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Left atrium (LA) modulates left ventricle (LV) filling and cardiac performance. We aimed to assess the effect of heart failure (HF) therapy on LA and LV function, and the relationship between LA/LV improvement and clinical outcome in acute HF with reduced LV ejection fraction (LVEF). Totally, 224 hospitalized patients with acute HF and LVEF 35% were enrolled and underwent echocardiography. They all received maximal tolerable doses of evidence-based medications. Patients received echocardiographic measurements at each visit including stroke volume, LVEF, LA minimal/maximal volume (LAV

Aims Chronic inflammation is linked to cancer. This study aims to evaluate the association between chronic rhinosinusitis (CRS) and nasopharyngeal carcinoma (NPC) through a Taiwanese nationwide database. Methods We used the National Health Insurance Research Database between January 1, 2003, and December 31, 2012. The starting date is either the date of the first clinical visit or the diagnosis of CRS. Patients were followed up until the first occurrence of target disease or the last date of medical record. Propensity score 1 to 2 matching was used to match pairs of patients with/without CRS. Results A total of 951 380 eligible patients were included in our study, with 36 210 patients diagnosed with CRS. After 1 to 2 propensity score matching, non-CRS cohort consisted of 69 258 patients and CRS cohort consisted of 34 629 patients. CRS was associated with the risk of developing NPC (adjusted OR = 2.23; 95% CI, 1.61-3.09). However, no significant association among CRS and NPC was observed in patients followed up for more than 1 year (adjusted OR = 1.16; 95% CI, 0.76-1.78). Conclusions Patients with CRS diagnosis have relationship with developing NPC within 1 year of follow-up, but not for longer intervals. The short-term association may be due to reversed causation or biased diagnosis. Accordingly, the study suggests CRS a weak role for NPC.

BACKGROUND: This study aimed to investigate the relationship between malnutrition and outcomes in patients with decompensated severe systolic heart failure (HF) focusing on clinical presentations and medication use. METHODS: This study prospectively enrolled 108 patients admitted for severe systolic HF with a left ventricular (LV) ejection fraction < 35%, low cardiac output, and high LV filling pressure. Five patients died during the index hospitalization, and the remaining 103 patients were followed up for 2 years. The primary endpoints were HF rehospitalization and all-cause mortality. Nutritional risk index (NRI) was calculated as (1.519 × serum albumin, g/L) + (41.7 × body weight/ideal body weight). RESULTS: Forty-four patients reached the study endpoints. An NRI ≤ 93 predicted events. The NRI ≤ 93 group had higher pulmonary artery systolic pressure, more edema over dependent parts, longer hospital stay, and more primary endpoints compared to the NRI > 93 group. The NRI ≤ 93 group received fewer evidence-based medications and more loop diuretics compared to the NRI > 93 group. NRI was an independent predictor of cardiovascular events [hazard ratio 0.902; 95% confidence interval (CI) 0.814-0.982 per 1 point increase; p = 0.012]. Low NRI was associated with a significantly higher use of loop diuretics [odds ratio (OR) 2.75; 95% CI 1.046-5.647; p = 0.004] and significantly lower use of beta blockers (OR 0.541; 95% CI 0.319-0.988; p = 0.002). CONCLUSIONS: Malnutrition assessed using the NRI was associated with cardiovascular events in the patients with severe systolic HF with low cardiac output and high LV filling pressure. Low NRI was associated with more diuretic and less beta blocker use.

BACKGROUND: Recent studies have shown that left atrial (LA) volume is a sensitive morphophysiological indicator of the severity of LV dysfunction and may also be a useful index of cardiovascular risk. In this study, we performed comparisons among left atrial (LA) functional parameters for predicting age-related diastolic dysfunction. METHODS: Echocardiography was performed in 2248 healthy participants with a low possibility of heart disease according to the decennium of age, and reference values were established. Progressive diastolic dysfunction paralleled increasing age and could be well identified by traditional and advanced echocardiographic parameters, including mitral inflow pattern, tissue Doppler parameters, and LA volume. RESULTS: Regarding LA functional parameters analyzed based on the decennium of age, left atrial ejection fraction (LAEF) and emptying fraction could not represent aging diastolic dysfunction well, but LA expansion index ((Vol(max) – Vol(min)) × 100% / Vol(min)) could. Vol(max) indicated maximal LA volume and Vol(min) indicated minimal LA volume. In assessments of diastolic dysfunction with receiver operating characteristic curve analysis, the best cut-off value of LA expansion index was < 100%, with an area under the curve (AUC) of 0.86, sensitivity of 80%, and specificity of 74%. LAEF < 30% (AUC 0.76, sensitivity 67%, specificity 70%) and LA emptying fraction < 50% (AUC 0.80, sensitivity 72%, specificity 71%) were also useful but performed less well. CONCLUSIONS: Compared with other LA functional parameters, LA expansion index can well represent age-related diastolic dysfunction.

Myocardial infarction and cerebral ischemic stroke are prominent causes of death worldwide. Platelets play major roles in these diseases, although they are anucleated cells, but also express the NF-κB. Pterostilbene (PTE) possesses some intriguing pharmacological properties, including the capacity to inhibit platelet activation. We investigated the inhibitory role of PTE in NF-κB-mediated signal events and compared the relative potency with that of classical NF-κB inhibitors. PTE and IκB kinase (IKK) inhibitor, BAY11-7082, and proteasome inhibitor, Ro106-9920, inhibited platelet aggregation, the activity of BAY11-7082 and PTE were similar, but Ro106-9920 was weak in this reaction. PTE and BAY11-7082 diminished NF-κB signaling molecules, including IKK, IκBα, and p65 phosphorylation, and reversed IκBα degradation. However, Ro106-9920 was only effective in diminishing p65 phosphorylation and reversing IκBα degradation. In investigating the role of Akt and NF-κB in cell signaling events, MK-2206 (an inhibitor of Akt) markedly abolished IKK and p65 phosphorylation, BAY11-7082 also reduced Akt phosphorylation. PTE exhibited more potent activity in vivo than did BAY11-7082 in acute pulmonary thromboembolism. In conclusion, we identified a distinctive activation pathway of NF-κB and Akt involved in PTE-mediated antiplatelet aggregation, and PTE demonstrated powerful activity as a prophylactic and as clinical therapy for cardiovascular diseases.

Familial hypercholesterolemia (FH) is an inherited autosomal dominant disorder of lipoprotein metabolism resulting in elevated serum levels of low-density lipoprotein cholesterol (LDL-C), which lead to increased risk for premature cardiovascular disease. The recognized cause is mutations of the low-density lipoprotein receptor (LDLR), apolipoprotein B (APOB), or proprotein convertase subtilisin/kexin type 9 genes. This study reviewed the literature in Han Chinese to investigate the frequency and spectrum of mutations that are recognized by molecular genetics as causes of FH, the clinical characteristics, and mutation detection rates of FH. MEDLINE, EMBASE, BIOSIS, Wanfang, CNKI, and FH websites, were reviewed through December 2014. Sixty-six studies met inclusion criteria. Totally, 143 different LDLR mutations were identified, including 134 point mutations and 9 large rearrangements; functional characteristics of 46 point mutations were studied. The 5 most frequent mutations included APOB 10579C>T, LDLR 986G>A, 1747C>T, 1879G>A, and 268G>A. Most of these mutations were reported in Southeast China, Hong Kong, and Taiwan. DNA detection rates of heterozygous FH were 6.5% to 77.5%, depending on the inclusion criteria and chosen screening method. With the economic growth and Western-like diet patterns being adopted over the past decade in municipalities in mainland China and Taiwan, the mean pretreatment concentration of LDL-C is higher among heterozygous FH patients reported since 2005 than in patients reported before 2005 (231 vs 196 mg/dL, P

Titration of evidence-based medications, important for treating heart failure (HF), is often underdosed by symptom-guided treatment. The aim of this study was to investigate, using echocardiographic parameters, stroke volume and left ventricular (LV) filling pressure to guide up-titration of medications, increasing prognostic benefits.A total of 765 patients with chronic HF and severely reduced LV ejection fractions (35%), referred from 2008 to 2016, were prospectively studied. Echocardiographic guidance was performed in 149 patients. LV filling pressure was assessed by left atrial expansion index, and stroke volume was estimated from diameter and time-velocity integral in the LV outflow tract. Up-titration of evidence-based medications and adjustment for side effects or worsening clinical conditions according to those parameters were performed. Propensity score matching was used to match pairs of patients with (n = 110) or without (n = 110) echocardiographic guidance. End points were 4-year frequencies of HF hospitalization and all-cause mortality.During a mean follow-up time of 4.1 years, rates of adverse events were 58 (52.7%) with no echocardiographic guidance and 36 (32.7%) with echocardiographic guidance (P .0001). Echocardiography provided effective guidance to reduce prescribing frequency and dose of diuretics and to promote evidence-based medication prescription. It reduced HF rehospitalization and all-cause mortality. By multivariate analysis, prognostic improvement was associated with up-titration of medications with echocardiographic guidance.There was a statistically significant difference in long-term prognosis between propensity score-matched pairs of patients with chronic severe HF with and without echocardiographic guidance. These findings need further validation in large prospective clinical trials.

Aims The power of left atrial (LA) parameters for predicting adverse events in relatively low-risk groups is not fully understood. This study investigated whether the LA expansion index predicts heart failure (HF) and all-cause mortality in subjects with dyspnoea. Methods and results Echocardiography was performed to identify causes of dypnoea in 1735 patients. The LA expansion index was calculated as (Volmax – Volmin) × 100%/Volmin, where Volmax was defined as the maximal LA volume and Volmin was defined as the minimal LA volume. The endpoints were 2-year frequencies of HF hospitalization and all-cause mortality. Over a median follow-up of 2.7 years, 91 participants reached endpoints. Rates of adverse events were exponentially proportional to the LA expansion index. For predicting adverse events, the LA expansion index was better than the maximal indexed LA volume and tissue Doppler parameters. Hospitalization for HF was independently associated with age, LVEF, pulmonary artery systolic pressure, LA expansion index, and history of prior HF. All-cause mortality was associated with age, pulmonary artery systolic pressure, and LA expansion index. Compared with the highest quartile of the LA expansion index, the lowest quartile had a 3.1-fold higher hazard of HF events and a 17.8-fold higher hazard of all-cause mortality. Conclusions The LA expansion index predicts adverse events in patients with dyspnoea. The prognostic power of the index exceeds that of other well-established echocardiographic parameters such as E/e' and maximal indexed LA volume. Trial registration NCT01171040.

Background Door-to-balloon (D2B) time is an important factor in the outcome of ST segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention. We aimed to use failure mode and effect analysis to reduce the D2B time for patients with STEMI and to improve clinical outcomes. Methods There were three stages in this study. In Stage 0, data collected from 2005–2006 was used to identify failures in the process, and during Stage 2 (2007) and Stage 3 (2008) the efficacy of intrahospital and interhospital strategies to reduce the D2B time were evaluated. This study enrolled 385 patients; 86 from 2005–2006; 80 in 2007; and 219 in 2008. Results By making improvements in these steps, the median D2B time was reduced from 146 min to 32 min for all patients. The proportion of patients with a D2B time of

BACKGROUND The left atrial (LA) expansion index for predicting atrial fibrillation (AF) in a relatively low-risk cohort is not fully understood. METHODS AND RESULTS In this prospective study of 2,200 dypnea patients, the LA expansion index was calculated as (Volmax-Volmin)×100%/Volmin, where Volmax was defined as maximum LA volume and Volmin was defined as minimum volume. The endpoints were 2-year frequency of AF, including both paroxysmal and persistent. Of the 180 participants (8.2%) who had AF attacks over a median follow-up of 2.7 years, 90 (4.1%) had at least 1 episode of persistent AF. Compared to patients with paroxysmal AF, those with persistent AF had a much lower LA expansion index (100±59% vs. 44±24%). LA expansion index was associated exponentially with the incidence of persistent AF. Independent predictors of AF included age, renal function impairment, pulmonary artery systolic pressure, and LA expansion index. Persistent AF, however, had significant independent associations only with prior heart failure, renal function impairment, diastolic dysfunction, and LA expansion index (odds ratio, 0.970; 95% confidence interval: 0.959-0.981 per 1% increase, P

Background Familial hypercholesterolemia (FH) is a heterogeneous autosomal dominant disease. The genetic heterogeneity of FH requires low-cost, high-throughput, and rapid mutation detection technology to efficiently integrate genetic screening into clinical practice. Objectives The aims of the study were to customize the MassARRAY assay to (1) establish an FH mutation assay panel, comprising known point mutations located on FH-causing genes and (2) test the feasibility of the assay for screening FH patients residing in Taiwan who fit the clinical criteria of FH diagnosis. Methods We designed a custom Agena iPLEX assay to detect 68 point mutations on FH-causing genes. First, the assay performance was verified by analyzing 180 previously sequenced subjects (120 with point mutations and 60 healthy controls), with the results being compared with those of Sanger DNA sequencing. Second, a blind study was carried out on 185 FH probands (44 definite FH and 141 probable/possible FH). Results In the first part of this study, only 1 discrepancy was found between the Agena iPLEX and Sanger sequencing genotyping results. In the blind study, a total of 62 probands with mutations were identified by both techniques. Five mutations were detected by Sanger sequencing assay only. The detection sensitivity and specificity rates of Agena iPLEX were 92.5% and 100%, respectively, in the blind study. The hands-on time for the Agena iPLEX assay was around 1 day. Conclusions The custom-designed Agena iPLEX assay has high specificity and sensitivity for FH genetic screening. Considering its low cost, rapidity, and flexibility, the assay has great potential to be incorporated into FH screening in Taiwan.

Diabetes mellitus (DM) is a strong risk factor of cardiovascular disease. To date, the impact of DM on outcomes after acute myocardial infarction (AMI) in Taiwan is undetermined. The aim of this study was to compare five-year outcomes after AMI in patients with and without diabetes in Taiwan.A nationwide cohort of 25,028 diabetic and 56,028 non-diabetic patients who were first hospitalized with AMI between 1996 and 2005 was enrolled through linkage with the Taiwan National Health Insurance research database. Patient mortality rates within 30 days after AMI, and 1, 3, and 5 years thereafter were compared.Length of hospital stay (8.9 ± 8.7 vs. 8.2 ± 8.0 days, p0.01) and medical cost during admission (in Taiwan dollars: $129,123 ± $158,073 vs. $121,631 ± $157,018, p0.01) were significantly higher in diabetic patients. The difference in mortality rate within 30 days was insignificant between diabetic and non-diabetic patients (18.1% vs. 17.6%, p = 0.06). Mortalities within 1 year (31.0% vs. 26.8%, p0.01), 3 years (42.4% vs. 34.7%, p0.01), and 5 years (50.6% vs. 41.1%, p0.01) were significantly higher in diabetic patients. In patients with AMI who underwent percutaneous coronary intervention (PCI) during index admission, the mortality rate within 30 days was insignificant (6.3% vs. 6.4%, p = 0.70) but mortalities within 1 year (15.2% vs. 11.6%, p0.01), 3 years (24.1% vs. 17.2%, p0.01), and 5 years (32.2% vs. 22.6%, p0.01) were significantly higher in diabetic patients.The average patient length of hospital stay and medical cost during admission were significantly higher in diabetic patients. Additionally, the difference in mortality rate within 30 days after AMI was insignificant between diabetic and non-diabetic patients. Also, long-term mortality after AMI was significantly higher in diabetic patients.Acute myocardial infarction; Diabetes mellitus; Length of hospital stay; Medical cost; Mortality; National health insurance.

Although there have been some studies focusing on the relationship between body mass index (BMI), coronary artery disease (CAD) and acute coronary syndrome, the clinical effects of BMI on outcomes after percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI) are not well known in a Taiwanese population.From January 2005 to December 2011, 1298 AMI patients who received PCI were enrolled from a single center in Taiwan. The patients were divided into 4 groups according to their BMI: underweight (BMI18.5 kg/m(2)); normal weight (18.5 ≤ BMI24 kg/m(2)); overweight (24 ≤ BMI27 kg/m(2)) and obese (BMI ≥ 27). All patients had been followed up for at least 12 months, and 30-day and 5-year all-cause and cardiovascular-cause mortality were compared among the study groups.The patients in the underweight group had a lower 30-day survival rate than the other 3 groups, and the underweight and normal weight patients had a lower 5-year survival rate than the overweight and obese patients. The multivariate regression analysis showed that Killip class ≥ 2, non-use of statin, older age, hemoglobin12 g/dl and chronic kidney disease, but not BMI, are independent predictors of all-cause mortality.In this present study, the major factors affecting long-term survival are lack of using statin and older age, but not obese paradox.Acute myocardial infarction; Mortality; Obesity; Percutaneous coronary intervention; Survival.

Patients with acute coronary syndrome and impaired renal function have been shown to have high mortality. However, there is scarce literature to date addressing the impact of diabetes mellitus (DM) and renal function on clinical outcomes of ST elevation myocardial infarction (STEMI) in Taiwan.This study enrolled 512 STEMI patients who received primary percutaneous coronary intervention. Patients were divided into 4 groups including group 1: patients without DM or CKD (nDM-nCKD); group 2: patients with DM but without CKD (DM-nCKD); group 3: patients with CKD but without DM (nDM-CKD); group 4: patients with DM and CKD (DM-CKD). Patients were also classified into four groups based on their estimated glomerular filtration rates (eGFR): stage 1 (eGFR ≥ 90 ml/min/1.73 m(2), n = 163), stage 2 (eGFR = 89-60 ml/min/1.73 m(2), n = 171), stage 3 (eGFR = 59-30 ml/min/1.73 m(2), n = 136), and stage 4 (eGFR30 ml/min/1.73 m(2), n = 42). The complication rates, length of hospital stay, and 30-day outcomes were analyzed.The patients in both the nDM-CKD group and DM-CKD group had higher incidences of hypotension, intra-aortic balloon counterpulsation use, and respiratory failure (p0.005). They had significantly longer hospital stay and 30-day mortality rates (p0.001). The patients with CKD stage 3 and 4 had longer hospital stay and higher 30-day mortality rates (p0.001). However, DM was not an independent factor on the length of hospital stay and 30-day mortality rates.STEMI patients with impaired renal function, but not DM, had significantly longer hospital stay and higher 30-day mortality rates.Chronic kidney disease; Diabetes mellitus; Mortality; Primary percutaneous coronary intervention; ST-segment elevation myocardial infarction.

Because of diastolic coupling between the left atrium and left ventricle, we hypothesized that left atrial (LA) function mirrors the diastolic function of left ventricle. The aims of this study were to assess whether LA volume parameters can be good indexes of left ventricular diastolic dysfunction. Six hundred fifty-nine patients underwent cardiac catheterization and measurements of left ventricular filling pressure (LVFP). Echocardiographic examinations including tissue Doppler and LA volumes were also assessed. Ratio of early diastolic mitral inflow velocity to early diastolic mitral annular velocity and LVFP tended to increase after progression of diastolic dysfunction. The inverse phenomenon existed in LA ejection and LA distensibility. LA distensibility was superior to LA ejection fraction and early diastolic mitral inflow velocity/early diastolic mitral annular velocity for identifying LVFP >15 mm Hg (areas under receiver operating characteristic curve 0.868, 0.834, and 0.759, respectively) and for differentiating pseudonormal from normal diastolic filling (areas under receiver operating characteristic curve 0.962, 0.907, and 0.741, respectively). Multivariate logistic regression showed that LA ejection fraction and LA distensibility were associated significantly with the presence of pseudonormal/restrictive ventricular filling. In conclusion, LA volume parameters can identify LVFP >15 mm Hg and differentiate among patterns of ventricular diastolic dysfunction. For assessing diastolic function LA parameters offer better performance than even tissue Doppler.

To evaluate multidetector computed tomographic (CT) images to investigate the prevalence, morphology, natural course, and prognostic effect of intramural blood pools (IBPs) in patients with acute intramural hematoma (IMH).Institutional review board approval and written informed consent were obtained. Sixty-five patients (41 men; mean age, 65.9 years ± 11.3 [standard deviation]) with acute IMH undergoing three or more multidetector CT examinations during follow-up for 12 months or longer (median = 18 months), except for those undergoing surgery (n = 16), were enrolled. Associated factors of developing and resorption of IBP in IMH were analyzed by using logistic regression.There were 40 IBPs in 10 patients at initial multidetector CT, and 15 new IBPs developed in 11 patients during follow-up. IBPs occurred most in the descending thoracic (55% [31 of 56]) and abdominal (41% [23 of 56]) aorta in 28% (18 of 65) of patients. During 33.8 months (range, 2.8-50 months) of follow-up in these 18 patients, 57% (32 of 56) of IBPs showed complete resorption in 15 patients, 29% (16 of 56) of IBPs showed incomplete resorption in eight patients, and 14% (eight of 56) of IBPs had interrupted follow-up because of surgery or death in three patients. Logistic regression showed that age younger than 70 years (odds ratio [OR], 8.74; 95% confidence interval [CI]: 1.03, 76.9) and IMH wall thickness greater than 10 mm (OR, 4.93; 95% CI: 1.04, 23.0) were associated with developing IBP at initial multidetector CT, while IBP with larger transmural diameter (OR, 1.16; 95% CI: 1.02, 1.31) and multidetector CT-demonstrated connection with intercostal or lumbar artery (63% [35 of 56]) (OR, 5.44; 95% CI: 1.43, 20.9) were associated with incomplete resorption.IBPs are frequently observed at multidetector CT in patients with IMH. They may resolve over time or appear during follow-up. These findings are not associated with a poor prognosis, and IBPs should be distinguished from ulcerlike projections.

Background: Although E/e' (the ratio of early diastolic mitral inflow velocity to early diastolic mitral annular velocity) is widely used to measure left ventricular filling pressure (LVFP), its accuracy is questionable in coronary artery disease patients. Methods and Results: Echocardiograms and LVFP were obtained from 174 patients with stable angina (Canadian Cardiovascular Society angina grade I-II) who had received interventions for angiography-confirmed coronary stenosis. Compared with single-vessel groups, the multiple-vessel group exhibited lower mitral annular velocities, higher LVFP, and stronger correlations between E/regional e' and LVFP. Additionally, stronger correlations between E/regional e' and LVFP existed in patients with systolic dysfunction or lower variation of myocardial performance index (MPI) among anterior, inferior and lateral borders of mitral annulus. Average e' was not superior to any regional e' for assessing LVFP by the E/e' method. E/e' and left atrial (LA) ejection fraction (EF) correlated linearly with LVFP, but the correlation between LA distensibility and LVFP was logarithmical. Compared with E/e', LA distensibility and LAEF were superior for identifying high LVFP. Conclusions: E/e' is not completely satisfactory for assessing LVFP in patients with stable angina, especially those with single-vessel disease, preserved systolic function or high MPI variation. For identifying high LVFP, LA distensibility and LAEF are better than E/e'. (Circ J 2011; 75: 1942-1950)

Familial hypercholesterolemia (FH) is commonly caused by mutations in the low-density lipoprotein receptor (LDLR), apolipoprotein B, and proprotein convertase subtilisin/kexin type 9 genes. The study aim was to investigate patients with FH in Taiwan, using molecular diagnostic methods, and compare the abnormalities in the small mutation and large DNA rearrangement subgroups. In total, 102 unrelated probands with FH were tested for mutations by exon-by-exon sequence analysis (EBESA) and multiple ligation-dependent probe amplification (MLPA). EBESA identified gene apolipoprotein B R3500W in 8 probands and 25 mis-sense, 5 nonsense, and 6 frameshift LDLR mutations in 52 probands; 11 were novel mutations. Of the 42 probands with mutations undetected by EBESA, 8 had abnormal MLPA patterns, including 2 with exon 6 to 18 deletions, 2 with exon 9 deletion, 1 with exon 6 to 8 deletions, 1 with exon 11 deletion, 1 with exon 3 to 5 duplications, and 1 with exon 7 to 12 duplications. Pedigree analysis showed mutation cosegregation with hypercholesterolemia in affected family members. Mean lipid profiles and rate of failure to lower LDL cholesterol100 mg/dl in response to rosuvastatin/ezetimibe treatment were similar in groups with abnormal MLPA patterns and groups carrying nonsense or frameshift mutations. In conclusion, frequency of large LDLR rearrangement was approximately 8% in Taiwanese patients with FH. The response to statin drugs differed between probands with abnormal MLPA patterns and probands carrying mis-sense or undetected mutations.

Echocardiograms and left ventricular (LV) filling pressure were obtained from 95 patients with chronic severe mitral regurgitation (MR) and 16 patients with acute severe MR. All patients underwent catheterization for preoperative examinations and LV filling pressure measurements. A total of 52 age-, gender- and co-morbidity–matched patients with negative coronary angiographic results served as the controls. Echocardiography, including assessment of left atrial (LA) distensibility, was performed simultaneously. LA distensibility correlated logarithmically with the LV filling pressure. However, the early-diastolic mitral inflow velocity divided by the early-diastolic mitral annular velocity (mitral E/E′) correlated linearly with the LV filling pressure. Bivariate correlation analysis revealed that LV filling pressure correlated positively with the maximum and minimum indexed LA volume, as well as the E/E′, but the LV filling pressure correlated negatively with LA distensibility, LA ejection fraction, and LV ejection fraction. However, the MR regurgitation volume was associated only with the maximum and minimum indexed LA volume. Receiver operating characteristic curve analysis indicated that LA distensibility was not inferior to E/E′ for identifying a LV filling pressure >15 mm Hg. However, to identify acute severe MR, LA distensibility was superior to E/E′. In conclusion, LA distensibility, as is E/E′, is a valuable diastolic parameter. In patients with severe MR, it offers adequate power to assess the LV filling pressure and to identify acute severe MR.

Background: Tissue Doppler imaging (TDI) data for acute inferior myocardial infarction (MI) patients who have received primary percutaneous coronary intervention (PCI) are sparse. Methods and Results: One hundred and sixty-five patients received primary PCI for acute inferior MI were enrolled. Right ventricular infarction (RVI) was defined as a culprit lesion proximal to the right ventricular branch of right coronary artery (RCA). Echocardiograms and TDI were obtained within 6 h after primary PCI. The prevalence of multi-vessel disease in the RCA-P culprit group (50%) was higher than that in other groups (39% of RCA-D culprit, 43% of left circumflex artery (LCX) culprit). The myocardial performance index (MPI) of the lateral tricuspid annulus provides discriminatory power for identifying RVI, whereas systolic velocity (Sm) of the lateral tricuspid annulus does not. Lateral mitral annular MPI divided by the lateral tricuspid annular MPI is a reliable index for identifying a culprit lesion (>1.06 predicts culprit over LCX

Evaluating right ventricular dysfunction, pulmonary artery systolic pressure (PASP), and exercise tolerance is critical in patients with systemic lupus erythematosus (SLE) because of the high mortality rate in such patients with pulmonary arterial hypertension (PAH). The aim of this study was to use the flow propagation velocity (FPV) of early diastolic tricuspid inflow to evaluate exercise tolerance and PAH severity and to predict readmission in patients with SLE.A total of 66 patients with SLE with or without PAH and 30 healthy control subjects were enrolled. Controls were age-matched to patients with SLE and without PAH. All patients completed the 6-minute walking distance (6MWD) test and underwent standard echocardiography. Tricuspid FPV was measured in the modified parasternal short-axis view using the color M-mode technique. PAH was defined as PASP35 mm Hg using the tricuspid regurgitant method.Patients with SLE and PAH had significantly lower tricuspid FPVs and 6MWDs than patients in the other 2 groups (both P values.001). Tricuspid FPV was well correlated with 6MWD (r = 0.748, P.001). In multivariate analysis, right atrial pressure was the only independent factor affecting tricuspid FPV (R(2) = 0.394, P.001), and 6MWD was affected only by tricuspid FPV and PASP (R(2) = 0.629, P.001). Patients with SLE who had been readmitted had lower tricuspid FPVs than those who had not (P = .035). Furthermore, FPVor = 35.4 cm/s predicted 6MWDor = 350 m and a lower 1-year readmission rate with good sensitivity and specificity.The tricuspid FPV technique provides a simple method for predicting exercise tolerance, the severity of PAH, and readmission among patients with SLE.

Background— We used diffusion-tensor cardiac MR to investigate myocardial microstructure changes, including tissue integrity (mean diffusivity [MD], fractional anisotropy) and fiber architecture (helix angles) in patients with recent myocardial infarction (MI). This study aimed to investigate the sequential changes of myocardial microstructure and its relationships with changes of macrostructure and function of the left ventricle post-MI. Methods and Results— Seventeen patients (age, 55.1�11.5 years; all men) participated in the follow-up study. Diffusion-tensor cardiac MR, cine gradient echo for left ventricle function, and late gadolinium enhancement for viability were measured from recent to chronic MI (median interval, 191 days). When compared with the remote zone, the infarct-adjacent zone showed overall increase of MD (2-way MANOVA, F 1,16 =36.3; P 1,16 =5.8; P =0.029), and decrease of mean helix angles (F 1,16 =62.0; P 1,16 =22.6; P 1,16 =7.8; P =0.013). Multiple linear regression showed that the improvement of wall thickening in the infarct-adjacent zone correlated with sequential decrease of MD in the infarct-adjacent zone ( r =−0.70; P =0.002) and increase of mean helix angles (ie, more right-handed helical myofiber reorientation, predominantly subendocardial location) in the remote zone ( r =0.60; P =0.011). Likewise, wall thickening in the remote zone correlated with MD in the remote zone ( r =−0.72; P =0.001) and mean helix angles in the infarct-adjacent zone ( r =0.72; P =0.001). Conclusion— Diffusion-tensor cardiac MR suggests that sequential zonal improvement of tissue integrity and fiber architecture remodeling both associate with sequential recovery of zonal wall thickening of the left ventricle from recent to chronic MI.

The aim of this study was to investigate the potential relationships between the carotid intima media thickness (carotid IMT), high sensitive C-reactive protein (hsCRP), and cholesterol burden in heterozygous familial hypercholesterolemia (FH) subjects. Thirty-two genetically-verified heterozygous patients with FH and 34 healthy controls were recruited into our study in Taiwan. We measured conventional risk factors, hsCRP, and carotid IMT of study subjects. The cholesterol-year score was used to estimate the lifetime cholesterol burden. Subjects with heterozygous FH had significantly elevated total cholesterol, elevated low-density lipoprotein cholesterol, and increased carotid IMT compared with control subjects. Carotid IMT correlated well with the cholesterol-year score. In patients with FH, univariate analysis showed that hsCRP was highly correlated with carotid IMT. Multiple linear regression analysis indicated that hsCRP was the only independent predictor of carotid IMT in patients with FH. In conclusion, patients with heterozygous FH had significantly higher carotid IMT and the level of hsCRP was independently associated with atherosclerotic progression. (R: 0.639, R(2): 0.408, p0.001).

Background Recent studies revealed that multidetector computed tomography late enhancement (MDCT-LE) is a reliable technique for detecting necrotic and scarred myocardial tissue. The aims of the study were to identify infarcted myocardium using MDCT-LE protocol in patients after myocardial infarction (MI) and assess viability in resting wall motion abnormalities. Methods One hundred one patients with previous MI (62 ± 13 years, 1-6 months after MI) underwent MDCT-LE (15 minutes after contrast medium administration), rest-redistribution thallium single photon emission computed tomography (Tl-SPECT), and dobutamine echocardiography (DbE). In a 17-segment model, infarcted myocardium detected by MDCT-LE was categorized as none, 1%-25%, 26%-50%, 51%-75%, or >75% segmental extent and was compared with decreased uptake of Tl-SPECT and contractile function by DbE on per patient and segmental basis in a blinded fashion. Results By per patient analysis, MDCT-LE identified the presence of infarcted myocardium in 97 patients (96%), and Tl-SPECT decreased uptake in 88 patients (87%), (P = .02). By per segment analysis, the concordance for detecting infarcted myocardium was good (κ value = 0.792). In segments with resting wall motion abnormalities (N = 486), there was moderate concordance in assessing viability (κ value between MDCT and Tl-SPECT = 0.555, MDCT and DbE = 0.498, Tl-SPECT and DbE = 0.478) with predefined MDCT-LE threshold of 50% segmental extent. Among segments with MDCT-LE >75% segmental extent, the proportion designated nonviable by Tl-SPECT and DbE reached 87.8% and 92.2%, respectively. Conclusions Multidetector computed tomography late enhancement is accurate in identifying the presence and extent of infarcted myocardium. Its segmental extent has good correlation with the magnitude of thallium decreased uptake and can predict contractile reserve. Multidetector computed tomography late enhancement can be an alternative to assess viability.

The objective of this study was to develop tissue Doppler parameters that could be used to differentiate right ventricular (RV) volume overload from RV pressure overload. The RV-pressure-overload group consisted of 40 patients with severe pulmonary hypertension, and the RV-volume-overload group consisted of 40 patients who had an atrial septal defect without evidence of right-to-left shunt, significant pulmonary hypertension, or Eisenmenger's complex. Another 40 healthy subjects were enrolled and served as a control group. Routine echocardiography and tissue Doppler imaging were performed. RV myocardial performance index was determined based on data collected during tissue Doppler imaging over the lateral tricuspid annulus. In patients with RV pressure overload, tissue Doppler parameters showed characteristically lower systolic velocity over the tricuspid annulus (RV myocardial systolic wave [Sm]) and longer isovolumic relaxation time (RV-IVRT). Nevertheless, in patients with RV volume overload, RV-Sm increased significantly, but early-diastolic velocity over tricuspid annulus was relatively low. In conclusion, RV-MPI, RV-Sm/early-diastolic velocity over tricuspid annulus, and RV-IVRT/RV-Sm were all useful to differentiate RV pressure overload from volume overload, although RV-IVRT/RV-Sm was the best parameter, with excellent sensitivity and specificity.

Background Accurate, non-invasive characterization of culprit lesions in patients after acute myocardial infarction (AMI) remains challenging. In this prospective study, multidetector row computed tomography (MDCT) is used to assess culprit and active complex lesions in patients early after AMI. Methods and Results We enrolled 103 patients with first non ST-elevation AMI who underwent 64-slices MDCT and conventional coronary angiography (CCAG). The definition of culprit lesion, stable non-culprit lesions and non-culprit active complex lesions was based on the findings of CCAG. The lesions were analyzed with MDCT data. In culprit lesions (n=103), luminal artery stenosis, remodeling index, plaque area and burden were significantly higher than non-culprit lesions (n=129). Multivariate discriminant analysis showed that MDCT density could discriminate culprit from non-culprit lesions. Receiver-operator characteristic curve analysis identified the optimal cutoff value of lesion density for discrimination between culprit and non-culprit lesion as 49.6 Hounsfield units (HU); this value was associated with a sensitivity, specificity and accuracy of 88.4%, 87.4%, and 87.9%, respectively. The MDCT in the stable non-culprit lesions (81.8±15.5 HU) was significantly higher than that in culprit lesions or non-culprit active complex lesions (33.2±13.8 and 48.3±15.7 HU, p

Shear stress protects endothelium from a variety of risk factors for vascular disease. Here, we demonstrate a novel mechanism whereby shear stress inhibited reactive oxygen species (ROS)-triggered signaling cascades in endothelial cells. Stimulation of bovine aortic endothelial cells (BAECs) with H(2)O(2) induced a 3.07-fold increase in p66(Shc) phosphorylation. This response was fully blocked by pretreatment of cells with specific JNK but not p38 or ERK MAP kinase inhibitor. Further study showed that knocking down of apoptosis signal-regulating kinase 1 (ASK1) by siRNA transfection in cells dramatically inhibited phosphorylation of JNK and p66(Shc) elicited by H(2)O(2). Pre-perfusion of BAECs cultured in silastic tubes with laminar flow generated by a servo-pump system for 30 min also significantly suppressed H(2)O(2)-induced phosphorylation of p66(Shc). This was accompanied by quantitatively similar inhibition of ASK1 and JNK phosphorylation and activation. These results suggested that shear stress protects endothelium against oxidant stress by suppression of ASK1-JNK-mediated p66(Shc) phosphorylation.

Introduction: Pulmonary arterial hypertension (PAH) is a progressive disorder characterized by the increased vascular resistance and the remodeling of pulmonary arteries. Evidences of accumulated inflammatory cells in the lung suggested that chronic inflammation might play a role in PAH. Regenerative cell therapy emerged as a potential treatment for PAH through regulating the host’s immune response. Hypothesis: The secretome of induced pluripotent stem cells (iPSCs) was investigated for their preventive and therapeutic effects in the pathogenesis of monocrotaline (MCT)-induced PAH rat. Methods: PAH was developed by the subcutaneous injection of MCT in rats. The conditioned medium of cultured iPSCs (iPSC CM) was applied daily in prevention (an hour after MCT injection) or reversal (14 days after MCT injection) by IP injection throughout the full 28 days of experiment. The effects of iPSC CM were interpreted by the analyses of systolic pressure (RVSP) and the hypertrophy index of right ventricle, also the regulation of inflammation in lung and the underlying mechanism. Results: Both prevention and reversal, the hemodynamic values of RVSP and hypertrophy index were significantly improved in MCT-induced PAH rats after iPSC CM treatment. Attenuated expression of pro-inflammatory M1 macrophage markers was observed in either the lung of MCT-induced PAH rats or in co-cultured human M1 macrophages after iPSC CM treatment. To investigate the potential molecules secreted by iPSCs into iPSC CM, two major ingredients, named α1-antitrypsin and feutin-a, were identified by protein mass spectrometry and confirmed by western blotting with specific antibodies. Both components were mentioned to be involved in the anti-inflammatory effects observed in various lung diseases. Conclusions: In this study, iPSC CM represented therapeutic benefits on MCT-induced PAH rats though attenuating inflammation. Molecules exhibit anti-inflammatory potential existed in the iPSC CM, such as α1-antitrypsin and feutin-a, might hold the promise as new therapeutics of regenerative cell therapy via paracrine mechanism.

The power of left atrial (LA) parameters for predicting left ventricular (LV) filling pressure and adverse events in acute heart failure (HF) with severe LV dysfunction, either sinus rhythm or atrial fibrillation (AF), is not fully understood.Echocardiography was performed in 141 patients with acute decompensated congestive HF and LV ejection fraction35%, including 42 with permanent AF. The LA expansion index was calculated as (Volmax - Volmin) × 100%/Volmin, where Volmax was defined as maximal and Volmin as minimal LA volume. Of 141 patients, invasive LV filling pressures within 12 hours of LA expansion index measurement were available in 109. The end points were 3-year frequencies of HF hospitalization and all-cause mortality. Over a median follow-up of 3.1 years, 74 participants (52.5%) reached the end points (sinus vs AF group: 48.5% vs 61.9%, respectively; P = .047). Multivariate analysis revealed that adverse events of both groups were only independently associated with age and LA expansion index. Rates of adverse events were proportional to LA expansion index. There was a good logarithmic relationship between LA expansion index and LV filling pressure, regardless of presence or absence of AF.LV filling pressure can be estimated well by LA expansion index, with or without AF. The LA expansion index predicts adverse events in HF patients with severe systolic dysfunction. (ClinicalTrials.gov number: NCT01307722).

AIM Whole exome sequencing (WES) is a recently developed method for discovering rare mutations associated with hereditary disorders. However, the feasibility and utilization of this method in identifying familial hypertriglyceridemia is not well known. The purpose of the study was to identify the genetic locus that causes hypertriglyceridemia and assess its prevalence in Taiwanese subjects with hypertriglyceridemia. METHODS We performed WES among two individuals with hypertriglyceridemia and one control subject in an index family (22 members). Based on the WES findings, we extended the study to genotype 65 unrelated adult index patients with a fasting serum triglyceride level of ＞ 500 mg/dL and 125 normal controls using polymerase chain reaction. RESULTS Using WES alignment, variant calling and annotation, 15 presumptive causal variants were initially identified, including 13 cases by the autosomal dominant model and two cases by the autosomal recessive model. Only APOA5 c.553 G ＞ T (rs2075291), resulting in the amino acid mutation Gly185Cys, co-segregated well with hypertriglyceridemia in terms of autosomal recessive inheritance (homozygote TT: mean triglyceride level: 1,071 mg/dL vs non TT (GT and GG): mean triglyceride level: 118 mg/dL; p ＜ 0.001) in the index family. In the unrelated cohorts, the frequency of the TT genotype of rs2075291 was 12.3% in the hypertriglyceridemic group; however, no TT genotype was found in the control group. CONCLUSIONS Our results demonstrate that WES is feasible for identifying the genetic locus that causes hypertriglyceridemia. The TT genotype of APOA5 c.553G ＞ T acts as an important indicator of hypertriglyceridemia in patients in Taiwan.

The slope of the preload recruitable stroke work relationship (Mw) is a highly linear, load-insensitive contractile index. To investigate whether Mwcan be determined from a single steady-state beat, 45 patients were studied during cardiac catheterization. Single-beat Mw(SBMw) was calculated directly from the baseline stroke work and baseline left ventricular (LV) end-diastolic volume (EDVB), and the volume-axis intercept (Vw) was estimated as k × EDVB+ ( k − 1) × LVwall, where k is the ratio of the epicardial shell volumes corresponding to Vwand EDVBand LVwallis the wall volume. The mean of individual k values was 0.72 ± 0.04, which correlated with LV mass significantly ( r = 0.60, P < 0.001). SBMwcalculated from a constant k of 0.7 predicted Mwwell ( r = 0.88, P < 0.0001), and the prediction improved slightly when k was estimated from individual LV mass ( r = 0.93, P < 0.0001). Subgroup analyses revealed that the single-beat technique also worked in patients with small or large LV mass or volume or with regional wall motion abnormalities. The absolute change in SBMwafter dobutamine infusion also correlated with that in Mw. In conclusion, Mwcan be estimated from a steady-state beat without alteration of preload.

The left ventricular (LV) end-systolic pressure-volume relation (ESPVR) is a load-insensitive method for evaluating LV contractility, which needs invasive measurement. Some noninvasive methods substitute peak aortic pressure (Ps) for end-systolic LV pressure by assuming there is no difference between these pressures. However, this assumption has not been directly validated. With conductance catheter and dual micromanometers, ESPVRs and the slope (EesLv) were constructed from simultaneous LV pressures (LVP) and volumes, aortic pressures (AOP) and LV volumes (Ees(AO)), and Ps and LV end-ejection volumes (VEE) (Ees(PP-EEV)) during preload reduction in 50 subjects. The ratio of steady-state P(s) over V(EE) (P(S)/V(EE)) was also checked. AOP and LVP displayed differences of 11 +/- 6 and -30 +/- 12 mm Hg at the onset and end-ejection, respectively, and -2 +/- 4 mm Hg at end-systole. Ees(AO) and Ees(LV) were nearly identical: Ees(AO) = 0.97 x Ees(LV) + 0.05, r2 = 0.99. Ees(PP-EEV) correlated with EesLV (EesPP-EEV = 0.57 x EesLV + 0.61, r2 = 0.46) but with much more scatter. Ps/V(EE) correlated worst with Ees(LV). Central AOP can be substituted for LVP to derive EesLV. Other estimation methods yield weaker and poor correlations to directly measured Ees.

Aims Since natriuretic peptide and troponin are associated with renal prognosis and left atrial (LA) parameters are indicators of subclinical cardiovascular abnormalities, this study investigated whether LA expansion index can predict renal decline. Methods and results This study analysed 733 (69% male) non-diabetic patients with sinus rhythm, preserved systolic function, and estimated glomerular filtration rate (eGFR) higher than 60 mL/min/1.73 m2. In all patients, echocardiograms were performed and LA expansion index was calculated. Renal function was evaluated annually. The endpoint was a downhill trend in renal function with a final eGFR of 3 mL/min/1.73 m2. The median follow-up time was 5.2 years, and 57 patients (7.8%) had renal function declines (19 had rapid renal declines, and 38 had incidental renal dysfunction). Events were associated with left ventricular mass index, LA expansion index, and heart failure during the follow-up period. The hazard ratio was 1.426 (95% confidence interval, 1.276–1.671; P

Background Hypertrophic cardiomyopathy (HCM) is a common genetic cardiac disorder associated with sudden death, heart failure, and stroke. The aim of the present study was to evaluate the prevalence and types of mutations in symptomatic patients with HCM in Taiwan. Methods Thirty-eight HCM index patients (mean age 60 ± 16 years) underwent systematic mutation screening of eight sarcomeric genes: β-myosin heavy chain ( MYH7 ), myosin-binding protein C ( MYBPC3 ), troponin T ( TNNT2 ), troponin I ( TNNI3 ), myosin ventricular regulatory light chain 2 ( MYL2 ), myosin ventricular essential light chain 1 ( MYL3 ), α-tropomyosin ( TPM1 ), and cardiac α-actin ( ACTC ), using direct DNA sequencing. In silico programs predicted damaging amino acids. In the positive families, genotype–phenotype correlation studies were done. Results Overall, 13 mutations were identified in 13 index patients (34.2%). The three most frequently mutated genes were MYH7 , MYBPC3 , and TNNT2 . One patient carried double mutations. Five mutations ( MYH7 R147S; MYBPC3 R597Q; MYBPC3 W1007R; TNNI3 E124Q; MYL3 R63C) were novel; all were missense mutations. Analysis using in silico tools showed near consensus to classify these five novel mutations as pathological. Family pedigree analysis showed the presence of cosegregation in at least two affected members in each proband family, but incomplete penetrance in young family members with a positive genotype. Conclusions We identified 13 HCM pedigrees, including 5 carrying novel mutations and 1 with a double mutation. The three most commonly mutated genes were MYH7 , MYBPC3 , and TNNT2 . These results, together with genetic counseling, could lead to earlier diagnosis and better management of family members at risk of HCM.

Objectives The goal of this study was to develop and validate a method to estimate left ventricular end-systolic elastance (Ees) in humans from noninvasive single-beat parameters. Background Left ventricular end-systolic elastance is a major determinant of cardiac systolic function and ventricular-arterial interaction. However, its use in heart failure assessment and management is limited by lack of a simple means to measure it noninvasively. This study presents a new noninvasive method and validates it against invasively measured Ees. Methods Left ventricular end-systolic elastance was calculated by a modified single-beat method employing systolic (Ps) and diastolic (Pd) arm-cuff pressures, echo-Doppler stroke volume (SV), echo-derived ejection fraction (EF) and an estimated normalized ventricular elastance at arterial end-diastole (ENd): Ees(sb)= [Pd− (ENd(est)× Ps× 0.9)[/(ENd(est)× SV). The ENdwas estimated from a group-averaged value adjusted for individual contractile/loading effects; Ees(sb)estimates were compared with invasively measured values in 43 patients with varying cardiovascular disorders, with additional data recorded after inotropic stimulation (n = 18, dobutamine 5 to 10 μg/kg per min). Investigators performing noninvasive analysis were blinded to the invasive results. Results Combined baseline and dobutamine-stimulated Eesranged 0.4 to 8.4 mm Hg/ml and was well predicted by Ees(sb)over the full range: E es = 0.86 × E es ( sb )+ 0.40 (r = 0.91, SEE = 0.64, p < 0.00001, n = 72). Absolute change in Ees(sb)before and after dobutamine also correlated well with invasive measures: E es ( sb ): ΔE es = 0.86 × ΔE es ( sb )+ 0.67 (r = 0.88, p < 0.00001). Repeated measures of Ees(sb)over two months in a separate group of patients (n = 7) yielded a coefficient of variation of 20.3 ± 6%. Conclusions The Eescan be reliably estimated from simple noninvasive measurements. This approach should broaden the clinical applicability of this useful parameter for assessing systolic function, therapeutic response and ventricular-arterial interaction.

Little information is available concerning the effect of late coronary stenting in patients with recent myocardial infarction, especially long-term results. We retrospectively reviewed our results of 57 stent placements in 52 consecutive patients who received stents at an infarct-related lesion 24 hr to 30 days after an acute myocardial infarctions (median, 14 days). The average age was 67 years; 90% were male. Two patients who suffered from acute stent thrombosis received revascularization again and two early deaths were due to refractory cardiogenic shock before discharge. Mean patient clinical follow-up was 18.3 ± 6.5 months. There were 1 subacute stent thrombosis, 1 cardiogenic death, and 10 patients (20.8%) in total suffering from angina class II to IV. Angiographic follow-up was performed in 36 patients (80%) at a mean of 7.5 ± 3.1 months. Of these 36 patients, only 1 (3% of the total population undergoing follow-up angiography) had reocclusion at follow-up, but restenosis existed in 18 patients (50%). We conclude that there is still relatively high incidence of angiographic recurrence that is often silent in long-term follow-up, though the long-term result of late stenting in recent MI is low incidence of reocclusion. Cathet. Cardiovasc. Intervent. 47:423–429, 1999. © 1999 Wiley-Liss, Inc.

Epicardial adipose tissue (EAT) is considered to play a role in the pathogenesis of coronary atherosclerosis. However, whether total EAT volume or location-specific EAT thickness may be a better predictor of obstructive coronary artery disease (CAD) is inconclusive. We investigated whether the total volume or location-specific thickness of EAT measured on computed tomography (CT) could be a useful marker of CAD on top of clinical risk factors and Agatston score. Two hundred eight consecutive subjects with clinical suspicion of CAD receiving coronary arterial calcium (CAC)-scoring CT and CT coronary angiography were retrospectively divided into 2 groups: an obstructive CAD group (n = 97) and a nonobstructive CAD group (n = 111). Total EAT volume and EAT thicknesses at different locations were measured on CAC-scoring CT. Left atrioventricular groove (AVG) EAT thickness was the sole EAT measurement that showed association with increasing number of vessels exhibiting ≥50% stenosis (p for trend0.001). Logistic regression showed that left AVG EAT thickness was the most important EAT predictor of obstructive CAD (odds ratio 1.16, 95% confidence interval 1.04 to 1.29, p = 0.006; optimal threshold ≥15 mm, odds ratio 4.62, 95% confidence interval 2.24 to 9.56, p0.001). Adding left AVG EAT thickness on top of clinical risk factors plus Agatston score improved prediction of obstructive CAD (area under the curve from 0.848 to 0.912, p = 0.002). In conclusion, excessive left AVG EAT adiposity is an important risk factor for obstructive CAD, independent of clinical risk factors and Agatston score. However, further trials are needed in investigation of combined assessment of location-specific EAT thickness and Agatston score on CAC scan as to whether this biomarker could improve CAD risk stratification in the general population.

Background Sixty-four and more-slice cardiac CT provides rapid and high quality coronary CT angiography for the majority of clinical needs of non-invasive evaluation of coronary artery. However, the recent advance of whole-heart coronary MRA has been able to provide high-quality of coronary MRA and also myocardial image in a reasonable scan time. The purpose of this study was to evaluate the clinical indication and the feasibility of coronary MRA with 32-channel coil at 3T scanner.

Pulmonary arterial hypertension (PAH) is characterized by progressive increases in vascular resistance and the remodeling of pulmonary arteries. The accumulation of inflammatory cells in the lung and elevated levels of inflammatory cytokines in the bloodstream suggest that inflammation may play a role in PAH. In this study, the benefits of induced pluripotent stem cells (iPSCs) and iPSC-conditioned medium (iPSC CM) were explored in monocrotaline (MCT)-induced PAH rats. We demonstrated that both iPSCs and iPSC CM significantly reduced the right ventricular systolic pressure and ameliorated the hypertrophy of the right ventricle in MCT-induced PAH rats in models of both disease prevention and disease reversal. In the prevention of MCT-induced PAH, iPSC-based therapy led to the decreased accumulation of inflammatory cells and down-regulated the expression of the IL-1β, IL-6, IL-12α, IL-12β, IL-23 and IFNγ genes in lung specimens, which implied that iPSC-based therapy may be involved in the regulation of inflammation. NF-κB signaling is essential to the inflammatory cascade, which is activated via the phosphorylation of the NF-κB molecule. Using the chemical inhibitor specifically blocked the phosphorylation of NF-κB, and in vitro assays of cultured human M1 macrophages implied that the anti-inflammation effect of iPSC-based therapy may contribute to the disturbance of NF-κB activation. Here, we showed that iPSC-based therapy could restore the hemodynamic function of right ventricle with benefits for preventing the ongoing inflammation in the lungs of MCT-induced PAH rats by regulating NF-κB phosphorylation.

Mitral regurgitation (MR) of even mild severity affects the prognosis of patients with acute coronary syndrome (ACS). The present study retrospectively analyzed 1,142 patients with ACS and MR of varying severity. Of the 95 patients with severe MR, 57 (60%) underwent primary percutaneous coronary intervention only and 38 (40%) underwent coronary artery bypass grafting (CABG) and mitral valve replacement (MVR). The severity of MR was significantly associated with the risk of heart failure but not with in-hospital or long-term mortality. In patients with severe MR, in-hospital mortality was no greater in those treated with CABG and MVR than in those treated with percutaneous coronary intervention alone. However, the incidence of long-term hard events (heart failure and all-cause mortality) was lower in those who had received the combined treatment. Multivariate analysis showed that, compared to percutaneous coronary intervention alone, CABG combined with MVR at the acute phase of ACS resulted in a significantly improved prognosis (odds ratio 0.172, 95% confidence interval 0.046 to 0.649, p = 0.009), even after adjusting for age, left ventricular filling pressure, and ejection fraction. In conclusion, the severity of MR in patients with ACS is associated with long-term heart failure events. Even at the acute phase of ACS, CABG combined with MVR results in an acceptable in-hospital mortality rate. The combined strategy also reduced the long-term hard events.

The purpose of the study was to investigate dual-phase MDCT for assessing obstructive lesions and the extent and severity of the subtending myocardium at risk in patients presenting with chest pain syndromes 9 or more months after having undergone revascularization for the treatment of ST-segment elevation myocardial infarction (STEMI).Dual-phase 64-MDCT was performed on 135 patients with recurring chest symptoms 9 months or more after revascularization (mean ± SD, 23 ± 11 months after index invasive angiogram for treatment of STEMI). Obstructive lesions (≥ 50% stenosis) were detected by MDCT angiography and the extent of myocardium at risk was detected by delayed phase 3D myocardium maps. A myocardium at-risk score based on MDCT findings was defined as the extent of myocardium at risk governed by the coronary lesion and weighted by lesion severity. Results were compared with stress-redistribution (201)Tl-SPECT and invasive angiography.In restenotic, new, progressive, and previously obstructive lesions that are not currently progressive, analysis of assessable segments (1966/2025, 97.1%) obtained true-positive detection rates of 88.1%, 88.6%, 82.9%, and 100%, respectively; false-negative detection rates were 5.3%, 1.6%, 2.9%, and 8.8%. In 124 patients (91.9%) in whom all segments were assessable, the MDCT-based myocardium at-risk score correlated with the SPECT-based summed difference score (SDS) (r = 0.841, p0.001). For detecting SPECT-based SDS ≥ 1 and SDS3, areas under the receiver operating characteristic curve for the MDCT-based myocardium at-risk score were 0.874 (95% CI, 0.805-0.942) and 0.938 (95% CI, 0.895-0.981), with optimal cutoff values of 2.68 and 5.01, respectively.Dual-phase MDCT is useful in detecting different patterns of obstructive lesions and the extent of myocardium at risk as an alternative for therapeutic planning in patients presenting with late symptoms after treatment for acute myocardial infarction.

Familial hypercholesterolemia (FH) is an autosomal dominant disease caused by mutations in low-density lipoprotein receptor (LDLR), apolipoprotein B-100 (APOB), and proprotein convertase subtilisin/kexin type 9 (PCSK9) genes. This study investigated FH patients carrying common mutations in Taiwan and compared them to FH southeastern Asians. Causal FH mutations were identified by exon-by-exon sequencing with/without multiplex ligation-dependent probe amplification among 208 Taiwanese with clinically diagnosed FH. Haplotype analyses among probands and family members were undertaken using TaqMan® Assays. Totally, LDLR mutations were found in 118 probands, consisting of 61 different loci, and APOB 10579C>T mutations in 12 probands. Three mutations (64delG, 1661C>T, and 2099A>G) were novel. LDLR 986G>A (13.1%), 1747C>T (10.8%), and APOB 10579C>T (9.2%) were common mutations with no differences in phenotypes. LDLR 1747C>T associated with one haplotype (CAAGCCCCATGG/(dTA)n-112nt); LDLR 986G>A with two. APOB 10579C>T associated with the same LDLR binding-domain pattern in Taiwanese and southeastern Asians. We concluded that LDLR 986G>A, 1747C>T and APOB 10579C>T are common mutations, with combined frequency of approximately 33%. The presence of different haplotypes associated with FH common mutations in Taiwan indicates multiple historical migrations, probable multiple recurrent origins from southern China, and haplotype homologies reflect the presence of common ancestors in southern China.

Atrial fibrillation (AF), a common complication after coronary artery bypass graft surgery (CABG), is associated with prolonged hospital stay. This prospective study assessed the accuracy of left atrial parameters and additional preoperative characteristics for predicting post-CABG AF and in-hospital mortality.A total of 197 patients without hemodynamic-significant valvular problems, who received isolated CABG, were enrolled. Echocardiography was performed before CABG.Compared with patients without post-CABG AF, those with post-CABG AF were older (71 vs 64 years, p0.0001), had a higher incidence of CABG during index hospitalization of acute myocardial infarction and preoperative respiratory failure requiring ventilator support, lower left ventricular ejection fraction (0.41 vs 0.48, p0.0001), lower left atrial expansion index (52.2% vs 93.3%, p0.0001), and higher left ventricular filling pressure (24.2 vs 19.1 mm Hg, p0.0001). Multivariate analysis of preoperative variables showed that independent predictors of AF included age (odds ratio [OR], 1.064; 95% confidence interval [CI], 1.022 to 1.107 per 1-year increase; p 0.002), maximal indexed left atrial volume (OR, 1.026; 95% CI, 1.002 to 1.051 per 1 mL/m2 increase; p 0.037) and left atrial expansion index (OR, 0.981; 95% CI, 0.962 to 0.998 per 1% increase; p 0.029). The left atrial expansion index was also significantly associated with in-hospital mortality (OR, 0.982; 95% CI, 0.951 to 0.996 per 1% increase; p 0.042). Incidence of post-CABG AF in patients with left atrial expansion index less than 120% progressively increased as left atrial expansion index decreased.Left atrial expansion index independently predicts post-CABG AF and in-hospital mortality.