tachycardia may present as atypical atrial flutter on the surface ECG.

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A 62-year-old man with a history of surgical therapy for papillary thyroid carcinoma was admitted because of chest pain, dyspnea on effort, pretibial edema, and slight fever. An electrocardiogram showed ST segment elevation in the precordial leads and low voltage in the limb leads. A large solid mass was demonstrated in both ventricles, with pericardial effusion, by echocardiography, thoracic computed tomography scan, transesophageal echocardiography, and angiography. A punch biopsy of the tumor revealed metastasic papillary carcinoma. During radiation therapy, the patient suddenly died of ventricular fibrillation. At autopsy, the tumor occupied almost the entire right ventricular cavity, expanding toward the main trunk of the pulmonary artery with a mobile peduncle and it had infiltrated the left ventricular wall through the interventricular septum. Microscopic examination confirmed metastatic papillary thyroid carcinoma. Only 2 other cases of cardiac metastases of papillary thyroid carcinoma have been reported and this case is the first report of metastases in both ventricles with a mobile right ventricular pedunculated tumor.

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Cardiogenic shock developed in a 72-year-old Japanese woman during combination therapy with verapamil and atenolol for recurrent supraventricular arrhythmia. She had coronary atherosclerosis, liver cirrhosis and brady-cardia-tachycardia syndrome. Despite of the high-dose catecholamines and counterpulsation, she progressively deteriorated. Bolus administration of intravenous calcium chloride(CaCl₂) immediately resolved her hemodynamic collapse.

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Although the long-term survival of patients suffering from coronary spasm is usually excellent, serious complications can develop, such as disabling pain, myocardial infarction, ventricular tachyarrhythmias, atrioventricular block and sudden cardiac death. A 40-year-old man who had intractable chest pain from coronary artery spasm suffered ventricular fibrillation and an acute anterior myocardial infarction upon first admission. The patient underwent a coronary angiogram. which revealed a spontaneous focal spasm at the proximal left anterior descending coronary artery(LAD). He was treated by the combination of nitrate and calcium channel blocker, but continued to complain of severe chest pain despite intensive medical therapy and he had to be treated in the emergency room 5 times during an 8-month follow-up period. An ergonovine coronary angiogram was performed and an intracoronary ultrasound examination, which revealed a focal spasm at the same site of the proximal LAD with a small amount of localized eccentric atheromatous plaque. A coronary artery stent was placed in the proximal LAD and his symptoms resolved. A follow-up coronary angiogram was performed 3 years after stenting and the stent remained patent without any in-stent restenosis or spasm.

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Three-dimensional imaging using electron-beam computed tomography(EBCT) has been used to assess static anatomical information in heart disease. With volume rendering, differences in objects can be distinguished through selection of the shape of opacity and color curves for CT values. If there is a difference between the CT values for arterial and venous blood, differences in opacity and color between them can be set. In a newborn baby with a left to right cardiac shunt across the ventricular septal defect(VSD), EBCT could depict arterial blood crossing the VSD into the right ventricle.

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