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The lipid-lowering and anti-atherosclerotic effects of atorvastatin (10 mg/day) were investigated by measuring changes in the levels of oxidized low-density lipoprotein (LDL), serum lipids (total cholesterol [TC], LDL-cholesterol [LDL-C] and triglycerides [TG]), and in the protein adiponectin. This was undertaken in 22 patients with ischaemic heart disease and serum LDL-C levels > 100 mg/dl. After 3 months of therapy, atorvastatin significantly decreased serum lipids, oxidized LDL was reduced from 457.0 +/- 148.6 to 286.9 +/- 88.5 nmol/l, and adiponectin increased from 9.7 +/- 7.4 to 13.9 +/- 9.98 microg/ml. No significant correlation was observed between adiponectin and LDL-C, TG and high-density lipoprotein cholesterol. Atorvastatin therapy was not associated with side-effects, such as myalgia and gastrointestinal disorders, and did not give abnormal laboratory test results. It is concluded that atorvastatin decreases serum lipid and oxidized LDL levels, and increases adiponectin levels in patients with ischaemic heart disease.

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Cardiac involvement is an important prognostic factor in sarcoidosis, but reliable indicators of mortality risk in cardiac sarcoidosis are unstudied in a large number of patients. To determine the significant predictors of mortality and to assess the efficacy of corticosteroids, we analyzed clinical findings, treatment, and prognosis in 95 Japanese patients with cardiac sarcoidosis. Twenty of these 95 patients had cardiac sarcoidosis proven by autopsy; none of these patients had received corticosteroids. We assessed 12 clinical variables as possible predictors of mortality by Cox proportional hazards model in 75 steroid-treated patients. During the mean follow-up of 68 months, 29 patients (73%) died of congestive heart failure and 11 (27%) experienced sudden death. Kaplan-Meier survival curves showed 5-year survival rates of 75% in the steroid-treated patients and of 89% in patients with a left ventricular ejection fraction > or = 50%, whereas there was only 10% 5-year survival rate in autopsy subjects. There was no significant difference in survival curves of patients treated with a high initial dose (> 30 mg) and a low initial dose (> or = 30 mg) of prednisone. Multivariate analysis identified New York Heart Association functional class (hazard ratio 7.72 per class I increase, p = 0.0008), left ventricular end-diastolic diameter (hazard ratio 2.60/10 mm increase, p = 0.02), and sustained ventricular tachycardia (hazard ratio 7.20, p = 0.03) as independent predictors of mortality. In conclusion, the severity of heart failure was one of the most significant independent predictors of mortality for cardiac sarcoidosis. Starting corticosteroids before the occurrence of systolic dysfunction resulted in an excellent clinical outcome. A high initial dose of prednisone may not be essential for treatment of cardiac sarcoidosis.

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The present study was designed to determine whether the wall thickening seen in acute myocarditis is caused by interstitial edema. The study group comprised 25 patients (idiopathic myocarditis, 17; eosinophilic myocarditis, 8) in whom acute myocarditis was diagnosed histologically and who underwent echocardiography and endomyocardial biopsy during both the acute and convalescent phases. The following echocardiographic parameters were measured: interventricular septum and left ventricular posterior wall thickness, left ventricular end-diastolic dimension, and left ventricular ejection fraction. Based on the myocardial biopsy specimens, the degree of interstitial edema was classified into 3 grades [(-), 1(+), 2(+)] and the transverse diameter of cardiac myocytes was measured using light microscopy. The thickness of both the interventricular septum and left ventricular wall decreased from 14.3+/-3.7 mm and 13.3+/-2.4 mm in the acute phase to 9.7+/-1.7 mm (p<0.001) and 10.2+/-1.7 mm (p<0.0001), respectively, in the convalescent phase. Edema was present in 22 patients (88.0%) in the acute phase, but in the convalescent phase, edema was present in only 7 patients (28.0%), indicating a significant reduction in the degree of edema (p<0.0001). Cardiac myocyte diameter did not differ significantly between the acute (13.6+/-1.1 microm) and convalescent (13.8+/-1.8 microm) phases.

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The pathogenesis of unstable angina pectoris (UAP) following percutaneous transluminal coronary angioplasty (PTCA) or directional coronary atherectomy (DCA) has not been adequately investigated, so the present study aimed to determine whether thrombi are present in restenotic lesions. The study group comprised 14 patients (16 arterial branches) with angina pectoris in whom either PTCA or DCA was performed and who had developed UAP associated with restenosis, and who then underwent DCA of the restenosed lesion (R-UAP group). The control groups comprised individuals with UAP undergoing DCA with no prior history of PTCA or DCA (P-UAP group; n=29, 29 branches), patients with acute myocardial infarction (AMI group; n=34, 34 branches), and patients with stable angina pectoris (SAP group; n=31, 33 branches). The presence of thrombi was determined by light microscopy of histologic specimens. Thrombus was present in only 1 of the 16 (6.3%) branches in the R-UAP group. 21 of the 29 (72.4%) branches in the P-UAP group, and in 25 of the 34 (73.5%) in the AMI group. In the SAP group, it was detected in only 2 of the 33 (7.1%) branches. The incidence of thrombus was significantly lower in the R-UAP group than in the P-UAP group. In conclusion, the role of thrombus is limited in causing post-interventional UAP at restenosed sites.

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A new cationic monoazaporphyrin, zinc 2-aza-8,12,13,17-tetraethyl-2,3,7,18-tetramethylporphyrinium iodide 3 was synthesized. Photodynamic activity of 3 in degradation of 2',3'-isopropylideneguanosine 4 was compared with 2-aza-8,12,13,17-tetraethyl-3,7,18-trimethylporphyrin 1, zinc 2-aza-8,12,13,17-tetraethyl-3,7,18-trimethylporphyrin 2, and hematoporphyrin 5. The quarternary ammonium 3 showed a remarkable increase of photodynamic activity compared with 5, although no appreciable difference in the activity was observed between 1 and 5.

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In patients with primary atrioventricular (AV) conduction disturbances, lesions are commonly believed to be limited to the conduction system. In the present study, myocardial lesions were analyzed histologically in patients with AV conduction disturbances to determine the presence of myocarditis. We studied 50 patients with second or third degree AV block in whom the cause was not clear (AVB group). Endomyocardial biopsy was performed from the right ventricle and examined by light microscopy. Tissue specimens also were obtained from 12 normal hearts at autopsy as a control group (N group). The diagnosis of myocarditis was based on the Dallas criteria. The myocyte transverse diameter was 15.4+/-4.1 microm in the AVB group and 11.7+/-3.1 microm in the N group (P<0.01). The fibrosis area ratio also was significantly higher in the AVB group than in the N group (10.1+/-6.7% vs 5.1+/-2.0%). The mean number of lymphocytes per 400-fold magnified field was significantly greater in the AVB group than in the N group (1.9+/-1.6 vs 1.3+/-0.4). In addition, disorganization of the cardiac myocytes was noted in 8 patients in the AVB group (16%), myocyte disarrangement in 39 patients (78%), myocytolysis in 23 patients (46%), and nuclear deformity in 21 patients (42%). Myocarditis was diagnosed in 3 of the 50 patients (6%). The present study demonstrates that myocardial lesions can be detected in a large proportion of patients with AV conduction disturbances. Furthermore, myocarditis is present in 6% of the cases.

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In this report, we describe 5 patients with cholesterol atheroembolic renal failure. In 3 of the 5 patients, combined therapy with corticosteroids and plasma exchange was performed. These 3 patients survived, with 2 showing an improvement in renal function. The 2 remaining patients died of multifactorial causes. The literature on therapy for cholesterol atheroembolic renal failure is reviewed and the efficacy of combined therapy by use of corticosteroids and plasma exchange is evaluated.

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Heart failure rarely develops in the setting of hypertrophic cardiomyopathy (HCM). Because of this, cardiac muscle cell disorganization (CD), which is a histologic characteristic of HCM, is not believed to be responsible for the development of systolic dysfunction. The aim of the present study was to clarify whether CD can cause systolic dysfunction and ventricular dilation in patients with HCM. Sixteen hearts from patients with HCM obtained at autopsy were divided into two groups: group A (n = 11), without biventricular dilation, and group B (n = 5), with dilation. Specimens consisting of transverse and longitudinal tissue sections of the ventricles were prepared, and the extent of CD and interstitial fibrosis was quantified, using light microscopy. None of the patients in group A had had chronic congestive heart failure, while all of the patients in group B had died of congestive heart failure. In group B, CD was not limited to the interventricular septum. Rather, diffuse CD was observed in both ventricular free walls. The extent of CD was significantly greater in group B than in group A, while the degree of interstitial fibrosis was similar in the two groups (13.6% in group A vs 14.6% in group B). These results suggest that CD may be responsible for systolic dysfunction and ventricular dilation.

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BACKGROUND: It has yet to be determined whether withdrawing beta-blocker therapy from patients with dilated cardiomyopathy (DCM) is safe. METHODS: The influence of tapering and then stopping metoprolol was clarified in 13 patients with DCM who had been receiving this agent for >/=30 months. RESULTS: Seven of the 13 patients deteriorated, including 4 who died suddenly or of congestive heart failure during the 4-month period after metoprolol cessation. CONCLUSION: In patients with DCM in whom beta-blocker therapy is effective, withdrawal of these agents may lead to death. We conclude that beta-blockers should not be stopped in this patient group.

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Many studies have previously confirmed high TNFalpha (tumor necrosis factor-alpha) production in sarcoidosis, and have shown that TNFalpha plays an important role in granuloma formation. We investigated TNFA and TNFB (lymphotoxin-alpha) gene polymorphisms in 26 cardiac sarcoidosis patients of Japanese origin. These studies revealed a significant increase in the more uncommon TNFA2 allele in the patient group, suggesting that the TNFA gene controls the genetic susceptibility to cardiac sarcoidosis.

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BACKGROUND: An early diagnosis of cardiac sarcoidosis is important, particularly when considering the need for administering corticosteroid therapy. However, no reports are available on the success rate of diagnosis on the basis of biopsy findings in patients with cardiac sarcoidosis. This study investigated the diagnostic success rate of histologic evaluation of endomyocardial biopsy specimens in patients with this disease. METHODS AND RESULTS: Right ventricular endomyocardial biopsy was performed in 26 patients in whom cardiac sarcoidosis was strongly suspected according to the Diagnostic Criteria of Sarcoidosis, plus abnormalities on the electrocardiogram, cardiac radionuclide images, or in left ventricular wall motion. A mean of 4.0 sites were sampled per patient. In each case we determined whether a definitive diagnosis of cardiac sarcoidosis could be made histologically. Noncaseating granulomas were found in only 5 (19.2%) of the 26 cases, thus permitting a histologic diagnosis of cardiac sarcoidosis. A histologic diagnosis was made in 4 (36.4%) of 11 patients who exhibited a dilated cardiomyopathy-like clinical picture, in contrast to only 1 (6.7%) of 15 patients in whom conduction disturbances were the major clinical feature and whose left ventricular ejection fraction was within normal limits. CONCLUSIONS: The diagnostic rate achieved with biopsy in cardiac sarcoidosis is low; the patients with sarcoidosis and evidence of significant cardiac involvement should be treated for cardiac sarcoidosis despite negative myocardial biopsies for this disease.

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Percutaneous cardiopulmonary support was used in 9 patients with fulminant myocarditis and cardiogenic shock. Although 2 of the patients died, 7 improved and were able to resume social activities. Percutaneous cardiopulmonary support should be administered routinely to patients with fulminant myocarditis developing into cardiogenic shock.

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In the present study, clinical findings of 15 patients with cardiac sarcoidosis presenting as dilated cardiomyopathy were compared with those of 30 consecutive patients with idiopathic dilated cardiomyopathy. The sarcoidosis patients had different clinical features, including female predominance, a high incidence of grave conduction disturbance and abnormal wall thickness, uneven wall motion abnormalities, and perfusion defects preferentially affecting the anteroseptal and apical regions, and poor prognosis compared with those with idiopathic dilated cardiomyopathy.

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A national survey of endomyocardial biopsy procedures was conducted in Japan. Questionnaires were mailed to 852 institutions and statistical analysis of the 213 completed questionnaires (25.0% of the total) was performed. Cardiac biopsies were being performed at 134 of these institutions (62.9%), representing a 5.5-fold increase over 1980. A total of 19,964 cardiac biopsies have been performed in Japan. Specimens were obtained from the right ventricle at 113 institutions, and from the left ventricle at 76 centers. The Konno-Sakakibara bioptome was used at 32 institutions, whereas the long sheath method was used at 98 institutions. Sixty of the institutions (44.8%) had encountered ventricular wall perforation. The perforation rate of the two ventricles combined was 0.7% (147 of 19,964 cases), with a mortality rate of 0.05% (10 of 19,964 cases). Endomyocardial biopsy has become widespread in Japan, and its safety was ascertained by this national survey.

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In Japan the majority of sarcoidosis-related deaths are due to cardiac sarcoidosis. One of the most common electrocardiographic abnormalities in patients with this disease is atrioventricular block. This study surveyed the incidence of cardiac sarcoidosis in Japanese patients (40 men and 49 women; mean age, 69.1 years) with high-degree atrioventricular block who were admitted to the hospital to receive a permanent pacemaker. We excluded cases in which sarcoidosis had been diagnosed from the involvement of other organs. Patients with the characteristic signs of sarcoidosis underwent echocardiography, radionuclide imaging, and biopsy. Ten cases (11.2%) of cardiac sarcoidosis were diagnosed, most frequently in women aged 40 to 69 years (8 of 25, 32%). Thus the possibility of cardiac sarcoidosis should be carefully considered in middle-aged or elderly Japanese women who show high-degree atrioventricular block.

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In studies of all the layers of autopsied hearts from patients with chronic myocarditis, local clusters of lymphocytes are frequently noted, in contrast with hearts obtained from patients with acute myocarditis. Myocardial biopsy specimens, however are no larger than about 2mm x 3mm. With this in mind, the present study was undertaken to determine whether chronic myocarditis can be diagnosed by endomyocardial biopsy. Specimens were obtained from seven patients in whom chronic myocarditis was confirmed by the clinical course and by autopsy findings. In H&E stained specimens, sites corresponding to the biopsy sites in both ventricles (right ventricular free wall, right ventricular side of the ventricular septum, left ventricular lateral wall) were selected at random (five sites each from the right and left ventricles in each patient) and examined under a light microscope. A mean of 5 or more lymphocytes per visual field (by light microscopy at 400-fold magnification), a proposed quantitative diagnostic criterion of myocarditis, was noted in the right ventricle in three patients (5 lymphocytes in two patients and 6 in one patient) and in the left ventricle in one patient (5 lymphocytes). Also, when the presence of lymphocyte clusters, considered to be a characteristic feature of chronic myocarditis, was determined, clusters of 20 or more lymphocytes per visual field were found in the same patients as those mentioned above, namely, in three patients (42.8%) in the right ventricle, as mentioned above, and in one patient (14.3%) in the left ventricle. At the sites of these lymphocyte clusters. findings such as degenerative changes of the myocardial cells and interstitial fibrosis were also associated, making possible a diagnosis of myocarditis. Therefore, in chronic myocarditis, even if five specimens are obtained by right ventricular biopsy, in approximately one half of patients the diagnosis of chronic myocarditis will be missed because of sampling errors.

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We report a case of diabetic ketoacidosis (DKA) complicated by acute myocarditis, which was confirmed by cardiac biopsy. A 26-year-old man was hospitalized with severe DKA. On admission, nonspecific ST-T change was noted on the electrocardiogram (ECG). The patient's levels of creatine phosphokinase (CPK) and glutamic oxaloacetic transaminase were slightly elevated, but he did not complain of chest discomfort or symptoms of heart disease. On the first day after admission, ST-T elevation was noted on ECG during treatment of DKA. By cardiac angiography and cardiac biopsy, coronary heart disease was ruled out and postmyocarditic change was histologically confirmed. An episode of upper respiratory viral infection before the onset of acute diabetes suggested that the patient suffered from viral-induced myocarditis and consequent development of IDDM. This possibility was confirmed by the clinical course of ECG change, with elevated CPK and lactate dehydrogenase and a slightly elevated antibody titer for echovirus.

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