Most of the pathophysiological actions of angiotensin II (Ang II) are mediated through the Ang II type 1 (AT₁) receptor, a member of the seven-transmembrane G protein-coupled receptor family. Essentially, AT₁ receptor signaling is beneficial for organismal survival and procreation, because it is crucial for normal organ development, and blood pressure and electrolyte homeostasis. On the other hand, AT₁ receptor signaling has detrimental effects, such as promoting various aging-related diseases that include cardiovascular diseases, diabetes, chronic kidney disease, dementia, osteoporosis, and cancer. Pharmacological or genetic blockade of AT₁ receptor signaling in rodents has been shown to prevent the progression of aging-related phenotypes and promote longevity. In this way, AT₁ receptor signaling exerts antagonistic and pleiotropic effects according to the ages and pathophysiological conditions. Here we review the pleiotropic effects of AT₁ receptor signaling in cardiovascular homeostasis and aging.

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Obesity has dramatically increased throughout the world, and has become one of the chief healthcare problems in many societies. Evidence has emerged that adipose tissue dysfunction associated with obesity is critically involved in the development of cardiovascular and metabolic disorders. In this review, we delineate the link between adipose tissue abnormalities and systemic metabolic dysfunction in patients with cardio-metabolic diseases and discuss the underlying mechanisms.

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We investigated the relationships between the ratio of serum n-3 polyunsaturated fatty acids (n-3PUFAs: eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]) to n-6PUFA (arachidonic acid [AA]) and the prevalence of coronary artery disease (CAD), and assessed the association of the ratio of serum n-3 to n-6 PUFAs with atherosclerosis-related markers.
This study was designed as a hospital-based cross-sectional study of 649 consecutive outpatients who had undergone regular examinations between April 2009 and October 2009. We divided the patients into 5 groups based on the quintiles of the EPA/AA ratio or quintiles of the DHA/AA ratio to determine independent factors for the prevalence of CAD.
In multivariate logistic regression analyses after adjustment for coronary risk factors and serum n-3PUFAs levels to minimize confounding factors to the extent possible because the serum levels of EPA and DHA showed a strong correlation (r = 0.812, P < 0.0001), the group with the highest EPA/AA ratio had a lower probability of CAD prevalence (odds ratio: 0.328, 95% confidence interval: 0.113 to 0.956, P = 0.041), but this was not true for the DHA/AA ratio. Multivariate analysis showed an increase in the EPA/AA ratio, but not in the DHA/AA ratio, was associated with effects on atherosclerosis-related markers, especially triglyceride-rich lipoproteins, high-density lipoprotein cholesterol (HDL-C) containing apolipoprotein A-1, and leukocyte count in an anti-atherogenic direction.
The results suggest a higher EPA/AA ratio, but not a higher DHA/AA ratio, might be associated with a lower prevalence of CAD and improvements of triglyceride metabolism and HDL metabolism, and systemic inflammation.

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Several studies have shown that various chemokines are more highly expressed in atherosclerotic plaques than in normal vessel walls. In the present study, we investigated the relationship between coronary atherosclerosis and noteworthy chemokines, including interferon-inducible protein of 10 kD (IP-10); monocyte chemoattractant protein 1 (MCP-1); regulated on activation, normal T-cell expressed and secreted (RANTES); and high-sensitivity C-reactive protein (hsCRP), an established marker of atherosclerotic disease. We studied 28 patients who underwent coronary angiography because of suspected coronary artery disease (CAD). CAD was defined as stenosis of more than 50% of the vessel diameter on coronary angiograms. Blood samples were obtained both from the aorta and the coronary sinus (CS) just before coronary angiography. Relative to CAD (−) patients, those who were CAD (+) tended to have higher plasma concentrations of IP-10 in the aorta, as well as significantly higher transcoronary concentration gradients of circulating IP-10. There were no significant differences between the two groups in aortic plasma concentrations or transcoronary concentration gradients of MCP-1, RANTES, and hsCRP. Furthermore, both the aortic plasma concentrations and transcoronary concentration gradients of IP-10 correlated with the Gensini score (r = 0.58 and r = 0.63, respectively, P < 0.01), while the plasma MCP-1, RANTES, and serum hsCRP concentrations did not. This study suggests that IP-10 is a good surrogate marker of coronary atherosclerosis.

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Late gadolinium enhancement magnetic resonance imaging (LGE-MRI) has been established as a modality to detect myocardial infarction (MI). However, the use of gadolinium contrast is limited in patients with advanced renal dysfunction. Although the signal intensity (SI) of infarct area assessed by cine MRI is low in some patients with prior MI, the prevalence and clinical significance of low SI has not been evaluated. The aim of this study was to evaluate how low SI assessed by cine MRI may relate to the myocardial viability in patients with prior MI. Fifty patients with prior MI underwent both cine MRI and LGE-MRI. The left ventricle was divided into 17 segments. The presence of low SI and the wall motion score (WMS) of each segment were assessed by cine MRI. The transmural extent of infarction was evaluated by LGE-MRI. LGE was detected in 329 of all 850 segments (39%). The low SI assessed by cine MRI was detected in 105 of 329 segments with LGE (32%). All segments with low SI had LGE. Of all 329 segments with LGE, the segments with low SI showed greater transmural extent of infarction (78 [72 - 84] % versus 53 [38 - 72] %, P < 0.01), thinner wall (4.0[3.1 - 4.8] mm versus 6.5 [5.2 - 8.1] mm, P < 0.01), and higher WMS (4.0 [4.0 - 4.0] versus 2.0 [2.0 - 3.0], P < 0.01). The low SI assessed by cine MRI may be effective for detecting poorly viable myocardium in patients with prior MI.

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Ezetimibe has been reported to provide significant incremental reduction in low-density-lipoprotein cholesterol (LDL-C) when added to a statin; however, its effect on coronary atherosclerosis has not yet been evaluated in detail. The aim of this study was to investigate the add-on effect of ezetimibe to a statin on coronary atherosclerosis evaluated by intravascular ultrasound (IVUS).
In this prospective randomized open-label study, a total of 51 patients with stable coronary artery disease (CAD) requiring percutaneous coronary intervention (PCI) were enrolled, and assigned to a combination group (n = 26, rosuvastatin 5 mg/day + ezetimibe 10 mg/day) or a monotherapy group (n = 25, rosuvastatin 5 mg/day). Volumetric IVUS analyses were performed at baseline and 6 months after the treatment for a non-PCI site. LDL-C level was significantly reduced in the combination group (-55.8%) versus that in the monotherapy group (-36.8%; P = 0.004). The percent change in plaque volume (PV), the primary endpoint, appeared to decrease more effectively in the combination group compared with the monotherapy group (-13.2% versus -3.1%, respectively, P = 0.050). Moreover, there was a significant group × time interaction in the effects of the two treatments on PV (P = 0.021), indicating the regressive effect of the combination therapy on PV was greater than that of monotherapy for subtly different values of baseline PV in the two treatment groups. Moreover, percent change in PV showed positive correlations with percent change of LDL-C (r = 0.384, P = 0.015).
Intensive lipid-lowering therapy with ezetimibe added to usual-dose statin may provide significant incremental reduction in coronary plaques compared with usual-dose statin monotherapy.

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The discriminative ability of the widely used CHADS2 and CHA2DS2-VASc scores for risk stratification of thromboembolism in atrial fibrillation (AF) is known as modest. Some echocardiographic parameters are known risk factors for thromboembolism. This study aimed to evaluate whether combining echocardiographic parameters with CHADS2 and CHA2DS2-VASc scores can improve the predictive power for embolic risk in AF.
A total of 526 (F/M = 83/433, mean age = 57.6 ± 10.7 years) patients with non-valvular AF were enrolled. The predictability for left atrial (LA) thrombus or dense spontaneous echo contrast (SEC) using clinical scores or echocardiographic parameters or combining clinical scores and echocardiographic parameters was calculated and compared.
Dense SEC or thrombus was present in 51 patients. The predicting powers of the CHADS2 and CHADS2-VASc scores for the presence of dense SEC or thrombus were modest (c-statistics 0.65 and 0.68, respectively, 95% confidence interval [CI] 0.61-0.69 and 0.64-0.74, respectively, both P < 0.001). Impaired LA function was the most descriptive predictor for the presence of thrombus or dense SEC among echocardiographic parameters. Combining impaired LA function (LA emptying fraction < 30%) with the CHADS2 and CHA2DS2-VASc scores showed the improvement of predictive power in detecting dense SEC or thrombus (c-statistics 0.78 and 95% CI 0.74-0.81 and c-statistics 0.77 and 95% CI 0.73-0.81, respectively, both P < 0.001).
Adding LA functional markers to the CHADS2 or CHA2DS2-VASc score improved the predictive value of the presence of thrombus or dense SEC. In clinical situations, anticoagulation should be considered to prevent embolism in patients with low-risk scores when they have LA dysfunction.

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We sought to evaluate the impact of biventricular (BiV) pacing with ventricular fusion by intrinsic atrioventricular nodal (AVN) conduction (BiV + intrinsic pacing) on clinical outcomes in patients with chronic heart failure (CHF) receiving cardiac resynchronization therapy (CRT).
A total of 44 patients were randomized to receive either BiV or BiV + intrinsic pacing for one month. Echocardiographic optimization was performed for the BiV pacing mode, while the BiV + intrinsic pacing mode was achieved by titrating AV delay under electrocardiography (ECG) monitoring. Symptoms, quality of life, ECG, echocardiography, and cardiovascular events were recorded at baseline and the end of the follow-up for each pacing mode.
Patients undergoing BiV + intrinsic pacing mode had shorter QRS duration compared to those with conventional BiV pacing (118.4 ± 21.6 ms versus 146.4 ± 5.3 ms, P < 0.0001). Also, these patients had improved echocardiographic left ventricular fractional shortening (LVFS) (17.4 ± 5.9 versus 15.7 ± 4.9, P = 0.019), higher left ventricular ejection fraction (LVEF) (35.5 ± 9.7 versus 32.7 ± 9.7, P = 0.048), longer 6-minute walk test (6MWT) (372.5 ± 80.9 m versus 328.7 ± 108.9 m, P = 0.0001), and better Minnesota Living with Heart Failure Questionnaire (MLHFQ) scores (12.5 ± 6.6 versus 18.2 ± 12.3, P = 0.0001).
Treating CHF patients with BiV+intrinsic pacing resulted in improved cardiac function and quality of life. BiV + intrinsic pacing can be used in CHF patients with sinus rhythm and normal AV nodal conduction to improve CRT efficacy.

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The aim of our study was to determine the characteristics and value of plasma von Willebrand factor antigen (vWF: Ag) levels after off-pump coronary artery bypass grafting (OPCAB) surgery in predicting the risk of cardiovascular ischemic events.
A retrospective cohort analysis of 203 non-ST-segment elevation myocardial infarction patients was performed. Patients were divided into a poor recovery group and a stable condition group according to whether ischemic events occurred or not within 90 days postoperatively. The level of vWF: Ag was detected using a blood coagulation analyzer. SPSS17.0 statistical software was used for data analysis. The Friedman rank sum test and Mann-Whitney U test were used for intra-group and inter-group data analysis, respectively. The diagnostic performance of vWF: Ag was evaluated by receiver operating characteristic (ROC) curve analysis.
Plasma vWF: Ag levels at postoperative days 14, 30, 60, and 90 in the poor recovery group were significantly higher than those at the corresponding time points in the stable group. The area under the ROC curve in diagnosing adverse events was 0.927 (95% CI: 0.867~0.987) with 96.6% sensitivity and 58.6% specificity when the cut-off value of vWF: Ag was 233% at postoperative day 30.
The changing characteristics of plasma vWF: Ag sensitively reflect the degree of vascular endothelial injury of OP-CAB patients and might serve as a surrogate marker of the adverse event of non-ST segment elevation myocardial infarction.

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Although we recently demonstrated that opening of a native aortic valve (AV) after left ventricular assist device (LVAD) implantation is a sufficient condition to prevent development of aortic insufficiency (AI), its preoperative predictors remain unknown. Data were obtained from 58 patients who had been treated with continuous flow LVAD for ≥ 6 months at our institute between 2006 and 2014. Opening of native AV was accomplished in 21 patients (36%) at postoperative 6 months. Uni/Multivariate logistic regression analyses demonstrated that a preoperative lower cumulative dose of β-blocker was the only independent predictor for postoperative opening of native AV (P = 0.020, OR 0.905) at the cutoff level of 4.5g (equivalent dose of carvedilol), calculated by an ROC analysis. Prevalence of native AV opening was increased gradually along with improvement of LV ejection fraction only in patients with preoperative insufficient β-blocker treatment during postoperative 6 months (P < 0.05 for both). Patients with opening of native AV had higher exercise capacity and a lower re-admission rate than those with closed native AV during 2-year LVAD support (5% versus 44%, P < 0.05). Opening of native AV during LVAD support is profoundly associated with LV reverse remodeling especially in patients with insufficient preoperative β-blocker exposure probably due to their better responsiveness to combination therapy with β-blocker and LVAD. Patients who accomplished native AV opening can enjoy better exercise performance and avoid re-admission due to cardiovascular events.

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Although conventional cardiac troponin T (cTnT) and I (cTnI) markers have been reported to predict adverse outcome in dilated cardiomyopathy (DCM), the usefulness of a new-generation high-sensitivity assay of cardiac troponin T (hs-cTnT) compared with these conventional biomarkers is unclear.
We performed clinical evaluation including measurements of troponin markers in 54 patients with DCM under a clinically stable condition. At baseline, the serum concentration of hs-cTnT was 0.014 ± 0.016 ng/mL and 17 (31%) of the patients showed abnormal hs-cTnT values (> 0.014 ng/mL). During a mean follow-up period of 5.1 ± 1.6 years, there were 16 cardiac events: heart failure death in 6 patients, sudden cardiac death in 2 patients, and hospitalization for heart failure in 8 patients. Patients with abnormal hs-cTnT or abnormal cTnT (> 0.01 ng/mL) values had significantly more frequent cardiac events than did those with normal hs-cTnT or cTnT values. On the other hand, abnormal cTnI (> 0.03 ng/mL) value did not reach statistical significance for these adverse events. Multivariate analysis showed that only an abnormal hs-cTnT value was an independent predictor of all cardiac events (HR: 5.68, P = 0.003). When the patients were divided into 4 groups according to the degree of hs-cTnT levels, the clinical course was significantly worse in patients with higher hs-cTnT values.
These results suggest that the serum concentration of hs-cTnT provides better risk stratification in DCM patients.

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In this study, we evaluated the prognostic value of plasma galectin-3 levels in patients with coronary heart disease (CHD) and chronic heart failure (HF) and selected 261 CHD patients who were consecutively admitted to our hospital. The enrolled chronic HF patients included HF patients with preserved ejection fraction (HFpEF) and reduced ejection fraction (HFrEF). Patients without HF served as the control group. Galectin-3 and B-type natriuretic peptide (BNP) levels were determined and the primary endpoint was the composite of all-cause mortality and rehospitalization with 12-month follow-up. Plasma galectin-3 levels were higher in HF patients compared with non-HF patients (P < 0.001). Receiver operating characteristic (ROC) analyses for diagnosis of HF showed that galectin-3 had the greatest area under the curve (AUC) of 0.756 (P < 0.001), with an optimal cutoff of 10.8 ng/mL, yielding a sensitivity of 81.7% and a specificity of 61.7%. Follow-up ROC analyses of galectin-3 for outcome prediction showed an optimal cutoff of 17.8 ng/ mL, yielding a sensitivity of 97.3% and a specificity of 77.6%. Galectin-3 yielded an AUC of 0.899 (P < 0.001), whereas the AUC of BNP was 0.633 (P = 0.022). Galectin-3 led to an AUC of 0.931 (P < 0.001) for HFpEF and an AUC of 0.882 (P < 0.001) for HFrEF. Cox proportional hazards regression analysis revealed that galectin-3 was an independent prognostic predictor for chronic HF, especially for HFpEF patients (RR: 1.231, 95% CI: 1.066-1.442). In summary, plasma galectin-3 levels were increased in CHD HF patients and were an independent predictor of all-cause mortality and rehospitalization. In HFpEF patients galectin-3 levels correlated stronger with outcomes than in HFrEF patients.

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Ultrafiltration (UF) is an alternative strategy to diuretic therapy for the treatment of patients with decompensated heart failure. The impact of UF in decompensated heart failure with renal insufficiency remains unclear. A literature search was conducted for randomized controlled trials (RCTs) that investigated the use of UF in decompensated heart failure patients with renal insufficiency.
Seven RCTs with 569 participants were eligible for analysis. There was significantly more 48 hour weight loss (WMD 1.59, 95% CI 0.32 to 2.86; P = 0.01; I2 = 68%) and 48 hour fluid removal (WMD 1.23, 95% CI 0.63 to 1.82; P < 0.0001; I2 = 43%) in the UF group compared to the control group. Serum creatinine (WMD 0.05; 95% CI -0.23 to 0.33; P = 0.61; I2 = 77%) and serum creatinine changes (WMD 0.05; 95% CI -0.15 to 0.26; P = 0.61; I2 = 77%) were similar between the UF and control groups. All-cause mortality (OR 0.95; 95% CI 0.58 to 1.55; P = 0.83; I2 = 0.0%) and all-cause rehospitalization (OR 0.97; 95% CI 0.49 to 1.92; P = 0.94; I2 = 52%) were also similar between the UF and control groups. Adverse events such as infection, anemia, hemorrhage, worsening heart failure, and other cardiac disorders did not differ significantly between the UF and control groups.
UF is an effective and safe therapeutic strategy and produces greater weight loss and fluid removal without affecting renal function, mortality, or rehospitalization in patients with decompensated heart failure complicated by renal insufficiency.

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Acute aortic dissection (AAD) is a life-threatening cardiovascular disease with high mortality. Hypertension is a well known risk factor of AAD. There have been previous reports about the association between circadian variation of blood pressure (BP) and cardiovascular events. However, little is known about the association between the onset-time of AAD and circadian variation of BP. The purpose of this study was to clarify the characteristics of circadian variation of BP in AAD and its relation to the onset-time of this disease. This study included type B spontaneous AAD patients who were referred to our institution and treated conservatively between January 2008 and June 2013. Patients with type A AAD, secondary to trauma, and type B AAD which preceded surgical intervention were excluded. Data were retrospectively collected from the hospital medical records. Sixty-eight patients with type B AAD were enrolled. The distribution of the circadian pattern in the study patients was as follows: extreme-dipper, 0% (none); dipper, 20.6% (n = 14); nondipper, 50% (n = 34); riser, 29.4% (n = 20). Non-dipper and riser patterns were more frequently observed compared with other population studies reported previously. Moreover, no patient in the dipper group had night-time onset while 31.5% of the patients in the absence of nocturnal BP fall group (non-dipper and riser) did (P = 0.01). Absence of a nocturnal BP fall was frequently seen in AAD patients. Absence of a nocturnal BP fall may be a risk factor of AAD. Circadian variation of BP may also affect the onset-time of type B AAD.

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The left atrial appendage (LAA) represents one of the major sources of cardiac thrombi responsible for embolic stroke in patients with atrial fibrillation (AF). The aim of the present study was to evaluate LAA structure and functions by transesophageal echocardiography (TEE) in patients with AF to investigate the possible association between the different LAA morphologies and the patients’ history of ischemic cerebral stroke. We included 50 patients with non-valvular AF (29 chronic, 21 paroxysmal), 24 patients (13 men) without stroke; and 26 patients (9 men) with a history of ischemic stroke. All patients underwent TEE evaluation of LAA morphology and functions. Compared to patients without stroke, patients with ischemic stroke had significantly higher CHADS2 scores (4.19 ± 0.89 versus 1.67 ± 1.13; P < 0.001) and C-reactive protein levels (8.3 ± 1.6 versus 7.6 ± 0.83 mg/L; P = 0.023), and lower peak filling (21.7 ± 11.3 versus 31.2 ± 9.5 cm/second; P = 0.033) and emptying (22.2 ± 9.7 versus 33.4 ± 13.4 cm/second, P = 0.030) velocities. Triangular LAA morphology had a higher prevalence in patients with stroke (36% versus 12% in non-stroke group); and in half of them an LAA thrombus was present. LAA thrombi were detected in 9 patients (18%) with stroke and in 5 patients (10%) without stroke. On multivariate logistic regression analysis, age (OR = 1.202 [1.042–1.585]; P = 0.041), LAA orifice diameter (OR = 1.275 [1.102–1.748]; P = 0.028), and triangular LAA morphology (OR = 4.53 [1.629–8.381]; P = 0.011) were significantly and independently associated with ischemic stroke in AF patients. LAA morphology evaluated by TEE may be useful for predicting ischemic cerebral stroke in patients with non-valvular AF, especially in those with a low CHADS2 score.

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There are many published articles on the effects of the antithrombolytic function of platelet glycoprotein IIb/IIIa inhibitors (GP IIb/IIIa inhibitors) in myocardial infarction. However, few studies have explored the effects and optimal concentration of tirofibans in diminishing the extent of myocardial reperfusion injury (RI).
Rats received 120 minutes of coronary ligation and 180 minutes of reperfusion. The rats were then divided into 7 groups based on the concentration of tirofiban administered intravenously 30 minutes prior to coronary reperfusion to the end of reperfusion. The ratio of myocardial necrotic area to area at risk (AAR), and myocardial malondialdehyde (MDA) and plasma myeloperoxidase (MPO) activities were measured. The apoptotic index (AI) was the percentage of myocytes positive for terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) out of all myocytes stained by 4’, 6-diamidino-2-phenylindole (DAPI).
The ratio of myocardial necrotic area to AAR significantly decreased in all tirofiban subgroups. The MDA activity for tirofiban concentrations of 2 and 5 ug/kg/minute showed a slight reduction. MPO activity was significantly decreased at a tirofiban concentration of 2 ug/kg/minute. The AI was significantly decreased at a tirofiban concentration of ≥ 0.4 ug/kg/minute.
The results indicate that a tirofiban can significantly ameliorate the cardiac RI and myocyte apoptosis in rats.

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Although the relationship between arteriosclerosis and inflammatory response has been recognized in recent years, little is known regarding the change in plasma Nogo-B in coronary artery disease (CAD). Thus, we investigated the expression levels of Nogo-B in CAD patients and examined this relation with disease stages. We recruited 92 CAD patients including 64 with acute coronary syndromes (ACS) and 28 with stable angina pectoris (SAP) cases and 28 healthy controls. The serum concentrations of Nogo-B were measured by enzyme-linked immunosorbent assay (ELISA). The plasma Nogo-B level was significantly higher in patients with ACS and SAP when compared with the healthy controls (both P < 0.05). Multivariate logistic regression analysis revealed that the level of Nogo-B was associated with CAD (odds ratio 1.006, 95% CI: 1.000-1.013, P < 0.05). In conclusion, an increased plasma Nogo-B level may be associated with CAD.

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Insulin resistance (IR) is a pathophysiological condition and is associated with cardiovascular risk factors including heart failure. However, studies demonstrating myocardial abnormalities in the early phases of IR are limited. The aim of this study was to investigate myocardial function in otherwise healthy individuals with IR.
Individuals with IR who were free of cardiovascular risk factors and healthy controls were included. Stress echocardiography with tissue Doppler imaging (TDI) was performed. Systolic and diastolic TDI waves were compared in both groups.
A total of 77 individuals (51 with IR and 26 controls) were included in our study. The tissue early flow (e’)/atrial contraction (a’) ratio at rest was significantly lower in the IR group (P = 0.003). The annular early flow (E)/e’ ratio, a predictor of left ventricular filling pressure, was similar in both groups at rest (P = 0.522). After exercise, e’/a’ impairment became more prominent in the IR group (P < 0.001); whereas the E/e’ ratio was also significantly lower (7.6 ± 1.8 versus 6.7 ± 0.9; P = 0.007) in the IR group.
Myocardial involvement seems to occur in patients with IR, before the appearance of other cardiovascular risk factors. Exercise induced diastolic worsening may be a predictor of reduced compliance and increased ventricular stiffness. More detailed prospective studies are required for more precise results.

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Speckle tracking echocardiography (STE) has been reported to be a promising technique for evaluating right ventricular (RV) function in the clinical setting. On the other hand, the usefulness of STE for RV evaluation in small animal models has not been clarified, although the rat model is among the most commonly used animal models to develop novel effective treatments against pulmonary hypertension and RV heart failure (HF).
We validated the use of STE and conventional echocardiographic variables for evaluating RV functions in a rat model by comparing the echocardiographic values of RVHF rats (n = 12) induced by monocrotaline injection with those of control rats (n = 12).
Most conventional echocardiographic variables demonstrated that RVHF rats have significant RV dysfunction. The area under the curve (AUC) values to distinguish RV dysfunction in RVHF rats from normal RV function in control rats using fractional area change (FAC), tricuspid annular plane systolic excursion (TAPSE), RV myocardial performance index (MPI), peak tissue Doppler tricuspid annular velocities at systole (Sa), and at early diastole (Ea) were 0.71, 0.98, 0.79, 0.92, and 0.91, respectively. However, using STE analysis for RV evaluation, limited reproducibility was observed (variability 19–37 %, ICC 0.74–0.88) and the only circumferential strain showed significantly lower absolute values (P = 0.039, AUC = 0.76).
To evaluate RV function in rat models, circumferential strain may be useful, however, the reproducibility and diagnostic utility were limited. Conventional echocardiographic variables such as TAPSE, tissue Doppler Sa, and Ea have superior diagnostic utility.

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Platelet–derived growth factor (PDGF) is implicated in the pathogenesis of pulmonary arterial hypertension (PAH). Imatinib, a PDGF-receptor tyrosine kinase inhibitor, improved hemodynamics, but serious side effects and drug discontinuation are common when treating PAH. A drug delivery system using nanoparticles (NPs) enables the reduction of side effects while maintaining the effects of the drug. We examined the efficacy of imatinib-incorporated NPs (Ima-NPs) in a rat model and in human PAH-pulmonary arterial smooth muscle cells (PASMCs). Rats received a single intratracheal administration of PBS, FITC-NPs, or Ima-NPs immediately after monocrotaline injection. Three weeks after monocrotaline injection, intratracheal administration of Ima-NPs suppressed the development of pulmonary hypertension, small pulmonary artery remodeling, and right ventricular hypertrophy in the rat model of monocrotaline-induced PAH. We also examined the effects of imatinib and Ima-NPs on PDGF-induced proliferation of human PAH-PASMCs by ³H-thymidine incorporation. Imatinib and Ima-NPs significantly inhibited proliferation after 24 hours of treatment. Ima-NPs significantly inhibited proliferation compared with imatinib at 24 hours after removal of these drugs. Delivery of Ima-NPs into lungs suppressed the development of MCT-induced PAH by sustained antiproliferative effects on PAS-MCs.

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The left internal thoracic artery (LITA) is considered the most reliable coronary artery bypass grafting conduit due to its high rate of long-term patency. LITA grafts are extremely durable and associated complications are infrequent. We present a case with spontaneous spiral dissection of a LITA graft to the left anterior descending artery, which was assessed by optical coherence tomography (OCT) and intravascular ultrasound (IVUS). OCT was superior in visualizing the disrupted flap, false lumen, and intramural hematoma, but it did not visualize the full extent of the vessel wall. In contrast, IVUS allowed more complete and deeper vessel visualization, and thus better appreciation of the extent of intramural hematoma. Combined use of these two modalities provides complementary details on imaging of a LITA dissection.

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An error appeared in the article titled “Fulminant Type 1 Diabetes Mellitus and Fulminant Viral Myocarditis: A Case Report and Literature Review” by Nobumasa Ohara, et al. (Vol. 56, No. 2, 239-244, 2015) “herpes simple virus” should be replaced by “herpes simplex virus” on page 242 line 27.

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