Optimizing simulated interviews and feedback to maximize medical students' self-efficacy in real time.

BACKGROUND: Self-efficacy is crucial in improving medical students' communication skills. This study aims to clarify where medical students' self-efficacy is greatest following an interview with a simulated patient and subsequent feedback. METHODS: A total of 162 medical students (109 men, 53 women) in their fourth or fifth year at a university in Japan participated in this study. The degree of self-efficacy in medical interviewing was measured before and after a medical interview with a simulated patient, and after the subsequent feedback session. RESULTS: ANOVA analysis revealed that self-efficacy for medical interviews was higher after both the interview and the feedback session than before the interview. Among all three time points, self-efficacy was highest after the feedback session. CONCLUSIONS: Feedback following a simulated interview with a simulated patient is important to improve the self-efficacy of medical students when learning medical interviewing skills.

Pulmonary Artery Diameter Predicts Lung Injury After Balloon Pulmonary Angioplasty in Patients With Chronic Thromboembolic Pulmonary Hypertension.

Balloon pulmonary angioplasty (BPA) has been an attractive strategy for chronic thromboembolic pulmonary hypertension (CTEPH), even though it occasionally causes lung injury. However, predictive factors of lung injury after BPA have not been established. Pulmonary artery (PA) dilatation is often observed in patients with pulmonary hypertension. We investigated the association between PA diameter and complications after BPA.The subjects were 19 CTEPH patients who underwent BPA. Patients were divided into two groups: patients with lung injury including asymptomatic lung infiltration on computed tomography (CT) images or mild hemoptysis (group L, n = 9) and no complications (group N, n = 10). PA diameter was measured on CT and corrected by the body surface area (PA diameter index).There were no significant differences in hemodynamic indices or the number of treated vessels between the two groups. Right, left, and main PA diameter indices were higher in group L than in group N. Among the clinical variables, the right, left, and main PA diameter indices were significant predictors for lung injury caused by BPA (right PA: OR 1.819, 95%CI 1.056-3.135, P < 0.05; left PA: OR 1.857, 95%CI 1.091-3.159, P < 0.05; main PA: OR 1.399, 95%CI 1.001-1.956, P < 0.05).The PA diameter index can be used to effectively predict the risk of lung injury after BPA.

The CHA2DS2-VASc score as a predictor of high mortality in hospitalized heart failure patients.

AIMS: Atrial fibrillation (AF) is common in patients with heart failure (HF). CHA2DS2-VASc score was originally employed as a risk assessment tool for stroke in patients with AF; however, it has recently been used to predict not only stroke but also various cardiovascular diseases beyond the original AF field. We aimed to verify the CHA2DS2-VASc score as a risk assessment tool to predict mortality in patients with HF. METHODS AND RESULTS: Consecutive 1011 patients admitted for treatment of HF were divided into three groups based on their CHA2DS2-VASc scores: score 1-3 group (n = 317), score 4-6 group (n = 549) and score 7-9 group (n = 145). Of the 1011 HF patients, 387 (38.3%) had AF. We compared patient characteristics among the three groups and prospectively followed for all-cause mortality. Although left ventricular ejection fraction was similar among all three groups, all-cause mortality was higher in the score 4-6 group and score 7-9 group than in the score 1-3 group (37.9 and 29.3% vs. 15.1%, log-rank P < 0.001). In the multivariable Cox proportional hazard analysis, the CHA2DS2-VASc score 7-9 was an independent predictor of all-cause mortality (all HF patients: hazard ratio (HR) 1.822, P = 0.011; HF patients with AF: HR 1.951, P = 0.031; HF patients without AF: HR 2.215, P = 0.033). CONCLUSIONS: The CHA2DS2-VASc score was an independent predictor of all-cause mortality in HF patients with or without AF. This comprehensive risk assessment score may help identify HF patients who are at high risk for mortality in HF patient.

Association between levels of anti-angiogenic isoform of vascular endothelial growth factor A and pulmonary hypertension.

BACKGROUNDS: Pulmonary hypertension (PH) is characterized by elevated pulmonary arterial pressure due to vasoconstriction and remodeling of the pulmonary microvasculature. Vascular endothelial growth factor (VEGF) is a key contributor for angiogenesis and vasculogenesis. VEGF165b is recently identified as an anti-angiogenic splicing variant of VEGF. The aim of this study was to examine the association between circulating levels of VEGF165b in PH patients under consideration with classifications of PH. METHODS AND RESULTS: We measured plasma levels of VEGF165b in the PH group (pulmonary artery hypertension [PAH], n=26; chronic thromboembolic pulmonary hypertension [CTEPH], n=13) and control group (n=30). Circulating levels of VEGF165b were higher in PH group than controls (97.1 vs. 53.3pg/ml, P<0.01). The multiple regression analysis demonstrated that the independent factor to determine the plasma levels of VEGF165b was the presence of PH (P=0.04). Next, we focused on differences in VEGF165b levels and classifications of PH. Plasma VEGF165b level was higher only in idiopathic PAH (n=9) than in control (137.1 vs. 53.3pg/ml, P<0.01), but not in PH related to collagen disease (n=7), congenital heart disease (n=10) and CTEPH (n=13). CONCLUSIONS: We demonstrated associations between circulating levels of VEGF165b and classifications of PH. VEGF165b, anti-angiogenic isoform, might contribute to the pathophysiology in PH, especially in idiopathic PAH. The level of plasma VEGF165b might be a novel marker that reflects the pathological conditions in patients with PH.

Familial hypertrophic obstructive cardiomyopathy with the GLA E66Q mutation and zebra body.

BACKGROUND: Fabry disease is caused by mutations in the α-galactosidase A (GLA) gene, which is located in X-chromosome coding for the lysosomal enzyme of GLA. Among many gene mutations, E66Q mutation is under discussion for its pathogenicity because there is no clinical report showing pathological evidence of Fabry disease with E66Q mutation. CASE PRESENTATION: A 65-year-old Japanese female was referred to our hospital for chest discomfort on effort. Transthoracic echocardiography showed severe left ventricular (LV) hypertrophy with LV outflow obstruction. Maximum LV outflow pressure gradient was 87 mmHg, and Valsalva maneuver increased the pressure gradient up to 98 mmHg. According to medical interview, one of her younger sister and a nephew died suddenly at age 42 and 36, respectively. Another younger sister also presented LV hypertrophy with outflow obstruction. Maximum LV outflow pressure gradient was 100 mmHg, and the E66Q mutation was detected similar to the case. Endomyocardial biopsy specimens presented vacuolation of cardiomyocytes, in which zebra bodies were detected by electron microscopic examination. Although the enzymatic activity of GLA was within normal range, the c. 196G>C nucleotide change, which lead to the E66Q mutation of GLA gene, was detected. We initially diagnosed her as cardiac Fabry disease based on the findings of zebra body. However, immunostaining showed few deposition of globotriaosylceramide in left ventricular myocardium, and gene mutations in the disease genes for hypertrophic cardiomyopathy (HCM), MYBPC3 and MYH6, were detected. Although the pathogenicity of the E66Q mutation cannot be ruled out, hypertrophic obstructive cardiomyopathy (HOCM) was more reasonable to explain the pathophysiology in the case. CONCLUSIONS: This is the confusable case of HOCM with Fabry disease with the GLA E66Q mutation. We have to take into consideration the possibility that some patients with the E66Q mutation may have similar histological findings of Fabry disease, and should be examed the possibility for harboring gene mutations associated with HCM.

Associations With Eicosapentaenoic Acid to Arachidonic Acid Ratio and Mortality in Hospitalized Heart Failure Patients.

BACKGROUND: Intake of n-3 polyunsaturated fatty acids (n-3 PUFAs) lowers the risk of atherosclerotic cardiovascular events, particularly ischemic heart disease. In addition, the ratio of eicosapentaenoic acid (EPA; n-3 PUFA) to arachidonic acid (AA; n-6 PUFA) has recently been recognized as a risk marker of cardiovascular disease. In contrast, the prognostic impact of the EPA/AA ratio on patients with heart failure (HF) remains unclear. METHODS AND RESULTS: A total of 577 consecutive patients admitted for HF were divided into 2 groups based on median of the EPA/AA ratio: low EPA/AA (EPA/AA <0.32 mg/dl, n = 291) and high EPA/AA (EPA/AA ≥0.32, n = 286) groups. We compared laboratory data and echocardiographic findings and followed cardiac mortality. Although body mass index, blood pressure, B-type natriuretic peptide, hemoglobin, estimated glomerular filtration rate, total protein, albumin, sodium, C-reactive protein, and left ventricular ejection fraction did not differ between the 2 groups, cardiac mortality was significantly higher in the low EPA/AA group than in the high EPA/AA group (12.7 vs 5.9%, log-rank P = .004). Multivariate Cox proportional hazard analysis revealed that the EPA/AA ratio was an independent predictor of cardiac mortality (hazard ratio 0.677, 95% confidence interval 0.453-0.983, P = .041) in patients with HF. CONCLUSION: The EPA/AA ratio was an independent predictor of cardiac mortality in patients with HF; therefore, the prognosis of patients with HF may be improved by taking appropriate management to control the EPA/AA balance.

Intravascular ultrasound predictors of acute side branch occlusion in coronary artery bifurcation lesions just after single stent crossover.

OBJECTIVES: We aimed to assess the intravascular ultrasound (IVUS) predictors of acute side branch (SB) occlusions just after single stent crossover in percutaneous coronary intervention (PCI) for coronary bifurcation lesions. BACKGROUND: PCI for bifurcation lesions remains technically challenging and has more clinical complications such as SB occlusion than non-bifurcation lesions. Although single stent crossover is the most common approach in treating bifurcation lesions, the predictors of acute SB occlusion are unclear. METHODS: Single stent crossover was performed on 174 patients with a total of 272 bifurcation lesions who were enrolled in this study. Each patient also underwent pre-PCI IVUS in a major vessel (MV). SB was defined as ostium diameter of ≥1.5 mm measured by IVUS, and occluded SB was defined as a thrombolysis in myocardial infarction flow grade of ≤2 just after stent implantation. We defined the SB diameter ratio as ostial SB total diameter (media-to-media) divided by ostial SB luminal diameter (intima-to-intima). RESULTS: There were 52 SBs in the occluded group (19.1%). There were no significant differences in baseline characteristics between the SB occluded and non-SB occluded groups. Logistic-regression analysis revealed that the thickness of MV plaque on the bilateral sides of SB at the junction site and the SB diameter ratio were independent predictors of SB occlusion just after stent implantation. CONCLUSIONS: In the IVUS observation, the MV plaque thickness at the junction site and the SB diameter ratio are predictors of acute SB occlusion just after single stent crossover.

ENDOGENOUS CARBON MONOXIDE CONCENTRATION IN BLOOD ELEVATES IN ACUTE CORONARY SYNDROME OF NONSMOKER POPULATION.

BACKGROUND: Carbon monoxide (CO) was previously only considered as a highly toxic pollutant since it binds to hemoglobin with high affinity. Recently, however, it has been recognized as a signaling molecule with regulatory roles in many physiological and pathophysiological processes within the cardiovascular system. The aim of this study was to clarify the behavior of CO in patients with acute coronary syndrome (ACS). METHODS: We assessed 235 patients with suspected ACS, 98 smokers (88 male, 62 ± 14 years) and 137 nonsmokers (77 male, 72 ± 13 years), who had undergone emergent cardiac catheterization and blood sampling for calculation of carboxyhemoglobin (COHb). Patients were categorized into 4 groups: smoking patients with ACS (n=77), smoking patients without ACS (n=21), non-smoking patients with ACS (n=97), and non-smoker patients without ACS (n=40). We investigated whether biomarkers were related to COHb levels. RESULTS: LogCOHb was significantly higher in the smoking patients compared to non-smoking patients (0.30 ± 0.12 vs. 0.45 ± 0.18, P < 0.01). Interestingly, among the non-smoking patients, COHb was increased in the ACS patients compared to the non ACS patients (0.31 ± 0.12 vs. 0.25 ± 0.12 P < 0.01). In contrast, among the smoking patients, there was no difference in COHb between the ACS and non-ACS patients (0.45 ± 0.18 vs. 0.44 ± 0.18, n.s.). There were no correlations between COHb and any of the biomarkers. CONCLUSIONS: These results suggest that endogenous CO may be useful to assess the risk of cardiovascular stress.

STENTING STRATEGY AND FOLLOW-UP RESULTS OF MULTI-CENTER REGISTRY IN FUKUSHIMA CITY FOR LEFT MAIN CORONARY ARTERY DISEASE: BARE METAL STENT VERSUS DRUG-ELUTING STENT.

An appropriate treatment strategy for left main trunk (LMT) lesions is still controversial in the drug-eluting stent (DES) era. Consecutive LMT stenting cases (n = 155) between January 2008 and January 2013 in 4 hospitals in Fukushima city were retrospectively analyzed. We excluded the patients suffering from cardiogenic shock before the stenting procedure. Among those cases, 60 patients had acute coronary syndrome, and remaining 95 had stable angina pectoris. Out of 155 cases, 45 patients were treated with bare metal stents (BMSs) and 110 patients were treated with DESs. All cases were succeeded in the initial procedure. Mean stent size of BMS was 3.85 ± 0.34 mm while that of DES was 3.46 ± 0.17 mm (P<0.001). At the follow up coronary angiography (255-day on average), % stenosis of BMS group was 26.6 ± 15.0% and that of DES group was 20.4 ± 12.6% (P = 0.006). The mean observation period for clinical events was 738.8 ± 480.3 days. Major adverse cardiac events-free rates for each group were compared and no significant differences were evident between the 2 groups (11.1% vs. 19.1%, ns). The present study demonstrated that use of BMSs would be a viable option in the treatment of LMT lesions when it is possible to use a large-sized stent (>3.5 mm).

Worsening late-acquired incomplete stent apposition after sirolimus-eluting stent implantation for a chronic total occlusion lesion.

A 70-year-old man underwent percutaneous coronary intervention (PCI) using sirolimus-eluting stent (SES) at the just proximal site of left anterior descending coronary artery. Six months after SES implantation, he suffered from late stent thrombosis. Intravascular ultrasound (IVUS) images demonstrated positive remodeling of the vessel, indicating late-acquired incomplete stent apposition (ISA). An angioplasty with a bigger balloon was performed to obtain sufficient stent struts apposition. Twenty-six months after the second PCI, he developed ST-elevation myocardial infarction and his CAG showed re-occlusion of the SES. Optical coherence tomography showed ISA and IVUS revealed further enlargement of the coronary artery around the SES.

Sudden cardiac arrest associated with an anomalous aortic origin of the left coronary artery from the opposite sinus of valsalva.

A 13-year-old boy was brought to our hospital after recovering from ventricular fibrillation that occurred after an episode of chest pain during training with his soccer team. Subsequent 64-slice multidetector computed tomography revealed the left coronary artery arising from the right sinus of Valsalva, which coursed between the ascending aorta and root of the main pulmonary artery. Surgical correction including unroofing of the left coronary ostium and pulmonary artery translocation was performed successfully. One year later, he remained asymptomatic and was back on his soccer team.

Significance of soluble lectin-like oxidized LDL receptor-1 levels in systemic and coronary circulation in acute coronary syndrome.

BACKGROUND: Soluble lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) level is a novel biomarker for diagnosis of acute coronary syndrome (ACS); however, this level in the coronary circulation has yet to be examined. METHODS: Twenty-seven consecutive patients with ACS and 40 patients with effort angina pectoris (EAP) undergoing percutaneous coronary intervention (PCI) had levels of soluble LOX-1 and LOX-1 index measured in paired blood samples from aorta (Ao) and coronary sinus (CS) just prior to the PCI. RESULTS: We found positive correlations between soluble LOX-1 levels in the Ao and CS in both ACS and EAP patients (P < 0.01, for both). The soluble LOX-1 levels in the Ao and CS were higher in ACS than in EAP patients (P < 0.01, for both). The levels of soluble LOX-1 and LOX-1 index of the CS were significantly greater than those of the Ao in both ACS and EAP patients (P < 0.01, for both). Receiver operating characteristic curves for ACS detection demonstrated high sensitivity and specificity for the soluble LOX-1 and LOX-1 index with no differences between the Ao and CS. CONCLUSIONS: The present study showed that circulating soluble LOX-1 originates from coronary circulation and soluble LOX-1 and LOX-1 index are useful biomarkers for ACS.

Serum tenascin-C level is associated with coronary plaque rupture in patients with acute coronary syndrome.

Tenascin-C, a large oligometric glycoprotein of the extracellular matrix, increases the expression of matrix metalloproteinases that lead to plaque instability and rupture, resulting in acute coronary syndrome (ACS). We hypothesized that a high serum tenascin-C level is associated with plaque rupture in patients with ACS. Fifty-two consecutive ACS patients who underwent emergency percutaneous coronary intervention (PCI) and, as a control, 66 consecutive patients with stable angina pectoris (SAP) were enrolled in this study. Blood samples were obtained from the ascending aorta just prior to the PCI procedures. After coronary guide-wire crossing, intravascular ultrasonography (IVUS) was performed for assessment of plaque characterization. Based on the IVUS findings, ACS patients were assigned to two groups according to whether there was ruptured plaque (ruptured ACS group) or not (nonruptured ACS group). There were 23 patients in the ruptured group and 29 patients in the nonruptured group. Clinical characteristics and IVUS measurements did not differ between the two groups. Tenascin-C levels were significantly higher in the ruptured ACS group than in the SAP group, whereas there was no significant difference between the nonruptured ACS and SAP groups. Importantly, in the ruptured ACS group, tenascin-C levels were significantly higher than in the nonruptured ACS group (71.9 ± 34.9 vs 50.5 ± 20.5 ng/ml, P < 0.005). Our data demonstrate that tenascin-C level is associated with pathologic conditions in ACS, especially the presence of ruptured plaque.

A case of acute myocardial infarction during perioperative period of non-cardiac surgery in a patient with antiphospholipid syndrome and a history of coronary artery bypass surgery.

A 65-year-old woman underwent coronary artery bypass surgery and was diagnosed with antiphospholipid syndrome (APS) at the same time in 1985. She was admitted to our hospital to undergo mastectomy for left breast cancer in 2012. She was put on intravenous infusion of heparin and stopped receiving both antiplatelet agents and warfarin. The operation was performed without complications, and antithrombotic therapy was restarted one day after the operation. On day 6 postoperative, she complained of sudden chest pain and on examination she was diagnosed with acute myocardial infarction. The culprit lesion was in a saphenous vein graft and coronary intervention was performed. .

Deep seating of 5 Fr. guiding catheter across the stenosis with 5 in 7 method was effective for severely calcified lesion.

A 57-year-old male with end stage renal disease underwent coronary angiography (CAG). The CAG revealed two vessel disease with severe calcification. A week after the percutaneous coronary intervention (PCI) to the left anterior descending coronary artery (LAD), we performed PCI to the right coronary artery (RCA). Because of the calcification, no devices could be crossed. We then performed 5 in 7 method using Heartrail ST01, and inserted it across the stenosis, with dilatation balloon at the distal RCA as anchoring. Finally we managed to implant two stents. We report that 5 in 7 method and deep seating of 5 Fr. guiding catheter were effective for the severely calcified lesion.

Left ventricular plasty improved cardiac function in a case of takotsubo cardiomyopathy with persistent aneurysm.

A 72-year-old woman was admitted to a local hospital due to repeated chest pain in December 2011. On admission, blood tests showed elevation of cardiac enzyme and B-type natriuretic peptide levels. Electrocardiography showed ST-segment elevation in almost all leads. Echocardiography showed akinesis in left ventricular (LV) apex, and hyperkinesis in basal LV. Urgent cardiac catheterization was performed. Coronary angiography showed no significant organic stenosis and the acetylcholine provocation test did not evoke coronary spasm. The left ventriculography revealed marked akinesis of the apical ballooning with hyperkinesis of the basal LV segments, suggesting takotsubo cardiomyopathy. Following the diagnosis, she started treatment for LV dysfunction with standard pharmacotherapy including beta blocker, aldosterone receptor blocker, and angiotensin-converting enzyme inhibitor. Even after 3 months, echocardiography demonstrated that LV wall motion was not recovered, and her symptoms of heart failure were not improved. Based on these findings, we considered that surgical LV plasty was necessary for the treatment of cardiac dysfunction in this patient. She underwent surgical operation (aneurysma resection and LV volume reduction) in April 2011. Pathological examination of the excised myocardial tissue from the aneurysm revealed damaged cardiomyocytes replaced with interstitial fibrosis and adipose tissue. After surgery, her LV systolic function and clinical symptoms dramatically improved. .

A reduction of coronary flow reserve is associated with chronic kidney disease and long-term cardio-cerebrovascular events in patients with non-obstructive coronary artery disease and vasospasm.

BACKGROUND: Coronary flow reserve (CFR) provides essential information about the coronary microvasculature. Chronic kidney disease (CKD) is a risk factor for cardio-cerebrovascular diseases. We hypothesized that low CFR is associated with CKD and long-term cardio-cerebrovascular events in the patients without obstructive coronary artery diseases and vasospasm. METHOD AND RESULTS: In this study, 73 patients suspected with coronary artery disease but had no epicardial coronary stenosis and vasospasm were enrolled. There were 13 CKD patients and CFR was measured using the Doppler flow wire methods in the left anterior descending artery. CFR was significantly lower in CKD group than non-CKD group (3.13 ± 0.6 vs. 4.00 ± 1.1, P = 0.007). From multivariate logistic regression analysis, the independent factor associated with the presence of CKD was only CFR (odds ratio 3.85, 95% confidence interval 1.27-11.70, P = 0.017). In the patients with low CFR (≤ 2.8), cardio-cerebrovascular events were more common than those with normal CFR (CFR > 2.8). Besides, in the patients who had both low CFR and CKD, long-term cardio-cerebrovascular events were more likely to occur than those with normal CFR or non-CKD. CONCLUSIONS: Our data suggest that low CFR is associated with CKD and cardio-cerebrovascular events in the patients without coronary stenosis and vasospasm.

Dilated phase of hypertrophic cardiomyopathy caused by two different sarcomere mutations, treated with surgical left ventricular reconstruction and cardiac resynchronization therapy with a defibrillator.

We herein report the case of a 61-year-old woman with dilated phase of hypertrophic cardiomyopathy (D-HCM) who had been diagnosed with HCM 17 years previously. On admission, her left ventricle (LV) had marked dilation, dyssynchrony with diffuse severe hypokinesis, and ventricular tachycardia. She had two mutations in the cardiac myosin binding protein-C gene, which were suspected to be the causes of the D-HCM. We performed LV reconstruction surgery and cardiac resynchronization therapy with a defibrillator for her drug-resistant severe heart failure. After surgery, her New York Heart Association class dramatically improved, and she has not been re-hospitalized since these treatments.