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A 37-year-old woman developed deep venous thrombosis (DVT) of the left lower extremity at 8 weeks of gestation during her second pregnancy. There was no personal or family history of thrombosis. She received intravenous heparin, but heparin resistance was noted. The plasma antithrombin activity decreased to 45% in the acute phase, and it remained low postpartum. Her mother also had low plasma antithrombin activity (46%), and genetic testing revealed a heterozygous SERPINC1 mutation. Even without a family history of thrombosis, we should suspect hereditary antithrombin deficiency in patients with initial DVT and perform thorough investigation.

A 30-year-old woman was referred to our hospital to undergo an evaluation for suspected Brugada syndrome. She showed no symptoms, but had a strong family history of sudden cardiac death. During observation, Holter electrocardiography (ECG), which had been performed to investigate her symptoms of occasional dizziness, showed a sinus node dysfunction with an occasional long sinus pause. An implantable cardioverter defibrillator (ICD) was therefore put in place, and bradycardia pacing from the ICD relieved those symptoms during the subsequent 18-month follow-up. The patient completed two pregnancies during the follow-up period. No symptomatic changes occurred during the pregnancies, but ECG indicated that an ST segment elevation in the right precordial leads was attenuated during the second and third trimesters of both pregnancies.

An 81-year-old man presented with shortness of breath and was referred to our hospital with suspected acute pulmonary embolism. Enhanced computed tomography revealed a right aberrant subclavian artery with a thrombosed Kommerell diverticulum (KD), as well as deep vein thrombosis in the left leg and bilateral pulmonary artery thrombosis. Thrombosis in the KD disappeared after one month of anticoagulation treatment with rivaroxaban. Thrombosis of a KD is a rare condition that may cause distal emboli and subclavian steal syndrome, although this syndrome was not present in this case. Rivaroxaban is an effective anticoagulant for treating thrombosis of a KD.

The aim of this study was to evaluate the association of functional mitral regurgitation (FMR), preserved or reduced ejection fraction (EF), and ischemic or nonischemic origin with outcomes in patients discharged alive after hospitalization for acute decompensated heart failure (HF). Of the 4,842 patients enrolled in the Acute Decompensated Heart Failure Syndromes (ATTEND) registry, 3,357 patients were evaluated to assess the association of FMR, preserved or reduced EF, and ischemic or nonischemic origin with the primary end point (all-cause death and readmission for HF after discharge). At the time of discharge, FMR was assessed semiquantitatively (classified as none, mild, or moderate to severe) by color Doppler analysis of the regurgitant jet area. According to multivariable analysis, in the ischemic group, either mild or moderate to severe FMR in patients with a preserved EF had a significantly higher risk of the primary end point than patients without FMR (hazard ratio [HR] 1.60; 95% confidence interval [CI] 1.12 to 2.29; p = 0.010 and HR 1.98; 95% CI 1.30 to 3.01; p = 0.001, respectively). In patients with reduced EF with an ischemic origin, only moderate to severe FMR was associated with a significantly higher risk of the primary end point (HR 1.67; 95% CI 1.11 to 2.50; p = 0.014). In the nonischemic group, there was no significant association between FMR and the primary end point in patients with either a preserved or reduced EF. In conclusion, among patients with acute decompensated HF with a preserved or reduced EF, the association of FMR with adverse outcomes may differ between patients who had an ischemic or nonischemic origin of HF.

Background: In our experience, the change in body weight (BW) during hospitalization varies greatly in patients with acute decompensated heart failure (HF). Since the clinical significance of a change in BW is not clear, we investigated whether a change in BW could predict mortality. Methods: We retrospectively enrolled 130 patients (72 males; aged 68 ± 10 years) who were hospitalized due to acute decompensated HF and followed for 2 years after discharge. The change in the BW index during hospitalization (ΔBWI) was calculated as (BW at hospital admission minus BW at hospital discharge)/body surface area at hospital discharge. Results: The patients were divided into quartiles according to ΔBWI, and the 2-year mortality rates in the quartiles with the lowest, second, third and highest ΔBWI were 18.8%, 12.1%, 3.1% and 9.1%, respectively. In a multivariate Cox proportional hazards analysis after adjusting for variables with a P value less than 0.05, ΔBWI was independently associated with 2-year mortality (P = 0.0002), and the quartile with the lowest ΔBWI had a higher relative risk (RR) for 2-year mortality than the quartile with the highest ΔBWI (RR: 7.46, 95% confidence interval: 1.03 - 53.99, P = 0.04). Conclusion: In conclusion, ΔBWI was significantly associated with 2-year mortality after discharge, which indicates that ΔBWI might be a simple predictor of prognosis in acute decompensated HF. J Clin Med Res. 2017;9(3):200-206 doi: https://doi.org/10.14740/jocmr2890w

An 81-year-old man was admitted to our hospital with abdominal distension due to refractory ascites of unknown origin. He subsequently died of aspiration pneumonia. Autopsy revealed a diagnosis of biphasic malignant peritoneal mesothelioma (MPM) containing both epithelioid and sarcomatous components. The diagnosis of MPM is often difficult because serum tumor markers, imaging studies, and the cytology of ascites may not provide enough information. Accordingly, peritoneal biopsy is necessary in order to diagnose MPM based on the histological and immunohistochemical findings.

A 26-year-old male suffered sustained chest pain. Electrocardiogram showed ST-segment elevation in the anteroseptal wall and reciprocal ST-segment change in the inferior wall. The troponin-I level and the white blood cell count were elevated. We gave a diagnosis of acute myocardial infarction. He underwent urgent coronary angiography, which revealed 90% diffuse stenosis in the middle right coronary artery and total occlusion in the proximal left anterior descending coronary artery (LAD). Since the electrocardiogram indicated that the culprit lesion was in the proximal LAD, we performed percutaneous coronary intervention. The coronary flow in the LAD was classified as thrombolysis in myocardial infarction trial 3. His coronary risk factors were obesity, smoking, family history, hypertension and diabetes, in addition to heterozygous familial hypercholesteremia (FH). Herein, we describe the case of a young patient with acute anteroseptal myocardial infarction and discuss the potential importance of controlling cholesterol levels in FH.

A 31-year-old female with an 18-year history of systemic lupus erythematosus (SLE) complained of epigastralgia and consulted the emergency outpatient department at our hospital. Her physical examination revealed tenderness at the scrobiculus cordis, which was a non-specific symptom of coronary heart disease (CHD). We ultimately gave a diagnosis of acute myocardial infarction based on coronary angiography and performed percutaneous coronary intervention. Although pre-interventional intravascular ultrasound demonstrated distinct atherosclerotic lesions in the coronary arteries, there were no atherosclerotic lesions in other systemic arteries. Although CHD in young SLE patients is a significant cause of morbidity and premature death, it tends to be misdiagnosed because their symptoms may be non-specific. In addition, this case highlights the fact that even SLE patients with no systemic atherosclerosis are at risk for the development of CHD. .

A 44-year-old woman had a 15-year history of asthma and had recently been treated for sinusitis and unidentified limb eruption. She had presented at a nearby clinic with inspiratory chest pain one week before hospitalization, and was diagnosed as having eosinophilic pneumonia based on peripheral blood eosinophilia and ground glass opacities in the right lung field, without pericardial effusion, as detected by chest computed tomography. She additionally presented with a feeling of chest tightness, and extensive pericardial effusion appeared within a week. She developed heart failure on admission, and we performed pericardiocentesis. We gave a clinical diagnosis of acute probable myopericarditis as the cause of pericardial effusion based on pleuritic chest pain, pericardial effusion, and elevation of cardiac enzymes, as well as eosinophilic granulomatosis with polyangiitis (EGPA) based on eosinophilia, her history of sinusitis, asthma, and migratory pulmonary opacities. We initiated oral prednisone 25 mg daily and pericardial effusion disappeared. In patients with EGPA, cardiac involvement is more serious than the involvement of other organs, and is associated with a poor prognosis. In this report we describe a rare case of EGPA complicated with progressive pericardial effusion and discuss the importance of the early diagnosis and treatment of EGPA. Learning objective: Eosinophilic granulomatosis with polyangiitis (EGPA), or Churg Strauss syndrome, is a multisystem disorder. It is important for patients with EGPA complicated with cardiac involvement to be diagnosed and treated early because cardiac involvement may lead to a fatal outcome.>