Comparison of the incidence of depression before and after endovascular treatment in patients with lower limb peripheral artery disease.

Depression is a chronic illness that affects mood, physical health, and overall vitality and quality of life. Depression has been associated with an increased risk of all-cause and cardiovascular mortality among patients with peripheral arterial disease (PAD). Therefore, this study aimed to compare the incidence of depression before and after endovascular treatment in patients with lower limb PAD. This is an important clinical issue considering the worldwide increase in PAD with the aging population and the known negative impact of depression on recovery. This was a retrospective sub-analysis of data from the Tokyo Peripheral Vascular Intervention Study using the TOMA-CODE registry. The presence and extent of depressive symptoms were evaluated using the patient health questionnaire (PHQ-9), with a depressive tendency score of ≥ 5. The PHQ-9 score was evaluated before endovascular treatment (EVT) and at 4 (± 1) weeks after EVT. The study population consisted of 87 patients who completed the PHQ-9 before EVT, with 76 completing the post-EVT PHQ-9. Of these 76, 19 had a pre-EVT score ≥ 5. Overall, there was no difference in the pre- and post-EVT scores (P = 0.091). There was no significant change in the 19 patients with a pre-EVT score ≥ 5 (mean 9.2 ± 4.4); however, there was a tendency to improve in the pre- to post-EVT score (mean, 6.9 ± 5.2; P = 0.059). Diabetes was a significant negative factor for pre- to post-EVT score improvement (P = 0.023). Overall, symptoms of depression showed the tendency to improve at 30 days post-EVT. However, diabetes was associated with lower improvement in symptoms.

[The case of an octogenarian who died of acute myocardial infarction complicated with acute pulmonary embolism from a right ventricular thrombus].

An 86-year-old female on dialysis experienced a decrease in blood pressure and worsening of her respiratory condition during dialysis, for which she visited our emergency unit. She was admitted to our Department of Cardiology with a diagnosis of acute myocardial infarction complicated with heart failure because of anterior wall of left ventricular dysfunction, positive troponin T levels and negative T wave on a precordial lead electrocardiogram. On the same day, she underwent coronary angiography and stenting at left anterior descending artery #7 with 99% stenosis. She also showed an elevated D-dimer level on admission, and contrast-enhanced computed tomography (CT) was performed the day after admission, considering the likelihood of respiratory failure due to pulmonary thromboembolism. However, the findings were negative. On the 4th day of hospitalization, she showed marked hypoxemia. Her D-dimer level was further elevated, and when she underwent enhanced CT again, there was no evidence of deep vein thrombosis, but thrombus in the pulmonary artery and apex of right ventricle was noted. She was therefore diagnosed with acute pulmonary embolism due to thrombosis from the right ventricle rather than from a deep vein. She rapidly received anticoagulant therapy and non-invasive positive pressure ventilation therapy for respiratory failure, but she entered cardiopulmonary arrest and quickly died. She was suspected to have been complicated with a right ventricular infarction and an acute anterior wall myocardial infarction, resulting in a large thrombus along the apex of the right ventricle. This case of both myocardial infarction and pulmonary embolism is very rare, and we report it here with consideration.

Brugada syndrome and idiopathic left ventricular tachycardia unmasked by exercise and a class Ic drug.

The patient was a 33-year-old male. Twenty years ago, he underwent radiofrequency catheter ablation for idiopathic sustained monomorphic ventricular tachycardia (VT) with an RBBB and superior axis pattern. The VT was inducible by programmed stimulation and entrained by rapid pacing. At this presentation, he developed palpitation and VT with the same morphology at the peak exercise on a treadmill with appearance of typical ECG pattern for Brugada syndrome (BrS). Pilsicainide induced the typical ECG pattern and premature ventricular beats (PVBs) of the same morphology as VT. The relationship between BrS and VT of left ventricular origin was discussed.

Optimal cut-off value of preprocedural geriatric nutritional risk index for predicting the clinical outcomes of patients undergoing endovascular revascularization for peripheral artery disease.

BACKGROUND: Malnutrition measured by the geriatric nutritional risk index (GNRI) was reported to be associated with poor prognosis for patients with peripheral artery disease (PAD). However, the optimal cut-off value of preprocedural GNRI for critical limb ischemia (CLI) and intermittent claudication (IC) is unknown. We aimed to determine its optimal cut-off value for CLI or IC patients requiring endovascular revascularization. METHODS: We explored data of 2246 patients (CLI: n = 1061, IC: n = 1185) registered in the Tokyo-taMA peripheral vascular intervention research COmraDE (TOMA-CODE) registry, which prospectively enrolled consecutive PAD patients who underwent endovascular revascularization in 34 hospitals in Japan from August 2014 to August 2016. The optimal cut-off values of GNRI were assessed by the survival classification and regression tree (CART) analyses, and the survival curve analyses for major adverse cardiovascular and limb events (MACLEs) were performed for these cut-off values. RESULTS: In addition to the first cut-off value of 96.2 in CLI and 85.6 in IC, the survival CART provided an additional cut-off value of 78.2 in CLI and 106.0 in IC for further risk stratification. The survival curve was significantly stratified by the GNRI-based malnutrition status in both CLI [high risk: 47.7% (51/107), moderate: 30.1% (118/392), and low: 10.2% (53/520), log-rank p < 0.001] and IC [high risk: 14.3% (7/49), moderate: 4.5% (29/646), and low: 0.5% (2/407), log-rank p < 0.001]. The multivariate Cox-proportional hazard analysis showed that a higher GNRI was significantly associated with a better outcome in both CLI [hazard ratio (HR) per 1-point increase: 0.97, 95% CI: 0.96-0.98, p < 0.001] and IC (HR: 0.94, 95% CI: 0.91-0.97, p < 0.001). CONCLUSIONS: Preprocedural nutritional status significantly stratified future events in patients with PAD. Given that the optimal cut-off value of GNRI in CLI was almost 10-points lower than that of IC, using a disease-specific cut-off value is important for risk stratification.

Cardiogenic shock induced by bisoprolol in a patient with CYP2D6 variant. A case report.

A 66-year-old man was admitted for congestive heart failure with tachycardiac atrial fibrillation (AF). Heart failure was improved by diuretics, but control of heart rate by verapamil was insufficient, and bisoprolol was prescribed. After taking 2.5 mg of bisoprolol, he developed a general malaise followed by sinus bradycardia and shock. In addition to catecholamines, the patient was treated with intra-aortic balloon pumping and a pacemaker. With intensive therapy, the general condition was improved, and acute elevation of liver enzymes after bisoprolol was normalized by the 17th hospital day. The blood sample taken 30 h after the intake of bisoprolol showed abnormally high levels. Although the patient was CYP2D6*10 heterozygote, the precise mechanism for excess accumulation of bisoprolol and refractory shock remains unknown. .

Brugada syndrome combined with monomorphic ventricular tachycardia and atrioventricular nodal reentrant tachycardia.

A 41-year-old man developed sustained monomorphic ventricular tachycardia (VT) with a left bundle branch block and inferior axis pattern during treadmill exercise concomitantly with unmasking of the typical Brugada electrocardiography (ECG) pattern. The typical ECG phenotype was provoked by a class IC drug. VT was not inducible with programmed electrical stimulation, but premature ventricular beat and non-sustained VT with the same morphology increased in frequency with isoproterenol treatment. Additionally, atrioventricular nodal reentrant tachycardia (AVNRT) was induced by electrical stimulation and VT and AVNRT were treated by radiofrequency catheter ablation.