The management of antithrombotics during the periendoscopic period is traditionally represented as a doubleedged sword for cardiologists and endoscopists. Appropriate administration prevents thromboembolic events, whereas excessive administration provokes bleeding events. Therefore, cardiologists and endoscopists must consider the risks of bleeding and thromboembolism in individual cases, before deciding whether to continue antithrombotic use. Several guidelines exist concerning antithrombotic management in Asian and Western countries. These guidelines generally classify procedural bleeding risk and thromboembolic risk into high risk and low risk groups and recommend that the two risks be weighed when managing a given patient. Moreover, they generally do not recommend interrupting antithrombotics during the periendoscopic period unless absolutely necessary; however, the details surrounding this point differ among the guidelines after several revisions. In this review, we describe the present state, problems, and future perspectives concerning the management of antithrombotics in patients with cardiovascular disease undergoing gastrointestinal endoscopy.

The usefulness of coronary magnetic resonance angiography (cMRA) has been reported, although the difference in the diagnostic accuracy of different protocols has not been established.

We compared conventional coronary angiography (CAG) and cMRA, conducted within 6 months in 24 consecutive patients between September 2012 and July 2014. Three cMRA protocols were examined, cMRA1, free-breathing wholeheart coronary angiography (WHCA) without contrast; cMRA2, free-breathing WHCA with contrast; and cMRA3, breath-hold steady-state free precession with contrast using a 3.0 T scanner. Image quality was graded on a 4-point scale: 1) nonassessable; 2) assessable, fair vessel contrast; 3) assessable, good vessel contrast; and 4) assessable, excellent vessel contrast. Significant narrowing of the coronary arteries was visually assessed.

Stenosis was observed in 34 segments, with a prevalence of 10.3%. For cMRA1, cMRA2, and cMRA3, the numbers of assessable segments were 245 (74.2%), 287 (87.0%), and 164 (49.7%), respectively (P < 0.001 by the McNemar test). For assessable segments, the sensitivity, specificity, positive predictive value, and negative predictive value were 89.3%, 99.1%, 92.6%, and 98.6% for cMRA1, 90.0%, 98.1%, 84.4%, and 98.8% for cMRA2, and 76.5%, 93.9%, 59.1%, and 97.1% for cMRA3, respectively. For the assessable segments, the image quality score was better with cMRA2 than with the other two protocols.

cMRA is a useful modality to rule out coronary artery disease, especially the cMRA2 protocol, which performed better than the other two protocols.

It is unknown whether there has been any change in the causes of death for acute ST-segment elevation myocardial infarction (STEMI) in the era of aggressive reperfusion. We analyzed the direct causes of in-hospital death in patients with STEMI treated with primary percutaneous coronary intervention (PCI) in a tertiary referral center over the past 10 years.

We retrospectively analyzed 878 STEMI patients treated with primary PCI in our hospital between January 2005 and December 2014. There were no significant changes in the age and sex of patients, but the prevalence of hypertension and smoking decreased. STEMI severity increased with more patients in Killip classification > 2. The number of out-ofhospital cardiac arrest events also increased over the 10 years. Symptom onset-to-door time did not change in the 10year study period. The care quality was improved with shorter door-to-balloon time for primary PCI and increased use of dual antiplatelet therapy. The all-cause in-hospital mortality was 9.1%, which did not vary over the 10 years. Multivariable analysis showed that Killip classification > 2 was the most important determinant of death. Cardiogenic shock was the major cause of cardiovascular death. There was an increase in non-cardiovascular causes of death in the most recent 3 years, with infection being a major problem.

Despite improvement in care quality for STEMI, the in-hospital mortality did not decrease in this tertiary referral center over these 10 years due to increased disease severity and non-cardiovascular causes of death.

A J-shaped or U-shaped curve phenomenon might exist between systolic blood pressure (SBP) or pulse pressure (PP) at admission and in-hospital mortality in Japanese patients with acute myocardial infarction (AMI) undergoing primary percutaneous coronary intervention (PCI). However, data regarding a relationship between mean blood pressure (MBP) at admission and in-hospital outcome in AMI patients undergoing primary PCI are still lacking in Japan.

A total of 1,413 primary PCI-treated AMI patients were classified into quintiles based on admission MBP (< 79 n = 283, 79-91 n = 285, 92-103 n = 285, 104-115 n = 279, and ≥ 116 mmHg n = 281). Patients with MBP < 79 mmHg had a significantly higher in-hospital mortality, while mortality was not significantly different among the other quintiles: 16.6% (< 79), 4.9% (79-91), 3.9% (92-103), 3.2% (104-115), and 5.0% (≥ 116 mmHg). On multivariate analysis, Killip class ≥ 3 at admission, LMT or multivessels as culprit lesions, admission MBP < 79 mmHg, and age were independent positive predictors of in-hospital mortality, whereas hypercholesterolemia and TIMI 3 flow before/after PCI were negative predictors, while the other MBP categories were not.

These results suggest that admission MBP < 79 mmHg might be associated with in-hospital death, and the in-hospital prognostic effects of MBP, the steady component of blood pressure, at admission might be different from those of SBP or PP, the pulsatile component of blood pressure, at admission in Japanese AMI patients undergoing primary PCI.

Red blood cell distribution width (RDW) can predict mortality in cardiovascular disease. However, the underlying mechanisms of the beneficial prognostic marker remain unknown. The purpose of this study was to investigate whether the RDW is related to impaired exercise tolerance and exercise training (ET) effect on RDW in patients with coronary artery disease (CAD).

Seventy-eight patients who underwent ET by supervised bicycle ergometer during 3 weeks served as the ET group whereas 30 patients who did not undergo ET were the control group. Exercise stress test with cardiopulmonary analysis was performed in the ET group. Peak oxygen uptake (from 14.1 ± 4.0 to 15.1 ± 3.8 mL/kg/minute, P < 0.05) significantly increased in the ET group. Although RDW and serum erythropoietin concentration (EP) before the observation period did not differ between the ET and control groups, RDW (from 44.4 ± 4.7 to 43.4 ± 3.8 fL, P < 0.01) and EP (from 27.9 ± 15.8 to 22.9 ± 8.2 mIU/mL, P < 0.005) significantly decreased in the ET group, however, these parameters did not change in the control group. In the ET group, RDW was negatively correlated with peak oxygen uptake (r = -0.55, P < 0.01) and the changes in RDW before and after ET were positively correlated with the changes in EP (r = 0.39, P < 0.005).

Thus, ET increases exercise tolerance and decreases RDW in association with increased oxygen uptake in patients with CAD.

Non-ST segment elevation acute coronary syndrome (NSTE-ACS) can be difficult to diagnose accurately, especially in the hyper-acute phase. Non-ECG-gated contrast-enhanced computed tomography (non-ECG-gated CE-CT) has been used in many institutions for screening acute chest pain. Although early defects (EDs) observed in non-ECG-gated CE-CT have been reported as a sign of acute myocardial ischemia, the precise diagnostic value of this sign for acute coronary syndrome has not been fully elucidated. We investigated the usefulness of non-ECG-gated CE-CT for the diagnosis of NSTE-ACS. We retrospectively reviewed 556 patients who were hospitalized for acute-onset chest pain and who underwent emergent coronary angiography. Non-ECG-gated CE-CT was performed in 23 of these patients. Two readers independently analyzed CT images using a 5-point scale. Of the 23 patients, 13 were diagnosed with NSTE-ACS. The remaining 10 patients were diagnosed with other conditions. The sensitivity, specificity, positive predictive value, and negative predictive value, respectively, of EDs on non-ECG-gated CE-CT to detect NSTE-ACS were 84.6%, 90%, 91.7%, and 81.8%. The identification of EDs was consistent between the two readers. Non-ECG-gated CE-CT may be useful not only to triage patients with chest pain by ruling out other conditions, but also to accurately diagnose NSTE-ACS.

Revascularization therapy such as percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) should be considered for heart failure with reduced ejection fraction (HFrEF). However, revascularization therapy does not always improve left ventricular ejection fraction (LVEF). The purpose of this study was to investigate the determinants of LVEF improvement following revascularization in HFrEF patients. From 2,229 consecutive decompensated heart failure patients, a total of 47 HFrEF patients who underwent revascularization were included in the analysis. Improvement of LVEF was defined as [(LVEF during chronic phase) – (LVEF during acute phase)] ≥ 10%. Univariate and multivariate logistic regression analyses were applied to investigate the determinants of LVEF improvement. The prevalence of revascularization by PCIs including chronic total occlusion (CTO) was significantly greater in the improved EF group (45.0%) as compared to the non-improved EF group (11.1%) (P = 0.02). Multivariate logistic regression analysis revealed that revascularization by PCIs including CTO was the significant determinant of the LVEF improvement after adjusting for confounding factors (OR 5.43, 95% CI 1.06-27.74, P = 0.04). Optimal medical therapy (angiotensin-converting enzyme (ACE) inhibitor and/or angiotensin II receptor blocker (ARB) and beta-blockers) was less frequently prescribed in patients with CABG (50.0% for ACE inhibitor and/or ARB and 41.7% for beta-blocker) than in patients without CABG (94.3% for both) (P < 0.01 and P < 0.001, respectively). In conclusion, revascularization by PCIs including CTO was the significant determinant of LVEF improvement in HFrEF patients. Our results underscore the importance of optimal medical therapy even if patients receive complete revascularization such as CABG.

Discrimination between paroxysmal and persistent atrial fibrillation (PAF and persistent AF) is important for determining the therapeutic strategy in patients with new-onset AF. We evaluated various clinical factors and P wave morphology to discriminate PAF and persistent AF patients in patients with new-onset AF.

The study population consisted of 79 patients with new-onset AF (70.3 ± 10.8 years, female:male 33:46) who were retrospectively selected from 8,632 AF patients in the Kitasato University Hospital ECG storing system. PAF (n = 38) and persistent AF (n = 41) patients were diagnosed by whether the initial PAF episode continued for 1 week. The P wave morphologies were analyzed using the most recent 12 lead-ECG recording of sinus rhythm. P wave dispersion was defined as the difference between the maximum and minimum durations of all leads. Along with these data, various clinical factors were evaluated and compared between PAF and persistent AF patients.

Multivariate analysis identified P wave dispersion (56.6 ± 14.8 versus 66.5 ± 12.8 msec, P = 0.002) and left atrial dimension (LAD: 40.2 ± 7.0 versus 47.7 ± 8.2 mm, P < 0.001) as independent factors for discrimination between PAF and persistent AF patients. Combining these two parameters achieved a specificity of 88.9%, a positive predictive value of 81.8%, a sensitivity of 95.3%, and a negative predictive value of 88.9%.

In patients with new-onset AF, P wave dispersion and LAD were independent factors for discrimination between PAF and persistent AF.

Interatrial block (IAB) is associated with an increased risk of atrial fibrillation (AF). The aim of this retrospective study was to investigate the association of a combination of IAB and the CHADS₂ score, an AF-related risk score for ischemic stroke, with new onset AF in patients in sinus rhythm. A total of 1,571 patients (803 males, 768 females; mean age: 58 ± 16 years) were included in this study. IAB was defined as a P-wave duration > 120 ms in the 12-lead electrocardiogram, and a high CHADS₂ score as ≥ 2 points. During the mean follow-up period of 4.8 ± 0.7 years, new onset AF occurred in 122 patients (16.1 per 1,000 patient-years). The incidence of new onset AF was 4.0 per 1,000 patient-years in patients with no IAB and a low CHADS₂ score, and 44.0 per 1,000 patient-years in patients with IAB and a high CHADS₂ score. In multivariate Cox regression analysis, the hazard ratio for IAB and a high CHADS₂ score compared with no IAB and a low CHADS₂ score was 12.18 (95% confidence interval: 6.22–23.87, P < 0.001), after adjustment for age, sex, coronary artery disease, valvular heart disease, smoking, medications, and echocardiographic parameters. In conclusion, IAB and a high CHADS₂ score independently and synergistically predict new onset AF in patients in sinus rhythm, indicating an approximately 12-fold higher risk in patients with both IAB and a high CHADS₂ score. Patients meeting these criteria should have more aggressive early intervention to prevent AF.

To investigate the genotype frequencies of cytochrome P450, family2, subfamily C, polypeptide19 (CYP2C19); P2Y₁₂ receptor; and glycoprotein IIIa polymorphisms in patients with coronary heart disease and their impact on clopidogrel responsiveness and major adverse cardiac events (MACEs).

A total of 146 coronary heart disease patients of Han ethnicity, on a clopidogrel regimen, were enrolled. Polymerase chain reaction and DNA sequencing were used to detect the genotype and allelic frequencies of CYP2C19 (^*2,^*3,^*17), P2Y12 (C34T, G52T, T744C) and GPIIIa (T1565C) polymorphisms. Clinical and laboratory data were compared between the high on-treatment platelet reactivity (HTPR) versus normal groups.

HTPR was identified in 35 (24%) patients. CYP2C19^*2 (G681A) polymorphism was found to be significantly associated with HTPR (P < 0.05). A allele frequencies were significantly higher in the HTPR group versus the normal group (P < 0.05). On logistic regression analysis, CYP2C19^*2 (G681A) polymorphism was found to be an independent risk factor associated with HTPR. No link could be established between genetic polymorphisms and recurrence of MACEs, or between HTPR and recurrence of MACEs.

The genetic polymorphisms in CYP2C19^*2 were closely associated with HTPR. The frequency of the A allele of CYP2C19^*2 was significantly associated with HTPR, with A allele carriers being more likely to develop HTPR.

The vasopressin type-2 antagonist tolvaptan (TLV) has clinical advantages including amelioration of congestion and normalization of hyponatremia in patients with decompensated heart failure (HF). However, there have been no studies on the cost-effectiveness of TLV therapy. We enrolled 60 consecutive hospitalized patients with stage D HF who received TLV [TLV (+) group], and 60 propensity score-matched HF patients without TLV treatment [TLV (-) group]. We excluded 54 patients who died or received cardiac replacement therapy within 1 year, and finally enrolled 32 patients who received TLV and 34 who did not, who were followed for > 1 year. Among 45 aquaporin-defined responders, whose urine aquaporin-2 relative to plasma arginine vasopressin level was > 1.4 × 10³ L/g Cre, the TLV (+) group required significantly lower total medical expenses and shorter lengths of stay (LOS) compared with the TLV (-) group [11.2 (1.233.3) versus 31.2 (2.2-71.4) × 10⁵ JPY/year, P < 0.001; 30 (0-304) versus 70 (20-221) days, P = 0.030]. In contrast, among the remaining 21 aquaporin-defined non-responders, medical expenses and LOS were comparable irrespective of TLV administration (P = 0.087 and P = 0.407). In conclusion, TLV therapy may reduce total medical expenses in aquaporin-defined responders with stage D HF.

Tolvaptan (TLV), an arginine vasopressin type 2 antagonist, has been shown to play a role in ameliorating symptomatic congestion and normalizing diluted hyponatremia in patients with congestive heart failure (HF). However, most evidence was derived from patients with HF with reduced ejection fraction (HFrEF), and the clinical efficacy of TLV in patients with HF with preserved ejection fraction (HFpEF) remains uncertain. In this study, we retrospectively enrolled 60 in-hospital patients with stage D HF, who had received TLV to treat symptomatic congestion at our institute between 2011 and 2013. As a control group, we also enrolled 60 background-matched HF patients who did not receive TLV therapy. Patients with HFpEF (n = 29), whose left ventricular ejection fraction was > 45%, had higher age and a lower urine aquaporin-2 level relative to the plasma arginine vasopressin concentration compared with those with HFrEF (n = 91). TLV therapy significantly reduced the 2-year readmission rates in both the HFrEF and HFpEF populations (P < 0.05 for both), indicating that TLV therapy may improve the long-term prognosis not only in patients with HFrEF but also in those with HFpEF.

Visit-to-visit variability (VVV) in blood pressure (BP) has been shown to be a predictor of cardiovascular events. It is unknown whether CR can improve VVV in BP as well as reducing BP. We enrolled 84 patients who had cardiovascular disease (CVD) and participated in a 3-month CR program. We measured systolic and diastolic BP (SBP and DBP), pulse pressure (PP), and heart rate (HR) before exercise training at each visit and determined VVV in BP or HR expressed as the standard deviation of the average BP or HR. Patients who had uncontrolled BP at baseline and who did not change their antihypertensive drugs throughout the study period showed a significant reduction of both SBP and DBP with a decrease in PP after 3 months. Patients who did not change their antihypertensive drugs were divided into larger (L-) and smaller (S-) VVV in the SBP groups and L- and S-VVV in the DBP groups according to the average value of VVV in SBP or DBP. In the L-VVV in the SBP and DBP groups, VVV in SBP and DBP in the 1st month was significantly decreased after the 3rd month in both groups. HR at baseline was significantly decreased after 3 months. In addition, CR induced a significant increase in the level of high-density lipoprotein cholesterol (HDL-C) in blood. In conclusion, CR improved VVV in BP in patients with L-VVV in BP and evoked a significant reduction in HR and an increase in HDL-C. These effects due to the CR program may be cardioprotective.

The neutrophil-to-lymphocyte (N/L) ratio has been associated with poor outcomes in patients with cardiovascular diseases, but it has not been studied in elderly patients with chronic heart failure (CHF).

In this study, we analyzed 1355 elderly patients admitted with CHF. A multivariate logistic regression model was used to assess the independent association of the N/L ratio with chronic kidney disease (CKD). The patients were then divided into tertiles according to the N/L ratios. We used Cox regression analysis to assess the association between the N/L ratio and subsequent major cardiovascular events (MCE), including cardiac death and rehospitalization for heart failure.

In the multiple logistic regression analysis, the N/L ratio was identified as a risk factor for CKD in elderly patients with CHF (odds ratio [OR] = 1.170, 95% confidence interval [CI] 1.054 to 1.298, P = 0.003). The median follow-up period was 18 months. In a multivariate analysis with the lowest tertile as the reference, the highest tertile of the N/L ratio remained significantly associated with MCE (hazard ratio [HR] = 1.425, 95% CI 1.109 to 1.832, P = 0.006), cardiac death (HR = 1.747, 95% CI 1.032 to 2.958, P = 0.038), and rehospitalization for heart failure (HR = 1.461, 95% CI 1.108 to 1.927, P = 0.007).

In elderly patients with CHF, the N/L ratio is one of the important risk factors for CKD and the highest tertile of the N/L ratio is associated with an increased risk for MCE.

This retrospective study aimed to investigate the predictive value of biomarkers for in-hospital mortality of patients with Stanford type A acute aortic dissection (AAD).

AAD is a life-threatening disease with an incidence of about 2.6-3.6 cases per 100,000/year.

A total of 67 consecutive Stanford type A AAD patients admitted to hospital were divided into a deceased group and survival group. The baseline information of the patients between two groups was systematically compared, followed by examination of the electrocardiograms (ECG). Based on the follow-up during hospitalization, we investigated the simultaneous assessment of indexes like fragmented QRS complex (fQRS), admission systolic blood pressure (SBP), aortic diameter, surgical management, troponin I (TnI), white blood cell (WBC) count, N-terminal pro-brain natriuretic peptide (NT-proBNP), and D-dimer.

The levels of TnI and NT-proBNP, WBC counts, and rate of fQRS (+) in patients of the deceased group were significantly higher than those in the survival group. The male sex (hazard ratio, 10.88; P = 0.001), admission SBP (hazard ratio, 0.98; P = 0.012), NT-proBNP (hazard ratio, 1.00; P = 0.001), and WBC count (hazard ratio, 1.10; P = 0.033) were independently related with in-hospital death. As a single marker, WBC count had the highest sensitivity at 84.6% (specificity 65.9%).

Admission SBP, NT-proBNP, and WBC count were potential independent risk factors of in-hospital death in Stanford type A AAD patients. WBC count may be a more accurate predictor of type A AAD than either alone.

This study aimed to investigate the independent and joint association of blood pressure (BP), homocysteine (Hcy), and fasting blood glucose (FBG) levels with brachial-ankle pulse wave velocity (baPWV, a measure of arterial stiffness) in Chinese hypertensive adults.

The analyses included 3967 participants whose BP, Hcy, FBG, and baPWV were measured along with other covariates. Systolic BP (SBP) was analyzed as 3 categories (SBP < 160 mmHg; 160 to 179 mmHg; ≥ 180 mmHg); Hcy as 3 categories (< 10 μmol/L; 10 to 14.9 μmol/L; ≥ 15.0 μmol/L) and FBG: normal (FBG < 5.6 mmol/L), impaired (5.6 mmol/L ≤ FBG < 7.0 mmol/L), and diabetes mellitus (FBG ≥ 7.0 mmol/L). We performed linear regression analyses to evaluate their associations with baPWV with adjustment for covariables.

When analyzed individually, BP, Hcy, and FBG were each associated with baPWV. When BP and FBG were analyzed jointly, the highest baPWV value (mean ± SD: 2227 ± 466 cm/s) was observed in participants with FBG ≥ 7.0 mmol/L and SBP ≥ 180 mmHg (β = 432.5, P < 0.001), and the lowest baPWV value (mean ± SD: 1692 ± 289 cm/s) was seen in participants with NFG and SBP < 160 mmHg. When Hcy and FBG were analyzed jointly, the highest baPWV value (2072 ± 480 cm/s) was observed in participants with FBG ≥ 7.0 mmol/L and Hcy ≥ 15.0 μmol/L (β = 167.6, P < 0.001), while the lowest baPWV value (mean ± SD: 1773 ± 334 cm/s) was observed in participants with NFG and Hcy < 10 μmol/L.

In Chinese hypertensive adults, SBP, Hcy, and FBG are individually and jointly associated with baPWV.

Our findings underscore the importance of identifying individuals with multiple risk factors of baPWV including high SBP, FBG, and Hcy.

Thrombotic microangiopathy (TMA) is a rare but lethal multisystem disease characterized by peripheral thrombocytopenia, microangiopathic hemolytic anemia, fever, and various stages of renal and neurological dysfunctions.^1,2) The causes of TMA are mainly thrombotic thrombocytopenic purpura (TTP) or hemolytic-uremic syndrome (HUS), and cases of TMA related to myelodysplastic syndrome (MDS) are quite rare. Herein, we report a case of acute myocardial infarction (AMI) caused by TMA which is strongly suspected to have a relationship to MDS, and discuss the treatment of our patient who needed antiplatelet or anticoagulant therapy after AMI, while on the other hand, had pancytopenia and a bleeding event due to MDS.

Fabry disease, an X-linked lysosomal storage disorder due to α-galactosidase A deficiency, is associated with dysfunction of various cell types and results in a systemic vasculopathy. We describe a 29-year-old woman with Fabry disease presenting with severe cardiac and renal manifestations. Gene analysis demonstrated a novel mutation (K391E) in the GLA gene. Enzyme replacement therapy (ERT) was started with agalsidase-β after confirming the diagnosis of Fabry disease, resulting in normalization of LV systolic function and improvement of renal function. As early therapy is crucial for preventing life-threatening sequelae, clinicians should consider Fabry disease in young patients presenting with cardiac and renal disease without any likely causes.

The patient was a 26 year-old man who was referred to our hospital in June 2011 because of severe heart failure. At age 24 years, he was found to have Becker muscular dystrophy. He received enalapril for cardiac dysfunction; however, he had worsening heart failure and was thus referred to our hospital. Echocardiography showed enlargement of the left ventricle, with a diastolic dimension of 77 mm and ejection fraction of 19%. His condition improved temporarily after an infusion of dobutamine and milrinone. He was then administered amiodarone for ventricular tachycardia; however, he subsequently developed hemoptysis. Amiodarone was discontinued and corticosteroid pulse therapy was administered followed by oral prednisolone (PSL). His creatinine phosphokinase (CPK) level and cardiomegaly improved after the corticosteroid therapy. The PSL dose was reduced gradually, bisoprolol was introduced, and the catecholamine infusion was tapered. A cardiac resynchronization device was implanted; however, the patient’s condition gradually worsened, which necessitated dobutamine infusion for heart failure. We readministered 30 mg PSL, which decreased the CPK level and improved the cardiomegaly. The dobutamine infusion was discontinued, and the patient was discharged. He was given 7.5 mg PSL as an outpatient, and he returned to normal life without exacerbation of the heart failure. There are similar reports showing that corticosteroids are effective for skeletal muscle improvement in Duchenne muscular dystrophy; however, their effectiveness for heart failure has been rarely reported. We experienced a case of Becker muscular dystrophy in which corticosteroid therapy was effective for refractory heart failure.

Aortitis is broadly divided into infectious and non-infectious etiologies, each with distinct treatment implications. We present the case of a patient who sustained a type A aortic dissection during urgent coronary angiography for acute coronary syndrome. Clinical findings and events during the procedure raised suspicion for an underlying vascular disorder; however, the diagnosis of staphylococcal aortitis was not made until pathological examination of resected tissue. Clues to the diagnosis of infectious aortitis noted throughout the patient’s clinical course are detailed as are potential consequences of diagnostic delays and treatment decisions, underscoring the difficulties in recognizing and managing the condition. In addition, we describe a previously unreported complication of cardiac catheterization in the setting of an infectious aortopathy.

A 22-year-old male was admitted to our hospital with deep vein thrombosis that was complicated by antithrombin deficiency. This deficiency was refractory to anticoagulation therapy. Although catheter-directed thrombolysis could not reperfuse the total occlusion in the left deep vein, a combination of thrombectomy, catheter-directed thrombolysis, and antithrombin concentrate treatment was able to dissolve the clots and ameliorate the blood flow into the left deep vein. Antithrombin concentrate administration would be effective in the treatment of antithrombin deficiency with medical refractory deep vein thrombosis.

Factor V Leiden (FVL) mutation is the most common hereditary thrombophilia. Association of this mutation with venous thrombosis is well established. However, there are several conflicting results regarding the association of FVL with arterial thrombosis, acute coronary syndrome, and intracardiac thrombosis. In this case report, we present a 44-yearold male patient with a medical history of both arterial and venous thrombosis who came to our emergency department with chest pain. After the initial evaluation he was diagnosed as having acute coronary syndrome and transthoracic echocardiography revealed an intracardiac apical thrombus. Coronary angiography showed non-critical stenosis. Thrombophilia panel was studied and the patient was found to be heterozygotic for FVL mutation. An apical thrombus was extracted surgically because of the high risk of systemic embolization.