Sodium-Glucose Cotransporter-2 Inhibitors in Heart Failure with Malnutrition, Frailty, Sarcopenia, or Cachexia.

(1) Background: In patients with heart failure (HF) and impaired nutritional status or decreased muscle mass, sodium-glucose cotransporter-2 inhibitors (SGLT2is) may worsen these conditions and result in poor prognosis, especially worsening of frailty. We aimed to investigate the relationship between SGLT2is and clinical outcomes, including frailty-related events, in patients with HF and malnutrition, frailty, sarcopenia, or cachexia. (2) Methods: In this retrospective observational cohort study, a global federated health research network provided data on patients with HF and malnutrition, frailty, sarcopenia, or cachexia from January 2016 to December 2021. We investigated the incidence of the composite endpoint of death or frailty-related events within one year. (3) Results: Among 214,778 patients included in the analysis, 4715 were treated with SGLT2is. After propensity score matching, 4697 patients in the SGLT2is group were matched with 4697 patients in the non-SGLT2is groups. The incidence of the composite endpoint, mortality, and frailty-related events was lower in the SGLT2is group than in the non-SGLT2is group (composite endpoint, 65.6% versus 77.6%, p < 0.001; mortality, 17.4% vs. 35.5%, p < 0.001; frailty-related events, 59.4% vs. 64.3%, p < 0.001). (4) Conclusions: Patients with HF and malnutrition, frailty, sarcopenia, or cachexia had a high incidence of death and frailty-related events. SGLT2is were associated with a lower incidence of these events.

Diuretic and renal effects of angiotensin receptor-neprilysin inhibitor in patients hospitalized for acute heart failure.

In patients hospitalized for acute decompensation of heart failure (HF), the impact of angiotensin receptor-neprilysin inhibitor (ARNI) on diuresis and renal function has not been fully investigated. Patients with HF and reduced ejection fraction who were hospitalized for acute decompensation and newly initiated ARNI after hemodynamic stabilization were enrolled. Changes in urine volume (UV), body weight, estimated glomerular filtration rate (eGFR), and urine N-acetyl-beta-d-glucosaminidase (uNAG) levels before and after ARNI initiation were investigated. Changes in the diuretic response [DR, calculated as urine volume/(intravenous furosemide volume/40 mg)], N-terminal pro-brain natriuretic peptide (NT-proBNP), hematocrit, and plasma volume (PV) were also evaluated. A total of 60 patients were enrolled. ARNI was initiated at a median of 6 [5, 7] days after hospitalization. After initiation of ARNI, body weight, NT-proBNP, and PV decreased. UV and DR increased only on the day of ARNI initiation (delta UV 400 ± 957 ml and delta DR 1100 ± 3107 ml/40 mg furosemide) and then decreased to baseline levels. In the multivariable linear regression analysis, younger age, higher BMI, and higher NT-proBNP levels were significantly associated with greater UV after ARNI initiation. eGFR and uNAG did not significantly change after the initiation of ARNI [delta eGFR -1.7 ± 12.0 mL/min/1.73 m2 and delta uNAG 2.0 (-5.6, 6.9) IU/L]. In patients hospitalized for HF, the initiation of ARNI was associated with a small and transient increase in UV and DR, and was not associated with worsening of renal function or tubular injury.

Possible Neoangiogenesis in Achilles Tendon Xanthoma with Familial Hypercholesterolemia: A Novel Approach to Achilles Tendon Xanthoma.

Achilles tendon xanthoma (ATX) is one of the typical features of familial hypercholesterolemia (FH). The morphological evaluation of ATX by X-ray radiography is widely recognized; however, the utility of other imaging modalities remains unclear. We herein report two cases of FH in which Doppler ultrasound imaging demonstrated a microvascular flow in ATX that only rarely could be observed in normal Achilles tendons. Neoangiogenesis accompanies chronic inflammation and it may play an important role in the deposition of cholesterol crystals leading to ATX. In addition to the morphological evaluation of ATX, the assessment of neoangiogenesis may therefore be essential for the evaluation of ATX.

Comparison of 0.9-mm and 1.4-mm catheters in excimer laser coronary angioplasty for acute myocardial infarction.

Excimer laser coronary angioplasty (ELCA) is a unique revascularization modality that can vaporize plaque and thrombus. Compared to thrombus aspiration therapy, ELCA is reported to provide better microcirculation and reduced peripheral embolism in treatment for acute coronary syndrome. Excimer laser catheters come in various sizes, and we sought to compare the 0.9- and 1.4-mm-diameter catheters. We retrospectively enrolled 90 acute myocardial infarction (AMI) patients who underwent primary percutaneous coronary intervention with excimer laser from August 2013 to March 2017 in our hospital. Patients were grouped by diameter of catheter that had been used, the 0.9 mm group (n = 51) and 1.4 mm group (n = 39). We evaluated myocardial perfusion, procedural success rate, short-term outcome, lesion crossability, and complications between the two groups. The percentage of patients whose final thrombolysis in myocardial infarction (TIMI) grade was 3 (0.9 mm 86.3% vs 1.4 mm 89.7% p = 0.75) and final myocardial blush grade (MBG) was 3 (0.9 mm 72.5% vs 1.4 mm 69.2% p = 0.82) was similarly high for both groups. Procedural success rate, in-hospital major adverse cardiac events (MACE), lesion crossability, and complications were also similar. This study showed that efficacy of 0.9 and 1.4 mm excimer laser catheter was equivalent in ELCA for AMI patients. If one takes into account lesion crossability, debulking effects, and the stunned platelets phenomenon, the 0.9 mm excimer laser catheter is sufficient for ELCA in AMI patients.

Sodium Bicarbonate-Ascorbic Acid Combination for Prevention of Contrast-Induced Nephropathy in Chronic Kidney Disease Patients Undergoing Catheterization.

BACKGROUND: Sodium bicarbonate and ascorbic acid have been proposed to prevent contrast-induced nephropathy (CIN). The present study evaluated the effect of their combined use on CIN incidence.Methods and Results:We prospectively enrolled 429 patients with chronic kidney disease (CKD: baseline estimated glomerular filtration rate <60 mL/min/1.73 m2) prior to elective coronary catheterization. CIN was defined as absolute (≥0.5 mg/dL) or relative (≥25%) increase in serum creatinine within 72 h. In the saline hydration (n=218) and combined sodium bicarbonate+ascorbic acid (n=211) groups, a total of 1,500-2,500 mL 0.9% saline was given before and after the procedure. In addition, the combination group received 20 mEq sodium bicarbonate and 3 g ascorbic acid i.v. before the procedure, followed by 2 g ascorbic acid after the procedure and a further 2 g after 12 h. There were no significant differences between the basic characteristics and contrast volume in the 2 groups. CIN occurred in 19 patients (8.7%) in the saline group, and in 6 patients (2.8%) in the combined treatment group (P=0.008). CONCLUSIONS: Combined sodium bicarbonate and ascorbic acid could prevent CIN following catheterization in CKD patients.

A case of severe aortic valve stenosis including triple-vessel ischemic heart disease in which multidisciplinary percutaneous coronary intervention and balloon aortic valvuloplasty relieved low cardiac output syndrome.

The patient was an 80-year-old man with low cardiac output syndrome associated with triple-vessel ischemic heart disease and severe aortic stenosis (AS). Deeming the patient unprepared for surgery because of his deteriorated general condition, we decided to perform revascularization with a percutaneous coronary intervention associated with intra-aortic balloon pump (IABP) and treat the severe AS with percutaneous balloon aortic valvuloplasty (BAV). Complete revascularization was successfully achieved and BAV was performed, improving the aortic valve area from 0.58 to 0.92 cm(2) and the pressure gradient from 41 to 26 mmHg. Postoperative hemodynamics improved, and the IABP was successfully removed.

Macroreentrant atrial tachycardia in patients without previous atrial surgery or catheter ablation: clinical and electrophysiological characteristics of scar-related left atrial anterior wall reentry.

INTRODUCTION: Macroreentrant atrial tachycardia (MRAT) has been described most frequently in patients with prior cardiac surgery. Left atrial tachycardia and flutter are common in patients who undergo atrial fibrillation ablation; however, few reports describe left atrial MRAT involving the regions of spontaneous scarring. Here, we describe left atrial MRAT in patients without prior cardiac surgery or catheter ablation (CA) and discuss the clinical and electrophysiological characteristics of tachycardia and outcome of CA. METHODS AND RESULTS: An electrophysiological study and CA were performed in 6 patients (3 men; age 76 ± 6 years) with MRAT originating from the left atrial anterior wall (LAAW). No patient had a history of cardiac surgery or CA in the left atrium. Spontaneous scars (areas with bipolar voltage ≤ 0.05 mV) were observed in all patients. The activation map showed a figure-eight circuit with loops around the mitral annulus (4 counterclockwise and 2 clockwise) and a low-voltage area with LAAW scarring. The mean tachycardia cycle length was 303 ± 49 milliseconds. The conduction velocity was significantly slower in the isthmus between the scar in the LAAW and the mitral annulus than in the lateral mitral annulus (0.17 ± 0.05 m/s vs 0.94 ± 0.35 m/s; P = 0.003). Successful ablation of the isthmus caused interruption of the tachycardia and rendered it noninducible in all patients. CONCLUSION: Spontaneous LAAW scarring is an unusual cause of MRAT, showing activation patterns with a figure-eight configuration. Radiofrequency CA is a feasible and effective treatment in such cases.

Various morphologies of bidirectional ventricular tachycardia caused by aconite "Torikabuto" poisoning.

A 43-year-old man presented with nausea. The patient developed ventricular fibrillation (VF), which was refractory to antiarrhythmic drugs and defibrillation. A coronary angiogram showed no coronary artery stenosis. We recorded various fatal arrhythmias, including bidirectional ventricular tachycardia (BVT). The presence of multiple types of BVTs that were refractory to drugs such as adenosine triphosphate, isoproterenol, verapamil, propranolol, and pilsicainide, and easily recurred after defibrillation indicated aconite poisoning. After persisting for 24 h, VF spontaneously resolved and sinus rhythm was restored. Laboratory data revealed lethal concentrations of aconitine. To the best of our knowledge, this is the first report of aconite poisoning-induced BVTs manifesting with multiple morphologies on 12-lead electrocardiogram. The arrhythmogenic effects of aconitine are well recognized. In addition to causing VT and VF, aconitine also can cause BVT. Aconitine can lead to delayed afterdepolarization which has an important role in triggering and maintaining BVT. However, in this case, the concentration of aconitine was high enough to render these drugs ineffective. Prompt application of percutaneous cardio-pulmonary support, which was continued until the aconitine was metabolized, proved successful in this case and should be considered as a management approach in cases of severe aconite poisoning.

Takotsubo (ampulla-shaped) cardiomyopathy associated with microscopic polyangiitis.

Recently, a cardiac disorder characterized by ballooning and hypokinesis at the apex has been described as takotsubo (ampulla-shaped) cardiomyopathy. We encountered a patient with a rare case of takotsubo cardiomyopathy associated with microscopic polyangiitis. A 70-year-old woman suddenly presented with ventricular dysfunction during the active phase of microscopic polyangiitis. The findings on echocardiograms and electrocardiograms were consistent with those of takotsubo cardiomyopathy. The ventricular dysfunction completely resolved after treatment with 40 mg/day of prednisolone and methylprednisolone pulse therapy. This unique type of cardiomyopathy can be a complication of microscopic polyangiitis.