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The patient was a 63-year-old man with drug-resistant atrial fibrillation who developed coronary spasm during cryoballoon ablation (CBA). CBA was started from the left inferior pulmonary vein. ST elevations in II, III, and aVf, with reciprocal ST depressions in V2-5, occurred in association with chest pain just after balloon rewarming and deflation, and the patient's blood pressure fell to 50 mmHg. Coronary angiography revealed 90% diffuse stenosis from the orifice of segment 1 to segment 4 in the right coronary artery. The stenosis and ST elevations improved after the intracoronary injection of nitroglycerine. Using continuous peripheral intravenous coronary vasodilation, we electrically isolated the other pulmonary veins with CBA without incident.

Left ventricular (LV) systolic dysfunction independently predicts mortality in patients with ST-elevation myocardial infarction (STEMI). However, deterioration of LV diastolic function in STEMI patients has not been well studied. Furthermore, long-term follow-up in patients with LV diastolic

Tako-tsubo cardiomyopathy, also called transient left ventricular apical ballooning, is a clinical entity first described in Japan. This syndrome is triggered by emotional or physical stress and mimics an acute coronary syndrome, although the coronary arteries are essentially normal. Recently, several reports have described variant forms of tako-tsubo cardiomyopathy, such as inverted tako-tsubo and mid-ventricular ballooning cardiomyopathy. We describe a case herein of an 87-year-old woman who presented a variant form of tako-tsubo cardiomyopathy complicated by syncope. Our findings may contribute to an elucidation of the mechanism underlying tako-tsubo cardiomyopathy.

We report a rare case of Holter monitoring documenting the onset of tako-tsubo cardiomyopathy in a 70-year-old woman. The patient experienced sudden chest discomfort after a quarrel in her hospital stay. Follow-up echocardiography on day 22 revealed a marked improvement of left ventricular apical akinesis. Angiographic examination at discharge showed neither coronary artery disease nor left ventricular asynergy.

A 53-year-old-male developed atrioventricular block in January 2001. A chest X-ray and laboratory tests, including serum angiotensin converting enzyme, were normal. The patient underwent permanent pacemaker implantation and attended for semiannual follow-up after discharge since the etiology of advanced atrioventricular block remains unknown. One year later, the patient was diagnosed with uveitis related to sarcoidosis. No clinical finding specific to cardiac sarcoidosis was notable at that time. Four years after onset, the patient developed congestive heart failure. An echocardiogram revealed diffuse LV hypokinesis, but no asymmetric interventricular septal thinning. Laboratory tests showed normal angiotensin converting enzyme. Noncaseating granuloma was not confirmed by transbronchial biopsy. Despite normal myocardial uptake of gallium-67, uptake of 18 F-Fluorodeoxyglucose increased in the myocardium. Nevertheless, clinical manifestations did not match the criteria for cardiac sarcoidosis. Prednisolone was administered daily. Two months after tapering dosage, the patient developed multiple organ failure and died. Post mortem histological findings were consistent with cardiac sarcoidosis. We experienced great difficulty in detecting cardiac involvement in the early stage of sarcoidosis. A specific method with greater sensitivity is required to diagnose cardiac involvement in the early stages of sarcoidosis.

This study compares serum markers of myocardial damage incurred during radiofrequency catheter ablation (RFCA).Blood was sampled from 34 patients with atrial flutter (n = 16), atrioventricular nodal reentrant tachycardia (AVNRT; n = 13), and Wolff-Parkinson-White syndrome (WPW; n = 5) to measure creatine kinase MB subfraction (CK-MB), human heart-type fatty acid protein (h-FABP), and cardiac troponin T (cTnT) values at baseline and after RFCA. The controls comprised 12 patients without significant elevation of all myocardial markers during electrophysiological study (EPS) without RFCA. h-FABP values did not elevate significantly, whereas CK-MB and cTnT demonstrated significant change after RFCA (P0.001). Neither peak h-FABP nor CK-MB correlated with following RFCA parameters: delivery duration, number of RFCA discharges, and cumulative RFCA energy. In contrast, correlations were significant between mean peak values of cTnT and these RFCA parameters (all P0.05). The sensitivity (71.6%) and specificity (35.6%) of h-FABP were inferior to those of cTnT (93.3% and 89.8%, respectively).h-FABP is an insensitive and less specific marker of myocardial damage in RFCA much along the lines of CK-MB and when compared with the proven accuracy of cTnT.

We experienced two cases of renal infarction with atrial fibrillation who presented with acute abdominal pain. On initial urinalysis, both patients showed no hematuria, but the plasma lactate dehydrogenase level was markedly elevated with little or no rise in plasma transaminases. Their diagnosis was confirmed by contrast-enhanced CT of the abdomen on the second and third days of the crisis. We immediately initiated anticoagulant therapy, resulting in successful prevention of new embolism. Contrast-enhanced CT should be considered if abdominal symptoms develop in patients with atrial fibrillation. Renal infarction could be diagnosed in the early course, even in cases with incomplete occlusion of the renal arteries and normal renal function. (Hypertens Res 2004; 27: 523-526)

Prognostic value of nonlinear heart rate dynamics in hemodialysis patients with coronary artery disease. Background Although altered nonlinear heart rate dynamics predicts death in patients with coronary artery disease (CAD), its prognostic value in chronic hemodialysis patients with CAD is unknown. Methods We analyzed 24-hour electrocardiogram for nonlinear heart rate dynamics and heart rate variability in a retrospective cohort of 81 chronic hemodialysis patients with CAD. Results During a follow-up period of 31 ± 20months, 19 cardiac and 8 noncardiac deaths were observed. Cox hazards model, including diabetes, left ventricular ejection fraction, and the number of diseased coronary arteries, revealed that abnormal α 2 (defined as both increase and decrease in α 2 because of its J curve relationship with cardiac mortality), decreased approximate entropy and decreased heart rate variability (triangular index and ultra-low frequency power) were significant and independent predictors of cardiac death. No significant and independent predictive power for noncardiac death was observed in either the heart rate dynamics or the heart rate variability measures. The predictive power of α 2 and approximate entropy was independent of that of triangular index and ultra-low frequency power. Combinations of two categories of measures improved the predictive accuracy; overall accuracy of approximate entropy + ultra-low frequency power for cardiac death was 87%. Conclusion Altered nonlinear heart rate dynamics are independent predictors of cardiac death in chronic hemodialysis patients with CAD and their combinations with decreased heart rate variability provide clinically useful markers for risk stratification.

The purpose of this study was to investigate the clinical significance of the reverse redistribution (RR) phenomenon on technetium-99m (99mTc)-tetrofosmin myocardial single photon emission computed tomography (SPECT) performed at rest. Twenty-five patients underwent myocardial SPECT 3 weeks after the onset of acute myocardial infarction. Myocardial images were acquired at 40 min (early) and 4 h (delayed) after the injection of 740 MBq of 99mTc-tetrofosmin. The regional myocardial uptake of the tracer in 26 segments of the left ventricular (LV) wall was visually scored from 0 (no activity) to 3 (normal activity), and then the RR was defined as a decrease of more than 1 point in the activity score on the delayed image compared with that on the early image. Regions with an activity score of 3 on both the early and delayed images were defined as normal, and those with a score of 0 or 1 on the early image were considered to have a fixed defect. The regional myocardial 99mTc-tetrofosmin uptake and washout rate were also quantitatively assessed in each region. In addition, exercise stress electrocardiograph-gated SPECT with 99mTc-tetrofosmin was performed within 1 week of the rest study, and the percent count increase (%CI) during myocardial contraction in each corresponding region was studied. RR was observed in 18 of the 25 patients. The regional washout rate of 99mTc-tetrofosmin was significantly higher in the RR regions (45.0±3.8%) than in either the normal regions (36.4±4.1%, p

We report a rare case of an 83-year-old woman with tako-tsubo cardiomyopathy, who presented with variable forms of left ventricular dysfunction during her clinical course. The distribution regional wall-motion abnormalities of the left ventricle on echocardiography had changed from a mid-ventricular ballooning type to the apical ballooning type 3 days from the onset. We suggest that these findings may indicate a new or variant entity of tako-tsubo cardiomyopathy.

Tako-tsubo cardiomyopathy is a stress-related cardiomyopathy which occurs in postmenopausal women after severe emotional stress. Although no evidence supporting specific treatment with tako-tsubo cardiomyopathy has been established, the prognosis is considered favorable with normalization of wall motion abnormalities within weeks. In addition, recurrence of this syndrome seems to be rare. Now, we report a recurrent case of tako-tsubo cardiomyopathy complicated by cardiogenic shock after repeated emotional stress.

Tako-tsubo cardiomyopathy is a rare, stress-related cardiomyopathy that occurs in postmenopausal women after emotional or physiological stressors. The prognosis is favorable with normalization of wall motion abnormalities within weeks. We report a rare case of tako-tsubo cardiomyopathy complicated by a left thrombus. Coronary angiography showed normal coronary arteries, although the echocardiography demonstrated the ballooning of the apex with hyperkinesis of the base in addition to a left ventricular thrombus. It is thought that this thrombus may have been caused by left ventricular dyskinesis. After short-term anticoagulant therapy, echocardiography revealed complete resolution of the left ventricular thrombus.

In smooth muscle of the circumflex coronary artery of guinea-pig, acetylcholine (ACh, 10−6 M) produced an endothelium-dependent hyperpolarization consisting of two components. An initial component that occurs in the presence of ACh and a slow component that developed after ACh had been withdrawn. Each component of the hyperpolarization was accompanied by an increase in membrane conductance. Indomethacin (5×10−6 M) or diclofenac (10−6 M), both inhibitors of cyclooxygenase, abolished only the slow hyperpolarization. The initial hyperpolarization was not inhibited by diclofenac nor by nitroarginine, an inhibitor of nitric oxide synthase. Both components of the ACh-induced hyperpolarization were abolished in the presence of atropine (10−6 M) or high-K solution ([K+]0=29.4 mM). The interval between ACh-stimulation required to generate an initial hyperpolarization of reproducible amplitude was 20 min or greater, but it was reduced to less than 5 min after inhibiting cyclooxygenase activity. Conditioning stimulation of the artery with substance P (10−7 M) also caused a long duration (about 20 min) inhibition of the ACh-response. The amplitude of the hyperpolarization generated by Y-26763, a K+-channel opener, was reproducible within 10 min after withdrawal of ACh. Exogenously applied prostacyclin (PGI2) hyperpolarized the membrane and reduced membrane resistance in concentrations over 2.8×10−9M. At concentrations below threshold for hyperpolarization and when no alteration of membrane resistance occurred, PGI2 inhibited the initial component of the ACh-induced hyperpolarization. It is concluded that endothelial prostanoids, possibly PGI2, have an inhibitory action on the release of endothelium-derived hyperpolarizing factor. British Journal of Pharmacology (1999) 126, 1–10; doi:10.1038/sj.bjp.0702254

Aims The aim of this study was to evaluate the role of matrix metalloproteinases (MMPs) for the prediction of long-term maintenance of sinus rhythm (SR) after cardioversion in atrial fibrillation (AF). Methods and results The study comprised 102 patients with AF. Pharmacological cardioversion was attempted for a 4-week period with anti-arrhythmic drugs in all patients. Those who failed medication underwent electrical cardioversion. Blood samples for biomarkers and echocardiographic data were obtained at baseline. Thirty-four patients (33.3%) converted to SR by pharmacological ( n = 22) and electrical ( n = 12) cardioversion and maintained it (SR group). The remaining 68 patients were refractory to the AF (RAF) group including recurrence ( n = 22) and unsuccessful treatment ( n = 46) after electrical/pharmacological cardioversion. Refractory AF was significantly associated with the duration of AF, hypertension, left atrial diameter, brain natriuretic peptide, MMP-2, and tissue inhibitor of MMP-2. For both multivariable logistic regression analysis and stepwise forward selection procedure, the duration of AF >5 months [odds ratio (OR) 15.32] and MMP-2 >767.0 ng/mL (OR 4.84) were significantly associated with RAF. Conclusion Our study suggests that elevated MMP-2 and longer AF duration increased the risk for difficulty in restoring SR in AF patients. Stratification of subjects according to the MMP-2 level may therefore be important for the effective management of AF.

BACKGROUND Conventional risk factors for thoracic aortic aneurysm including dissection (TAA) are thought to include age, arteriosclerosis, and hypertension. In addition, evidence suggests that genetic factors play a role in the development of this condition. The purpose of the present study was to identify genetic variants that confer susceptibility to TAA in hypertensive subjects. METHODS Study subjects comprised 1,351 hypertensive individuals: 88 patients with TAA and 1,263 subjects without this condition. The genotypes for 142 polymorphisms of 119 candidate genes were determined by a method that combines the PCR and sequence-specific oligonucleotide probes with suspension array technology. RESULTS Evaluation of genotype distributions by the chi2-test and subsequent multivariable logistic regression analysis with adjustment for covariates revealed that the 3949T-->G (3' untranslated region) polymorphism of the thrombospondin-2 gene (THBS2; odds ratio, 4.6), the -110A-->C polymorphism of the heat shock 70-kDa protein 8 gene (HSPA8; odds ratio, 0.4), the C-->T (Pro198Leu) polymorphism of the glutathione peroxidase 1 gene (GPX1; odds ratio, 0.3), the -6G-->A polymorphism of the angiotensinogen gene (AGT; odds ratio, 0.3), and the -850C-->T polymorphism of the tumor necrosis factor gene (TNF; odds ratio, 0.5) were significantly (P < 0.05) associated with TAA. CONCLUSIONS The variant allele of THBS2 is a risk factor for TAA in hypertensive patients, whereas the variant alleles of HSPA8, GPX1, AGT, and TNF are protective against this condition. Determination of genotypes for these polymorphisms may prove informative for assessment of the genetic risk for TAA.

Although several environmental factors, including a high-calorie diet and physical inactivity, influence the development of type 2 diabetes mellitus, genetic factors have been shown to contribute to individual susceptibility to this condition. The purpose of the present study was to identify gene polymorphisms that confer susceptibility or resistance to type 2 diabetes mellitus, and thereby to contribute to assessment of the genetic risk for this condition. The study population comprised 5259 unrelated Japanese individuals (2980 men, 2279 women), including 1640 subjects with type 2 diabetes mellitus (1071 men, 569 women) and 3619 controls (1909 men, 1710 women). The genotypes for 94 polymorphisms of 67 genes were determined with a method that combines the polymerase chain reaction and sequence-specific oligonucleotide probes with suspension array technology. Evaluation of genotype distributions by the chi-square test revealed that the 13989-->G (Ile118Val) polymorphism of the cytochrome P450, subfamily IIIA, polypeptide 4 gene (CYP3A4) was significantly (false discovery rate, 0.000009) associated with the prevalence of type 2 diabetes mellitus. Multivariable logistic regression analysis with adjustment for age and sex also revealed that the 13989-->G (Ile118Val) polymorphism of CYP3A4 was significantly (P=0.00002) associated with the prevalence of type 2 diabetes mellitus, with the AG genotype being protective against this condition. Genotyping for CYP3A4 may thus prove informative for assessment of the genetic risk for type 2 diabetes mellitus.

Introduction. Hypertriglyceridemia is an important risk factor for coronary heart disease. The purpose of the present study was to identify gene polymorphisms associated with hypertriglyceridemia (serum triglyceride concentration, ≥1.65 mmol/L) for assessment of the genetic risk for this condition. Methods. A total of 5206 individuals from two independent populations was examined: Subject panel A comprised 3787 individuals who either visited outpatient clinics of or were admitted to the participating hospitals because of various symptoms or for a health checkup; subject panel B comprised 1419 community-dwelling elderly individuals. The genotypes for 100 polymorphisms of 65 candidate genes were determined by a method that combines the polymerase chain reaction and sequence-specific oligonucleotide probes with suspension array technology. Given the multiple comparisons of genotypes with hypertriglyceridemia, we adopted the criterion of a false discovery rate (FDR) of Results. Evaluation of genotype distributions by the chi-square test and subsequent multivariable logistic regression analysis with adjustment for age and sex revealed that seven polymorphisms [−1131T→ C, −3A→G, and 553G→T (Gly185Cys) of APOA5 ; 1100C→T of APOC3 ; 85T→C of APOA1 ; 41A→G (Glu14Gly) of ACAT2 ; C→G (Ser47Stop) of LPL ] were significantly (FDR < 0.05) associated with hypertriglyceridemia in subject panel A. To validate these associations, we examined the same polymorphisms in subject panel B. The six polymorphisms of APOA5 , APOC3 , APOA1 , and LPL , but not that of ACAT2 , were again significantly associated with hypertriglyceridemia. Serum triglyceride concentrations differed significantly ( P< 0.05, ANOVA) among genotypes of each of these six polymorphisms in both subject panels. The three polymorphisms of APOA5 were in linkage disequilibrium. Conclusions. Polymorphisms of APOA5 , APOC3 , APOA1 , and LPL are determinants of hypertriglyceridemia. Genotyping of these polymorphisms may prove informative for assessment of the genetic risk for hypertriglyceridemia and may contribute to the personalized prevention of this condition.

Introduction. A low serum concentration of HDL-cholesterol and a high serum concentration of LDL-cholesterol are risk factors for atherosclerosis. Our goal was to identify genetic variants that confer susceptibility to a low serum concentration of HDL-cholesterol ( Methods. A total of 5213 individuals from two independent populations was examined: Subject panel A comprised 3794 individuals who either visited outpatient clinics of or were admitted to the participating hospitals because of various symptoms or for a health checkup; subject panel B comprised 1419 community-dwelling elderly individuals. The genotypes for 100 polymorphisms of 65 candidate genes were determined. Given the multiple comparisons of genotypes with these conditions, we adopted the criterion of a false discovery rate (FDR) of Results. Examination of genotype distributions by the chi-square test and subsequent multivariable logistic regression analysis with adjustment for age and sex revealed that six [−1131T→C, −3A→G, and 553G→T (Gly185Cys) of APOA5 ; −250G→A and −515C→T of LIPC ; 13989A→G (Ile119Val) of CYP3A4 ] and three [4070C→T (Arg158Cys) and 3932T→C (Cys112Arg) of APOE ; 190G→A (Val64Ile) of CCR2 ] polymorphisms were significantly (FDR < 0.05) associated with low HDL-cholesterol and high LDL-cholesterol, respectively, in subject panel A. To validate these associations, we examined the same polymorphisms in subject panel B. The three polymorphisms of APOA5 and two polymorphisms of APOE were significantly associated with low HDL-cholesterol and high LDL-cholesterol, respectively. The serum concentrations of HDL-cholesterol and LDL-cholesterol differed significantly ( P < 0.01, ANOVA) among genotypes of the corresponding polymorphisms in both subject panels. The polymorphisms of APOA5 and APOE were each in linkage disequilibrium. Conclusions. Polymorphisms of APOA5 and APOE are determinants of low HDL-cholesterol and high LDL-cholesterol, respectively. Genotyping of these polymorphisms may prove informative for prediction of the genetic risk for these conditions.

Introduction: Aneurysms and dissections at the thoracic aorta (TAA) are the leading causes of mortality and morbidity in the United States and Japan. Although hypertension is a major risk for TAA, several studies have indicated that genetic factors also influence the structural formation of TAA. The purpose of the present study was to identify gene polymorphisms associated with TAA among hypertensive patients for assessment of the genetic risk for this condition. Methods: This case-control study comprised 1351 hypertensive individuals, including 88 subjects with TAA and 1263 without any cardiovascular complications. The genotypes for 142 polymorphisms of 121 candidate genes were determined by a method that combines the polymerase chain reaction and sequence-specific oligonucleotide probes with suspension array technology. Results: Evaluation of genotype distributions by the chi-square test and subsequent multivariable logistic regression analysis with adjustment for age, sex, body mass index, and prevalence of smoking, diabetes mellitus, hypercholesterolemia, and metabolic syndrome revealed that the T→G (3′ UTR) polymorphism of the thrombospondin 2 gene ( THBS2 ; odds ratio, 4.7) is significantly (P < 0.05) associated with TAA in hypertensive subjects, with the variant G allele representing a risk factor for this condition. Furthermore, the -110A→C polymorphism of heat-shock 70-kD protein 8 gene ( HSPA8 ; odd ratio, 0.3), the C→T (Pro198Leu) polymorphism of the glutathione peroxidase gene ( GPX1 ; odds ratio, 0.3), the -6G→A polymorphism of angiotensin 1 gene ( AGT ; odds ratio, 0.3), and the -850C→T polymorphism of tumor necrosis factor gene ( TNF ; odds ratio, 0.5) were significantly associated with this condition, with the variant allele of each polymorphism being protective against this condition. A stepwise forward selection procedure revealed that polymorphisms of THBS2 , HSPA8 , GPX1 , AGT , and TNF significantly affected the prevalence of TAA. Conclusions: Genetic variant of THBS2 may be a risk factor for TAA in hypertensive patients, whereas variants of HSPA8 , GPX1 , AGT , and TNF may be protective against this condition. Determination of genotypes for these polymorphisms may prove informative for assessment of the genetic risk for TAA.

Aims Our study aims to investigate the pathophysiologic mechanism underlying tako-tsubo cardiomyopathy using F-18 fluorodeoxyglucose (FDG) positron emission tomography (PET). Methods and results Fifteen patients with tako-tsubo cardiomyopathy were enrolled in this study. Plasma catecholamines, cardiac troponin T (cTnT), and D-dimer were serially evaluated in all patients. Thallium-201 (201Tl) single-photon emission computed tomography (SPECT) and F-18 FDG PET were performed in 10 and eight patients, respectively. Emotional or physical stress occurred in 12 (80.0%) patients. ST-T segment abnormalities existed in all patients. Thirteen patients exhibited mildly elevated cTnT, although coronary angiography did not reveal significant stenosis in any patient. Endomyocardial biopsy specimens ( n = 9) demonstrated contraction-band necrosis ( n = 4) and mononuclear cell infiltration ( n = 3). The levels of norepinephrine and epinephrine peaked on admission (744 ± 452 and 140 ± 166 pg/mL, respectively). There was severely reduced uptake at the apex on F-18 FDG PET image, despite slightly reduced uptake of 201Tl. Elevation of D-dimer was observed in nine patients. Conclusion The extent of metabolic defect involving apical akinetic area was more severe than perfusion abnormality. Our data suggest that sudden emotional or physical stress may cause a catecholamine-induced metabolic disorder in the myocardium, which is probably central to this syndrome.

Hyperlipidemia or dyslipidemia is one of the most important risk factors for coronary heart disease. The purpose of the present study was to identify gene polymorphisms for assessment of the genetic risk for myocardial infarction (MI) in individuals with low or high serum concentrations of high- density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol, or triglyceride (TG), thereby contributing to the personalized prevention of MI in such individuals. The study population comprised 2682 unrelated Japanese individuals (1796 men, 886 women), including 1113 subjects (869 men, 244 women) with MI and 1569 controls (927 men, 642 women). The genotypes for 164 polymorphisms of 137 candidate genes were determined by a method that combines the polymerase chain reaction and sequence-specific oligonucleotide probes with suspension array technology. Multivariable logistic regression analyses and stepwise forward selection procedures revealed that seven different polymorphisms were significantly (P0.005) associated with MI in individuals with low or high serum concentrations of HDL- or LDL-cholesterol or of TG: the 190T --C (Trp64Arg) polymorphism of ADRB3 in individuals with low HDL-cholesterol; the 1018C --T (Thr145Met) polymorphism of GP1BA, the A --G (Ile646Val) polymorphism of AKAP10, and the -55C --T polymorphism of UCP3 in individuals with high HDL-cholesterol; the -603A --G polymorphism of F3 and the -11377C --G polymorphism of ADIPOQ in individuals with low LDL-cholesterol; the 1018C --T polymorphism of GP1BA in individuals with low TG; and the 4G --5G polymorphism of PAI1 in individuals with high TG. No polymorphism was associated with MI in individuals with high LDL-cholesterol. These results suggest that polymorphisms associated with MI may differ among individuals with different lipid profiles. Stratification of subjects according to lipid profiles may thus be important for personalized prevention of MI based on genetic information.

Atrial fibrillation (AF) may result from an electric conduction disturbance, increased hemodynamic stress, ischemia, inflammation, or remodeling in atria. Although genetic epidemiological studies have identified several genetic variants as risk factors for AF, the genetic determinants of this condition remain largely unknown. The purpose of the present study was to identify gene polymorphisms that confer susceptibility to lone AF. The study population comprised 1069 unrelated Japanese individuals, including 196 subjects with chronic lone AF and 873 controls. The genotypes for 40 polymorphisms of 32 candidate genes were determined by a method that combines the polymerase chain reaction and sequence-specific oligonucleotide probes with suspension array technology. Multivariable logistic regression analysis with adjustment for age, sex, body mass index, and the prevalence of smoking, hypertension, diabetes mellitus, and hyperchole-sterolemia as well as a stepwise forward selection procedure revealed that the -1306C-->T polymorphism of the matrix metalloproteinase 2 gene (MMP2) and the -592A-->C polymorphism of the interleukin 10 gene (IL10) were significantly (false discovery rate of

The purpose of the present study was to assess the genetic risk for myocardial infarction (MI) in individuals with or without conventional coronary risk factors and thereby to contribute to the personalized prevention of MI in such individuals. The study population comprised 3483 unrelated Japanese individuals (1913 men, 1570 women). The 1192 subjects with MI (926 men, 266 women) and 2291 controls (987 men, 1304 women) either had or did not have conventional coronary risk factors, including hypertension, hypercholesterolemia, and diabetes mellitus. The genotypes for 164 polymorphisms of 137 candidate genes were determined by a method that combines the polymerase chain reaction and sequence-specific oligonucleotide probes with suspension array technology. Multivariable logistic regression analysis and a stepwise forward selection procedure revealed that nine different polymorphisms were significantly (P

The authors encountered a very rare case of paradoxical brain embolism resulting from pulmonary arteriovenous fistula and coincident pulmonary embolism. Enhanced computed tomography was useful for diagnosing this infrequent condition.

Hypertriglyceridemia accompanied by low levels of high-density lipoprotein cholesterol (HDL-C) is a risk factor for coronary artery disease. High-density lipoprotein 2 (HDL2) and 3 (HDL3) are believed to suppress the progress of atherosclerosis through reverse cholesterol transport. As a result, peripheral tissues can be protected against excessive accumulation of cholesterol. Although bezafibrate is known to accelerate the increase of HDL-C, results are not standardized regarding increases of HDL3 and HDL2 subfractions.This study assessed the effects of bezafibrate on serum triglyceride (TG) fractional clearance rate (K2) and HDL2 and HDL3 cholesterol (HDL2-C and HDL3-C, respectively) levels in patients with primary hypertriglyceridemia (serum TG ≥150 mg/dL).Outpatients with primary hypertriglyceridemia were enrolled in this 8-week study conducted at the Third Department of Internal Medicine, Nagoya City University Hospital (Nagoya, Japan). Oral bezafibrate was administered at a dose of 400 mg/d (200-mg tablet BID, morning and evening) for 8 weeks. After 8 weeks, serum levels of total cholesterol (TC), TG, HDL-C, HDL2-C, and HDL3-C were measured. A fat emulsion tolerance test to assess K2 and measurements of plasma lipoprotein lipase (LPL) mass, LPL activity, and hepatic triglyceride lipase (HTGL) activity in postheparin plasma were performed before bezafibrate administration and after the course of treatment.Sixteen patients (10 men, 6 women; mean [SD] age, 54 [12] years [range, 30-69 years]; mean [SD] body mass index, 23 [2] kg/m(2)) entered the study. The following findings were observed in male and female patients after 8 weeks of treatment. A statistically significant reduction was observed in mean serum TG level (P0.01). Significant increases were seen in HDL-C, HDL2-C, and HDL3-C (all P0.01), K2 (P0.01), and in plasma LPL mass (P0.01) and LPL activity (P0.05). TC level and HTGL activity did not change significantly. No adverse effects related to the use of bezafibrate were documented.In this study, bezafibrate treatment resulted in significant decreases in serum TG level and significant increases in HDL2-C and HDL3-C levels and plasma LPL mass and activity. We hypothesize that bezafibrate may increase HDL3-C by promoting TG-rich lipoprotein catabolism and may increase HDL2-C by promoting the conversion of HDL3 to HDL2.

In patients with myocardial infarction (MI), an expansion of the remote normal regions of the left ventricle is often observed. However, the characteristics of such regions are not fully understood. Thus, we investigated this issue from the standpoint of myocardial oxidative metabolism using (11)C-acetate PET.In 33 patients with recent MI (24 not receiving beta-blockers, 9 receiving beta-blockers) and 12 age-matched normal control subjects, (11)C-acetate dynamic myocardial PET scanning was performed at rest. Time-activity curves of (11)C-acetate in 5-7 regions of interest (ROIs) on the midventricular transaxial image in each subject were generated, and the clearance rate constant (K(mono)) in each ROI was calculated by monoexponential fitting as an index of myocardial oxidative metabolism. The left ventricular (LV) end-diastolic volume index as an index of LV remodeling and the heart rate. pressure product were obtained in all subjects.The LV end-diastolic volume index was significantly larger in patients with MI without beta-blockers than in normal control subjects (101 +/- 22.5 vs. 61.6 +/- 12.8 mL x m(-2); P0.001). There was no significant difference in the heart rate x pressure product between the patients with MI without beta-blockers and the normal control subjects (8,229 +/- 1,503 vs. 8,311 +/- 1,311 mm Hg x min(-1)). The K(mono) in remote normal regions was significantly greater in patients with MI without beta-blockers even when compared with the highest K(mono) on the anteroseptal wall of the left ventricle in normal control subjects (0.078 +/- 0.022 vs. 0.065 +/- 0.007 min(-1); P0.01). In contrast, the heart rate. pressure product (6,911 +/- 1,135 mm Hg x min(-1)) and the K(mono) (0.054 +/- 0.009 min(-1)) in remote normal regions were significantly less in patients with beta-blockers than in those without beta-blockers (P0.001). No significant difference in the LV end-diastolic volume index was found between the MI patients with and without beta-blockers. Multivariate regression analysis showed that beta-blockers significantly and directly decreased the K(mono) in remote normal regions after adjusting the effect of the heart rate x pressure product, although the prime determinant of the K(mono) in such regions was the heart rate x pressure product.Myocardial oxidative metabolism in remote normal regions is accelerated in the left ventricles with remodeling after acute MI. Therapy using beta-blockers normalizes the myocardial oxidative metabolism in such regions through the reduction of the heart rate x pressure product and their direct effect on the myocardium.

We report the case of a 62-year-old man with recurrent arterial embolisms to his arms caused by a thrombosis of the ascending aorta. He had developed a left brachial artery embolism 8 years previously, but presented with a right brachial artery embolus on this occasion. A clot-like mass was seen in the ascending aorta on computed tomography without significant atherosclerosis. Magnetic resonance imaging identified multiple asymptomatic cerebral infarctions. Therefore, we surgically removed the thrombus in the ascending aorta, which was an organized fibrin clot. Pathologically, atherosclerosis and plaque formation were evident at the intima where the clot attached. Clot formation was considered to be due to local arteriosclerosis.We report a case of thrombosis of the ascending aorta causing multiple and recurrent arterial embolisms. The patient had no evidence of coagulation disorders, and arteriosclerotic risk factors such as hypertension, diabetes mellitus, and dyslipidemia were absent. Thus, thrombosis may develop in patients without traditional risk factors.