Peripartum cardiomyopathy in patients with psychiatric disorders successfully treated with bromocriptine: Two case reports.

Peripartum cardiomyopathy (PPCM) is a rare disorder in which left ventricular systolic dysfunction and heart failure symptoms occur during the peripartum period. Inhibition of prolactin secretion by bromocriptine mediates beneficial effects on cardiac function in PPCM. Mental disorders are also associated with the onset of PPCM. Psychiatric medications for mental disorders would affect serotonin production and tryptophan and dopamine metabolism, and they are associated with PPCM. Conversely, bromocriptine affects psychiatric symptoms; therefore, the treatment of PPCM complicated by mental disorders using bromocriptine may be difficult. Herein, we report cases of two patients with PPCM and mental disorders successfully treated with bromocriptine therapy. The first case involved a 33-year-old woman with a history of atypical depression and anxiety disorder, who developed PPCM with a left ventricular ejection fraction (LVEF) of 19 %. The second case was that of a 42-year-old woman with a history of bipolar and panic disorders who developed PPCM with an LVEF of 18 %. Both patients were administered bromocriptine; however, psychiatric symptoms did not worsen and cardiac function improved. We also review the literature on the relationship between PPCM and mental disorders. Learning objective: Mental disorders and psychiatric medications may be associated with the onset of peripartum cardiomyopathy (PPCM). Although bromocriptine has beneficial effects on PPCM, it has also been reported to increase the risk of worsening psychiatric symptoms; therefore, the efficacy and safety of bromocriptine in PPCM patients with mental disorders is controversial. Our cases showed that bromocriptine can be used safely without worsening psychiatric symptoms in PPCM with mental disorders.

Cardiac Arrest Due to Brugada Syndrome Associated With Influenza Infection: A Case Report and Literature Review.

A 38-year-old Japanese male with no significant medical history but a family history of sudden cardiac death was referred for cardiac arrest. He had a fever (40°C) one day before his visit. His wife reported that he groaned while unconscious, which prompted a referral to the authors' hospital. He was febrile and experienced ventricular fibrillation in the emergency department. After the resolution of ventricular fibrillation, electrocardiography revealed a right bundle branch block with ST-segment elevation in leads V1-3, consistent with a Brugada electrocardiographic pattern; he also tested positive for influenza A infection. Antiarrhythmic and antipyretic agents were administered, and peramivir was initiated; a fatal arrhythmia did not occur. A cardioverter-defibrillator was implanted, and the patient was discharged without complications. Brugada syndrome is a genetic disease that causes fatal cardiac arrhythmias, with fever recognized to induce the Brugada electrocardiographic pattern. The mechanism of the Brugada-type electrocardiographic pattern, right bundle branch block, and ST-segment elevation in the right precordial leads is considered to be the result of an outward shift of ionic currents during early repolarization, causing a marked abbreviation of the action potential in epicardial cells of the right ventricle. Activation and inactivation kinetics for early sodium currents are faster at higher temperatures. To date, there have only been four published reports describing Brugada-like electrocardiographic changes associated with fever related to influenza infection, and this is the first report of cardiac arrest. Since influenza infection can cause high fever and trigger the fetal arrhythmia of Brugada syndrome, it is important to shorten the duration of the fever. Anti-influenza therapy may be considered in patients who have a history of sudden cardiac arrest in the family, as influenza may influence the development of the Brugada ECG pattern in these individuals. The authors also review the literature on Brugada-like electrocardiographic changes induced by influenza infection. Physicians should be aware that Brugada's electrocardiographic pattern and cardiac arrest can be caused by febrile episodes, including those related to influenza infection.

Anti-factor Xa activity, prothrombin time, and activated partial thromboplastin time in patients treated with factor Xa inhibitors.

The regimens for factor Xa (FXa) inhibitors (apixaban, edoxaban, and rivaroxaban) vary with venous thromboembolism (VTE) or non-valvular atrial fibrillation (NVAF). The dosage and duration of FXa inhibitor therapy also differ. However, the distribution of anti-factor Xa activity (AXA) values, prothrombin time (PT), and activated partial thromboplastin time (APTT) in patients administered each FXa inhibitor has not fully been assessed. Trough and peak AXA values, PT, and APTT were measured in 85 patients taking apixaban, 105 patients taking edoxaban, and 27 patients taking rivaroxaban. The patients were further divided into three groups based on the dosage. Each FXa inhibitor showed various ranges of AXA values, and twice-daily use resulted in higher absolute AXA values than once-daily use. AXA values and PT for 20 mg apixaban at both trough and peak times were significantly higher than those for 5 mg or 10 mg. AXA values for 60 mg edoxaban at peak time were significantly higher than those for 15 mg or 30 mg. AXA values for 30 mg of rivaroxaban at both trough and peak times were significantly higher than those for 10 mg or 15 mg. In a nonlinear regression model of the relationship between AXA and PT or APTT, PT was positively correlated with AXA values for each FXa inhibitor. This study obtained trough and peak levels of AXA, PT, and APTT in patients with VTE or NVAF who were administered apixaban, edoxaban, and rivaroxaban.

Impact of Renal Function on Anti-factor Xa Activity Concentrations with Edoxaban Use in Patients with Non-valvular Atrial Fibrillation.

BACKGROUND: Chromogenic anti-factor Xa activity (AXA) assay is used to measure the pharmacodynamics of factor Xa inhibitors, including edoxaban. Although AXA concentrations in patients with non-valvular atrial fibrillation using edoxaban have been reported, the impact of renal function on AXA concentrations with edoxaban use in patients with non-valvular atrial fibrillation has not been fully assessed. METHODS: Trough and peak AXA concentrations were measured in 93 patients with non-valvular atrial fibrillation taking edoxaban (73.6 ± 11.2 years, 48 were male). The patients were divided into three groups: patients with moderate renal dysfunction (creatinine clearance 15-49 mL/min), mild renal dysfunction (creatinine clearance 50-95 mL/min), and normal renal function (creatinine clearance > 95 mL/min). Both trough and peak AXA concentrations were assessed among the groups according to the edoxaban dose (30 or 60 mg). RESULTS: At a 30-mg dose, patients with moderate renal dysfunction showed significantly higher trough AXA concentrations than patients with mild renal dysfunction or normal renal function. At a 60-mg dose, patients with mild renal dysfunction showed significantly higher trough AXA concentrations than patients with normal renal function. Peak AXA concentrations were not significantly different between the groups. Creatinine clearance was significantly and negatively correlated with trough AXA concentrations at a 60-mg dose, whereas the correlation of creatinine clearance with AXA concentrations was borderline significant at a 30-mg dose. No correlation was found between creatinine clearance and peak AXA concentrations at either dose. CONCLUSIONS: Creatinine clearance tends to be negatively correlated with trough AXA concentrations in patients with non-valvular atrial fibrillation taking edoxaban, while renal function is not correlated with peak AXA concentrations.

Nivolumab-induced Myositis and Myocarditis with Positive Anti-titin Antibody and Anti-voltage-gated Potassium Channel Kv1.4 Antibody.

Immune checkpoint inhibitors (ICIs) are complicated by immune-related adverse events (irAEs), such as myositis, myocarditis, and myasthenia gravis (MG). Anti-titin antibody and anti-voltage-gated potassium channel Kv1.4 antibody are anti-striated antibodies that are frequently detected in MG patients with myositis and/or myocarditis. However, the clinical relationship between positive anti-striated antibodies and irAEs of ICIs remains unknown. We herein report a case of nivolumab-induced myositis and myocarditis with positive anti-titin antibody and anti-voltage-gated potassium channel Kv1.4 antibody in a patient with non-small-cell lung cancer. We also review reported cases of positive anti-striated antibodies related to irAEs of ICIs.

Coagulation markers in patients with venous thromboembolism treated with 10 mg apixaban twice daily.

Apixaban is used to treat venous thromboembolism (VTE) at 10 mg twice daily (BID) for 7 days, followed by 5 mg BID without dose adjustment, and non-valvular atrial fibrillation (NVAF) at 5 mg BID or 2.5 mg BID with dose adjustment criteria (DAC) including age, body weight, and renal function. The anti-factor Xa activity (AXA), prothrombin time (PT), and activated partial thromboplastin time (APTT) in patients with VTE receiving 10 mg BID of apixaban remains unclear. Twenty-six patients (70.8±15.4 years, 10 males) with VTE receiving 10 mg BID of apixaban were enrolled. The patients were divided into two groups based on whether they met the DAC of NVAF: DAC group (n=8) and non-DAC group (n=18). Trough and peak AXA values, PT, and APTT were measured at 10 mg BID dosage and then at 5 mg BID dosage. Coagulation markers in recipients of 10 mg BID therapy were significantly higher than those of 5 mg BID recipients. A significant and strong positive correlation was observed between AXA and PT at trough and peak times. The AXA values and PT in the DAC group were significantly higher than those in the non-DAC group. No significant inter-group differences were seen in APTT. This study provides the first report of AXA distribution in VTE patients receiving 10 mg BID of apixaban. Our findings indicate that coagulation markers may differ in patients with VTE-prescribed higher doses of apixaban and a DAC may be warranted in such patients.

Wellens syndrome in a young woman with coronary artery vasculitis.

We report the case of a 30-year-old woman who was referred to our hospital with chest pain. An electrocardiogram showed biphasic T-wave inversions in leads V2-4 compared with that done 2 years ago, suggesting Wellens syndrome, and an emergent coronary angiography revealed significant stenosis of the proximal left anterior descending artery due to coronary artery vasculitis. Although acute coronary syndrome in the young is very rare, coronary artery vasculitis should be considered as a possible etiology, especially in young women with chest pain.

A case of cardiac amyloidosis in an elderly Japanese patient with amyloidogenic transthyretin Val122Ile variant.

A 76-year-old Japanese man with a history of stomach cancer and chronic atrial fibrillation was referred to our department with left atrial thrombus. He had a history of gastric amyloidosis diagnosed by a pathological specimen of the stomach; however, further examination for amyloidosis was not performed. The patient displayed clinical signs and symptoms of heart failure and echocardiography showed a thick left ventricular wall. Since cardiac amyloidosis was suspected, the patient underwent cardiac magnetic resonance imaging and 99mTc-pyrophosphate scintigraphy. These results are consistent with transthyretin amyloidosis (ATTR amyloidosis). DNA analysis of transthyretin (TTR) was performed and a heterozygous Val122Ile mutation was identified. Notably, his only son requested the analysis; however, no mutations were noted. ATTR Val122Ile is one of the mutations in TTR that are associated with hereditary amyloidosis, causing severe cardiomyopathy. The prevalence of the ATTR Val122Ile mutation is 3.9% in the African-American population. However, the occurrence of this mutation in Asian populations is very rare. This is the second reported case of the ATTR Val122Ile variant in Japan and the first case tested including familial genes. .

[Caseous Calcification of Mitral Valve Annulus;Report of a Case].

We report a case of an 80-year-old female presenting with a mitral valve tumor. Postoperatively, pathologic diagnosis was caseous calcification of the mitral annulus. In surgery, she successfully underwent a mitral valve replacement with a 20 mm mechanical valve. The importance of correctly making a preoperative diagnosis cannot be over-emphasized. Technical discussion on possibility of mitral valve repair and patient-prosthesis mismatch after mitral valve replacement is also made.

Fenestration using a scoring balloon Scoreflex® as troubleshooting for acute vessel closure due to intramural hematoma complication in percutaneous coronary intervention.

This case report demonstrated the usefulness of scoring balloon when luminal narrowing occurred after balloon angioplasty in the left circumflex artery due to coronary intramural hematoma. Although a stent was placed, coronary flow was not improved. We intended to make a fenestra between the true lumen and the hematoma using a scoring balloon (Scoreflex® 2.0 × 10 mm, OrbusNeich, Tokyo, Japan) which was dilated in the distal segment of the branch. Angiograms showed restoration of TIMI-3 flow with a long dissection spanning from distal of the stent to the scored area. After 3 months and 1 year, follow-up coronary angiograms demonstrated occluded false lumen and good coronary flow in the treated vessel.

Presence of structural heart disease and left ventricular dysfunction predict hospitalizations for new-onset heart failure after right ventricular apical pacing.

AIMS: Long-standing right ventricular apical pacing (RVAP) may result in impaired left ventricular (LV) function and systolic heart failure (HF) in selected patients. However, which patients are susceptible to those harmful effects is unknown. METHODS AND RESULTS: In 367 consecutive patients undergoing pacemaker implantations (PMIs) and RVAP, the clinical, laboratory, and echocardiographic data before the PMIs, electrocardiographic parameters [baseline and paced QRS duration (QRSd)], and echocardiography were analysed. The cumulative per cent of those ventricularly paced (Cum%VP) was >90% in all subjects. During a mean follow-up period of 113±69 months, the occurrence of HF requiring hospitalization for the intravenous administration of HF medications was found in 60 patients (16%; HF group), but not in the remaining 307 (84%; no-HF group). The prevalence of structural heart disease (SHD; P<0.0001), cardiothoracic ratio (P<0.0001), baseline left atrial size (P=0.0001), LV end-diastolic volume (P<0.005) and end-systolic volume (P<0.0005), LV mass index (P<0.001), and baseline and paced QRSd (both for P<0.001) were greater in the HF group than in the no-HF group. Inversely, the LV ejection fraction (LVEF) in the HF group was smaller than that in the no-HF group (P<0.001). The multivariate Cox regression analysis revealed that the presence of SHD [hazard ratio (HR)=3.12; 95% confidence interval (CI), 1.7-5.7; P<0.001] and the LVEF (<40%; HR=2.57; 95% CI, 1.09-6.07; P<0.05) were associated with hospitalizations due to HF after RVAP. CONCLUSION: The presence of SHD and an impaired LV systolic function before the PMI may predict hospitalizations due to HF after RVAP.

Positive influence of aging on the occurrence of fat replacement in the right ventricular myocardium determined by multislice-CT in subjects with atherosclerosis.

PURPOSE: We evaluated predictors of fat replacement (FR) in the right-ventricular-myocardium (RVM) determined by MSCT in atherosclerotics not receiving anti-arrhythmia drugs and evaluated the relationship between the presence of FR in the RVM and the occurrence of ventricular premature beats (VPB). MATERIALS AND METHODS: 120-consecutive-atherosclerotics (101-males, 11-85 years) not receiving anti-arrhythmia drugs for VPB, who underwent MSCT for evaluating atherosclerosis and Holter-ECG within one-month, were retrospectively analyzed for FR in the RVM and its relationship with age, body mass index (BMI), and occurrence of VPB. RESULTS: 31-subjects had FR in RVM (18-males; median 67 years), and 89 did not (53-males, median 56 years). Median age was significantly higher in subjects with FR in RVM (P<0.01). The median BMI was 23.0 in subjects with FR and 23.0 in those without (not significant). Average number of VPB by Holter-ECG was 1445 in 31 subjects with FR. Without FR, the average number of VPB was 995. The difference in the numbers of VPB was not significant (P=0.73). A logistic-regression-model using age, male sex and BMI indicated that age was associated with an increased incidence of FR in the RVM (relative risk=1.055, 95% CI 1.019-1.092, P<0.05). CONCLUSIONS: Age but not BMI is significantly associated with the presence of FR in the RVM. Aging might have a positive influence on the occurrence of FR in the RVM as determined by MSCT in atherosclerotics, but FR in the RVM had no influence on the occurrence of VPB.

ATP-induced dormant pulmonary veins originating from the carina region after circumferential pulmonary vein isolation of atrial fibrillation.

INTRODUCTION: Elimination of transient pulmonary vein recurrences (dormant PVs) induced by an ATP injection and ablation at the PV carina region is an effective strategy for atrial fibrillation (AF) ablation. The relationship between dormant PVs and the PV carina region has not been evaluated. METHODS: A total of 212 consecutive symptomatic AF patients underwent circumferential PV electrical isolation (CPVEI) with a double lasso technique. They were divided into 2 groups in a retrospective review; Group 1: those given an ATP injection during an intravenous isoproterenol infusion after the CPVEI (n = 106), and Group 2: those in which it was not given after the CPVEI (n = 106). Radiofrequency energy was applied at the earliest dormant PV activation site identified using a Lasso catheter on the CPVEI line and then PV carina region if it was ineffective. RESULTS: After a successful PVEI, 54 patients (51%) in Group 1 had PV reconnections during an ATP injection. Acute PVEI sites were observed on the carina region within the CPVEI line in the right PVs (16%) and left PVs (10%). Dormant PVs were reisolated at the carina region in the right PVs (23%) and left PVs (26%). The distribution of the dormant PV sites, except for the RIPV, significantly differed from that of the acute PVEI sites (P < 0.05). Further, AF recurred significantly in the Group 2 patients as compared to those in Group 1 during 16 +/- 6.1 months of follow-up (P < 0.05). CONCLUSION: PV carina region origins may partly be responsible for an acute PVEI and potential recurrences.

Change in blood pressure just after initiation of cardiac resynchronization therapy predicts long-term clinical outcome in patients with advanced heart failure.

BACKGROUND: The aim of this study was to retrospectively investigate the long-term effect of cardiac resynchronization therapy (CRT) and to clarify the useful predictors of clinical outcome. Methods and Results The study group comprised 43 patients with advanced heart failure who underwent CRT (10 females; 66+/-10 years): 23 were in sinus rhythm (SR group) and 20 had chronic atrial fibrillation (AF group). The clinical parameters and echocardiographic data were evaluated before and after CRT. There were no significant differences in the clinical parameters, echocardiographic data at baseline or frequency of responders between the 2 groups. In both groups, the clinical characteristics at baseline did not differ between the responders and non-responders. A prompt rise in systolic blood pressure (SBP) just after CRT was observed more often in responders than in non-responders, and SBP rise > or =5 mmHg was the only significant independent predictor of a CRT responder (P=0.0033). Furthermore, there was a significant difference in the event-free survival between patients with and without SBP rise > or =5 mmHg, demonstrated by Kaplan-Meier method, at 2 years of follow-up (P=0.045). Conclusion A prompt BP rise just after CRT may predict short- and long-term clinical improvement in CRT recipients.

Hemangioma located just above the left main coronary artery, in a subject who had cardiac arrest due to ventricular fibrillation, led to a diagnosis of Brugada syndrome.

We report the case of a 38-year-old Asian man with a pericardial hemangioma on the left main coronary artery. The patient presented initially at our hospital after cardiopulmonary resuscitation following an episode of ventricular fibrillation (VF). Because of spontaneous coved-type ST segment elevation on the higher intercostal space V1 to V2 in a 12-lead electrocardiogram, documented VF in the absence of structural heart disease, and a family history of sudden death, he was diagnosed with Brugada syndrome. Transesophageal echocardiography showed a smooth-surfaced mass with well-demarcated borders, directly above the left main coronary artery. Computed tomography confirmed the presence of the mass, which showed no enhancement at early phase, but did demonstrate homogenous enhancement at delay phase by contrast material. There were no findings from either the nuclear medicine or the tumor marker investigations which indicated that the mass located just above the main coronary arteries was malignant. Therefore, taken together, these findings suggested that the tumor might be a pericardial hemangioma. The relationship between the location of the hemangioma just above the left main coronary artery and the occurrence of VF was not clear, i.e. whether the presence of the hemangioma caused the stimulation of the left main coronary artery and as a result, led to the spasm of the left main coronary artery and the occurrence of VF. Furthermore, as the tumor did not extend into any of the adjacent structures, such as the coronary arteries or the right ventricular outflow tract, surgical resection was not performed; instead, the patient received a dual chamber implantable cardioverter-defibrillator.

Angiosarcoma in the right atria demonstrated by fusion images of multislice computed tomography and positron emission tomography using F-18 Fluoro-Deoxyglucose.

Primary cardiac tumors are rare. In this report, using fusion images of multislice computed tomography (MSCT) and positron emission tomography (PET) using F-18 Fluoro-Deoxyglucose, we could diagnose, morphologically, the location, size and extent of the tumor, and degree of blood flow from the feeding artery (by MSCT) and establish that this cardiac tumor was malignant (by PET) before surgical operation. Histologically, the tumor was diagnosed as a cardiac angiosarcoma.

Remarkable thickening of right atrial wall in subjects with cardiac amyloidosis complicated with sick sinus syndrome.

We observed a 63-year old male with cardiac amyloidosis who presented with the clinical symptoms of sick sinus syndrome and dyspnea and abnormal thickening of the right atrial wall, which extended to the junction of the superior vena cava. This may explain the relationship of abnormal thickening of the right atrium which extends to the junction of the superior vena cava and right atrium with amyloid deposits in the sinus node and occurrence of sick sinus syndrome.

Occurrence of de novo sustained monomorphic ventricular tachycardia induced after percutaneous transluminal alcohol septal myocardial ablation for hypertrophic obstructive cardiomyopathy.

We report here a 75-year-old male with hypertrophic obstructive cardiomyopathy of de novo sustained monomorphic ventricular tachycardia (VT) after successful percutaneous transluminal alcohol septal myocardial ablation (PTSMA). In this case history, the necrotic induced by the PTSMA procedure might represent a region of slow conduction that is a circuit of re-entry and therefore stimulation might be spread around. Therefore, the basis of the sustained monomorphic VT was thought to be the presence of a focal necrotic area, itself a complication arising from the PTSMA procedures. In conclusion, the PTSMA procedure may have caused a de novo episode of ventricular arrhythmia.

Epidemiology of fat replacement of the right ventricular myocardium determined by multislice computed tomography using a logistic regression model.

PURPOSE: We frequently observe fat replacement (FR) of the anterior wall of the right ventricular myocardium (RVM), but its epidemiological significance is not clear. METHODS AND MATERIALS: 49 consecutive subjects (28 males, 36-83 years old, median 67) underwent enhanced ECG-gated multislice CT (Light speed ultra 16, General Electrics, WI) and we retrospectively analyzed the presence of FR of RVM. A logistic model for predicting FR of RVM was constructed using age, sex, hypertension [HT], diabetes mellitus [DM], hyperlipidemia [HL] smoking, obesity (body mass index >25.0) and calcified and non-calcified plaques of coronary arteries (CA). RESULTS: FR of RVM was detected in 21 subjects (12 males, 51-78 years old, median 67), 76% of whom had HT, 38% DM, 43% HL, 48% smoking history, 52% were obese, and 76% had calcified and 24% had non-calcified plaques of CA. Only obesity was significantly higher in FR (p<0.05). A logistic regression model showed, although there was a close association between obesity and an increased incidence of FR, it did not reach statistical significance (p=0.0515, relative risk 5.11). CONCLUSIONS: Obesity is significantly more common in cases of FR, and despite a negative multivariable analysis, may influence FR in the RVM. FR in obesity may occur independently of clinically-significant arrhythmia, which is different from ARVC. Thus, even with FR, obesity must be considered as a diagnosis before ARVC.